Posttraumatic Stress Disorder
Posttraumatic Stress Disorder for the Defense
By Bill Masters
Wallace, Klor & Mann, P.C.
Little Miss Muffet
Sat on a tuffet,
Eating some curds and whey.
Along came a spider,
And sat down beside her,
And frightened Miss Muffet away.
Nursery Rhyme
I. Posttraumatic Stress Disorder
A. Introduction
1. “Posttraumatic Stress Disorder” Defined
Posttraumatic stress disorder (PTSD) is, very generally, the psychological diagnosis given someone who has persistent difficulty psychologically coping with an unusually threatening experience, to a degree that interferes with his or her ability to function socially or occupationally. More specifically, PTSD is defined in the “DSM-IV-TR,” the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders, the diagnostic bible of specialists in mental health care in the United States.
In the DSM-IV-TR, PTSD consists of six basic criteria: The individual must (1) experience a traumatic event; (2) suffer cognitive dysfunction; (3) suffer behavioral dysfunction; (4) have autonomic nervous system arousal; (5) have this constellation of symptoms last more than one month; and (6) have clinically significant impairment in social function.
2. PTSD as a Bane for the Defense
For the defense, PTSD is a bane. To borrow from Shakespeare, “it harrows [us] with fear and wonder.” That fear is securely rooted in the realization that the diagnostic criteria for PTSD are basically subjective and that any disorder consisting of subjective criteria is bound to spawn frivilous litigation. The only relief from this fear springs from an appreciation of the refreshing skepticism with which many jurors, usually lacking higher education, view psychologists and psychiatrists with their black bags of amorphous diagnostic categories.
For plaintiffs’ lawyers, claims for PTSD are bliss. Simply, these claims are of the kind that can be molded into forms appealing to juries. They arise from trauma that can produce reactions with highly variable latency periods. They can result in chronic injury. They can be blamed for any or every subsequent negative life event. And they largely lack objective criteria of disproof.
As a result, PTSD is a diagnosis much abused. Abuses occur through the actions of unprincipled plaintiffs, psychological experts, and lawyers. Of possible ways by which these people may abuse the diagnosis of PTSD, the following are the most obvious: (1) an illegitimate diagnosis; (2) a legitimate diagnosis but exaggerated symptoms; and (3) legitimate symptoms and a legitimate diagnosis, but an illegitimate prognosis. As would be expected, the motives for abusing the diagnostic category PTSD are many, including: (1) plaintiff’s fraud or plaintiff’s factitious disorder; (2) lawyer “overreaching” driven by greed or overzealousness; (3) expert overreaching driven by greed, overzealousness, or ideological axe-grinding; and (4) expert incompetence.
In the end, in the context of litigation, PTSD as a diagnostic category causes two basic problems. First, it fails, for the most part, to separate those with psychological symptoms with PTSD from those with psychological symptoms but without PTSD, the true positives from the false positives, the wheat from the chaff. Second, it also seems to invite false claims, the claims of malingerers and those with factitious disorders––in short, it provides an enticement to lie, to fake, to scam, to seek that which is undeserved. But not to despair: the cure is a stalwart and savvy defense lawyer.
B. History of PTSD
Long ago, certain clusters of symptoms or syndromes were recognized to be associated with severe stress. These syndromes had a variety of names: “shell shock,” “battle fatigue,” “combat fatigue,” and “traumatic neurosis.” Eventually psychiatrists and psychologists began to seek to discern the essence of these various psychological maladies. That effort culminated in 1952 in the Diagnostic and Statistical Manual (DSM). Since then, PTSD, as a diagnostic category, has evolved through successive editions and revisions of the DSM. Understanding this evolution is important because many of the psychological studies used by plaintiffs’ experts at trial were conducted using the different conceptualizations of PTSD in the DSM-III, DSM-III-R, or DSM-IV.
1. DSM-I (1952)
Under the heading “Transient Situational Personality Disorders,” the DSM-I identified a mental disorder entitled “Gross Stress Reaction.” Gross stress reaction was characterized as primarily transient reaction to severe or extreme stress such as that experienced in combat or in civilian catastrophe.
2. DSM-II (1968)
In 1968, the DSM-I was replaced by the DSM-II, which lacked the mental disorder characterized in the DSM-I as “Gross Stress Reaction.” But it did have a disorder under the heading of “Transient Situational Disturbances” characterized as “Adjustment Reaction to Adult Life.” An example of this disorder was stated to be the “resentment with depressive tone associated with an unwanted pregnancy and manifested by hostile complaints and suicidal gestures,” or “the fear associated with military combat and manifested by trembling, running and hiding.”
3. DSM-III (1980)
In 1980, the DSM-II was replaced by the DSM-III, which reintroduced the mental disorder formerly identified under the DSM I as “Gross Stress Reaction” identifying it as “PTSD.”
In the DSM-III, PTSD was characterized more elaborately than it was in the DSM-II, but still required, as it did in the DSM-II, an “extreme stressor,” that is, a stressor that would evoke significant symptoms of distress in “almost everyone.” These symptoms were placed in three categories: (1) re-experiencing the trauma; (2) a numbing of responsiveness to the environment; and (3) increased arousal.
4. DSM-III-R (1987)
In 1987, the DSM-III was revised. The DSM-III-R continued and further amplified the concept of “PTSD,”
characterizing it as a patterned symptomatic response to an event “outside the range of usual human experience . . . markedly distressing to almost everyone.” As in the DSM-III, in the DSM-III-R the symptoms of PTSD were arranged in three categories: (1) re-experiencing the trauma; (2) a numbing of responsiveness to the environment; and (3) increased arousal. But in the DSM-III-R some criteria in the version of PTSD in the DSM-III were deleted from or moved or added to different categories of symptoms.
5. DSM-IV (1994)
In 1994, the DSM-III-R was replaced by the DSM-IV.
In the DSM-IV, PTSD is characterized essentially as it was in the DSM-III-R, except for Criteria A and C. Now, in the DSM-IV, Criterion A provides as follows:
“A. The person has been exposed to a traumatic event in which both of the following were present:
“(1) The person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others.
“(2) The person’s response involved intense fear, helplessness, or horror. Note: In children, this may be expressed instead by disorganized or agitated behavior.”
This formulation of Criterion A removes the element of objectivity inherent in that criterion in the DSM-III and DSM-III-R. Now someone who is hypersensitive to a less than extreme event is eligible for a diagnosis of PTSD.
The DSM-IV also changes Criterion C. Unlike in the DSM-III-R, in the DSM-IV, Criterion C requires both a persistent avoidance of stimuli associated with trauma and a numbing of general responsiveness rather than one or the other.
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As is apparent, over the years from the DSM-I in 1952 to the DSM-IV in 1994, PTSD, as a concept, has evolved. This 40-year evolution has resulted from a variety of forces––epistemological, sociological, and political. Preeminent among these varied forces are the sociological and political, particularly the sequelae of the Vietnam War and feminist activism.
From 1950 to 1970, little research occurred into the traumatic stress response. But in the 1960s, with escalation of the Vietnam War and the growing awareness of the troubling symptom profiles of some combatants, research into the stress response was revived. As a result of this intensified research, the variety of symptoms that regularly follow trauma were more thoroughly identified.
In the 1970s, 1980s, and 1990s, the feminist movement focused on empowering women. An aspect of that movement has been characterized as the “sexual wars.” In this war of the sexes, the feminist call to arms was the thesis that many if not most men sexually abuse females of all ages. To curb this abuse, feminists armed themselves with criminal and civil laws. On the civil side, assigning a psychological disorder such as PTSD as a consequence of the abuse provides the “victim” or “survivor” with a remedy in court for damages. Having a civil action for damages enables the victim not only to curb the abuse but also to effect a transfer of wealth and to acquire power through threats of use of the legal system. Consistent with this goal, basing the mental disorder on subjective complaints and on a stressor, the severity of which is in the eye of the victim, opens the door to almost anyone who wants the entitlements associated with being labeled a “victim.”
C. Diagnostic Criteria of PTSD
The current diagnostic criteria for PTSD are found in the DSM-IV (also called the DSM-IV-TR) or, alternatively, in the International Classification of Diseases (10th Rev.) (the ICD-10).
1. DSM-IV (1994) [DSM-IV-TR (2000)]
In this country, PTSD is defined according to the specific stressor (criterion A) and symptom criteria (Criteria B, C, and D) provided in the DSM-IV. Those criteria are as follows:
“A. The person has been exposed to a traumatic event in which both of the following were present:
“(1) the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others; and
“(2) the person’s response involved intense fear, helplessness, or horror. Note: In children, this may be expressed instead by disorganized or agitated behavior.
“B. The traumatic event is persistently re-experienced in one (or more) of the following ways:
“(1) recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions. Note: In young children, repetitive play may occur in which themes or aspects of the trauma are expressed;
“(2) recurrent distressing dreams of the event. Note: In children, there may be frightening dreams without recognizable content;
“(3) acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and disassociative flashback episodes, including those that occur on awakening or when intoxicated). Note: In young children, trauma-specific reenactment may occur;
“(4) intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event; and
“(5) physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event.
“C. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by three (or more) of the following:
“(1) efforts to avoid thoughts, feelings, or conversations associated with the trauma;
“(2) efforts to avoid activities, places, or people that arouse recollections of the trauma;
“(3) inability to recall an important aspect of the trauma;
“(4) markedly diminished interest or participation in significant activities;
“(5) feeling of detachment or estrangement from others;
“(6) restricted range of affect (e.g., unable to have loving feelings); and
“(7) sense of a foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span).
“D. Persistent symptoms of increased arousal (not present before the trauma), as indicated by two (or more) of the following:
“(1) difficulty falling or staying asleep;
“(2) irritability or outbursts of anger;
“(3) difficulty concentrating;
“(4) hypervigilance; and
“(5) exaggerated startle response.
“E. Duration of the disturbance (symptoms in Criteria B, C, and D) is more than one month.
“F. The disturbance caused clinically significant distress or impairment in social, occupational, or other important areas of functioning.”
2. ICD-10
The ICD-10 provides another classificatory scheme for PTSD.
In the ICD-10, the criteria for PTSD are similar to, but in important respects different from, those criteria provided for PTSD in the DSM-IV. Indeed, the level of concordance between the criteria in the DSM-IV for PTSD and those in the ICD-10 is low. (The level of concordance is the percentage of cases with a positive diagnosis on either classification system that have a positive diagnosis on both classification systems.) For PTSD, the concordance was 35 percent, with the ICD-10 identifying cases at twice the frequency of the DSM-IV.
The defense should expect a plaintiffs’ expert to select whichever set of criteria will result in a diagnosis of PTSD.
But in the United States, it is standard to use the criteria in the DSM-IV-TR.
D. Analysis of PTSD Criteria
The criteria for PTSD expressed as Criteria A through E in the DSM-IV-TR bear detailed analysis to disclose nuances useful in fashioning a defense against a claim for alleged PTSD.
1. Criterion A – The Illusion of Objectivity
Criterion A is the gatekeeper to a diagnosis of PTSD. It has two subparts: Subpart (1) provides a limiting description of the kinds of events that can qualify as traumatic stressors. Subpart (2) provides a limiting description of the kinds of subjective responses to the event to establish that the event was in fact traumatic. More specifically, Criterion A provides:
“The person has been exposed to a traumatic event in which both of the following were present:
“(1) the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others;
“(2) the person’s response involved intense fear, helplessness, or horror. Note: In children, this may be expressed instead by disorganized or agitated behavior.”
Subpart (1) describes the kind of event that needs to be experienced as traumatic. It has pretensions of being “objective.” That is, this diagnostic criterion is not dependent entirely on the plaintiff’s subjective experience. Yet the criterion is so broad––that is, “the person was confronted with an event that involved a threat to the physical integrity of others”––that any event threatening to cause physical injury appears to qualify.
Events that are mere threats to “physical integrity” are usually considered by psychologists and psychiatrists to include all experiences of sexual assault or sexual molestation, not just those in which the victim perceives a threat of violence.
But, arguably, less significant events may be included as well, including a spectrum of events causing soft tissue injuries. For instance, Susie Trisikell confronted a small chuckhole in the path of her 25-speed Italian racing bicycle during Cycle Oregon, a chuckhole that, if ridden over, would threaten her with a bilateral strain of her gluteus maximus. Unless the phrase “physical integrity” is a term of art with an extraordinary meaning, a sprained gluteus maximus is a disruption of Susie’s “physical integrity.”
There are further ambiguities. For instance, “hindsight traumatization” from prior personal exposure to an originally nontraumatic event does not accord with the spirit of Criterion A. Yet it is not ruled out conceptually. Nor is Criterion A meant to include more indirect and impersonal experiences such as hearing a news report of a catastrophe occurring to strangers. Even so, conceptually, individuals with extreme reactions to minor trauma may qualify under Criterion A of the DSM-IV.
Somewhat in conflict with the stated DSM-IV criteria, the commentary on PTSD in the DSM-IV indicates that the stressor must be extremely traumatic. Examples include military combat, violent personal assault, severe automobile accidents, and learning about a serious injury to a family member or close friend.
As is apparent, Criterion A is a logically disjointed composition, obviously the work of a committee composed of people with opposite views, and probably represents a political compromise. Unfortunately, it is a compromise that plays into the hands of the plaintiffs’ bar, the alleged “victims” they represent, and advocacy groups, which want a shift in focus in Criterion A from the nature of the stressor to the reaction of the person, thereby increasing the subjectivity of the criterion.
* * *
Subpart (2) of Criterion A is unabashedly subjective. This requirement was designed “to qualify [for a diagnosis of PTSD] individuals making high-magnitude attributions to low-magnitude events” and thus to qualify those events as well. Regrettably, no reliable method exists to verify that an individual indeed reacted to the event with intense fear, helplessness, or horror; a plaintiff need only say that she did.
* * *
Although 38 percent of the population is exposed to catastrophic stress, only about 9.2 percent react with the symptoms characterizing PTSD.
No one knows why some people are vulnerable to catastrophic stress and others not. But risk factors for vulnerability are said to include previous exposure to unusual stress, maladaptive coping mechanisms, other adjustment problems, childhood separations, family history of antisocial behavior, being female, and having a diagnosis of borderline personality disorder.
Virtually everyone is exposed to minor stress during life, with birth being probably the first such exposure. Most people weather these stressors without developing PTSD. Yet some purportedly do develop PTSD. It is not clear why.
Following are examples highlighting the interplay between Subpart (1) and Subpart (2) of Criterion A:
Selma Bodie was told by her male employer that her work performance was substandard and that she had 60 days to improve her performance or be terminated. At that, Selma had a nervous breakdown. Would it make a difference if Selma was employed as a daycare provider, a lawyer, or a terrorist? Selma may have had an extreme reaction to that stressful news, but the stressor does not qualify under Subpart (1) of Criterion A.
* * *
Al Noid, who had been rear-ended twice in the last two months, was stopped at a stop sign in his residential neighborhood when he was rear-ended again by Lester Fourget, who was traveling ten miles an hour. Al reacted with intense fear and hopelessness. Although Al satisfied Subpart (2) of Criterion A, he probably did not satisfy Subpart (1); but he will assert that he had concern about his “physical integrity.”
* * *
Jill Owt was an attorney with five children whose husband had died unexpectedly three years earlier. Jill had an enormous occupational workload representing disadvantaged women in cases of domestic violence. Her work, besides its volume, was very stressful. Not only did she feel the strain of empathizing with abused women, but many of the women she represented had personality disorders causing a strain in their working relationship. Besides her occupational workload, she had to care for five children. Not surprisingly, apart from her job and caring for her children, she had no life. About six months ago, she began to receive complaints from her coworkers and family that she was forgetful, that she could not stay on task, that she was irritable and had frequent outbursts of anger, that she never seemed to smile anymore and increasingly wanted to be alone, and that her usually careful attention to detail and interest in helping others was waning. Although Jill has responded to the stress with intense hopelessness, she has not satisfied Subpart (1) of Criterion A.
2. Criteria B, C, and D – Symptoms in Search of a Trauma
Sometime after the traumatic event, a plaintiff must have certain kinds of symptoms to qualify for a diagnosis of PTSD. This constellation of symptoms must develop for the first time after the trauma. That is, within a reasonable time before the traumatic event, the plaintiff must have had none of the required set of symptoms described in Criteria C and D on which are based the diagnosis of PTSD.
As a rule, psychological symptoms are of four basic kinds: (1) cognition (thoughts); (2) emotions (feelings); (3) sensations (pain); and (4) behaviors (affects and actions). With those categories in mind, in reading these following PTSD symptom criteria, always ask, what might be the day-to-day manifestations or instantiations of these categories of symptoms? This task is the crucial transition from abstraction to concrete example, the process of integrating theory and experience.
* * *
3. Criterion B – Cognitive Symptoms
Criterion B requires that the traumatic event be mentally “persistently re-experienced.” This is a cognitive manifestation of PTSD. Of the three symptom criteria (Criteria B, C, and D in the DSM-IV), Criterion B is the most specific and is thus the most useful to the defense in distinguishing PTSD from other mental disorders.
“B. The traumatic event is persistently re-experienced in one (or more) of the following ways:
“(1) recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions [cognitive]. Note: In young children, repetitive play may occur in which themes or aspects of the trauma are expressed;
“(2) recurrent distressing dreams of the event. Note: In children, there may be frightening dreams without recognizable content [cognitive];
“(3) acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative flashback episodes, including those that occur on awakening or when intoxicated) [behavioral and emotional]. Note: In young children, trauma-specific reenactment may occur;
“(4) intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event [cognitive and emotional]; and
“(5) physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event [behavioral].”
The symptoms in Criterion B (re-experiencing or intrusion symptoms) are called “phasic,” in that they are manifested only from time to time.
B(1): The recollections must be “recurrent.” They must be “intrusive.” And they must be “distressing.” These recollections are not merely bad memories. They are memories that come to consciousness despite efforts to keep them from awareness.
These recollections may occur somatically. For example, they may become manifest as urinary urgency, foot pain, chest pain, or headaches.
B(2): The dreams must be “recurrent.” And they must be “distressing.” A few nightmares do not satisfy this criterion. Qualifying dreams usually represent the traumatic event symbolically, not literally. For instance, not satisfying this criterion are “dreams or recurrent nightmares of falling off a cliff.”
These dreams are in the nature of a fantasy and not linked to traumatic experiences. Nor are “dreams of monsters or other threatening fantasy figures, or anxiety dreams related to conflicts or fears involving daily living rather than traumatic exposure.”
B(3): The behavior or emotion that the traumatic events were recurring includes “illusions,” “hallucinations,” and “dissociative flashbacks.” An “illusion” is a misperception or misinterpretation of a real external stimulus, such as hearing the rustling of leaves as the sound of voices. An “hallucination” is a sensory perception that has the compelling sense of reality of a true perception but that occurs without external stimulation of the relevant sensory organ. Transient hallucinatory experiences may occur in people without mental disorders.
What is a dissociative “flashback?” A “flashback” is a recurrence of a memory, feeling, or perceptual experience from the past. “Dissociation” is a disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment. Thus, “dissociative flashback” would be a flashback that is not placed in historical context but is experienced out of context as though the recurring memory, feeling, or perception were being lived in the immediate moment.
B(4): The psychological distress must be “intense.” And the cues of that distress must resemble or symbolize the traumatic event. The psychological distress is often manifested as anxiety, anger, or “dysphoria” (depression or unhappiness). Phenomena not meeting these criteria for distress are “the sad feeling experienced at anniversaries of a trauma, but ones that do not impede ongoing function.”
B(5): “Physiological reactivity” to cues may include heart rate, skin conductance, blood pressure, and forehead electromyogram (EMG). This criterion is more objective than other symptom criteria for PTSD in the DSM-IV. Even so, some of these physiologic reactions may be simulated in those without PTSD.
4. Criterion C – Behavioral Symptoms
Criterion C requires that the plaintiff respond to environmental stimuli differently from how she did before her traumatic experience. First, she needs to persistently avoid stimuli associated with the traumatic event. Second, she needs to be generally less responsive to other kinds of stimuli. These are behavioral manifestations of PTSD.
“C. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by three (or more) of the following:
“(1) efforts to avoid thoughts, feelings, or conversations associated with the trauma [behavior re: internal cues];
“(2) efforts to avoid activities, places, or people that arouse recollections of the trauma [behavior re: external cues];
“(3) inability to recall an important aspect of the trauma [cognitive];
“(4) markedly diminished interest or participation in significant activities [emotional and cognitive];
“(5) feeling of detachment or estrangement from others [emotional];
“(6) restricted range of affect [behavioral and emotional]; and
“(7) sense of a foreshortened future [cognitive and emotional].”
The symptoms of Criterion C (avoidance symptoms) are called “tonic,” in that they are manifested most of the time. Defense counsel should also note that Criterion C has a conjunctive requirement, one arm of which––numbing––must not have preexisted the trauma. So a sound defense strategy would be to establish that the plaintiff’s history before the trauma involved a numbing of general responsiveness from, for example, depression.
Criteria C(1) and C(2) are characteristic symptoms of “phobia,” an anxiety disorder. Criteria C(4), C(5), C(6), and C(7) are characteristic symptoms of mood disorders, such as dysthymia and major depression, and of certain personality disorders, such as borderline personality disorder. A diagnosis of PTSD in a plaintiff satisfying three of Criteria C(4), C(5), C(6), and C(7), but not either Criterion C(1) or C(2) would be more suspect than a diagnosis based on C(1) and C(2).
Phenomena not qualifying as psychogenic amnesia include “forgetting minor details, or [having a] head injury, alcohol-induced ‘blackouts,’ or other neurological memory failures.”
Also not meeting the criterion are “changes in activity due to physical limitations, or the severe anhedonia of depression.”
5. Criterion D – Autonomic Arousal
Criterion D requires that the plaintiff have persistent symptoms of increased arousal. This is an autonomic nervous system manifestation of PTSD.
“D. Persistent symptoms of increased arousal (not present before the trauma), as indicated by two (or more) of the following:
“(1) difficulty falling or staying asleep [behavioral];
“(2) irritability or outbursts of anger [emotional and behavioral];
“(3) difficulty concentrating [cognitive];
“(4) hypervigilance [cognitive and behavioral]; and
“(5) exaggerated startle response [behavioral].”
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The symptoms of Criterion D are characteristic of mood disorders, anxiety disorders, and certain personality disorders. These symptoms to the extent relied on to diagnose PTSD cannot have been present before the trauma.
The set of arousal symptoms in Criterion D are a mixture of tonic and phasic symptoms. Tonic arousal symptoms include insomnia and hypervigilance. Phasic arousal symptoms include exaggerated startle response and physiologic reactivity upon exposure to events that symbolize or resemble an aspect of the traumatic event.
6. Criterion E – Duration
Criterion E requires that the plaintiff’s symptoms (stated in Criteria B, C, and D) persist for more than one month. If the symptoms do not persist for one month, then the appropriate diagnosis is “acute stress disorder.”
7. Criterion F – Effect
Criterion F requires that the plaintiff’s symptoms be clinically significant––that is, produce noticeable distress or impair function in everyday activities.
II. Structuring a Defense
A claim for PTSD can be defended on a variety of bases. First, the defense may challenge the “evidential reliability” of PTSD as a diagnostic entity. Second, it may challenge the expertise of the proffered expert who has diagnosed PTSD. Third, it may assert that the diagnosis of PTSD is inaccurate because one or more of the diagnostic criteria have not been satisfied, or it may assert that the expert who diagnosed PTSD has failed to rule out other more prevalent disorders that may better account for the plaintiff’s clinical profile. Fourth, it may assert that the plaintiff is malingering. Fifth, the defense may assert that although the plaintiff appears to have PTSD, PTSD was caused by events for which the defendant is not responsible. And sixth, it may attempt to minimize the damages that the plaintiff seeks to recover for PTSD.
Selecting the bases upon which to defend should be judicious, accounting for the facts and the potential attitudes of the jury, and avoiding the “shotgun approach,” a strategy that the jury tends to perceive as a desperate and defensive grasping at straws.
A. PTSD as a Valid Diagnostic Category
“Epidemiologists like to count cases; doctors like to treat cases; and modern insurance companies will only pay for cases.”
R. E. Kendall, M.D.
“The concept of a case is a chimera existing only in the mind of the investigator.”
J. Copeland, M.D.
1. Introduction
PTSD is a diagnostic category. Whether that or any other diagnostic category is useful is gauged by the twin concepts of “validity” and “reliability.” The term “validity” refers to the objective quality of the category––that is, whether or not that category in fact measures what it purports to measure. The term “reliability” refers to the subjective quality of the category––whether or not there is intersubjective agreement from observation to observation (intra-observer agreement) and from observer to observer (inter-observer agreement) that the classification applies.
Any diagnostic category, to be considered accurate, should be validated. Determining “validity” usually requires an observationally direct or reductionistic standard of reference against which to measure the accuracy of the diagnostic category.
For example, the diagnosis of brain tumor on the basis of symptoms of impaired neurological function can be verified by the identification of the tumor through MRI, CT scan, or biopsy (surgery and histological inspection). The logical direction of this process of validation is that the relatively nonspecific but more obvious phenomena either act as a symbol for or point to less obvious but more specific pathognomonic phenomena. So to claim that a procedure is valid is to be able to provide justifications that the validator is more epistemologically secure than the procedure itself. This appeal to firmer ground is an aspect of empiricism.
But a basic problem in any process of validation is this: the theory, principle, or procedure investigated will always be underdetermined by the data. As a result, a logical and epistemic space exists in which will be at play that activity called “interpretation.” That means that the process of validation is a process of assessing an interpretation in light of other interpretations. Usually in that process, a number of interpretations may be offered. And, unfortunately, no one will have an impeccable gold standard by which to assess the merits of those various and often competing interpretations. So the process of validation becomes a process of circumferentially narrowing that logical and epistemic space through a process of argumentation or persuasion. That process of argumentation is always open-ended. And so validity is always a matter of degree. As the great biologist Edward O. Wilson wisely observed:
“Few claims in science, and particularly those entailing concepts, are accepted as final. But as evidence piles upon evidence and theories interlock more firmly, certain bodies of knowledge do gain universal acceptance.
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“[Yet] no objective yardstick exists on which to mark these degrees of acceptance; there is no body of external objective truth by which they can be calibrated. There is only warranted assertibility, to use William James’ phrase, within which particular descriptions of reality grow ever more congenial to scientists until objections cease.”
The point is, validation is a process that is both scientific and rhetorical, and so requires both evidence and argument.
A variety of measures of validity exist: “face” validity, “descriptive” validity, “predictive” validity, and “construct” validity. Some are more forceful warrants than others. Face validity is expert consensus that a diagnostic category (or set of diagnostic criteria), on its face, captures accurately a specific clinical pattern of signs and symptoms.
Face validity is the appearance to those in a position to know from having observed patients that the descriptive criteria accurately resemble what is seen in patients. Less approvingly, face validity is merely the clinical, but untested, impressions of clinicians that a characteristic configuration of signs and symptoms exist. Behind the use of face validity is the assumption that other more powerful kinds of validity exist, even if not yet demonstrated.
Descriptive validity is the extent to which the characteristic features of a diagnosis are shown to be unique, setting that diagnosis apart from other diagnostic categories and, importantly, with the joint occurrence of the characteristic signs and symptoms in a heterogeneous group being more common than would be expected by chance alone.
In the context of psychological disorders, descriptive validity seeks to confirm that the behavioral manifestations of interest do not occur randomly, but cluster meaningfully into “syndromes,” a grouping of symptoms or signs that recurrently appear temporally together in many persons.
Predictive validity is the extent to which the diagnostic classification is associated with a specific course of the manifestation of disease or response to treatment.
One expects something in the future to be probabilistically determined when a person meets current criteria for the disorder.
Construct validity is the presence of evidence supporting theoretical models explaining the etiology or pathogenesis of the disease or disorder.
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In an important article entitled Establishment of Diagnostic Validity in Psychiatric Illness: Its Application to Schizophrenia,
Drs. Eli Robins and Samuel. Guze identified a respected method for developing the foregoing types of validity for psychological disorders, using five kinds of studies: (1) descriptive studies of clinical phenomena; (2) laboratory studies defining unique parameters of the disorder, including chemical, physiological, radiological, anatomical, or psychological factors; (3) studies to identify variables that delimit the boundary conditions for the inclusion of patients with the disorder and the exclusion of patients who do not have the disorder; (4) long-term follow-up studies of patients to determine whether there is variability in outcome and to see whether the original cohort of patients present with the same or a different disorder; and (5) family studies to ascertain the degree to which the same disorder occurs in families.
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The most problematic aspect of validating psychological disorders is the lack of a “gold standard,” “the test or procedure used to define the true state of the patient.”
As a result, the effort to validate a psychological disorder entails an admixture of judgments of both fact and value. To validate a psychological disorder, the investigators need to develop data through painstaking studies. But these data are only one variable in a matrix of judgments that together result in a diagnostic category. For example, data provide an answer if there is agreement about what the question is. Yet if the experts cannot agree about the proper construct of a psychological disorder, they cannot agree on the proper validators. If different validators validate different constructs, empirical criteria are unavailable to decide which validators are most important. That is, there are no metacriteria. For instance, expert consensus determines what standard constitutes the “gold” standard, the bedrock of any epistemological inquiry. But empirical data cannot decide whether two possibly related syndromes should be considered as (1) one disorder without subtype status, (2) one disorder with subtype status, (3) two different disorders in the same diagnostic grouping (e.g., mood disorders, anxiety disorders), or (4) two different disorders in different diagnostic groupings.
As one psychiatrist eloquently stated:
“Psychiatric diagnosis is, above all, a convention. Thus, even when an ‘atheoretical view’ and the use of the ‘best available knowledge’ suggest that a disorder is potentially valid, the ‘product’ should be ‘cleared’ by several interest groups before the official printing of the label. From such a process, the new disorder emerges cosmetically assembled for mass marketing (see, for instance, the recent controversy surrounding DSM-III-R’s masochistic personality and premenstrual syndromes).”
2. Kinds of Evidence Adduced for Validity of PTSD
Although PTSD is a stated diagnostic category in the DSM, is it a “valid” diagnostic category? For example, is PTSD merely a label for the aggravation by trauma of preexisting psychopathology?
Are the mental disorders designated as co-morbid with PTSD truly co-morbid, or are they instead the only disorders present, with PTSD being an artifact? In 1984, two highly respected psychiatrists, Drs. Goodwin and Guze, experts in validation of psychological disorders, wrote the following about the DSM-III’s “post-traumatic stress disorder, delayed type”:
“This has the same clinical features as the post-accident anxiety syndrome, but the symptoms do not appear until at least six months after the trauma. In 1980 the Veterans Administration announced that post-traumatic stress disorder, delayed type, was a compensable disorder.
* * *.
“Many veterans responded by filing claims based on their belief that they suffered from post-traumatic stress disorder, delayed type, related to traumatic war experiences. The symptoms of the disorder were well-publicized in the media and in brochures distributed by national service organizations. Rarely before had so many claimants presented themselves to psychiatric examiners having read printed symptom checklists describing the diagnostic features of the disorder for which they sought compensation. Some psychiatrists were offended by the ‘mechanical litany of complaints recited by a well-read claimant.’ The decision to award compensation was made even more difficult by the almost total lack of evidence that ‘post-traumatic stress disorder, delayed type’ exists as a clinical entity.”
Yet, today, say experts in PTSD, significant agreement exists that PTSD is valid.
(After all, it is enshrined in the DSM-IV.) So for the defense a challenge to a diagnosis of PTSD on the grounds that PTSD is not a valid diagnostic category has little or no hope of success. Even so, a critical look at the evidence purportedly validating PTSD does have some value. For if that evidence is shown to be weak or preliminary, confidence in any diagnosis of PTSD will be undermined.
In 1987, coincident with publication of the DSM-III-R, Drs. Keane and Wolfe published an article entitled Post-Traumatic Stress Disorder: Evidence for Diagnostic Validity and Methods of Psychological Assessment.
This article discussed the evidence for the validity of the PTSD construct in terms of the criteria provided by Drs. Robins and Guze. Drs. Keane and Wolfe note that “PTSD has been criticized by Goodwin and Guze and other authors for a lack of evidence that supports its existence as a diagnosis distinct from already existing categories (e.g. depression, dysthymia )[;] however, a number of recently completed studies provide supporting evidence for the validity of the PTSD diagnosis.” In the conclusion of the article, the authors note that “laboratory studies that discriminate PTSD from other psychological disorders comprise the bulk of the available evidence; definitive longitudinal studies and family studies have yet to be conducted and will provide much-needed new information on the degree to which PTSD circumscribes a unique disorder.”
As presented below, the laboratory-based data on the validity of PTSD as a diagnostic category to which they refer stem from three sources: (a) psychophysiological assessment studies, (b) psychometric studies, and (c) experimentally designed laboratory studies.
a. Psychophysiological Assessment Studies
Drs. Keane and Wolfe cited six psychophysiological assessment studies.
This collection of studies has some obvious limitations. Only three of these six studies were published. All dealt with war veterans, mostly Vietnam veterans.
b. Psychometric Studies
Drs. Keane and Wolfe cited three studies published in the early 1980s. But these three studies had limited value.
First, all three studies involved Vietnam combat veterans. Second, the psychometric measures involved “self-reports,” a relatively unreliable way to acquire information.
c. Direct Laboratory Testing
Drs. Keane and Wolfe cited one study involving direct laboratory testing.
This study also has obvious limitations. First, it was unpublished. And second, it dealt with Vietnam combat veterans. Obviously, the findings in studies involving combat veterans need to be replicated with noncombat populations to gain credibility and to ensure validity.
* * *
Three years later, in 1990, Drs. Wolfe and Keane published a review article entitled Diagnostic Validity of Posttraumatic Stress Disorder,
repeatedly cited as the definitive resource by other authors on the validity of PTSD. Their article indicates that “efforts to validate the diagnosis of PTSD are currently evolving rapidly.” (This review is dated 1990, four years before the publication of the DSM-IV in 1994.) The authors organize those efforts into “four content areas: (1) empirical efforts in diagnosis (based extensively on a variety of assessment procedures); (2) model-building attempts (emphasizing phenomenology and conceptual formulations); (3) focused biologic and physiologic approaches (reflecting the search for intrinsic biologic or centrally [central nervous system] mediated markers); and (4) epidemiologic approaches (examining disease distributions across populations).”
d. Empirical Efforts
The support for the diagnosis of PTSD has been primarily provided by procedures assessing PTSD clinically. These procedures are (i) descriptive (or case interviews), (ii) psychometric tests, and (iii) laboratory tests. Psychological assessment is considered best achieved through the “multimodal approach,” that is, through use of a comprehensive, structured assessment “battery.” These batteries consist of individual tests or structured interviews, designed to characterize the disorder and distinguish it from other serious psychological disturbances and to obtain clear-cut estimates of past and current functional abilities in a wide range of skills felt to be impacted in the development of trauma disorders.
But these batteries have flaws that tend to undermine their validity. First, the individual diagnostic instruments that make up the “battery” are based on studies of combat-related PTSD. (Those individual instruments include the Mississippi Scale for Combat-Related Posttraumatic Stress Disorder and the PTSD subscales of the MMPI.) Drs. Keane and Wolfe note that “the task remains to evaluate their utility for civilian PTSD populations.”
One instrument developed with civilian populations is the Impact of Event Scale (IES). This instrument was developed with the PTSD criteria of the DSM-III (not with the PTSD criteria of the DSM-III-R or DSM-IV). The authors note that it has a “reasonable degree of clinical and face validity,” citing the study of J. Schwarzwald et al., Validation of the Impact of Event Scale for Psychological Sequelae of Combat.
Again, this is a study cited as a warrant for use of an instrument with civilian populations “validated” through studies of combat veterans.
Second, there are few standardized, examiner-administered formats for interviews to identify PTSD. Two types of interview formats exist for use in PTSD: (i) generic psychiatric interviews and (ii) PTSD symptom-focused interviews:
i. Generic Psychiatric Interviews
The three most common psychiatric interview formats in 1990 included the Structured Clinical Interview for DSM-III-R; the Schedule for Affective Disorders and Schizophrenia; and the Diagnostic Interview Schedule. Yet these interviews lack comparative data sets to substantiate rates of diagnostic sensitivity and specificity, and “no widespread, comparative studies using diverse traumatized populations have been conducted to permit comparisons of diagnostic sensitivity and accuracy.”
ii. PTSD Symptom-Focused Interviews
Of the few such symptom-focused interviews, most have been developed with Vietnam combat veterans. The most well known are the Jackson Structured Interview for Combat-Related PTSD and the Brecksville Interview for PTSD. “No comparative data [are] available yet about the diagnostic utility of these interviews for other groups of trauma victims.” “And validational accomplishments in non combat-related PTSD are at a relatively early stage.”
e. Models in PTSD
Drs. Keane and Wolfe contrast two conceptual models of PTSD: the “reductionistic” model with the “interactive model.” Both models appear to have been derived from studies of combat veterans. The “reductionistic” model of etiology, say the authors, was popular in the earlier years and focused on the severity of the stressor, almost exclusively in Vietnam combat veterans. The more recent “interactive model” focuses on the importance of variables other than the traumatic stressor in producing PTSD, such as disposition, “personality,” “background,” and “context.” To verify this model, the authors cite four studies.
Yet these four studies again focus on combat veterans. Finally, the authors note, and this is important, “there is a need to expand diagnostic and validational approaches from Vietnam combat veterans to varying ‘victim classes’.” “As these efforts proceed,” the authors continue, “critical advances in identifying individual, categorical, and generic aspects of trauma syndromes can be expected.”
Again, Drs. Keane and Wolfe seem to be buying validity on credit.
f. Biologic–Physiologic Approaches
Some investigators have attempted to identify specific biologic, biochemical, neuroendocrinologic, or physiologic alterations in those with PTSD. Yet Drs. Keane and Wolfe note that nothing definitive has been developed for biochemical, neuroendocrinological, or pharmacological responses to validate PTSD. On the dimension of physiology, they note that some investigations have demonstrated “compelling diagnostic information on PTSD” with the presence of heart rate reactivity in certain PTSD patients that significantly distinguishes them from both well-adjusted controls and patients with other severe psychological disorders. The authors cite a previously discussed study,
as well as two additional studies.
All three studies involve only select groups of Vietnam veterans, not the general civilian population. This distressing fact tempers the external validity of these studies because, as the authors later remark, “very limited knowledge is currently available about the degree to which disparate victim classes are similar in their development and manifestation of trauma symptomatology.”
g. Epidemiologic Approaches
Drs. Keane and Wolfe report that several epidemiologic studies have attempted to document the prevalence of PTSD in the general population and in Vietnam veterans. Then they report that methodological differences in these studies, likely responsible for different end points, raise diagnostic questions and caution that more research in this area is needed. Epidemiologic studies investigate an endpoint, in this case PTSD, which is presupposed to be a valid diagnostic category. On that basis, it is difficult to see how the results of these studies validate PTSD.
* * *
In 1990, Robert W. Bulter et al. remarked that “a considerable amount of evidence has been accumulated [mostly involving Vietnam combat veterans] in support of the overall validity of PTSD as a diagnostic entity[; yet] much of this evidence . . . is based on self-report measures.”
Six years later, in 1996, one academic psychiatrist remarked that “we have not progressed beyond a face validity for PTSD, meaning it is on the level of first impressions of clinicians who are simply trying to identify a disorder . . . [and] due to the high comorbidity present with the diagnosis of PTSD, we remain distant from being able to attest to the uniqueness of this one diagnostic grouping or to its having a predictive validity.”
3. Stressors
Controversy exists whether an extreme traumatic stressor should be necessary for PTSD. Some advocate that Subpart (1) of Criterion A be abolished or reformulated in favor of purely subjective perception of the magnitude of the stressor instead of the more tightly and objectively defined current requirement.
In 1990, an exhaustive review of existing studies on the stressor criterion conducted in preparation of the DSM-IV indicated that the magnitude of the stressor was directly proportional to the risk of developing PTSD.
What constitutes the magnitude of the stressor? An adequate topology is not yet available. Generic characteristics, however, include magnitude, rate of change, duration, unpredictability, unpreparedness, and lack of prior experience. Data on this aspect of Criterion A are important to the defense. The defense is immediately interested in PTSD alleged to have arisen from stressors for which the alleged “victim” can seek legal redress. The defense is not immediately concerned, then, with PTSD from war, natural disasters, political imprisonment, or torture, but is rather concerned with PTSD from motor vehicle accidents, from harassment at the place of employment, from sexual assault, and from exposure while on the job to traumatic stressors (firefighters, police, and health care providers).
Stressors of low magnitude may create a risk of developing PTSD. But in 1990, no data were available to confirm that link. This is an important finding for the defense. Simply, the defense is often faced with claims for alleged PTSD based on stressors of low magnitude, such as the minor automobile accident or niggling harassment in the workplace.
Subpart (2) of Criterion A, the subjective evaluation of the traumatic event, was probably designed “to qualify individuals making high-magnitude attributions to low-magnitude events and thus to qualify those events as well” as causing PTSD. Yet Subpart (2) is weakly supported as correlating with PTSD. The data on this criterion were noted to be “highly confounded and largely unreplicated.”
This is also an important finding for the defense. Many claims for PTSD are based on the assertion that although the stressor may seem minor to most people, it was devastating to the plaintiff who was particularly frightened by the event.
In 1995, Rachael Yehuda et al. published a paper entitled Conflict Between Current Knowledge About Posttraumatic Stress Disorder and Its Original Conceptual Basis, in which they remarked that “many recent findings are inconsistent with the notion that traumatic events are the primary cause of symptoms and challenge the idea of PTSD as a typical stress response.”
They reached an important conclusion: PTSD following a traumatic event is the exception rather than the rule. “Among those who are exposed to very severe and prolonged trauma, there is usually a substantial number of individuals who do not develop PTSD or other psychiatric illnesses.” That is, “decompensation following trauma is neither a random process nor an outcome entirely predictable by the nature of the traumatic event.” “As such,” the authors go on to conclude, “the emergence of PTSD following exposure to a trauma may represent the manifestation of an underlying diathesis [constitutional predisposition to certain disorders] rather than a normative adaptation to environmental challenge.” That is, people with PTSD were abnormal before developing PTSD; they are the so-called “eggshell” plaintiffs. This conclusion may contradict the finding in 1990 that Subpart (2) of Criterion A has little or no empirical support, a conclusion that may move the nosology of PTSD in a direction less helpful to the defense.
4. Symptoms
PTSD comprises three sets of symptoms: (a) persistent re-experiencing of the trauma (one symptom is needed); (b) persistent avoidance and numbing (three symptoms are needed); and (c) persistent increased arousal (two symptoms are needed). Do these sets of symptoms reflect an underlying and identifiable symptom structure, or are they simply arbitrary groupings of symptoms?
a. Factor Analysis
The answer to that question is sought from both “factor analytic” studies and “longitudinal” studies of victims of trauma. In 1991, Drs. Davidson and Foa remarked that “in preparation for the DSM-IV, the work group has also considered the validity of the diagnostic criteria for posttraumatic stress disorder . . . [and] literature reviews have concluded that among veterans and disaster victims, . . . the emergent factor loadings broadly correspond with the intrusive, avoidance, and hyperarousal clusters found in DSM-III-R.”
But these authors provided no citation to these factor analytic studies.
A major limitation of most studies of PTSD is that they are retrospective and so may confuse cause and effect. As a result, “investigators of posttraumatic stress disorder (PTSD) [have] difficulty in determining the relative contributions to its etiology of the traumatic experience and of preexisting psychopathology in the victim of the trauma.” “From a research standpoint, keeping the stressor as a part of the diagnosis builds in a confound that makes it impossible to empirically assess PTSD as a response.”
Much of the criticism about the symptom criteria of PTSD is that too many symptoms are required to define PTSD. For instance, some advocate reducing the number of avoidance symptoms from three to two. Obviously, this proposal does not help the defense.
Some advocate separating the avoidance symptoms from the numbing symptoms, placing each in separate categories. They believe the numbing symptoms are central to the diagnosis of PTSD and better than other symptoms at distinguishing those with PTSD from those without PTSD. Some relatively recent factor analytic studies support the position that the avoidance and numbing criteria of Criterion C should be separated into distinct categories.
That would be a step in a direction favorable to the defense in that it raises the bar to diagnosis of PTSD.
Some factor analytic studies have found weak factor loadings for PTSD items reflecting memory difficulties. This evidence could be helpful to the defense in undermining the validity of the so-called “repressed memory syndrome.”
Thirteen factor analytic studies of PTSD symptoms have been published:
DSM-III: Eight of these factor analytic studies concern the DSM-III. These eight studies factor analyzed heterogeneous item pools, consisting of items assessing a subset of DSM-III-R or DSM-IV PTSD symptoms mixed with items assessing other symptoms. As a result, analyses of the item pools make it difficult to identify PTSD factors. There may have been too few PTSD items to reliably identify PTSD factors, and identification of these factors may be obscured by the inclusion of items assessing other types of symptoms.
DSM-III-R and DSM-IV: The five studies based on the criteria of DSM-III-R or DSM-IV are not in complete agreement.
b. Psychophysiologic Responses
Because virtually all the indicia of PTSD are “symptoms” (that is, subjective reports from the patient of this or that cognition, emotion, or behavior) the Holy Grail for PTSD researchers and devotees is a biological marker (a sign) that more objectively distinguishes those with PTSD from those without PTSD. In this regard, arguably two somewhat objective indicia of PTSD could make the diagnosis of PTSD more objective and less dependent on the patient’s self-reports. These criteria are found in Section B(5), “physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event,” and D(5), “exaggerated startle response.”
Neither of these criteria [B(5) and D(5)] is necessary to the diagnosis of PTSD, but if their validity is established, each, if present, may make the diagnosis of PTSD difficult to refute. Obviously, the defense should expect plaintiffs’ experts to focus on these two criteria in an effort to validate their diagnoses of PTSD.
What empirical support is there for these two criteria? There is nothing impressive. A number of studies have been conducted that purport to attach psychological significance to physiologic signals. These studies concern the “phasic” aspects of PTSD and are considered biological because the dependent variable is biological. The idea behind these alleged biological indicia of PTSD is that the traumatic event is an unconditional stimulus, and later stimuli associated with the traumatic event act as conditioned stimuli to elicit conditioned responses in the form of these two physiologic responses.
But this psychophysiological process is not that straightforward. That is, a variety of irrelevant individual differences or other nuisance factors can affect psychophysiological responses. The result is often ambiguity about the link between psychophysiological responses and psychological constructs. To reduce the ambiguities, investigators should explicitly incorporate procedures for testing alternate hypotheses. They should also incorporate multiple physiological responses. They should examine the pattern of responsivity over time. (Though important, the reliability of psychophysiological responses recorded on a single occasion is rarely assessed or reported.) And they should adopt standardized procedures. If a psychophysiological response truly assessed individual differences, significant test-retest stability should exist across various measurements. Yet, as a rule, the temporal stability of psychophysiological responses has been low.
i. Physiologic Reactivity on Exposure to Cues
A number of studies concern the effect of environmental cues on various autonomic physiologic responses, such as heart rate and skin conductance. This literature is described by PTSD insiders as “robust” and “considerable” and as supporting the usefulness of psychophysiological techniques for diagnosing and characterizing PTSD. Yet a closer examination of these studies and their methodologies creates significant concern about the clinical value of tests for physiologic responses in diagnosing PTSD, especially in civilian populations.
Dr. Keane et al. noted that these foregoing psychophysiologic studies have “methodological limitations” that preclude definitive conclusions about diagnostic accuracy. First, a high PTSD base rate exists in studies using psychophysiologic variables to classify participants relative to diagnostic status. Second, nearly all studies of reactivity to trauma-relevant cues include a major comparison group composed of well-adjusted combat veterans, typically volunteers. Comparison with these groups can inflate diagnostic hit rates by capitalizing on the myriad differences irrespective of PTSD status. Third, there has been a failure to adequately demonstrate cross-validation of the classification equations. Most studies have not attempted cross-validation on an independent sample or had too few participants to adequately test stability of the prediction equations. Fourth, the studies have not used multivariate analytic methods to investigate classification accuracy because sample sizes have been too small.
Moreover, as many as 40 percent of patients with PTSD do not show the expected elevation in reactivity to trauma cues. In fact, one researcher highlighted a trend across studies that indicates better performance in identifying individuals who do not qualify for an interview-based PTSD diagnosis than in identifying those who do qualify for the diagnosis. Obviously, all in all cumulating the results of a number of defectively designed studies does not add up to the results of a well-designed study.
ii. Exaggerated Startle Response
Exaggerated startle in PTSD is suggested to be a conditioned emotional response to stimuli reminiscent of the trauma. In 1990, Robert W. Bulter et al. noted that “remarkably little work has been directed toward validating the presence of exaggerated startle response in PTSD.”
Including exaggerated startle as a feature of PTSD in the DSM-III in 1980 was primarily the result of data from “case studies.” Case studies, as a form of evidentiary warrant, are generally insufficient to establish a cause-and-effect relationship between eyeblink startle and PTSD.
Subsequently conducted were laboratory studies of the eyeblink startle response in those diagnosed with PTSD. The results of those studies are ambiguous. As late as 1996, C. A. Morgan et al. remarked that “at this time there are not enough data to make inferences about the nature of the pathophysiology of PTSD, as measured by the startle response, from one patient population to another.”
What was true in 1996 is true today.
5. Chronicity
PTSD has generally been found to remain present for at least one year in about half of the cases. Data about the chronicity of PTSD are obtained from cross-sectional studies and prospective studies.
a. Cross-Sectional Studies
A number of cross-sectional studies indicate that stress-related symptoms persist years after the trauma.
b. Prospective Studies
Most prospective studies have shown a decrease in psychological stress-related symptoms over time.
6. Delayed Onset
In the DSM-IV, if onset of symptoms is at least six months after the stressor, the PTSD is characterized as “with delayed onset.” The distinction between “acute” versus “delayed” PTSD is based on uncontrolled clinical observations, that is, case studies.
PTSD with delayed onset is extremely rare. Indeed, some psychiatrists and psychologists doubt its validity, attributing reports of delayed onset to prestressor psychopathology, drug abuse, factitious disorder, and malingering.
7. Validity of Other Traumatic Response Syndromes
O misery! The things I have suffered, cause enough for deep lamentations! O you cursed sons of a hateful mother, a plague on you!
Euripides, Medea
What should such fellows as I do crawling between heaven and earth? We are arrant knaves all; believe none of us.
Shakespeare, Hamlet, III, i, 128
a. Introduction
A number of so-called disorders with elements of PTSD have been created and labeled for sociopolitical purposes. Prominent among them are “Complex Posttraumatic Stress Disorder,” the “Battered Woman Syndrome,” and the “Repressed Memory Syndrome.” Although a challenge to PTSD as defined in the DSM-IV on the grounds of validity is likely to be unsuccessful, a challenge to these nonstandard, often politically motivated syndromes is more likely to be successful.
These nonstandard traumatic response syndromes cannot be adequately understood without understanding the social context in which they have arisen. In short, traumatic response syndromes have become a handmaiden of the “gender” politics of the so-called “Cultural Left.” That is, a cadre of radical feminists have used and continue to use these diagnostic categories to fight, with passionate intensity, for their comrades against omnipresent patriarchal oppressors, who apparently are to them, among other things, all too frequently pervasive sexual abusers and systematic traumatizers of women and children. Because these traumatic response syndromes label someone––a victim––with a chronic psychological injury as the result of trauma often instituted by a victimizer, they are a weapon. Like any weapon, they can be used for good or ill, as a shield or sword, for remediation of legitimate individual loss or to achieve ulterior ideological or political goals.
For the defense, the battle is with that subclass of psychological therapists who have decided to use these various trauma response syndromes, including PTSD, under the guise of remedying an individual psychological loss to effect politicosocial change (akin to the state use in the old USSR of psychiatric diagnoses to neutralize political dissidents). This is the therapist who couldn’t care less whether or not the trauma response syndrome as a construct or as a diagnosis is valid. They are therapists who are completely and perversely insensitive to the number of false positive diagnoses of sexual abuse that their nosological concepts and diagnostic techniques generate, even though for those falsely accused of sexually abusing someone, the consequences of such a misdiagnosis are personally and socially devastating.
These therapists are relatively easy to identify. They tend to speak the jargon of the “neo-Marxist” (or “Cultural Leftist”): “dominant classes,” “secret, conspiratorial efforts to dominate the weak and dependent,” “dominating cultures,” “privileging,” “underclasses,” “oppressors,” “victims,” “historical forces,” “evil deterministic environments.” Whereas Marx spoke of insidious deterministic economic forces, these neo-Marxists speak of the insidious forces of gender. Whereas Marxists had the capitalistic manifesto, the neo-Marxists have the cultural manifesto, an array of ill-conceived handbooks on “victim or survivor syndromes.”
In their discourse, these therapists invariably tell highly crafted, stylized stories of victimization, ignoring or suppressing other equally resonant stories that would tend to cast these so-called “victims” in a less favorable light. An example is the psychotherapist who sees all men as victimizers and all women as victims. The upshot is that the worldview of these therapists is seen to be tenaciously biased and reductionistic: all the ills of this world are the fault of men.
Listen, for example, to the militant tone of feminist therapist Dr. Judith Herman:
“Violence is a routine part of women’s sexual and domestic lives. . .. For most of the twentieth century, it was the study of combat veterans that led to the development of a body of knowledge about traumatic disorders. Not until the women’s liberation movement of the 1970’s was it recognized that the most common post-traumatic disorders are those not of men in war but of women in civilian life.
* * *
“… Man’s discovery that his genitalia could serve as a weapon to generate fear must rank as one of the most important discoveries of prehistoric times, along with the use of fire and the first crude stone axe. From prehistoric times to the present, I believe, rape has played a critical function. It is nothing more or less than a conscious process of intimidation by which all men keep all women in a state of fear.
“The systematic study of psychological trauma therefore depends on the support of a political movement. . . . Advances in the field occur only when they are supported by a political movement powerful enough to legitimate any alliance between investigators and patients and to counteract the ordinary social processes of silencing and denial.”
b. Complex Posttraumatic Stress Disorder
Complex posttraumatic stress disorder is the creation of feminist therapist Dr. Judith Herman. It is, for all practical purposes, designed to apply to, in Dr. Herman’s words, “those subjected to totalitarian systems in sexual and domestic life”––that is, all women in patriarchal societies. This syndrome has not been validated and by its terms could encompass virtually any mental disorder or transient malady of any woman in our society.
Considerable controversy exists over the purported connection between severe, chronic childhood trauma and PTSD. Most consider such early childhood traumatic experiences as merely a risk factor for later PTSD. Others consider such traumatic experiences as producing a form of PTSD, which they wanted included in the DSM-IV under the rubric Disorder of Extreme Stress Not Otherwise Specified (DESNOS), or “Complex PTSD.” Critics of both positions point out that although early or extremely severe trauma in childhood often results in significant mental illness, that illness seems to be different in kind from PTSD. Indeed, that mental illness is reflected in a pattern of self-abuse, dissociation, chronic affective and personality changes, and a tendency to being repeatedly victimized. This pattern is more closely allied with the dissociative disorders and certain personality disorders like borderline personality disorder or the proposed “self-defeating personality disorder.”
Complex PTSD or DESNOS was considered in field trials for the DSM-IV. During those trials, the investigators examined the reliability, validity, internal consistency, and overlap of Complex PTSD with PTSD. The result was that, currently, Complex PTSD is not listed in Appendix B of the DSM-IV under Criteria Sets and Axes Provided for Further Study.
c. The Battered Woman Syndrome
The battered woman syndrome (BWS) identifies and describes “patterns of responses and perceptions characteristic of women who have been subjected to continuous physical or psychological abuse by their mates.”
The pattern typically includes psychophysiological stress, lowered self-esteem, learned helplessness, and idealization of the abuser. Its essence is that the battered woman is psychologically compelled to commit violence against the victimizer (usually her husband or boyfriend) or against someone else at the direction of the victimizer. Basically, BWS is a concept used by criminal defense and plaintiffs’ lawyers to exculpate their female clients, either to have them acquitted of violent domestic crimes or to obtain monetary verdicts in their favor against their husbands or boyfriends.
An interesting example of this defense occurred in the criminal defense of Karla Homolka, a Canadian model who assisted her boyfriend, Paul Bernardo, in kidnapping, sexually abusing, and strangling teenage girls. When Bernardo was torturing his victims upstairs in his home, Homolka, as she recalls, went downstairs to blow-dry her hair because “I didn’t want to stay upstairs.” Shortly later, she and Bernardo went to her parents’ house for Easter dinner, and she gave Bernardo a card wishing Happy Easter “to the most wonderful man in the whole wide world.” When prosecuted, in her defense, Homolka claimed she was beaten into submission and blackmailed by Bernardo into helping him fulfill his fantasies of having “sex slaves.”
Defense counsel will rarely defend a woman alleged to have battered her spouse in a case in which BWS arises. The more likely event is that the defense will be defending a third party alleged to be responsible for a traumatic event causing PTSD in an individual who has also been battered by her spouse. Then the issue arises whether the PTSD-like symptoms were caused by the battering or instead by the alternative traumatic event.
BWS resembles PTSD and is often used in conjunction with PTSD. Indeed, an expert may describe BWS as a “subset of PTSD.”
Yet to the extent that BWS is something other than PTSD, it has not been validated as a psychological disorder and is not listed in the DSMIVTR.
d. Repressed Memory Syndrome
Repressed memory syndrome (RMS) is a cluster of symptoms, many overlapping with those of PTSD, in which is prominent the phenomenon known as “dissociative amnesia.”
Dissociative amnesia is an “inability to recall important personal information, usually of a traumatic or stressful nature, that is too extensive to be explained by ordinary forgetfulness.” So with reference to PTSD, what the patient has is the inability to recall the traumatic event, which would satisfy the requirement of Subpart (1) of Criterion A.
The traumatic event is “remembered” many years later, usually with the help of, or at least the suggestion of, a dogged and dedicated therapist, who largely presumes that the trauma existed either because of the patient’s gender or because of the nature of the patient’s psychological or physical symptoms. The sociopolitical dimension of RMS is that the trauma is typically female childhood sexual abuse purportedly inflicted by a male, usually a member of the victim’s family, and the dogged therapist is usually a radical feminist (a “Cultural Leftist”). Indeed, a variety of highly respected specialists in mental health care have remarked that the increased use in clinical practice in America of the idea of “repression” is the result of desire for social changes rather than a product of scientific progress.
Repressed memory of traumatic events or conditions is a clinical phenomenon described in several places in the DSM-IV: for instance, PTSD, acute stress disorder, somatization disorder, and dissociative amnesia. The traumatic event may be childhood sexual abuse. But this phenomenon of “repressed memory” or “dissociative amnesia” should be distinguished, some say, from “repressed” or “recovered” memory syndrome. The repressed memory syndrome is defined as “the propensity of some victims of major trauma to experience complete absence of awareness or memory of a traumatic event from the time of its occurrence until a period of years thereafter.”
Distinguish the repressed memory syndrome from the false memory syndrome, defined as “a condition in which a person’s identity and interpersonal relationships are centered around a memory of traumatic experience which is objectively false but in which the person strongly believes.”
This dispute over “repressed memory” is relevant to claims for PTSD when the claimant is alleging a recovered memory (a memory theretofore unrecovered owing to dissociative amnesia) of sexual or physical abuse, whether during childhood or adulthood, and that abuse is alleged to have resulted in PTSD. If an individual with dissociative amnesia of childhood sexual abuse has a clinical profile (a cluster of nonspecific symptoms) satisfying the criteria of PTSD, then she is diagnosed with “PTSD.” If she does not satisfy those criteria and does not satisfy the criteria of acute stress disorder or somatization disorder, she will be diagnosed with dissociative amnesia. But she should not be diagnosed with repressed memory syndrome, which is not a validated clinical entity and which is not listed in the DSMIVTR.
The defense lawyer may be enlisted on either side of this dispute over repressed memories: (1) the defense lawyer may defend the alleged sexual abuser when sued by the alleged victim or (2) the defense lawyer may defend the therapist who is accused of committing malpractice by implanting false memories of childhood sexual abuse.
The underlying premises of the repressed memory syndrome are (1) that the initial memory for a trauma is fixed or indelible; (2) that the memory is not conscious; that is, it is “repressed,” until years later when, through a variety of therapeutic techniques (“memory work”), it becomes conscious; and (3) that these therapeutic techniques do not confound the process of recovering these indelible memories. Yet these three assumptions are not supported by the weight of evidence.
The first assumption is not only unsupported but contradicted by the experimental evidence. That research indicates that memory is not fixed and indelible, remaining over time remarkably accurate, but is rather malleable and subject to the misinformation effect, the process of distorting memory through integrating false post-event information into subsequent accounts of the event. Indeed, painstaking, thoughtful research has shown that entire scenes of stressful events can be fabricated and then inserted in another’s memory.
The second assumption is also not supported by the experimental evidence. The psychological process of repression is merely a hypothesis. Not surprisingly, studies cited to support that hypothesis of repressed memory are not of a high methodological quality. Many of them have not even been published. Many, if published, have not been published in peer-reviewed journals or journals reviewed by those outside the repressed memory establishment (an ideologically motivated group with weak scientific credentials).
Most, if not all, conclusions supporting RMS rest on “case studies.” Case studies are anecdotal, unrepeatable, uncontrolled, unrepresentative, subjectively interpreted, and not amenable to statistical analysis. The case study is thus useful only in two situations: First, it can generate some fresh conjecture that is then amenable to empirical testing. Second, the case embodies an effective refutation of a particular hypothesis. But case studies are insufficient to establish the relationship of cause and effect.
If psychologists and psychiatrists are to understand how well they can predict, they must rely on prospective (not retrospective) studies involving careful record keeping. The proper study design to investigate dissociative amnesia must have these features: (1) the study group must have unequivocally documented trauma; (2) all the subjects must have been abused while older than age 5; (3) all subjects must be interviewed about their past history of trauma; (4) subjects who denied abuse on the general interview must receive a clarification interview in which they are directly asked about the known abuse. If some failed to recollect the abuse, this would suggest repression.
Prospective studies have failed to demonstrate that dissociative amnesia results from trauma. In these prospective studies, the investigators have followed up victims of a known past traumatic event and then assessed their memories at the time of evaluation, eliminating the problem of recall bias. These prospectively designed studies are vastly superior to the retrospectively designed studies, relied upon by the cadre of repressed memory therapists. In those retrospective studies, the subjects did not display amnesia at the time of index evaluation, but were believed to have experienced amnesia in the past. As a result, these retrospective studies have serious methodological limitations, especially the limitation of “recall bias.”
* * *
Drs. Harrison Pope and Judith Hudson et al. analyzed the available prospective studies in great detail and found that “when trauma victims were asked directly about their known experience, they consistently reported memories.” “Non-reporting was encountered only in those studies where the investigators failed to ask subjects directly about the event.” “Such non-reporting must not be assumed to reflect amnesia: a large literature has shown that when not asked directly interviewees will frequently not disclose sensitive autobiographical information that they actually remember.” “Among the prospective studies . . ., non-reporting by trauma victims could be readily explained by ordinary and well-established processes without the need to postulate a novel process such as ‘dissociative amnesia’.”
Moreover, Drs. Kendall and Tackett, in a comprehensive review examining 45 studies of 3,369 victims of sexual abuse, describe no evidence of dissociative amnesia.
The third assumption––that therapeutic techniques used with RMS patients do not confound the process of recovering these memories––is also unsupported by the evidence. Therapists can implant false memories of abuse. This process of “implanting memories” is partly due to the fact that biographical memory is a reconstructive process in which memories are not retrieved unchanged, but rather “reconstructed and elaborated by all kinds of subsequent influences.”
First, the therapist focuses on exceedingly prevalent, nonspecific symptoms that are both ontologically and epistemologically subjective. To many of these therapists, the “factoid” of sexual abuse is written in the patients’ symptoms. No memory of abuse or independent verification of abuse is required. “The inference of a history of childhood sexual abuse, based solely on adult mental behavioral symptoms, is impermissible on both scientific and logical grounds.” “Scientifically, such an inference is impermissible because there is no empirical evidence for a specific association between child-sexual abuse and these symptoms.” “But even if such associations were established empirically, the inference of childhood sexual abuse from adult psychological symptoms would remain logically impermissible because such an inference violates normative rules of deductive reasoning (it is, in fact, an example of the common logical error of affirming the consequent).”
Next, the therapist sets about to convince the patient that these problems have a single pathogenesis: childhood sexual abuse. To do this, RMS therapists use techniques well recognized for their ability to increase suggestibility and for their potential for creating pseudomemories, including: (1) hypnosis; (2) age regression; (3) guided visualization; (4) relaxation; (5) group processes; (6) role-playing; (7) leading questioning techniques; (8) teaching patients to classify frankly speculative or confabulated scenarios as memories; (9) sexualized dream interpretation; (10) body memory interpretation; (11) aggressive sodium amytal interviews; and (12) misleading bibliotherapy.
These are dangerous techniques. If an overzealous or unscrupulous therapist can implant false memories of a traumatic event such that the alleged victim begins to have intrusive memories of the supposed event, then a claim of PTSD can be manufactured from suggestion and fantasy, not from the result of fact. What is of concern is the apparent “observer bias” involved in those who diagnose these “disorders.” All scientifically oriented investigators are familiar with the phenomenon of “observer bias.” That is, the observers see what they want to see, not what is before their eyes. This bias is suspected to be at the bottom of many claims of recovered memories of sexual and physical abuse.
No better evidence exists on the play of observer bias than the kinds of “survivors” who profess to have repressed memories of abuse. There are four distinct groups of “survivors” involved in this repressed memory game: (1) the religious fundamentalists who believe that almost all females have been victims of satanic rituals; (2) the gender feminists who believe they have been victims of childhood sexual abuse by close male family members; (3) the science fiction trekkies who believe they have been abducted and sexually abused by space aliens; and (4) the counterculturalists under the influence of Eastern religions who believe in reincarnation and who believe they were abused in past lives. The belief of repressed memory therapists in satanic ritual abuse, alien abductions, and abuse in past lives constitutes the reductio ad absurdum in this entire therapeutic field.
A recent review of the literature for clinical studies on repression of childhood sexual abuse finds only four studies—all of which are seriously flawed, leading the reviewers, Drs. Pope and Hudson of the Harvard Medical School, to conclude:
“[P]resent evidence is insufficient to permit the conclusion that individuals can ‘repress’ memories of childhood sexual abuse . . .. This finding is surprising, since many writers have suggested that there is a high prevalence of repression in the population.
. . . .
“It might be argued that this dearth of studies is due to the difficulty of documenting trauma and demonstrating amnesia. But if repression affects even a small fraction of abused individuals, one would expect hundreds of thousands, if not millions, of current cases in the United States alone, and even larger numbers worldwide.”
B. Reliability of Diagnosing PTSD
1. Introduction
Reliability (or “precision”) refers to consistency among those who assess accuracy.
That is, “reliability” refers to (1) whether those who measure a variable agree from observation to observation or measurement to measurement on the values of that variable and (2) whether different clinicians measuring, examining, or assessing the same variable obtain similar values. Proffered clinical evidence is unreliable if a series of clinical assessments exist on an aspect of the diagnosis and these assessments are, for the most part, different.
Reliability does not imply validity. Simply, although phenomena such as symptoms are observed consistently, nothing guarantees that these symptoms in fact measure what they purport to measure. Even so, “reliability” is an indicator of “validity.” That is, if a symptom or sign is unreliable, it has questionable validity. For example, if our clocks did not generally agree with one another, we could not use them to measure time. Our clocks would not measure falsely; they would not measure at all.
Reliability, then, is a necessary but not a sufficient criterion for validity.
In fields such as psychology, where the symptoms and signs and diagnostic constructs are somewhat resistant to external validation, reliability or consistency between assessments becomes extremely important. So is, it follows, the measurement or determination of consistency. As a rule, determining the reliability of clinical assessments requires a study in “clinical epidemiology.” By means of such a study, a clinician can assess whether or not successive clinical observations of symptoms, signs, and test results are consistent. That assessment is often reported as the observed intraobserver agreement and the observed interobserver agreement. The range of such observed agreement would be from 0 percent (or none) to 100 percent (or complete agreement). In fact, it is most always less than 100 percent.
Yet it would be a mistake to equate the measured “observed agreement” with the “clinical agreement.” The two are different. Simply, a certain portion of the “observed agreement” is due to chance, not due to clinical skill or brute clinical facts. That portion of “observed agreement” beyond chance is called actual agreement. Ideally, “actual agreement” should equal potential agreement, the state of complete agreement. Yet that ideal is not usually achieved. The index of how well actual agreement beyond chance approximates potential agreement beyond chance is called “kappa.”
kappa = Actual Agreement Beyond Chance
Potential Agreement Beyond Chance
A kappa of 0 is the worst possible and of 1.0 is the best possible score. Some attach the following qualitative terms to kappas:
.0 – .2 = slight
.2 – .4 = fair
.4 – .6 = moderate
.6 – .8 = substantial
.8 – 1.0 = almost perfect to perfect
2. Multimodal Approach
Given the diagnostic category of PTSD as set forth in the DSM-IV, is that category “reliably” identified by psychiatrists and psychologists in those with PTSD? If it is not, then any particular diagnosis of PTSD is unreliable and the PTSD construct or category itself will be unreliable, given that the gold standard whether someone has or does not have PTSD is still the clinical assessment of symptoms.
Maximizing diagnostic reliability is achieved through an approach to diagnosis called the multimodal approach.
This comprehensive approach to diagnosis incorporates information obtained from a variety of sources—clinical interviews, psychometrics, and psychophysiological assessment—allowing the diagnostician to consider the extent to which the results of these various measures converge on or diverge from a diagnostic hypothesis.
The challenge to a diagnosis of PTSD on the grounds that it is unreliable is often a viable and very important defense, perhaps the most important defense. When a plaintiff’s expert fails to use methods designed to enhance reliability, such as a structured interview, the defense should argue that the diagnosis is unreliable. To develop this line of attack, the defense should first establish the importance of the reliability of the diagnosis. Next, it should establish that various instruments have been developed to increase the probability of reliability in diagnosing PTSD. In doing so, the defense should emphasize the need for these instruments arising in the psychiatric field owing to a concern that diagnostic processes without them have been considered unreliable. But note this caution: merely because the plaintiff’s expert used a psychometric test to assess PTSD is no guarantee that the assessment is reliable. The psychometric test may lack the qualities considered necessary to make that test reliable. Then, finally, the defense should demonstrate that these instruments were not used in this case.
Following are the qualities of good psychometric tests: (1) high inter-rater reliability; (2) high test-retest consistency (rtt); (3) high internal consistency [the test will be internally consistent if each item measures the same variable; and the best measure of internal consistency is Cronbach’s alpha, which measures the average correlation between the set of test items and any other set measuring the same variable; ideally Cronbach’s alpha should be 1, a perfect correlation]; (4) low standard error of measurement; (5) good evidence of validity, especially construct validity; and (6) high discriminatory power [measured by Ferguson’s delta; a good test will emphasize individual differences and so show a large scatter of scores; when that occurs, delta approaches 1].
For every psychometric test, norms must be identified to establish the relationship of any individual score on that test to the scores of the normative population. These norms should be based on large and representative samples of the relevant population. And essential to accurate sampling is understanding the characteristics of the population sampled. Is that population the general population (in Detroit, Michigan; in Portland, Oregon?); Vietnam veterans; women who have been raped; firefighters; etc.?
Most psychometric instruments have been standardized on Vietnam combat veterans. So the defense then needs to establish that Vietnam combat veterans cannot be considered comparable to civilian populations.
It is also important to understand how the traumatic event was defined and what is the range of those traumatic events. And it is important to know what criteria were used to define PTSD: those in the DSM-III, DSM-III-R, or DSM-IV. The validity of measures of PTSD may also vary with type of trauma, co-morbid disorders, ethnic background, or chronicity.
3. Standardized Psychometric Instruments to Assess PTSD
A “psychometric instrument” is a device that has been standardized and validated to assess a particular psychological function or identify a particular psychological disorder.
A psychometric instrument may range (1) from a so-called “structured self-report measure,” a questionnaire like the MMPI-2; (2) to a structured series of questions to be asked in a patient interview; (3) to a neuropsychological test such as the Halstead-Reitan Battery; or (4) to a projective test such as the Rorschach inkblot.
Each of these kinds of instruments is available to aid in the diagnosis of PTSD. Yet a score on one of these psychometric instruments alone is not sufficient to warrant a diagnosis of PTSD. As indicated earlier, reliability in diagnosing PTSD is maximized through what is called a “multimodal” approach. This multimodal approach entails use of “multiple assessments, including information from multiple sources (self-report and family members) collected through multiple methods (interviews and psychometric measures) over multiple contacts.” An expert who fails to adopt the multimodal approach to diagnosis is cutting corners.
a. Structured Self-Report Measures
Self-report measures are questionnaires that the patient, with pen or pencil, answers. Many of these questionnaires have been standardized on samples of Vietnam veterans with combat-related PTSD. As a result, they cannot be assumed to apply to patients with civilian-related PTSD.
i. MMPI and MMPI-2
(A) Subscales
The Minnesota Multiphasic Personality Inventory (MMPI) has the Keane PTSD subscale (PK-MMPI), a well-researched subscale with reference to combat veterans, but not to civilian populations.
The PK Scale has 46 items that differentiate 100 male veterans with PTSD from 100 male veterans with psychiatric diagnoses other than PTSD. The PK-MMPI was researched in the context of the PTSD criteria of the DSM-III, however, not the DSM-III-R or DSM-IV. The Keane PTSD subscale has been reworked for use in the MMPI-2.
Besides the Keane PTSD subscale, the MMPI-2 also includes a new PTSD subscale, the Schlenger and Kulka PTSD scale (PS-MMPI-2).
The PS Scale has 60 items and was developed by contrasting item responses of healthy Vietnam veterans with PTSD. But this new subscale was not tested on civilian populations.
Clinicians should be very cautious of diagnosing any plaintiff with PTSD based on scores on these two subscales. A recent study of the validity of these two PTSD scales concluded as follows:
“We believe that it is important to construe the MMPI-2 PTSD scales as indices of general psychological distress and not simply of PTSD. When PK or PS are highly elevated, the presence of PTSD can be suspected as a possible source of distress, but PTSD should not be diagnosed on the basis of test performance alone.”
(B) Clinical Profile Analysis
Analysis of patterns of elevations of clinical scales of the MMPI sometimes helps to identify psychological disorders. Some work has been done to distinguish combat veterans with PTSD from control groups. In one study, a pattern of 8-2/2-8 clinical scale evaluations distinguished combat veterans from controls.
Yet these findings do not confidently apply to civilian PTSD populations.
ii. Millon Clinical Multiaxial Inventory
(A) MCMI and MCMI-II
The earlier MCMI and MCMI-II lacked a PTSD scale. As a result, PTSD symptoms were easily misinterpreted as evidence of a dysfunctional personality. The MCMI and MCMI-II are best used to establish personality disorders co-morbid with PTSD.
(B) MCMI-III
Millon Clinical Multiaxial Inventory is now in its third version, the MCMI-III. The MCMI-III contains a PTSD scale (the R scale within the “clinical syndromes” group). Although the PTSD scale is loosely tied to the DSM-IV criteria, it includes a majority of items not directly associated with diagnostic criteria in the DSM-IV, such as items examining sadness, feelings of worthlessness, and rapid mood changes. Only 6 of 16 R scale items actually tap current PTSD criteria. For these and other reasons, PTSD cannot be diagnosed based solely on an MCMI-III R score.
iii. Mississippi Scale for PTSD
(A) Mississippi Scale for Combat-Related PTSD
The Mississippi scale for combat-related PTSD is a 35-item instrument developed to measure PTSD in combat veterans.
It has excellent reliability for detecting combat-induced PTSD.
(B) The Civilian Mississippi Scale (CMS)
The Civilian Mississippi Scale was developed to assess PTSD in civilian populations.
It contains 11 re-experiencing and situational avoidance items, 11 withdrawals and numbing items, 8 arousal items, and 5 guilt and suicidality items.
(C) Revised Civilian Mississippi Scale (RCMS)
The RCMS has 30 items. It is anchored in undefined past trauma, referred to “as the event.” All items are rated on a 5-point scale (1 = not at all true; 5 = extremely true). Research is still needed, however, to assess the convergent and divergent validity of these scales.
iv. Impact Event Scale
(A) Impact Event Scale
Although widely used, the Impact Event Scale (IES) was developed in response to the PTSD criteria of the DSM-III.
So the IES taps intrusive and avoidant, but not hyperarousal, symptoms. Because it does not assess all PTSD criteria, it cannot establish a diagnosis. If used, the IES should be considered only a screen for the presence of non-arousal-related posttraumatic stress.
(B) Impact Event Scale––Revised
The IES-R contains six new hyperarousal items and an additional item to parallel DSM-IV criteria.
Both IES and IES-R were developed as research measures and lack the requisite normative data associated with modern clinical tests.
v. Penn Inventory
The Penn Inventory for PTSD is a 26-item scale.
Each item is composed of four sentences scored 0 to 3 representing different levels of a feeling or thought. This inventory is not validated on civilian PTSD populations. And further research is needed to document its overall utility.
vi. Symptom Checklist-90 (SCL-90)
The SCL-90 is widely used.
It is a 90-item self-report symptom inventory. All items are scored on a 5-point scale (0 = not at all; 4 = extremely). A 28-item scale has been derived from the 90 items that discriminates between crime victims with and without PTSD, referred to now as the CR-PTSD scale. It is reliable, but not yet validated. Until it is independently validated, its precision for measuring PTSD remains uncertain.
vii. Los Angeles-Symptom Checklist (LASC)
LASC is a 43-item measure of posttraumatic stress.
Seventeen of these items measure the re-experiencing, avoidance, and hyperarousal criteria of PTSD as defined in the DSM-III-R. Symptoms are rated by how much they are a problem (0 = no problem; 4 = extreme problems). A PTSD diagnosis is “suggested” if the relevant symptoms are endorsed at a “2” or higher. LASC should be used only to screen for, not to diagnose, PTSD.
viii. PTSD Symptom Scale – Self-Report
(A) PTSD Symptom Scale – Self-Report (PSS- R)
PSS-SR is a 17-item measure designed to assess PTSD symptoms in rape victims.
All 17 items are related to rape. Responses to the items are on a 4-point scale (0 = not at all; 3 = very much).
(B) Modified Symptom Scale – Self-Report (MPSS-SR)
The MPSS-SR is designed for general trauma populations.
ix. Posttraumatic Stress Diagnostic Scale (PDS)
The PDS was designed to adopt the PSS-SR for general clinical use.
It is considered “an excellent choice as a PTSD screener.” It has four parts: part I surveys exposure to traumatic events; part II examines characteristics of what the respondent believes was the most traumatic event; part III lists DSM-IV symptom criteria; and part IV considers how the symptoms have interfered with daily activities.
x. Purdue PTSD Questionnaire
(A) Purdue PTSD Questionnaire (PTSD)
The Purdue PTSD is a 15-item measure keyed to the DSM-III PTSD criteria and is designed to measure combat-related PTSD.
(B) Purdue PTSD Questionnaire – Revised (PPTSD-R)
The PTSD-R has 17 items keyed to the DSM-III-R PTSD criteria. It is designed to tap PTSD in general trauma populations.
b. Clinical Structured Interviews
A common way to assess whether someone has PTSD is for the psychiatrist or psychologist, with the DSM-IV criteria for PTSD in mind, to ask the person a series of questions about her history and current cognitive, behavioral, and emotional status. And then, with that information, the diagnostician decides, based on a “clinical impression,” whether the patient has PTSD. This diagnostic process is considered outdated and “unreliable.”
Diagnostic state of the art is the “structured” interview, a set or series of structured questions posed by an examiner to the patient.
These structured interviews ideally increase the likelihood of covering all relevant symptoms and thereby decrease the chance of diagnostic error. Questions in these structured interviews are dictated by internally logical or consistent rules that govern the content of the questions, the order in which the topics are covered, and the specific kinds of information sought.
Yet not all these interviews link specific traumatic events to specific traumatic symptoms. For an accurate DSM-IV diagnosis, at least one trauma must be specifically associated with all required diagnostic symptoms. In any event, nationally recognized experts on PTSD, in critiquing studies about PTSD, have criticized many of these studies for using clinical instead of structured interviews. As a result, on the basis of these written critiques, a forensic expert who fails to use a structured interview may be impeached on cross-examination.
i. Structured Clinical Interview (SCID)
SCID is the most thoroughly researched and widely used structured clinical interview. Accordingly, among structured interviews, it is considered the “gold standard.”
It has high inter-rater reliability. And it is strongly correlated with other psychometrically generated indices of PTSD, such as the Mississippi Scale, Impact of Event Scale, and Keane PTSD Scale of the MMPI. The limitation of SCID for diagnosing PTSD is that it yields only dichotomous information about the presence or absence of each symptom criteria. Moreover, formal, large-sample psychometric studies have not been performed on the SCID-PTSD module. It has been “validated” only on smaller samples of Vietnam combat veterans.
ii. Clinician-Administered PTSD Scale (CAPS)
An increasingly popular instrument, CAPS consists of 17 clinician-administered questions to assess the frequency and intensity of the DSM-III-R and DSM-IV symptoms of PTSD.
It has a 5-point (0 to 4) rating scale. Frequency and intensity ratings may be summed for each symptom to yield a severity score (0 to 8) and across symptoms to yield scores for the re-experiencing, avoidance and numbing, and hyperarousal clusters. A total PTSD severity score may be computed by summing across ratings for all 17 symptoms. CAPS, however, was validated on Vietnam combat veterans. It has not been validated on civilian PTSD populations.
iii. Posttraumatic Stress Disorder Interview (PTSD-I)
This interview, developed using the criteria of the DSM-III-R, was validated on male Vietnam combat veterans.
It has not been validated on civilian PTSD populations. PTSD-I is able to provide both dichotomous diagnostic decisions and continuous data for the set of symptoms. But it cannot produce valid, lifetime diagnoses.
iv. Diagnostic Interview Schedule (DIS)
For PTSD, this interview is not reliable and has not been validated on civilian populations. In a large sample study, DIS-PTSD module achieved a sensitivity of only 21.5, a specificity of 97.9, and a kappa of .26.
No forensic expert should be using the structured interview to diagnose PTSD.
v. Structured Interview for PTSD (SI-PTSD)
This interview is structured on the PTSD criteria in the DSM-III, not the DSM-III-R or DSM-IV. Whatever validity it has is confined to studies of combat veterans. A DSM-III-R version is available, but data on this version are sparse.
vi. Anxiety Disorders Interview–Revised PTSD Module (ADIS-R PTSD)
ADIS-R is not the best interview for PTSD. But it is helpful, in the process of differential diagnosis, in distinguishing PTSD from other anxiety disorders.
* * *
When interviewing a plaintiff, a forensic expert should be expected to use a structured interview. Currently the two interviews available are SCID-PTSD or CAPS revised for DSM-IV. Both are validated on Vietnam combat veterans and hence subject to criticism when applied to civilians. Yet that flaw is a lesser shortcoming than not using a structured interview.
* * *
c. Projective Techniques
Projective techniques consist of a set of ambiguous stimuli (such as an inkblot) that subjects are asked to describe or explain. The responses to these ambiguous stimuli are considered to indicate something about the psychological makeup of the individual rather than about the stimuli.
i. Rorschach Inkblot Test
The Rorschach inkblot test is a “projective” technique. It consists of ten standard inkblots, a set of relatively freeform stimuli to which the individual may respond in any manner chosen. The Rorschach is considered by some to be ideally suited for assessing PTSD in that it is believed to bypass conscious cognitive and affective experience or resistance and tap “unconscious” mental processes, revealing underlying anxiety.
A serious limitation of the Rorschach is that limited studies exist on civilian PTSD populations. Moreover, projective tests have poor reliability and validity and could never meet the criteria of scientific measurement as defined in the so-called “hard” sciences. Repeatedly, as a result, the scientific status of the Rorschach has been called into question.
ii. Stroop Interference Task
The Stroop Interference Task is also a projective technique. In this test, the patient is presented with words of varying emotional intensity printed in different colors. The patient is asked, under timed conditions, to name the colors of these printed words. When attention is directed only to the print color of the word, the meaning of the words impinges on the mind of the patient. Words with greater emotional impact take slightly longer to mentally process, thus slowing the patient’s report of the word’s print color. Inferences about the patient’s psychological functioning are drawn from these delayed responses.
Limited studies on this measure exist on civilian PTSD populations.
d. Questionnaires About Traumatic Events
A variety of questionnaires have been designed to inquire into Criterion A of PTSD.
i. Traumatic Events Questionnaire (TEQ)
The Traumatic Events Questionnaire inquires about 11 stressors.
These stressors are combat; large fires or explosions; serious industrial or farm accidents; sexual assault or rape; natural disasters; violent crimes; witnessing mutiliations, killings, or serious accidents; other life-threatening experiences; violent or unexpected death of a loved one; any other traumatic events; and an “event can’t tell” (an event so traumatic that the patient can’t describe it.)
ii. Traumatic Stress Schedule (TSS)
The Traumatic Stress Schedule inquires about ten potentially traumatic events.
These events are combat; robbery or theft involving force; physical assault; sexual assault; loss of a loved one through accident, homicide, or suicide; personal injury or property loss as a result of fire; personal or property loss as a result of severe weather or disaster; forced evacuation or otherwise learning of an imminent danger or hazard in the environment; a motor vehicle accident causing injury to one or more passengers; and any other event that is terrifying or shocking.
iii. Potential Stressful Events Interview
The Potential Stressful Events Interview has items about the type of stressor, the objective-behavioral characteristics of the stressor, and subjective reactions to the stressor.
Types of stressors evaluated are war-zone or combat experiences; serious accidents associated with motor vehicles, work, or elsewhere; natural disasters; serious illnesses; childhood sexual abuse; childhood sexual assaults; other forced sexual contact; aggravated physical assaults (i.e., involving a weapon); simple physical assaults; other situations involving serious injury; other situations involving fear of injury or death; witnessing serious injury or death; and other extraordinarily stressful events.
iv. Traumatic Events Scale (TES)
The Traumatic Events Scale (TES) assesses 30 interpersonal and environmental traumas.
Behaviors alleged to be traumatic stressors range from uninvited physical contact (kissing, hugging, patting, stroking, rape) to offensive verbal remarks (sexual allusions, dirty jokes, unsolicited phone calls) to nonverbal, nontouching behavior (leering, hand gestures, pictures or posters, graffiti).
C. Expertise to Diagnose PTSD
The nature of the expert’s qualifications has two basic ramifications. First, at the threshold is whether the expert is sufficiently qualified to diagnose PTSD. Second, across the threshold is the issue of the relative degree of expertise between the plaintiff’s expert and the defendant’s expert. That is, is the expert for one of the parties more impressively credentialed than the other?
1. Nature of Expertise
a. Mental Health Field
The expert should have expertise in the field of mental health. In that field, an expert is apt to be either a psychiatrist or a psychologist. A psychiatrist is a medical doctor who has had four years of college, four years of medical school, and some postgraduate training in the field of mental health. The psychiatrist may have an M.D. or a D.O. A psychologist has had four years of college and usually some graduate school. The psychologist could have a master’s degree or a Ph.D. in psychology. Psychoanalysts are usually psychiatrists or psychologists, although not necessarily, who have completed extensive advanced training in psychoanalytic theory and its methods of treatment.
Those with a Master’s in Social Work (MSW) are also appearing as experts to diagnose PTSD. Plaintiffs’ counsel have found that these mental health practitioners are inexpensive and malleable. Aggressive defense counsel should mount a Daubert challenge to the use of an MSW, as insufficiently schooled and trained to conduct a meaningful differential diagnosis as to PTSD.
The plaintiff’s expert could also be a physician who does not practice psychiatry. For instance, the expert could be a neurologist, board-certified in both neurology and psychiatry. A neurologist board-certified in psychiatry is not apt to have significant clinical experience in psychiatry let alone in specifically diagnosing PTSD, although defense counsel should expect most courts to allow them to testify about PTSD.
b. Clinical Experience
Whether the expert is a psychiatrist or psychologist, the expert should have clinical experience in diagnosing PTSD. As the DSM-IV notes, “the diagnostic categories, criteria, and textual descriptions [in the DSM-IV] are meant to be employed by individuals with appropriate clinical training and experience in diagnosis.”
c. Licensure
The expert should also be licensed to practice clinically in some state in the United States. Moreover, that clinical practice should have included or presently include the diagnosis of PTSD. Of course, implicit in that requirement is the further requirement that the expert’s clinical practice include diagnosing mental disorders that constitute the set of differential diagnoses for PTSD.
2. Levels of Expertise
Not only is the nature of expertise important but so also is the level or depth of that expertise in any effort to persuade judges and juries on relevant issues in the fields of psychiatry and psychology.
A recently licensed psychologist who has diagnosed PTSD in only one patient will obviously be less persuasive than a psychiatrist, all other things being equal, for whom PTSD has been a life’s work.
a. Board Certification
For the defense, if the expert is a physician, that physician should be board-certified.
Certification reflects a general level of expertise in psychiatry. If the plaintiff’s expert is not also board-certified, then the defense may exploit this difference in qualifications. A physician who is board-certified is different from a physician who is board-eligible. A physician who is board-eligible has completed the prerequisites posed by one or more of the 24 specialty boards, but has either failed the certification examination or declined to be examined.
In medicine, of the 24 American specialty boards, one is relevant in the clinical field of psychiatry.
This is the American Board of Psychiatry and Neurology. That board currently issues eight types of certificates. The certificates relevant in cases involving PTSD are psychiatry, child and adolescent psychiatry, and forensic psychiatry. A certificate in psychiatry is a prerequisite for obtaining a certificate in forensic psychiatry and child and adolescent psychiatry.
The examination for certification has two parts: (1) a written examination using the DSM-IV as the primary authority on psychiatric diagnostic nomenclature and (2) an oral examination divided into two one-hour examinations in clinical psychiatry.
The American Board of Professional Psychology (ABPP) awards a diploma for the psychologist who has demonstrated proficiency in the fields of industrial counseling, clinical or forensic psychology, and clinical neuropsychology. Reasons exist to discount the value of being board-certified or of being a diplomat in clinical or forensic psychology. But discounting those qualifications has no strategic value if the defense is also relying on those added qualifications, as it should be, to impress the jury. When one party has, as an expert, a psychiatrist and the other party has a psychologist, the party with the psychiatrist should exploit that difference. That is, the psychiatrist, having been trained as a physician, can be presented as someone with broader knowledge of the alternate diagnoses possibly responsible for the plaintiff’s symptoms.
The defense should explain in some detail the qualifications of its experts. The more explanation, the more likely the judge or jury will be to understand the significance of those qualifications. For instance, the typical exchange between attorney and physician over the physician’s qualification of board certification is as follows:
“Q: Doctor, are you board-certified in psychiatry?
“A: Yes, I have been board-certified since 1985.”
After this somewhat elliptical exchange, the jury, and many judges, may wonder about the meaning of board certification and why it’s significant. As a result, the defense should pursue the following, more elaborate explanation:
“Q: Doctor, are you board-certified in psychiatry?
“A: Yes.
“Q: Who issues the certification?
“A: The American Board of Psychiatry and Neurology.
“Q: Who is on the board?
“A: Psychiatrists and neurologists preeminent in their medical fields.
“Q: Why was the board established?
“A: That board was established to ‘establish and improve standards for the teaching and practice of psychiatry and neurology’ and to ‘improve the quality of health.’
“Q: When were you board-certified?
“A: I was board-certified in 1985.
“Q: What is board certification?
“A: Board certification in psychiatry and neurology is an acknowledgment by the American Board of Psychiatry and Neurology that I have attained a high level of knowledge in this medical specialty.
“Q: What specifically did you have to do to become board-certified?
“A: First I needed to have postgraduate medical training in an accredited program. Next I needed to pass a grueling written and oral examination.
“Q: Are all psychiatrists board-certified?
“A: No.”
b. Publications
The defense will want to impress the judge or jury with the depth of its expert’s knowledge by referring to the expert’s publications. Obtain a bibliography of articles the expert has published at least within the last ten years. Do the same for the plaintiff’s experts. The more publications on the issues in the litigation, the more qualified the expert will appear to be to the judge or jury. If, however, the focus of these articles in the bibliography of the plaintiff’s expert is on topics other than those involved in some aspect of the litigation, the defense will want to exploit that shortcoming.
Yet plaintiffs do appreciate the rhetorical value of an expert with publications on the litigated scientific and medical issues. In fact, plaintiffs’ experts often undertake concerted efforts to enhance their list of publications on those litigated issues solely for purposes of appearing more knowledgeable to the judge or jury. But be watchful for the expert with a resume of “duplicate” and “salami” publications. A “duplicate” publication occurs when the results of a single study appear in more than one journal. A “salami” publication occurs when small slices of the work are submitted as separate papers. Unfortunately, the psychological community appears particularly fond of duplicate and salami publications.
Also consider the articles that the plaintiff’s expert has cited as references in her own articles. Some of these articles may be helpful to the defense. As to those articles, at trial, the expert will have difficulty explaining why she can selectively choose articles’ bibliographies that support her opinion in court and disregard those that undermine that opinion.
“Q: Doctor, in 1987 you published an article in the American Journal of Psychiatry. True?
“A: Yes.
“Q: Today, you have cited that article in support of your opinion that defendant’s product, alphabet soup, causes an atypical disease you call ‘tangled mind syndrome.’ True?
“A: Yes.
“Q: In that same article, in the bibliography, you cite with approval an article by Dr. Derrida entitled ‘The Alpha & Omega of the Posttraumatic Stress Disorder.’ That article appeared in the peer-reviewed journal The New England Journal of Medicine. True?
“A: Yes.
“Q: In that article, which you found sufficiently authoritative to cite in support of your article, the author states that a case study is insufficient evidence to establish general causation. True?
“A: Well, I thought so then.”
c. Treating Psychiatrists or Psychologists
The treating psychiatrist is the plaintiff’s biased ally for therapeutic reasons. At the same time, ironically, the treating psychiatrist will be perceived by the jury as the more believable or unbiased expert witness. This irony is a problem for the defense. To overcome this difficulty, the defense will need to explain to the jury the nature of the therapeutic relationship between the plaintiff and the treating psychiatrist and why, for purposes of trial, that relationship impairs the objectivity of the treating physician. If the treating psychiatrist were objective, he or she would probably damage the painstakingly created “therapeutic alliance.” That is, the plaintiff would feel betrayed when information the plaintiff relayed to the psychiatrist that the plaintiff considers intimate and confidential is disclosed during the course of the expert’s testimony.
Ethically, treating psychiatrists are advised not to testify as forensic experts on behalf of a patient. For instance, the American Academy of Psychiatry and the Law advises that “a treating psychiatrist should generally avoid agreeing to be an expert witness or to perform an evaluation of his patient for legal purposes because a forensic evaluation usually requires that other people be interviewed and testimony may adversely affect the therapeutic relationship” (American Academy of Psychiatry and the Law 1991).
D. Failure to Satisfy Criteria of PTSD
1. One or More Criteria Not Satisfied
Most often, a challenge to a claim for PTSD will involve the defense that the plaintiff fails to satisfy one or more of the criteria of PTSD, as identified in the DSM-IV. Expect the plaintiff’s expert to describe attributes of the plaintiff’s cognition, emotion, or behavior that only facially satisfy the requisite diagnostic criteria. In this process, the plaintiff’s expert will probably describe an aspect of the plaintiff’s cognition, emotion, or behavior in the belief that that description satisfies the criteria when, in fact, it does not. For example, the plaintiff’s expert may testify that the plaintiff often reflects anxiously about the motor vehicle accident, with the expert expecting erroneously that that description satisfies Criterion B(1) requiring “recurrent and intrusive distressing recollections of the event.” Merely thinking or reflecting anxiously about the traumatic event is usually insufficient to meet the re-experiencing criteria. The plaintiff must experience unwanted, unbidden, and distressing memories of the event. For another example, the plaintiff may testify that his avoidance symptoms occurred initially a year from the time of the trauma, believing that he has thereby satisfied Criterion C. Although re-experiencing symptoms may develop months or years after trauma, avoidance symptoms have usually been present from the time of trauma.
2. Use of DSM-IV in Forensic Settings
Two aspects of the DSM make it a potent weapon in the hands of the overzealous or unscrupulous expert: (1) the DSM is only a “guideline” and (2) the priority of “clinical judgment” in diagnosing PTSD.
a. DSM Is Only a “Guideline”
The DSM-IV appears to establish necessary and sufficient or definitional criteria for a diagnosis. If a plaintiff satisfies the required criteria, she has the disorder; otherwise, she does not. Yet it is stated repeatedly in the DSM-IV that it is only a guideline.
So what appear in the DSM-IV to be definitional criteria are merely evidential, thereby providing the expert significant discretion in formulating a diagnosis. The DSM-IV notes that “the exercise of clinical judgment may justify giving a certain diagnosis to an individual even though the clinical presentation falls just short of meeting the full criteria for the diagnosis as long as the symptoms that are present are persistent and severe.”
A plaintiffs’ expert is always looking for ploys to water down the inclusionary criteria and thicken the exclusionary criteria of the disorder.
b. Subsyndromal PTSD
The term subsyndromal PTSD refers to a subset or subcluster of symptoms of PTSD. Technically, someone with subsyndromal PTSD does not have PTSD. Yet recognize that the full criterial set for PTSD in the DSM-IV is not definitional but evidential. So having the full set of criteria for PTSD is good evidence that the individual has “PTSD.” Having a subset of the criteria for PTSD is evidence but not good evidence that the individual has PTSD.
The defense needs to be alert to the clinician who too readily diagnoses PTSD when the plaintiff fails to fulfill all the required criteria under the DSM-IV. Obviously, when the clinician too readily diagnoses PTSD based on an incomplete set of symptoms, people without PTSD but with mood or anxiety disorders will probably be diagnosed with PTSD only for purposes of litigation.
3. Differentials Not Ruled Out
a. Differential Diagnosis
Many psychological maladies share symptoms with PTSD. For that reason, care is required to distinguish those psychological conditions from PTSD. That process is accomplished through a differential diagnosis. In general, differential diagnosis is a process––a systematic review of the clinician’s diagnostic hypothesis in light of the signs and symptoms––to determine whether that diagnostic hypothesis best fits those data. In this process, the clinician considers other diagnostic hypotheses––diseases or disorders that might apply––and with those hypotheses in mind looks for data, perhaps overlooked, that might satisfy those alternate diagnostic hypotheses.
b. Failure to Perform Differential Diagnosis
A diagnosis of PTSD can be undermined if the plaintiff’s expert failed to perform a differential diagnosis in the process of diagnosing PTSD. As a rule, assuming that the expert is properly qualified, the expert’s guiding principle is to assess how probable is each potential diagnosis given the plaintiff’s symptoms and signs, a thought process captured in the maxim that “common disorders occur commonly,” or, more metaphorically, “when you hear hoofbeats, think of horses, not zebras.”
c. Likely Differentials
A differential diagnosis should consider disorders that share some of the cognitive, emotional, and behavioral criteria of PTSD. On that basis, a differential diagnosis should consider the following alternate psychological conditions or disorders on both Axis I and Axis II of the DSM-IV.
On Axis I: (1) mood disorders; (2) anxiety disorders other than PTSD; (3) somatoform disorders; (4) adjustment disorders; (5) dissociative identity disorder; (6) attention-deficit hyperactivity disorder; (7) post-concussion syndrome; (8) bereavement; (9) drug and alcohol abuse; (10) brief reactive psychosis; (11) dissociative amnesia; (12) dissociative fugue; (13) schizophrenia; (14) depersonalization disorder; and (15) mixed anxiety-depressive disorder.
On Axis II: (16) borderline personality disorder; and (17) antisocial personality disorder.
i. Mood Disorders
PTSD may be characterized by (1) markedly diminished interest or participation in significant activities; (2) feelings of detachment or estrangement from others; and (3) restricted range of effect, as well as by (4) difficulty sleeping; (5) irritability; and (6) difficulty concentrating. Major depression can be characterized by similar symptoms, such as (1) markedly diminished interest or pleasure in all, or almost all, activities most of the day; (2) insomnia or hypersomnia; (3) psychomotor agitation; (4) diminished ability to think or concentrate.
So if someone with preexisting depression is exposed to a Criterion A stressor, that person could claim to have PTSD on the basis of the symptoms from the preexisting depression. It would be up to the clinician to rule out that preexisting depression before diagnosing PTSD. Moreover, an individual subject to a Criterion A stressor may develop depression rather than PTSD. So the clinician should also endeavor to rule out depression developing after exposure to the stressor.
ii. Anxiety Disorders
The anxiety disorders include panic attacks, phobias, obsessive-compulsive disorder, acute stress disorder, generalized anxiety disorder, and substance-induced anxiety disorder. Because anxiety is invariably present in PTSD, the clinician should rule out each of these anxiety disorders before diagnosing PTSD.
- Panic Attacks
There are three types of panic attacks: (1) unexpected; (2) situationally bound; and (3) situationally predisposed. Panic attacks that occur in “panic disorder” are “unexpected.” Panic attacks that occur in PTSD are situationally bound or predisposed in that the panic attacks are cued by stimuli recalling the stressor.
- Phobias
A specific phobia is a marked and persistent fear (and avoidance) of clearly discernible, circumscribed objects or situations. In contrast to the kind of avoidance characterizing specific phobia, the avoidance in PTSD follows a life-threatening stressor and is accompanied by additional features such as re-experiencing the trauma and restricted affect.
- Obsessive-Compulsive Disorder
In obsessive-compulsive disorder, the recurrent intrusive thoughts are experienced as inappropriate and are not related to an experienced traumatic event.
- Acute Stress Disorder
Acute stress disorder (ASD) is distinguished from PTSD in that in ASD the symptoms occur and resolve within four weeks of the traumatic event.
(E) Generalized Anxiety Disorder
Generalized anxiety disorder (GAD) is characterized by relatively persistent excessive anxiety and worry for a period of at least six months accompanied by at least three additional symptoms such as restlessness, being easily fatigued, difficulty concentrating, irritability, and disturbed sleep. Many of these symptoms also occur in PTSD. So GAD could be erroneously labeled as PTSD. But GAD is not diagnosed if the anxiety occurs exclusively during the course of PTSD.
iii. Somatoform Disorders
As in PTSD, in somatization disorder, symptoms may include hallucinations and dissociative symptoms such as amnesia. But unlike somatization disorder, PTSD requires, in addition to a severe trauma, persistent symptoms of increased arousal and persistent avoidance of stimuli associated with the trauma.
iv. Adjustment Disorders
An adjustment disorder is the development of clinically significant emotional or behavioral symptoms within three months after onset of any identifiable psychosocial stressor. The symptoms must resolve within six months of the termination of the stressor. PTSD is characterized by the presence of an extreme stressor and a specific constellation of symptoms, and may not develop within three months after onset of the stressor and may not resolve within six months of termination of the stressor.
v. Dissociative Identity Disorder
Dissociative identity disorder (DID) is characterized by the presence of two or more distinct identities or personality states each with its own relatively enduring pattern of attributes, involving perceiving, relating to, and thinking about the environment and self. A feature of DID is amnesia, a symptom that may be present in PTSD. Those with DID may also manifest posttraumatic symptoms such as nightmares, flashbacks, startle responses, or full-blown PTSD.
vi. Attention-Deficit Hyperactivity Disorder
Attention-deficit hyperactivity disorder (ADHD) is characterized by a persistent pattern of inattention or hyperactivity—that is, by impulsivity that is more frequent and severe than is observed in individuals at a comparable level of development. Symptoms of hyperactivity, impulsivity, or inattention that cause impairment must have been present before age seven. PTSD is characterized by persistent symptoms of increased arousal manifested as irritability or outbursts of anger, difficulty concentrating, hypervigilance, or exaggerated startle response. But unlike the symptoms of ADHD, these symptoms occur in the context of a trauma.
vii. Post-Concussion Syndrome
Post-concussion syndrome (PCS) is characterized by an acquired impairment in cognitive functioning, accompanied by specific neurobehavioral symptoms that occur from closed head injury of sufficient severity to produce a significant cerebral concussion. The concussion may be manifested by loss of consciousness, posttraumatic amnesia, and, less commonly, posttraumatic onset of seizures. PTSD is characterized by many of the same kinds of symptoms and behaviors. Given that both disorders occur in the context of a trauma, PCS might be confused with PTSD. In PTSD, the differentiating factor is likely to be Criterion B, that the traumatic event be persistently re-experienced in one of a variety of possible ways.
viii. Bereavement
Bereavement is catalogued in the DSM-IV under “Additional Conditions That May Be a Focus of Clinical Attention.” Bereavement is used when the focus of clinical attention is a reaction to the death of a loved one. Some of the symptoms of bereavement include those present in PTSD, such as hallucinations, insomnia, markedly diminished interest in significant activities, and difficulty concentrating. If the death of the loved one was attendant to a traumatic stressor under Criterion A of PTSD, then bereavement may be confused with PTSD if PTSD does not also develop.
ix. Drug and Alcohol Abuse
Drug and alcohol abuse can result in a variety of disorders that share symptoms or behaviors with PTSD. Substance and alcohol abuse can induce amnesia, hallucinations, mood disorders, and anxiety disorders. All these symptoms may also be present in someone with PTSD.
x. Brief Psychotic Disorder
Brief psychotic disorder is a disturbance that involves the sudden onset of at least one of the following psychotic symptoms: delusions, hallucinations, disorganized speech, or grossly disorganized or catatonic behavior. PTSD is characterized by hallucinations in which the individual acts or feels as if the traumatic event were recurring. PTSD is distinguishable from brief psychotic disorder in that PTSD occurs in the context of a trauma and is attended by other symptoms and behaviors such as persistent avoidance of stimuli associated with the trauma and persistent symptoms of increased arousal.
xi. Dissociative Amnesia
Dissociative amnesia is characterized by an inability to recall important personal information, usually of a traumatic or stressful nature, that is too extensive to be explained by normal forgetfulness. In PTSD there can be amnesia for the traumatic event. If the amnesia occurs during the course of PTSD, dissociative amnesia is not diagnosed.
xii. Dissociative Fugue
Dissociative fugue is characterized by sudden, unexpected travel away from home or one’s customary place of work, accompanied by either an inability to recall one’s past and confusion about personal identity or the assumption of a new identity. PTSD is a constellation of symptoms that may coexist with dissociative fugue.
xiii. Schizophrenia
Schizophrenia is characterized by certain symptoms such as delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior, affective flattening, “alogia” (an impoverishment in thinking inferred from observing speech), or “avolition” (an inability to initiate and persist in goal-directed activities) that have a duration of at least a month and that interfere with social or occupational functioning. PTSD may also involve hallucinations, affective flattening, avolition, and disorganized behavior.
xiv. Depersonalization Disorder
Depersonalization disorder is characterized by persistent or recurrent episodes of “depersonalization,” defined as a feeling of detachment or estrangement from oneself. Depersonalization is a common experience, and depersonalization disorder should thus be diagnosed only if the symptoms are sufficiently severe to cause marked distress or impairment in functioning. Because depersonalization is associated with many other mental disorders such as PTSD, depersonalization disorder should not be diagnosed separately when the symptoms occur only during a panic attack or as part of PTSD.
xv. Mixed Anxiety-Depressive Disorder
Mixed anxiety-depressive disorder is characterized by a persistent or recurrent dysphoric mood lasting at least one month accompanied by additional symptoms that also must persist for at least one month, including at least four of the following: concentration or memory difficulties, sleep disturbance, fatigue or low energy, irritability, worry, being easily moved to tears, hypervigilance, anticipating the worse, hopelessness or pessimism about the future, and low self-esteem or feelings of worthlessness.
PTSD is characterized by symptoms and behaviors found in both depression and anxiety disorders. PTSD would be distinguishable from mixed anxiety-depressive disorder by Criterion B in which the traumatic event is persistently re-experienced in a variety of ways. Even so, it would be difficult to differentiate someone who had mixed anxiety-depressive disorder and who experienced a traumatic event, minor or otherwise, from someone who had genuine PTSD.
xvi. Borderline Personality Disorder
Borderline personality disorder (BPD) is characterized by a pervasive pattern of instability of interpersonal relationships, self-image, and affects, and marked impulsivity beginning in early adulthood and present in a variety of contexts. Among the possible indicia of BPD are the symptoms of transient stress-related dissociation, frequent displays of temper, and affective instability due to a marked reactivity of mood, including anxiety.
PTSD is often characterized by dissociation, outbursts of anger, and affective instability. Unlike BPD, PTSD requires a traumatic event and that the traumatic event be persistently re-experienced. If an individual with BPD were to be subjected to a traumatic event, however, it would be difficult to determine whether that event resulted in PTSD or merely occurred in the context of BPD.
xvii. Antisocial Personality Disorder
Antisocial personality disorder (APD) is characterized by a pervasive pattern of deceit and manipulation, beginning in childhood and continuing into adulthood. APD is similar to narcissistic personality disorder in that people with each disorder tend to be tough-minded, glib, superficial, exploitative, and unempathic. But unlike those with NPD, those with APD are not as needy for the admiration and envy of others. APD is also similar to BPD in that each is characterized by an attempt to manipulate, but those with BPD manipulate to gain nurturance, whereas those with APD manipulate to gain power and profit.
Because APD is characterized by impulsivity and irritability, characteristics also found in those with PTSD, APD should be ruled out in diagnosing PTSD. APD and PTSD can coexist in an individual, but when an individual is diagnosed with APD, the prospect of malingered PTSD should be considered before diagnosing PTSD.
d. Bayes’ Theorem
As is apparent from the foregoing, diagnosis is complicated by the fact that a set of symptoms may not be “specific” for any particular disorder, but may instead be a manifestation of any number of different disorders. The diagnostician’s art is in being able to determine out of this array of possible disorders which, if any, apply to this particular patient. So the diagnostician’s principal inquiry is, what is the probability of this particular diagnostic hypothesis given these symptoms? This inquiry may be symbolized as follows: Pr(DH|S), with “Pr” representing “probability,” “DH” representing “diagnostic hypothesis,” the vertical line representing “given” what follows or “assuming the truth of” what follows, and “S” representing symptoms found in this particular patient.
The defense and jury should realize that Pr(DH|S) does not equal Pr(S|DH). Pr(S|DH) represents the probability of the symptoms occurring assuming the truth of the diagnostic hypothesis. That is, if 100 patients are known to have the disorder prescribed by the diagnostic hypothesis, how many of the 100 patients have the particular symptoms described by S? If, say, 90 patients have those particular symptoms, the probability of these symptoms given the disorder is 90 percent. But from this it is not correct to infer that if those symptoms are found in a patient, it is 90 percent probable that she has the disorder. That is, it is not correct to infer Pr(DH⎪S). Despite the invalidity of that inference, that is the inference most people would tend to draw.
What the diagnostician seeks is Pr(DHS). That probability can often be assessed with Bayes’ Theorem. Bayes’ Theorem is a fundamental tool of “inductive inference,” providing a way to reason backward from effects (evidence such as signs and symptoms) to their causes (trauma). It offers a powerful and uniform way of thinking about the extent to which evidence confirms a theory of causation. What follows is the general form of Bayes’ Theorem:
Pr(DH|S) = Pr(S|DH)Pr(DH)
Pr (S)
In this theorem, Pr(DH|S) is the conditional probability of the diagnostic hypothesis (DH) being true given the evidence or symptoms (S). (This conditional probability can be thought of as the probability-of-DH-on-the-assumption-that-S-is-true.) This probability is known as the posterior probability. Pr(DH) is the probability of the diagnostic hypothesis before the events causing the symptoms. This probability is known as the prior probability or “base rate.” That is, it is the probability of the diagnostic hypothesis in the absence of the subsequently developing symptoms. Pr(S) is the probability of the symptoms. That is, it is the probability of observing this evidence. Pr(S|DH) is the “conditional probability” of the symptoms being true, assuming that the diagnostic hypothesis is true. This probability is known as the likelihood.
Bayes’ Theorem is more easily understood if expressed in terms of “odds” rather than in terms of “probability.” Here is the odds ratio form of Bayes’ Theorem:
Post evidence odds = Pre-evidence odds x Likelihood ratio
The pre-evidence odds of the disorder is the probability before the evidence that the plaintiff has the disorder divided by the probability before the evidence that the plaintiff does not have the disorder. The “likelihood ratio” (LR) measures the contribution of the evidence. When the evidence is present, the likelihood ratio is the true positive rate divided by the false positive rate. If the evidence is absent, the likelihood ratio is the false negative rate divided by the true negative rate. The post-evidence odds of the disorder is the product of the pre-evidence odds of the disorder and the likelihood ratio. The probability of the disorder given the evidence is the quotient of the post-evidence odds divided by 1 plus the post-evidence odds.
If Pr(DH) is low, Pr(DH|S) may be low even if Pr(S|DH) is high. For example, if the likelihood of the evidence given the plaintiff’s diagnostic hypothesis [Pr(S|DH)] is 80 percent and the prior probability or “base rate” of that hypothesis is, generously stated in favor of the plaintiff, 1 percent, then the probability of that hypothesis being true given the evidence is .8 multiplied by .01 or .008 or, in terms of percentage, .8 percent. That is a very unimpressive number. If, for the sake of argument, the likelihood of the evidence given the defendant’s diagnostic hypothesis is only 20 percent and the prior probability of that hypothesis is, conservatively stated, 10 percent, then the probability of that hypothesis being true given the evidence is .2 multiplied by .10 or .02 or, in terms of percentage, 2 percent. Obviously, the probability of the defendant’s hypothesis being true (2 percent) is significantly greater than the probability of the plaintiff’s hypothesis being true (.8 percent) given the available evidence.
Now, if the plaintiff were to demonstrate that the likelihood of the evidence given its hypothesis was 90.55 percent assuming the same value for the base rate, the probability of its hypothesis being true given the evidence would be .9055 multiplied by .01 or .009055 or, in terms of percentage .905 percent, and the probability of the defendant’s hypothesis being true given the evidence would be .0945 multiplied by .10 or .00945 or, in terms of percentage, .945 percent. Still, even on these terms, the probability of the defendant’s hypothesis being true given the evidence is greater (although by a very small amount) than the probability of the plaintiff’s hypothesis being true.
e. The Problem of Co-morbidity
The stressors that lead to PTSD place an individual at risk for developing psychiatric disorders related to but distinct from PTSD. “One of the most consistent findings in studies of PTSD . . . is that the great majority of sufferers fulfill the diagnostic criteria for other disorders in addition to those for PTSD.” These related but distinct psychiatric disorders include anxiety disorders, mood disorders, substance abuse disorders, somatoform disorders, and personality disorders. So expect that whenever the defense asserts that the plaintiff’s symptom profile is consistent with a mental disorder other than PTSD, the plaintiff will respond that the mental disorder is “co-morbid” with PTSD and probably the result of the traumatic stressor or the result of the plaintiff’s having to endure the symptoms of PTSD. “Co-morbidity” is defined as the concurrent occurrence of two or more mental disorders.
Also expect that whenever the defense responds that the mental disorder preexisted the traumatic stressor, the plaintiff will assert that the symptoms were risk factors predisposing the plaintiff to PTSD when the plaintiff eventually encountered the traumatic stressor.
f. Incidence and Prevalence of PTSD
Knowing the incidence and prevalence of PTSD is important in assessing the likelihood that a diagnosis of PTSD is valid. When a number of possible diagnoses may accommodate the patient’s clinical findings or profile, the diagnostician may need to assess the likelihood of each possible diagnosis. To do that, the diagnostician will need to know the prevalence of the alternative diagnosis in the relevant population. This is the “prior probability” or “base rate” of the disorder. With those data on prevalence and with Bayes’ Theorem, the diagnostician may then determine which of the alternate diagnoses is most likely.
Studies of the prevalence of PTSD may examine two kinds of populations: (1) populations at risk, such as combat veterans and disaster victims, and (2) the general population. Rates of PTSD in individuals exposed to trauma range from 5 percent to 11 percent. “Current rates” of PTSD in nonveterans is estimated to be 1.2 percent in men and 0.3 percent in women. And the “lifetime prevalence” of PTSD in the general population is estimated to be 8 percent.
- Man-Made Disasters
5 percent
- Large-Scale Transportation Accidents
12 percent
- Emergency Worker Exposure to Trauma
3–32 percent
- Rape and Sexual Assault
12–14 percent
- Spousal Battery
13 percent
- Child Abuse
6–62 percent
- Witnessing Death or Serious Injury of Family Member or Friend
Male Vietnam Veterans 15 percent
Female Vietnam Veterans 9 percent
- Violent Crimes, Deaths, or Accidents
7–11 percent
- Motor Vehicle Accidents
8–46 percent
* * *
4. Malingering
“… the lady doth protest too much.”
Shakespeare
a. Introduction
For the most part, an assumption underlying the process of diagnosis in the DSM is that the patient, when relating her symptoms, is motivated to tell the truth. Yet in some contexts, including cases in which the claimant alleges PTSD, that assumption is unrealistic. And so the DSM provides that in considering the diagnosis of PTSD, the diagnostician must rule out malingering in situations involving financial remuneration, benefit eligibility, and litigation.
Although the incidence of malingered psychiatric symptoms after injury is unknown, follow-up studies on people considered 100 percent disabled indicate that about 40 percent of those showed no disability whatsoever one year after determination of their disability.
So it is safe to assume that “malingering” plaintiffs are legion. If evidence of “faking bad” (that is, trying to appear impaired) exists, then no conclusions should be drawn about any dysfunction.
b. Definition of “Malingering”
The term “malingering” has a specific meaning in the DSM. “The essential feature of malingering is the intentional production of false or grossly exaggerated physical or psychological symptoms, motivated by external incentives, such as avoiding military duty, avoiding work, obtaining financial compensation, evading criminal prosecution, or obtaining drugs.”
Be careful to distinguish between “pure malingering,” “partial malingering,” and “false imputation.” “Pure malingering” is the feigning of disease when it does not exist at all. Pure malingering is uncommon in PTSD. “Partial malingering” is the conscious exaggeration of existing symptoms or the fraudulent allegation that prior genuine symptoms are still present. Partial malingering is quite common. In PTSD, “false imputation” is ascribing actual symptoms to a cause consciously recognized as having no relationship to the symptoms.
c. Labeling Plaintiff as a Malingerer
Most treating physicians or psychologists do not even try to rule out malingering. Treating physicians or psychologists accept the patient’s word and if they have suspicions are loath to disclose them. Simply, physicians, especially psychiatrists, are usually taught to sympathize with and believe their patients. This attitude is usually consistent with the physician’s objective to treat the patient, not to thwart the patient’s economic interests. When a physician has doubt about what a patient has said, the physician will have a tendency to presume dysfunction, not malingering. That is, for physicians it is worse to overlook a disorder than to overdiagnose it, unless the appropriate treatment is dangerous. Moreover, most physicians realize that if they do not adopt this attitude, many patients will leave them. So if a physician believes that a patient is malingering, he will merely not provide her with the standard treatment, and send her away, without creating an embarrassing entry in the patient’s chart that the patient is malingering. Clinicians are also reluctant to label someone a malingerer for fear of legal liability. To avoid that pitfall, clinicians are cautioned to merely state that no objective evidence exists to support the claimant’s subjective complaints.
Even so, when clear evidence of malingering is presented, the clinician should characterize the plaintiff’s behavior as malingering. Clear evidence is provided (1) when, while the patient believes he is unobserved, he is caught doing what he claimed he could not do; or (2) when the patient actively confesses that he is faking.
d. Detecting Malingering
Detecting malingering or faking often involves nothing more than assessing whether the plaintiff’s behavior is other than what would be expected in the circumstances. Satisfactorily determining whether the plaintiff’s behavior is inconsistent with expectations requires some time observing how the plaintiff behaves in appropriate circumstances. Unfortunately, usually only a limited opportunity exists to observe the patient by the jury, by the defendant’s expert, or by the plaintiff’s nontreating expert. Even if the plaintiff’s expert observes such behavior, she will not expose the plaintiff. The plaintiff’s nontreating expert not only will not attempt to detect malingering, but too often will be a willing conspirator in promoting the plaintiff’s malingering in an effort to achieve monetary recovery in litigation. The only check on malingering is the defendant’s lawyer or medical or psychological expert.
i. Red Flags
Malingering should be strongly suspected if any combination of the following is noted: (1) poor work record; (2) prior incapacitating injuries; (3) discrepant capacity for work and recreation; (4) unvarying, repetitive dreams; (5) antisocial personality traits (not necessarily full-blown APD); (6) overidealized functioning before trauma; (7) evasiveness; (8) inconsistency in symptom presentation; (9) lack of cooperation during the diagnostic evaluation and in complying with the prescribed treatment regimen; (10) marked discrepancy between the person’s claimed stress or disability and the objective findings; and (11) medicolegal context of presentation (e.g., the person is referred by an attorney to the clinician for examination).
For example, with respect to item (4), malingerers are unlikely to volunteer information about nightmares. But when they do, they tend to claim that they have repetitive dreams, which always reenact the traumatic event in exactly the same way. Genuine nightmares from trauma usually show variations on the theme of the traumatic event.
ii. Other Indicia of Malingering
A number of tests for malingering have been developed in some standard neuropsychological tests or batteries of tests.
For instance, usually in a psychological or psychiatric IME, the plaintiff will be given an MMPI. (Nowadays, however, the MMPI-2 is the test commonly administered.) The MMPI can be used to establish malingering in PTSD; indeed, it is the most validated psychological test to ascertain malingered mental illness. It can help distinguish claimants with true PTSD from those with functional disorders.
Also review the plaintiff’s answers to the MMPI test questions for inconsistencies. For example, the examinee may be malingering if she has testified that she has not abused alcohol, but answers yes to questions 264 and 489 in the MMPI-2: (264) “I have used alcohol excessively” and (489) “I have a drug or alcohol problem.”
Through your consulting expert, develop the significance of the various scales on those tests that expose malingering. These scales are as follows:
> MMPI:
? Scale > 30 raw score points
T-R Index > 4
Carelessness Scale > 4
F Scale > 15
Lacher & Wrobel Critical Items > 83
Wiener & Harmon Obvious and Subtle Items
Wales & Seeman Obvious Items > 99 and Subtle Items < 46
Dissimulation (Ds) raw score > 21
> MMPI-2:
F Scale
Back-Page F Scale (Fb) T-Score > 80
True Response Inconsistency Scale raw score > 12
Lees-Haley Fake Bad Scale > 20
Assessing the validity of the plaintiff’s responses to the items of the MMPI-2 involves three basic steps.
First, the total number of items that the plaintiff fails to answer is ascertained. If the plaintiff omits more than 30 items, the “profile,” as it is called, is probably invalid. Second, if the plaintiff has answered an acceptable number of items, the “consistency” with which the plaintiff answered the items in the MMPI-2 is then ascertained. (Consistency in endorsing items verifies that the plaintiff has endorsed the items reliably; the items must be answered consistently before determining the accuracy with which the plaintiff has answered the items.) Third, if the plaintiff passes the preceding two steps, the “accuracy” of the answers must be verified.
Consistency measures devised for the MMPI-2 are the Variable Response Inconsistency Scale (VRIN) consisting of semantically similar pairs of items and the True Response Inconsistency Scale (TRIN) consisting of item pairs that are opposite in content but keyed in the same direction.
(A) Variable Response Inconsistency Scale (VRIN)
VRIN consists of 67 pairs of items that have similar or opposite item content.
These pairs of items are scored if the plaintiff is inconsistent in responding to them. When the scores on VRIN are 7 or lower, or 16 or higher, a high probability exists that the client has answered or endorsed the items consistently or inconsistently, respectively.
(B) True Response Inconsistency Scale (TRIN)
TRIN consists of 23 pairs of items.
TRIN is similar to VRIN except that the scored response is either true or false to both items in each pair of items. High scores on TRIN reflect plaintiffs who tend to be “yea-sayers” and low scores reflect plaintiffs who are “nay-sayers” regardless of item content. Scores on TRIN are not used to determine whether the plaintiff has answered the items consistently.
It is very difficult for plaintiffs to fake the MMPI-2 as if they have a “specific” mental disorder. So plaintiffs answering the items inaccurately will usually over-report psychopathology in general rather than specifically. Over-reporting of psychopathology on the MMPI-2 can be assessed by the “Obvious and Subtle” subscales, Critical items, the F and FB Scales, and the F-K Dissimulation Index.
(C) Wiener and Harmon Obvious and Subtle Subscales
On five scales in the MMPI-2, the items to be endorsed can be classified as either items indicating obvious emotional disturbance or items subtle (not obvious) for emotional disturbance. Plaintiffs who over-report emotional disturbance will tend to answer the obvious but not the subtle items as indicating emotional disturbance. Those five scales on the MMPI are 2(D), 3(Hy), 4(Pd), 6(Pa), and 9(Ma). A plaintiff who achieves T scores of 80 or more on all five obvious scales and T scores near 50 on all five subtle scales is trying to over-report. The T scores for each of the obvious and subtle subscales is calculated, their difference is determined on each clinical scale, and these differences are totaled into a single overall measure. A total T score difference above whatever criterion is used to identify over-reporting of psychopathology is presumptive rather than definitive evidence of over-reporting. Beyond that criterion, it is necessary to verify that the plaintiff is over-reporting psychopathology rather than actually experiencing severe psychopathology.
(D) Lachar and Wrobel Critical Items
A set of “critical items” is thought to require careful scrutiny if answered in the deviant direction. A plaintiff who is trying to over-report psychopathology would be expected to endorse a large number of these items. Normal individuals endorse 16 to 23 percent of these critical items on average, whereas psychiatric patients endorse 32 to 36 percent on average.
- F-K Dissimulation Index
The raw score of the F Scale minus the raw score of the K Scale is used to assess the accuracy of item endorsement. If the F-K Dissimulation Index was greater than +9, the profile is designated as over-reporting.
- The F Scale
The F Scale consists of 60 items selected to detect unusual or atypical ways of answering test items. It consists of items that no more than 10 percent of an early subsample of the Minnesota normative sample answered in the deviant direction. An MMPI-2 raw score between 16 and 22 may indicate an invalid profile. A raw score above 23 probably indicates an invalid profile.
- The FB Scale
The FB Scale consists of 40 items on the MMPI-2 that no more than 10 percent of the MMPI-2 normative sample answered in the deviant direction. The items in the FB Scale are analogous to those of the F scale except that they are placed in the second half of the test. Again, as with the F Scale, a raw score of 16 to 22 may indicate an invalid profile. A raw score above 23 probably indicates an invalid profile.
- Lees-Haley Fake Bad Scale
The Lees-Haley Fake Bad Scale consists of 43 items on the MMPI-2.
Of these items, 18 are to be answered “true” and 25 to be answered “false.” Those items to be answered “true” include the following:
“11. People should try to understand their dreams and be guided by or take warning from them.”
“18. I am very seldom troubled by constipation.”
“31. I have nightmares every few nights.”
“506. I am a high-strung person.”
Those items to be answered “false” include the following:
“12. I enjoy detective or mystery stories.”
“41. I have had periods of days, weeks or months when I couldn’t take care of things because I couldn’t ‘get going.'”
“57. I am a very sociable person.”
“374. At periods my mind seems to work more slowly than usual.”
“561. I usually have enough energy to do my work.”
A score of 20 is used to identify malingering from nonmalingering plaintiffs.
(I) The Infrequency-Psychopathology Scale, F(p)
The Infrequency-Psychopathology Scale consists of 27 items on the MMPI2.
Of the 27, 18 are keyed true and 9 keyed false. These items are distinctive in that they are endorsed infrequently by both those who are normal and those with mental disorders. These items reflect severe psychotic symptoms, very unusual habits, and highly amoral attitudes, and they identify confusion. The higher the F(p) score, the more likely it is that the plaintiff has faked bad on the MMPI-2. T scores over 100 on the F(p) are very strong indicators of faking.
The F(p) scale can be used as an adjunct to the interpretation of F and FB Scales. If the F Scale is elevated, examine the VRIN score. If VRIN is elevated beyond a T score of 80, the F score is likely elevated due to random responding. If the VRIN is not elevated, examine TRIN. If TRIN is greater than 100, the F score is probably elevated due to acquiescence or nay-saying.
If both VRIN and TRIN are not elevated, examine F(p). If F(p) is elevated, the elevated F score is probably due to faking.
5. Factitious Disorder
The DSM-IV diagnostic criteria for factitious disorder are as follows:
“A. Intentional production or feigning of physical or psychological signs or symptoms.
“B. The motivation for the behavior is to assume the sick role.
“C. External incentives for the behavior (such as economic gain, avoiding legal responsibility, or improving physical well-being, as in malingering) are absent.”
Factitious disorder differs from malingering in that the motivation for producing symptoms in malingering is an external incentive, whereas in factitious disorder external incentives are absent. Factitious disorder is suggested when there is evidence of an intrapsychic need to maintain the sick role.
E. Alternate Causation of PTSD
A plaintiff may have PTSD, but that PTSD may have been caused by a stressor other than that stressor for which the defendant is alleged to be responsible. The defense will want to consider these two options: (1) whatever the plaintiff has, she had it before the alleged stressor, or (2) whatever the plaintiff has, she developed it after but not from the alleged stressor. Establishing this defense on causation requires identifying (1) a history of symptoms compatible with PTSD and (2) an exposure to a qualifying stressor. The defense may discover––for instance, through psychiatric records––that the plaintiff had the symptoms of PTSD before the alleged trauma. Or the defense may discover that the plaintiff was subjected to a stressor more objectively extreme than the stressor alleged to have caused the plaintiff’s current complaints, thereby raising the possibility that the plaintiff’s complaints arose from the earlier, more extreme trauma.
1. Delayed Onset
The specter of an intervening stressor between the stressor for which the defendant is allegedly responsible and the manifestation of symptoms is particularly probable given that PTSD can have a delayed onset, defined to be “at least 6 months after the stressor.” For the defense, the concept of delayed-onset PTSD is nettlesome. A plaintiff involved in a motor vehicle accident who has no complaints or symptoms constituting PTSD before a visit with a lawyer may afterwards develop PTSD after being referred to and consulting with a psychologist or psychiatrist recommended by that lawyer.
2. Childhood Abuse
Much is heard about the high incidence and prevalence of childhood abuse, particularly sexual abuse.
If these reports of sexual abuse are accurate, these high rates for incidence and prevalence are important for the defense. Simply, childhood physical and sexual abuse may result in PTSD. Many who were abused as children developed PTSD as children. PTSD, incipient in childhood, may become chronic, persisting into adulthood.
Plaintiffs’ experts on PTSD will attempt to turn weaknesses in their positions into strengths. For example, if the plaintiff has a history of child abuse, and studies are introduced reflecting that child abuse results in PTSD with the defense arguing that if the plaintiff has PTSD, it resulted from child abuse, and studies indicate that PTSD is underdiagnosed in those who were abused as children, the plaintiff’s expert will argue that the plaintiff’s prior PTSD merely sensitized the plaintiff to PTSD from the motor vehicle accident.
Childhood abuse is also associated with certain personality disorders. Those personality disorders include antisocial personality disorder, borderline personality disorder, and dissociative identity disorder. If there is a high prevalence of childhood abuse and that abuse is associated with these personality disorders, there should be a high prevalence of these personality disorders. This fact is significant because the symptoms of these personality disorders sometimes mimic the symptoms of PTSD.
3. Sensitization Hypothesis
If abused as a child, the plaintiff will raise what is called the “sensitization hypothesis.” That hypothesis is that previous exposure to trauma sensitizes an individual to subsequent trauma, thereby placing that individual at greater risk for developing PTSD. Based on this hypothesis, the plaintiff will argue that her childhood trauma, while not resulting in PTSD in childhood, sensitized her to the alleged trauma precipitated by the defendant, resulting currently in PTSD.
4. “Eggshell” Plaintiff
Increasing evidence indicates that PTSD is not a normal reaction to extraordinary events but an abnormal reaction to both ordinary and extraordinary events. That is, PTSD is the response of the “eggshell” plaintiff. In traditional thinking, the magnitude of the stressor should be directly proportional to the risk of developing PTSD. But research indicates that “there is as yet no direct support for the validity of the . . . distinction between extraordinary stressors . . . and more ordinary stressors.”
No threshold appears to exist. So low-magnitude events may give rise to PTSD.
But this line of thinking may prove too much. If the plaintiff has a predisposition to PTSD owing to emotional fragility, the plaintiff would be expected to have developed PTSD from any number of minor traumas both before and after the alleged trauma for which the defendant is alleged to be responsible. So when the plaintiff predicates her claim for PTSD on a stressor that seems somewhat ordinary, asserting that she is a highly susceptible individual, the so-called eggshell plaintiff, then the defense should be developed that any number of events in the plaintiff’s past could be responsible for her current symptoms. For instance, the defense may want to assert that the alleged stressor for which the defendant is allegedly responsible is merely an “external cue” that merely “symbolizes” or “resembles” the true preexisting traumatic event. (See Criteria B(4) & B(5).)
5. Risk Factors for PTSD
Some people have qualities that predispose them to develop PTSD.
These predisposing qualities include: (1) combat exposure; (2) socioeconomic status as a child; (3) psychiatric symptoms of depression or anxiety; (4) childhood abuse; (5) legal education; (6) being a woman; (7) substance abuse; and (8) antisocial behavior.
That people can have a predisposition to PTSD helps in assessing the merits or demerits of claim for PTSD. If the plaintiff has these predisposing qualities, then the likelihood increases that his or her diagnosis of PTSD is legitimate or malingered (viz., legal education, antisocial behavior). But having these predisposing qualities also increases the likelihood that although the diagnosis of PTSD is legitimate, the claim that the defendant caused the plaintiff’s PTSD is illegitimate in that the plaintiff’s PTSD probably developed from earlier traumas.
F. Limitation of Damages
If the plaintiff has PTSD caused by the defendant, the defense will want to limit the potential award of damages. Limiting damages involves demonstrating (1) that the disorder is not severely disabling; (2) that the disorder is not chronic; (3) that the disorder can be successfully treated; or (4) that the treatment is inexpensive.
1. Level of Disability
The definition of “mental disorder” in the DSM-IV requires that there be clinically significant impairment or distress. For the defense, that level of disability needs to be minimized, if possible. This effort involves a factual investigation into the plaintiff’s claims of impairment.
2. Chronicity
Every defense lawyer fears the word “chronic” when uttered by a plaintiff’s medical or psychological expert. A diagnosis of chronicity usually carries with it the prospect for a significant award of damages. This prospect is particularly upsetting because the standard for diagnosing chronicity is often so arbitrary and so deliberately oblivious to future prospects of recovery or remission. Nowhere is that set of concerns more applicable than in the diagnosis of chronicity in PTSD.
Under the DSM-IV, PTSD is characterized as chronic if the symptoms have persisted for three months. As a consequence, in litigated cases, the plaintiff will have a diagnosis of chronicity by the time the complaint is filed. The issue for the defense will be to establish a remission rate for those diagnosed with chronic PTSD and to convince the jury that the plaintiff will recover.
If PTSD becomes chronic, without treatment, it will probably persist for decades.
It has been estimated that at least one-third of those with PTSD do not recover. People with chronic PTSD will also be likely to develop a deleterious change in personality, with severe functional incapacity.
Yet PTSD is also compatible with remarkable functional recovery.
Indeed, without treatment, the severity of PTSD symptoms seems to decrease over time. A number of post-trauma factors play a significant role in prognosis: (1) early treatment with sharing and validation of the victim’s experience; (2) early and continuing social support; (3) exposure to therapeutic groups with other PTSD victims; (4) avoidance of retraumatization; (5) avoidance of activities that interrupt or prevent treatment.
In tort law, a plaintiff who is injured through the fault of another is denied recovery for damages for that injury to the extent that the plaintiff could have reasonably avoided those injuries. This law is relevant to claims for tortiously induced PTSD. Research indicates that early treatment of PTSD substantially reduces the risk that the PTSD will become chronic. As a result, a plaintiff who develops PTSD but who fails to seek early treatment should not recover damages for chronic PTSD if the weight of evidence is that the plaintiff’s PTSD would not be chronic had she sought early treatment.
3. Effectiveness of Treatment
In the context of litigation, whether or not a purported disorder is treated is an important question. Treatment not only establishes the amount of special damages but often is a multiplicand in a rule of thumb for determining general damages. Treatment is also an indication whether the diagnosis itself is genuine and whether the plaintiff has made an effort to avoid or mitigate the consequences of her injuries. A plaintiff diagnosed with a serious but treatable disorder who is not prescribed treatment or who does not seek treatment is rightfully suspect.
But be sensitive to the timing of this defense. If this shortcoming in the plaintiff’s case is raised before trial, do not be surprised to find that the plaintiff will begin some form of treatment by the time trial begins. Indeed, expect to learn that the plaintiff is undertaking treatment involving fairly potent drugs in order to give her claim an aura of legitimacy.
The two prominent treatments for PTSD are psychotherapy (talk) and pharmacotherapy (drugs). These two forms of treatment are not mutually exclusive.
a. Psychotherapy
Psychotherapy is the talking cure. It may be (1) individual psychotherapy, involving behavioral, cognitive, or psychodynamic techniques; or (2) group therapy. Despite the old saw “talk is cheap,” psychotherapy is typically protracted and expensive at $70+ per hour. Moreover, the effectiveness of this kind of therapy, apart from placebo effects, has not been established through controlled clinical trials.
Attempts to assess the effectiveness of psychodynamic psychotherapy have had significant methodological flaws, including lack of controls, lack of adequate assessment of outcome, and vaguely described treatments.
“Exposure” therapy is the most studied and supported therapeutic treatment technique for PTSD.
This kind of therapy seeks to produce habituation of emotional responses by instructing the patient to describe the event as if it were happening in the present while visualizing it; this exposure to the traumatic memory is continued until emotional reactions to the traumatic memory decrease.
Prolonged imaginal and in vivo exposure is claimed to reduce symptoms by allowing patients to realize that contrary to their mistaken ideas: (1) being in objectively safe situations that remind one of the trauma is not dangerous; (2) remembering the trauma is not equivalent to experiencing it again; (3) anxiety does not remain indefinitely in the presence of feared situations or memories, but rather it decreases even without avoidance or escape; and (4) experiencing anxiety and PTSD symptoms does not lead to loss of control. Some studies have arguably supported the effectiveness of prolonged exposure in treating PTSD.
“Eye Movement Desensitization and Reprocessing” is a form of exposure therapy.
This form of therapy consists in a patient focusing on a disturbing image or memory and related emotions and cognitions while the therapist waves a finger across the patient’s visual field with the patient tracking the finger. After each sequence, the patient indicates his or her level of distress. Yet existing studies on the effectiveness of this treatment have been methodologically flawed.
A cognitive therapy called anxiety management is based on the premise that pathological anxiety stems from deficits in skills in managing anxiety.
Managing anxiety provides patients with a repertoire of such strategies, such as relaxation training, positive self-statements, breathing training, biofeedback, social skills training, and distraction techniques. Existing studies support the effectiveness of anxiety management (stress inoculation training) in female assault victims; the effectiveness of anxiety management in other groups of trauma victims remains to be assessed.
b. Pharmacotherapy
Pharmacotherapy is sometimes helpful in reversing the biological abnormalities associated with PTSD. Drugs used in treating PTSD include antidepressants, anxiolytics, carbamazepine, lithium, and neuroleptics.
i. Antidepressants
Antidepressants, particularly the tricyclics and the serotonin reuptake inhibitors, are frequently used to treat PTSD.
These drugs are used to control dysphoria, sleep disturbance, and nightmares. Yet, as to PTSD, no satisfactory controlled clinical trials exist establishing the clinical efficacy of these drugs.
ii. Tricyclics
Imipramine, amitriptyline, and desipramine have been tested as treatments for PTSD.
iii. Monoamine Oxidase Inhibitors (MAOI)
Phenelzine has been tested as a treatment for PTSD.
iv. Selective Serotonin Reuptake Inhibitors (SSRI)
SSRIs have become the medications of choice for PTSD. They are most effective in the treatment of numbing and hyperarousal symptoms.
v. Anxiolytics
Anxiolytics are also frequently used to treat PTSD.
These anxiolytics include the antidepressants, MAOIs; sympatholytics such as proprandol and clonidine; and benzodiazepines such as diazepam and prazolam. These drugs are used to treat explosive behavior and nightmares. Yet, again, no satisfactory controlled clinical trials exist confirming the direct efficacy of these drugs.
vi. Carbamazepine
Carbamazepine (Tegretol) is an anti-convulsant that counters limbic “kindling,” a process by which neuroanatomic structures become increasingly sensitized following repeated exposure to electrical stimulation.
This drug is used to treat “flashbacks,” nightmares, and intrusive recall. Carbamazepine has had some success in treating those with PTSD, but additional controlled experimental trials are needed.
vii. Lithium
Lithium is a potent drug and is used by some to treat PTSD.
This drug is used to treat loss of control and impulsiveness. But no published systematic double-blind clinical trials of lithium treatment exist for PTSD.
viii. Neuroleptics
Neuroleptics are anti-psychotic drugs that typically block post-synaptic dopamine receptors in the central nervous system. Trade names for these neuroleptics include Thorazine, Navane, Haldol, and Clozaril. These drugs are used to treat dissociative and psychotic symptoms. These potent drugs were widely used in the 1960s and 1970s to treat Vietnam veterans with PTSD. But now they are not routinely used to treat PTSD.
4. Cost of Treatment
The cost of medications is often less than the cost of psychotherapy.
* * *
When the plaintiff seeks recovery of special damages, which include a substantial component for treatment for PTSD, the defense should be aware of what methodologically sound studies, if any, support the effectiveness of that kind of treatment. If none exist, then that point ought to be brought to the attention of the jury and the treatment characterized as unnecessary.
Yet, in attempting to limit damages, the defense is faced with a potential pitfall: proving that certain treatments are ineffective and hence unnecessary may leave the impression that the plaintiff’s PTSD is untreatable and hence chronic. In this regard, recent studies involving a significant sample of Vietnam veterans have disclosed that prolonged and intensive hospital treatment (medications, group and individual therapy, behavioral therapy, and family therapy) for chronic PTSD had no long-term beneficial effects on the veterans’ symptoms.
G. Special Issues of Interest in Litigation
1. PTSD From Activities in the Workplace
Claims are proliferating for discrimination or sexual harassment in the workplace. For the most part, the alleged harassment will be considered offensive but not severely traumatic. Yet on occasion, a plaintiff will assert that the discriminating or harassing behavior was so traumatic that it resulted in PTSD.
In the process, the plaintiff will assert that although the offensive behavior did not involve an event involving actual or threatened death or serious injury, it did involve a threat to her “physical integrity.” (The alleged stressor will not appear to fit with the severe stressors listed in the commentary of the DSM-IV or with the stressors listed in the various standardized trauma questionnaires or inventories.) The plaintiff will further assert that she is hypersensitive to the putative stressor, and that is why a stressor that might have caused the ordinary person to be merely upset or angry caused the plaintiff to develop PTSD.
The difficulty with the plaintiff’s position is that if the plaintiff is so hypersensitive to this kind of alleged behavior, she, not having been born yesterday, will have probably been subjected to similar behavior in the past and, if so, should have developed PTSD on those occasions as well. An inquiry into the plaintiff’s history will probably reveal that she has been subjected to stressors that would be viewed objectively as more traumatizing than the alleged incidents of sexual harassment in the workplace.
2. PTSD From Motor Vehicle Accidents
The stressors people most frequently encounter that might constitute a basis for a PTSD claim are those arising from motor vehicle accidents. Motor vehicle accidents have been found to be the single leading cause of PTSD in the general population, with the reported rates of PTSD in victims of serious motor vehicle accidents ranging from 8 percent to 46 percent.
From a plaintiff’s perspective, what better adjunct to a claim for personal injuries from a motor vehicle accident than a claim for psychological injuries, encouraging juror sympathies and boosting an otherwise pedestrian award for damages into the stratosphere?
Although the commentary in the DSM-IV on PTSD remarks that PTSD may arise from motor vehicle accidents, those accidents need to be “severe automobile accidents,” presumably to qualify the stressor under Criterion A. Yet, despite that commentary, Criterion A in the DSM-IV has in Subpart (2) a subjective component that many plaintiffs will argue enables them to qualify under Criterion A for PTSD even though many would not consider the automobile accident in which those plaintiffs were involved to be “severe.” Indeed, in some studies, trauma and injury-related characteristics, such as accident and injury severity and subjective perception of a threat to life, were not found to be associated with PTSD at one year.
The significance of this finding is that “injured victims of traffic accidents are at considerable risk for development of PTSD even when they are only mildly injured.”
As a result, the defense needs to be familiar with the studies of PTSD arising from motor vehicle accidents.
A number of studies have been conducted concerning PTSD from motor vehicle accidents.
These studies are primarily concerned with (1) the rate of PTSD from motor vehicle accidents of varying degrees of severity, (2) the cut point at which the symptoms of PTSD tend either to resolve or to become chronic, and (3) the risk factors for developing PTSD from motor vehicle accidents. Yet drawing conclusions about the risk of psychiatric morbidity after motor vehicle accidents is difficult for a number of reasons. Primarily, the studies lack uniformity, including inconsistencies across measurement (severity of accident), time elapsed from the motor vehicle accidents, and the absence of systematic longitudinal follow-up.
3. PTSD Overlying Preexisting Psychological Disorders
A plaintiff who has been diagnosed with PTSD may very well have preexisting psychological disorders presenting with symptoms and behaviors constituting elements of PTSD. Obvious examples of such preexisting disorders are, on Axis I, mood and generalized anxiety disorders and, on Axis II, borderline or antisocial personality disorders. When this co-morbidity occurs, the defense will need to have these different disorders demarcated.
Plaintiffs will assert that disorders co-morbid with PTSD are the result of PTSD. Those disorders include substance-abuse disorders, depression, and anxiety. Unfortunately, little is known about the chronological order between the onset of PTSD and the onset of co-morbid disorders.
Criterion C (3 or more) and D (2 or more) must be satisfied before a plaintiff can be diagnosed with PTSD. Both criteria require that the target symptoms not have been present before the trauma. As a result, if the plaintiff has preexisting depression or personality disorder that is manifest through symptoms characterized in Criterion C (particularly C(3) through C(7)) or D, the plaintiff may have difficulty establishing that she developed PTSD from the trauma without some sleight of hand from her expert.
4. Subtle Presentations of PTSD
A subtle presentation of PTSD has been defined as a situation in which “a person shows some signs and symptoms [of PTSD], but reports no previous traumatic events, no qualifying emotional reaction to these events, or obvious links between previous trauma and current psychological difficulties.”
(This is another, less loaded way to describe the “repressed memory syndrome.”)
When the plaintiff presents this way, expect the plaintiff’s therapist or expert to adopt one of two diagnostic solutions: (1) base a diagnosis of PTSD on obvious signs and symptoms alone, assuming that a symptomatic individual in fact must be failing to disclose a relevant trauma, or (2) link the person’s suffering arbitrarily to a qualifying event, although the person makes no such connection.
This diagnostic maneuver may be camouflaged through use of a variety of diagnostic instruments such as a structured interview (viz., the Clinician-Administered PTSD Scale) or psychometric test (viz., the MMPI-II) or a self-report PTSD scale (viz., Impact of Event Scale) followed by administration of various diagnostic tools used to assess the obstacles of reporting trauma, such as a dissociation scale or substance-abuse survey or social desirability or defensiveness scale. But in the end the clinician will remark that “the connection of symptoms to trauma is always an inferential process rather than purely an introspective one[;] in subtle cases, it thus is reasonable to explore the individual’s perceptions about the likelihood of symptoms being connected to the trauma separately from the perceptions that the symptoms do occur.”
5. Inflated Base Rates of PTSD
a. PTSD
Calculating the “positive predictive value” of various symptoms for PTSD requires knowledge of the prevalence or base rate of PTSD in the relevant population. The lower the base rate, the less likely those symptoms are to predict PTSD in this particular plaintiff. The higher the base rate, the more likely those symptoms are to predict PTSD in this plaintiff.
This is a mathematical relationship well known to ideologues who want to use PTSD as a tool to reconstruct society. They endeavor to overstate the base rate of PTSD in categories of trauma of particular interest to their social agenda—childhood abuse, rape, spousal abuse, and so on. For instance, estimates of the prevalence of childhood sexual abuse range from 6 percent to 62 percent. Many of these estimates are inflated as a result of using poor methodologies in conducting surveys and epidemiologic studies. For example, in one notorious study investigating the incidence of incest, the author instructed interviewers to ask, “How upset were you by this experience––extremely upset, somewhat upset, or not very upset?” Obviously, this question did not allow for the possibility that the experience caused no upset. The author also defined “incest” too broadly, to include any attempted sexual contact between relatives, no matter how distant the relationship, before the age of 18. Moreover, interviewers were biased by ten hours of pre-interview indoctrination about the horrors of rape and incest.
b. Traumatic Events
Another numerical value important to the defense is the ratio of those who develop PTSD from exposure to a traumatic event to all those exposed to that kind of traumatic event. The fewer people developing PTSD from exposure to that kind of traumatic event, the less likely it is that the plaintiff has PTSD from that kind of exposure.
6. PTSD in Children
This chapter on PTSD has not specifically discussed PTSD in children. Children with PTSD often have different symptoms from adults with PTSD.
As the DSM-IV recognizes under Criteria B(1), B(2), and B(3):
“(1) recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions. Note: In young children, repetitive play may occur in which themes or aspects of the trauma are expressed;
“(2) recurrent distressing dreams of the event. Note: In children, there may be frightening dreams without recognizable content;
“(3) acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative flashback episodes, including those that occur on awakening or when intoxicated). Note: In young children, trauma-specific reenactment may occur;
“(4) intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event; and
“(5) physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event.”
Psychometric instruments have been developed to assess PTSD in children. Reviews of these instruments should be consulted when undertaking the defense of a case involving a child or adolescent with PTSD.
Endnotes
1 American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders (4th ed. 2000).
2 The twentieth-century philosopher Ludwig Wittgenstein articulated the skepticism with which laypeople view psychiatry, even though psychiatry has moved from the formulations of Freud to a more biologically based endeavor. I. Bouveresse, Wittgenstein Reads Freud The Myth of the Unconscious 26-27 (1995); L. Wittgenstein, Lectures, Cambridge 1932-1935: From the Notes of Alice Ambrose and Margaret MacDonald (Alice Ambrose ed., 1979).
3 John P. Wilson, The Historical Evolution of PTSD Diagnostic Criteria: From Freud to DSM-IV, 7 J. Traumatic Stress 681-98 (1994).
4 Diagnostic and Statistical Manual of Mental Disorders 40 (1st ed. 1952).
“Under conditions of great or unusual stress, a normal personality may utilize established patterns of reaction to deal with overwhelming fear. The patterns of such reactions differ from those of neurosis or psychosis chiefly with respect to clinical history, reversibility of reaction, and its transient character. When promptly and adequately treated, the condition may clear rapidly. It is also possible that the condition may progress to one of the neurotic reactions. If the reaction persists, this term is to be regarded as a temporary diagnosis to be used only until a more definitive diagnosis is established.”
“This diagnosis is justified only in situations in which the individual has been exposed to severe physical demands or extreme emotional stress, such as in combat or in civilian catastrophe (fire, earthquake, explosion, etc.). In many instances this diagnosis applies to previously more or less ‘normal’ persons who have experienced intolerable stress.
“The particular stress involved will be specified as (1) combat or (2) civilian catastrophe.”
5 Diagnostic and Statistical Manual of Mental Disorders 49 (2d ed. 1968).
6 Diagnostic and Statistical Manual of Mental Disorders 236 (3d ed. 1980).
“A. Existence of a recognizable stressor that would evoke significant symptoms of distress in almost everyone.
“B. Reexperiencing of the trauma as evidenced by at least one of the following:
“(1) Recurrent and intrusive recollections of the event.
“(2) Recurrent dreams of the event.
“(3) Sudden acting or feeling as if the traumatic event were re-occurring because of an association with an environmental or ideational stimulus.
“C. Numbing of responsiveness to or reduced involvement with the external world, beginning some time after the trauma, as shown by at least one of the following:
“(1) Markedly diminished interest in one or more significant activities
“(2) Feeling of detachment or estrangement from others
“(3) Constricted affect
“D. At least two of the following symptoms that were not present before the trauma:
“(1) Hyperalertness or exaggerated startle
“(2) Sleep disturbance
“(3) Guilt about surviving when others have not, or about behavior required for survival
“(4) Memory impairment or trouble concentrating
“(5) Avoidance of activities that arouse recollection of the traumatic event
“(6) Intensification of symptoms by exposure to events that symbolize or resemble the traumatic event
” Post-trauamatic stress disorder, acute.
“‘Post-traumatic stress disorder, acute’ was characterized as having an onset of symptoms within six months of the trauma and a duration of symptoms less than six months.
” Post-traumatic stress disorder, chronic or delayed
“‘Post-traumatic stress disorder, chronic or delayed’ was characterized as having a duration of symptoms six months or more (chronic) and/or an onset of symptoms at least six months after the trauma (delayed).”
7 Diagnostic and Statistical Manual of Mental Disorders 247 (3d rev. ed. 1987).
“A. The person has experienced an event that is outside the range of usual human experience and that would be markedly distressing to almost anyone, e.g., serious threat to one’s life or physical integrity; serious threat or harm to one’s children, spouse, or other close relatives and friends; sudden destruction of one’s home or community; or seeking another person who has recently been, or is being, seriously injured or killed as the result of an accident or physical violence.
“B. The traumatic event is persistently reexperienced in at least one of the following ways:
“(1) recurrent and intrusive distressing recollections of the event (in young children, repetitive play in which themes or aspects of the trauma are expressed)
“(2) recurrent distressing dreams of the event
“(3) sudden acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative [flashback] episodes, even those that occur upon awakening or when intoxicated)
“(4) intense psychological distress at exposure to events that symbolize or resemble an aspect of the traumatic event, including anniversaries of the trauma
“C. Persistent avoidance of stimuli associated with the trauma or numbing of general responsiveness (not present before the trauma), as indicated by at least three of the following:
“(1) efforts to avoid thoughts or feelings associated with the trauma
“(2) efforts to avoid activities or situations that arouse recollections of the trauma
“(3) inability to recall an important aspect of the trauma (psychogenic amnesia)
“(4) markedly diminished interest in significant activities (in young children, loss of recently acquired developmental skills such as toilet training or language skills)
“(5) feeling of detachment or estrangement from others
“(6) restricted range of affect, e.g., unable to have loving feelings
“(7) sense of a foreshortened future, e.g., does not expect to have a career, marriage, or children, or a long life
“D. Persistent symptoms of increased arousal (not present before the trauma), as indicated by at least two of the following:
“(1) difficulty falling or staying asleep
“(2) irritability or outbursts of anger
“(3) difficulty concentrating
“(4) hypervigilance
“(5) exaggerated startle response
“(6) physiologic reactivity upon exposure to events that symbolize or resemble an aspect of the traumatic event (e.g., a woman who was raped in an elevator breaks out in a sweat when entering any elevator)
“E. Duration of the disturbance (symptoms in B, C, and D) at least one month.
“Specify delayed onset if the onset of symptoms was at least six months after the trauma.”
8 As to those criteria moved, D(5) in the DSM-III was moved to C(2) in the DSM-III-R. D(6) in the DSM-III was moved to B(4) in the DSM-III-R. As to those criteria deleted, D(3) in the DSM-III was deleted from the DSM-III-R. As to those criteria added, Criteria C(1), C(2), C(3), C(7), and D(2) were added to the DSM-III-R.
The distinction between acute and chronic PTSD in the DSM III was deleted in the DSM-III-R. In the DSM-III-R, the symptoms must persist one month for the disturbance to be characterized as PTSD. Otherwise, the disturbance is characterized as “acute stress reaction.”
9 Diagnostic and Statistical Manual of Mental Disorders (4th ed. 1994). The text of the DSM-IV was revised in 2000 and is called, for short, the DSM-IV-TR.
Judith A. Lyons & Terence M. Keane, Keane PTSD Scale: MMPI & MMPI-2 Update, 5 J. Traumatic Stress 111-17 (1992).
10 The DSM-IV also added Criterion F. But this change is not significant. Criterion F was implicit in the DSM-III and DSMIIIR. In addition, in the DSM-IV the distinction between acute and chronic PTSD was reinstated. But in the DSM-IV, the distinction is predicated on a duration of symptoms of less than three months but more than one month for acute PTSD and three or more months for chronic PTSD.
11 L. Stephen O’Brien, Traumatic Events and Mental Health (1998).
12 For a discussion about the role of the International Classification of Diseases and the DSM, refer to pages xxiv, xxv, xxvi, and xxix in DSM-IV-TR.
13 The ICD-10 provides the following definition of PTSD:
“Post-traumatic Stress Disorder
“Arises as a delayed or protracted response to a stressful event or situation (of either brief or long duration) of an exceptionally threatening or catastrophic nature, which is likely to cause pervasive distress in almost anyone. Predisposing factors, such as personality traits (e.g. compulsive, asthenic) or previous history of neurotic illness, may lower the threshold for the development of the syndrome or aggravate its course, but they are neither necessary nor sufficient to explain its occurrence. Typical features include episodes of repeated reliving of the trauma in intrusive memories (‘flashbacks’), dreams or nightmares, occurring against the persisting background of a sense of ‘numbness’ and emotional blunting, detachment from other people, unresponsiveness to surroundings, anhedonia, and avoidance of activities and situations reminiscent of the trauma. There is usually a state of autonomic hyperarousal and hypervigilance, an enhanced startle reaction, and insomnia. Anxiety and depression are commonly associated with the above symptoms and signs, and suicidal ideation is not infrequent. The onset follows the trauma with a latency period that may range from a few weeks to months. The course is fluctuating but recovery can be expected in the majority of cases. In a small proportion of cases the condition may follow a chronic course over many years, with eventual transition to an enduring personality change (F62.0).”
International Statistical Classification of Disease and Related Health Problems (10th rev. ed. 1992).
Norman Sartorius et al., Progress Toward Achieving a Common Language in Psychiatry, II: Results From the International Field Trials of the ICD-10 Diagnostic Criteria for Research for Mental and Behavioral Disorders, 152 Am. J. Psychiatry 1427-37 (1995).
14 Lorna Peters et al., A Comparison of ICD-10 and DSM-IV Criteria for Post-Traumatic Stress Disorder, 12 J. Traumatic Stress 335-43 (1998).
15 Gavin Andrews et al., Classification in Psychiatry: ICD-10 versus DSM-IV, 174 Brit. J. Psychiatry 3-5 (1999).
16 See Diagnostic and Statistical Manual of Mental Disorders 463-64 (4th rev. ed. 2000).
17 I. Pilowsky, Minor Accidents and Major Psychological Trauma: A Clinical Perspective, 8 Stress Med. 77-78 (1992).
Danny Koren et al., Acute Stress Response and Posttraumatic Stress Disorder in Traffic Accident Victims: A One-Year Prospective; Follow-Up Study, 156 Am. J. Psychiatry 367-73 (1999) (“injured victims of traumatic events, traffic accidents in our case, are at considerable risk for development of PTSD even when they are only mildly injured”).
A problem with studies assessing the correlation between the severity of motor vehicle accidents and PTSD is that no adequate measure of “severity” exists. Edward B. Blanchard & Edward J. Hickling, After the Crash, Assessment & Treatment of Motor Vehicle Accident Survivors 15 (“there are no validated scales of accident severity”).
Joel Paris, Does Stress Cause Posttraumatic Stress Disorder?, 44 Can. J. Psychiatry 20 (1999).
18 DSM-IV-TR at 463-64.
Following are examples in which PTSD might be an expected reaction to an extreme stressor.
“On the morning of May 5, the Army of the Potomac halted and began to form its line of battle . . .. The Confederate Army under General Lee had moved into their path. Artillery shells fell on the Sixth Corps headquarters as Sedgwick hastily sent his infantry to the right through the wooded countryside. . . . A New Jersey infantry regiment came jogging past the corps headquarters. Tom Hyde, one of Sedgwick’s aides-de-camp, was standing near Wendell [Holmes], fiddling with his horse’s bridle, when a shell took off the head of a New Jersey man. The head struck Hyde, bursting, and he was knocked down, covered with blood and brains; even his mouth, gaping in surprise was filled.”
–T. Hyde, “Following the Creek Cross” (1894), in S. Novick, The Life of Oliver Wendell Holmes 184-85 (1989).
“Lieutenant Larry Gwin of Alpha Company recalls that late that night one of Alpha’s men crawled into the American perimeter. ‘Sergeant James A. Mullartey from our 1st Platoon made it back to our lines. His story: The NVA had been shooting our wounded. One came up to him, stuck a pistol in his mouth, and fired. The bullet exited the back of his throat, knocked him out and they left him for dead. He survived and when he woke up at night he started crawling to us.'”
–H. G. Moore & J. L. Galloway, We Were Soldiers Once. . .and Young 334 (1993).
Children in medieval and early renaissance Europe routinely witnessed public executions, some of which were unspeakably brutal. For instance, executions of those convicted of treason involved the following brutalities: the miscreant was hanged until he lost consciousness; then he was revived; then he had his privates cut off and stuffed into his mouth; then he had his stomach cut open, and then, while he was still alive, his intestines were tossed in a cauldron of boiling water; then his heart was plucked from his chest and held up to his face; then he was beheaded; the head was then parboiled; and finally placed on a pike. Would not a child, having witnessed that, be expected by today’s standards to develop PTSD? Did those children develop PTSD?
19 Naomi Breslau et al., Traumatic Events and Posttraumatic Stress Disorder in an Urban Population of Young Adults, 48 Archives Gen. Psychiatry 216-22 (1991).
20 Arieh Y. Shaleu et al., Predictors of PTSD in Injured Trauma Survivors: A Prospective Study, 153 Am. J. Psychiatry 219-25 (1996); Naomi Breslau et al., Risk Factors for PTSD-Related Traumatic Events: A Prospective Analysis, 152 Am. J. Psychiatry 529-35 (1995); Sara A. Freedman et al., Predictors of Chronic Post-Traumatic Stress Disorder, 174 Brit. J. Psychiatry 353-59 (1999).
21 Robert I. Simon, Toward the Development of Guidelines in the Forensic Psychiatric Examination of Posttraumatic Stress Disorder in Litigation 42 (1995).
Ekkehard Othmer & Sieglinde C. Othmer, “The Clinical Interview Using DSM-IV,” in 2, The Difficult Patient: Post-Traumatic Stress ch. 3 (1994); David A. Tomb, The Phenomenology of Post-Traumatic Stress Disorder, 17 Psychiatric Clinics N. Am. 237-50 (1994).
Loren Pankratz, Patients Who Deceive 168-69 (1998).
22 Daniel S. Weiss, “Structured Clinical Interview Techniques,” in Assessing Psychological Trauma and PTSD 499 (John P. Wilson & Terence M. Keane eds., 1997).
23 Id.
24 Id. at 400.
25 Id. at 501.
26 Id. at 502.
27 Robert L. Spitzer & Jerome C. Wakefield, DSM-IV Diagnostic Criterion for Clinical Significance: Does It Help Solve the False Positive Problem?, 156 Am. J. Psychiatry 1856-64 (1999).
28 Stephen V. Faraone & Ming T. Tsuang, Measuring Diagnostic Accuracy in the Absence of a “Gold Standard,” 151 Am. J. Psychiatry 650-57 (1994).
29 Edward O. Wilson, Consilience 64 (1998).
30 Naomi Breslau & Glenn C. Davis, Posttraumatic Stress Disorder, the Stressor Criterion, 175 J. Nervous & Mental Disease 255-75 (1987); Mardi J. Horowitz et al., Diagnosis of Posttraumatic Stress Disorder, 175 J. Nervous & Mental Disease 267-68 (1987).
31 Naomi Breslau & Glenn C. Davis, Posttraumatic Stress Disorder, the Stressor Criterion, 175 J. Nervous & Mental Disease 255-75 (1987); Mardi J. Horowitz et al., Diagnosis of Posttraumatic Stress Disorder, 175 J. Nervous & Mental Disease 267-68 (1987).
32 Naomi Breslau & Glenn C. Davis, Posttraumatic Stress Disorder, the Stressor Criterion, 175 J. Nervous & Mental Disease 255-75 (1987); Mardi J. Horowitz et al., Diagnosis of Posttraumatic Stress Disorder, 175 J. Nervous & Mental Disease 267-68 (1987).
33 Naomi Breslau & Glenn C. Davis, Posttraumatic Stress Disorder, the Stressor Criterion, 175 J. Nervous & Mental Disease 255-75 (1987); Mardi J. Horowitz et al., Diagnosis of Posttraumatic Stress Disorder, 175 J. Nervous & Mental Disease 267-68 (1987); Editorial, The Validation of Psychiatric Diagnosis: New Models and Approaches, 152 Am. J. Psychiatry 161-62 (1995).
34 126 Am. J. Psychiatry 983-87 (1970); Eli Robins & Samuel B. Guze, Establishment of Diagnostic Validity in Psychiatric Illness: Its Application to Schizophrenia, 126 Am. J. Psychiatry 107-11 (1970).
35 Editorial, The Validation of Psychiatric Diagnosis: New Models and Approaches, 152 Am. J. Psychiatry 161-62 (1995).
36 Stuart A. Kirk & Herb Kutchins, The Selling of DSM, the Rhetoric of Science in Psychiatry 235-42 (1992); Samuel B. Guze, Review of the Diagnostic and Statistical Manual of Mental Disorders, 152 Am. J. Psychiatry 1228 (4th ed. 1995) (“very few of the hundreds of diagnostic categories have been satisfactorily validated according to these criteria”).
37 Editorial, What Is PTSD?, 154 Am. J. Psychiatry 143-45 (1997).
38 D.W. Goodwin & S.B. Guze, Psychiatric Diagnosis (1984); Samuel B. Guze, Review of the Diagnostic and Statistical Manual of Mental Disorders, 152 Am. J. Psychiatry 1228 (4th ed. 1995) (“very few of the hundreds of diagnostic categories have been satisfactorily validated according to these criteria”).
39 Jonathan Davidson et al., Validity and Reliability of the DSM-III Criteria for Posttraumatic Stress Disorder, 177 J. Nervous & Mental Disease 336-41 (1989); Landy F. Sparr, Post-Traumatic Stress Disorder, Does It Exist?, 13 Neurologic Clinics 413-29 (1995).
40 43 J. Clinical Psychology 32-43 (1987).
41 Id. at 35-36.
42 See generally Scott P. Orr & Danny G. Kalonpek, “Psychophysiological Assessment of Posttraumatic Stress Disorder,” in Assessing Psychological Trauma and PTSD 69 (John P. Wilson & Terence M. Keane eds., 1997).
43 D. Dobbs & W. P. Wilson, Observations on Persistence of War Neurosis, Diseases of the Nervous System 21: 686-91 (1960) (a pre-PTSD study of the psychophysiological responses of combat veterans to relevant combat stimuli described as resembling those of a conditional emotional response; no specific data on the “PTSD” group were presented and no specific comparisons to this group to the two control groups were made).
E. B. Blanchard et al., The Development of a Psychophysiological Assessment Procedure for PTSD in Vietnam Veterans, 54 Psychiatric Q. 220-28 (1982) (psychophysiological responses to standardized sounds of combat discriminated Vietnam veterans with PTSD from age- and gender-matched comparison group; the comparison group was nonveterans, a fact that compromises the value of this study in that the study lacks positive control groups, such as non-PTSD combat veterans with anxiety disorders).
P. F. Malloy et al., Validation of a Multimethod Assessment of PTSD in Vietnam Veterans, 51 J. Consulting & Clinical Psychology 488-94 (1983) (used standardized audiovisual cues to demonstrate that male Vietnam veterans with PTSD not involved in combat were more responsive to the combat cues than either psychiatrically impaired veterans without PTSD or well-adjusted veterans; the utility of this study was compromised by the fact that these psychiatrically impaired veterans were noncombat veterans—it may not be surprising that persons with no prior exposure to combat would be unresponsive to combat-related stimuli).
T. P. Pallmeyer, Refining and Testing an Assessment Procedure for PTSD in Vietnam Veterans (unpublished, 1985).
R. J. Gerardi, Fakeability of Psychophysiological Assessment of PTSD (unpublished, 1986).
J. Knight et al., Empirical Validation of DSM-III Criteria for PTSD (unpublished, 1984).
44 T. M. Fairbank et al., Some Preliminary Data on the Psychological Characteristics of Vietnam Veterans with PTSD, 51 J. Consulting & Clinical Psychology 912-19 (1983).
W. E. Penk et al., Adjustment Differences Among Male Substance Abusers Varying in Degree of Combat Experience in Vietnam, 49 J. Consulting & Clinical Psychology 426-37 (1981).
T. M. Keane et al., Empirical Development of an MMPI Subscale for the Assessment of Combat-Related PTSD, 62 J. Consulting & Clinical Psychology 888-91 (1984).
45 Zimering et al., PTSD in Vietnam Veterans: An Empirical Evaluation of the Diagnostic Criteria (unpublished, 1984).
46 M.E. Wolfe & A.D. Mosnaim, Posttraumatic Stress Disorder Etiology, Phenomenology, and Treatment 49-63 (1990).
47 Id. at 53.
48 55 J. Consulting & Clinical Psychology 251-56 (1987).
49 Jessica Wolfe & Terence M. Keane, “Diagnostic Validity of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder 54 (Marion E. Wolf & Aron D. Mosnaim eds., 1990).
50 In this area, the DSM-IV committee cited six articles published during or after 1990.
S. Solomon & G. J. Canino, Appropriateness of the DSM-III-R Criteria for Posttraumatic Stress Disorder, 31 Comp. Psychiatry 227-37 (1990); P. Steinglass & E. Gerrity, Natural Disasters and Posttraumatic Stress Disorder: Short-term vs. Long-term Recovery in Two Disaster Affected Communities, 20 J. Applied Soc. Psychological 1746-65 (1990); Green et al., Buffalo Creek Survivors in the Second Decade: Stability of Stress Symptoms, 60 Am. J. Orthopsychiatry 43-54 (1990); D. G. Kilpatrick & H. S. Resnick, “Posttraumatic Stress Disorder Associated With Exposure to Criminal Victimization in Clinical and Community Populations,” in Posttraumatic Stress Disorder: DSM-IV and Beyond 113-43 (J.R.T. Davidson & E. B. Foa eds., 1993) (a review article that does not cite any basic research article published during or after 1990); Nader et al., Children’s PTSD Reactions One Year After a Sniper Attack on Their School, 147 Am. J. Psychiatry 1526-30 (1990); B. O. Rothbaum & E. B. Foa, “Subtypes of Posttraumatic Stress Disorder and Duration of Symptoms,” in Posttraumatic Stress Disorder: DSM-IV and Beyond 23-36 (J.R.T. Davidson & E. B. Foe eds., 1993) (a review article that does not cite any basic research article published during or after 1990, except to K. Nader et al. cited above).
51 In this area, the DSM-IV committee cited no basic research articles published during or after 1990.
Pitman et al., Psychophysiologic Assessment of Post-traumatic Stress Disorder Imagery in Vietnam Combat Veterans, 44 Archives Gen. Psychiatry 970-75 (1987); B. Van der Kolk & M. Greenberg, “The Psychobiology of the Trauma Response: Hyperarousal, Constriction, and Addiction to Traumatic Reexposure,” in Psychological Trauma 63-87 (B. Van der Kolk ed., 1987); Z. Solomon & M. Mikulincer, Combat Stress Reactions, Post-traumatic Stress Disorder, and Social Adjustment: A Study of Israeli Veterans, 175 J. Nervous & Mental Disease 277-85 (1987); L. Kolb, A Neuropsychological Hypothesis Explaining Post-Traumatic Stress Disorders, 144 Am. J. Psychiatry 989-95 (1987).
52 Jessica Wolfe & Terence M. Keane, “Diagnostic Validity of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder 58 (Marion E. Wolfe & Aron D. Mosnaim eds., 1990).
53 P. F. Malloy et al., Validation of a Multimethod Assessment of Posttraumatic Stress Disorders in Vietnam Veterans, 51 J. Consulting & Clinical Psychology 488-94 (1983).
54 E. B. Blanchard et al., Cardiac Response to Relevant Stimuli as an Adjunctive Tool for Diagnosing Posttraumatic Stress Disorder in Vietnam Veterans, 17 Behavior Therapy 592-606 (1986).
55 R. K. Pittman et al., Psychophysiologic Assessment of Post-traumatic Stress Disorder Imagery in Vietnam Combat Veterans, 44 Archives Gen. Psychiatry 970-75 (1987) (adapted ideographic methods for studying emotion in order to compare the psychophysiological response (skin conductance, heart rate, and EMG) of male Vietnam veterans with and without PTSD to individually tailored imagery scripts, which contained stimulus, response, and meaning propositions that depicted, among others, the two most stressful combat experiences recalled by the veteran, with results demonstrating greater reactivity to imagery-based trauma cues for the PTSD group relative to the non-PTSD comparison group; the utility of this study was compromised by the fact that the comparison group did not include non-PTSD psychiatric patients who were combat veterans).
56 In this area, the DSM-IV committee cited two basic research articles published during or after 1990. J.R.T. Davidson et al., Posttraumatic Stress Disorder in the Community: An Epidemiologic Study, 21 Psychological Med. 713-21 (1991); I. Winfield et al., Sexual Assault and Psychiatric Disorders Among a Community Sample of Women, 147 Am. J. Psychiatry 335-41 (1990); A. Frances, Problems in Defining Clinical Significance in Epidemiological Studies, 55 Archives Gen. Psychiatry 119 (1998).
57 Robert W. Butler et al., Physiological Evidence of Exaggerated Startle Response in a Subgroup of Vietnam Veterans With Combat-Related PTSD, 147 Am. J. Psychiatry 1308-12 (1990).
58 Carl P. Malmquist, “The Use and Misuse of Psychiatry,” in Sexual Harassment Cases, 26 Psychiatric Annals 149-56, 153 (1996).
59 John S. March, “What Constitutes a Stressor? The ‘Criterion A’ Issue,” in Posttraumatic Stress Disorder DSM-IV and Beyond ch 3 (Jonathan R. T. Davidson & Edna B. Foa eds., 1993); Naomi Breslau & Glenn C. Davis, Posttraumatic Stress Disorder, the Stressor Criterion, 175 J. Nervous & Mental Disease 255-75 (1987).
60 Id. at 46.
61 152 Am J. Psychiatry 1705-13 (1995).
62 Jonathan R. T. Davidson & Edna B. Foa, Refining Criteria for Posttraumatic Stress Disorder, 42 Hosp. & Community Psychiatry 259, 261 (1991). For a general discussion of “factor analysis,” see Paul Kline, The New Psychometrics 52-69 (1998).
63 Susan D. Solomon & Glorisa J. Canino, Appropriateness of DSM-III-R Criteria for Posttraumatic Stress Disorder, 31 Comprehensive Psychiatry 227, 235 (1990).
64 Daniel W. King et al., Confirmatory Factor Analysis of the Clinician-Administered PTSD Scale: Evidence for the Dimensionality of Posttraumatic Stress Disorder, 10 Psychological Assessment 90, 91 (1998).
65 T. M. Keane et al., Mississippi Scale for Combat-Related Post-Traumatic Stress Disorder: Three Studies in Reliability and Validity, 56 J. Consulting & Clinical Psychology 85-90 (1988); J. Davidson et al., Validity and Reliability of the DSM-III Criteria for Posttraumatic Stress Disorder, 177 J. Nervous & Mental Disease 336-41 (1989) (a principal components factor analysis extracted three factors: (1) arousal and intrusiveness; (2) survival guilt, detachment-estrangement, reduced interest, and avoidance of reminders; and (3) decreased sleep, impaired concentration and memory, and constricted affect); L. A. King & D. W. King, Latent Structure of the Mississippi Scale for Combat-Related Post-Traumatic Stress Disorder: Exploratory and Higher Order Confirmatory Factor Analyses, 1 Assessment 275-91 (1994); D. Lauterbach et al., Properties of the Civilian Version of the Mississippi PTSD Scale, 10 J. Traumatic Stress 499-513 (1997); M. W. McFall et al., Reliability and Validity of the Mississippi Scale for Combat-Related Posttraumatic Stress Disorder, 2 Psychological Assessment 114-21 (1990); S. M. Silver & C. U. Iacono, Factor-Analytic Support for DSM-III’s Post-Traumatic Stress Disorder for Vietnam Veterans, 40 J. Clinical Psychology 5-14 (1984); D. L. Vreven et al., The Civilian Version of the Mississippi PTSD Scale: A Psychometric Evaluation, 8 J. Traumatic Stress 91-109 (1995); C. G. Watson et al., A Factor Analysis of the DSM-III Post-Traumatic Stress Disorder Criteria, 47 J. Clinical Psychology 205-14 (1991); Daniel W. King et al., Confirmatory Factor Analysis of the Clinician-Administered PTSD Scale: Evidence for the Dimensionality of Posttraumatic Stress Disorder, 10 Psychological Assessment 90-96 (1998); Charles G. Watson et al, A Factor Analysis of the DSM-III Post-Traumatic Stress Disorder Criteria, 47 J. Clinical Psychology 205-14 (1991); Steven M. Silver & C. U. Iancono, Factor-Analytic Support for DSM-III’s Post-Traumatic Stress Disorder for Vietnam Veterans, J. Clinical Psychology 5-14 (1984).
66 T. M. Keane, “Symptomatology of Vietnam Veterans With Post-Traumatic Stress Disorder,” in Posttraumatic Stress Disorder: DSM-IV and Beyond 99-111 (J.R.T. Davidson & E. B. Foe eds., 1993) (this study suggested four factors: (1) intrusive experiences, restriction of affect, and hypervigilance; (2) reactivity, avoidance, and startle; (3) irritability and impairment of concentration; (4) diminished interest in activities and feelings of detachment; but there are weaknesses in the study: small sample; factor loadings not presented; subjectivity involved in interpreting the scree plot, and likely range restriction of scores as a result of confining the sample to people with PTSD).
E. B. Foa et al., Arousal, Numbing and Intrusion: Symptom Structure of PTSD Following Assault, 152 Am. J. Psychiatry 116-120 (1995) (the study extracted three factors: (1) arousal-avoidance, (2) numbing, and (3) intrusion; but the investigators failed to describe the method used to determine the number of factors to subtract (some methods tend to overextract factors)).
L. A. King et al., The Los Angeles Symptom Checklist: A Self-Report Measure of Posttraumatic Stress Disorder, 2 Assessment 1-17 (1995) (this study produced three factors: (1) most PTSD symptoms, (2) somatic anxiety symptoms, and (3) interpersonal difficulties).
S. Taylor et al., The Structure of Post-Traumatic Stress Symptoms, 107 J. Abnormal Psychology 154-60 (1998) (the findings of this study using civilian victims of motor vehicle accidents and military personnel stationed in Bosnia were that DSM-IV PTSD symptoms are composed of two factors: (1) intrusion or avoidance and (2) hyperarousal or numbing; it was postulated that intrusions give rise to avoidance and hyperarousal gives rise to numbing).
D. W. King et al., Confirmatory Factor Analysis of the Clinician-Administered PTSD Scale: Evidence for the Dimensionality of Posttraumatic Stress Disorder, 10 Psychological Assessment 90-96 (1998) (the results favored a four-factor solution of (1) intrusion, (2) effortful avoidance, (3) emotional numbing, and (4) hyperarousal.
67 A. J. Tomarken, A Psychometric Perspective on Psychophysiological Measures, 7 Psychological Assessment 387-95 (1995).
J. T. Cacioppo & L. G. Tassinary, Inferring Psychological Significance From Physiological Signas, 45 Am. Psychologist 16-28 (1990).
68 D. Dobbs & W. P. Wilson, Observations on Persistence of War Neurosis, 21 Diseases of Nervous System 686-91 (1960) (a pre-PTSD study of the psychophysiological responses of combat veterans to relevant combat stimuli described as resembling those of a conditional emotional response; no specific data on the “PTSD” group were presented and no specific comparisons to this group to the two control groups were made).
E. B. Blanchard et al., The Development of a Psychophysiological Assessment Procedure for PTSD in Vietnam Veterans, 54 Psychiatric Q. 220-28 (1982) (psychophysiological responses to standardized sounds of combat discriminated Vietnam veterans with PTSD from age- and gender-matched comparison group; the comparison group was nonveterans, a fact that compromises the value of this study in that the study lacks positive control groups, such as non-PTSD combat veterans with anxiety disorders).
P. F. Malloy et al., Validation of a Multimethod Assessment of PTSD in Vietnam Veterans, 51 J. Consulting & Clinical Psychology 488-94 (1983) (used standardized audiovisual cues to demonstrate that male Vietnam veterans with PTSD noncombat veterans were more responsive to the combat cues than either psychiatrically impaired veterans without PTSD or well-adjusted veterans; the utility of this study was compromised by the fact that these psychiatrically impaired veterans were noncombat veterans—it may not be surprising that persons with no prior exposure to combat would be unresponsive to combat-related stimuli).
E. B. Blanchard et al., Cardiac Response to Relevant Stimuli as an Adjunctive Tool for Diagnosing Posttraumatic Stress Disorder in Vietnam Veterans, 17 Behavior Therapy 592-606 (1986) [see also a replication study by E. B. Blanchard et al., Cardiac Response to Relevant Stimuli as an Adjunct in Diagnosing Post-Traumatic Stress Disorder: Replication and Extension, 20 Behavior Therapy 535-43 (1989)] (A sample of male Vietnam veterans was examined for heart-rate responses to standardized “emotionally meaningful combat sounds” (helicopters, AK-47 firing, mortars and screaming wounded). The findings were that (1) “on a group basis,” the resting or baseline heart rate of veterans with PTSD is higher than that of comparison groups [a finding contradicted by a later, more sophisticated study: R. K. Pitman et al., Psychophysiologic Responses to Combat Imagery of Vietnam Veterans with Posttraumatic Stress Disorder Versus Other Anxiety Disorders, 99 J. Abnormal Psychology 49-54 (1990)] and (2) “on a group basis,” veterans with PTSD show greater increases in heart rate to relevant combat stimuli than do comparison groups. The authors limit the finding to Vietnam veterans as a group, not as individuals, that is, the means of individual scores, not the individual scores. Obviously, this limits the usefulness of heart-rate responses as a diagnostic tool to assess the status of any individual. The authors remark that “absolute levels of HR either during a resting baseline or while the individual is listening to combat sounds do not provide a very good individual discrimination.”).
T. P. Pallmeyer et al., The Psychophysiology of Combat-Induced Post-traumatic Stress Disorder in Vietnam Veterans, 24 Behav. Res. & Therapy 645-52 (1986) (This study included five psychiatric combat controls, but had no measure of severity of combat exposure, and only one of the five had a diagnosis in the same category as PTSD, namely, generalized anxiety; although these five non-PTSD psychiatric subjects appeared less physiologically responsive than the PTSD subjects to the standard auditory, combat-related stimulus, this finding was statistically significant at only one of the several stimulus intensity levels. Studies of Vietnam combat veterans may not be generalizable to civilian victims of trauma for a variety of reasons, including (1) PTSD symptoms in combat victims have persisted for years; (2) combat veterans with PTSD were frequently exposed to combat trauma; (3) the nature or intensity of the trauma may be a factor in producing PTSD symptoms; (4) combat veterans have been male.).
R. K. Pitman et al., Psychophysiologic Responses to Combat Imagery of Vietnam Veterans with Posttraumatic Stress Disorder Versus Other Anxiety Disorders, 99 J. Abnormal Psychology 49-54 (1990) (A very small sample of seven Vietnam combat veterans with PTSD were compared to seven combat veterans without PTSD but with some form of anxiety disorder (phobia, panic disorder, generalized anxiety disorder, and obsessive-compulsive disorder). All subjects were presented with 11 scripts––five individualized scripts and six standardized scripts. The five individualized scripts consisted of two of the individual’s most stressful combat experiences, a precombat experience, a positive experience and a neutral experience. The six standardized scripts consisted of two neutral experiences, a combat experience (an incoming mortar and rocket attack), a positive experience, an action experience, and a fear experience (public speaking). When these scripts were presented to the subjects, the subjects were measured for skin conductance, EMG, and heart rate. The results were that neither group was very responsive to the standard combat experience or the standard fear experience or the individual scripts, except for the individualized combat scripts: The PTSD group had significant “group” differences [mean scores] for skin conductance and EMG. But the researchers did not report the individual scores. The implication of not reporting individual scores is that some individuals without PTSD scored higher on the measurements of skin conductance and EMG than did some individuals with PTSD, a fact that significantly reduces the diagnostic value of these psychophysiological measurements. Pitman and colleagues have striven to fill in the gaps of this research program. One gap was the failure to use adequate control groups. Another gap was the failure to use subjects with PTSD other than Vietnam combat veterans.).
A. Y. Shalev et al., Psychophysiologic Assessment of Traumatic Imagery in Israeli Civilian Patients with Posttraumatic Stress Disorder, 150 Am. J. Psychiatry 620-24 (1993) (This study had two sample groups: 13 people with PTSD from a variety of traumatic events and 13 without who had been subjected to traumatic events similar to those in the PTSD group. The groups differed significantly for heart rate and EMG responses but not for skin conductance. The “combined” physiologic responses of the PTSD and non-PTSD groups (means) differed significantly during imagery of the personal traumatic scripts. The physiologic responses to imagery of the personal traumatic event of the female PTSD subjects were about 33 percent higher than those of the male subjects. The study is not clear, however, about how well the test identified individuals with PTSD or without PTSD. The authors do mention using a discriminant function empirically derived from studies of Vietnam combat veterans to identify the present subjects with PTSD, with a resulting sensitivity of 69 percent and specificity of 77 percent. Individual scores were not presented to enable the reader to determine whether some individuals with PTSD had lower scores on the measurement variables (EMG, heart rate, and skin conductance) than did some individuals without PTSD. The assumption is that some did, thereby compromising the diagnostic value of these psychophysiologic tests. Another problem with the study is the differential physiologic responses of women compared to men that would affect the mean value used as the measure of comparison. The mean values of the subjects with PTSD could be elevated over those of the subjects without PTSD owing to the contribution of the women with PTSD. Another problem is that in previous studies with Vietnam combat veterans, the differentiating psychophysiologic response was skin conductance, but in the present study it was not. A final problem is using the responses to different kinds of traumatic stressors. The physiologic response of someone with PTSD who was subject to terrorist attacks could be expected to significantly elevate the mean of the group with PTSD over the mean of those without PTSD who were subjected to less terrifying stressors such as motor vehicle accidents. (The nature of the motor vehicle accident was not specified for either group.)).
E. B. Blanchard et al., Psychophysiology of Posttraumatic Stress Disorder Related to Motor Vehicle Accidents: Replication and Extension, 64 J. Consulting & Clinical Psychology 742-51 (1996) (this study had four sample groups: three groups of motor vehicle accident victims with PTSD, with subsyndromal PTSD, and without PTSD and a group of motor vehicle accident subjects. The participants were cued with two idiosyncratic audiotapes and one standardized videotape. The two audiotapes were designed to capture the participant’s experience with his or her motor vehicle accident. The results were that, only as to audiotape 1, only mean heart rate (out of the four physiologic responses: heart rate, skin conductance, EMG, diastolic blood pressure) successfully discriminated motor vehicle accident victims with PTSD from other motor vehicle accident victims and controls. The authors note that for “these data to have clinical utility, one would hope there were not only mean differences in reactivity but also distributional differences such that one could distinguish the individual case into different diagnostic groups based on the responses.” Using a cutoff score of +2 beats per minute or greater, the authors found a sensitivity of 69.4 percent and a specificity of 66.7 percent in distinguishing PTSD from subsyndromal PTSD and an overall specificity of 77.6 percent in distinguishing PTSD from all motor vehicle accident victims. This study has significant flaws. First, there was no apparent effort to control for medication and drug use. Second, the control group did not include positive controls without PTSD who had anxiety disorders. Third, there was no apparent effort to control for litigation effects in the exposure group. Fourth, there was no apparent effort to match the severity of the motor vehicle accident to the findings of PTSD, except to eliminate at the outset “minor ‘fender benders.'” Fifth, no breakout of sex differences appeared for those diagnosed with PTSD or subdromal PTSD or no PTSD. (There was a greater proportion of women to men in the motor vehicle accident group than in the non-motor vehicle accident group.) Sixth, only audiotape 1 seemed to produce the desired response even though both audiotapes 1 and 2 were designed to capture the participant’s experience of his or her motor vehicle accident, with only “slight variations” between the tapes.).
S. P. Orr et al., Psychophysiologic Assessment of Women with Posttraumatic Stress Disorder Resulting From Childhood Sexual Abuse, 66 J. Consulting & Clinical Psychology 906-13 (1998) (There were three sample groups: a group with current PTSD from childhood sexual abuse, a group that once had PTSD from childhood sexual abuse, and a group that never had PTSD. Judged against the DSM-III-R criteria, the sensitivity of the physiologic responsiveness during personal sexual abuse imagery was 66 percent and the specificity 78 percent and a prior discriminant function (developed with Vietnam combat veterans) classified 66 percent of the current group, 42 percent of the lifetime group, and 22 percent of the never group as responders during sexual-abuse imagery. Investigators also performed univariate pairwise comparisons between groups, none of which were significant except for corrugator EMG in which the mean of the lifetime group was greater than the mean of the never group. An unexpected difference emerged across groups for the personal neutral script, with a larger mean for the lifetime group. The investigators compared the means of the various groups, not the individual responses. As a result, some of the “current PTSD” subjects may have had responses lower than some of the “never” subjects. When only medication- or drug-free subjects were analyzed, the differences failed to reach statistical significance. The investigators speculated that that result was due to the reduced power from the small sample size. The current group had more comorbid pathology, including more subjects with anxiety disorders, than did the other groups. This could be a confounding factor. The control group should include positive controls who never had PTSD but who have anxiety disorders such as generalized anxiety disorder in order to determine whether PTSD is distinguishable from other anxiety disorders. The current group also had significantly more drug and medication use than the other groups, another potential confounder. A variety of medications, drugs, and other substances can influence physiologic responses. Beta-blockers can reduce heart rate. Anticholinergics elevate resting heart rate. Use of or withdrawal from nicotine, caffeine, and alcohol can influence physiologic responses nonuniformly. Indeed, little is known about the impact of many medications and substances on physiologic response.).
T.M. Keane et al., Utility of Psychophysiological Measurement in the Diagnosis of Posttraumatic Stress Disorder: Results from a Department of Veterans Affairs Cooperative Study, 66 J. Consulting & Clinical Psychology 914-23 (1998) (This study using a large sample was designed to determine the extent to which psychophysiological measures can predict the presence or absence of PTSD as determined by a gold standard diagnostic interview, the Structured Clinical Interview for DSM-III-R. The authors conclude that the results of the study “provide definitive support for a positive association between psychophysiological responsitivity to cues depicting traumatic war-zone experiences and combat-related PTSD.” Yet they note that “classification rates based on psychophysiological response were lower than those reported previously” and that there was a “statistically significant reduction in PTSD probability scores on retesting.”).
69 R. W. Butler et al., Physiological Evidence of Exaggerated Startle Response in a Subgroup of Vietnam Veterans With Combat-Related PTSD, 147 Am. J. Psychiatry 1308-12 (1990).
70 There are a number of published studies of acoustic startle in PTSD:
E. M. Ornitz & R. S. Pynoos, Startle Modulation in Children with Posttraumatic Stress Disorder, 146 Am. J. Psychiatry 866-70 (1989).
R. W. Butler et al., Physiological Evidence of Exaggerated Startle Response in a Subgroup of Vietnam Veterans With Combat-Related PTSD, 147 Am. J. Psychiatry 1308-12 (1990) (The subjects were 38 male Vietnam veterans with self-reported combat experience. No assessment was made of the extent or nature of that combat experience. Of the 38, 20 were diagnosed with chronic PTSD; the other 18 were used as controls. Thirty-five percent of the subjects (seven with PTSD and six without PTSD) were eliminated from the analysis because they were considered to be “non-responders” (even though they had substantial startle responses), leaving a remaining sample of 13 with PTSD and 12 without PTSD. Acoustic startle stimuli (40-msec noise bursts at different sound levels: 85, 90, 95, 100, 110, 116 dB(A)) and tactile startle stimuli were administered. Acoustic startle was measured by eyeblink EMG amplitude. The magnitude of each startle response was defined as the largest of the peak values beginning between 20 and 80 msec after onset of the startle stimulus, expressed in digital units. The results were that the PTSD group exhibited significantly higher eyeblink EMG amplitudes, measured nonparametrically, than the control group only at 85 dB(A) and 100 dB(A). No significant differences were found between the two groups in response to tactile stimuli. This study has significant limitations. First, the PTSD group had significantly greater combat experience than the control group. Second, alcohol and drug use may have been a confounder. Third, the sample sizes were small. Fourth, the control group lacked adequate positive controls, that is, combat veterans without PTSD who have anxiety disorders. Fifth, the authors noted that “it is too early to state where the measure [of acoustic startle] will have diagnostic utility.” The database needs extending and the findings need to be cross-validated.).
A. Y. Shalev et al., Physiologic Responses to Loud Tones in Israeli Post-Traumatic Stress Disorder Patients, 49 Archives Gen. Psychiatry 870-75 (1992) (The subjects were a PTSD group (14), an anxiety-disorder group (14), a past-trauma group without PTSD (15), and a no-trauma group (19). Psychoactive medications were being used by the PTSD group (benzodrazepines (7) and antidepressants (5)); and the anxiety group (benzodrazepines (6), antidepressants (5), and neuroleptics (1)). The stimuli were 15 95-dB (sound pressure level), 1000-Hz, 500-msec pure tones with 0-msec rise and fall times. The physiological data response was left orbicularis oculi EMG, skin conductance, and heart rate. The results were that there were no significant group effects for any of the EMG measures. There was a “nonsignificant” “trend” toward a larger skin conductance response in subjects with PTSD. There was a larger accelerative heart-rate response in subjects with PTSD.).
C. A. Morgan et al., Yohimbine Facilitated Acoustic Startle in Combat Veterans With Posttraumatic Stress Disorder, 117 Psycho-pharmacology 466-71 (1995).
C. A. Morgan et al., Fear-Potentiated Startle in Posttraumatic Stress Disorder, 38 Biological Psychiatry 378-85 (1995) (This was a study designed to determine whether “fear-potentiated” startle responses are increased in Vietnam combat veterans. The subjects were male Vietnam combat veterans with PTSD (12) and male healthy volunteers (10). Three of the PTSD group did not complete the testing because of panic attacks. Five of the remaining nine in the PTSD group had comorbid panic disorder. The subjects were stimulated with an acoustic startle consisting of a 40 msec burst of white noise at 106 dB(A). The physiologic response was right orbicularis oculi EMG. The subjects were under threat of receiving an electric shock during the startle stimulus. The result was that on average the startle response was larger in the PTSD group compared to the control group.).
S. P. Orr et al., Physiologic Responses to Loud Tones in Vietnam Veterans With Posttraumatic Stress Disorder, 104 J. Abnormal Psychology 75-82 (1995) (The subjects were 56 male Vietnam veterans with combat experience. Of these, 37 were diagnosed with PTSD, and 19 diagnosed without PTSD used as controls. The physiologic measures were left orbicularis oculi EMG, skin conductance, and heart rate. The stimuli were 15 95-dB (sound pressure level), 1000-Hz, 500-msec pure tones with 0-msec rise and fall times. The results were a significant “group” difference in orbicularis oculi EMG response, no significant group difference in skin conductance response, and a significantly larger heart rate response in those with PTSD. The present results do not replicate the Shalev et al. (1992) findings of overall greater skin conductance responsivity in PTSD. The authors note that “if anxiety or fear is responsible for the exaggerated startle response in PTSD, a similar response should also be present in individuals with generalized anxiety disorder [but] we are not aware of any studies that have examined the eyeblink startle response in individuals with the disorder.”).
C. Grillon et al., Baseline Startle Amplitude and Prepulse Inhibition in Vietnam Veterans With Posttraumatic Stress Disorder, 64 Psychiatry Res. 169-78 (1996).
C. A. Morgan et al., Startle Reflex Abnormalities in Women With Sexual Assault-Related Posttraumatic Stress Disorder, 154 Am. J. Psychiatry 1076-80 (1997) (The subjects were female civilians with sexual-assault-related PTSD (13); and female civilians without PTSD and without sexual assault (16). The stimuli was two pulse alone 240-msec duration bursts of white noise at 92 dB(A) and 102 dB(A); and one prepulse plus pulse 230-msec duration burst of 20-dB(A) white noise 120 msec before a 40-msec duration 102-dB(A) pulse. The physiologic response was right and left orbicularis oculi EMG. The results were that the overall startle response was not significantly greater in the PTSD subjects than in the comparison subjects. A startle response was greater in the PTSD group than in the comparison group for the left eye but not the right eye but only in response to the 102-dB(A) startle stimuli in block and 92-dB(A) startle stimuli in block. “The implications for lateralization in PTSD are not clear.” The findings of an exaggerated startle response to the 92-dB(A) stimulus in women with PTSD differs from startle response in men, who have not reported exaggerated startle responses to soft tones (90-95 dB). This study has significant limitations. First, the study did not include either a trauma-exposed control group or measures of autonomic reactivity. Second, the small numbers of women in the samples preclude meaningful conclusions about gender differences.).
C. A. Morgan et al., Exaggerated Acoustic Startle Reflex in Gulf War Veterans With Posttraumatic Stress Disorder, 153 Am. J. Psychiatry 64-68 (1996) (The subjects were (1) Gulf War veterans with PTSD (10); combat comparison subjects (7); and civilian comparison subjects (15). The physiologic response was left orbicularis oculi EMG; the stimulus was 40-msec burst of white noise with a near instantaneous use time at the following five intensities: 90, 96, 102, 108, 114 dB(A). The results were that the Gulf War veterans with PTSD, as a group, had larger amplitudes of eyeblink reflex than did the controls. The magnitude of the startle response was greater in the PTSD group than in the civilian group only at 108 dB(A) and 114 dB(A). No significant differences occurred at 90 and 96 dB(A). The magnitude of the startle response in the PTSD subjects was significantly greater than in the combat controls at 96 dB(A), 102 dB(A), 108 dB(A), and 114 dB(A). There are obvious limitations to this study. First, what accounts for the failure of the PTSD subject to have increased startle over the civilian controls at all the same intensities that the PTSD subjects had increased startle in relation to the non-PTSD combat controls? Second, the control group lacked positive controls with anxiety disorders.).
S. P. Orr et al., Physiologic Responses to Non-Startling Tones in Vietnam Veterans with Post-traumatic Stress Disorder, 73 Psychiatry Res. 103-07 (1997) (the subjects were medication-free Vietnam combat veterans divided into a PTSD group (20) and a non-PTSD group (19). The stimuli consisted of 15 86-dB(A) (sound pressure level), 1000-Hz, 500-msec pure tones, with 40-msec rise and fall tones. The physiologic response was left orbicularis oculi EMG skin conductance and heart rate. The results were that the PTSD group had higher average heart rate than the non-PTSD control group, but no differences existed in EMG or skin conductance between the two groups. The authors noted that the heart rate findings were not a consequence of elevated sympathetic activity given the lack of a difference in skin conductance and EMG.).
S. P. Orr et al., Physiologic Responses to Loud Tones in Israeli Veterans of the 1973 Yom Kippur War, 41 Biological Psychiatry 319-26 (1997) (The subjects were Israeli veterans of the Yom Kippur War divided into a PTSD group (19) and a non-PTSD group (74). The stimuli were 15 95-dB(A) (sound pressure level), 1000-Hz, 500-msec pure tones with 0-msec rise and fall times. The physiologic response was left orbicularis oculi EMG, skin conductance, and heart rate levels. The results were no significant group differences in EMG or skin conductance, but a larger magnitude response in heart rate in the PTSD group compared with the non-PTSD group, which was marginally significant.).
A. Y. Shalev et al., Auditory Startle Responses in Help-Seeking Trauma Survivors, 69 Psychiatry Res. 1-7 (1997) (The subjects were medication-free help-seeking trauma survivors divided into a PTSD group (30) with trauma from a variety of sources and a past-trauma control group without PTSD (28), also with trauma from a variety of sources. The stimuli was 15 consecutive 95-d-B(A), 500-msec, 1000-Hz tones with 0-msec rise and fall times. The physiologic response was left orbicularis oculi EMG, skin conductance, and heart rate. The results were that the PTSD subjects had higher than average EMG responses and higher skin conductance responses than the controls. No difference existed on the variable of heart rate.).
L. J. Metzger et al., Physiologic Reactivity to Startling Tones in Women With Posttraumatic Stress Disorder, 108 J. Abnormal Psychology 347-52 (1999) (The subjects were a group with current PTSD (21); a group with past PTSD (23), and a group that had never had PTSD (13). The current group had more comorbid disorders than the other groups, ranging from depression and anxiety to drug dependence. Those in current group (11) were taking more psychotropic autonomically active medications than those in the other groups. The stimuli were 15 95-dB(A), 1000-Hz, 500-msec pure tones with 0-msec rise and fall times. The physiologic measures were left orbicularis oculi EMG, skin conductance, and heart rate. The results were as follows: Heart Rate Response: Women with current PTSD from childhood sexual abuse produced significantly larger accelerative heart rate responses to startling tones than women with childhood sexual abuse without PTSD. Women with lifetime but not current PTSD had larger heart rate responses than women with current PTSD. Skin Conductance Response: Women with current PTSD from childhood sexual abuse produced slower absolute habituation of skin conductance response magnitudes to startling tones than women with childhood sexual abuse without PTSD. Women with lifetime but not current PTSD had greater skin conductance response magnitudes than women with current PTSD. EMG Response: no group differences found.).
71 G. Goldstein et al., Survivors of Imprisonment in the Pacific Theater During World War II, 144 Am. J. Psychiatry 1210-13 (1987); W. W. Eaton et al., Impairment in Holocaust Survivors After 33 Years: Data From an Unbiased Community Sample, 139 Am. J. Psychiatry 773-77 (1982); B. L. Green et al., Buffalo Creek Survivors in the Second Decade: Stability of Stress Symptoms, 60 Am. J. Orthopsychiatry 43-54 (1990); B. L. Green et al., Identifying Survivors at Risk: Long-Term Impairment Following the Beverly Hills Supper Club Fire, 53 J. Consulting & Clinical Psychology 672-78 (1985); R. L. Leopold & H. Dillon, Psycho-Anatomy of a Disaster: A Long Term Study of Post-Traumatic Neuroses in Survivors of Marine Explosion, 119 Am. J. Psychiatry 913-21 (1963); B. Gersons, Patterns of PTSD Among Police Officers Following Shooting Incidents: A Two-Dimensional Model and Treatment Implications, 2 J. Traumatic Stress 247-57 (1989).
72 B. L. Green et al., Identifying Survivors at Risk: Long-Term Impairment Following the Beverly Hills Supper Club Fire, 53 J. Consulting & Clinical Psychiatry 672-78 (1985).
B. L. Green et al., Buffalo Creek Survivors in the Second Decade: Comparison with Unexposed and Non-Litigant Groups, 20 J. Applied Soc. Psychology 1033-50 (1990).
S. M. Southwick et al., Trauma-Related Symptoms in Veterans of Operation Desert Storm: A Preliminary Report, 150 Am. J. Psychiatry 1524-28 (1993).
S. M. Southwick et al., Trauma-Related Symptoms in Veterans of Operation Desert Storm: A 2-Year Follow-Up, 152 Am. J. Psychiatry 1150-55 (1995) (the overall severity of PTSD symptoms as measured by the Mississippi scale and the DSM-III-R-based PTSD scale increased in severity over two years, with the greatest change occurring between one month and six months; it should be noted that 22 of the 84 participants who initially completed assessments dropped out in the two-year follow-up).
R. J. Ursano et al., Acute and Chronic Post-Traumatic Stress Disorder in Motor Vehicle Accident Victims, 156 Am. J. Psychiatry 589-95 (1999).
73 C. Van Dyke et al., Posttraumatic Stress Disorder: A Thirty-Year Delay in a World War II Veteran, 142 Am. J. Psychiatry 1070-73 (1985) (reporting that a decorated WWII veteran developed PTSD 30 years after the WWII-related combat stressor).
74 A. Ehlers et al., Psychological Predictors of Chronic Post-Traumatic Stress Disorder After Motor Vehicle Accidents, 107 J. Abnormal Psychology 508-19 (1998).
75 Judith L. Herman, Trauma and Recovery 9, 28, 30 (1992).
Dr. Herman’s less articulate but equally destructive comrades include Ellen Bass and Laura Davis, whose book, The Courage to Heal: A Guide for Women Survivors of Child Sexual Abuse (3d ed. 1994), has become the bible of the repressed-memory movement.
Daniel A. Furber & Suzanna Sherry, Beyond All Reason, The Radical Assault on Truth in American Law 95-117 (1997); Glen O. Gabbard, Patients Who Hate, 52 Psychiatry 96-106 (1989).
76 The suggested criteria of Complex PTSD are as follows:
(1) A history of subjection to totalitarian control over a prolonged period (months to years). Examples include hostages, prisoners of war, concentration-camp survivors, and survivors of some religious cults. Examples also include those subjected to totalitarian systems in sexual and domestic life, including survivors of domestic battering, child physical or sexual abuse, and organized sexual exploitation.
(2) Alterations in affect regulation, including
persistent dysphoria
chronic suicidal preoccupation
self-injury
explosive or extremely inhibited anger (may alternate)
compulsive or extremely inhibited sexuality (may alternate)
(3) Alterations in consciousness, including
amnesia or hyperamnesia for traumatic events
transient dissociative episodes
depersonalization/derealization
reliving experiences, either in the form of intrusive posttraumatic stress disorder symptoms or in the form of reminative preoccupation
(4) Alterations in self-perception, including
sense of helplessness or paralysis of initiative
shame, guilt, and self-blame
sense of defilement or stigma
sense of complete difference from others (may include sense of specialness, utter aloneness, belief no other person can understand, or nonhuman identity)
(5) Alterations in perception of perpetrator, including
preoccupation with relationship with perpetrator (includes preoccupation with revenge)
unrealistic attribution of total power to perpetrator (caution: victim’s assessment of power realities may be more realistic than clinician’s)
idealization of paradoxical gratitude
sense of special or supernatural relationship
acceptance of belief system or rationalization of perpetrator
(6) Alterations in relations with others, including
isolation with withdrawal
disruption in intimate relationships
repeated search for rescuer (may alternate with isolation and withdrawal)
persistent distrust
repeated failures of self-protection
(7) Alterations in systems of meaning
loss of sustaining faith
sense of hopelessness and despair
77 L. E. Walker, The Battered Woman Syndrome (1984); Donald G. Dutton & Susan Painter, The Battered Woman Syndrome: Effects of Severity and Intermittency of Abuse, 63 Am. J. Orthopsychiatry 614-22 (1993).
78 R. A. Schuller & N. Micmar, Battered Woman Syndrome Evidence in the Courtroom, 16 Law & Hum. Behav. 273-91 (1992).
79 State v. Stevens, 970 P.2d 215 (Or. 1998) (testimony that the battered-woman syndrome is a variety of posttraumatic stress disorder); Millie C. Astin et al., Posttraumatic Stress Disorder and Childhood Abuse in Battered Women: Comparisons With Maritally Distressed Women, 63 J. Consulting & Clinical Psychology 308-12 (1995).
80 Diana M. Elliot & John Briere, Posttraumatic Stress Associated With Delayed Recall of Sexual Abuse: A General Population Study, 8 J. Traumatic Stress 629-47 (1995); Linda M. Williams, Recovered Memories of Abuse in Women With Documented Child Sexual Victimization Histories, 8 J. Traumatic Stress 649-73 (1995); R. Joseph, The Neurology of Traumatic “Dissociative” Amnesia: Commentary and Literature Review, 23 Child Abuse & Neglect 715-27 (1999); Bessel A. van der Kolk & Rita Fisler, Dissociation and the Fragmentary Nature of Traumatic Memories: An Overview and Exploratory Study, 8 J. Traumatic Stress 505-25 (1995); Harrison G. Pope et al., Questionable Validity of “Dissociative Amnesia” in Trauma Victims, 172 Brit. J. Psychiatry 210-15 (1998); Cathy Spatz Widom & Robin L. Shepard, Accuracy of Adult Recollections of Childhood Victimization: Part 1. Childhood Physical Abuse, 8 Psychological Assessment 412-21 (1996); Cathy Spatz Widom & Suzanne Morris, Accuracy of Adult Recollections of Childhood Victimization: Part 2. Childhood Sexual Abuse, 9 Psychological Assessment 34-46 (1997); S. Brandon J. Boakes et al., Recovered Memories of Childhood Sexual Abuse, 172 Brit. J. Psychiatry 296-307 (1998); Scott P. Orr et al., Psychophysiologic Assessment of Women With Posttraumatic Stress Disorder Resulting From Childhood Sexual Abuse, 66 J. Consulting & Clinical Psychology 906-13 (1998); Jonathan W. Schooler et al., “Taking the Middle Line: Can We Accommodate Both Fabricated and Recovered Memories of Sexual Abuse?,” in Recovered Memories and False Memories (Martin A. Conway ed., 1997); Naomi Breslau et al., Previous Exposure to Trauma and PTSD Effects of Subsequent Trauma: Results From the Detroit Area Survey of Trauma, 156 Am. J. Psychiatry 902-07 (1999); Judith Lewis Herman & Emily Schatzow (Women’s Mental Health Collective), Recovery and Verification of Memories of Childhood Sexual Trauma, 4 Psychoanalytic Psychology 1-14 (1987); John Briere & Jon Conte, Self-Reported Amnesia for Abuse in Adults Molested as Children, 6 J. Traumatic Stress 21-31 (1993); Linda Meyer Williams, Recall of Childhood Trauma: A Prospective Study of Women’s Memories of Child Sexual Abuse, 62 J. Consulting & Clinical Psychology 1167-76 (1994).
81 E.g., Daniel L. Schacter, Searching for Memory ch. 9 (1996); Paul R. McHugh, Psychotherapy Awry, American Scholar, Winter 1994; Fred H. Frankel, Discovering New Memories in Psychotherapy—Childhood Revisited, Fantasy, or Both?, 333 New Eng. J. Med. 591-94 (1995); William H. Anderson, Letter to Editor, 334 New Eng. J. Med. 274 (1996).
82 Elizabeth Bass & Laura Davis, The Courage to Heal (1988).
83 Kenneth S. Pope, Memory, Abuse & Science: Questioning Claims About the False Memory Epidemic, 51 Am. Psychologist 957-74 (1996); Alan W. Scheflin & David Spiegel, From Courtroom to Couch, Working With Repressed Memory & Avoiding Lawsuits, 21 Psychiatric Clinics N. Am. 847-67 (1998).
84 John F. Kihlstrom, Memory, Abuse, and Science, Am. Psychologist 994-95 (Sept. 1997); Kenneth S. Pope, Science as Careful Questioning: Are Claims of a False Memory Syndrome Epidemic Based on Empirical Evidence?, Am. Psychologist 997-1006 (Sept. 1997); Frederick Crews, The Memory Wars, Freud’s Legacy in Dispute (1995).
85 Elizabeth Loftus & Katherine Ketcham, The Myth of Repressed Memory: False Memories and Allegations of Sexual Abuse (1994); Daniel L. Schacter, Searching for Memory, The Brain, the Mind, and the Past ch. 9 (1996); Elizabeth F. Loftus, The Price of Bad Memories, Skeptical Inquirer, Mar./Apr. 1998, at 23-24; Daniel L. Schacter, Implicit Memory: History and Current Status, 13 J. Experimental Psychology: Learning, Memory & Cognition 501-18 (1987); Ethel Spector Person & Howard Klar, Establishing Trauma: The Difficulty Distinguishing Between Memories & Fantasies, 42 J. Am. Psychoanalytic Ass’n 1055-81 (1994); Elizabeth F. Loftus et al., Forgetting Sexual Trauma: What Does It Mean When 38% Forget?, 62 J. Consulting & Clinical Psychology 1177-81 (1994); Elizabeth F. Loftus et al., Memories of Childhood Sexual Abuse, Remembering & Repressing, 18 Psychology of Women Q. 67-84 (1994); Patricia J. Bauer, What Do Infants Recall of Their Lives? Memory for Specific Events by One- to Two-Year-Olds, 51 Am. Psychologist 29-41 (1996); Daniel Schacter, Memory Wars, 272 Scientific Am. 135-39 (1995).
86 J. K. Briere, Methodological Issues in the Study of Sexual Abuse Effects, 60 J. Consulting & Clinical Psychology 196-203 (1992).
D. O. Femina et al., Child Abuse: Adolescent Records vs. Adult Recall, 145 Child Abuse & Neglect 227-31 (1990) (69 adults with documented histories of childhood physical abuse were interviewed about their childhood abuse. 26 responded in ways not reflecting their histories. When 8 of these subjects were re-interviewed, they acknowledged their abuse and admitted withholding information about their abuse in their first interview.).
S. N. Gold et al., Degrees of Repression of Sexual Abuse Memories, 49 Am. Psychologist 441-42 (1994).
P. M. Coons et al., “Repressed Memories in Patients with Dissociative Disorder: Literature Review, Controlled Study and Treatment Recommendations,” in 16 Review of Psychiatry 11: 153 to 11: 172 (L. J. Dickstein et al. eds., 1997).
L. M. Williams, Recall of Childhood Trauma. A Prospective Study of Women’s Memories of Child Sexual Abuse, 62 J. Consulting & Clinical Psychology 1167-76 (1994).
J. Briere & J. Conte, Self-Reported Amnesia for Abuse in Adults Molested as Children, 6 J. Traumatic Stress 21-31 (1993) (267 of 450 subjects said there was a time between the forced sexual experience and their 18th birthday when they could not remember the forced sexual experience. The subjects were recruited by their therapists (selection bias). None of the abuse was corroborated. The subject’s response was ambiguous. Did they merely forget? Did they repress the experience? Some subjects may have been influenced by suggestion because all were in therapy with therapists who were part of an informal sexual abuse treatment referral network.).
J. L. Herman & E. Schatzow, Recovery and Verification of Memories of Childhood Sexual Trauma, 4 Psychoanalytic Psychology 1-14 (1987) (This was a case series of 53 women treated by the authors in time-limited group therapy for “incest survivors.” Fourteen had severe amnesia; but some had this during the period of normal childhood amnesia. Only 21 of the 53 obtained corroborating evidence of the incest, but it is unclear whether any of the 21 had severe amnesia.).
L. M. Williams, Recall of Childhood Trauma. A Prospective Study of Women’s Memories of Child Sexual Abuse, 62 J. Consulting & Clinical Psychology 1167-76 (1994) (129 women who had been brought as children (10 months old to 12 years old) to a hospital emergency room for treatment after reported sexual abuse were interviewed as adults and asked whether they had been sexually abused. 49 did not report the abuse. These 49 were considered to have amnesia. 25 of these 49 experienced the abuse at age 6 or younger. These 25 may represent normal childhood amnesia. The remaining nonreporters may merely have forgotten or may not want to discuss the issue with the researchers.).
J. W. Schooler et al., “Taking the Middle Line: Can We Accommodate Both Fabricated and Recovered Memories of Sexual Abuse?,” in Recovered Memories and False Memories (M. A. Conway ed., 1997).
D. M. Elliot & J. Briere, Posttraumatic Stress Associated with Delayed Recall of Sexual Abuse: A General Population-Study, 8 J. Trauma Stress 629-47 (1995).
D. M. Elliot, Trauma to Events: Prevalence and Delayed Recall in the General Population, 65 J. Consulting & Clinical Psychology 811-20 (1997).
C. S. Widom & S. Morris, Accuracy of Adult Recollections of Childhood Victimization: Part 2. Childhood Sexual Abuse, 8 Psychological Assessment 412-21 (1997).
C. Bagley, Validity of a Short Measure of Child Sexual Abuse, 66 Psychological Rep. 449-50 (1990).
B. A. Van der Kolk & R. Fisler, Dissociation and the Fragmentary Nature of Traumatic Memories: Overview and Exploratory Study, 8 J. Trauma Stress 505-25 (1995).
Shirley Feldman-Summers & Kenneth S. Pope, The Experience of “Forgetting” Childhood Abuse: A National Survey of Psychologists, 62 J. Consulting & Clinical Psychology 636-39 (1994).
Elizabeth F. Loftus, The Reality of Repressed Memories, 48 Am. Psychologist 518-37 (1993).
David S. Holmes, “The Evidence of Repression: An Examination of Sixty Years of Research,” in Repression and Dissociation ch. 4 (Jerome L. Singer ed., 1990).
87 Harrison G. Pope, Jr. & James I. Hudson, Can Memories of Childhood Sexual Abuse Be Repressed?, 25 Psychological Med. 121-26 (1995).
Harrison G. Pope, Jr. & James I. Hudson, Can Individuals “Repress” Memories of Childhood Sexual Abuse? An Examination of the Evidence, 25 Psychiatric Annals 715-25 (1995).
John Briere, Methodological Issues in the Study of Sexual Abuse Effects, 60 J. Consulting & Clinical Psychology 196-203 (1992).
“To demonstrate dissociative amnesia, investigators should interview and follow-up people who experience a well-documented trauma. These people must be at least six years old at the time of the trauma and free of neurological problems such as head injury or drug intoxication. The traumatic event must be too important to the individual to plausibly be lost by ordinary forgetfulness. If some of the victims do not report memories on an initial interview, they must participate in a clarification interview in which they should be asked whether they remember the specific event that they are known to have experienced. Although this last step might be criticized as over-cueing, data show that any lesser approach risks mis-classifying many people who actually remember. . . .[U]ntil studies meeting these criteria appear, dissociative amnesia remains unproven.”
88 L. C. Terr, Chowchilla Revisited: The Effects of Psychic Trauma Four Years After a School-bus Kidnapping, 140 Am. J. Psychiatry 1543-50 (1983).
L. C. Terr et al., Children’s Memories in the Wake of Challenger, 153 Am. J. Psychiatry 618-25 (1996).
W. A. Wagenaar & J. Groeneweg, The Memory of Concentration Camp Survivors, 4 Applied Cognitive Psychology 77-87 (1990).
C. S. Widom & R. L. Shepard, Accuracy of Adult Recollection of Childhood Victimization. Part 1: Childhood Physical Abuse, 8 Psychological Assessment 412-21 (1996).
C. S. Widom & S. Morris, Accuracy of Adult Recollections of Childhood Victimization. Part 2: Childhood Sexual Abuse, 9 Psychological Assessment 34-46 (1997).
L. M. Williams, Recall Childhood Trauma. A Prospective Study of Women’s Memories of Child Sexual Abuse, 62 J. Consulting & Clinical Psychology 1167-76 (1994).
C. Bagley, Child Sexual Abuse and Mental Health in Adolescents and Adults: British and Canadian Perspectives (1995).
A. W. Burgess et al., Memory Presentations of Childhood Sexual Abuse, 33 J. Psychosocial Nursing 9-16.
D. D. Femina et al., Child Abuse: Adolescent Recovers v. Adult Recall, 145 Child Abuse & Neglect 227-31 (1990).
R. L. Leopold & H. Dillon, Psycho-anatomy of a Disaster: A Long Term Study of Post-traumatic Neuroses in Survivors of a Marine Explosion, 119 Am. J. Psychiatry 913-21 (1963).
U. Malt, The Long-term Psychiatric Consequences of Accidental Injury: A Longitudinal Study of 107 Adults, 153 Brit. J. Psychiatry 810-18 (1988).
C. Peterson & M. Bell, Children’s Memory for Trauma Injury, 67 Child Development 3045-70 (1996).
L. C. Terr, Children of Chowchilla: A Study of Psychic Trauma, 34 Psychoanalytic Study of the Child 552-623 (1979).
Chris R. Brewin et al., Psychopathology and Early Experience: A Reappraisal of Retrospective Reports, 113 Psychological Bull. 82-98 (1993).
89 H. G. Pope et al., Questionable Validity of ‘Dissociative Amnesia’ in Trauma Victims, 172 Brit. J. Psychiatry 210-15 (1998).
90 K. A. Kendall-Tackett et al., Impact of Sexual Abuse on Children: A Review and Synthesis of Recent Empirical Studies, 113 Psychological Bull. 164-80 (1993).
91 Elizabeth A. Feigon & Joseph deRivera, “Recovered Memory” Therapy: Profession at a Turning Point, 39 Comprehensive Psychiatry 338-44 (1998).
Scott P. Orr et al., Psychophysiologic Assessment of Women With Posttraumatic Stress Disorder Resulting From Childhood Sexual Abuse, 66 J. Consulting & Clinical Psychology 909-13 (1998).
Christine A. Courtois, “Delayed Memories of Child Sexual Abuse: Critique of the Controversy and Clinical Guidelines,” in Recovered Memories and False Memories (Martin A. Conway ed., 1997).
Fred H. Frankel, Discovering New Memories in Psychotherapy—Childhood Revisited, Fantasy, or Both?, 333 New Eng. J. Med. 591-94 (1995).
Elizabeth F. Loftus & Jacqueline E. Pickrell, The Formation of False Memories, 25 Psychiatric Annals 720-25 (1995).
Daniel L. Schacter, Searching for Memory, The Brain, the Mind, and the Past ch. 9 (1996).
92 John F. Kihlstrom, Memory, Abuse, and Science, Am. Psychologist 994-95 (Sept. 1997).
93 The AMA has issued a statement on RMS with these recommendations.:
“1. That the AMA recognize that few cases in which adults make accusations of childhood sexual abuse based on recovered memories can be proved or disproved and it is not yet known how to distinguish true memories from imagined events in these cases.
“2. That the AMA encourage physicians to address the therapeutic needs of patients who report memories of childhood sexual abuse and that these needs exist quite apart from the truth or falsity of any claims.
“3. The AMA considers recovered memories of childhood sexual abuse to be of uncertain authenticity, which should be subject to external verification. The use of recovered memories is fraught with problems of potential misapplication.
“4. That the AMA encourage physicians treating possible adult victims of childhood abuse to subscribe to the Principles of Medical Ethics when treating the patients and that psychiatrists pay particular attention to the Principles of Medical Ethics with Annotations Especially Applicable to Psychiatry.”
This last recommendation concerns, as the AMA noted,
“[T]he role of the therapist in developing new memories. It is well-established for example that a trusted person such as a therapist can influence an individual’s reports, which would include memories of abuse. Indeed, as the issue of repressed memories has grown, there have been reports of therapists advising patients that their symptoms are indicative—not merely suggestive—of having been abused, even when the patient denies having been abused. Other research has shown that repeated questioning may lead individuals to report events that in fact never occurred. Unfortunately, the dynamics that underlie an individual’s suggestibility are only beginning to be understood.”
An article by Fred Frankel of the Harvard Medical School in the New England Journal of Medicine accurately surveys the issues involved in RMS:
“The new-found confidence in the accuracy of long-delayed recall may have been engendered by . . . the influence of the feminist movement. . . . Women in distress, with a wide range of symptoms from anxiety and depression to sexual dysfunction, came to be regarded as victims of trauma even in the absence of memories of the events themselves.”
“[P]roof of the existence of dissociation or repression is weak . . .. The question is whether we can accept as valid, without corroboration, stories that emerge for the very first time in therapy, totally unsuspected until then by patients now in their 30s and 40s.”
“[A] number of parents . . . reported being denied access to a family meeting with the therapist who had validated their adult child’s memories, unless the parents admitted in advance that they were guilty . . .. I was [also] familiar with a series of reports by authors with academic appointments that appeared to be methodologically unpersuasive.”
“The paper cited by Herman and Schatzow, although widely cited as providing evidence corroborating reports of long-forgotten trauma, has been criticized largely on two grounds: the suggestive context in which the memories were elicited and insufficient data. The women were reported to have confirmed their memories of trauma by checking with relatives, perpetrators, and available records. Except for the few illustrative case histories at the end of their article, however, Herman and Schatzow did not discuss the nature and the extent of the corroboration in any detail. Nor was it clear that the women who reported confirmation of their memories included any of those who had been unaware of the trauma before their group experience. The paper thus does not provide persuasive examples of accurate memories totally unsuspected until their discovery in therapy.”
“We thus see that even if dissociation or repression exists, the case for it at this stage rests largely on anecdotes and case reports.”
Bowman & Mertz, A Dangerous Direction: Legal Intervention and Sexual Abuse Survivor Therapy, 109 Harv. L. Rev. 551-639 (1996) (This article is a plea to plaintiffs’ lawyers to desist in suing therapists for malpractice who specialize in the repressed memory syndrome, citing all the highly suspect research by that cult of memory therapists. Characteristically, the authors do not suggest that plaintiffs’ attorneys desist in suing the alleged perpetrators of sexual abuse, even though the incidence of false positive diagnoses is extremely high.).
94 Harrison G. Pope, Jr. & James I. Hudson, Can Memories of Childhood Sexual Abuse Be Repressed?, 25 Psychological Med. 121-26 (1995).
95 B. S. Everitt, The Cambridge Dictionary of Statistics 283 (1998).
96 L. Wittgenstein provided this analogy in one of his notebooks.
97 Steven N. Allen, Psychological Assessment of Post-Traumatic Stress Disorder, Psychometrics, Current Trends, and Future Directions, 17 Psychiatric Clinics N. Am. 327-49 (1994).
Jessica Wolfe & Terence M. Keane, “Diagnostic Validity of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder 52 (Marion E. Wolf & Aron D. Mosnaim eds., 1990); Terence Keane et al., Post-Traumatic Stress Disorder: Evidence for Diagnostic Validity and Methods of Psychological Assessment, 43 J. Clinical Psychology 32-43 (1987).
98 Lee J. Cronbach, Coefficient Alpha and the Internal Structure of Tests, 16 Psychometrika 297-334 (1951).
George A. Ferguson, On the Theory of Test Discrimination, 14 Psychometrika 61-68 (1949).
99 Richard A. Kulka et al., Assessment of Posttraumatic Stress Disorder in the Community: Prospects & Pitfalls From Recent Studies of Vietnam Veterans, 3 Psychological Assessment: J. Consulting & Clinical Psychology 547-60 (1991).
100 E. V. Berk et al., Traumatogenicity: Effects of Self-Reported Noncombat Trauma on MMPIs of Male Vietnam Combat and Non-Combat Veterans Treated for Substance Abuse, 45 J. Clinical Psychology 704-08 (1989).
R. Long et al., Chronicity: Adjustment Differences in Vietnam Combat Veterans Differing in Rates of Psychiatric Hospitalization, 45 J. Clinical Psychology 745-53 (1989).
W. E. Penk et al., Post-Traumatic Stress Disorder (PTSD): Issues of Utility, Traumatogenicity, Co-Morbidity, Teratogenicity vs. Psychogenicity, Ethnicity, “Gendericity” and Chronicity, 45 J. Clinical Psychology 688-90 (1989).
101 Frank W. Weathers et al., “Psychometric Theory in the Development of Posttraumatic Stress Disorder Assessment Tools,” in Assessing Psychological Trauma and PTSD, ch. 4 (John P. Wilson & Terence M. Keane eds., 1997).
Charles G. Watson, Psychometric Posttraumatic Stress Disorder Measurement Techniques: A Review, 2 Psychological Assessment: J. Consulting & Clinical Psychology 460-69 (1990).
Assessing Psychological Trauma and PTSD (John P. Wilson & Terence M. Keane eds., 1997).
102 John Briere, Psychological Assessment of Adult Posttraumatic States 107-12 (1997).
Terence M. Keane et al., Utility of Psychophysiological Measurement in the Diagnosis of Posttraumatic Stress Disorder: Results From a Department of Veterans Affairs Cooperative Study, 66 J. Consulting & Clinical Psychology 914-23 (1998).
Terence M. Keane et al., Post-Traumatic Stress Disorder: Evidence for Diagnostic Validity and Methods of Psychological Assessment, 43 J. Clinical Psychology 32-43 (1987).
103 John Briere, Psychological Assessment of Adult Posttraumatic States 109 (1997).
Brett T. Litz et al., Similarities and Differences Between MMPI & MMPI-2 Applications to the Assessment of Posttraumatic Stress Disorder, 57 J. Personality Assessment 238-53 (1991).
104 Harold R. Miller et al., What’s in a Name? The MMPI-2 PTSD Scales, 51 J. Clinical Psychology 626-61 (1995).
105 John Briere, Psychological Assessment of Adult Posttraumatic States 108 (1997).
106 John Briere, Psychological Assessment of Adult Posttraumatic States 112-17 (1997).
107 John Briere, Psychological Assessment of Adult Posttraumatic States 133-34 (1997).
Terence M. Keane et al., Mississippi Scale for Combat-Related Posttraumatic Stress Disorder: Three Studies in Reliability and Validity, 56 J. Consulting & Clinical Psychology 85-90 (1988).
Miles E. McFall et al., Reliability and Validity of Mississippi Scale for Combat-Related Posttraumatic Stress Disorder, 2 J. Consulting & Clinical Psychiatry 114-21 (1990).
108 Dawn L. Vreven et al., The Civilian Version of the Mississippi PTSD Scale: A Psychometric Evaluation, 8 J. Traumatic Stress 91-109 (1995).
John Briere, Psychological Assessment of Adult Posttraumatic States 134-35 (1997).
Dean Lauterbach et al., Psychometric Properties of the Civilian Version of the Mississippi PTSD Scale, 10 J. Traumatic Stress 499-513 (1997).
109 Fran H. Norris & Julia L. Perilla, The Revised Civilian Mississippi Scale for PTSD: Reliability, Validity, and Cross-Language Stability, 9 J. Traumatic Stress 285-98 (1996).
John Briere, Psychological Assessment of Adult Posttraumatic States 135 (1997).
110 John Briere, Psychological Assessment of Adult Posttraumatic States 130-32 (1997).
111 John Briere, Psychological Assessment of Adult Posttraumatic States 131 (1997).
112 John Briere, Psychological Assessment of Adult Posttraumatic States 131 (1997).
D. S. Weiss et al., Predicting Symptomatic Distress in Emergency Services Personnel, 63 J. Consulting & Clinical Psychology 361-68 (1995).
C. R. Marmar et al., Characteristics of Emergency Services Personnel Related to Peritraumatic Dissociation During Critical Incident Exposure, 153 Am. J. Psychiatry 94-102 (1996).
113 John Briere, Psychological Assessment of Adult Posttraumatic States 138 (1997).
Melvyn Hammarberg, Penn Inventory for Posttraumatic Stress Disorder: Psychometric Properties, 4 Psychological Assessment 67-76 (1992).
114 John Briere, Psychological Assessment of Adult Posttraumatic States 118-19 (1997).
115 John Briere, Psychological Assessment of Adult Posttraumatic States 132-33 (1997).
116 John Briere, Psychological Assessment of Adult Posttraumatic States 135-36 (1997).
117 S. A. Falsetti, The Modified PTSD Symptom Scale: A Brief Self-Report Measure of Post-traumatic Stress Disorder, 17 Behavior Therapist 66-67 (1993).
John Briere, Psychological Assessment of Adult Posttraumatic States 136 (1997).
118 John Briere, Psychological Assessment of Adult Posttraumatic States 136-37 (1997).
119 John Briere, Psychological Assessment of Adult Posttraumatic States 137-38 (1997).
120 D. Lauterbach & S. Vranna, Three Studies on the Reliability and Validity of a Self-Report Measure of Posttraumatic Stress, 3 Assessment 17-5 (1996).
John Briere, Psychological Assessment of Adult Posttraumatic States 137-38 (1997).
121 John Briere, Psychological Assessment of Adult Posttraumatic States 96-98 (1997).
Charles G. Watson et al., The PTSD Interview: Rationale, Description, Reliability, and Concurrent Validity of a DSM-III-Based Technique, 47 J. Clinical Psychology 179-88 (1991).
Daniel S. Weiss, “Structured Clinical Interview Techniques,” in International Handbook of Traumatic Stress Syndromes 179-87 (John P. Wilson & Beverley Raphael eds., 1993).
Jessica Wolfe & Terence M. Keane, “Diagnostic Validity of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder 54 (Marion E. Wolfe & Aron D. Mosnaim eds., 1990).
122 John Briere, Psychological Assessment of Adult Posttraumatic States 98 (1997).
123 John Briere, Psychological Assessment of Adult Posttraumatic States 101-02 (1997).
Dudley David Blake et al., The Development of a Clinician-Administered PTSD Scale, 8 J. Traumatic Stress 75-89 (1995).
124 Daniel S. Weiss, “Structured Clinical Interview Techniques,” in Assessing Psychological Trauma and PTSD 506-07 (John P. Wilson & Terence M. Keane eds., 1997).
125 Daniel S. Weiss, “Structured Clinical Interview Techniques,” in Assessing Psychological Trauma and PTSD 505 (John P. Wilson & Terence M. Keane eds., 1997).
John Briere, Psychological Assessment of Adult Posttraumatic States 99 (1997).
126 John Briere, Psychological Assessment of Adult Posttraumatic States 100 (1997).
Daniel S. Weiss, “Structured Clinical Interview Techniques,” in Assessing Psychological Trauma and PTSD 506 (John P. Wilson & Terence M. Keane eds., 1997).
127 Daniel S. Weiss, “Structured Clinical Interview Techniques,” in Assessing Psychological Trauma and PTSD 506 (John P. Wilson & Terence M. Keane eds., 1997).
John Briere, Psychological Assessment of Adult Posttraumatic States 99-100 (1997).
128 Patti Levin, “Assessing Posttraumatic Stress Disorder With the Rorschach Projective Technique,” in International Handbook of Traumatic Stress Syndromes 189-200 (John P. Wilson & Beverley Raphael eds., 1993).
129 J. M. Wood et al., The Comprehensive System for the Rorschach: A Critical Examination, 7 Psychological Sci. 3-10 (1996); L. R. Aiken, Personality Assessment: Methods and Practice (1996).
John Briere, Psychological Assessment of Adult Posttraumatic States 120-26 (1997).
Patti Levin & Bruce Reis, “Use of the Rorschach in Assessing Trauma,” in Assessing Psychological Trauma and PTSD ch. 9 (John P. Wilson & Terence M. Keane eds., 1997).
Scott O. Lilienfeld, Projective Measures of Personality and Psychopathology, How Well Do They Work?, Skeptical Inquirer, Sept./Oct. 1999, at 32-39.
Irving B. Weiner, Some Observations on the Validity of the Rorschach Inkblot Method, 8 Psychological Assessment 206-13 (1996).
130 Jeffrey A. Knight, “Neuropsychological Assessment in Posttraumatic Stress Disorder, in Assessing Psychological Trauma and PTSD 475-76 (John P. Wilson & Terence M. Keane eds., 1997).
131 John Briere, Psychological Assessment of Adult Posttraumatic States 83 (1997).
132 John Briere, Psychological Assessment of Adult Posttraumatic States 83-84 (1997).
133 John Briere, Psychological Assessment of Adult Posttraumatic States 84-85 (1997).
134 John Briere, Psychological Assessment of Adult Posttraumatic States 85 (1997).
135 David Faust & Jay Ziskin, The Expert Witness in Psychology and Psychiatry, 241 Science 31 (1988); Steven N. Allen, Psychological Assessment of Post-Traumatic Stress Disorder, 17 Psychiatric Clinics of N. Am. 327 (1994).
136 1 The Official ABMS Directory of Board Certified Medical Specialists (31st ed. 1999).
137 Id.
138 Ethical Principles of Psychologists and Code of Conduct, 47 Am. Psychologist 1597 (1992); American Academy of Psychiatry & the Law: Ethical Guidelines for the Practice of Forensic Psychiatry (1991); Robert I. Simon, “Toward the Development of Guidelines in the Forensic Psychiatric Examination of Posttraumatic Stress Disorder in Claimants,” in Posttraumatic Stress Disorder in Litigation 63-66 (Robert I. Simon ed., 1995).
139 DSM-IV-TR, Use of Clinical Judgment, at xxxii.
140 Id.
A differential diagnosis means different things to different people. To some it may mean an exhaustive list, not probabilistically ordered, of diagnoses that could explain a set of clinical findings. To others, it may mean a short list of diagnoses remaining after a large bulk of clinical data has been evaluated. To others, it may mean a probabilistically ordered list of potential diagnoses.
141 Arthur S. Blank, Jr., Clinical Detection, Diagnosis, and Differential Diagnosis of Post-Traumatic Stress Disorder, 17 Psychiatric Clinics of N. Am. 351-83 (1994).
Deborah A. Zarin & Felton Earls, Diagnostic Decision Making in Psychiatry, 150 Am. J. Psychiatry 197-206 (1993).
David Faust & Jay Ziskin, The Expert Witness in Psychology and Psychiatry, 241 Science 31-35 (1988).
142 John G. Gunderson & Alex N. Sabo, The Phenomenological and Conceptual Interface Between Borderline Personality Disorder and PTSD, 150 Am. J. Psychiatry 19-27 (1993).
Steven L. Shearer et al., Frequency and Correlates of Childhood Sexual and Physical Abuse Histories in Adult Female Borderline Inpatients, 147 Am. J. Psychiatry 214-16 (1990).
Susan N. Ogata et al., Childhood Sexual and Physical Abuse in Adult Patients With Borderline Personality Disorder, 147 Am. J. Psychiatry 1008-13 (1990).
Bessel A. van der Kolk & Onno van der Hart, Pierre Janet and the Breakdown of Adaptation in Psychological Trauma, 146 Am. J. Psychiatry 1530-40 (1989).
143 David Malakoff, Bayes Offers a “New” Way to Make Sense of Numbers, 286 Science 1460-64 (1999); Colin Howson & Peter Urbach, Bayesian Reasoning in Science, 350 Science 371-74 (1991).
144 J. R. T. Davidson et al., Posttraumatic Stress Disorder in the Community: An Epidemiological Study, 21 Psychological Medicine 713-21 (1991) (the lifetime prevalence of PTSD in the Piedmont region of North Carolina (using the criteria of the DSM-III measured by the Diagnostic Interview Scale) was 1.3 percent).
J. E. Helzer et al., Post-Traumatic Stress Disorder in the General Population: Findings of the Epidemiologic Catchment Area Study, 317 New Eng. J. Medicine 630-34 (1987) (the lifetime prevalence of PTSD in the St. Louis area (using the criteria of the DSM-III measured by the Diagnostic Interview Scale) was 1.0 percent).
J. H. Shore et al., Community Patterns of Posttraumatic Stress Disorders, 177 J. Nervous & Mental Disease 681-85 (1989) (the lifetime prevalence of PTSD (using the criteria of the DSM-III measured by Diagnostic Interview Schedule, criticized as lacking sensitivity to traumatic stress) was for men 2.9 percent (including combat-induced PTSD) and for women 3.3 percent).
R. S. Pynoos et al., Life Threat and Posttraumatic Stress in School-Age Children, 44 Archives Gen. Psychiatry 1057-63 (1987).
R. C. Kessler et al., Posttraumatic Stress Disorder in the National Comorbidity Survey, 52 Archives Gen. Psychiatry 1048-60 (1995) (The lifetime prevalence of PTSD (using the criteria of the DSM-III-R, measured by a modified version of the Composite International Diagnostic Interview and a modified version of the Revised Diagnostic Interview Schedule) was 7.8 percent (10.45 percent in women and 5.0 percent in men). Lifetime prevalence of exposure to trauma for men was 60.7 percent and for women 51.2 percent.).
F. H. Norris, Epidemiology of Trauma: Frequency and Impact of Different Potentially Traumatic Events on Different Demographic Groups, 60 J. Consulting & Clinical Psychology 409-18 (1992) (the prevalence of current not lifetime PTSD in 250 persons (not drawn randomly) from four southern cities (using the criteria of the DSM-III-R, measured by “The Traumatic Stress Schedule,” denied by the author) was 7.4 percent: 6.0 percent for men and 8.8 percent for women).
N. Breslau et al., Traumatic Events and Posttraumatic Stress Disorder in an Urban Population of Young Adults, 48 Archives Gen. Psychiatry 216-22 (1991) (The lifetime prevalence of PTSD (using the criteria of the DSM-III-R measured by NIMH Diagnostic Interview Schedule Version III-Revised to be more sensitive to traumatic stress) was 9.55 percent (11.3 percent in women and 5.6 percent in men). The lifetime prevalence of exposure to traumatic events qualifying for the DSM-III-R stressor criterion in this sample of young adults was 39.1 percent. The lifetime prevalence of DSM-III-R PTSD was 9.2 percent.).
Ronald C. Kessler et al., Posttraumatic Stress Disorder in the National Comorbidity Survey, 52 Archives Gen. Psychiatry 1048-60 (1995).
Jonathan R. T. Davidson & John A. Fairbank, “The Epidemiology of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder, DSM-IV and Beyond ch. 8 (J. R. T. Davidson & Edna B. Foa eds., 1993).
J. R. T. Davidson et al., Post Traumatic Stress Disorder in the Community: An Epidemiological Study, 21 Psychological Med. 1-9 (1991).
J. E. Helzer et al., Post Traumatic Stress Disorder in the General Population, 317 New Eng. J. Med. 1630-34 (1987).
DSM-IV-TR at 466.
145 Rachel Yehuda et al., Impact of Cumulative Lifetime Trauma and Recent Stress on Current Posttraumatic Stress Disorder Symptoms in Holocaust Survivors, 152 Am. J. Psychiatry 1815-18 (1995).
Rachel Yehuda et al., Vulnerability to Posttraumatic Stress Disorder in Adult Offspring of Holocaust Survivors, 155 Am. J. Psychiatry 1163-71 (1998).
Bonnie L. Green et al., Buffalo Creek Survivors in the Second Decade: Stability of Stress Symptoms, 60 Am. J. Orthopsychiatry 43-54 (1990).
Bonnie L. Green et al., Identifying Survivors at Risk: Long-Term Impairment Following the Beverly Hills Supper Club Fire, 53 J. Consulting & Clinical Psychology 672-78 (1985).
Bonnie L. Green et al., Buffalo Creek Survivors in the Second Decade: Comparison With Unexposed and Nonlitigant Groups, 20 J. Applied Soc. Psychology 1033-50 (1990).
Bonnie L. Green, “Disasters and Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder, DSM-IV and Beyond ch. 5 (J. R. T. Davidson & Edna B. Foa eds., 1993).
146 Bonnie L. Green, “Disasters and Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder, DSM-IV and Beyond ch. 5 (J. R. T. Davidson & Edna B. Foa eds., 1993).
Penny Dixon et al., Peripheral Victims of the Herald of Free Enterprise Disaster, 66 Brit. J. Med. Psychology 193-202 (1993).
147 A. C. McFarlane, The Aetiology of Post Traumatic Morbidity: Predisposing, Precipitating and Perpetuating Factors, 154 Brit. J. Psychiatry 221-28 (1989).
Dieter Wagner et al., Prevalence of Symptoms of Posttraumatic Stress Disorder in German Professional Firefighters, 155 Am. J. Psychiatry 1727-32 (1998).
Robert J. Ursano et al., Posttraumatic Stress Disorder and Identification in Disaster Workers, 156 Am. J. Psychiatry 353-59 (1999).
148 Bonnie L. Green, “Recent Research Findings on the Diagnosis of Posttraumatic Stress Disorder, Prevalence, Course, Comorbidity, and Risk,” in Posttraumatic Stress Disorder in Litigation ch. 2 (Robert L. Simon ed., 1995).
Dean G. Kilpatrick & Heidi S. Resnick, “Posttraumatic Stress Disorder Associated With Exposure to Criminal Victimization in Clinical and Community Populations,” in Posttraumatic Stress Disorder, DSM-IV and Beyond ch. 7 (J. R. T. Davidson & Edna B. Foa eds., 1993).
I. Winfield et al., Sexual Assault and Psychiatric Disorders Among Women in a Community Population, 147 Am. J. Psychiatry 335-41 (1990).
B. O. Rothbaum et al., A Prospective Examination of Post-Traumatic Stress Disorder in Rape Victims, 5 J. Traumatic Stress 455-75 (1992).
F. H. Norris, Epidemiology of Trauma: Frequency and Impact of Different Potentially Traumatic Events on Different Demographic Groups, 60 J. Consulting & Clinical Psychology 409-18 (1992).
Idee Winfield et al., Sexual Assault and Psychiatric Disorders Among a Community—Sample of Women, 147 Am. J. Psychiatry 335-41 (1990).
Glenn Craig Davis & Naomi Breslau, Post-Traumatic Stress Disorder in Victims of Civilian Trauma and Criminal Violence, 17 Psychiatric Clinics of N. Am. 289-99 (1994).
Chris R. Brewin et al., Acute Stress Disorder and Posttraumatic Stress Disorder in Victims of Violent Crime, 156 Am. J. Psychiatry 360-66 (1999).
Ned Rodriguez et al., Posttraumatic Stress Disorder in Adult Female Survivors of Childhood Sexual Abuse: A Comparison Study, 65 J. Consulting & Clinical Psychology 53-59 (1997).
149 F. H. Norris, Epidemiology of Trauma: Frequency and Impact of Different Potentially Traumatic Events on Different Demographic Groups, 60 J. Consulting & Clinical Psychology 409-18 (1992).
150 Lenore M. Williams, Recall of Childhood Trauma: A Prospective Study of Women’s Memories of Child Sexual Abuse, 62 J. Consulting & Clinical Psychology 1167-76 (1994); D. E. Russell, Sexual Exploitation: Rape, Child Sexual Abuse, and Sexual Harassment (1984); D. Finkelhor, Sexually Victimized Children (1979); S. D. Peters et al., “Prevalence,” in A Sourcebook on Child Sexual Abuse 15-59 (D. Finkelhor et al. eds., 1986); M. H. Stinson & S. S. Hendrick, Reported Childhood Sexual Abuse in University Counseling Center Clients, 39 J. Counseling Psychology 370-74 (1992); G. E. Wyatt, The Sexual Abuse of Afro-American and White-American Women in Childhood, 9 Child Abuse & Neglect 507-19 (1985); D. Stephen Lindsay & J. Don Read, Psychotherapy and Memories of Childhood Sexual Abuse: A Cognitive Perspective, 8 Applied Cognitive Psychology 281-338 (1994).
151 Dean G. Kilpatrick & Heidi S. Resnick, “Posttraumatic Stress Disorder Associated With Exposure to Criminal Victimization in Clinical and Community Populations,” in Posttraumatic Stress Disorder, DSM-IV and Beyond ch. 7 (J. R. T. Davidson & Edna B. Foa eds., 1993).
Naomi Breslau et al., Posttraumatic Events and Posttraumatic Stress Disorder in an Urban Population of Young Adults, 48 Archives Gen. Psychiatry 216-22 (1991).
152 F. H. Norris, Epidemiology of Trauma: Frequency and Impact of Different Potentially Traumatic Events on Different Demographic Groups, 60 J. Consulting & Clinical Psychology 409-18 (1992).
Edward B. Blanchard & Edward J. Hickling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors 16-19, 21-34 (1997).
153 Alan Fontana & Robert Rosenbeck, Effects of Compensation-Seeking on Treatment Outcomes Among Veterans With Posttraumatic Stress Disorder, 186 J. Nervous & Mental Disease 223-30 (“Among inpatients in programs designed programmatically to provide an extremely long length of stay (100 days on average), the motivation to apply for or to maintain compensation status appeared to inhibit improvement.”).
Paul Ekman & Maureen O’Sullivan, Who Can Catch a Liar?, 46 Am. Psychologist 921-30 (1991).
154 David Faust, The Detection of Deception, 13 Neurologic Clinics 255-65 (1995).
155 Phillip J. Resnick, “Guidelines for the Evaluation of Malingering in Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder in Litigation ch. 6 (Robert L. Simon ed., 1995).
156 John A. Fairbank et al., Psychometric Detection of Fabricated Symptoms of Posttraumatic Stress Disorder, 142 Am. J. Psychiatry 501-03 (1985).
Stephen T. Perconte & Anthony J. Goreczny, Failure to Detect Fabricated Posttraumatic Stress Disorder With the Use of the MMPI in a Clinical Population, 147 Am. J. Psychiatry 1057-60 (1990).
Paul R. Lees-Haley, Efficacy of MMPI-2 Validity Scales and MCMI-II Modifier Scales for Detecting Spurious PTSD Claims: F, F-K, Fake Bad Scale, Ego Strength, Subtle-Obvious Subscales DIS, and DEB, 48 J. Clinical Psychology 681-89 (1992).
157 Roger L. Greene, The MMPI-2/MMPI, An Interpretive Manual 50 (1991).
158 Id. at 68.
159 R. S. Epstein, Avoidant Symptoms Cloaking the Diagnosis of PTSD in Patients With Severe Accidental Injury, J. Traumatic Stress 451-58 (1993) (15 motor vehicle accident victims were followed who had been admitted to a regional trauma center. (They were interviewed periodically over nine months.) Four individuals initially met diagnostic criteria for PTSD; two others, who had partial PTSD, went on to meet delayed-onset criteria during the follow-up interval. Thus, it appears that PTSD secondary to motor vehicle accidents can have a delayed onset.).
M. M. Green et al., Undiagnosed Post-Traumatic Stress Disorder Following Motor Vehicle Accidents, 159 Med. J. Australia 529-34 (1993) (24 motor vehicle accident victims were followed over an 18-month period. Between the initial and 18th month assessments, five individuals who were not initially diagnosed with PTSD had developed symptoms severe enough to warrant a diagnosis of PTSD. It should be noted that these five participants with delayed-onset PTSD were diagnosed with borderline PTSD at the initial interview (none of those who were initially symptom-free went on to develop delayed-onset PTSD in this study). The participants were interviewed at only these two time points, making it impossible to determine whether they would have met criteria for delayed-onset PTSD by DSM-III-R standards. These five individuals were delayed in their development of the disorder in the sense that they did not meet criteria in the month after the trauma.).
R. Mayou et al., Psychiatrist Consequences of Road Traffic Accidents, 307 Brit. Med. J. 647-51 (1993) (a consecutive series of accident victims were followed who had sought medical attention after their accidents (N = 188). These accident victims were prospectively followed over a one-year period. Five individuals met criteria for PTSD three months post-trauma, eight met criteria at both the 3- and 12-month interviews, and six met criteria at the 12-month interview only. At least 6 of the 19 participants with PTSD would have met criteria for delayed-onset PTSD. It was found that poor social, medical, and occupational outcome was associated with increased psychological morbidity at one year.).
B. L. Green et al., Buffalo Creek Survivors in the Second Decade: Stability of Stress Symptoms, 60 Am. J. Orthopsychiatry 43-54 (1990) (This study reported 14-year follow-up data on a sample of individuals exposed to the devastating Buffalo Creek Dam collapse of 1972. Of those who participated in the follow-up portion of the study, 11 percent had delayed-onset PTSD. The only differentiating characteristic in the delayed-onset group in this sample was ethnicity. Caucasians were more likely than African-Americans to meet the diagnostic criteria shortly after the trauma; however, being African-American put participants at a higher risk for developing delayed-onset PTSD. Attempting to draw inferences about the nature of delayed-onset PTSD from this study would be difficult given the long interval between initial assessment and follow-up, as well as potential problems with retrospective bias.).
A. C. McFarlane, The Longitudinal Course of Posttraumatic Morbidity: The Range of Outcomes and Their Predictors, 176 J. Nervous & Medical Disease 30-39 (1988) (This study reported prospective questionnaire data on a sample of 469 Australian firefighters over a 29-month period. Of the final 315 firefighters who participated in a follow-up, 62 showed delayed onset of PTSD (20 percent). There was a statistically significant effect for the delayed-onset group to avoid thinking about their trauma shortly after the fire. Discriminate function analyses revealed that neuroticism and the impact of attending debriefing meetings were the best predictors of delayed-onset PTSD.).
T. C. Buckley et al., A Prospective Examination of Delayed Onset PTSD Secondary to Motor Vehicle Accidents, 105 J. Abnormal Psychology 617-25 (1996) (This study, another “salami” publication by this group, used 158 victims of motor vehicle accidents. Of 158 motor vehicle accident victims who had sought medical treatment within three days of the accident, on initial evaluation of PTSD one to four months post-accident, 62 met the criteria of PTSD under the DSM-III-R as measured by CAPS and 96 did not. Of the 96, seven developed PTSD during the one-year follow-up interval, with the average interval from accident to development of PTSD being 8.5 months. All of the seven had “subsyndromal PTSD” at initial evaluation (meeting clusters B and D but not C). 71 percent (five of those who developed delayed-onset PTSD] were involved in litigation.).
160 Paul R. Lees-Haley, Efficacy of MMPI-2 Validity Scales & MCMI-II Modifier Scales for Detecting Spurious PTSD Claims: F, F-K, Fake Bad Scale, Ego Strength, Subtle-Obvious Subscales, DIS & DEB, 48 J. Clinical Psychology 681-89 (1992); Paul R. Lees-Haley et al., A Fake Bad Scale on the MMPI-2 for Personal Injury Claimants, 68 Psychological Rep. 203-10 (1991).
161 Otfried Spreen & Esther Strauss, A Compendium of Neuropsychological Tests 625 (1998); P. A. Abrisi & J. S. Ben-Porath, An MMPI-2 Infrequent Response Scale for Use With Psychopathological Populations: The Infrequency—Psychopathology Scale F(p), 7 Psychological Assessment 424-31 (1995); P. A. Abrisi & J. S. Ben-Porath, Characteristics of the MMPI-2 F(p) Scale as a Function of Diagnosis in an Inpatient Sample of Veterans, 9 Psychological Assessment 102-05 (1997).
162 Landy Sparr & Loren D. Pankratz, Factitious Posttraumatic Stress Disorder, 140 Am. J. Psychiatry 1016-19 (1983); Loren Pankratz, Patients Who Deceive 169 (1998); J. A. Fairbank et al., Psychometric Detection of Fabricated Symptoms of PTSD, 142 Am. J. Psychiatry 501-03 (1985); J. E. Lynn & M. Belza, Factitious Posttraumatic Stress Disorder: The Veteran Who Never Got to Vietnam, 35 Hosp. & Community Psychiatry 697-701 (1984).
163 R. S. Epstein, Avoidant Symptoms Cloaking the Diagnosis of PTSD in Patients With Severe Accidental Injury, J. Traumatic Stress 451-58 (1993) (15 motor vehicle accident victims were followed who had been admitted to a regional trauma center. (They were interviewed periodically over nine months.) Four individuals initially met diagnostic criteria for PTSD; two others, who had partial PTSD, went on to meet delayed-onset criteria during the follow-up interval. Thus, it appears that PTSD secondary to motor vehicle accidents can have a delayed onset.).
M. M. Green et al., Undiagnosed Post-Traumatic Stress Disorder Following Motor Vehicle Accidents, 159 Med. J. Australia 529-34 (1993) (24 motor vehicle accident victims were followed over an 18-month period. Between the initial and 18th month assessments, five individuals who were not initially diagnosed with PTSD had developed symptoms severe enough to warrant a diagnosis of PTSD. It should be noted that these five participants with delayed-onset PTSD were diagnosed with borderline PTSD at the initial interview (none of those who were initially symptom-free went on to develop delayed-onset PTSD in this study). The participants were interviewed at only these two time points, making it impossible to determine whether they would have met criteria for delayed-onset PTSD by DSM-III-R standards. These five individuals were delayed in their development of the disorder in the sense that they did not meet criteria in the month after the trauma.).
R. Mayou et al., Psychiatrist Consequences of Road Traffic Accidents, 307 Brit. Med. J. 647-51 (1993) (A consecutive series of accident victims were followed who had sought medical attention after their accidents (N = 188). These accident victims were prospectively followed over a one-year period. Five individuals met criteria for PTSD three months post-trauma, eight met criteria at both the 3- and 12-month interviews, and six met criteria at the 12-month interview only. At least 6 of the 19 participants with PTSD would have met criteria for delayed-onset PTSD. It was found that poor social, medical, and occupational outcome was associated with increased psychological morbidity at one year.).
B. L. Green et al., Buffalo Creek Survivors in the Second Decade: Stability of Stress Symptoms, 60 Am. J. Orthopsychiatry 43-54 (1990) (This study reported 14-year follow-up data on a sample of individuals exposed to the devastating Buffalo Creek Dam collapse of 1972. Of those who participated in the follow-up portion of the study, 11 percent had delayed-onset PTSD. The only differentiating characteristic in the delayed-onset group in this sample was ethnicity. Caucasians were more likely than African-Americans to meet the diagnostic criteria shortly after the trauma; however, being African-American put participants at a higher risk for developing delayed-onset PTSD. Attempting to draw inferences about the nature of delayed-onset PTSD from this study would be difficult given the long interval between initial assessment and follow-up, as well as potential problems with retrospective bias.).
A. C. McFarlane, The Longitudinal Course of Posttraumatic Morbidity: The Range of Outcomes and Their Predictors, 176 J. Nervous & Medical Disease 30-39 (1988) (This study reported prospective questionnaire data on a sample of 469 Australian firefighters over a 29-month period. Of the final 315 firefighters who participated in a follow-up, 62 showed delayed onset of PTSD (20 percent). There was a statistically significant effect for the delayed-onset group to avoid thinking about their trauma shortly after the fire. Discriminate function analyses revealed that neuroticism and the impact of attending debriefing meetings were the best predictors of delayed-onset PTSD.).
T. C. Buckley et al., A Prospective Examination of Delayed Onset PTSD Secondary to Motor Vehicle Accidents, 105 J. Abnormal Psychology 617-25 (1996) (This study, another “salami” publication by this group, used 158 victims of motor vehicle accidents. Of 158 motor vehicle accident victims who had sought medical treatment within three days of the accident, on initial evaluation of PTSD one to four months post-accident, 62 met the criteria of PTSD under the DSM-III-R as measured by CAPS and 96 did not. Of the 96, seven developed PTSD during the one-year follow-up interval, with the average interval from accident to development of PTSD being 8.5 months. All of the seven had “subsyndromal PTSD” at initial evaluation (meeting clusters B and D but not C). 71 percent (five of those who developed delayed-onset PTSD) were involved in litigation.).
164 See endnote 150.
165 Rachel Yehuda et al., Conflict Between Current Knowledge About Posttraumatic Stress Disorder and Its Original Conceptual Basis, 152 Am. J. Psychiatry 1705-13 (1995); Chris R. Brewin et al., Meta-Analysis of Risk Factors for Posttraumatic Stress Disorder in Trauma-Exposed Adults, 68 J. Consulting & Clinical Psychology 748-66 (2000).
166 Arieh Y. Shaleu et al., Predictors of PTSD in Injured Trauma Survivors: A Prospective Study, 153 Am. J. Psychiatry 219-25 (1996).
Naomi Breslau et al., Risk Factors for PTSD-Related Traumatic Events: A Prospective Analysis, 152 Am. J. Psychiatry 529-35 (1995).
Sara A. Freedman et al., Predictors of Chronic Post-Traumatic Stress Disorder, 174 Brit. J. Psychiatry 353-59 (1999).
167 DSM-IV-TR at 466; 2 DSM-IV Sourcebook 588-90 (1996); Edward B. Blanchard & Edward J. Hickling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors ch. 7 (1997); Arthur S. Blank, Jr., “The Longitudinal Course of Posttraumatic Stress,” in Posttraumatic Stress Disorder DSM-IV & Beyond 3-22 (Jonathan R. T. Davidson & Edna B. Foa eds., 1993); Bonnie L. Green, “Recent Research Findings on the Diagnosis of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder in Litigation ch. 2 (Robert I. Simon ed., 1995).
168 DSM-IV-TR at 466; 2 DSM-IV Sourcebook 588-90 (1996); Edward B. Blanchard & Edward J. Hickling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors ch. 7 (1997); Arthur S. Blank, Jr., “The Longitudinal Course of Posttraumatic Stress,” in Posttraumatic Stress Disorder DSM-IV & Beyond 3-22 (Jonathan R. T. Davidson & Edna B. Foa eds., 1993); Bonnie L. Green, “Recent Research Findings on the Diagnosis of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder in Litigation ch. 2 (Robert I. Simon ed., 1995).
169 S. D. Solomon et al., Efficacy of Treatment for Post-Traumatic Stress Disorder, 268 J. Am. Med. Ass’n 633-38 (1992).
Jeffrey J. Sherman, Effects of Psychotherapeutic Treatments for PTSD: A Meta-Analysis of Controlled Clinical Trials, 11 J. Traumatic Stress 413-35 (1998).
170 S. D. Solomon et al., Efficacy of Treatment for Post-Traumatic Stress Disorder, 268 J. Am. Med. Ass’n 633-38 (1992).
171 D. Brom et al., Brief Psychotherapy for Post-Traumatic Stress Disorder, 57 J. Consulting & Clinical Psychology 607-12 (1989).
E. B. Foa & N. J. Kozak, Emotional Processing of Fear: Exposure to Corrective Information, 99 Psychological Bull. 20-35 (1986).
E. G. Peniston, EMG Biofeedback-Assisted Desensitization Treatment for Vietnam Combat Veterans’ Post-Traumatic Stress Disorder, 9 Clinical Biofeedback & Health 35-41 (1986).
172 K. Kuch, Treatment of PTSD Following Automobile Accidents, 10 Behavior Therapist 224-42 (1987).
K. Kuch et al., Post-Traumatic Stress Disorder After Car Accidents, 30 Can. J. Psychiatry 426-27 (1985).
173 Edward B. Blanchard & Edward J. Hickling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors 211-20 (1997); S. D. Solomon et al., Efficacy of Treatment for Post-Traumatic Stress Disorder, 268 J. Am. Med. Ass’n 633-38 (1992); Edna B. Foa et al., “Posttraumatic Stress Disorder,” in 2 Treatment of Psychiatric Disorders 1499-1519 (Glen O. Gabbard ed., 1995).
174 S. D. Solomon et al., Efficacy of Treatment for Post-Traumatic Stress Disorder, 268 J. Am. Med. Ass’n 633-38 (1992).
L. J. Veronen & D. G. Kilpatrick, “Stress Management for Rape Victims,” in Stress Reduction and Prevention 341-74 (D. Meichenbaum & M. E. Jaremko eds., 1983).
Edna Foa & N. J. Kozak, Emotional Processing of Fear: Exposure to Corrective Information, 99 Psychological Bull. 20-35 (1986).
Edna B. Foa et al., “Posttraumatic Stress Disorder,” in 2 Treatment of Psychiatric Disorders 1499-1519 (Glen O. Gabbard ed., 1995).
175 Julia B. Frank et al., “Antidepressants in the Treatment of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder, Etiology, Phenomenology & Treatment ch. 14 (Marion E. Wolf & Aron D. Mosnaim eds., 1990).
176 J. Davidson et al., Treatment of Posttraumatic Stress Disorder With Amitriptyline and Placebo, 47 Archives Gen. Psychiatry 259-66 (1990); C. Reist et al., Controlled Trial of Desipramine in 18 Men With Posttraumatic Stress Disorder, 146 Am. J. Psychiatry 513-16 (1976).
177 J. B. Frank et al., A Randomized Clinical Trial of Phenelzine and Imipramine for Posttraumatic Stress Disorder, 1145 Am. J. Psychiatry 1289-91 (1988).
T. R. Kosten et al., Pharmacotherapy for Posttraumatic Stress Disorder Using Phenelzine or Imipramine, 179 J. Nervous & Mental Disease 366-70 (1988).
178 Edna B. Foa et al., “Posttraumatic Stress Disorder,” in 2 Treatment of Psychiatric Disorders 1499-1519 (Glen O. Gabbard ed., 1995).
179 Matthew J. Friedman, “Interrelationships Between Biological Mechanisms and Pharmacotherapy of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder 215-17 (Marion E. Wolf & Aron D. Mosnaim eds., 1990).
180 A. Steven Lipper, “Carbamazepine in the Treatment of Posttraumatic Stress Disorder: Implications for the Kindling Hypothesis,” in Posttraumatic Stress Disorder, Etiology, Phenomenology, and Treatment ch. 15 (Marion E. Wolf & Aron D. Mosnaim eds., 1990).
181 Matthew J. Friedman, “Interrelationships Between Biological Mechanisms and Pharmacotherapy of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder 215-17 (Marion E. Wolf & Aron D. Mosnaim eds., 1990).
182 A well-known psychiatrist has remarked that:
“This report, which brings into doubt not only the treatment but the nature of the underlying ‘disease,’ has produced many agonized debates within the VA. Enthusiasts for PTSD argue that the investigators somehow missed the patients’ ‘real’ states of mind while at the same time over-looking subtle but nonetheless positive responses to treatment. They have also stepped up the search for biological evidence of brain changes produced by the emotional trauma of combat—changes that might validate chronic PTSD as a distinct condition and justify characterizing certain patients as its victims regardless of whether a successful treatment yet exists for it. In the psychiatric journals, reports of such a ‘biological marker’ come and go.
“Yet while we await final word on chronic PTSD, the skeptics—both within and without the VA system—would appear to hold much the stronger hand. They have pointed, for example, to analogous research on war veterans in Israel. According to Israeli psychiatrists, long-term treatment in hospitals has the unfortunate tendency of making battle-trauma victims hypersensitive to their symptoms and, by encouraging them to concentrate on the psychological wounds of combat, distracts their attention from the ‘here-and-now’ problems of adjusting to peace-time demands and responsibilities.
. . . .
“When a patient’s reaction does not follow this standard course, one need hardly leap to conclude he is suffering from an ‘abnormal’ or ‘chronic’ or ‘delayed’ form of PTSD. More likely, the culprit will be a separate and complicating condition like (most commonly) major depression, with its cardinal symptoms of misery, despair, and self-recrimination. In this condition, memories of past losses, defeats, or traumas are reawakened, giving content and justification to diminished attitudes about oneself. But such memories should hardly be confused with the cause of the depression itself, which can and should be treated for what it is. America’s war veterans, who are entitled to our respect and support, surely deserve better than to be maintained in a state of chronic invalidism.” Paul R. McHugh, How Psychiatry Lost Its Way, Commentary 35 (Dec. 1999).
183 Carl P. Malmquist, The Use and Misuse of Psychiatry in Sexual Harassment Cases, 26 Psychiatric Annals 149-56 (1996).
184 Edward B. Blanchard & Edward J. Hinkling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors 16-19, 21-34 (1997).
185 Margaret M. Green et al., Undiagnosed Post-traumatic Stress Disorder Following Motor Vehicle Accidents, 159 Med. J. Australia 529-34 (1993); A. Feinstein & R. Dolan, Predictors of Post-traumatic Stress Disorder Following Physical Trauma: An Examination of the Stressor Criterion, 21 Psychological Med. 85-91 (1991); R. Mayo et al., Psychiatric Consequences of Road Traffic Accidents, 307 Brit. Med. J. 647-51 (1993); A. Burstein, Posttraumatic Stress Disorder (letter), 46 J. Clinical Psychiatry 554 (1985).
186 Danny Koren et al., Acute Stress Response and Posttraumatic Stress Disorder in Traffic Accident Victims: A One-Year Prospective; Follow-Up Study, 156 Am. J. Psychiatry 367-73 (1999) (“injured victims of traumatic events, traffic accidents in our case, are at considerable risk for development of PTSD even when they are only mildly injured”).
A problem with studies assessing the correlation between the severity of motor vehicle accidents and PTSD is that no adequate measure of “severity” exists. Edward B. Blanchard & Edward J. Hinkling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors 15 (1997) (“there are no validated scales of accident severity”).
187 Edward B. Blanchard, Psychiatric Morbidity Associated With Motor Vehicle Accidents, 183 J. Nervous & Mental Disease 495-504 (1995).
Klaus Kuch et al., Posttraumatic Stress Disorder and Motor Vehicle Accidents: A Multidisciplinary Overview, 41 Can. J. Psychiatry 429-34 (1996).
Douglas L. Delahanty et al., Acute and Chronic Distress and Posttraumatic Stress Disorder as a Function of Responsibility for Serious Motor Vehicle Accidents, 65 J. Consulting & Clinical Psychology 560-67 (1997).
Allison G. Harvey et al., The Relationship Between Acute Stress Disorder and Posttraumatic Stress Disorder: A Prospective Evaluation of Motor Vehicle Accident Survivors, 66 J. Consulting & Clinical Psychology 507-12 (1998).
Paul Stallard et al., Prospective Study of Post-Traumatic Stress Disorder in Children Involved in Road Traffic Accidents, 317 Brit. Med. J. 1619-23 (1998).
Margaret M. Green et al., Undiagnosed Post-Traumatic Stress Disorder Following Motor Vehicle Accidents, 159 Med. J. Australia 529-34 (1993).
Edward B. Blanchard et al., Psychological Morbidity Associated With Motor Vehicle Accidents, 32 Behav. Res. & Therapy 283-90 (1994).
Allan Burstein, Posttraumatic Stress Disorder in Victims of Motor Vehicle Accidents, 40 Hosp. & Community Psychiatry 295-97 (1989).
Edward B. Blanchard et al., Psychophysiology of Posttraumatic Stress Disorder Related to Motor Vehicle Accidents: Replication and Extension, 64 J. Consulting & Clinical Psychology 742-51 (1996).
Danny Koren et al., Acute Stress Response and Posttraumatic Stress Disorder in Traffic Accident Victims: A One-Year Prospective, Follow-Up Study, 156 Am. J. Psychiatry 367-73 (1999).
Todd C. Buckley et al., A Prospective Examination of Delayed Onset PTSD Secondary to Motor Vehicle Accidents, 105 J. Abnormal Psychology 617-25 (1996).
Edward B. Blanchard et al., Effects of Litigation Settlements on Posttraumatic Stress Symptoms in Motor Vehicle Accidents, 11 J. Traumatic Stress 337-54 (1998).
Edward B. Blanchard et al., Prediction of Remission of Acute Posttraumatic Stress Disorder in Motor Vehicle Accident Victims, 10 J. Traumatic Stress 215-34 (1997).
Edward B. Blanchard & Edward J. Hickling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors (1997).
188 A. Blaszczynski et al., Psychiatric Morbidity Following Motor Vehicle Accidents: A Review of Methodological Issues, 39 Comprehensive Psychiatry 111-21 (1998) (a review of the studies on the relationship between motor vehicle accidents and psychiatric illness, criticizing the studies for a variety of significant methodological shortcomings, such as (1) failure to provide ratings of the severity of injury; (2) failure to use randomly selected subjects, using a disproportionate number of women and using subjects referred for medicolegal assessment; (3) failure to control for involvement in litigation; and (4) failure to specify well-defined diagnostic endpoints).
K. Kuch et al., Post-Traumatic Stress Disorder After Car Accidents, 30 Can. J. Psychiatry 426-27 (1985) (Thirty subjects involved in motor vehicle accidents were referred to a “behavioral medicine service” for a medicolegal opinion or for treatment. (The study group is the product of obvious selection bias.) There were no controls. The severity of the motor vehicle accidents was not clearly described or quantified. These subjects were evaluated under the criteria of the DSM-III, and all were found to have PTSD. Behavioral treatment was considered very successful for these subjects.).
A. Burstein, Posttraumatic Stress Disorder in Victims of Motor Vehicle Accidents, 40 Hosp. & Community Psychiatry 95-297 (1989) (The author reports his experience with 70 of his patients involved in motor vehicle accidents who were diagnosed with PTSD under the criteria of the DSM-III. There were no controls. Nor is the severity of the motor vehicle accidents described. The author remarks that it is difficult to identify those with PTSD from motor vehicle accidents for a variety of reasons: (1) the individuals are too embarrassed to report psychiatric symptoms; (2) physicians overlook psychiatric symptoms; (3) post-concussion symptoms are similar to the symptoms of PTSD and so may mask the PTSD. Subgroups of PTSD patients may be difficult to manage: those with intense feelings of re-experiencing the accident and who have poor impulse control (e.g., alcoholics, antisocial personalities, and the demented).).
E. J. Hickling et al., Motor Vehicle Accidents, Headaches, and Post-traumatic Stress Disorder: Assessment Findings in a Consecutive Series, 32 Headache 147-51 (1992) (Twenty individuals with “post-traumatic” headaches from motor vehicle accidents with suspected psychological problems were referred to a psychologist for treatment of their headaches. (A substantial likelihood of selection bias exists as a result.) Nineteen of these individuals were given psychiatric diagnoses. Of those, 15 had PTSD; 14 had a mood disorder, including 10 with major depression. For all but one, neurological exams were normal.).
E. J. Hickling, Post-traumatic Stress Disorder and Motor Vehicle Accidents, 6 J. Anxiety Disorders 83-304 (1992).
D. Brom et al., Victims of Traffic Accidents: Incidence and Prevention of Posttraumatic Stress Disorders, 49 J. Clinical Psychiatry 131-40 (1993) (Eighty-three individuals in the monitoring group (reflecting a response rate of 36 percent and with a subsequent dropout rate of 24 percent) and sixty-eight in the intervention group (reflecting a response rate of 13 percent with a subsequent dropout rate of 16 percent) involved in moderately serious to serious motor vehicle accidents in the Netherlands. These individuals were examined one and six months after the accident. After one month, 50 percent in the monitoring group and 75 percent in the intervention group showed no or hardly any symptoms, 28 percent in the monitoring group and 17 percent in the intervention group had moderate symptoms, and the remaining 22 percent in the monitoring group and 8 percent in the intervention group had reasonably severe symptoms of intrusion and avoidance. After six months, 82 percent had no symptoms; 10 percent had moderate symptoms and 8 percent had severe symptoms.).
R. Mayou et al., Psychiatric Consequences of Road Traffic Accidents, 307 Brit. Med. J. 647-51 (1993) (All subjects aged 18-70 living in Oxfordshire who had been traffic accident victims seen at the emergency room (188 subjects) were categorized into three categories: (1) multiple-injury victims who had been occupants of motor vehicles in accidents; (2) multiple-injury victims who had been motorcycle drivers or passengers; (3) whiplash-injury victims who had no other physical injury. These subjects were interviewed soon after the accident, at three months, and at six months. At the first assessment, 41 percent had elevated anxiety or depression. Eighteen percent had acute distress syndrome with horrific intrusive memories of the accident. Most subjects reported good psychological outcome at one year. Nineteen people (11 percent) satisfied the DSM-III-R criteria for PTSD. Eight individuals had PTSD at 3 and 12 months, five at 3 months only and six at 12 months only.).
M. M. Green et al., Undiagnosed Posttraumatic Stress Disorder Following Motor Vehicle Accidents, 159 Med. J. Australia 529-34 (1993) (Sixty-nine Australian adults hospitalized after motor vehicle accidents were evaluated four weeks and 18 months after the accident. The sample was biased toward people with more severe injuries who required prolonged hospitalization. At four weeks, of the 24 subjects evaluated, two were diagnosed with PTSD. At 18 months, of these subjects, one still had PTSD and the other could not be contacted. Five other individuals now were diagnosed with PTSD. Those at risk for PTSD were not predicted by the severity of their injuries or the nature of the accident but only by the perceived threat to their lives. No consideration was given to the efforts of seeking financial compensation; the rate of recruitment was low (52 percent), and the measure of disability may have been inadequate.).
E. B. Blanchard et al., Effects of Litigation Settlements on Posttraumatic Stress Symptoms in Motor Vehicle Accident Victims, 11 J. Trauma Stress 337-54 (1998) (50 motor vehicle accident victims who sought medical treatment were referred or self-referred for the study. A control group of non-motor vehicle accident subjects was constituted (40 people). Forty-six percent had PTSD and 20 percent had sub-syndromal PTSD. Previous major depression seemed to predispose the formerly depressed individual to develop PTSD. The high rate of PTSD is probably the result of selection (referral bias). The authors instructed referral sources to refer all motor vehicle accident victims rather than just those evaluated as having psychological difficulties.).
E. B. Blanchard et al., The Impact of Severity of Physical Injury and Perception of Life Threat in the Development of Post-traumatic Stress Disorder in Motor Vehicle Accident Victims, 33 Behavior Res. & Therapy 529-34 (1995) (98 motor vehicle accident victims sought medical help within a week of the accident and were referred to the authors for evaluation by local doctors or through ads in the newspaper. The subjects were evaluated with a structured clinical interview (CAPS). Only the measure of life threat or fear of death significantly predicted PTSD. The extent of the injury is a significant predictor of PTSD, but it lacks specificity.).
E. B. Blanchard et al., Psychiatric Morbidity Associated with Motor Vehicle Accidents, 183 J. Nervous & Mental Disease 495-504 (1995) (This study used 158 adults who had been in a recent motor vehicle accident and sought medical attention within a week of the accident. Subjects were evaluated one to four months after the motor vehicle accident. Sixty-one percent of the sample did not have PTSD. Of the remainder, four variables significantly predicted PTSD: (1) a prior major depressive episode; (2) fear of dying in the motor vehicle accident; (3) the extent of injury, and (4) whether the motor vehicle accident victims had contacted a lawyer, but the direction of casualty is not known.).
R. A. Bryant et al., Initial Posttraumatic Stress Responses Following Motor Vehicle Accidents, 9 J. Trauma Stress 3-234 (1996) (This study used 114 subjects involved in motor vehicle accidents (82 men and 32 women) in whom posttraumatic responses were assessed using the Impact of Event Scale (which cannot diagnose PTSD over an eight-month period after the motor vehicle accident). 25 percent and 18 percent reported extreme and moderate intrusive symptoms, respectively, and 18 percent and 32 percent reported extreme and moderate avoidance symptoms, respectively. The severity of the accident was not disclosed or quantified.).
A. Y. Shalev et al., Predictors of PTSD in Injured Trauma Survivors: A Prospective Study, 153 Am. J. Psychiatry, 219-25 (1996) (61 individuals subjected to traumatic stressors participated in a prospective study on PTSD. 51 completed the study. Of the 51, 27 had been involved in recent motor vehicle accidents. The severity of the motor vehicle accidents was not specified. Of the 51, 13 (25.5 percent) developed PTSD (DSM-III-R) at six-month assessment. (The number of motor vehicle accident victims who developed PTSD was not identified.) The authors noted that trauma severity did not predict PTSD.).
E. B. Blanchard et al., Who Develops PTSD From Motor Vehicle Accidents?, 34 Behav. Res. & Therapy 1-10 (1996) (158 recent motor vehicle accident victims seeking medical attention (but not from the authors) were compared with 93 nonaccident controls. Structured clinical interviews were used by trained clinicians to assess psychiatric status. 62 individuals (39.2 percent) had PTSD (DSM-III-R) and 45 (28.5 percent) had subsyndromal PTSD. 51 (32.3 percent) had no psychological problems. A major limitation of this study is likely selection bias.).
K. Kuch et al., Posttraumatic Stress Disorder and Motor Vehicle Accidents: A Multidisciplinary Overview, 41 Can. J. Psychiatry 429-34 (1996) (This is a literature review of recent studies on prevalence, symptom profile, and outcome of PTSD. The authors remark that “functional complaints may be reinforced inadvertently by clinicians interested in [PTSD].” “A retrospective study of [the] ferry crew after the Herald of Free Enterprise disaster” disclosed that “three years after the accident, same crew members presented with symptoms of PTSD, who had had no direct contact with the disaster, with bereaved relatives, or with rescuers.”).
D. L. Delahanty et al., Acute and Chronic Distress and Posttraumatic Stress Disorder as a Function of Responsibility for Serious Motor Vehicle Accidents, 656 J. Clinical & Consulting Psychology 560-67 (1997) (subjects who felt responsible for the motor vehicle accident had lower rates of PTSD from the accident than did those who believed another was responsible for the accident).
A. G. Harvey & R. A. Bryant, The Relationship Between Acute Stress Disorder and Posttraumatic Stress Disorder: A Prospective Evaluation of Motor Vehicle Accident Survivors, 66 J. Consulting & Clinical Psychology 507-12 (1998) (a study designed to prospectively examine the relationship between acute dissociation, acute stress disorder (ASD), and PTSD in motor vehicle accident victims. 92 subjects involved in motor vehicle accidents who sought treatment at a hospital were assessed between 2 and 26 days post-trauma. Of the 92, 71 had a follow-up assessment six months post-trauma. On initial assessment, 13 percent had ASD and 20 percent had subclinical ASD. At six months, 25 percent had PTSD and 10 percent had subclinical PTSD. 22 percent of those with ASD initially did not have PTSD six months later. Acute dissociative symptoms are important precursors of long-term PTSD, but they are not sufficient to adequately identify those at risk of developing chronic PTSD. The ASD criteria performed better in predicting the absence of PTSD than in predicting its presence.).
A. G. Harvey & R. A. Bryant, The Relationship Between Acute Stress Disorder and Posttraumatic Stress Disorder: A Two-Year Prospective Evaluation, 67 J. Consulting & Clinical Psychology 985-88 (1999) (This is a two-year follow-up of the study described by Harvey et al. in 1998 in which 92 motor vehicle accident “survivors” were assessed within one month post-trauma and 11 were assessed six months post-trauma. In this current study, 56 were assessed two years post-trauma (a 61 percent retention rate). At the two-year follow-up, 63 percent with a diagnosis of ASD met the full criteria for PTSD. Of those participants with neither full nor subsyndromal ASD, 9 percent met the full criteria for PTSD. Symptoms that had a strong positive predictive power for developing chronic PTSD were emotional numbing, depersonalization, a sense of reliving the trauma, and motor restlessness. The authors note that the current ASD criteria are not optimal and not significantly superior to PTSD criteria in predicting chronic PTSD. The authors caution, however, that the conclusions from their findings cannot be generalized to other trauma populations.).
P. Stallard et al., Prospective Study of Post-traumatic Stress Disorder in Children Involved in Road Traffic Accidents, 317 Brit. Med. J. 1619-23 (1998) (119 children involved in motor vehicle accidents who had sought medical treatment were evaluated. 41 (34.5 percent) had PTSD. Neither the type of incident nor the nature and severity of physical injuries were related to the degree of psychological distress. Some of the children with PTSD were involved in minor accidents.).
K. A. H. Mirza et al., Post-traumatic Stress Disorder in Children and Adolescents Following Road Traffic Accidents, 172 Brit. J. Psychiatry 443-47 (1998) (119 children and adolescents between 8 and 16 years of age from emergency department of a hospital were evaluated for symptoms of PTSD at four weeks and six months. No control groups were established. Accident severity was not defined. But the degree of physical injury was measured. At four weeks, 23 percent had severe PTSD, 6 percent had moderate PTSD, and 19 percent had mild PTSD. At six months, 13 had severe PTSD, 2 individuals had moderate PTSD, and 4 had mild PTSD.).
E. B. Blanchard et al., Prediction of Remission of Acute Posttraumatic Stress Disorder in Motor Vehicle Accident Victims, 10 J. Traumatic Stress 215-34 (1997) (This is another “salami” publication using this research group’s 158 victims of motor vehicle accidents. The sample, predominantly women, was not randomly selected. A motor vehicle accident was defined arbitrarily as “serious” if the “victim” sought medical attention. (No well-recognized studies exist for quantifying the seriousness of a MVA.) PTSD was assessed using the criteria of the DSM-III-R measured by Clinician-Administered PTSD scale. On initial assessment, 62 had PTSD, 45 had “sub-syndromal” PTSD, and 51 had “non-PTSD.” Slightly over half with PTSD had remitted completely or partially by six months, or eight to ten months post-motor vehicle accident. Five percent of those with sub-syndromal PTSD developed PTSD at six months. A good proportion of the remission can be predicted with three classes of variables: (1) overall degree of severity of the symptoms at initial assessment; (2) aspects of the extent of physical injury and relative recovery from the injuries; and (3) whether a family member had experienced a new trauma during the six-month follow-up.).
E. B. Blanchard et al., Effects of Litigation Settlements on Posttraumatic Stress Symptoms in Motor Vehicle Accident Victims, 11 J. Trauma Stress 337-54 (1998) (158 victims of motor vehicle accidents (108 women and 50 men) who sought medical attention within 48 hours of the accident were assessed for PTSD one to four months after the accident (using the criteria of the DSM-III-R measured by the structured clinical interview for DSM-III-R) (another in a series of “salami” publications on PTSD by this group of researchers using the same sample of 158 victims of motor vehicle accidents). 132 subjects were followed 6 months and 12 months later. Of these, 67 had filed litigation and 65 had not filed litigation. 18 in the original group were minors, 13 of whom did not file litigation. Litigants had higher PTSD symptom scores measured by CAPS, showed higher levels of subjective distress, and were more impaired than nonlitigants. Litigants who had settled by the 12-month follow-up remained more psychologically distressed than those who never litigated, but did not have statistically significant differences in posttraumatic stress symptoms. Litigants who settled improved significantly on function but continued to have psychological distress. Litigants who settled within the year of follow-up were more severely injured than those who did not settle and those who did not litigate.).
D. Koren et al., Acute Stress Response and Posttraumatic Stress Disorder in Traffic Accident Victims: A One-Year Prospective, Follow-Up Study, 156 Am. J. Psychiatry 367-73 (1999) (99 motor vehicle accident victims and 21 non-motor vehicle accident controls were prospectively followed for one year. The motor vehicle accident group was recruited from orthopedic hospital wards with mild to moderate physical injury requiring hospitalization for at least two days, and the controls from those seeking elective surgery. The dropout rate at one year was 25 percent (25/99) for the motor vehicle accident group. At one year, 32 percent had PTSD. Assessment for PTSD was not made before this time, but assessment of “PTSD symptoms” (but not PTSD) was made one week after hospitalization. From this study, the authors reached several conclusions: (1) the PTSD diagnosis among traffic accident victims was not significantly associated with any of the accident-related characteristics, including severity of injury, objective responsibility, subjective sense of guilt, and initiation of litigation; (2) previous psychiatric morbidity, especially anxiety and affective disorders, was associated with chronic PTSD; (3) no association existed between PTSD and the major characteristics of the traumatic stressor; (4) symptoms stabilized about three months post-motor vehicle accident; so three months rather than one month might be a more appropriate cutoff for the transition from acute stress disorder to PTSD; (5) PTSD appears to be an abnormal response to traumatic events in predisposed individuals; (6) mildly injured individuals in motor vehicle accidents are at considerable risk for PTSD; and (7) DSM-III-R Scale for Severity of PTSD Symptomatology and Impact of Event Scale scores at three months were the best predictors of PTSD at one year.).
R. J. Ursano et al., Acute and Chronic Posttraumatic Stress Disorder in Motor Vehicle Accident Victims, 156 Am. J. Psychiatry 589-95 (1999) (This is purportedly the only systematic long-term prospective study using structured clinical interviews to examine motor vehicle accident-related PTSD in the general population. 122 subjects involved in a motor vehicle accident and 42 controls were followed for 12 months. The motor vehicle accident subjects were recruited from a metropolitan hospital (50 percent participation rate) and from police reports of “serious” motor vehicle accidents (25 percent participation rate). A “serious” motor vehicle accident was not defined. The controls recruited from emergency rooms were treated for minor injuries from non-motor vehicle accidents. Dropout rates were at six months 23 from motor vehicle accident group and at twelve months a total of 36 from the motor vehicle accident group, leaving 86 motor vehicle accident subjects remaining (about a 30 percent dropout rate). From the study, the authors reached several conclusions: (1) PTSD is a common outcome after a serious motor vehicle accident; after one month, 34.4 percent had PTSD; after three months, 25.2 percent had PTSD (defined as chronic PTSD in the DSM-IV); after six months, 18.2 percent had PTSD; after nine months, 17.6 percent had PTSD; and after 12 months, 14 percent had PTSD; (2) previous trauma was not a risk factor but previous PTSD was a risk factor for motor vehicle accident-related PTSD; (3) chronic PTSD may be more accurately diagnosed at six months than at three months; (4) women have nearly a five times greater risk for motor vehicle accident-related PTSD but not a greater risk for chronic PTSD; and (5) individuals with a history of a major anxiety disorder are more at risk for motor vehicle accident-related acute and chronic PTSD. Individuals with a history of major depression are more at risk for acute but not chronic motor vehicle accident-related PTSD.).
A. Ehlers et al., Psychological Predictors of Chronic Posttraumatic Stress Disorder After Motor Vehicle Accidents, 107 J. Abnormal Psychology 508-19 (1998) (967 patients recruited from an emergency room in an English hospital (67.1 percent of the total patients recruited) were assessed initially and at three months or initially at one year or initially at three months and at one year using DSM-IV criteria measured by the Posttraumatic Stress Symptom Scale; at three months 23.1 percent met DSM-IV criteria for PTSD, and at one year 16.5 percent met the criteria. About half the participants met the re-experiencing, hyperarousal, and disability criteria, but far fewer also met the avoidance and numbing criteria. 6.2 percent of those who did not have PTSD at three months had PTSD at one year. Injury severity was not significantly related to PTSD diagnosis; the greatest predictors of chronic or delayed-onset PTSD were persistent health problems and financial problems owing to the accident. Although not proposed by the authors as a reason for this correlation, the reason may be a function of compensation seeking.).
T. C. Buckley et al., A Prospective Examination of Delayed Onset PTSD Secondary to Motor Vehicle Accidents, 105 J. Abnormal Psychology 617-25 (1996).
Alex Blaszczynski et al., Psychiatric Morbidity Following Motor Vehicle Accidents: A Review of Methodological Issues, 39 Comprehensive Psychiatry 111-21 (1998).
189 W. Jake Jacobs & Constance Dalenberg, Subtle Presentations of Post-Traumatic Stress Disorder, 21 Psychiatric Clinics N. Am. 835-45 (1998).
190 W. Jake Jacobs & Constance Dalenberg, Subtle Presentations of Post-Traumatic Stress Disorder, 21 Psychiatric Clinics N. Am. 835, 843 (1998).
191 These studies reported a prevalence rate for all sexual abuse at about 28 percent for girls under age 14 and 38 percent for girls under age 18.
D. E. Russell, Sexual Exploitation: Rape, Child Sexual Abuse, and Sexual Harassment (1984).
G. E. Wyatt, The Sexual Abuse of Afro-American and White American Women in Childhood, 9 Child Abuse & Neglect 231-40 (1985).
192 Paul R. Silva et al., Stress and Vulnerability to Posttraumatic Stress Disorder in Children and Adolescents, 157 Am. J. Psychiatry 1229-35 (2000).
Kathleen A. Kendall-Tackett et al., Impact of Sexual Abuse on Children: A Review and Synthesis of Recent Empirical Studies, 113 Psychological Bull. 164-80 (1993).
Lenore C. Terr, Childhood Traumas: An Outline and Overview, 148 Am. J. Psychiatry 10-20 (1991).
John S. March et al., Cognitive-Behavioral Psychotherapy for Children and Adolescents With Posttraumatic Stress Disorder After a Single-Incident Stressor, 37 J. Am. Acad. Child Adolescent Psychiatry 585-93 (1998).
Judith A. Cohen et al., Summary of the Practice Parameters for the Assessment and Treatment of Children and Adolescents With Posttraumatic Stress Disorder, 37 J. Am. Acad. Child Adolescent Psychiatry 997-1001 (1998).
Allison E. Dubner & Robert W. Motta, Sexually and Physically Abused Foster Care Children and Posttraumatic Stress Disorder, 67 J. Consulting & Clinical Psychology 367-73 (1999).
Jason L. Anthony et al., Dimensionality of Posttraumatic Stress Disorder Symptoms in Children Exposed to Disaster: Results From Confirmatory Factor Analyses, 108 J. Abnormal Psychology 326-36 (1999).
193 Richard J. McNally, Assessment of Posttraumatic Stress Disorder in Children, 3 Psychological Assessment: J. Consulting & Clinical Psychology 531-37 (1991).
Posttraumatic Stress Disorder for the Defense
By Bill Masters
Wallace, Klor & Mann, P.C.
Little Miss Muffet
Sat on a tuffet,
Eating some curds and whey.
Along came a spider,
And sat down beside her,
And frightened Miss Muffet away.
Nursery Rhyme
I. Posttraumatic Stress Disorder
A. Introduction
1. “Posttraumatic Stress Disorder” Defined
Posttraumatic stress disorder (PTSD) is, very generally, the psychological diagnosis given someone who has persistent difficulty psychologically coping with an unusually threatening experience, to a degree that interferes with his or her ability to function socially or occupationally. More specifically, PTSD is defined in the “DSM-IV-TR,” the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders, the diagnostic bible of specialists in mental health care in the United States.
In the DSM-IV-TR, PTSD consists of six basic criteria: The individual must (1) experience a traumatic event; (2) suffer cognitive dysfunction; (3) suffer behavioral dysfunction; (4) have autonomic nervous system arousal; (5) have this constellation of symptoms last more than one month; and (6) have clinically significant impairment in social function.
2. PTSD as a Bane for the Defense
For the defense, PTSD is a bane. To borrow from Shakespeare, “it harrows [us] with fear and wonder.” That fear is securely rooted in the realization that the diagnostic criteria for PTSD are basically subjective and that any disorder consisting of subjective criteria is bound to spawn frivilous litigation. The only relief from this fear springs from an appreciation of the refreshing skepticism with which many jurors, usually lacking higher education, view psychologists and psychiatrists with their black bags of amorphous diagnostic categories.
For plaintiffs’ lawyers, claims for PTSD are bliss. Simply, these claims are of the kind that can be molded into forms appealing to juries. They arise from trauma that can produce reactions with highly variable latency periods. They can result in chronic injury. They can be blamed for any or every subsequent negative life event. And they largely lack objective criteria of disproof.
As a result, PTSD is a diagnosis much abused. Abuses occur through the actions of unprincipled plaintiffs, psychological experts, and lawyers. Of possible ways by which these people may abuse the diagnosis of PTSD, the following are the most obvious: (1) an illegitimate diagnosis; (2) a legitimate diagnosis but exaggerated symptoms; and (3) legitimate symptoms and a legitimate diagnosis, but an illegitimate prognosis. As would be expected, the motives for abusing the diagnostic category PTSD are many, including: (1) plaintiff’s fraud or plaintiff’s factitious disorder; (2) lawyer “overreaching” driven by greed or overzealousness; (3) expert overreaching driven by greed, overzealousness, or ideological axe-grinding; and (4) expert incompetence.
In the end, in the context of litigation, PTSD as a diagnostic category causes two basic problems. First, it fails, for the most part, to separate those with psychological symptoms with PTSD from those with psychological symptoms but without PTSD, the true positives from the false positives, the wheat from the chaff. Second, it also seems to invite false claims, the claims of malingerers and those with factitious disorders––in short, it provides an enticement to lie, to fake, to scam, to seek that which is undeserved. But not to despair: the cure is a stalwart and savvy defense lawyer.
B. History of PTSD
Long ago, certain clusters of symptoms or syndromes were recognized to be associated with severe stress. These syndromes had a variety of names: “shell shock,” “battle fatigue,” “combat fatigue,” and “traumatic neurosis.” Eventually psychiatrists and psychologists began to seek to discern the essence of these various psychological maladies. That effort culminated in 1952 in the Diagnostic and Statistical Manual (DSM). Since then, PTSD, as a diagnostic category, has evolved through successive editions and revisions of the DSM. Understanding this evolution is important because many of the psychological studies used by plaintiffs’ experts at trial were conducted using the different conceptualizations of PTSD in the DSM-III, DSM-III-R, or DSM-IV.
1. DSM-I (1952)
Under the heading “Transient Situational Personality Disorders,” the DSM-I identified a mental disorder entitled “Gross Stress Reaction.” Gross stress reaction was characterized as primarily transient reaction to severe or extreme stress such as that experienced in combat or in civilian catastrophe.
2. DSM-II (1968)
In 1968, the DSM-I was replaced by the DSM-II, which lacked the mental disorder characterized in the DSM-I as “Gross Stress Reaction.” But it did have a disorder under the heading of “Transient Situational Disturbances” characterized as “Adjustment Reaction to Adult Life.” An example of this disorder was stated to be the “resentment with depressive tone associated with an unwanted pregnancy and manifested by hostile complaints and suicidal gestures,” or “the fear associated with military combat and manifested by trembling, running and hiding.”
3. DSM-III (1980)
In 1980, the DSM-II was replaced by the DSM-III, which reintroduced the mental disorder formerly identified under the DSM I as “Gross Stress Reaction” identifying it as “PTSD.”
In the DSM-III, PTSD was characterized more elaborately than it was in the DSM-II, but still required, as it did in the DSM-II, an “extreme stressor,” that is, a stressor that would evoke significant symptoms of distress in “almost everyone.” These symptoms were placed in three categories: (1) re-experiencing the trauma; (2) a numbing of responsiveness to the environment; and (3) increased arousal.
4. DSM-III-R (1987)
In 1987, the DSM-III was revised. The DSM-III-R continued and further amplified the concept of “PTSD,”
characterizing it as a patterned symptomatic response to an event “outside the range of usual human experience . . . markedly distressing to almost everyone.” As in the DSM-III, in the DSM-III-R the symptoms of PTSD were arranged in three categories: (1) re-experiencing the trauma; (2) a numbing of responsiveness to the environment; and (3) increased arousal. But in the DSM-III-R some criteria in the version of PTSD in the DSM-III were deleted from or moved or added to different categories of symptoms.
5. DSM-IV (1994)
In 1994, the DSM-III-R was replaced by the DSM-IV.
In the DSM-IV, PTSD is characterized essentially as it was in the DSM-III-R, except for Criteria A and C. Now, in the DSM-IV, Criterion A provides as follows:
“A. The person has been exposed to a traumatic event in which both of the following were present:
“(1) The person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others.
“(2) The person’s response involved intense fear, helplessness, or horror. Note: In children, this may be expressed instead by disorganized or agitated behavior.”
This formulation of Criterion A removes the element of objectivity inherent in that criterion in the DSM-III and DSM-III-R. Now someone who is hypersensitive to a less than extreme event is eligible for a diagnosis of PTSD.
The DSM-IV also changes Criterion C. Unlike in the DSM-III-R, in the DSM-IV, Criterion C requires both a persistent avoidance of stimuli associated with trauma and a numbing of general responsiveness rather than one or the other.
* * *
As is apparent, over the years from the DSM-I in 1952 to the DSM-IV in 1994, PTSD, as a concept, has evolved. This 40-year evolution has resulted from a variety of forces––epistemological, sociological, and political. Preeminent among these varied forces are the sociological and political, particularly the sequelae of the Vietnam War and feminist activism.
From 1950 to 1970, little research occurred into the traumatic stress response. But in the 1960s, with escalation of the Vietnam War and the growing awareness of the troubling symptom profiles of some combatants, research into the stress response was revived. As a result of this intensified research, the variety of symptoms that regularly follow trauma were more thoroughly identified.
In the 1970s, 1980s, and 1990s, the feminist movement focused on empowering women. An aspect of that movement has been characterized as the “sexual wars.” In this war of the sexes, the feminist call to arms was the thesis that many if not most men sexually abuse females of all ages. To curb this abuse, feminists armed themselves with criminal and civil laws. On the civil side, assigning a psychological disorder such as PTSD as a consequence of the abuse provides the “victim” or “survivor” with a remedy in court for damages. Having a civil action for damages enables the victim not only to curb the abuse but also to effect a transfer of wealth and to acquire power through threats of use of the legal system. Consistent with this goal, basing the mental disorder on subjective complaints and on a stressor, the severity of which is in the eye of the victim, opens the door to almost anyone who wants the entitlements associated with being labeled a “victim.”
C. Diagnostic Criteria of PTSD
The current diagnostic criteria for PTSD are found in the DSM-IV (also called the DSM-IV-TR) or, alternatively, in the International Classification of Diseases (10th Rev.) (the ICD-10).
1. DSM-IV (1994) [DSM-IV-TR (2000)]
In this country, PTSD is defined according to the specific stressor (criterion A) and symptom criteria (Criteria B, C, and D) provided in the DSM-IV. Those criteria are as follows:
“A. The person has been exposed to a traumatic event in which both of the following were present:
“(1) the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others; and
“(2) the person’s response involved intense fear, helplessness, or horror. Note: In children, this may be expressed instead by disorganized or agitated behavior.
“B. The traumatic event is persistently re-experienced in one (or more) of the following ways:
“(1) recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions. Note: In young children, repetitive play may occur in which themes or aspects of the trauma are expressed;
“(2) recurrent distressing dreams of the event. Note: In children, there may be frightening dreams without recognizable content;
“(3) acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and disassociative flashback episodes, including those that occur on awakening or when intoxicated). Note: In young children, trauma-specific reenactment may occur;
“(4) intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event; and
“(5) physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event.
“C. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by three (or more) of the following:
“(1) efforts to avoid thoughts, feelings, or conversations associated with the trauma;
“(2) efforts to avoid activities, places, or people that arouse recollections of the trauma;
“(3) inability to recall an important aspect of the trauma;
“(4) markedly diminished interest or participation in significant activities;
“(5) feeling of detachment or estrangement from others;
“(6) restricted range of affect (e.g., unable to have loving feelings); and
“(7) sense of a foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span).
“D. Persistent symptoms of increased arousal (not present before the trauma), as indicated by two (or more) of the following:
“(1) difficulty falling or staying asleep;
“(2) irritability or outbursts of anger;
“(3) difficulty concentrating;
“(4) hypervigilance; and
“(5) exaggerated startle response.
“E. Duration of the disturbance (symptoms in Criteria B, C, and D) is more than one month.
“F. The disturbance caused clinically significant distress or impairment in social, occupational, or other important areas of functioning.”
2. ICD-10
The ICD-10 provides another classificatory scheme for PTSD.
In the ICD-10, the criteria for PTSD are similar to, but in important respects different from, those criteria provided for PTSD in the DSM-IV. Indeed, the level of concordance between the criteria in the DSM-IV for PTSD and those in the ICD-10 is low. (The level of concordance is the percentage of cases with a positive diagnosis on either classification system that have a positive diagnosis on both classification systems.) For PTSD, the concordance was 35 percent, with the ICD-10 identifying cases at twice the frequency of the DSM-IV.
The defense should expect a plaintiffs’ expert to select whichever set of criteria will result in a diagnosis of PTSD.
But in the United States, it is standard to use the criteria in the DSM-IV-TR.
D. Analysis of PTSD Criteria
The criteria for PTSD expressed as Criteria A through E in the DSM-IV-TR bear detailed analysis to disclose nuances useful in fashioning a defense against a claim for alleged PTSD.
1. Criterion A – The Illusion of Objectivity
Criterion A is the gatekeeper to a diagnosis of PTSD. It has two subparts: Subpart (1) provides a limiting description of the kinds of events that can qualify as traumatic stressors. Subpart (2) provides a limiting description of the kinds of subjective responses to the event to establish that the event was in fact traumatic. More specifically, Criterion A provides:
“The person has been exposed to a traumatic event in which both of the following were present:
“(1) the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others;
“(2) the person’s response involved intense fear, helplessness, or horror. Note: In children, this may be expressed instead by disorganized or agitated behavior.”
Subpart (1) describes the kind of event that needs to be experienced as traumatic. It has pretensions of being “objective.” That is, this diagnostic criterion is not dependent entirely on the plaintiff’s subjective experience. Yet the criterion is so broad––that is, “the person was confronted with an event that involved a threat to the physical integrity of others”––that any event threatening to cause physical injury appears to qualify.
Events that are mere threats to “physical integrity” are usually considered by psychologists and psychiatrists to include all experiences of sexual assault or sexual molestation, not just those in which the victim perceives a threat of violence.
But, arguably, less significant events may be included as well, including a spectrum of events causing soft tissue injuries. For instance, Susie Trisikell confronted a small chuckhole in the path of her 25-speed Italian racing bicycle during Cycle Oregon, a chuckhole that, if ridden over, would threaten her with a bilateral strain of her gluteus maximus. Unless the phrase “physical integrity” is a term of art with an extraordinary meaning, a sprained gluteus maximus is a disruption of Susie’s “physical integrity.”
There are further ambiguities. For instance, “hindsight traumatization” from prior personal exposure to an originally nontraumatic event does not accord with the spirit of Criterion A. Yet it is not ruled out conceptually. Nor is Criterion A meant to include more indirect and impersonal experiences such as hearing a news report of a catastrophe occurring to strangers. Even so, conceptually, individuals with extreme reactions to minor trauma may qualify under Criterion A of the DSM-IV.
Somewhat in conflict with the stated DSM-IV criteria, the commentary on PTSD in the DSM-IV indicates that the stressor must be extremely traumatic. Examples include military combat, violent personal assault, severe automobile accidents, and learning about a serious injury to a family member or close friend.
As is apparent, Criterion A is a logically disjointed composition, obviously the work of a committee composed of people with opposite views, and probably represents a political compromise. Unfortunately, it is a compromise that plays into the hands of the plaintiffs’ bar, the alleged “victims” they represent, and advocacy groups, which want a shift in focus in Criterion A from the nature of the stressor to the reaction of the person, thereby increasing the subjectivity of the criterion.
* * *
Subpart (2) of Criterion A is unabashedly subjective. This requirement was designed “to qualify [for a diagnosis of PTSD] individuals making high-magnitude attributions to low-magnitude events” and thus to qualify those events as well. Regrettably, no reliable method exists to verify that an individual indeed reacted to the event with intense fear, helplessness, or horror; a plaintiff need only say that she did.
* * *
Although 38 percent of the population is exposed to catastrophic stress, only about 9.2 percent react with the symptoms characterizing PTSD.
No one knows why some people are vulnerable to catastrophic stress and others not. But risk factors for vulnerability are said to include previous exposure to unusual stress, maladaptive coping mechanisms, other adjustment problems, childhood separations, family history of antisocial behavior, being female, and having a diagnosis of borderline personality disorder.
Virtually everyone is exposed to minor stress during life, with birth being probably the first such exposure. Most people weather these stressors without developing PTSD. Yet some purportedly do develop PTSD. It is not clear why.
Following are examples highlighting the interplay between Subpart (1) and Subpart (2) of Criterion A:
Selma Bodie was told by her male employer that her work performance was substandard and that she had 60 days to improve her performance or be terminated. At that, Selma had a nervous breakdown. Would it make a difference if Selma was employed as a daycare provider, a lawyer, or a terrorist? Selma may have had an extreme reaction to that stressful news, but the stressor does not qualify under Subpart (1) of Criterion A.
* * *
Al Noid, who had been rear-ended twice in the last two months, was stopped at a stop sign in his residential neighborhood when he was rear-ended again by Lester Fourget, who was traveling ten miles an hour. Al reacted with intense fear and hopelessness. Although Al satisfied Subpart (2) of Criterion A, he probably did not satisfy Subpart (1); but he will assert that he had concern about his “physical integrity.”
* * *
Jill Owt was an attorney with five children whose husband had died unexpectedly three years earlier. Jill had an enormous occupational workload representing disadvantaged women in cases of domestic violence. Her work, besides its volume, was very stressful. Not only did she feel the strain of empathizing with abused women, but many of the women she represented had personality disorders causing a strain in their working relationship. Besides her occupational workload, she had to care for five children. Not surprisingly, apart from her job and caring for her children, she had no life. About six months ago, she began to receive complaints from her coworkers and family that she was forgetful, that she could not stay on task, that she was irritable and had frequent outbursts of anger, that she never seemed to smile anymore and increasingly wanted to be alone, and that her usually careful attention to detail and interest in helping others was waning. Although Jill has responded to the stress with intense hopelessness, she has not satisfied Subpart (1) of Criterion A.
2. Criteria B, C, and D – Symptoms in Search of a Trauma
Sometime after the traumatic event, a plaintiff must have certain kinds of symptoms to qualify for a diagnosis of PTSD. This constellation of symptoms must develop for the first time after the trauma. That is, within a reasonable time before the traumatic event, the plaintiff must have had none of the required set of symptoms described in Criteria C and D on which are based the diagnosis of PTSD.
As a rule, psychological symptoms are of four basic kinds: (1) cognition (thoughts); (2) emotions (feelings); (3) sensations (pain); and (4) behaviors (affects and actions). With those categories in mind, in reading these following PTSD symptom criteria, always ask, what might be the day-to-day manifestations or instantiations of these categories of symptoms? This task is the crucial transition from abstraction to concrete example, the process of integrating theory and experience.
* * *
3. Criterion B – Cognitive Symptoms
Criterion B requires that the traumatic event be mentally “persistently re-experienced.” This is a cognitive manifestation of PTSD. Of the three symptom criteria (Criteria B, C, and D in the DSM-IV), Criterion B is the most specific and is thus the most useful to the defense in distinguishing PTSD from other mental disorders.
“B. The traumatic event is persistently re-experienced in one (or more) of the following ways:
“(1) recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions [cognitive]. Note: In young children, repetitive play may occur in which themes or aspects of the trauma are expressed;
“(2) recurrent distressing dreams of the event. Note: In children, there may be frightening dreams without recognizable content [cognitive];
“(3) acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative flashback episodes, including those that occur on awakening or when intoxicated) [behavioral and emotional]. Note: In young children, trauma-specific reenactment may occur;
“(4) intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event [cognitive and emotional]; and
“(5) physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event [behavioral].”
The symptoms in Criterion B (re-experiencing or intrusion symptoms) are called “phasic,” in that they are manifested only from time to time.
B(1): The recollections must be “recurrent.” They must be “intrusive.” And they must be “distressing.” These recollections are not merely bad memories. They are memories that come to consciousness despite efforts to keep them from awareness.
These recollections may occur somatically. For example, they may become manifest as urinary urgency, foot pain, chest pain, or headaches.
B(2): The dreams must be “recurrent.” And they must be “distressing.” A few nightmares do not satisfy this criterion. Qualifying dreams usually represent the traumatic event symbolically, not literally. For instance, not satisfying this criterion are “dreams or recurrent nightmares of falling off a cliff.”
These dreams are in the nature of a fantasy and not linked to traumatic experiences. Nor are “dreams of monsters or other threatening fantasy figures, or anxiety dreams related to conflicts or fears involving daily living rather than traumatic exposure.”
B(3): The behavior or emotion that the traumatic events were recurring includes “illusions,” “hallucinations,” and “dissociative flashbacks.” An “illusion” is a misperception or misinterpretation of a real external stimulus, such as hearing the rustling of leaves as the sound of voices. An “hallucination” is a sensory perception that has the compelling sense of reality of a true perception but that occurs without external stimulation of the relevant sensory organ. Transient hallucinatory experiences may occur in people without mental disorders.
What is a dissociative “flashback?” A “flashback” is a recurrence of a memory, feeling, or perceptual experience from the past. “Dissociation” is a disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment. Thus, “dissociative flashback” would be a flashback that is not placed in historical context but is experienced out of context as though the recurring memory, feeling, or perception were being lived in the immediate moment.
B(4): The psychological distress must be “intense.” And the cues of that distress must resemble or symbolize the traumatic event. The psychological distress is often manifested as anxiety, anger, or “dysphoria” (depression or unhappiness). Phenomena not meeting these criteria for distress are “the sad feeling experienced at anniversaries of a trauma, but ones that do not impede ongoing function.”
B(5): “Physiological reactivity” to cues may include heart rate, skin conductance, blood pressure, and forehead electromyogram (EMG). This criterion is more objective than other symptom criteria for PTSD in the DSM-IV. Even so, some of these physiologic reactions may be simulated in those without PTSD.
4. Criterion C – Behavioral Symptoms
Criterion C requires that the plaintiff respond to environmental stimuli differently from how she did before her traumatic experience. First, she needs to persistently avoid stimuli associated with the traumatic event. Second, she needs to be generally less responsive to other kinds of stimuli. These are behavioral manifestations of PTSD.
“C. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by three (or more) of the following:
“(1) efforts to avoid thoughts, feelings, or conversations associated with the trauma [behavior re: internal cues];
“(2) efforts to avoid activities, places, or people that arouse recollections of the trauma [behavior re: external cues];
“(3) inability to recall an important aspect of the trauma [cognitive];
“(4) markedly diminished interest or participation in significant activities [emotional and cognitive];
“(5) feeling of detachment or estrangement from others [emotional];
“(6) restricted range of affect [behavioral and emotional]; and
“(7) sense of a foreshortened future [cognitive and emotional].”
The symptoms of Criterion C (avoidance symptoms) are called “tonic,” in that they are manifested most of the time. Defense counsel should also note that Criterion C has a conjunctive requirement, one arm of which––numbing––must not have preexisted the trauma. So a sound defense strategy would be to establish that the plaintiff’s history before the trauma involved a numbing of general responsiveness from, for example, depression.
Criteria C(1) and C(2) are characteristic symptoms of “phobia,” an anxiety disorder. Criteria C(4), C(5), C(6), and C(7) are characteristic symptoms of mood disorders, such as dysthymia and major depression, and of certain personality disorders, such as borderline personality disorder. A diagnosis of PTSD in a plaintiff satisfying three of Criteria C(4), C(5), C(6), and C(7), but not either Criterion C(1) or C(2) would be more suspect than a diagnosis based on C(1) and C(2).
Phenomena not qualifying as psychogenic amnesia include “forgetting minor details, or [having a] head injury, alcohol-induced ‘blackouts,’ or other neurological memory failures.”
Also not meeting the criterion are “changes in activity due to physical limitations, or the severe anhedonia of depression.”
5. Criterion D – Autonomic Arousal
Criterion D requires that the plaintiff have persistent symptoms of increased arousal. This is an autonomic nervous system manifestation of PTSD.
“D. Persistent symptoms of increased arousal (not present before the trauma), as indicated by two (or more) of the following:
“(1) difficulty falling or staying asleep [behavioral];
“(2) irritability or outbursts of anger [emotional and behavioral];
“(3) difficulty concentrating [cognitive];
“(4) hypervigilance [cognitive and behavioral]; and
“(5) exaggerated startle response [behavioral].”
* * *
The symptoms of Criterion D are characteristic of mood disorders, anxiety disorders, and certain personality disorders. These symptoms to the extent relied on to diagnose PTSD cannot have been present before the trauma.
The set of arousal symptoms in Criterion D are a mixture of tonic and phasic symptoms. Tonic arousal symptoms include insomnia and hypervigilance. Phasic arousal symptoms include exaggerated startle response and physiologic reactivity upon exposure to events that symbolize or resemble an aspect of the traumatic event.
6. Criterion E – Duration
Criterion E requires that the plaintiff’s symptoms (stated in Criteria B, C, and D) persist for more than one month. If the symptoms do not persist for one month, then the appropriate diagnosis is “acute stress disorder.”
7. Criterion F – Effect
Criterion F requires that the plaintiff’s symptoms be clinically significant––that is, produce noticeable distress or impair function in everyday activities.
II. Structuring a Defense
A claim for PTSD can be defended on a variety of bases. First, the defense may challenge the “evidential reliability” of PTSD as a diagnostic entity. Second, it may challenge the expertise of the proffered expert who has diagnosed PTSD. Third, it may assert that the diagnosis of PTSD is inaccurate because one or more of the diagnostic criteria have not been satisfied, or it may assert that the expert who diagnosed PTSD has failed to rule out other more prevalent disorders that may better account for the plaintiff’s clinical profile. Fourth, it may assert that the plaintiff is malingering. Fifth, the defense may assert that although the plaintiff appears to have PTSD, PTSD was caused by events for which the defendant is not responsible. And sixth, it may attempt to minimize the damages that the plaintiff seeks to recover for PTSD.
Selecting the bases upon which to defend should be judicious, accounting for the facts and the potential attitudes of the jury, and avoiding the “shotgun approach,” a strategy that the jury tends to perceive as a desperate and defensive grasping at straws.
A. PTSD as a Valid Diagnostic Category
“Epidemiologists like to count cases; doctors like to treat cases; and modern insurance companies will only pay for cases.”
R. E. Kendall, M.D.
“The concept of a case is a chimera existing only in the mind of the investigator.”
J. Copeland, M.D.
1. Introduction
PTSD is a diagnostic category. Whether that or any other diagnostic category is useful is gauged by the twin concepts of “validity” and “reliability.” The term “validity” refers to the objective quality of the category––that is, whether or not that category in fact measures what it purports to measure. The term “reliability” refers to the subjective quality of the category––whether or not there is intersubjective agreement from observation to observation (intra-observer agreement) and from observer to observer (inter-observer agreement) that the classification applies.
Any diagnostic category, to be considered accurate, should be validated. Determining “validity” usually requires an observationally direct or reductionistic standard of reference against which to measure the accuracy of the diagnostic category.
For example, the diagnosis of brain tumor on the basis of symptoms of impaired neurological function can be verified by the identification of the tumor through MRI, CT scan, or biopsy (surgery and histological inspection). The logical direction of this process of validation is that the relatively nonspecific but more obvious phenomena either act as a symbol for or point to less obvious but more specific pathognomonic phenomena. So to claim that a procedure is valid is to be able to provide justifications that the validator is more epistemologically secure than the procedure itself. This appeal to firmer ground is an aspect of empiricism.
But a basic problem in any process of validation is this: the theory, principle, or procedure investigated will always be underdetermined by the data. As a result, a logical and epistemic space exists in which will be at play that activity called “interpretation.” That means that the process of validation is a process of assessing an interpretation in light of other interpretations. Usually in that process, a number of interpretations may be offered. And, unfortunately, no one will have an impeccable gold standard by which to assess the merits of those various and often competing interpretations. So the process of validation becomes a process of circumferentially narrowing that logical and epistemic space through a process of argumentation or persuasion. That process of argumentation is always open-ended. And so validity is always a matter of degree. As the great biologist Edward O. Wilson wisely observed:
“Few claims in science, and particularly those entailing concepts, are accepted as final. But as evidence piles upon evidence and theories interlock more firmly, certain bodies of knowledge do gain universal acceptance.
* * *
“[Yet] no objective yardstick exists on which to mark these degrees of acceptance; there is no body of external objective truth by which they can be calibrated. There is only warranted assertibility, to use William James’ phrase, within which particular descriptions of reality grow ever more congenial to scientists until objections cease.”
The point is, validation is a process that is both scientific and rhetorical, and so requires both evidence and argument.
A variety of measures of validity exist: “face” validity, “descriptive” validity, “predictive” validity, and “construct” validity. Some are more forceful warrants than others. Face validity is expert consensus that a diagnostic category (or set of diagnostic criteria), on its face, captures accurately a specific clinical pattern of signs and symptoms.
Face validity is the appearance to those in a position to know from having observed patients that the descriptive criteria accurately resemble what is seen in patients. Less approvingly, face validity is merely the clinical, but untested, impressions of clinicians that a characteristic configuration of signs and symptoms exist. Behind the use of face validity is the assumption that other more powerful kinds of validity exist, even if not yet demonstrated.
Descriptive validity is the extent to which the characteristic features of a diagnosis are shown to be unique, setting that diagnosis apart from other diagnostic categories and, importantly, with the joint occurrence of the characteristic signs and symptoms in a heterogeneous group being more common than would be expected by chance alone.
In the context of psychological disorders, descriptive validity seeks to confirm that the behavioral manifestations of interest do not occur randomly, but cluster meaningfully into “syndromes,” a grouping of symptoms or signs that recurrently appear temporally together in many persons.
Predictive validity is the extent to which the diagnostic classification is associated with a specific course of the manifestation of disease or response to treatment.
One expects something in the future to be probabilistically determined when a person meets current criteria for the disorder.
Construct validity is the presence of evidence supporting theoretical models explaining the etiology or pathogenesis of the disease or disorder.
* * *
In an important article entitled Establishment of Diagnostic Validity in Psychiatric Illness: Its Application to Schizophrenia,
Drs. Eli Robins and Samuel. Guze identified a respected method for developing the foregoing types of validity for psychological disorders, using five kinds of studies: (1) descriptive studies of clinical phenomena; (2) laboratory studies defining unique parameters of the disorder, including chemical, physiological, radiological, anatomical, or psychological factors; (3) studies to identify variables that delimit the boundary conditions for the inclusion of patients with the disorder and the exclusion of patients who do not have the disorder; (4) long-term follow-up studies of patients to determine whether there is variability in outcome and to see whether the original cohort of patients present with the same or a different disorder; and (5) family studies to ascertain the degree to which the same disorder occurs in families.
* * *
The most problematic aspect of validating psychological disorders is the lack of a “gold standard,” “the test or procedure used to define the true state of the patient.”
As a result, the effort to validate a psychological disorder entails an admixture of judgments of both fact and value. To validate a psychological disorder, the investigators need to develop data through painstaking studies. But these data are only one variable in a matrix of judgments that together result in a diagnostic category. For example, data provide an answer if there is agreement about what the question is. Yet if the experts cannot agree about the proper construct of a psychological disorder, they cannot agree on the proper validators. If different validators validate different constructs, empirical criteria are unavailable to decide which validators are most important. That is, there are no metacriteria. For instance, expert consensus determines what standard constitutes the “gold” standard, the bedrock of any epistemological inquiry. But empirical data cannot decide whether two possibly related syndromes should be considered as (1) one disorder without subtype status, (2) one disorder with subtype status, (3) two different disorders in the same diagnostic grouping (e.g., mood disorders, anxiety disorders), or (4) two different disorders in different diagnostic groupings.
As one psychiatrist eloquently stated:
“Psychiatric diagnosis is, above all, a convention. Thus, even when an ‘atheoretical view’ and the use of the ‘best available knowledge’ suggest that a disorder is potentially valid, the ‘product’ should be ‘cleared’ by several interest groups before the official printing of the label. From such a process, the new disorder emerges cosmetically assembled for mass marketing (see, for instance, the recent controversy surrounding DSM-III-R’s masochistic personality and premenstrual syndromes).”
2. Kinds of Evidence Adduced for Validity of PTSD
Although PTSD is a stated diagnostic category in the DSM, is it a “valid” diagnostic category? For example, is PTSD merely a label for the aggravation by trauma of preexisting psychopathology?
Are the mental disorders designated as co-morbid with PTSD truly co-morbid, or are they instead the only disorders present, with PTSD being an artifact? In 1984, two highly respected psychiatrists, Drs. Goodwin and Guze, experts in validation of psychological disorders, wrote the following about the DSM-III’s “post-traumatic stress disorder, delayed type”:
“This has the same clinical features as the post-accident anxiety syndrome, but the symptoms do not appear until at least six months after the trauma. In 1980 the Veterans Administration announced that post-traumatic stress disorder, delayed type, was a compensable disorder.
* * *.
“Many veterans responded by filing claims based on their belief that they suffered from post-traumatic stress disorder, delayed type, related to traumatic war experiences. The symptoms of the disorder were well-publicized in the media and in brochures distributed by national service organizations. Rarely before had so many claimants presented themselves to psychiatric examiners having read printed symptom checklists describing the diagnostic features of the disorder for which they sought compensation. Some psychiatrists were offended by the ‘mechanical litany of complaints recited by a well-read claimant.’ The decision to award compensation was made even more difficult by the almost total lack of evidence that ‘post-traumatic stress disorder, delayed type’ exists as a clinical entity.”
Yet, today, say experts in PTSD, significant agreement exists that PTSD is valid.
(After all, it is enshrined in the DSM-IV.) So for the defense a challenge to a diagnosis of PTSD on the grounds that PTSD is not a valid diagnostic category has little or no hope of success. Even so, a critical look at the evidence purportedly validating PTSD does have some value. For if that evidence is shown to be weak or preliminary, confidence in any diagnosis of PTSD will be undermined.
In 1987, coincident with publication of the DSM-III-R, Drs. Keane and Wolfe published an article entitled Post-Traumatic Stress Disorder: Evidence for Diagnostic Validity and Methods of Psychological Assessment.
This article discussed the evidence for the validity of the PTSD construct in terms of the criteria provided by Drs. Robins and Guze. Drs. Keane and Wolfe note that “PTSD has been criticized by Goodwin and Guze and other authors for a lack of evidence that supports its existence as a diagnosis distinct from already existing categories (e.g. depression, dysthymia )[;] however, a number of recently completed studies provide supporting evidence for the validity of the PTSD diagnosis.” In the conclusion of the article, the authors note that “laboratory studies that discriminate PTSD from other psychological disorders comprise the bulk of the available evidence; definitive longitudinal studies and family studies have yet to be conducted and will provide much-needed new information on the degree to which PTSD circumscribes a unique disorder.”
As presented below, the laboratory-based data on the validity of PTSD as a diagnostic category to which they refer stem from three sources: (a) psychophysiological assessment studies, (b) psychometric studies, and (c) experimentally designed laboratory studies.
a. Psychophysiological Assessment Studies
Drs. Keane and Wolfe cited six psychophysiological assessment studies.
This collection of studies has some obvious limitations. Only three of these six studies were published. All dealt with war veterans, mostly Vietnam veterans.
b. Psychometric Studies
Drs. Keane and Wolfe cited three studies published in the early 1980s. But these three studies had limited value.
First, all three studies involved Vietnam combat veterans. Second, the psychometric measures involved “self-reports,” a relatively unreliable way to acquire information.
c. Direct Laboratory Testing
Drs. Keane and Wolfe cited one study involving direct laboratory testing.
This study also has obvious limitations. First, it was unpublished. And second, it dealt with Vietnam combat veterans. Obviously, the findings in studies involving combat veterans need to be replicated with noncombat populations to gain credibility and to ensure validity.
* * *
Three years later, in 1990, Drs. Wolfe and Keane published a review article entitled Diagnostic Validity of Posttraumatic Stress Disorder,
repeatedly cited as the definitive resource by other authors on the validity of PTSD. Their article indicates that “efforts to validate the diagnosis of PTSD are currently evolving rapidly.” (This review is dated 1990, four years before the publication of the DSM-IV in 1994.) The authors organize those efforts into “four content areas: (1) empirical efforts in diagnosis (based extensively on a variety of assessment procedures); (2) model-building attempts (emphasizing phenomenology and conceptual formulations); (3) focused biologic and physiologic approaches (reflecting the search for intrinsic biologic or centrally [central nervous system] mediated markers); and (4) epidemiologic approaches (examining disease distributions across populations).”
d. Empirical Efforts
The support for the diagnosis of PTSD has been primarily provided by procedures assessing PTSD clinically. These procedures are (i) descriptive (or case interviews), (ii) psychometric tests, and (iii) laboratory tests. Psychological assessment is considered best achieved through the “multimodal approach,” that is, through use of a comprehensive, structured assessment “battery.” These batteries consist of individual tests or structured interviews, designed to characterize the disorder and distinguish it from other serious psychological disturbances and to obtain clear-cut estimates of past and current functional abilities in a wide range of skills felt to be impacted in the development of trauma disorders.
But these batteries have flaws that tend to undermine their validity. First, the individual diagnostic instruments that make up the “battery” are based on studies of combat-related PTSD. (Those individual instruments include the Mississippi Scale for Combat-Related Posttraumatic Stress Disorder and the PTSD subscales of the MMPI.) Drs. Keane and Wolfe note that “the task remains to evaluate their utility for civilian PTSD populations.”
One instrument developed with civilian populations is the Impact of Event Scale (IES). This instrument was developed with the PTSD criteria of the DSM-III (not with the PTSD criteria of the DSM-III-R or DSM-IV). The authors note that it has a “reasonable degree of clinical and face validity,” citing the study of J. Schwarzwald et al., Validation of the Impact of Event Scale for Psychological Sequelae of Combat.
Again, this is a study cited as a warrant for use of an instrument with civilian populations “validated” through studies of combat veterans.
Second, there are few standardized, examiner-administered formats for interviews to identify PTSD. Two types of interview formats exist for use in PTSD: (i) generic psychiatric interviews and (ii) PTSD symptom-focused interviews:
i. Generic Psychiatric Interviews
The three most common psychiatric interview formats in 1990 included the Structured Clinical Interview for DSM-III-R; the Schedule for Affective Disorders and Schizophrenia; and the Diagnostic Interview Schedule. Yet these interviews lack comparative data sets to substantiate rates of diagnostic sensitivity and specificity, and “no widespread, comparative studies using diverse traumatized populations have been conducted to permit comparisons of diagnostic sensitivity and accuracy.”
ii. PTSD Symptom-Focused Interviews
Of the few such symptom-focused interviews, most have been developed with Vietnam combat veterans. The most well known are the Jackson Structured Interview for Combat-Related PTSD and the Brecksville Interview for PTSD. “No comparative data [are] available yet about the diagnostic utility of these interviews for other groups of trauma victims.” “And validational accomplishments in non combat-related PTSD are at a relatively early stage.”
e. Models in PTSD
Drs. Keane and Wolfe contrast two conceptual models of PTSD: the “reductionistic” model with the “interactive model.” Both models appear to have been derived from studies of combat veterans. The “reductionistic” model of etiology, say the authors, was popular in the earlier years and focused on the severity of the stressor, almost exclusively in Vietnam combat veterans. The more recent “interactive model” focuses on the importance of variables other than the traumatic stressor in producing PTSD, such as disposition, “personality,” “background,” and “context.” To verify this model, the authors cite four studies.
Yet these four studies again focus on combat veterans. Finally, the authors note, and this is important, “there is a need to expand diagnostic and validational approaches from Vietnam combat veterans to varying ‘victim classes’.” “As these efforts proceed,” the authors continue, “critical advances in identifying individual, categorical, and generic aspects of trauma syndromes can be expected.”
Again, Drs. Keane and Wolfe seem to be buying validity on credit.
f. Biologic–Physiologic Approaches
Some investigators have attempted to identify specific biologic, biochemical, neuroendocrinologic, or physiologic alterations in those with PTSD. Yet Drs. Keane and Wolfe note that nothing definitive has been developed for biochemical, neuroendocrinological, or pharmacological responses to validate PTSD. On the dimension of physiology, they note that some investigations have demonstrated “compelling diagnostic information on PTSD” with the presence of heart rate reactivity in certain PTSD patients that significantly distinguishes them from both well-adjusted controls and patients with other severe psychological disorders. The authors cite a previously discussed study,
as well as two additional studies.
All three studies involve only select groups of Vietnam veterans, not the general civilian population. This distressing fact tempers the external validity of these studies because, as the authors later remark, “very limited knowledge is currently available about the degree to which disparate victim classes are similar in their development and manifestation of trauma symptomatology.”
g. Epidemiologic Approaches
Drs. Keane and Wolfe report that several epidemiologic studies have attempted to document the prevalence of PTSD in the general population and in Vietnam veterans. Then they report that methodological differences in these studies, likely responsible for different end points, raise diagnostic questions and caution that more research in this area is needed. Epidemiologic studies investigate an endpoint, in this case PTSD, which is presupposed to be a valid diagnostic category. On that basis, it is difficult to see how the results of these studies validate PTSD.
* * *
In 1990, Robert W. Bulter et al. remarked that “a considerable amount of evidence has been accumulated [mostly involving Vietnam combat veterans] in support of the overall validity of PTSD as a diagnostic entity[; yet] much of this evidence . . . is based on self-report measures.”
Six years later, in 1996, one academic psychiatrist remarked that “we have not progressed beyond a face validity for PTSD, meaning it is on the level of first impressions of clinicians who are simply trying to identify a disorder . . . [and] due to the high comorbidity present with the diagnosis of PTSD, we remain distant from being able to attest to the uniqueness of this one diagnostic grouping or to its having a predictive validity.”
3. Stressors
Controversy exists whether an extreme traumatic stressor should be necessary for PTSD. Some advocate that Subpart (1) of Criterion A be abolished or reformulated in favor of purely subjective perception of the magnitude of the stressor instead of the more tightly and objectively defined current requirement.
In 1990, an exhaustive review of existing studies on the stressor criterion conducted in preparation of the DSM-IV indicated that the magnitude of the stressor was directly proportional to the risk of developing PTSD.
What constitutes the magnitude of the stressor? An adequate topology is not yet available. Generic characteristics, however, include magnitude, rate of change, duration, unpredictability, unpreparedness, and lack of prior experience. Data on this aspect of Criterion A are important to the defense. The defense is immediately interested in PTSD alleged to have arisen from stressors for which the alleged “victim” can seek legal redress. The defense is not immediately concerned, then, with PTSD from war, natural disasters, political imprisonment, or torture, but is rather concerned with PTSD from motor vehicle accidents, from harassment at the place of employment, from sexual assault, and from exposure while on the job to traumatic stressors (firefighters, police, and health care providers).
Stressors of low magnitude may create a risk of developing PTSD. But in 1990, no data were available to confirm that link. This is an important finding for the defense. Simply, the defense is often faced with claims for alleged PTSD based on stressors of low magnitude, such as the minor automobile accident or niggling harassment in the workplace.
Subpart (2) of Criterion A, the subjective evaluation of the traumatic event, was probably designed “to qualify individuals making high-magnitude attributions to low-magnitude events and thus to qualify those events as well” as causing PTSD. Yet Subpart (2) is weakly supported as correlating with PTSD. The data on this criterion were noted to be “highly confounded and largely unreplicated.”
This is also an important finding for the defense. Many claims for PTSD are based on the assertion that although the stressor may seem minor to most people, it was devastating to the plaintiff who was particularly frightened by the event.
In 1995, Rachael Yehuda et al. published a paper entitled Conflict Between Current Knowledge About Posttraumatic Stress Disorder and Its Original Conceptual Basis, in which they remarked that “many recent findings are inconsistent with the notion that traumatic events are the primary cause of symptoms and challenge the idea of PTSD as a typical stress response.”
They reached an important conclusion: PTSD following a traumatic event is the exception rather than the rule. “Among those who are exposed to very severe and prolonged trauma, there is usually a substantial number of individuals who do not develop PTSD or other psychiatric illnesses.” That is, “decompensation following trauma is neither a random process nor an outcome entirely predictable by the nature of the traumatic event.” “As such,” the authors go on to conclude, “the emergence of PTSD following exposure to a trauma may represent the manifestation of an underlying diathesis [constitutional predisposition to certain disorders] rather than a normative adaptation to environmental challenge.” That is, people with PTSD were abnormal before developing PTSD; they are the so-called “eggshell” plaintiffs. This conclusion may contradict the finding in 1990 that Subpart (2) of Criterion A has little or no empirical support, a conclusion that may move the nosology of PTSD in a direction less helpful to the defense.
4. Symptoms
PTSD comprises three sets of symptoms: (a) persistent re-experiencing of the trauma (one symptom is needed); (b) persistent avoidance and numbing (three symptoms are needed); and (c) persistent increased arousal (two symptoms are needed). Do these sets of symptoms reflect an underlying and identifiable symptom structure, or are they simply arbitrary groupings of symptoms?
a. Factor Analysis
The answer to that question is sought from both “factor analytic” studies and “longitudinal” studies of victims of trauma. In 1991, Drs. Davidson and Foa remarked that “in preparation for the DSM-IV, the work group has also considered the validity of the diagnostic criteria for posttraumatic stress disorder . . . [and] literature reviews have concluded that among veterans and disaster victims, . . . the emergent factor loadings broadly correspond with the intrusive, avoidance, and hyperarousal clusters found in DSM-III-R.”
But these authors provided no citation to these factor analytic studies.
A major limitation of most studies of PTSD is that they are retrospective and so may confuse cause and effect. As a result, “investigators of posttraumatic stress disorder (PTSD) [have] difficulty in determining the relative contributions to its etiology of the traumatic experience and of preexisting psychopathology in the victim of the trauma.” “From a research standpoint, keeping the stressor as a part of the diagnosis builds in a confound that makes it impossible to empirically assess PTSD as a response.”
Much of the criticism about the symptom criteria of PTSD is that too many symptoms are required to define PTSD. For instance, some advocate reducing the number of avoidance symptoms from three to two. Obviously, this proposal does not help the defense.
Some advocate separating the avoidance symptoms from the numbing symptoms, placing each in separate categories. They believe the numbing symptoms are central to the diagnosis of PTSD and better than other symptoms at distinguishing those with PTSD from those without PTSD. Some relatively recent factor analytic studies support the position that the avoidance and numbing criteria of Criterion C should be separated into distinct categories.
That would be a step in a direction favorable to the defense in that it raises the bar to diagnosis of PTSD.
Some factor analytic studies have found weak factor loadings for PTSD items reflecting memory difficulties. This evidence could be helpful to the defense in undermining the validity of the so-called “repressed memory syndrome.”
Thirteen factor analytic studies of PTSD symptoms have been published:
DSM-III: Eight of these factor analytic studies concern the DSM-III. These eight studies factor analyzed heterogeneous item pools, consisting of items assessing a subset of DSM-III-R or DSM-IV PTSD symptoms mixed with items assessing other symptoms. As a result, analyses of the item pools make it difficult to identify PTSD factors. There may have been too few PTSD items to reliably identify PTSD factors, and identification of these factors may be obscured by the inclusion of items assessing other types of symptoms.
DSM-III-R and DSM-IV: The five studies based on the criteria of DSM-III-R or DSM-IV are not in complete agreement.
b. Psychophysiologic Responses
Because virtually all the indicia of PTSD are “symptoms” (that is, subjective reports from the patient of this or that cognition, emotion, or behavior) the Holy Grail for PTSD researchers and devotees is a biological marker (a sign) that more objectively distinguishes those with PTSD from those without PTSD. In this regard, arguably two somewhat objective indicia of PTSD could make the diagnosis of PTSD more objective and less dependent on the patient’s self-reports. These criteria are found in Section B(5), “physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event,” and D(5), “exaggerated startle response.”
Neither of these criteria [B(5) and D(5)] is necessary to the diagnosis of PTSD, but if their validity is established, each, if present, may make the diagnosis of PTSD difficult to refute. Obviously, the defense should expect plaintiffs’ experts to focus on these two criteria in an effort to validate their diagnoses of PTSD.
What empirical support is there for these two criteria? There is nothing impressive. A number of studies have been conducted that purport to attach psychological significance to physiologic signals. These studies concern the “phasic” aspects of PTSD and are considered biological because the dependent variable is biological. The idea behind these alleged biological indicia of PTSD is that the traumatic event is an unconditional stimulus, and later stimuli associated with the traumatic event act as conditioned stimuli to elicit conditioned responses in the form of these two physiologic responses.
But this psychophysiological process is not that straightforward. That is, a variety of irrelevant individual differences or other nuisance factors can affect psychophysiological responses. The result is often ambiguity about the link between psychophysiological responses and psychological constructs. To reduce the ambiguities, investigators should explicitly incorporate procedures for testing alternate hypotheses. They should also incorporate multiple physiological responses. They should examine the pattern of responsivity over time. (Though important, the reliability of psychophysiological responses recorded on a single occasion is rarely assessed or reported.) And they should adopt standardized procedures. If a psychophysiological response truly assessed individual differences, significant test-retest stability should exist across various measurements. Yet, as a rule, the temporal stability of psychophysiological responses has been low.
i. Physiologic Reactivity on Exposure to Cues
A number of studies concern the effect of environmental cues on various autonomic physiologic responses, such as heart rate and skin conductance. This literature is described by PTSD insiders as “robust” and “considerable” and as supporting the usefulness of psychophysiological techniques for diagnosing and characterizing PTSD. Yet a closer examination of these studies and their methodologies creates significant concern about the clinical value of tests for physiologic responses in diagnosing PTSD, especially in civilian populations.
Dr. Keane et al. noted that these foregoing psychophysiologic studies have “methodological limitations” that preclude definitive conclusions about diagnostic accuracy. First, a high PTSD base rate exists in studies using psychophysiologic variables to classify participants relative to diagnostic status. Second, nearly all studies of reactivity to trauma-relevant cues include a major comparison group composed of well-adjusted combat veterans, typically volunteers. Comparison with these groups can inflate diagnostic hit rates by capitalizing on the myriad differences irrespective of PTSD status. Third, there has been a failure to adequately demonstrate cross-validation of the classification equations. Most studies have not attempted cross-validation on an independent sample or had too few participants to adequately test stability of the prediction equations. Fourth, the studies have not used multivariate analytic methods to investigate classification accuracy because sample sizes have been too small.
Moreover, as many as 40 percent of patients with PTSD do not show the expected elevation in reactivity to trauma cues. In fact, one researcher highlighted a trend across studies that indicates better performance in identifying individuals who do not qualify for an interview-based PTSD diagnosis than in identifying those who do qualify for the diagnosis. Obviously, all in all cumulating the results of a number of defectively designed studies does not add up to the results of a well-designed study.
ii. Exaggerated Startle Response
Exaggerated startle in PTSD is suggested to be a conditioned emotional response to stimuli reminiscent of the trauma. In 1990, Robert W. Bulter et al. noted that “remarkably little work has been directed toward validating the presence of exaggerated startle response in PTSD.”
Including exaggerated startle as a feature of PTSD in the DSM-III in 1980 was primarily the result of data from “case studies.” Case studies, as a form of evidentiary warrant, are generally insufficient to establish a cause-and-effect relationship between eyeblink startle and PTSD.
Subsequently conducted were laboratory studies of the eyeblink startle response in those diagnosed with PTSD. The results of those studies are ambiguous. As late as 1996, C. A. Morgan et al. remarked that “at this time there are not enough data to make inferences about the nature of the pathophysiology of PTSD, as measured by the startle response, from one patient population to another.”
What was true in 1996 is true today.
5. Chronicity
PTSD has generally been found to remain present for at least one year in about half of the cases. Data about the chronicity of PTSD are obtained from cross-sectional studies and prospective studies.
a. Cross-Sectional Studies
A number of cross-sectional studies indicate that stress-related symptoms persist years after the trauma.
b. Prospective Studies
Most prospective studies have shown a decrease in psychological stress-related symptoms over time.
6. Delayed Onset
In the DSM-IV, if onset of symptoms is at least six months after the stressor, the PTSD is characterized as “with delayed onset.” The distinction between “acute” versus “delayed” PTSD is based on uncontrolled clinical observations, that is, case studies.
PTSD with delayed onset is extremely rare. Indeed, some psychiatrists and psychologists doubt its validity, attributing reports of delayed onset to prestressor psychopathology, drug abuse, factitious disorder, and malingering.
7. Validity of Other Traumatic Response Syndromes
O misery! The things I have suffered, cause enough for deep lamentations! O you cursed sons of a hateful mother, a plague on you!
Euripides, Medea
What should such fellows as I do crawling between heaven and earth? We are arrant knaves all; believe none of us.
Shakespeare, Hamlet, III, i, 128
a. Introduction
A number of so-called disorders with elements of PTSD have been created and labeled for sociopolitical purposes. Prominent among them are “Complex Posttraumatic Stress Disorder,” the “Battered Woman Syndrome,” and the “Repressed Memory Syndrome.” Although a challenge to PTSD as defined in the DSM-IV on the grounds of validity is likely to be unsuccessful, a challenge to these nonstandard, often politically motivated syndromes is more likely to be successful.
These nonstandard traumatic response syndromes cannot be adequately understood without understanding the social context in which they have arisen. In short, traumatic response syndromes have become a handmaiden of the “gender” politics of the so-called “Cultural Left.” That is, a cadre of radical feminists have used and continue to use these diagnostic categories to fight, with passionate intensity, for their comrades against omnipresent patriarchal oppressors, who apparently are to them, among other things, all too frequently pervasive sexual abusers and systematic traumatizers of women and children. Because these traumatic response syndromes label someone––a victim––with a chronic psychological injury as the result of trauma often instituted by a victimizer, they are a weapon. Like any weapon, they can be used for good or ill, as a shield or sword, for remediation of legitimate individual loss or to achieve ulterior ideological or political goals.
For the defense, the battle is with that subclass of psychological therapists who have decided to use these various trauma response syndromes, including PTSD, under the guise of remedying an individual psychological loss to effect politicosocial change (akin to the state use in the old USSR of psychiatric diagnoses to neutralize political dissidents). This is the therapist who couldn’t care less whether or not the trauma response syndrome as a construct or as a diagnosis is valid. They are therapists who are completely and perversely insensitive to the number of false positive diagnoses of sexual abuse that their nosological concepts and diagnostic techniques generate, even though for those falsely accused of sexually abusing someone, the consequences of such a misdiagnosis are personally and socially devastating.
These therapists are relatively easy to identify. They tend to speak the jargon of the “neo-Marxist” (or “Cultural Leftist”): “dominant classes,” “secret, conspiratorial efforts to dominate the weak and dependent,” “dominating cultures,” “privileging,” “underclasses,” “oppressors,” “victims,” “historical forces,” “evil deterministic environments.” Whereas Marx spoke of insidious deterministic economic forces, these neo-Marxists speak of the insidious forces of gender. Whereas Marxists had the capitalistic manifesto, the neo-Marxists have the cultural manifesto, an array of ill-conceived handbooks on “victim or survivor syndromes.”
In their discourse, these therapists invariably tell highly crafted, stylized stories of victimization, ignoring or suppressing other equally resonant stories that would tend to cast these so-called “victims” in a less favorable light. An example is the psychotherapist who sees all men as victimizers and all women as victims. The upshot is that the worldview of these therapists is seen to be tenaciously biased and reductionistic: all the ills of this world are the fault of men.
Listen, for example, to the militant tone of feminist therapist Dr. Judith Herman:
“Violence is a routine part of women’s sexual and domestic lives. . .. For most of the twentieth century, it was the study of combat veterans that led to the development of a body of knowledge about traumatic disorders. Not until the women’s liberation movement of the 1970’s was it recognized that the most common post-traumatic disorders are those not of men in war but of women in civilian life.
* * *
“… Man’s discovery that his genitalia could serve as a weapon to generate fear must rank as one of the most important discoveries of prehistoric times, along with the use of fire and the first crude stone axe. From prehistoric times to the present, I believe, rape has played a critical function. It is nothing more or less than a conscious process of intimidation by which all men keep all women in a state of fear.
“The systematic study of psychological trauma therefore depends on the support of a political movement. . . . Advances in the field occur only when they are supported by a political movement powerful enough to legitimate any alliance between investigators and patients and to counteract the ordinary social processes of silencing and denial.”
b. Complex Posttraumatic Stress Disorder
Complex posttraumatic stress disorder is the creation of feminist therapist Dr. Judith Herman. It is, for all practical purposes, designed to apply to, in Dr. Herman’s words, “those subjected to totalitarian systems in sexual and domestic life”––that is, all women in patriarchal societies. This syndrome has not been validated and by its terms could encompass virtually any mental disorder or transient malady of any woman in our society.
Considerable controversy exists over the purported connection between severe, chronic childhood trauma and PTSD. Most consider such early childhood traumatic experiences as merely a risk factor for later PTSD. Others consider such traumatic experiences as producing a form of PTSD, which they wanted included in the DSM-IV under the rubric Disorder of Extreme Stress Not Otherwise Specified (DESNOS), or “Complex PTSD.” Critics of both positions point out that although early or extremely severe trauma in childhood often results in significant mental illness, that illness seems to be different in kind from PTSD. Indeed, that mental illness is reflected in a pattern of self-abuse, dissociation, chronic affective and personality changes, and a tendency to being repeatedly victimized. This pattern is more closely allied with the dissociative disorders and certain personality disorders like borderline personality disorder or the proposed “self-defeating personality disorder.”
Complex PTSD or DESNOS was considered in field trials for the DSM-IV. During those trials, the investigators examined the reliability, validity, internal consistency, and overlap of Complex PTSD with PTSD. The result was that, currently, Complex PTSD is not listed in Appendix B of the DSM-IV under Criteria Sets and Axes Provided for Further Study.
c. The Battered Woman Syndrome
The battered woman syndrome (BWS) identifies and describes “patterns of responses and perceptions characteristic of women who have been subjected to continuous physical or psychological abuse by their mates.”
The pattern typically includes psychophysiological stress, lowered self-esteem, learned helplessness, and idealization of the abuser. Its essence is that the battered woman is psychologically compelled to commit violence against the victimizer (usually her husband or boyfriend) or against someone else at the direction of the victimizer. Basically, BWS is a concept used by criminal defense and plaintiffs’ lawyers to exculpate their female clients, either to have them acquitted of violent domestic crimes or to obtain monetary verdicts in their favor against their husbands or boyfriends.
An interesting example of this defense occurred in the criminal defense of Karla Homolka, a Canadian model who assisted her boyfriend, Paul Bernardo, in kidnapping, sexually abusing, and strangling teenage girls. When Bernardo was torturing his victims upstairs in his home, Homolka, as she recalls, went downstairs to blow-dry her hair because “I didn’t want to stay upstairs.” Shortly later, she and Bernardo went to her parents’ house for Easter dinner, and she gave Bernardo a card wishing Happy Easter “to the most wonderful man in the whole wide world.” When prosecuted, in her defense, Homolka claimed she was beaten into submission and blackmailed by Bernardo into helping him fulfill his fantasies of having “sex slaves.”
Defense counsel will rarely defend a woman alleged to have battered her spouse in a case in which BWS arises. The more likely event is that the defense will be defending a third party alleged to be responsible for a traumatic event causing PTSD in an individual who has also been battered by her spouse. Then the issue arises whether the PTSD-like symptoms were caused by the battering or instead by the alternative traumatic event.
BWS resembles PTSD and is often used in conjunction with PTSD. Indeed, an expert may describe BWS as a “subset of PTSD.”
Yet to the extent that BWS is something other than PTSD, it has not been validated as a psychological disorder and is not listed in the DSMIVTR.
d. Repressed Memory Syndrome
Repressed memory syndrome (RMS) is a cluster of symptoms, many overlapping with those of PTSD, in which is prominent the phenomenon known as “dissociative amnesia.”
Dissociative amnesia is an “inability to recall important personal information, usually of a traumatic or stressful nature, that is too extensive to be explained by ordinary forgetfulness.” So with reference to PTSD, what the patient has is the inability to recall the traumatic event, which would satisfy the requirement of Subpart (1) of Criterion A.
The traumatic event is “remembered” many years later, usually with the help of, or at least the suggestion of, a dogged and dedicated therapist, who largely presumes that the trauma existed either because of the patient’s gender or because of the nature of the patient’s psychological or physical symptoms. The sociopolitical dimension of RMS is that the trauma is typically female childhood sexual abuse purportedly inflicted by a male, usually a member of the victim’s family, and the dogged therapist is usually a radical feminist (a “Cultural Leftist”). Indeed, a variety of highly respected specialists in mental health care have remarked that the increased use in clinical practice in America of the idea of “repression” is the result of desire for social changes rather than a product of scientific progress.
Repressed memory of traumatic events or conditions is a clinical phenomenon described in several places in the DSM-IV: for instance, PTSD, acute stress disorder, somatization disorder, and dissociative amnesia. The traumatic event may be childhood sexual abuse. But this phenomenon of “repressed memory” or “dissociative amnesia” should be distinguished, some say, from “repressed” or “recovered” memory syndrome. The repressed memory syndrome is defined as “the propensity of some victims of major trauma to experience complete absence of awareness or memory of a traumatic event from the time of its occurrence until a period of years thereafter.”
Distinguish the repressed memory syndrome from the false memory syndrome, defined as “a condition in which a person’s identity and interpersonal relationships are centered around a memory of traumatic experience which is objectively false but in which the person strongly believes.”
This dispute over “repressed memory” is relevant to claims for PTSD when the claimant is alleging a recovered memory (a memory theretofore unrecovered owing to dissociative amnesia) of sexual or physical abuse, whether during childhood or adulthood, and that abuse is alleged to have resulted in PTSD. If an individual with dissociative amnesia of childhood sexual abuse has a clinical profile (a cluster of nonspecific symptoms) satisfying the criteria of PTSD, then she is diagnosed with “PTSD.” If she does not satisfy those criteria and does not satisfy the criteria of acute stress disorder or somatization disorder, she will be diagnosed with dissociative amnesia. But she should not be diagnosed with repressed memory syndrome, which is not a validated clinical entity and which is not listed in the DSMIVTR.
The defense lawyer may be enlisted on either side of this dispute over repressed memories: (1) the defense lawyer may defend the alleged sexual abuser when sued by the alleged victim or (2) the defense lawyer may defend the therapist who is accused of committing malpractice by implanting false memories of childhood sexual abuse.
The underlying premises of the repressed memory syndrome are (1) that the initial memory for a trauma is fixed or indelible; (2) that the memory is not conscious; that is, it is “repressed,” until years later when, through a variety of therapeutic techniques (“memory work”), it becomes conscious; and (3) that these therapeutic techniques do not confound the process of recovering these indelible memories. Yet these three assumptions are not supported by the weight of evidence.
The first assumption is not only unsupported but contradicted by the experimental evidence. That research indicates that memory is not fixed and indelible, remaining over time remarkably accurate, but is rather malleable and subject to the misinformation effect, the process of distorting memory through integrating false post-event information into subsequent accounts of the event. Indeed, painstaking, thoughtful research has shown that entire scenes of stressful events can be fabricated and then inserted in another’s memory.
The second assumption is also not supported by the experimental evidence. The psychological process of repression is merely a hypothesis. Not surprisingly, studies cited to support that hypothesis of repressed memory are not of a high methodological quality. Many of them have not even been published. Many, if published, have not been published in peer-reviewed journals or journals reviewed by those outside the repressed memory establishment (an ideologically motivated group with weak scientific credentials).
Most, if not all, conclusions supporting RMS rest on “case studies.” Case studies are anecdotal, unrepeatable, uncontrolled, unrepresentative, subjectively interpreted, and not amenable to statistical analysis. The case study is thus useful only in two situations: First, it can generate some fresh conjecture that is then amenable to empirical testing. Second, the case embodies an effective refutation of a particular hypothesis. But case studies are insufficient to establish the relationship of cause and effect.
If psychologists and psychiatrists are to understand how well they can predict, they must rely on prospective (not retrospective) studies involving careful record keeping. The proper study design to investigate dissociative amnesia must have these features: (1) the study group must have unequivocally documented trauma; (2) all the subjects must have been abused while older than age 5; (3) all subjects must be interviewed about their past history of trauma; (4) subjects who denied abuse on the general interview must receive a clarification interview in which they are directly asked about the known abuse. If some failed to recollect the abuse, this would suggest repression.
Prospective studies have failed to demonstrate that dissociative amnesia results from trauma. In these prospective studies, the investigators have followed up victims of a known past traumatic event and then assessed their memories at the time of evaluation, eliminating the problem of recall bias. These prospectively designed studies are vastly superior to the retrospectively designed studies, relied upon by the cadre of repressed memory therapists. In those retrospective studies, the subjects did not display amnesia at the time of index evaluation, but were believed to have experienced amnesia in the past. As a result, these retrospective studies have serious methodological limitations, especially the limitation of “recall bias.”
* * *
Drs. Harrison Pope and Judith Hudson et al. analyzed the available prospective studies in great detail and found that “when trauma victims were asked directly about their known experience, they consistently reported memories.” “Non-reporting was encountered only in those studies where the investigators failed to ask subjects directly about the event.” “Such non-reporting must not be assumed to reflect amnesia: a large literature has shown that when not asked directly interviewees will frequently not disclose sensitive autobiographical information that they actually remember.” “Among the prospective studies . . ., non-reporting by trauma victims could be readily explained by ordinary and well-established processes without the need to postulate a novel process such as ‘dissociative amnesia’.”
Moreover, Drs. Kendall and Tackett, in a comprehensive review examining 45 studies of 3,369 victims of sexual abuse, describe no evidence of dissociative amnesia.
The third assumption––that therapeutic techniques used with RMS patients do not confound the process of recovering these memories––is also unsupported by the evidence. Therapists can implant false memories of abuse. This process of “implanting memories” is partly due to the fact that biographical memory is a reconstructive process in which memories are not retrieved unchanged, but rather “reconstructed and elaborated by all kinds of subsequent influences.”
First, the therapist focuses on exceedingly prevalent, nonspecific symptoms that are both ontologically and epistemologically subjective. To many of these therapists, the “factoid” of sexual abuse is written in the patients’ symptoms. No memory of abuse or independent verification of abuse is required. “The inference of a history of childhood sexual abuse, based solely on adult mental behavioral symptoms, is impermissible on both scientific and logical grounds.” “Scientifically, such an inference is impermissible because there is no empirical evidence for a specific association between child-sexual abuse and these symptoms.” “But even if such associations were established empirically, the inference of childhood sexual abuse from adult psychological symptoms would remain logically impermissible because such an inference violates normative rules of deductive reasoning (it is, in fact, an example of the common logical error of affirming the consequent).”
Next, the therapist sets about to convince the patient that these problems have a single pathogenesis: childhood sexual abuse. To do this, RMS therapists use techniques well recognized for their ability to increase suggestibility and for their potential for creating pseudomemories, including: (1) hypnosis; (2) age regression; (3) guided visualization; (4) relaxation; (5) group processes; (6) role-playing; (7) leading questioning techniques; (8) teaching patients to classify frankly speculative or confabulated scenarios as memories; (9) sexualized dream interpretation; (10) body memory interpretation; (11) aggressive sodium amytal interviews; and (12) misleading bibliotherapy.
These are dangerous techniques. If an overzealous or unscrupulous therapist can implant false memories of a traumatic event such that the alleged victim begins to have intrusive memories of the supposed event, then a claim of PTSD can be manufactured from suggestion and fantasy, not from the result of fact. What is of concern is the apparent “observer bias” involved in those who diagnose these “disorders.” All scientifically oriented investigators are familiar with the phenomenon of “observer bias.” That is, the observers see what they want to see, not what is before their eyes. This bias is suspected to be at the bottom of many claims of recovered memories of sexual and physical abuse.
No better evidence exists on the play of observer bias than the kinds of “survivors” who profess to have repressed memories of abuse. There are four distinct groups of “survivors” involved in this repressed memory game: (1) the religious fundamentalists who believe that almost all females have been victims of satanic rituals; (2) the gender feminists who believe they have been victims of childhood sexual abuse by close male family members; (3) the science fiction trekkies who believe they have been abducted and sexually abused by space aliens; and (4) the counterculturalists under the influence of Eastern religions who believe in reincarnation and who believe they were abused in past lives. The belief of repressed memory therapists in satanic ritual abuse, alien abductions, and abuse in past lives constitutes the reductio ad absurdum in this entire therapeutic field.
A recent review of the literature for clinical studies on repression of childhood sexual abuse finds only four studies—all of which are seriously flawed, leading the reviewers, Drs. Pope and Hudson of the Harvard Medical School, to conclude:
“[P]resent evidence is insufficient to permit the conclusion that individuals can ‘repress’ memories of childhood sexual abuse . . .. This finding is surprising, since many writers have suggested that there is a high prevalence of repression in the population.
. . . .
“It might be argued that this dearth of studies is due to the difficulty of documenting trauma and demonstrating amnesia. But if repression affects even a small fraction of abused individuals, one would expect hundreds of thousands, if not millions, of current cases in the United States alone, and even larger numbers worldwide.”
B. Reliability of Diagnosing PTSD
1. Introduction
Reliability (or “precision”) refers to consistency among those who assess accuracy.
That is, “reliability” refers to (1) whether those who measure a variable agree from observation to observation or measurement to measurement on the values of that variable and (2) whether different clinicians measuring, examining, or assessing the same variable obtain similar values. Proffered clinical evidence is unreliable if a series of clinical assessments exist on an aspect of the diagnosis and these assessments are, for the most part, different.
Reliability does not imply validity. Simply, although phenomena such as symptoms are observed consistently, nothing guarantees that these symptoms in fact measure what they purport to measure. Even so, “reliability” is an indicator of “validity.” That is, if a symptom or sign is unreliable, it has questionable validity. For example, if our clocks did not generally agree with one another, we could not use them to measure time. Our clocks would not measure falsely; they would not measure at all.
Reliability, then, is a necessary but not a sufficient criterion for validity.
In fields such as psychology, where the symptoms and signs and diagnostic constructs are somewhat resistant to external validation, reliability or consistency between assessments becomes extremely important. So is, it follows, the measurement or determination of consistency. As a rule, determining the reliability of clinical assessments requires a study in “clinical epidemiology.” By means of such a study, a clinician can assess whether or not successive clinical observations of symptoms, signs, and test results are consistent. That assessment is often reported as the observed intraobserver agreement and the observed interobserver agreement. The range of such observed agreement would be from 0 percent (or none) to 100 percent (or complete agreement). In fact, it is most always less than 100 percent.
Yet it would be a mistake to equate the measured “observed agreement” with the “clinical agreement.” The two are different. Simply, a certain portion of the “observed agreement” is due to chance, not due to clinical skill or brute clinical facts. That portion of “observed agreement” beyond chance is called actual agreement. Ideally, “actual agreement” should equal potential agreement, the state of complete agreement. Yet that ideal is not usually achieved. The index of how well actual agreement beyond chance approximates potential agreement beyond chance is called “kappa.”
kappa = Actual Agreement Beyond Chance
Potential Agreement Beyond Chance
A kappa of 0 is the worst possible and of 1.0 is the best possible score. Some attach the following qualitative terms to kappas:
.0 – .2 = slight
.2 – .4 = fair
.4 – .6 = moderate
.6 – .8 = substantial
.8 – 1.0 = almost perfect to perfect
2. Multimodal Approach
Given the diagnostic category of PTSD as set forth in the DSM-IV, is that category “reliably” identified by psychiatrists and psychologists in those with PTSD? If it is not, then any particular diagnosis of PTSD is unreliable and the PTSD construct or category itself will be unreliable, given that the gold standard whether someone has or does not have PTSD is still the clinical assessment of symptoms.
Maximizing diagnostic reliability is achieved through an approach to diagnosis called the multimodal approach.
This comprehensive approach to diagnosis incorporates information obtained from a variety of sources—clinical interviews, psychometrics, and psychophysiological assessment—allowing the diagnostician to consider the extent to which the results of these various measures converge on or diverge from a diagnostic hypothesis.
The challenge to a diagnosis of PTSD on the grounds that it is unreliable is often a viable and very important defense, perhaps the most important defense. When a plaintiff’s expert fails to use methods designed to enhance reliability, such as a structured interview, the defense should argue that the diagnosis is unreliable. To develop this line of attack, the defense should first establish the importance of the reliability of the diagnosis. Next, it should establish that various instruments have been developed to increase the probability of reliability in diagnosing PTSD. In doing so, the defense should emphasize the need for these instruments arising in the psychiatric field owing to a concern that diagnostic processes without them have been considered unreliable. But note this caution: merely because the plaintiff’s expert used a psychometric test to assess PTSD is no guarantee that the assessment is reliable. The psychometric test may lack the qualities considered necessary to make that test reliable. Then, finally, the defense should demonstrate that these instruments were not used in this case.
Following are the qualities of good psychometric tests: (1) high inter-rater reliability; (2) high test-retest consistency (rtt); (3) high internal consistency [the test will be internally consistent if each item measures the same variable; and the best measure of internal consistency is Cronbach’s alpha, which measures the average correlation between the set of test items and any other set measuring the same variable; ideally Cronbach’s alpha should be 1, a perfect correlation]; (4) low standard error of measurement; (5) good evidence of validity, especially construct validity; and (6) high discriminatory power [measured by Ferguson’s delta; a good test will emphasize individual differences and so show a large scatter of scores; when that occurs, delta approaches 1].
For every psychometric test, norms must be identified to establish the relationship of any individual score on that test to the scores of the normative population. These norms should be based on large and representative samples of the relevant population. And essential to accurate sampling is understanding the characteristics of the population sampled. Is that population the general population (in Detroit, Michigan; in Portland, Oregon?); Vietnam veterans; women who have been raped; firefighters; etc.?
Most psychometric instruments have been standardized on Vietnam combat veterans. So the defense then needs to establish that Vietnam combat veterans cannot be considered comparable to civilian populations.
It is also important to understand how the traumatic event was defined and what is the range of those traumatic events. And it is important to know what criteria were used to define PTSD: those in the DSM-III, DSM-III-R, or DSM-IV. The validity of measures of PTSD may also vary with type of trauma, co-morbid disorders, ethnic background, or chronicity.
3. Standardized Psychometric Instruments to Assess PTSD
A “psychometric instrument” is a device that has been standardized and validated to assess a particular psychological function or identify a particular psychological disorder.
A psychometric instrument may range (1) from a so-called “structured self-report measure,” a questionnaire like the MMPI-2; (2) to a structured series of questions to be asked in a patient interview; (3) to a neuropsychological test such as the Halstead-Reitan Battery; or (4) to a projective test such as the Rorschach inkblot.
Each of these kinds of instruments is available to aid in the diagnosis of PTSD. Yet a score on one of these psychometric instruments alone is not sufficient to warrant a diagnosis of PTSD. As indicated earlier, reliability in diagnosing PTSD is maximized through what is called a “multimodal” approach. This multimodal approach entails use of “multiple assessments, including information from multiple sources (self-report and family members) collected through multiple methods (interviews and psychometric measures) over multiple contacts.” An expert who fails to adopt the multimodal approach to diagnosis is cutting corners.
a. Structured Self-Report Measures
Self-report measures are questionnaires that the patient, with pen or pencil, answers. Many of these questionnaires have been standardized on samples of Vietnam veterans with combat-related PTSD. As a result, they cannot be assumed to apply to patients with civilian-related PTSD.
i. MMPI and MMPI-2
(A) Subscales
The Minnesota Multiphasic Personality Inventory (MMPI) has the Keane PTSD subscale (PK-MMPI), a well-researched subscale with reference to combat veterans, but not to civilian populations.
The PK Scale has 46 items that differentiate 100 male veterans with PTSD from 100 male veterans with psychiatric diagnoses other than PTSD. The PK-MMPI was researched in the context of the PTSD criteria of the DSM-III, however, not the DSM-III-R or DSM-IV. The Keane PTSD subscale has been reworked for use in the MMPI-2.
Besides the Keane PTSD subscale, the MMPI-2 also includes a new PTSD subscale, the Schlenger and Kulka PTSD scale (PS-MMPI-2).
The PS Scale has 60 items and was developed by contrasting item responses of healthy Vietnam veterans with PTSD. But this new subscale was not tested on civilian populations.
Clinicians should be very cautious of diagnosing any plaintiff with PTSD based on scores on these two subscales. A recent study of the validity of these two PTSD scales concluded as follows:
“We believe that it is important to construe the MMPI-2 PTSD scales as indices of general psychological distress and not simply of PTSD. When PK or PS are highly elevated, the presence of PTSD can be suspected as a possible source of distress, but PTSD should not be diagnosed on the basis of test performance alone.”
(B) Clinical Profile Analysis
Analysis of patterns of elevations of clinical scales of the MMPI sometimes helps to identify psychological disorders. Some work has been done to distinguish combat veterans with PTSD from control groups. In one study, a pattern of 8-2/2-8 clinical scale evaluations distinguished combat veterans from controls.
Yet these findings do not confidently apply to civilian PTSD populations.
ii. Millon Clinical Multiaxial Inventory
(A) MCMI and MCMI-II
The earlier MCMI and MCMI-II lacked a PTSD scale. As a result, PTSD symptoms were easily misinterpreted as evidence of a dysfunctional personality. The MCMI and MCMI-II are best used to establish personality disorders co-morbid with PTSD.
(B) MCMI-III
Millon Clinical Multiaxial Inventory is now in its third version, the MCMI-III. The MCMI-III contains a PTSD scale (the R scale within the “clinical syndromes” group). Although the PTSD scale is loosely tied to the DSM-IV criteria, it includes a majority of items not directly associated with diagnostic criteria in the DSM-IV, such as items examining sadness, feelings of worthlessness, and rapid mood changes. Only 6 of 16 R scale items actually tap current PTSD criteria. For these and other reasons, PTSD cannot be diagnosed based solely on an MCMI-III R score.
iii. Mississippi Scale for PTSD
(A) Mississippi Scale for Combat-Related PTSD
The Mississippi scale for combat-related PTSD is a 35-item instrument developed to measure PTSD in combat veterans.
It has excellent reliability for detecting combat-induced PTSD.
(B) The Civilian Mississippi Scale (CMS)
The Civilian Mississippi Scale was developed to assess PTSD in civilian populations.
It contains 11 re-experiencing and situational avoidance items, 11 withdrawals and numbing items, 8 arousal items, and 5 guilt and suicidality items.
(C) Revised Civilian Mississippi Scale (RCMS)
The RCMS has 30 items. It is anchored in undefined past trauma, referred to “as the event.” All items are rated on a 5-point scale (1 = not at all true; 5 = extremely true). Research is still needed, however, to assess the convergent and divergent validity of these scales.
iv. Impact Event Scale
(A) Impact Event Scale
Although widely used, the Impact Event Scale (IES) was developed in response to the PTSD criteria of the DSM-III.
So the IES taps intrusive and avoidant, but not hyperarousal, symptoms. Because it does not assess all PTSD criteria, it cannot establish a diagnosis. If used, the IES should be considered only a screen for the presence of non-arousal-related posttraumatic stress.
(B) Impact Event Scale––Revised
The IES-R contains six new hyperarousal items and an additional item to parallel DSM-IV criteria.
Both IES and IES-R were developed as research measures and lack the requisite normative data associated with modern clinical tests.
v. Penn Inventory
The Penn Inventory for PTSD is a 26-item scale.
Each item is composed of four sentences scored 0 to 3 representing different levels of a feeling or thought. This inventory is not validated on civilian PTSD populations. And further research is needed to document its overall utility.
vi. Symptom Checklist-90 (SCL-90)
The SCL-90 is widely used.
It is a 90-item self-report symptom inventory. All items are scored on a 5-point scale (0 = not at all; 4 = extremely). A 28-item scale has been derived from the 90 items that discriminates between crime victims with and without PTSD, referred to now as the CR-PTSD scale. It is reliable, but not yet validated. Until it is independently validated, its precision for measuring PTSD remains uncertain.
vii. Los Angeles-Symptom Checklist (LASC)
LASC is a 43-item measure of posttraumatic stress.
Seventeen of these items measure the re-experiencing, avoidance, and hyperarousal criteria of PTSD as defined in the DSM-III-R. Symptoms are rated by how much they are a problem (0 = no problem; 4 = extreme problems). A PTSD diagnosis is “suggested” if the relevant symptoms are endorsed at a “2” or higher. LASC should be used only to screen for, not to diagnose, PTSD.
viii. PTSD Symptom Scale – Self-Report
(A) PTSD Symptom Scale – Self-Report (PSS- R)
PSS-SR is a 17-item measure designed to assess PTSD symptoms in rape victims.
All 17 items are related to rape. Responses to the items are on a 4-point scale (0 = not at all; 3 = very much).
(B) Modified Symptom Scale – Self-Report (MPSS-SR)
The MPSS-SR is designed for general trauma populations.
ix. Posttraumatic Stress Diagnostic Scale (PDS)
The PDS was designed to adopt the PSS-SR for general clinical use.
It is considered “an excellent choice as a PTSD screener.” It has four parts: part I surveys exposure to traumatic events; part II examines characteristics of what the respondent believes was the most traumatic event; part III lists DSM-IV symptom criteria; and part IV considers how the symptoms have interfered with daily activities.
x. Purdue PTSD Questionnaire
(A) Purdue PTSD Questionnaire (PTSD)
The Purdue PTSD is a 15-item measure keyed to the DSM-III PTSD criteria and is designed to measure combat-related PTSD.
(B) Purdue PTSD Questionnaire – Revised (PPTSD-R)
The PTSD-R has 17 items keyed to the DSM-III-R PTSD criteria. It is designed to tap PTSD in general trauma populations.
b. Clinical Structured Interviews
A common way to assess whether someone has PTSD is for the psychiatrist or psychologist, with the DSM-IV criteria for PTSD in mind, to ask the person a series of questions about her history and current cognitive, behavioral, and emotional status. And then, with that information, the diagnostician decides, based on a “clinical impression,” whether the patient has PTSD. This diagnostic process is considered outdated and “unreliable.”
Diagnostic state of the art is the “structured” interview, a set or series of structured questions posed by an examiner to the patient.
These structured interviews ideally increase the likelihood of covering all relevant symptoms and thereby decrease the chance of diagnostic error. Questions in these structured interviews are dictated by internally logical or consistent rules that govern the content of the questions, the order in which the topics are covered, and the specific kinds of information sought.
Yet not all these interviews link specific traumatic events to specific traumatic symptoms. For an accurate DSM-IV diagnosis, at least one trauma must be specifically associated with all required diagnostic symptoms. In any event, nationally recognized experts on PTSD, in critiquing studies about PTSD, have criticized many of these studies for using clinical instead of structured interviews. As a result, on the basis of these written critiques, a forensic expert who fails to use a structured interview may be impeached on cross-examination.
i. Structured Clinical Interview (SCID)
SCID is the most thoroughly researched and widely used structured clinical interview. Accordingly, among structured interviews, it is considered the “gold standard.”
It has high inter-rater reliability. And it is strongly correlated with other psychometrically generated indices of PTSD, such as the Mississippi Scale, Impact of Event Scale, and Keane PTSD Scale of the MMPI. The limitation of SCID for diagnosing PTSD is that it yields only dichotomous information about the presence or absence of each symptom criteria. Moreover, formal, large-sample psychometric studies have not been performed on the SCID-PTSD module. It has been “validated” only on smaller samples of Vietnam combat veterans.
ii. Clinician-Administered PTSD Scale (CAPS)
An increasingly popular instrument, CAPS consists of 17 clinician-administered questions to assess the frequency and intensity of the DSM-III-R and DSM-IV symptoms of PTSD.
It has a 5-point (0 to 4) rating scale. Frequency and intensity ratings may be summed for each symptom to yield a severity score (0 to 8) and across symptoms to yield scores for the re-experiencing, avoidance and numbing, and hyperarousal clusters. A total PTSD severity score may be computed by summing across ratings for all 17 symptoms. CAPS, however, was validated on Vietnam combat veterans. It has not been validated on civilian PTSD populations.
iii. Posttraumatic Stress Disorder Interview (PTSD-I)
This interview, developed using the criteria of the DSM-III-R, was validated on male Vietnam combat veterans.
It has not been validated on civilian PTSD populations. PTSD-I is able to provide both dichotomous diagnostic decisions and continuous data for the set of symptoms. But it cannot produce valid, lifetime diagnoses.
iv. Diagnostic Interview Schedule (DIS)
For PTSD, this interview is not reliable and has not been validated on civilian populations. In a large sample study, DIS-PTSD module achieved a sensitivity of only 21.5, a specificity of 97.9, and a kappa of .26.
No forensic expert should be using the structured interview to diagnose PTSD.
v. Structured Interview for PTSD (SI-PTSD)
This interview is structured on the PTSD criteria in the DSM-III, not the DSM-III-R or DSM-IV. Whatever validity it has is confined to studies of combat veterans. A DSM-III-R version is available, but data on this version are sparse.
vi. Anxiety Disorders Interview–Revised PTSD Module (ADIS-R PTSD)
ADIS-R is not the best interview for PTSD. But it is helpful, in the process of differential diagnosis, in distinguishing PTSD from other anxiety disorders.
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When interviewing a plaintiff, a forensic expert should be expected to use a structured interview. Currently the two interviews available are SCID-PTSD or CAPS revised for DSM-IV. Both are validated on Vietnam combat veterans and hence subject to criticism when applied to civilians. Yet that flaw is a lesser shortcoming than not using a structured interview.
* * *
c. Projective Techniques
Projective techniques consist of a set of ambiguous stimuli (such as an inkblot) that subjects are asked to describe or explain. The responses to these ambiguous stimuli are considered to indicate something about the psychological makeup of the individual rather than about the stimuli.
i. Rorschach Inkblot Test
The Rorschach inkblot test is a “projective” technique. It consists of ten standard inkblots, a set of relatively freeform stimuli to which the individual may respond in any manner chosen. The Rorschach is considered by some to be ideally suited for assessing PTSD in that it is believed to bypass conscious cognitive and affective experience or resistance and tap “unconscious” mental processes, revealing underlying anxiety.
A serious limitation of the Rorschach is that limited studies exist on civilian PTSD populations. Moreover, projective tests have poor reliability and validity and could never meet the criteria of scientific measurement as defined in the so-called “hard” sciences. Repeatedly, as a result, the scientific status of the Rorschach has been called into question.
ii. Stroop Interference Task
The Stroop Interference Task is also a projective technique. In this test, the patient is presented with words of varying emotional intensity printed in different colors. The patient is asked, under timed conditions, to name the colors of these printed words. When attention is directed only to the print color of the word, the meaning of the words impinges on the mind of the patient. Words with greater emotional impact take slightly longer to mentally process, thus slowing the patient’s report of the word’s print color. Inferences about the patient’s psychological functioning are drawn from these delayed responses.
Limited studies on this measure exist on civilian PTSD populations.
d. Questionnaires About Traumatic Events
A variety of questionnaires have been designed to inquire into Criterion A of PTSD.
i. Traumatic Events Questionnaire (TEQ)
The Traumatic Events Questionnaire inquires about 11 stressors.
These stressors are combat; large fires or explosions; serious industrial or farm accidents; sexual assault or rape; natural disasters; violent crimes; witnessing mutiliations, killings, or serious accidents; other life-threatening experiences; violent or unexpected death of a loved one; any other traumatic events; and an “event can’t tell” (an event so traumatic that the patient can’t describe it.)
ii. Traumatic Stress Schedule (TSS)
The Traumatic Stress Schedule inquires about ten potentially traumatic events.
These events are combat; robbery or theft involving force; physical assault; sexual assault; loss of a loved one through accident, homicide, or suicide; personal injury or property loss as a result of fire; personal or property loss as a result of severe weather or disaster; forced evacuation or otherwise learning of an imminent danger or hazard in the environment; a motor vehicle accident causing injury to one or more passengers; and any other event that is terrifying or shocking.
iii. Potential Stressful Events Interview
The Potential Stressful Events Interview has items about the type of stressor, the objective-behavioral characteristics of the stressor, and subjective reactions to the stressor.
Types of stressors evaluated are war-zone or combat experiences; serious accidents associated with motor vehicles, work, or elsewhere; natural disasters; serious illnesses; childhood sexual abuse; childhood sexual assaults; other forced sexual contact; aggravated physical assaults (i.e., involving a weapon); simple physical assaults; other situations involving serious injury; other situations involving fear of injury or death; witnessing serious injury or death; and other extraordinarily stressful events.
iv. Traumatic Events Scale (TES)
The Traumatic Events Scale (TES) assesses 30 interpersonal and environmental traumas.
Behaviors alleged to be traumatic stressors range from uninvited physical contact (kissing, hugging, patting, stroking, rape) to offensive verbal remarks (sexual allusions, dirty jokes, unsolicited phone calls) to nonverbal, nontouching behavior (leering, hand gestures, pictures or posters, graffiti).
C. Expertise to Diagnose PTSD
The nature of the expert’s qualifications has two basic ramifications. First, at the threshold is whether the expert is sufficiently qualified to diagnose PTSD. Second, across the threshold is the issue of the relative degree of expertise between the plaintiff’s expert and the defendant’s expert. That is, is the expert for one of the parties more impressively credentialed than the other?
1. Nature of Expertise
a. Mental Health Field
The expert should have expertise in the field of mental health. In that field, an expert is apt to be either a psychiatrist or a psychologist. A psychiatrist is a medical doctor who has had four years of college, four years of medical school, and some postgraduate training in the field of mental health. The psychiatrist may have an M.D. or a D.O. A psychologist has had four years of college and usually some graduate school. The psychologist could have a master’s degree or a Ph.D. in psychology. Psychoanalysts are usually psychiatrists or psychologists, although not necessarily, who have completed extensive advanced training in psychoanalytic theory and its methods of treatment.
Those with a Master’s in Social Work (MSW) are also appearing as experts to diagnose PTSD. Plaintiffs’ counsel have found that these mental health practitioners are inexpensive and malleable. Aggressive defense counsel should mount a Daubert challenge to the use of an MSW, as insufficiently schooled and trained to conduct a meaningful differential diagnosis as to PTSD.
The plaintiff’s expert could also be a physician who does not practice psychiatry. For instance, the expert could be a neurologist, board-certified in both neurology and psychiatry. A neurologist board-certified in psychiatry is not apt to have significant clinical experience in psychiatry let alone in specifically diagnosing PTSD, although defense counsel should expect most courts to allow them to testify about PTSD.
b. Clinical Experience
Whether the expert is a psychiatrist or psychologist, the expert should have clinical experience in diagnosing PTSD. As the DSM-IV notes, “the diagnostic categories, criteria, and textual descriptions [in the DSM-IV] are meant to be employed by individuals with appropriate clinical training and experience in diagnosis.”
c. Licensure
The expert should also be licensed to practice clinically in some state in the United States. Moreover, that clinical practice should have included or presently include the diagnosis of PTSD. Of course, implicit in that requirement is the further requirement that the expert’s clinical practice include diagnosing mental disorders that constitute the set of differential diagnoses for PTSD.
2. Levels of Expertise
Not only is the nature of expertise important but so also is the level or depth of that expertise in any effort to persuade judges and juries on relevant issues in the fields of psychiatry and psychology.
A recently licensed psychologist who has diagnosed PTSD in only one patient will obviously be less persuasive than a psychiatrist, all other things being equal, for whom PTSD has been a life’s work.
a. Board Certification
For the defense, if the expert is a physician, that physician should be board-certified.
Certification reflects a general level of expertise in psychiatry. If the plaintiff’s expert is not also board-certified, then the defense may exploit this difference in qualifications. A physician who is board-certified is different from a physician who is board-eligible. A physician who is board-eligible has completed the prerequisites posed by one or more of the 24 specialty boards, but has either failed the certification examination or declined to be examined.
In medicine, of the 24 American specialty boards, one is relevant in the clinical field of psychiatry.
This is the American Board of Psychiatry and Neurology. That board currently issues eight types of certificates. The certificates relevant in cases involving PTSD are psychiatry, child and adolescent psychiatry, and forensic psychiatry. A certificate in psychiatry is a prerequisite for obtaining a certificate in forensic psychiatry and child and adolescent psychiatry.
The examination for certification has two parts: (1) a written examination using the DSM-IV as the primary authority on psychiatric diagnostic nomenclature and (2) an oral examination divided into two one-hour examinations in clinical psychiatry.
The American Board of Professional Psychology (ABPP) awards a diploma for the psychologist who has demonstrated proficiency in the fields of industrial counseling, clinical or forensic psychology, and clinical neuropsychology. Reasons exist to discount the value of being board-certified or of being a diplomat in clinical or forensic psychology. But discounting those qualifications has no strategic value if the defense is also relying on those added qualifications, as it should be, to impress the jury. When one party has, as an expert, a psychiatrist and the other party has a psychologist, the party with the psychiatrist should exploit that difference. That is, the psychiatrist, having been trained as a physician, can be presented as someone with broader knowledge of the alternate diagnoses possibly responsible for the plaintiff’s symptoms.
The defense should explain in some detail the qualifications of its experts. The more explanation, the more likely the judge or jury will be to understand the significance of those qualifications. For instance, the typical exchange between attorney and physician over the physician’s qualification of board certification is as follows:
“Q: Doctor, are you board-certified in psychiatry?
“A: Yes, I have been board-certified since 1985.”
After this somewhat elliptical exchange, the jury, and many judges, may wonder about the meaning of board certification and why it’s significant. As a result, the defense should pursue the following, more elaborate explanation:
“Q: Doctor, are you board-certified in psychiatry?
“A: Yes.
“Q: Who issues the certification?
“A: The American Board of Psychiatry and Neurology.
“Q: Who is on the board?
“A: Psychiatrists and neurologists preeminent in their medical fields.
“Q: Why was the board established?
“A: That board was established to ‘establish and improve standards for the teaching and practice of psychiatry and neurology’ and to ‘improve the quality of health.’
“Q: When were you board-certified?
“A: I was board-certified in 1985.
“Q: What is board certification?
“A: Board certification in psychiatry and neurology is an acknowledgment by the American Board of Psychiatry and Neurology that I have attained a high level of knowledge in this medical specialty.
“Q: What specifically did you have to do to become board-certified?
“A: First I needed to have postgraduate medical training in an accredited program. Next I needed to pass a grueling written and oral examination.
“Q: Are all psychiatrists board-certified?
“A: No.”
b. Publications
The defense will want to impress the judge or jury with the depth of its expert’s knowledge by referring to the expert’s publications. Obtain a bibliography of articles the expert has published at least within the last ten years. Do the same for the plaintiff’s experts. The more publications on the issues in the litigation, the more qualified the expert will appear to be to the judge or jury. If, however, the focus of these articles in the bibliography of the plaintiff’s expert is on topics other than those involved in some aspect of the litigation, the defense will want to exploit that shortcoming.
Yet plaintiffs do appreciate the rhetorical value of an expert with publications on the litigated scientific and medical issues. In fact, plaintiffs’ experts often undertake concerted efforts to enhance their list of publications on those litigated issues solely for purposes of appearing more knowledgeable to the judge or jury. But be watchful for the expert with a resume of “duplicate” and “salami” publications. A “duplicate” publication occurs when the results of a single study appear in more than one journal. A “salami” publication occurs when small slices of the work are submitted as separate papers. Unfortunately, the psychological community appears particularly fond of duplicate and salami publications.
Also consider the articles that the plaintiff’s expert has cited as references in her own articles. Some of these articles may be helpful to the defense. As to those articles, at trial, the expert will have difficulty explaining why she can selectively choose articles’ bibliographies that support her opinion in court and disregard those that undermine that opinion.
“Q: Doctor, in 1987 you published an article in the American Journal of Psychiatry. True?
“A: Yes.
“Q: Today, you have cited that article in support of your opinion that defendant’s product, alphabet soup, causes an atypical disease you call ‘tangled mind syndrome.’ True?
“A: Yes.
“Q: In that same article, in the bibliography, you cite with approval an article by Dr. Derrida entitled ‘The Alpha & Omega of the Posttraumatic Stress Disorder.’ That article appeared in the peer-reviewed journal The New England Journal of Medicine. True?
“A: Yes.
“Q: In that article, which you found sufficiently authoritative to cite in support of your article, the author states that a case study is insufficient evidence to establish general causation. True?
“A: Well, I thought so then.”
c. Treating Psychiatrists or Psychologists
The treating psychiatrist is the plaintiff’s biased ally for therapeutic reasons. At the same time, ironically, the treating psychiatrist will be perceived by the jury as the more believable or unbiased expert witness. This irony is a problem for the defense. To overcome this difficulty, the defense will need to explain to the jury the nature of the therapeutic relationship between the plaintiff and the treating psychiatrist and why, for purposes of trial, that relationship impairs the objectivity of the treating physician. If the treating psychiatrist were objective, he or she would probably damage the painstakingly created “therapeutic alliance.” That is, the plaintiff would feel betrayed when information the plaintiff relayed to the psychiatrist that the plaintiff considers intimate and confidential is disclosed during the course of the expert’s testimony.
Ethically, treating psychiatrists are advised not to testify as forensic experts on behalf of a patient. For instance, the American Academy of Psychiatry and the Law advises that “a treating psychiatrist should generally avoid agreeing to be an expert witness or to perform an evaluation of his patient for legal purposes because a forensic evaluation usually requires that other people be interviewed and testimony may adversely affect the therapeutic relationship” (American Academy of Psychiatry and the Law 1991).
D. Failure to Satisfy Criteria of PTSD
1. One or More Criteria Not Satisfied
Most often, a challenge to a claim for PTSD will involve the defense that the plaintiff fails to satisfy one or more of the criteria of PTSD, as identified in the DSM-IV. Expect the plaintiff’s expert to describe attributes of the plaintiff’s cognition, emotion, or behavior that only facially satisfy the requisite diagnostic criteria. In this process, the plaintiff’s expert will probably describe an aspect of the plaintiff’s cognition, emotion, or behavior in the belief that that description satisfies the criteria when, in fact, it does not. For example, the plaintiff’s expert may testify that the plaintiff often reflects anxiously about the motor vehicle accident, with the expert expecting erroneously that that description satisfies Criterion B(1) requiring “recurrent and intrusive distressing recollections of the event.” Merely thinking or reflecting anxiously about the traumatic event is usually insufficient to meet the re-experiencing criteria. The plaintiff must experience unwanted, unbidden, and distressing memories of the event. For another example, the plaintiff may testify that his avoidance symptoms occurred initially a year from the time of the trauma, believing that he has thereby satisfied Criterion C. Although re-experiencing symptoms may develop months or years after trauma, avoidance symptoms have usually been present from the time of trauma.
2. Use of DSM-IV in Forensic Settings
Two aspects of the DSM make it a potent weapon in the hands of the overzealous or unscrupulous expert: (1) the DSM is only a “guideline” and (2) the priority of “clinical judgment” in diagnosing PTSD.
a. DSM Is Only a “Guideline”
The DSM-IV appears to establish necessary and sufficient or definitional criteria for a diagnosis. If a plaintiff satisfies the required criteria, she has the disorder; otherwise, she does not. Yet it is stated repeatedly in the DSM-IV that it is only a guideline.
So what appear in the DSM-IV to be definitional criteria are merely evidential, thereby providing the expert significant discretion in formulating a diagnosis. The DSM-IV notes that “the exercise of clinical judgment may justify giving a certain diagnosis to an individual even though the clinical presentation falls just short of meeting the full criteria for the diagnosis as long as the symptoms that are present are persistent and severe.”
A plaintiffs’ expert is always looking for ploys to water down the inclusionary criteria and thicken the exclusionary criteria of the disorder.
b. Subsyndromal PTSD
The term subsyndromal PTSD refers to a subset or subcluster of symptoms of PTSD. Technically, someone with subsyndromal PTSD does not have PTSD. Yet recognize that the full criterial set for PTSD in the DSM-IV is not definitional but evidential. So having the full set of criteria for PTSD is good evidence that the individual has “PTSD.” Having a subset of the criteria for PTSD is evidence but not good evidence that the individual has PTSD.
The defense needs to be alert to the clinician who too readily diagnoses PTSD when the plaintiff fails to fulfill all the required criteria under the DSM-IV. Obviously, when the clinician too readily diagnoses PTSD based on an incomplete set of symptoms, people without PTSD but with mood or anxiety disorders will probably be diagnosed with PTSD only for purposes of litigation.
3. Differentials Not Ruled Out
a. Differential Diagnosis
Many psychological maladies share symptoms with PTSD. For that reason, care is required to distinguish those psychological conditions from PTSD. That process is accomplished through a differential diagnosis. In general, differential diagnosis is a process––a systematic review of the clinician’s diagnostic hypothesis in light of the signs and symptoms––to determine whether that diagnostic hypothesis best fits those data. In this process, the clinician considers other diagnostic hypotheses––diseases or disorders that might apply––and with those hypotheses in mind looks for data, perhaps overlooked, that might satisfy those alternate diagnostic hypotheses.
b. Failure to Perform Differential Diagnosis
A diagnosis of PTSD can be undermined if the plaintiff’s expert failed to perform a differential diagnosis in the process of diagnosing PTSD. As a rule, assuming that the expert is properly qualified, the expert’s guiding principle is to assess how probable is each potential diagnosis given the plaintiff’s symptoms and signs, a thought process captured in the maxim that “common disorders occur commonly,” or, more metaphorically, “when you hear hoofbeats, think of horses, not zebras.”
c. Likely Differentials
A differential diagnosis should consider disorders that share some of the cognitive, emotional, and behavioral criteria of PTSD. On that basis, a differential diagnosis should consider the following alternate psychological conditions or disorders on both Axis I and Axis II of the DSM-IV.
On Axis I: (1) mood disorders; (2) anxiety disorders other than PTSD; (3) somatoform disorders; (4) adjustment disorders; (5) dissociative identity disorder; (6) attention-deficit hyperactivity disorder; (7) post-concussion syndrome; (8) bereavement; (9) drug and alcohol abuse; (10) brief reactive psychosis; (11) dissociative amnesia; (12) dissociative fugue; (13) schizophrenia; (14) depersonalization disorder; and (15) mixed anxiety-depressive disorder.
On Axis II: (16) borderline personality disorder; and (17) antisocial personality disorder.
i. Mood Disorders
PTSD may be characterized by (1) markedly diminished interest or participation in significant activities; (2) feelings of detachment or estrangement from others; and (3) restricted range of effect, as well as by (4) difficulty sleeping; (5) irritability; and (6) difficulty concentrating. Major depression can be characterized by similar symptoms, such as (1) markedly diminished interest or pleasure in all, or almost all, activities most of the day; (2) insomnia or hypersomnia; (3) psychomotor agitation; (4) diminished ability to think or concentrate.
So if someone with preexisting depression is exposed to a Criterion A stressor, that person could claim to have PTSD on the basis of the symptoms from the preexisting depression. It would be up to the clinician to rule out that preexisting depression before diagnosing PTSD. Moreover, an individual subject to a Criterion A stressor may develop depression rather than PTSD. So the clinician should also endeavor to rule out depression developing after exposure to the stressor.
ii. Anxiety Disorders
The anxiety disorders include panic attacks, phobias, obsessive-compulsive disorder, acute stress disorder, generalized anxiety disorder, and substance-induced anxiety disorder. Because anxiety is invariably present in PTSD, the clinician should rule out each of these anxiety disorders before diagnosing PTSD.
- Panic Attacks
There are three types of panic attacks: (1) unexpected; (2) situationally bound; and (3) situationally predisposed. Panic attacks that occur in “panic disorder” are “unexpected.” Panic attacks that occur in PTSD are situationally bound or predisposed in that the panic attacks are cued by stimuli recalling the stressor.
- Phobias
A specific phobia is a marked and persistent fear (and avoidance) of clearly discernible, circumscribed objects or situations. In contrast to the kind of avoidance characterizing specific phobia, the avoidance in PTSD follows a life-threatening stressor and is accompanied by additional features such as re-experiencing the trauma and restricted affect.
- Obsessive-Compulsive Disorder
In obsessive-compulsive disorder, the recurrent intrusive thoughts are experienced as inappropriate and are not related to an experienced traumatic event.
- Acute Stress Disorder
Acute stress disorder (ASD) is distinguished from PTSD in that in ASD the symptoms occur and resolve within four weeks of the traumatic event.
(E) Generalized Anxiety Disorder
Generalized anxiety disorder (GAD) is characterized by relatively persistent excessive anxiety and worry for a period of at least six months accompanied by at least three additional symptoms such as restlessness, being easily fatigued, difficulty concentrating, irritability, and disturbed sleep. Many of these symptoms also occur in PTSD. So GAD could be erroneously labeled as PTSD. But GAD is not diagnosed if the anxiety occurs exclusively during the course of PTSD.
iii. Somatoform Disorders
As in PTSD, in somatization disorder, symptoms may include hallucinations and dissociative symptoms such as amnesia. But unlike somatization disorder, PTSD requires, in addition to a severe trauma, persistent symptoms of increased arousal and persistent avoidance of stimuli associated with the trauma.
iv. Adjustment Disorders
An adjustment disorder is the development of clinically significant emotional or behavioral symptoms within three months after onset of any identifiable psychosocial stressor. The symptoms must resolve within six months of the termination of the stressor. PTSD is characterized by the presence of an extreme stressor and a specific constellation of symptoms, and may not develop within three months after onset of the stressor and may not resolve within six months of termination of the stressor.
v. Dissociative Identity Disorder
Dissociative identity disorder (DID) is characterized by the presence of two or more distinct identities or personality states each with its own relatively enduring pattern of attributes, involving perceiving, relating to, and thinking about the environment and self. A feature of DID is amnesia, a symptom that may be present in PTSD. Those with DID may also manifest posttraumatic symptoms such as nightmares, flashbacks, startle responses, or full-blown PTSD.
vi. Attention-Deficit Hyperactivity Disorder
Attention-deficit hyperactivity disorder (ADHD) is characterized by a persistent pattern of inattention or hyperactivity—that is, by impulsivity that is more frequent and severe than is observed in individuals at a comparable level of development. Symptoms of hyperactivity, impulsivity, or inattention that cause impairment must have been present before age seven. PTSD is characterized by persistent symptoms of increased arousal manifested as irritability or outbursts of anger, difficulty concentrating, hypervigilance, or exaggerated startle response. But unlike the symptoms of ADHD, these symptoms occur in the context of a trauma.
vii. Post-Concussion Syndrome
Post-concussion syndrome (PCS) is characterized by an acquired impairment in cognitive functioning, accompanied by specific neurobehavioral symptoms that occur from closed head injury of sufficient severity to produce a significant cerebral concussion. The concussion may be manifested by loss of consciousness, posttraumatic amnesia, and, less commonly, posttraumatic onset of seizures. PTSD is characterized by many of the same kinds of symptoms and behaviors. Given that both disorders occur in the context of a trauma, PCS might be confused with PTSD. In PTSD, the differentiating factor is likely to be Criterion B, that the traumatic event be persistently re-experienced in one of a variety of possible ways.
viii. Bereavement
Bereavement is catalogued in the DSM-IV under “Additional Conditions That May Be a Focus of Clinical Attention.” Bereavement is used when the focus of clinical attention is a reaction to the death of a loved one. Some of the symptoms of bereavement include those present in PTSD, such as hallucinations, insomnia, markedly diminished interest in significant activities, and difficulty concentrating. If the death of the loved one was attendant to a traumatic stressor under Criterion A of PTSD, then bereavement may be confused with PTSD if PTSD does not also develop.
ix. Drug and Alcohol Abuse
Drug and alcohol abuse can result in a variety of disorders that share symptoms or behaviors with PTSD. Substance and alcohol abuse can induce amnesia, hallucinations, mood disorders, and anxiety disorders. All these symptoms may also be present in someone with PTSD.
x. Brief Psychotic Disorder
Brief psychotic disorder is a disturbance that involves the sudden onset of at least one of the following psychotic symptoms: delusions, hallucinations, disorganized speech, or grossly disorganized or catatonic behavior. PTSD is characterized by hallucinations in which the individual acts or feels as if the traumatic event were recurring. PTSD is distinguishable from brief psychotic disorder in that PTSD occurs in the context of a trauma and is attended by other symptoms and behaviors such as persistent avoidance of stimuli associated with the trauma and persistent symptoms of increased arousal.
xi. Dissociative Amnesia
Dissociative amnesia is characterized by an inability to recall important personal information, usually of a traumatic or stressful nature, that is too extensive to be explained by normal forgetfulness. In PTSD there can be amnesia for the traumatic event. If the amnesia occurs during the course of PTSD, dissociative amnesia is not diagnosed.
xii. Dissociative Fugue
Dissociative fugue is characterized by sudden, unexpected travel away from home or one’s customary place of work, accompanied by either an inability to recall one’s past and confusion about personal identity or the assumption of a new identity. PTSD is a constellation of symptoms that may coexist with dissociative fugue.
xiii. Schizophrenia
Schizophrenia is characterized by certain symptoms such as delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior, affective flattening, “alogia” (an impoverishment in thinking inferred from observing speech), or “avolition” (an inability to initiate and persist in goal-directed activities) that have a duration of at least a month and that interfere with social or occupational functioning. PTSD may also involve hallucinations, affective flattening, avolition, and disorganized behavior.
xiv. Depersonalization Disorder
Depersonalization disorder is characterized by persistent or recurrent episodes of “depersonalization,” defined as a feeling of detachment or estrangement from oneself. Depersonalization is a common experience, and depersonalization disorder should thus be diagnosed only if the symptoms are sufficiently severe to cause marked distress or impairment in functioning. Because depersonalization is associated with many other mental disorders such as PTSD, depersonalization disorder should not be diagnosed separately when the symptoms occur only during a panic attack or as part of PTSD.
xv. Mixed Anxiety-Depressive Disorder
Mixed anxiety-depressive disorder is characterized by a persistent or recurrent dysphoric mood lasting at least one month accompanied by additional symptoms that also must persist for at least one month, including at least four of the following: concentration or memory difficulties, sleep disturbance, fatigue or low energy, irritability, worry, being easily moved to tears, hypervigilance, anticipating the worse, hopelessness or pessimism about the future, and low self-esteem or feelings of worthlessness.
PTSD is characterized by symptoms and behaviors found in both depression and anxiety disorders. PTSD would be distinguishable from mixed anxiety-depressive disorder by Criterion B in which the traumatic event is persistently re-experienced in a variety of ways. Even so, it would be difficult to differentiate someone who had mixed anxiety-depressive disorder and who experienced a traumatic event, minor or otherwise, from someone who had genuine PTSD.
xvi. Borderline Personality Disorder
Borderline personality disorder (BPD) is characterized by a pervasive pattern of instability of interpersonal relationships, self-image, and affects, and marked impulsivity beginning in early adulthood and present in a variety of contexts. Among the possible indicia of BPD are the symptoms of transient stress-related dissociation, frequent displays of temper, and affective instability due to a marked reactivity of mood, including anxiety.
PTSD is often characterized by dissociation, outbursts of anger, and affective instability. Unlike BPD, PTSD requires a traumatic event and that the traumatic event be persistently re-experienced. If an individual with BPD were to be subjected to a traumatic event, however, it would be difficult to determine whether that event resulted in PTSD or merely occurred in the context of BPD.
xvii. Antisocial Personality Disorder
Antisocial personality disorder (APD) is characterized by a pervasive pattern of deceit and manipulation, beginning in childhood and continuing into adulthood. APD is similar to narcissistic personality disorder in that people with each disorder tend to be tough-minded, glib, superficial, exploitative, and unempathic. But unlike those with NPD, those with APD are not as needy for the admiration and envy of others. APD is also similar to BPD in that each is characterized by an attempt to manipulate, but those with BPD manipulate to gain nurturance, whereas those with APD manipulate to gain power and profit.
Because APD is characterized by impulsivity and irritability, characteristics also found in those with PTSD, APD should be ruled out in diagnosing PTSD. APD and PTSD can coexist in an individual, but when an individual is diagnosed with APD, the prospect of malingered PTSD should be considered before diagnosing PTSD.
d. Bayes’ Theorem
As is apparent from the foregoing, diagnosis is complicated by the fact that a set of symptoms may not be “specific” for any particular disorder, but may instead be a manifestation of any number of different disorders. The diagnostician’s art is in being able to determine out of this array of possible disorders which, if any, apply to this particular patient. So the diagnostician’s principal inquiry is, what is the probability of this particular diagnostic hypothesis given these symptoms? This inquiry may be symbolized as follows: Pr(DH|S), with “Pr” representing “probability,” “DH” representing “diagnostic hypothesis,” the vertical line representing “given” what follows or “assuming the truth of” what follows, and “S” representing symptoms found in this particular patient.
The defense and jury should realize that Pr(DH|S) does not equal Pr(S|DH). Pr(S|DH) represents the probability of the symptoms occurring assuming the truth of the diagnostic hypothesis. That is, if 100 patients are known to have the disorder prescribed by the diagnostic hypothesis, how many of the 100 patients have the particular symptoms described by S? If, say, 90 patients have those particular symptoms, the probability of these symptoms given the disorder is 90 percent. But from this it is not correct to infer that if those symptoms are found in a patient, it is 90 percent probable that she has the disorder. That is, it is not correct to infer Pr(DH⎪S). Despite the invalidity of that inference, that is the inference most people would tend to draw.
What the diagnostician seeks is Pr(DHS). That probability can often be assessed with Bayes’ Theorem. Bayes’ Theorem is a fundamental tool of “inductive inference,” providing a way to reason backward from effects (evidence such as signs and symptoms) to their causes (trauma). It offers a powerful and uniform way of thinking about the extent to which evidence confirms a theory of causation. What follows is the general form of Bayes’ Theorem:
Pr(DH|S) = Pr(S|DH)Pr(DH)
Pr (S)
In this theorem, Pr(DH|S) is the conditional probability of the diagnostic hypothesis (DH) being true given the evidence or symptoms (S). (This conditional probability can be thought of as the probability-of-DH-on-the-assumption-that-S-is-true.) This probability is known as the posterior probability. Pr(DH) is the probability of the diagnostic hypothesis before the events causing the symptoms. This probability is known as the prior probability or “base rate.” That is, it is the probability of the diagnostic hypothesis in the absence of the subsequently developing symptoms. Pr(S) is the probability of the symptoms. That is, it is the probability of observing this evidence. Pr(S|DH) is the “conditional probability” of the symptoms being true, assuming that the diagnostic hypothesis is true. This probability is known as the likelihood.
Bayes’ Theorem is more easily understood if expressed in terms of “odds” rather than in terms of “probability.” Here is the odds ratio form of Bayes’ Theorem:
Post evidence odds = Pre-evidence odds x Likelihood ratio
The pre-evidence odds of the disorder is the probability before the evidence that the plaintiff has the disorder divided by the probability before the evidence that the plaintiff does not have the disorder. The “likelihood ratio” (LR) measures the contribution of the evidence. When the evidence is present, the likelihood ratio is the true positive rate divided by the false positive rate. If the evidence is absent, the likelihood ratio is the false negative rate divided by the true negative rate. The post-evidence odds of the disorder is the product of the pre-evidence odds of the disorder and the likelihood ratio. The probability of the disorder given the evidence is the quotient of the post-evidence odds divided by 1 plus the post-evidence odds.
If Pr(DH) is low, Pr(DH|S) may be low even if Pr(S|DH) is high. For example, if the likelihood of the evidence given the plaintiff’s diagnostic hypothesis [Pr(S|DH)] is 80 percent and the prior probability or “base rate” of that hypothesis is, generously stated in favor of the plaintiff, 1 percent, then the probability of that hypothesis being true given the evidence is .8 multiplied by .01 or .008 or, in terms of percentage, .8 percent. That is a very unimpressive number. If, for the sake of argument, the likelihood of the evidence given the defendant’s diagnostic hypothesis is only 20 percent and the prior probability of that hypothesis is, conservatively stated, 10 percent, then the probability of that hypothesis being true given the evidence is .2 multiplied by .10 or .02 or, in terms of percentage, 2 percent. Obviously, the probability of the defendant’s hypothesis being true (2 percent) is significantly greater than the probability of the plaintiff’s hypothesis being true (.8 percent) given the available evidence.
Now, if the plaintiff were to demonstrate that the likelihood of the evidence given its hypothesis was 90.55 percent assuming the same value for the base rate, the probability of its hypothesis being true given the evidence would be .9055 multiplied by .01 or .009055 or, in terms of percentage .905 percent, and the probability of the defendant’s hypothesis being true given the evidence would be .0945 multiplied by .10 or .00945 or, in terms of percentage, .945 percent. Still, even on these terms, the probability of the defendant’s hypothesis being true given the evidence is greater (although by a very small amount) than the probability of the plaintiff’s hypothesis being true.
e. The Problem of Co-morbidity
The stressors that lead to PTSD place an individual at risk for developing psychiatric disorders related to but distinct from PTSD. “One of the most consistent findings in studies of PTSD . . . is that the great majority of sufferers fulfill the diagnostic criteria for other disorders in addition to those for PTSD.” These related but distinct psychiatric disorders include anxiety disorders, mood disorders, substance abuse disorders, somatoform disorders, and personality disorders. So expect that whenever the defense asserts that the plaintiff’s symptom profile is consistent with a mental disorder other than PTSD, the plaintiff will respond that the mental disorder is “co-morbid” with PTSD and probably the result of the traumatic stressor or the result of the plaintiff’s having to endure the symptoms of PTSD. “Co-morbidity” is defined as the concurrent occurrence of two or more mental disorders.
Also expect that whenever the defense responds that the mental disorder preexisted the traumatic stressor, the plaintiff will assert that the symptoms were risk factors predisposing the plaintiff to PTSD when the plaintiff eventually encountered the traumatic stressor.
f. Incidence and Prevalence of PTSD
Knowing the incidence and prevalence of PTSD is important in assessing the likelihood that a diagnosis of PTSD is valid. When a number of possible diagnoses may accommodate the patient’s clinical findings or profile, the diagnostician may need to assess the likelihood of each possible diagnosis. To do that, the diagnostician will need to know the prevalence of the alternative diagnosis in the relevant population. This is the “prior probability” or “base rate” of the disorder. With those data on prevalence and with Bayes’ Theorem, the diagnostician may then determine which of the alternate diagnoses is most likely.
Studies of the prevalence of PTSD may examine two kinds of populations: (1) populations at risk, such as combat veterans and disaster victims, and (2) the general population. Rates of PTSD in individuals exposed to trauma range from 5 percent to 11 percent. “Current rates” of PTSD in nonveterans is estimated to be 1.2 percent in men and 0.3 percent in women. And the “lifetime prevalence” of PTSD in the general population is estimated to be 8 percent.
- Man-Made Disasters
5 percent
- Large-Scale Transportation Accidents
12 percent
- Emergency Worker Exposure to Trauma
3–32 percent
- Rape and Sexual Assault
12–14 percent
- Spousal Battery
13 percent
- Child Abuse
6–62 percent
- Witnessing Death or Serious Injury of Family Member or Friend
Male Vietnam Veterans 15 percent
Female Vietnam Veterans 9 percent
- Violent Crimes, Deaths, or Accidents
7–11 percent - Motor Vehicle Accidents
8–46 percent
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4. Malingering
“… the lady doth protest too much.”
Shakespeare
a. Introduction
For the most part, an assumption underlying the process of diagnosis in the DSM is that the patient, when relating her symptoms, is motivated to tell the truth. Yet in some contexts, including cases in which the claimant alleges PTSD, that assumption is unrealistic. And so the DSM provides that in considering the diagnosis of PTSD, the diagnostician must rule out malingering in situations involving financial remuneration, benefit eligibility, and litigation.
Although the incidence of malingered psychiatric symptoms after injury is unknown, follow-up studies on people considered 100 percent disabled indicate that about 40 percent of those showed no disability whatsoever one year after determination of their disability.
So it is safe to assume that “malingering” plaintiffs are legion. If evidence of “faking bad” (that is, trying to appear impaired) exists, then no conclusions should be drawn about any dysfunction.
b. Definition of “Malingering”
The term “malingering” has a specific meaning in the DSM. “The essential feature of malingering is the intentional production of false or grossly exaggerated physical or psychological symptoms, motivated by external incentives, such as avoiding military duty, avoiding work, obtaining financial compensation, evading criminal prosecution, or obtaining drugs.”
Be careful to distinguish between “pure malingering,” “partial malingering,” and “false imputation.” “Pure malingering” is the feigning of disease when it does not exist at all. Pure malingering is uncommon in PTSD. “Partial malingering” is the conscious exaggeration of existing symptoms or the fraudulent allegation that prior genuine symptoms are still present. Partial malingering is quite common. In PTSD, “false imputation” is ascribing actual symptoms to a cause consciously recognized as having no relationship to the symptoms.
c. Labeling Plaintiff as a Malingerer
Most treating physicians or psychologists do not even try to rule out malingering. Treating physicians or psychologists accept the patient’s word and if they have suspicions are loath to disclose them. Simply, physicians, especially psychiatrists, are usually taught to sympathize with and believe their patients. This attitude is usually consistent with the physician’s objective to treat the patient, not to thwart the patient’s economic interests. When a physician has doubt about what a patient has said, the physician will have a tendency to presume dysfunction, not malingering. That is, for physicians it is worse to overlook a disorder than to overdiagnose it, unless the appropriate treatment is dangerous. Moreover, most physicians realize that if they do not adopt this attitude, many patients will leave them. So if a physician believes that a patient is malingering, he will merely not provide her with the standard treatment, and send her away, without creating an embarrassing entry in the patient’s chart that the patient is malingering. Clinicians are also reluctant to label someone a malingerer for fear of legal liability. To avoid that pitfall, clinicians are cautioned to merely state that no objective evidence exists to support the claimant’s subjective complaints.
Even so, when clear evidence of malingering is presented, the clinician should characterize the plaintiff’s behavior as malingering. Clear evidence is provided (1) when, while the patient believes he is unobserved, he is caught doing what he claimed he could not do; or (2) when the patient actively confesses that he is faking.
d. Detecting Malingering
Detecting malingering or faking often involves nothing more than assessing whether the plaintiff’s behavior is other than what would be expected in the circumstances. Satisfactorily determining whether the plaintiff’s behavior is inconsistent with expectations requires some time observing how the plaintiff behaves in appropriate circumstances. Unfortunately, usually only a limited opportunity exists to observe the patient by the jury, by the defendant’s expert, or by the plaintiff’s nontreating expert. Even if the plaintiff’s expert observes such behavior, she will not expose the plaintiff. The plaintiff’s nontreating expert not only will not attempt to detect malingering, but too often will be a willing conspirator in promoting the plaintiff’s malingering in an effort to achieve monetary recovery in litigation. The only check on malingering is the defendant’s lawyer or medical or psychological expert.
i. Red Flags
Malingering should be strongly suspected if any combination of the following is noted: (1) poor work record; (2) prior incapacitating injuries; (3) discrepant capacity for work and recreation; (4) unvarying, repetitive dreams; (5) antisocial personality traits (not necessarily full-blown APD); (6) overidealized functioning before trauma; (7) evasiveness; (8) inconsistency in symptom presentation; (9) lack of cooperation during the diagnostic evaluation and in complying with the prescribed treatment regimen; (10) marked discrepancy between the person’s claimed stress or disability and the objective findings; and (11) medicolegal context of presentation (e.g., the person is referred by an attorney to the clinician for examination).
For example, with respect to item (4), malingerers are unlikely to volunteer information about nightmares. But when they do, they tend to claim that they have repetitive dreams, which always reenact the traumatic event in exactly the same way. Genuine nightmares from trauma usually show variations on the theme of the traumatic event.
ii. Other Indicia of Malingering
A number of tests for malingering have been developed in some standard neuropsychological tests or batteries of tests.
For instance, usually in a psychological or psychiatric IME, the plaintiff will be given an MMPI. (Nowadays, however, the MMPI-2 is the test commonly administered.) The MMPI can be used to establish malingering in PTSD; indeed, it is the most validated psychological test to ascertain malingered mental illness. It can help distinguish claimants with true PTSD from those with functional disorders.
Also review the plaintiff’s answers to the MMPI test questions for inconsistencies. For example, the examinee may be malingering if she has testified that she has not abused alcohol, but answers yes to questions 264 and 489 in the MMPI-2: (264) “I have used alcohol excessively” and (489) “I have a drug or alcohol problem.”
Through your consulting expert, develop the significance of the various scales on those tests that expose malingering. These scales are as follows:
> MMPI:
? Scale > 30 raw score points
T-R Index > 4
Carelessness Scale > 4
F Scale > 15
Lacher & Wrobel Critical Items > 83
Wiener & Harmon Obvious and Subtle Items
Wales & Seeman Obvious Items > 99 and Subtle Items < 46
Dissimulation (Ds) raw score > 21
> MMPI-2:
F Scale
Back-Page F Scale (Fb) T-Score > 80
True Response Inconsistency Scale raw score > 12
Lees-Haley Fake Bad Scale > 20
Assessing the validity of the plaintiff’s responses to the items of the MMPI-2 involves three basic steps.
First, the total number of items that the plaintiff fails to answer is ascertained. If the plaintiff omits more than 30 items, the “profile,” as it is called, is probably invalid. Second, if the plaintiff has answered an acceptable number of items, the “consistency” with which the plaintiff answered the items in the MMPI-2 is then ascertained. (Consistency in endorsing items verifies that the plaintiff has endorsed the items reliably; the items must be answered consistently before determining the accuracy with which the plaintiff has answered the items.) Third, if the plaintiff passes the preceding two steps, the “accuracy” of the answers must be verified.
Consistency measures devised for the MMPI-2 are the Variable Response Inconsistency Scale (VRIN) consisting of semantically similar pairs of items and the True Response Inconsistency Scale (TRIN) consisting of item pairs that are opposite in content but keyed in the same direction.
(A) Variable Response Inconsistency Scale (VRIN)
VRIN consists of 67 pairs of items that have similar or opposite item content.
These pairs of items are scored if the plaintiff is inconsistent in responding to them. When the scores on VRIN are 7 or lower, or 16 or higher, a high probability exists that the client has answered or endorsed the items consistently or inconsistently, respectively.
(B) True Response Inconsistency Scale (TRIN)
TRIN consists of 23 pairs of items.
TRIN is similar to VRIN except that the scored response is either true or false to both items in each pair of items. High scores on TRIN reflect plaintiffs who tend to be “yea-sayers” and low scores reflect plaintiffs who are “nay-sayers” regardless of item content. Scores on TRIN are not used to determine whether the plaintiff has answered the items consistently.
It is very difficult for plaintiffs to fake the MMPI-2 as if they have a “specific” mental disorder. So plaintiffs answering the items inaccurately will usually over-report psychopathology in general rather than specifically. Over-reporting of psychopathology on the MMPI-2 can be assessed by the “Obvious and Subtle” subscales, Critical items, the F and FB Scales, and the F-K Dissimulation Index.
(C) Wiener and Harmon Obvious and Subtle Subscales
On five scales in the MMPI-2, the items to be endorsed can be classified as either items indicating obvious emotional disturbance or items subtle (not obvious) for emotional disturbance. Plaintiffs who over-report emotional disturbance will tend to answer the obvious but not the subtle items as indicating emotional disturbance. Those five scales on the MMPI are 2(D), 3(Hy), 4(Pd), 6(Pa), and 9(Ma). A plaintiff who achieves T scores of 80 or more on all five obvious scales and T scores near 50 on all five subtle scales is trying to over-report. The T scores for each of the obvious and subtle subscales is calculated, their difference is determined on each clinical scale, and these differences are totaled into a single overall measure. A total T score difference above whatever criterion is used to identify over-reporting of psychopathology is presumptive rather than definitive evidence of over-reporting. Beyond that criterion, it is necessary to verify that the plaintiff is over-reporting psychopathology rather than actually experiencing severe psychopathology.
(D) Lachar and Wrobel Critical Items
A set of “critical items” is thought to require careful scrutiny if answered in the deviant direction. A plaintiff who is trying to over-report psychopathology would be expected to endorse a large number of these items. Normal individuals endorse 16 to 23 percent of these critical items on average, whereas psychiatric patients endorse 32 to 36 percent on average.
- F-K Dissimulation Index
The raw score of the F Scale minus the raw score of the K Scale is used to assess the accuracy of item endorsement. If the F-K Dissimulation Index was greater than +9, the profile is designated as over-reporting.
- The F Scale
The F Scale consists of 60 items selected to detect unusual or atypical ways of answering test items. It consists of items that no more than 10 percent of an early subsample of the Minnesota normative sample answered in the deviant direction. An MMPI-2 raw score between 16 and 22 may indicate an invalid profile. A raw score above 23 probably indicates an invalid profile.
- The FB Scale
The FB Scale consists of 40 items on the MMPI-2 that no more than 10 percent of the MMPI-2 normative sample answered in the deviant direction. The items in the FB Scale are analogous to those of the F scale except that they are placed in the second half of the test. Again, as with the F Scale, a raw score of 16 to 22 may indicate an invalid profile. A raw score above 23 probably indicates an invalid profile.
- Lees-Haley Fake Bad Scale
The Lees-Haley Fake Bad Scale consists of 43 items on the MMPI-2.
Of these items, 18 are to be answered “true” and 25 to be answered “false.” Those items to be answered “true” include the following:
“11. People should try to understand their dreams and be guided by or take warning from them.”
“18. I am very seldom troubled by constipation.”
“31. I have nightmares every few nights.”
“506. I am a high-strung person.”
Those items to be answered “false” include the following:
“12. I enjoy detective or mystery stories.”
“41. I have had periods of days, weeks or months when I couldn’t take care of things because I couldn’t ‘get going.'”
“57. I am a very sociable person.”
“374. At periods my mind seems to work more slowly than usual.”
“561. I usually have enough energy to do my work.”
A score of 20 is used to identify malingering from nonmalingering plaintiffs.
(I) The Infrequency-Psychopathology Scale, F(p)
The Infrequency-Psychopathology Scale consists of 27 items on the MMPI2.
Of the 27, 18 are keyed true and 9 keyed false. These items are distinctive in that they are endorsed infrequently by both those who are normal and those with mental disorders. These items reflect severe psychotic symptoms, very unusual habits, and highly amoral attitudes, and they identify confusion. The higher the F(p) score, the more likely it is that the plaintiff has faked bad on the MMPI-2. T scores over 100 on the F(p) are very strong indicators of faking.
The F(p) scale can be used as an adjunct to the interpretation of F and FB Scales. If the F Scale is elevated, examine the VRIN score. If VRIN is elevated beyond a T score of 80, the F score is likely elevated due to random responding. If the VRIN is not elevated, examine TRIN. If TRIN is greater than 100, the F score is probably elevated due to acquiescence or nay-saying.
If both VRIN and TRIN are not elevated, examine F(p). If F(p) is elevated, the elevated F score is probably due to faking.
5. Factitious Disorder
The DSM-IV diagnostic criteria for factitious disorder are as follows:
“A. Intentional production or feigning of physical or psychological signs or symptoms.
“B. The motivation for the behavior is to assume the sick role.
“C. External incentives for the behavior (such as economic gain, avoiding legal responsibility, or improving physical well-being, as in malingering) are absent.”
Factitious disorder differs from malingering in that the motivation for producing symptoms in malingering is an external incentive, whereas in factitious disorder external incentives are absent. Factitious disorder is suggested when there is evidence of an intrapsychic need to maintain the sick role.
E. Alternate Causation of PTSD
A plaintiff may have PTSD, but that PTSD may have been caused by a stressor other than that stressor for which the defendant is alleged to be responsible. The defense will want to consider these two options: (1) whatever the plaintiff has, she had it before the alleged stressor, or (2) whatever the plaintiff has, she developed it after but not from the alleged stressor. Establishing this defense on causation requires identifying (1) a history of symptoms compatible with PTSD and (2) an exposure to a qualifying stressor. The defense may discover––for instance, through psychiatric records––that the plaintiff had the symptoms of PTSD before the alleged trauma. Or the defense may discover that the plaintiff was subjected to a stressor more objectively extreme than the stressor alleged to have caused the plaintiff’s current complaints, thereby raising the possibility that the plaintiff’s complaints arose from the earlier, more extreme trauma.
1. Delayed Onset
The specter of an intervening stressor between the stressor for which the defendant is allegedly responsible and the manifestation of symptoms is particularly probable given that PTSD can have a delayed onset, defined to be “at least 6 months after the stressor.” For the defense, the concept of delayed-onset PTSD is nettlesome. A plaintiff involved in a motor vehicle accident who has no complaints or symptoms constituting PTSD before a visit with a lawyer may afterwards develop PTSD after being referred to and consulting with a psychologist or psychiatrist recommended by that lawyer.
2. Childhood Abuse
Much is heard about the high incidence and prevalence of childhood abuse, particularly sexual abuse.
If these reports of sexual abuse are accurate, these high rates for incidence and prevalence are important for the defense. Simply, childhood physical and sexual abuse may result in PTSD. Many who were abused as children developed PTSD as children. PTSD, incipient in childhood, may become chronic, persisting into adulthood.
Plaintiffs’ experts on PTSD will attempt to turn weaknesses in their positions into strengths. For example, if the plaintiff has a history of child abuse, and studies are introduced reflecting that child abuse results in PTSD with the defense arguing that if the plaintiff has PTSD, it resulted from child abuse, and studies indicate that PTSD is underdiagnosed in those who were abused as children, the plaintiff’s expert will argue that the plaintiff’s prior PTSD merely sensitized the plaintiff to PTSD from the motor vehicle accident.
Childhood abuse is also associated with certain personality disorders. Those personality disorders include antisocial personality disorder, borderline personality disorder, and dissociative identity disorder. If there is a high prevalence of childhood abuse and that abuse is associated with these personality disorders, there should be a high prevalence of these personality disorders. This fact is significant because the symptoms of these personality disorders sometimes mimic the symptoms of PTSD.
3. Sensitization Hypothesis
If abused as a child, the plaintiff will raise what is called the “sensitization hypothesis.” That hypothesis is that previous exposure to trauma sensitizes an individual to subsequent trauma, thereby placing that individual at greater risk for developing PTSD. Based on this hypothesis, the plaintiff will argue that her childhood trauma, while not resulting in PTSD in childhood, sensitized her to the alleged trauma precipitated by the defendant, resulting currently in PTSD.
4. “Eggshell” Plaintiff
Increasing evidence indicates that PTSD is not a normal reaction to extraordinary events but an abnormal reaction to both ordinary and extraordinary events. That is, PTSD is the response of the “eggshell” plaintiff. In traditional thinking, the magnitude of the stressor should be directly proportional to the risk of developing PTSD. But research indicates that “there is as yet no direct support for the validity of the . . . distinction between extraordinary stressors . . . and more ordinary stressors.”
No threshold appears to exist. So low-magnitude events may give rise to PTSD.
But this line of thinking may prove too much. If the plaintiff has a predisposition to PTSD owing to emotional fragility, the plaintiff would be expected to have developed PTSD from any number of minor traumas both before and after the alleged trauma for which the defendant is alleged to be responsible. So when the plaintiff predicates her claim for PTSD on a stressor that seems somewhat ordinary, asserting that she is a highly susceptible individual, the so-called eggshell plaintiff, then the defense should be developed that any number of events in the plaintiff’s past could be responsible for her current symptoms. For instance, the defense may want to assert that the alleged stressor for which the defendant is allegedly responsible is merely an “external cue” that merely “symbolizes” or “resembles” the true preexisting traumatic event. (See Criteria B(4) & B(5).)
5. Risk Factors for PTSD
Some people have qualities that predispose them to develop PTSD.
These predisposing qualities include: (1) combat exposure; (2) socioeconomic status as a child; (3) psychiatric symptoms of depression or anxiety; (4) childhood abuse; (5) legal education; (6) being a woman; (7) substance abuse; and (8) antisocial behavior.
That people can have a predisposition to PTSD helps in assessing the merits or demerits of claim for PTSD. If the plaintiff has these predisposing qualities, then the likelihood increases that his or her diagnosis of PTSD is legitimate or malingered (viz., legal education, antisocial behavior). But having these predisposing qualities also increases the likelihood that although the diagnosis of PTSD is legitimate, the claim that the defendant caused the plaintiff’s PTSD is illegitimate in that the plaintiff’s PTSD probably developed from earlier traumas.
F. Limitation of Damages
If the plaintiff has PTSD caused by the defendant, the defense will want to limit the potential award of damages. Limiting damages involves demonstrating (1) that the disorder is not severely disabling; (2) that the disorder is not chronic; (3) that the disorder can be successfully treated; or (4) that the treatment is inexpensive.
1. Level of Disability
The definition of “mental disorder” in the DSM-IV requires that there be clinically significant impairment or distress. For the defense, that level of disability needs to be minimized, if possible. This effort involves a factual investigation into the plaintiff’s claims of impairment.
2. Chronicity
Every defense lawyer fears the word “chronic” when uttered by a plaintiff’s medical or psychological expert. A diagnosis of chronicity usually carries with it the prospect for a significant award of damages. This prospect is particularly upsetting because the standard for diagnosing chronicity is often so arbitrary and so deliberately oblivious to future prospects of recovery or remission. Nowhere is that set of concerns more applicable than in the diagnosis of chronicity in PTSD.
Under the DSM-IV, PTSD is characterized as chronic if the symptoms have persisted for three months. As a consequence, in litigated cases, the plaintiff will have a diagnosis of chronicity by the time the complaint is filed. The issue for the defense will be to establish a remission rate for those diagnosed with chronic PTSD and to convince the jury that the plaintiff will recover.
If PTSD becomes chronic, without treatment, it will probably persist for decades.
It has been estimated that at least one-third of those with PTSD do not recover. People with chronic PTSD will also be likely to develop a deleterious change in personality, with severe functional incapacity.
Yet PTSD is also compatible with remarkable functional recovery.
Indeed, without treatment, the severity of PTSD symptoms seems to decrease over time. A number of post-trauma factors play a significant role in prognosis: (1) early treatment with sharing and validation of the victim’s experience; (2) early and continuing social support; (3) exposure to therapeutic groups with other PTSD victims; (4) avoidance of retraumatization; (5) avoidance of activities that interrupt or prevent treatment.
In tort law, a plaintiff who is injured through the fault of another is denied recovery for damages for that injury to the extent that the plaintiff could have reasonably avoided those injuries. This law is relevant to claims for tortiously induced PTSD. Research indicates that early treatment of PTSD substantially reduces the risk that the PTSD will become chronic. As a result, a plaintiff who develops PTSD but who fails to seek early treatment should not recover damages for chronic PTSD if the weight of evidence is that the plaintiff’s PTSD would not be chronic had she sought early treatment.
3. Effectiveness of Treatment
In the context of litigation, whether or not a purported disorder is treated is an important question. Treatment not only establishes the amount of special damages but often is a multiplicand in a rule of thumb for determining general damages. Treatment is also an indication whether the diagnosis itself is genuine and whether the plaintiff has made an effort to avoid or mitigate the consequences of her injuries. A plaintiff diagnosed with a serious but treatable disorder who is not prescribed treatment or who does not seek treatment is rightfully suspect.
But be sensitive to the timing of this defense. If this shortcoming in the plaintiff’s case is raised before trial, do not be surprised to find that the plaintiff will begin some form of treatment by the time trial begins. Indeed, expect to learn that the plaintiff is undertaking treatment involving fairly potent drugs in order to give her claim an aura of legitimacy.
The two prominent treatments for PTSD are psychotherapy (talk) and pharmacotherapy (drugs). These two forms of treatment are not mutually exclusive.
a. Psychotherapy
Psychotherapy is the talking cure. It may be (1) individual psychotherapy, involving behavioral, cognitive, or psychodynamic techniques; or (2) group therapy. Despite the old saw “talk is cheap,” psychotherapy is typically protracted and expensive at $70+ per hour. Moreover, the effectiveness of this kind of therapy, apart from placebo effects, has not been established through controlled clinical trials.
Attempts to assess the effectiveness of psychodynamic psychotherapy have had significant methodological flaws, including lack of controls, lack of adequate assessment of outcome, and vaguely described treatments.
“Exposure” therapy is the most studied and supported therapeutic treatment technique for PTSD.
This kind of therapy seeks to produce habituation of emotional responses by instructing the patient to describe the event as if it were happening in the present while visualizing it; this exposure to the traumatic memory is continued until emotional reactions to the traumatic memory decrease.
Prolonged imaginal and in vivo exposure is claimed to reduce symptoms by allowing patients to realize that contrary to their mistaken ideas: (1) being in objectively safe situations that remind one of the trauma is not dangerous; (2) remembering the trauma is not equivalent to experiencing it again; (3) anxiety does not remain indefinitely in the presence of feared situations or memories, but rather it decreases even without avoidance or escape; and (4) experiencing anxiety and PTSD symptoms does not lead to loss of control. Some studies have arguably supported the effectiveness of prolonged exposure in treating PTSD.
“Eye Movement Desensitization and Reprocessing” is a form of exposure therapy.
This form of therapy consists in a patient focusing on a disturbing image or memory and related emotions and cognitions while the therapist waves a finger across the patient’s visual field with the patient tracking the finger. After each sequence, the patient indicates his or her level of distress. Yet existing studies on the effectiveness of this treatment have been methodologically flawed.
A cognitive therapy called anxiety management is based on the premise that pathological anxiety stems from deficits in skills in managing anxiety.
Managing anxiety provides patients with a repertoire of such strategies, such as relaxation training, positive self-statements, breathing training, biofeedback, social skills training, and distraction techniques. Existing studies support the effectiveness of anxiety management (stress inoculation training) in female assault victims; the effectiveness of anxiety management in other groups of trauma victims remains to be assessed.
b. Pharmacotherapy
Pharmacotherapy is sometimes helpful in reversing the biological abnormalities associated with PTSD. Drugs used in treating PTSD include antidepressants, anxiolytics, carbamazepine, lithium, and neuroleptics.
i. Antidepressants
Antidepressants, particularly the tricyclics and the serotonin reuptake inhibitors, are frequently used to treat PTSD.
These drugs are used to control dysphoria, sleep disturbance, and nightmares. Yet, as to PTSD, no satisfactory controlled clinical trials exist establishing the clinical efficacy of these drugs.
ii. Tricyclics
Imipramine, amitriptyline, and desipramine have been tested as treatments for PTSD.
iii. Monoamine Oxidase Inhibitors (MAOI)
Phenelzine has been tested as a treatment for PTSD.
iv. Selective Serotonin Reuptake Inhibitors (SSRI)
SSRIs have become the medications of choice for PTSD. They are most effective in the treatment of numbing and hyperarousal symptoms.
v. Anxiolytics
Anxiolytics are also frequently used to treat PTSD.
These anxiolytics include the antidepressants, MAOIs; sympatholytics such as proprandol and clonidine; and benzodiazepines such as diazepam and prazolam. These drugs are used to treat explosive behavior and nightmares. Yet, again, no satisfactory controlled clinical trials exist confirming the direct efficacy of these drugs.
vi. Carbamazepine
Carbamazepine (Tegretol) is an anti-convulsant that counters limbic “kindling,” a process by which neuroanatomic structures become increasingly sensitized following repeated exposure to electrical stimulation.
This drug is used to treat “flashbacks,” nightmares, and intrusive recall. Carbamazepine has had some success in treating those with PTSD, but additional controlled experimental trials are needed.
vii. Lithium
Lithium is a potent drug and is used by some to treat PTSD.
This drug is used to treat loss of control and impulsiveness. But no published systematic double-blind clinical trials of lithium treatment exist for PTSD.
viii. Neuroleptics
Neuroleptics are anti-psychotic drugs that typically block post-synaptic dopamine receptors in the central nervous system. Trade names for these neuroleptics include Thorazine, Navane, Haldol, and Clozaril. These drugs are used to treat dissociative and psychotic symptoms. These potent drugs were widely used in the 1960s and 1970s to treat Vietnam veterans with PTSD. But now they are not routinely used to treat PTSD.
4. Cost of Treatment
The cost of medications is often less than the cost of psychotherapy.
* * *
When the plaintiff seeks recovery of special damages, which include a substantial component for treatment for PTSD, the defense should be aware of what methodologically sound studies, if any, support the effectiveness of that kind of treatment. If none exist, then that point ought to be brought to the attention of the jury and the treatment characterized as unnecessary.
Yet, in attempting to limit damages, the defense is faced with a potential pitfall: proving that certain treatments are ineffective and hence unnecessary may leave the impression that the plaintiff’s PTSD is untreatable and hence chronic. In this regard, recent studies involving a significant sample of Vietnam veterans have disclosed that prolonged and intensive hospital treatment (medications, group and individual therapy, behavioral therapy, and family therapy) for chronic PTSD had no long-term beneficial effects on the veterans’ symptoms.
G. Special Issues of Interest in Litigation
1. PTSD From Activities in the Workplace
Claims are proliferating for discrimination or sexual harassment in the workplace. For the most part, the alleged harassment will be considered offensive but not severely traumatic. Yet on occasion, a plaintiff will assert that the discriminating or harassing behavior was so traumatic that it resulted in PTSD.
In the process, the plaintiff will assert that although the offensive behavior did not involve an event involving actual or threatened death or serious injury, it did involve a threat to her “physical integrity.” (The alleged stressor will not appear to fit with the severe stressors listed in the commentary of the DSM-IV or with the stressors listed in the various standardized trauma questionnaires or inventories.) The plaintiff will further assert that she is hypersensitive to the putative stressor, and that is why a stressor that might have caused the ordinary person to be merely upset or angry caused the plaintiff to develop PTSD.
The difficulty with the plaintiff’s position is that if the plaintiff is so hypersensitive to this kind of alleged behavior, she, not having been born yesterday, will have probably been subjected to similar behavior in the past and, if so, should have developed PTSD on those occasions as well. An inquiry into the plaintiff’s history will probably reveal that she has been subjected to stressors that would be viewed objectively as more traumatizing than the alleged incidents of sexual harassment in the workplace.
2. PTSD From Motor Vehicle Accidents
The stressors people most frequently encounter that might constitute a basis for a PTSD claim are those arising from motor vehicle accidents. Motor vehicle accidents have been found to be the single leading cause of PTSD in the general population, with the reported rates of PTSD in victims of serious motor vehicle accidents ranging from 8 percent to 46 percent.
From a plaintiff’s perspective, what better adjunct to a claim for personal injuries from a motor vehicle accident than a claim for psychological injuries, encouraging juror sympathies and boosting an otherwise pedestrian award for damages into the stratosphere?
Although the commentary in the DSM-IV on PTSD remarks that PTSD may arise from motor vehicle accidents, those accidents need to be “severe automobile accidents,” presumably to qualify the stressor under Criterion A. Yet, despite that commentary, Criterion A in the DSM-IV has in Subpart (2) a subjective component that many plaintiffs will argue enables them to qualify under Criterion A for PTSD even though many would not consider the automobile accident in which those plaintiffs were involved to be “severe.” Indeed, in some studies, trauma and injury-related characteristics, such as accident and injury severity and subjective perception of a threat to life, were not found to be associated with PTSD at one year.
The significance of this finding is that “injured victims of traffic accidents are at considerable risk for development of PTSD even when they are only mildly injured.”
As a result, the defense needs to be familiar with the studies of PTSD arising from motor vehicle accidents.
A number of studies have been conducted concerning PTSD from motor vehicle accidents.
These studies are primarily concerned with (1) the rate of PTSD from motor vehicle accidents of varying degrees of severity, (2) the cut point at which the symptoms of PTSD tend either to resolve or to become chronic, and (3) the risk factors for developing PTSD from motor vehicle accidents. Yet drawing conclusions about the risk of psychiatric morbidity after motor vehicle accidents is difficult for a number of reasons. Primarily, the studies lack uniformity, including inconsistencies across measurement (severity of accident), time elapsed from the motor vehicle accidents, and the absence of systematic longitudinal follow-up.
3. PTSD Overlying Preexisting Psychological Disorders
A plaintiff who has been diagnosed with PTSD may very well have preexisting psychological disorders presenting with symptoms and behaviors constituting elements of PTSD. Obvious examples of such preexisting disorders are, on Axis I, mood and generalized anxiety disorders and, on Axis II, borderline or antisocial personality disorders. When this co-morbidity occurs, the defense will need to have these different disorders demarcated.
Plaintiffs will assert that disorders co-morbid with PTSD are the result of PTSD. Those disorders include substance-abuse disorders, depression, and anxiety. Unfortunately, little is known about the chronological order between the onset of PTSD and the onset of co-morbid disorders.
Criterion C (3 or more) and D (2 or more) must be satisfied before a plaintiff can be diagnosed with PTSD. Both criteria require that the target symptoms not have been present before the trauma. As a result, if the plaintiff has preexisting depression or personality disorder that is manifest through symptoms characterized in Criterion C (particularly C(3) through C(7)) or D, the plaintiff may have difficulty establishing that she developed PTSD from the trauma without some sleight of hand from her expert.
4. Subtle Presentations of PTSD
A subtle presentation of PTSD has been defined as a situation in which “a person shows some signs and symptoms [of PTSD], but reports no previous traumatic events, no qualifying emotional reaction to these events, or obvious links between previous trauma and current psychological difficulties.”
(This is another, less loaded way to describe the “repressed memory syndrome.”)
When the plaintiff presents this way, expect the plaintiff’s therapist or expert to adopt one of two diagnostic solutions: (1) base a diagnosis of PTSD on obvious signs and symptoms alone, assuming that a symptomatic individual in fact must be failing to disclose a relevant trauma, or (2) link the person’s suffering arbitrarily to a qualifying event, although the person makes no such connection.
This diagnostic maneuver may be camouflaged through use of a variety of diagnostic instruments such as a structured interview (viz., the Clinician-Administered PTSD Scale) or psychometric test (viz., the MMPI-II) or a self-report PTSD scale (viz., Impact of Event Scale) followed by administration of various diagnostic tools used to assess the obstacles of reporting trauma, such as a dissociation scale or substance-abuse survey or social desirability or defensiveness scale. But in the end the clinician will remark that “the connection of symptoms to trauma is always an inferential process rather than purely an introspective one[;] in subtle cases, it thus is reasonable to explore the individual’s perceptions about the likelihood of symptoms being connected to the trauma separately from the perceptions that the symptoms do occur.”
5. Inflated Base Rates of PTSD
a. PTSD
Calculating the “positive predictive value” of various symptoms for PTSD requires knowledge of the prevalence or base rate of PTSD in the relevant population. The lower the base rate, the less likely those symptoms are to predict PTSD in this particular plaintiff. The higher the base rate, the more likely those symptoms are to predict PTSD in this plaintiff.
This is a mathematical relationship well known to ideologues who want to use PTSD as a tool to reconstruct society. They endeavor to overstate the base rate of PTSD in categories of trauma of particular interest to their social agenda—childhood abuse, rape, spousal abuse, and so on. For instance, estimates of the prevalence of childhood sexual abuse range from 6 percent to 62 percent. Many of these estimates are inflated as a result of using poor methodologies in conducting surveys and epidemiologic studies. For example, in one notorious study investigating the incidence of incest, the author instructed interviewers to ask, “How upset were you by this experience––extremely upset, somewhat upset, or not very upset?” Obviously, this question did not allow for the possibility that the experience caused no upset. The author also defined “incest” too broadly, to include any attempted sexual contact between relatives, no matter how distant the relationship, before the age of 18. Moreover, interviewers were biased by ten hours of pre-interview indoctrination about the horrors of rape and incest.
b. Traumatic Events
Another numerical value important to the defense is the ratio of those who develop PTSD from exposure to a traumatic event to all those exposed to that kind of traumatic event. The fewer people developing PTSD from exposure to that kind of traumatic event, the less likely it is that the plaintiff has PTSD from that kind of exposure.
6. PTSD in Children
This chapter on PTSD has not specifically discussed PTSD in children. Children with PTSD often have different symptoms from adults with PTSD.
As the DSM-IV recognizes under Criteria B(1), B(2), and B(3):
“(1) recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions. Note: In young children, repetitive play may occur in which themes or aspects of the trauma are expressed;
“(2) recurrent distressing dreams of the event. Note: In children, there may be frightening dreams without recognizable content;
“(3) acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative flashback episodes, including those that occur on awakening or when intoxicated). Note: In young children, trauma-specific reenactment may occur;
“(4) intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event; and
“(5) physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event.”
Psychometric instruments have been developed to assess PTSD in children. Reviews of these instruments should be consulted when undertaking the defense of a case involving a child or adolescent with PTSD.
Endnotes
1 American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders (4th ed. 2000).
2 The twentieth-century philosopher Ludwig Wittgenstein articulated the skepticism with which laypeople view psychiatry, even though psychiatry has moved from the formulations of Freud to a more biologically based endeavor. I. Bouveresse, Wittgenstein Reads Freud The Myth of the Unconscious 26-27 (1995); L. Wittgenstein, Lectures, Cambridge 1932-1935: From the Notes of Alice Ambrose and Margaret MacDonald (Alice Ambrose ed., 1979).
3 John P. Wilson, The Historical Evolution of PTSD Diagnostic Criteria: From Freud to DSM-IV, 7 J. Traumatic Stress 681-98 (1994).
4 Diagnostic and Statistical Manual of Mental Disorders 40 (1st ed. 1952).
“Under conditions of great or unusual stress, a normal personality may utilize established patterns of reaction to deal with overwhelming fear. The patterns of such reactions differ from those of neurosis or psychosis chiefly with respect to clinical history, reversibility of reaction, and its transient character. When promptly and adequately treated, the condition may clear rapidly. It is also possible that the condition may progress to one of the neurotic reactions. If the reaction persists, this term is to be regarded as a temporary diagnosis to be used only until a more definitive diagnosis is established.”
“This diagnosis is justified only in situations in which the individual has been exposed to severe physical demands or extreme emotional stress, such as in combat or in civilian catastrophe (fire, earthquake, explosion, etc.). In many instances this diagnosis applies to previously more or less ‘normal’ persons who have experienced intolerable stress.
“The particular stress involved will be specified as (1) combat or (2) civilian catastrophe.”
5 Diagnostic and Statistical Manual of Mental Disorders 49 (2d ed. 1968).
6 Diagnostic and Statistical Manual of Mental Disorders 236 (3d ed. 1980).
“A. Existence of a recognizable stressor that would evoke significant symptoms of distress in almost everyone.
“B. Reexperiencing of the trauma as evidenced by at least one of the following:
“(1) Recurrent and intrusive recollections of the event.
“(2) Recurrent dreams of the event.
“(3) Sudden acting or feeling as if the traumatic event were re-occurring because of an association with an environmental or ideational stimulus.
“C. Numbing of responsiveness to or reduced involvement with the external world, beginning some time after the trauma, as shown by at least one of the following:
“(1) Markedly diminished interest in one or more significant activities
“(2) Feeling of detachment or estrangement from others
“(3) Constricted affect
“D. At least two of the following symptoms that were not present before the trauma:
“(1) Hyperalertness or exaggerated startle
“(2) Sleep disturbance
“(3) Guilt about surviving when others have not, or about behavior required for survival
“(4) Memory impairment or trouble concentrating
“(5) Avoidance of activities that arouse recollection of the traumatic event
“(6) Intensification of symptoms by exposure to events that symbolize or resemble the traumatic event
” Post-trauamatic stress disorder, acute.
“‘Post-traumatic stress disorder, acute’ was characterized as having an onset of symptoms within six months of the trauma and a duration of symptoms less than six months.
” Post-traumatic stress disorder, chronic or delayed
“‘Post-traumatic stress disorder, chronic or delayed’ was characterized as having a duration of symptoms six months or more (chronic) and/or an onset of symptoms at least six months after the trauma (delayed).”
7 Diagnostic and Statistical Manual of Mental Disorders 247 (3d rev. ed. 1987).
“A. The person has experienced an event that is outside the range of usual human experience and that would be markedly distressing to almost anyone, e.g., serious threat to one’s life or physical integrity; serious threat or harm to one’s children, spouse, or other close relatives and friends; sudden destruction of one’s home or community; or seeking another person who has recently been, or is being, seriously injured or killed as the result of an accident or physical violence.
“B. The traumatic event is persistently reexperienced in at least one of the following ways:
“(1) recurrent and intrusive distressing recollections of the event (in young children, repetitive play in which themes or aspects of the trauma are expressed)
“(2) recurrent distressing dreams of the event
“(3) sudden acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative [flashback] episodes, even those that occur upon awakening or when intoxicated)
“(4) intense psychological distress at exposure to events that symbolize or resemble an aspect of the traumatic event, including anniversaries of the trauma
“C. Persistent avoidance of stimuli associated with the trauma or numbing of general responsiveness (not present before the trauma), as indicated by at least three of the following:
“(1) efforts to avoid thoughts or feelings associated with the trauma
“(2) efforts to avoid activities or situations that arouse recollections of the trauma
“(3) inability to recall an important aspect of the trauma (psychogenic amnesia)
“(4) markedly diminished interest in significant activities (in young children, loss of recently acquired developmental skills such as toilet training or language skills)
“(5) feeling of detachment or estrangement from others
“(6) restricted range of affect, e.g., unable to have loving feelings
“(7) sense of a foreshortened future, e.g., does not expect to have a career, marriage, or children, or a long life
“D. Persistent symptoms of increased arousal (not present before the trauma), as indicated by at least two of the following:
“(1) difficulty falling or staying asleep
“(2) irritability or outbursts of anger
“(3) difficulty concentrating
“(4) hypervigilance
“(5) exaggerated startle response
“(6) physiologic reactivity upon exposure to events that symbolize or resemble an aspect of the traumatic event (e.g., a woman who was raped in an elevator breaks out in a sweat when entering any elevator)
“E. Duration of the disturbance (symptoms in B, C, and D) at least one month.
“Specify delayed onset if the onset of symptoms was at least six months after the trauma.”
8 As to those criteria moved, D(5) in the DSM-III was moved to C(2) in the DSM-III-R. D(6) in the DSM-III was moved to B(4) in the DSM-III-R. As to those criteria deleted, D(3) in the DSM-III was deleted from the DSM-III-R. As to those criteria added, Criteria C(1), C(2), C(3), C(7), and D(2) were added to the DSM-III-R.
The distinction between acute and chronic PTSD in the DSM III was deleted in the DSM-III-R. In the DSM-III-R, the symptoms must persist one month for the disturbance to be characterized as PTSD. Otherwise, the disturbance is characterized as “acute stress reaction.”
9 Diagnostic and Statistical Manual of Mental Disorders (4th ed. 1994). The text of the DSM-IV was revised in 2000 and is called, for short, the DSM-IV-TR.
Judith A. Lyons & Terence M. Keane, Keane PTSD Scale: MMPI & MMPI-2 Update, 5 J. Traumatic Stress 111-17 (1992).
10 The DSM-IV also added Criterion F. But this change is not significant. Criterion F was implicit in the DSM-III and DSMIIIR. In addition, in the DSM-IV the distinction between acute and chronic PTSD was reinstated. But in the DSM-IV, the distinction is predicated on a duration of symptoms of less than three months but more than one month for acute PTSD and three or more months for chronic PTSD.
11 L. Stephen O’Brien, Traumatic Events and Mental Health (1998).
12 For a discussion about the role of the International Classification of Diseases and the DSM, refer to pages xxiv, xxv, xxvi, and xxix in DSM-IV-TR.
13 The ICD-10 provides the following definition of PTSD:
“Post-traumatic Stress Disorder
“Arises as a delayed or protracted response to a stressful event or situation (of either brief or long duration) of an exceptionally threatening or catastrophic nature, which is likely to cause pervasive distress in almost anyone. Predisposing factors, such as personality traits (e.g. compulsive, asthenic) or previous history of neurotic illness, may lower the threshold for the development of the syndrome or aggravate its course, but they are neither necessary nor sufficient to explain its occurrence. Typical features include episodes of repeated reliving of the trauma in intrusive memories (‘flashbacks’), dreams or nightmares, occurring against the persisting background of a sense of ‘numbness’ and emotional blunting, detachment from other people, unresponsiveness to surroundings, anhedonia, and avoidance of activities and situations reminiscent of the trauma. There is usually a state of autonomic hyperarousal and hypervigilance, an enhanced startle reaction, and insomnia. Anxiety and depression are commonly associated with the above symptoms and signs, and suicidal ideation is not infrequent. The onset follows the trauma with a latency period that may range from a few weeks to months. The course is fluctuating but recovery can be expected in the majority of cases. In a small proportion of cases the condition may follow a chronic course over many years, with eventual transition to an enduring personality change (F62.0).”
International Statistical Classification of Disease and Related Health Problems (10th rev. ed. 1992).
Norman Sartorius et al., Progress Toward Achieving a Common Language in Psychiatry, II: Results From the International Field Trials of the ICD-10 Diagnostic Criteria for Research for Mental and Behavioral Disorders, 152 Am. J. Psychiatry 1427-37 (1995).
14 Lorna Peters et al., A Comparison of ICD-10 and DSM-IV Criteria for Post-Traumatic Stress Disorder, 12 J. Traumatic Stress 335-43 (1998).
15 Gavin Andrews et al., Classification in Psychiatry: ICD-10 versus DSM-IV, 174 Brit. J. Psychiatry 3-5 (1999).
16 See Diagnostic and Statistical Manual of Mental Disorders 463-64 (4th rev. ed. 2000).
17 I. Pilowsky, Minor Accidents and Major Psychological Trauma: A Clinical Perspective, 8 Stress Med. 77-78 (1992).
Danny Koren et al., Acute Stress Response and Posttraumatic Stress Disorder in Traffic Accident Victims: A One-Year Prospective; Follow-Up Study, 156 Am. J. Psychiatry 367-73 (1999) (“injured victims of traumatic events, traffic accidents in our case, are at considerable risk for development of PTSD even when they are only mildly injured”).
A problem with studies assessing the correlation between the severity of motor vehicle accidents and PTSD is that no adequate measure of “severity” exists. Edward B. Blanchard & Edward J. Hickling, After the Crash, Assessment & Treatment of Motor Vehicle Accident Survivors 15 (“there are no validated scales of accident severity”).
Joel Paris, Does Stress Cause Posttraumatic Stress Disorder?, 44 Can. J. Psychiatry 20 (1999).
18 DSM-IV-TR at 463-64.
Following are examples in which PTSD might be an expected reaction to an extreme stressor.
“On the morning of May 5, the Army of the Potomac halted and began to form its line of battle . . .. The Confederate Army under General Lee had moved into their path. Artillery shells fell on the Sixth Corps headquarters as Sedgwick hastily sent his infantry to the right through the wooded countryside. . . . A New Jersey infantry regiment came jogging past the corps headquarters. Tom Hyde, one of Sedgwick’s aides-de-camp, was standing near Wendell [Holmes], fiddling with his horse’s bridle, when a shell took off the head of a New Jersey man. The head struck Hyde, bursting, and he was knocked down, covered with blood and brains; even his mouth, gaping in surprise was filled.”
–T. Hyde, “Following the Creek Cross” (1894), in S. Novick, The Life of Oliver Wendell Holmes 184-85 (1989).
“Lieutenant Larry Gwin of Alpha Company recalls that late that night one of Alpha’s men crawled into the American perimeter. ‘Sergeant James A. Mullartey from our 1st Platoon made it back to our lines. His story: The NVA had been shooting our wounded. One came up to him, stuck a pistol in his mouth, and fired. The bullet exited the back of his throat, knocked him out and they left him for dead. He survived and when he woke up at night he started crawling to us.'”
–H. G. Moore & J. L. Galloway, We Were Soldiers Once. . .and Young 334 (1993).
Children in medieval and early renaissance Europe routinely witnessed public executions, some of which were unspeakably brutal. For instance, executions of those convicted of treason involved the following brutalities: the miscreant was hanged until he lost consciousness; then he was revived; then he had his privates cut off and stuffed into his mouth; then he had his stomach cut open, and then, while he was still alive, his intestines were tossed in a cauldron of boiling water; then his heart was plucked from his chest and held up to his face; then he was beheaded; the head was then parboiled; and finally placed on a pike. Would not a child, having witnessed that, be expected by today’s standards to develop PTSD? Did those children develop PTSD?
19 Naomi Breslau et al., Traumatic Events and Posttraumatic Stress Disorder in an Urban Population of Young Adults, 48 Archives Gen. Psychiatry 216-22 (1991).
20 Arieh Y. Shaleu et al., Predictors of PTSD in Injured Trauma Survivors: A Prospective Study, 153 Am. J. Psychiatry 219-25 (1996); Naomi Breslau et al., Risk Factors for PTSD-Related Traumatic Events: A Prospective Analysis, 152 Am. J. Psychiatry 529-35 (1995); Sara A. Freedman et al., Predictors of Chronic Post-Traumatic Stress Disorder, 174 Brit. J. Psychiatry 353-59 (1999).
21 Robert I. Simon, Toward the Development of Guidelines in the Forensic Psychiatric Examination of Posttraumatic Stress Disorder in Litigation 42 (1995).
Ekkehard Othmer & Sieglinde C. Othmer, “The Clinical Interview Using DSM-IV,” in 2, The Difficult Patient: Post-Traumatic Stress ch. 3 (1994); David A. Tomb, The Phenomenology of Post-Traumatic Stress Disorder, 17 Psychiatric Clinics N. Am. 237-50 (1994).
Loren Pankratz, Patients Who Deceive 168-69 (1998).
22 Daniel S. Weiss, “Structured Clinical Interview Techniques,” in Assessing Psychological Trauma and PTSD 499 (John P. Wilson & Terence M. Keane eds., 1997).
23 Id.
24 Id. at 400.
25 Id. at 501.
26 Id. at 502.
27 Robert L. Spitzer & Jerome C. Wakefield, DSM-IV Diagnostic Criterion for Clinical Significance: Does It Help Solve the False Positive Problem?, 156 Am. J. Psychiatry 1856-64 (1999).
28 Stephen V. Faraone & Ming T. Tsuang, Measuring Diagnostic Accuracy in the Absence of a “Gold Standard,” 151 Am. J. Psychiatry 650-57 (1994).
29 Edward O. Wilson, Consilience 64 (1998).
30 Naomi Breslau & Glenn C. Davis, Posttraumatic Stress Disorder, the Stressor Criterion, 175 J. Nervous & Mental Disease 255-75 (1987); Mardi J. Horowitz et al., Diagnosis of Posttraumatic Stress Disorder, 175 J. Nervous & Mental Disease 267-68 (1987).
31 Naomi Breslau & Glenn C. Davis, Posttraumatic Stress Disorder, the Stressor Criterion, 175 J. Nervous & Mental Disease 255-75 (1987); Mardi J. Horowitz et al., Diagnosis of Posttraumatic Stress Disorder, 175 J. Nervous & Mental Disease 267-68 (1987).
32 Naomi Breslau & Glenn C. Davis, Posttraumatic Stress Disorder, the Stressor Criterion, 175 J. Nervous & Mental Disease 255-75 (1987); Mardi J. Horowitz et al., Diagnosis of Posttraumatic Stress Disorder, 175 J. Nervous & Mental Disease 267-68 (1987).
33 Naomi Breslau & Glenn C. Davis, Posttraumatic Stress Disorder, the Stressor Criterion, 175 J. Nervous & Mental Disease 255-75 (1987); Mardi J. Horowitz et al., Diagnosis of Posttraumatic Stress Disorder, 175 J. Nervous & Mental Disease 267-68 (1987); Editorial, The Validation of Psychiatric Diagnosis: New Models and Approaches, 152 Am. J. Psychiatry 161-62 (1995).
34 126 Am. J. Psychiatry 983-87 (1970); Eli Robins & Samuel B. Guze, Establishment of Diagnostic Validity in Psychiatric Illness: Its Application to Schizophrenia, 126 Am. J. Psychiatry 107-11 (1970).
35 Editorial, The Validation of Psychiatric Diagnosis: New Models and Approaches, 152 Am. J. Psychiatry 161-62 (1995).
36 Stuart A. Kirk & Herb Kutchins, The Selling of DSM, the Rhetoric of Science in Psychiatry 235-42 (1992); Samuel B. Guze, Review of the Diagnostic and Statistical Manual of Mental Disorders, 152 Am. J. Psychiatry 1228 (4th ed. 1995) (“very few of the hundreds of diagnostic categories have been satisfactorily validated according to these criteria”).
37 Editorial, What Is PTSD?, 154 Am. J. Psychiatry 143-45 (1997).
38 D.W. Goodwin & S.B. Guze, Psychiatric Diagnosis (1984); Samuel B. Guze, Review of the Diagnostic and Statistical Manual of Mental Disorders, 152 Am. J. Psychiatry 1228 (4th ed. 1995) (“very few of the hundreds of diagnostic categories have been satisfactorily validated according to these criteria”).
39 Jonathan Davidson et al., Validity and Reliability of the DSM-III Criteria for Posttraumatic Stress Disorder, 177 J. Nervous & Mental Disease 336-41 (1989); Landy F. Sparr, Post-Traumatic Stress Disorder, Does It Exist?, 13 Neurologic Clinics 413-29 (1995).
40 43 J. Clinical Psychology 32-43 (1987).
41 Id. at 35-36.
42 See generally Scott P. Orr & Danny G. Kalonpek, “Psychophysiological Assessment of Posttraumatic Stress Disorder,” in Assessing Psychological Trauma and PTSD 69 (John P. Wilson & Terence M. Keane eds., 1997).
43 D. Dobbs & W. P. Wilson, Observations on Persistence of War Neurosis, Diseases of the Nervous System 21: 686-91 (1960) (a pre-PTSD study of the psychophysiological responses of combat veterans to relevant combat stimuli described as resembling those of a conditional emotional response; no specific data on the “PTSD” group were presented and no specific comparisons to this group to the two control groups were made).
E. B. Blanchard et al., The Development of a Psychophysiological Assessment Procedure for PTSD in Vietnam Veterans, 54 Psychiatric Q. 220-28 (1982) (psychophysiological responses to standardized sounds of combat discriminated Vietnam veterans with PTSD from age- and gender-matched comparison group; the comparison group was nonveterans, a fact that compromises the value of this study in that the study lacks positive control groups, such as non-PTSD combat veterans with anxiety disorders).
P. F. Malloy et al., Validation of a Multimethod Assessment of PTSD in Vietnam Veterans, 51 J. Consulting & Clinical Psychology 488-94 (1983) (used standardized audiovisual cues to demonstrate that male Vietnam veterans with PTSD not involved in combat were more responsive to the combat cues than either psychiatrically impaired veterans without PTSD or well-adjusted veterans; the utility of this study was compromised by the fact that these psychiatrically impaired veterans were noncombat veterans—it may not be surprising that persons with no prior exposure to combat would be unresponsive to combat-related stimuli).
T. P. Pallmeyer, Refining and Testing an Assessment Procedure for PTSD in Vietnam Veterans (unpublished, 1985).
R. J. Gerardi, Fakeability of Psychophysiological Assessment of PTSD (unpublished, 1986).
J. Knight et al., Empirical Validation of DSM-III Criteria for PTSD (unpublished, 1984).
44 T. M. Fairbank et al., Some Preliminary Data on the Psychological Characteristics of Vietnam Veterans with PTSD, 51 J. Consulting & Clinical Psychology 912-19 (1983).
W. E. Penk et al., Adjustment Differences Among Male Substance Abusers Varying in Degree of Combat Experience in Vietnam, 49 J. Consulting & Clinical Psychology 426-37 (1981).
T. M. Keane et al., Empirical Development of an MMPI Subscale for the Assessment of Combat-Related PTSD, 62 J. Consulting & Clinical Psychology 888-91 (1984).
45 Zimering et al., PTSD in Vietnam Veterans: An Empirical Evaluation of the Diagnostic Criteria (unpublished, 1984).
46 M.E. Wolfe & A.D. Mosnaim, Posttraumatic Stress Disorder Etiology, Phenomenology, and Treatment 49-63 (1990).
47 Id. at 53.
48 55 J. Consulting & Clinical Psychology 251-56 (1987).
49 Jessica Wolfe & Terence M. Keane, “Diagnostic Validity of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder 54 (Marion E. Wolf & Aron D. Mosnaim eds., 1990).
50 In this area, the DSM-IV committee cited six articles published during or after 1990.
S. Solomon & G. J. Canino, Appropriateness of the DSM-III-R Criteria for Posttraumatic Stress Disorder, 31 Comp. Psychiatry 227-37 (1990); P. Steinglass & E. Gerrity, Natural Disasters and Posttraumatic Stress Disorder: Short-term vs. Long-term Recovery in Two Disaster Affected Communities, 20 J. Applied Soc. Psychological 1746-65 (1990); Green et al., Buffalo Creek Survivors in the Second Decade: Stability of Stress Symptoms, 60 Am. J. Orthopsychiatry 43-54 (1990); D. G. Kilpatrick & H. S. Resnick, “Posttraumatic Stress Disorder Associated With Exposure to Criminal Victimization in Clinical and Community Populations,” in Posttraumatic Stress Disorder: DSM-IV and Beyond 113-43 (J.R.T. Davidson & E. B. Foa eds., 1993) (a review article that does not cite any basic research article published during or after 1990); Nader et al., Children’s PTSD Reactions One Year After a Sniper Attack on Their School, 147 Am. J. Psychiatry 1526-30 (1990); B. O. Rothbaum & E. B. Foa, “Subtypes of Posttraumatic Stress Disorder and Duration of Symptoms,” in Posttraumatic Stress Disorder: DSM-IV and Beyond 23-36 (J.R.T. Davidson & E. B. Foe eds., 1993) (a review article that does not cite any basic research article published during or after 1990, except to K. Nader et al. cited above).
51 In this area, the DSM-IV committee cited no basic research articles published during or after 1990.
Pitman et al., Psychophysiologic Assessment of Post-traumatic Stress Disorder Imagery in Vietnam Combat Veterans, 44 Archives Gen. Psychiatry 970-75 (1987); B. Van der Kolk & M. Greenberg, “The Psychobiology of the Trauma Response: Hyperarousal, Constriction, and Addiction to Traumatic Reexposure,” in Psychological Trauma 63-87 (B. Van der Kolk ed., 1987); Z. Solomon & M. Mikulincer, Combat Stress Reactions, Post-traumatic Stress Disorder, and Social Adjustment: A Study of Israeli Veterans, 175 J. Nervous & Mental Disease 277-85 (1987); L. Kolb, A Neuropsychological Hypothesis Explaining Post-Traumatic Stress Disorders, 144 Am. J. Psychiatry 989-95 (1987).
52 Jessica Wolfe & Terence M. Keane, “Diagnostic Validity of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder 58 (Marion E. Wolfe & Aron D. Mosnaim eds., 1990).
53 P. F. Malloy et al., Validation of a Multimethod Assessment of Posttraumatic Stress Disorders in Vietnam Veterans, 51 J. Consulting & Clinical Psychology 488-94 (1983).
54 E. B. Blanchard et al., Cardiac Response to Relevant Stimuli as an Adjunctive Tool for Diagnosing Posttraumatic Stress Disorder in Vietnam Veterans, 17 Behavior Therapy 592-606 (1986).
55 R. K. Pittman et al., Psychophysiologic Assessment of Post-traumatic Stress Disorder Imagery in Vietnam Combat Veterans, 44 Archives Gen. Psychiatry 970-75 (1987) (adapted ideographic methods for studying emotion in order to compare the psychophysiological response (skin conductance, heart rate, and EMG) of male Vietnam veterans with and without PTSD to individually tailored imagery scripts, which contained stimulus, response, and meaning propositions that depicted, among others, the two most stressful combat experiences recalled by the veteran, with results demonstrating greater reactivity to imagery-based trauma cues for the PTSD group relative to the non-PTSD comparison group; the utility of this study was compromised by the fact that the comparison group did not include non-PTSD psychiatric patients who were combat veterans).
56 In this area, the DSM-IV committee cited two basic research articles published during or after 1990. J.R.T. Davidson et al., Posttraumatic Stress Disorder in the Community: An Epidemiologic Study, 21 Psychological Med. 713-21 (1991); I. Winfield et al., Sexual Assault and Psychiatric Disorders Among a Community Sample of Women, 147 Am. J. Psychiatry 335-41 (1990); A. Frances, Problems in Defining Clinical Significance in Epidemiological Studies, 55 Archives Gen. Psychiatry 119 (1998).
57 Robert W. Butler et al., Physiological Evidence of Exaggerated Startle Response in a Subgroup of Vietnam Veterans With Combat-Related PTSD, 147 Am. J. Psychiatry 1308-12 (1990).
58 Carl P. Malmquist, “The Use and Misuse of Psychiatry,” in Sexual Harassment Cases, 26 Psychiatric Annals 149-56, 153 (1996).
59 John S. March, “What Constitutes a Stressor? The ‘Criterion A’ Issue,” in Posttraumatic Stress Disorder DSM-IV and Beyond ch 3 (Jonathan R. T. Davidson & Edna B. Foa eds., 1993); Naomi Breslau & Glenn C. Davis, Posttraumatic Stress Disorder, the Stressor Criterion, 175 J. Nervous & Mental Disease 255-75 (1987).
60 Id. at 46.
61 152 Am J. Psychiatry 1705-13 (1995).
62 Jonathan R. T. Davidson & Edna B. Foa, Refining Criteria for Posttraumatic Stress Disorder, 42 Hosp. & Community Psychiatry 259, 261 (1991). For a general discussion of “factor analysis,” see Paul Kline, The New Psychometrics 52-69 (1998).
63 Susan D. Solomon & Glorisa J. Canino, Appropriateness of DSM-III-R Criteria for Posttraumatic Stress Disorder, 31 Comprehensive Psychiatry 227, 235 (1990).
64 Daniel W. King et al., Confirmatory Factor Analysis of the Clinician-Administered PTSD Scale: Evidence for the Dimensionality of Posttraumatic Stress Disorder, 10 Psychological Assessment 90, 91 (1998).
65 T. M. Keane et al., Mississippi Scale for Combat-Related Post-Traumatic Stress Disorder: Three Studies in Reliability and Validity, 56 J. Consulting & Clinical Psychology 85-90 (1988); J. Davidson et al., Validity and Reliability of the DSM-III Criteria for Posttraumatic Stress Disorder, 177 J. Nervous & Mental Disease 336-41 (1989) (a principal components factor analysis extracted three factors: (1) arousal and intrusiveness; (2) survival guilt, detachment-estrangement, reduced interest, and avoidance of reminders; and (3) decreased sleep, impaired concentration and memory, and constricted affect); L. A. King & D. W. King, Latent Structure of the Mississippi Scale for Combat-Related Post-Traumatic Stress Disorder: Exploratory and Higher Order Confirmatory Factor Analyses, 1 Assessment 275-91 (1994); D. Lauterbach et al., Properties of the Civilian Version of the Mississippi PTSD Scale, 10 J. Traumatic Stress 499-513 (1997); M. W. McFall et al., Reliability and Validity of the Mississippi Scale for Combat-Related Posttraumatic Stress Disorder, 2 Psychological Assessment 114-21 (1990); S. M. Silver & C. U. Iacono, Factor-Analytic Support for DSM-III’s Post-Traumatic Stress Disorder for Vietnam Veterans, 40 J. Clinical Psychology 5-14 (1984); D. L. Vreven et al., The Civilian Version of the Mississippi PTSD Scale: A Psychometric Evaluation, 8 J. Traumatic Stress 91-109 (1995); C. G. Watson et al., A Factor Analysis of the DSM-III Post-Traumatic Stress Disorder Criteria, 47 J. Clinical Psychology 205-14 (1991); Daniel W. King et al., Confirmatory Factor Analysis of the Clinician-Administered PTSD Scale: Evidence for the Dimensionality of Posttraumatic Stress Disorder, 10 Psychological Assessment 90-96 (1998); Charles G. Watson et al, A Factor Analysis of the DSM-III Post-Traumatic Stress Disorder Criteria, 47 J. Clinical Psychology 205-14 (1991); Steven M. Silver & C. U. Iancono, Factor-Analytic Support for DSM-III’s Post-Traumatic Stress Disorder for Vietnam Veterans, J. Clinical Psychology 5-14 (1984).
66 T. M. Keane, “Symptomatology of Vietnam Veterans With Post-Traumatic Stress Disorder,” in Posttraumatic Stress Disorder: DSM-IV and Beyond 99-111 (J.R.T. Davidson & E. B. Foe eds., 1993) (this study suggested four factors: (1) intrusive experiences, restriction of affect, and hypervigilance; (2) reactivity, avoidance, and startle; (3) irritability and impairment of concentration; (4) diminished interest in activities and feelings of detachment; but there are weaknesses in the study: small sample; factor loadings not presented; subjectivity involved in interpreting the scree plot, and likely range restriction of scores as a result of confining the sample to people with PTSD).
E. B. Foa et al., Arousal, Numbing and Intrusion: Symptom Structure of PTSD Following Assault, 152 Am. J. Psychiatry 116-120 (1995) (the study extracted three factors: (1) arousal-avoidance, (2) numbing, and (3) intrusion; but the investigators failed to describe the method used to determine the number of factors to subtract (some methods tend to overextract factors)).
L. A. King et al., The Los Angeles Symptom Checklist: A Self-Report Measure of Posttraumatic Stress Disorder, 2 Assessment 1-17 (1995) (this study produced three factors: (1) most PTSD symptoms, (2) somatic anxiety symptoms, and (3) interpersonal difficulties).
S. Taylor et al., The Structure of Post-Traumatic Stress Symptoms, 107 J. Abnormal Psychology 154-60 (1998) (the findings of this study using civilian victims of motor vehicle accidents and military personnel stationed in Bosnia were that DSM-IV PTSD symptoms are composed of two factors: (1) intrusion or avoidance and (2) hyperarousal or numbing; it was postulated that intrusions give rise to avoidance and hyperarousal gives rise to numbing).
D. W. King et al., Confirmatory Factor Analysis of the Clinician-Administered PTSD Scale: Evidence for the Dimensionality of Posttraumatic Stress Disorder, 10 Psychological Assessment 90-96 (1998) (the results favored a four-factor solution of (1) intrusion, (2) effortful avoidance, (3) emotional numbing, and (4) hyperarousal.
67 A. J. Tomarken, A Psychometric Perspective on Psychophysiological Measures, 7 Psychological Assessment 387-95 (1995).
J. T. Cacioppo & L. G. Tassinary, Inferring Psychological Significance From Physiological Signas, 45 Am. Psychologist 16-28 (1990).
68 D. Dobbs & W. P. Wilson, Observations on Persistence of War Neurosis, 21 Diseases of Nervous System 686-91 (1960) (a pre-PTSD study of the psychophysiological responses of combat veterans to relevant combat stimuli described as resembling those of a conditional emotional response; no specific data on the “PTSD” group were presented and no specific comparisons to this group to the two control groups were made).
E. B. Blanchard et al., The Development of a Psychophysiological Assessment Procedure for PTSD in Vietnam Veterans, 54 Psychiatric Q. 220-28 (1982) (psychophysiological responses to standardized sounds of combat discriminated Vietnam veterans with PTSD from age- and gender-matched comparison group; the comparison group was nonveterans, a fact that compromises the value of this study in that the study lacks positive control groups, such as non-PTSD combat veterans with anxiety disorders).
P. F. Malloy et al., Validation of a Multimethod Assessment of PTSD in Vietnam Veterans, 51 J. Consulting & Clinical Psychology 488-94 (1983) (used standardized audiovisual cues to demonstrate that male Vietnam veterans with PTSD noncombat veterans were more responsive to the combat cues than either psychiatrically impaired veterans without PTSD or well-adjusted veterans; the utility of this study was compromised by the fact that these psychiatrically impaired veterans were noncombat veterans—it may not be surprising that persons with no prior exposure to combat would be unresponsive to combat-related stimuli).
E. B. Blanchard et al., Cardiac Response to Relevant Stimuli as an Adjunctive Tool for Diagnosing Posttraumatic Stress Disorder in Vietnam Veterans, 17 Behavior Therapy 592-606 (1986) [see also a replication study by E. B. Blanchard et al., Cardiac Response to Relevant Stimuli as an Adjunct in Diagnosing Post-Traumatic Stress Disorder: Replication and Extension, 20 Behavior Therapy 535-43 (1989)] (A sample of male Vietnam veterans was examined for heart-rate responses to standardized “emotionally meaningful combat sounds” (helicopters, AK-47 firing, mortars and screaming wounded). The findings were that (1) “on a group basis,” the resting or baseline heart rate of veterans with PTSD is higher than that of comparison groups [a finding contradicted by a later, more sophisticated study: R. K. Pitman et al., Psychophysiologic Responses to Combat Imagery of Vietnam Veterans with Posttraumatic Stress Disorder Versus Other Anxiety Disorders, 99 J. Abnormal Psychology 49-54 (1990)] and (2) “on a group basis,” veterans with PTSD show greater increases in heart rate to relevant combat stimuli than do comparison groups. The authors limit the finding to Vietnam veterans as a group, not as individuals, that is, the means of individual scores, not the individual scores. Obviously, this limits the usefulness of heart-rate responses as a diagnostic tool to assess the status of any individual. The authors remark that “absolute levels of HR either during a resting baseline or while the individual is listening to combat sounds do not provide a very good individual discrimination.”).
T. P. Pallmeyer et al., The Psychophysiology of Combat-Induced Post-traumatic Stress Disorder in Vietnam Veterans, 24 Behav. Res. & Therapy 645-52 (1986) (This study included five psychiatric combat controls, but had no measure of severity of combat exposure, and only one of the five had a diagnosis in the same category as PTSD, namely, generalized anxiety; although these five non-PTSD psychiatric subjects appeared less physiologically responsive than the PTSD subjects to the standard auditory, combat-related stimulus, this finding was statistically significant at only one of the several stimulus intensity levels. Studies of Vietnam combat veterans may not be generalizable to civilian victims of trauma for a variety of reasons, including (1) PTSD symptoms in combat victims have persisted for years; (2) combat veterans with PTSD were frequently exposed to combat trauma; (3) the nature or intensity of the trauma may be a factor in producing PTSD symptoms; (4) combat veterans have been male.).
R. K. Pitman et al., Psychophysiologic Responses to Combat Imagery of Vietnam Veterans with Posttraumatic Stress Disorder Versus Other Anxiety Disorders, 99 J. Abnormal Psychology 49-54 (1990) (A very small sample of seven Vietnam combat veterans with PTSD were compared to seven combat veterans without PTSD but with some form of anxiety disorder (phobia, panic disorder, generalized anxiety disorder, and obsessive-compulsive disorder). All subjects were presented with 11 scripts––five individualized scripts and six standardized scripts. The five individualized scripts consisted of two of the individual’s most stressful combat experiences, a precombat experience, a positive experience and a neutral experience. The six standardized scripts consisted of two neutral experiences, a combat experience (an incoming mortar and rocket attack), a positive experience, an action experience, and a fear experience (public speaking). When these scripts were presented to the subjects, the subjects were measured for skin conductance, EMG, and heart rate. The results were that neither group was very responsive to the standard combat experience or the standard fear experience or the individual scripts, except for the individualized combat scripts: The PTSD group had significant “group” differences [mean scores] for skin conductance and EMG. But the researchers did not report the individual scores. The implication of not reporting individual scores is that some individuals without PTSD scored higher on the measurements of skin conductance and EMG than did some individuals with PTSD, a fact that significantly reduces the diagnostic value of these psychophysiological measurements. Pitman and colleagues have striven to fill in the gaps of this research program. One gap was the failure to use adequate control groups. Another gap was the failure to use subjects with PTSD other than Vietnam combat veterans.).
A. Y. Shalev et al., Psychophysiologic Assessment of Traumatic Imagery in Israeli Civilian Patients with Posttraumatic Stress Disorder, 150 Am. J. Psychiatry 620-24 (1993) (This study had two sample groups: 13 people with PTSD from a variety of traumatic events and 13 without who had been subjected to traumatic events similar to those in the PTSD group. The groups differed significantly for heart rate and EMG responses but not for skin conductance. The “combined” physiologic responses of the PTSD and non-PTSD groups (means) differed significantly during imagery of the personal traumatic scripts. The physiologic responses to imagery of the personal traumatic event of the female PTSD subjects were about 33 percent higher than those of the male subjects. The study is not clear, however, about how well the test identified individuals with PTSD or without PTSD. The authors do mention using a discriminant function empirically derived from studies of Vietnam combat veterans to identify the present subjects with PTSD, with a resulting sensitivity of 69 percent and specificity of 77 percent. Individual scores were not presented to enable the reader to determine whether some individuals with PTSD had lower scores on the measurement variables (EMG, heart rate, and skin conductance) than did some individuals without PTSD. The assumption is that some did, thereby compromising the diagnostic value of these psychophysiologic tests. Another problem with the study is the differential physiologic responses of women compared to men that would affect the mean value used as the measure of comparison. The mean values of the subjects with PTSD could be elevated over those of the subjects without PTSD owing to the contribution of the women with PTSD. Another problem is that in previous studies with Vietnam combat veterans, the differentiating psychophysiologic response was skin conductance, but in the present study it was not. A final problem is using the responses to different kinds of traumatic stressors. The physiologic response of someone with PTSD who was subject to terrorist attacks could be expected to significantly elevate the mean of the group with PTSD over the mean of those without PTSD who were subjected to less terrifying stressors such as motor vehicle accidents. (The nature of the motor vehicle accident was not specified for either group.)).
E. B. Blanchard et al., Psychophysiology of Posttraumatic Stress Disorder Related to Motor Vehicle Accidents: Replication and Extension, 64 J. Consulting & Clinical Psychology 742-51 (1996) (this study had four sample groups: three groups of motor vehicle accident victims with PTSD, with subsyndromal PTSD, and without PTSD and a group of motor vehicle accident subjects. The participants were cued with two idiosyncratic audiotapes and one standardized videotape. The two audiotapes were designed to capture the participant’s experience with his or her motor vehicle accident. The results were that, only as to audiotape 1, only mean heart rate (out of the four physiologic responses: heart rate, skin conductance, EMG, diastolic blood pressure) successfully discriminated motor vehicle accident victims with PTSD from other motor vehicle accident victims and controls. The authors note that for “these data to have clinical utility, one would hope there were not only mean differences in reactivity but also distributional differences such that one could distinguish the individual case into different diagnostic groups based on the responses.” Using a cutoff score of +2 beats per minute or greater, the authors found a sensitivity of 69.4 percent and a specificity of 66.7 percent in distinguishing PTSD from subsyndromal PTSD and an overall specificity of 77.6 percent in distinguishing PTSD from all motor vehicle accident victims. This study has significant flaws. First, there was no apparent effort to control for medication and drug use. Second, the control group did not include positive controls without PTSD who had anxiety disorders. Third, there was no apparent effort to control for litigation effects in the exposure group. Fourth, there was no apparent effort to match the severity of the motor vehicle accident to the findings of PTSD, except to eliminate at the outset “minor ‘fender benders.'” Fifth, no breakout of sex differences appeared for those diagnosed with PTSD or subdromal PTSD or no PTSD. (There was a greater proportion of women to men in the motor vehicle accident group than in the non-motor vehicle accident group.) Sixth, only audiotape 1 seemed to produce the desired response even though both audiotapes 1 and 2 were designed to capture the participant’s experience of his or her motor vehicle accident, with only “slight variations” between the tapes.).
S. P. Orr et al., Psychophysiologic Assessment of Women with Posttraumatic Stress Disorder Resulting From Childhood Sexual Abuse, 66 J. Consulting & Clinical Psychology 906-13 (1998) (There were three sample groups: a group with current PTSD from childhood sexual abuse, a group that once had PTSD from childhood sexual abuse, and a group that never had PTSD. Judged against the DSM-III-R criteria, the sensitivity of the physiologic responsiveness during personal sexual abuse imagery was 66 percent and the specificity 78 percent and a prior discriminant function (developed with Vietnam combat veterans) classified 66 percent of the current group, 42 percent of the lifetime group, and 22 percent of the never group as responders during sexual-abuse imagery. Investigators also performed univariate pairwise comparisons between groups, none of which were significant except for corrugator EMG in which the mean of the lifetime group was greater than the mean of the never group. An unexpected difference emerged across groups for the personal neutral script, with a larger mean for the lifetime group. The investigators compared the means of the various groups, not the individual responses. As a result, some of the “current PTSD” subjects may have had responses lower than some of the “never” subjects. When only medication- or drug-free subjects were analyzed, the differences failed to reach statistical significance. The investigators speculated that that result was due to the reduced power from the small sample size. The current group had more comorbid pathology, including more subjects with anxiety disorders, than did the other groups. This could be a confounding factor. The control group should include positive controls who never had PTSD but who have anxiety disorders such as generalized anxiety disorder in order to determine whether PTSD is distinguishable from other anxiety disorders. The current group also had significantly more drug and medication use than the other groups, another potential confounder. A variety of medications, drugs, and other substances can influence physiologic responses. Beta-blockers can reduce heart rate. Anticholinergics elevate resting heart rate. Use of or withdrawal from nicotine, caffeine, and alcohol can influence physiologic responses nonuniformly. Indeed, little is known about the impact of many medications and substances on physiologic response.).
T.M. Keane et al., Utility of Psychophysiological Measurement in the Diagnosis of Posttraumatic Stress Disorder: Results from a Department of Veterans Affairs Cooperative Study, 66 J. Consulting & Clinical Psychology 914-23 (1998) (This study using a large sample was designed to determine the extent to which psychophysiological measures can predict the presence or absence of PTSD as determined by a gold standard diagnostic interview, the Structured Clinical Interview for DSM-III-R. The authors conclude that the results of the study “provide definitive support for a positive association between psychophysiological responsitivity to cues depicting traumatic war-zone experiences and combat-related PTSD.” Yet they note that “classification rates based on psychophysiological response were lower than those reported previously” and that there was a “statistically significant reduction in PTSD probability scores on retesting.”).
69 R. W. Butler et al., Physiological Evidence of Exaggerated Startle Response in a Subgroup of Vietnam Veterans With Combat-Related PTSD, 147 Am. J. Psychiatry 1308-12 (1990).
70 There are a number of published studies of acoustic startle in PTSD:
E. M. Ornitz & R. S. Pynoos, Startle Modulation in Children with Posttraumatic Stress Disorder, 146 Am. J. Psychiatry 866-70 (1989).
R. W. Butler et al., Physiological Evidence of Exaggerated Startle Response in a Subgroup of Vietnam Veterans With Combat-Related PTSD, 147 Am. J. Psychiatry 1308-12 (1990) (The subjects were 38 male Vietnam veterans with self-reported combat experience. No assessment was made of the extent or nature of that combat experience. Of the 38, 20 were diagnosed with chronic PTSD; the other 18 were used as controls. Thirty-five percent of the subjects (seven with PTSD and six without PTSD) were eliminated from the analysis because they were considered to be “non-responders” (even though they had substantial startle responses), leaving a remaining sample of 13 with PTSD and 12 without PTSD. Acoustic startle stimuli (40-msec noise bursts at different sound levels: 85, 90, 95, 100, 110, 116 dB(A)) and tactile startle stimuli were administered. Acoustic startle was measured by eyeblink EMG amplitude. The magnitude of each startle response was defined as the largest of the peak values beginning between 20 and 80 msec after onset of the startle stimulus, expressed in digital units. The results were that the PTSD group exhibited significantly higher eyeblink EMG amplitudes, measured nonparametrically, than the control group only at 85 dB(A) and 100 dB(A). No significant differences were found between the two groups in response to tactile stimuli. This study has significant limitations. First, the PTSD group had significantly greater combat experience than the control group. Second, alcohol and drug use may have been a confounder. Third, the sample sizes were small. Fourth, the control group lacked adequate positive controls, that is, combat veterans without PTSD who have anxiety disorders. Fifth, the authors noted that “it is too early to state where the measure [of acoustic startle] will have diagnostic utility.” The database needs extending and the findings need to be cross-validated.).
A. Y. Shalev et al., Physiologic Responses to Loud Tones in Israeli Post-Traumatic Stress Disorder Patients, 49 Archives Gen. Psychiatry 870-75 (1992) (The subjects were a PTSD group (14), an anxiety-disorder group (14), a past-trauma group without PTSD (15), and a no-trauma group (19). Psychoactive medications were being used by the PTSD group (benzodrazepines (7) and antidepressants (5)); and the anxiety group (benzodrazepines (6), antidepressants (5), and neuroleptics (1)). The stimuli were 15 95-dB (sound pressure level), 1000-Hz, 500-msec pure tones with 0-msec rise and fall times. The physiological data response was left orbicularis oculi EMG, skin conductance, and heart rate. The results were that there were no significant group effects for any of the EMG measures. There was a “nonsignificant” “trend” toward a larger skin conductance response in subjects with PTSD. There was a larger accelerative heart-rate response in subjects with PTSD.).
C. A. Morgan et al., Yohimbine Facilitated Acoustic Startle in Combat Veterans With Posttraumatic Stress Disorder, 117 Psycho-pharmacology 466-71 (1995).
C. A. Morgan et al., Fear-Potentiated Startle in Posttraumatic Stress Disorder, 38 Biological Psychiatry 378-85 (1995) (This was a study designed to determine whether “fear-potentiated” startle responses are increased in Vietnam combat veterans. The subjects were male Vietnam combat veterans with PTSD (12) and male healthy volunteers (10). Three of the PTSD group did not complete the testing because of panic attacks. Five of the remaining nine in the PTSD group had comorbid panic disorder. The subjects were stimulated with an acoustic startle consisting of a 40 msec burst of white noise at 106 dB(A). The physiologic response was right orbicularis oculi EMG. The subjects were under threat of receiving an electric shock during the startle stimulus. The result was that on average the startle response was larger in the PTSD group compared to the control group.).
S. P. Orr et al., Physiologic Responses to Loud Tones in Vietnam Veterans With Posttraumatic Stress Disorder, 104 J. Abnormal Psychology 75-82 (1995) (The subjects were 56 male Vietnam veterans with combat experience. Of these, 37 were diagnosed with PTSD, and 19 diagnosed without PTSD used as controls. The physiologic measures were left orbicularis oculi EMG, skin conductance, and heart rate. The stimuli were 15 95-dB (sound pressure level), 1000-Hz, 500-msec pure tones with 0-msec rise and fall times. The results were a significant “group” difference in orbicularis oculi EMG response, no significant group difference in skin conductance response, and a significantly larger heart rate response in those with PTSD. The present results do not replicate the Shalev et al. (1992) findings of overall greater skin conductance responsivity in PTSD. The authors note that “if anxiety or fear is responsible for the exaggerated startle response in PTSD, a similar response should also be present in individuals with generalized anxiety disorder [but] we are not aware of any studies that have examined the eyeblink startle response in individuals with the disorder.”).
C. Grillon et al., Baseline Startle Amplitude and Prepulse Inhibition in Vietnam Veterans With Posttraumatic Stress Disorder, 64 Psychiatry Res. 169-78 (1996).
C. A. Morgan et al., Startle Reflex Abnormalities in Women With Sexual Assault-Related Posttraumatic Stress Disorder, 154 Am. J. Psychiatry 1076-80 (1997) (The subjects were female civilians with sexual-assault-related PTSD (13); and female civilians without PTSD and without sexual assault (16). The stimuli was two pulse alone 240-msec duration bursts of white noise at 92 dB(A) and 102 dB(A); and one prepulse plus pulse 230-msec duration burst of 20-dB(A) white noise 120 msec before a 40-msec duration 102-dB(A) pulse. The physiologic response was right and left orbicularis oculi EMG. The results were that the overall startle response was not significantly greater in the PTSD subjects than in the comparison subjects. A startle response was greater in the PTSD group than in the comparison group for the left eye but not the right eye but only in response to the 102-dB(A) startle stimuli in block and 92-dB(A) startle stimuli in block. “The implications for lateralization in PTSD are not clear.” The findings of an exaggerated startle response to the 92-dB(A) stimulus in women with PTSD differs from startle response in men, who have not reported exaggerated startle responses to soft tones (90-95 dB). This study has significant limitations. First, the study did not include either a trauma-exposed control group or measures of autonomic reactivity. Second, the small numbers of women in the samples preclude meaningful conclusions about gender differences.).
C. A. Morgan et al., Exaggerated Acoustic Startle Reflex in Gulf War Veterans With Posttraumatic Stress Disorder, 153 Am. J. Psychiatry 64-68 (1996) (The subjects were (1) Gulf War veterans with PTSD (10); combat comparison subjects (7); and civilian comparison subjects (15). The physiologic response was left orbicularis oculi EMG; the stimulus was 40-msec burst of white noise with a near instantaneous use time at the following five intensities: 90, 96, 102, 108, 114 dB(A). The results were that the Gulf War veterans with PTSD, as a group, had larger amplitudes of eyeblink reflex than did the controls. The magnitude of the startle response was greater in the PTSD group than in the civilian group only at 108 dB(A) and 114 dB(A). No significant differences occurred at 90 and 96 dB(A). The magnitude of the startle response in the PTSD subjects was significantly greater than in the combat controls at 96 dB(A), 102 dB(A), 108 dB(A), and 114 dB(A). There are obvious limitations to this study. First, what accounts for the failure of the PTSD subject to have increased startle over the civilian controls at all the same intensities that the PTSD subjects had increased startle in relation to the non-PTSD combat controls? Second, the control group lacked positive controls with anxiety disorders.).
S. P. Orr et al., Physiologic Responses to Non-Startling Tones in Vietnam Veterans with Post-traumatic Stress Disorder, 73 Psychiatry Res. 103-07 (1997) (the subjects were medication-free Vietnam combat veterans divided into a PTSD group (20) and a non-PTSD group (19). The stimuli consisted of 15 86-dB(A) (sound pressure level), 1000-Hz, 500-msec pure tones, with 40-msec rise and fall tones. The physiologic response was left orbicularis oculi EMG skin conductance and heart rate. The results were that the PTSD group had higher average heart rate than the non-PTSD control group, but no differences existed in EMG or skin conductance between the two groups. The authors noted that the heart rate findings were not a consequence of elevated sympathetic activity given the lack of a difference in skin conductance and EMG.).
S. P. Orr et al., Physiologic Responses to Loud Tones in Israeli Veterans of the 1973 Yom Kippur War, 41 Biological Psychiatry 319-26 (1997) (The subjects were Israeli veterans of the Yom Kippur War divided into a PTSD group (19) and a non-PTSD group (74). The stimuli were 15 95-dB(A) (sound pressure level), 1000-Hz, 500-msec pure tones with 0-msec rise and fall times. The physiologic response was left orbicularis oculi EMG, skin conductance, and heart rate levels. The results were no significant group differences in EMG or skin conductance, but a larger magnitude response in heart rate in the PTSD group compared with the non-PTSD group, which was marginally significant.).
A. Y. Shalev et al., Auditory Startle Responses in Help-Seeking Trauma Survivors, 69 Psychiatry Res. 1-7 (1997) (The subjects were medication-free help-seeking trauma survivors divided into a PTSD group (30) with trauma from a variety of sources and a past-trauma control group without PTSD (28), also with trauma from a variety of sources. The stimuli was 15 consecutive 95-d-B(A), 500-msec, 1000-Hz tones with 0-msec rise and fall times. The physiologic response was left orbicularis oculi EMG, skin conductance, and heart rate. The results were that the PTSD subjects had higher than average EMG responses and higher skin conductance responses than the controls. No difference existed on the variable of heart rate.).
L. J. Metzger et al., Physiologic Reactivity to Startling Tones in Women With Posttraumatic Stress Disorder, 108 J. Abnormal Psychology 347-52 (1999) (The subjects were a group with current PTSD (21); a group with past PTSD (23), and a group that had never had PTSD (13). The current group had more comorbid disorders than the other groups, ranging from depression and anxiety to drug dependence. Those in current group (11) were taking more psychotropic autonomically active medications than those in the other groups. The stimuli were 15 95-dB(A), 1000-Hz, 500-msec pure tones with 0-msec rise and fall times. The physiologic measures were left orbicularis oculi EMG, skin conductance, and heart rate. The results were as follows: Heart Rate Response: Women with current PTSD from childhood sexual abuse produced significantly larger accelerative heart rate responses to startling tones than women with childhood sexual abuse without PTSD. Women with lifetime but not current PTSD had larger heart rate responses than women with current PTSD. Skin Conductance Response: Women with current PTSD from childhood sexual abuse produced slower absolute habituation of skin conductance response magnitudes to startling tones than women with childhood sexual abuse without PTSD. Women with lifetime but not current PTSD had greater skin conductance response magnitudes than women with current PTSD. EMG Response: no group differences found.).
71 G. Goldstein et al., Survivors of Imprisonment in the Pacific Theater During World War II, 144 Am. J. Psychiatry 1210-13 (1987); W. W. Eaton et al., Impairment in Holocaust Survivors After 33 Years: Data From an Unbiased Community Sample, 139 Am. J. Psychiatry 773-77 (1982); B. L. Green et al., Buffalo Creek Survivors in the Second Decade: Stability of Stress Symptoms, 60 Am. J. Orthopsychiatry 43-54 (1990); B. L. Green et al., Identifying Survivors at Risk: Long-Term Impairment Following the Beverly Hills Supper Club Fire, 53 J. Consulting & Clinical Psychology 672-78 (1985); R. L. Leopold & H. Dillon, Psycho-Anatomy of a Disaster: A Long Term Study of Post-Traumatic Neuroses in Survivors of Marine Explosion, 119 Am. J. Psychiatry 913-21 (1963); B. Gersons, Patterns of PTSD Among Police Officers Following Shooting Incidents: A Two-Dimensional Model and Treatment Implications, 2 J. Traumatic Stress 247-57 (1989).
72 B. L. Green et al., Identifying Survivors at Risk: Long-Term Impairment Following the Beverly Hills Supper Club Fire, 53 J. Consulting & Clinical Psychiatry 672-78 (1985).
B. L. Green et al., Buffalo Creek Survivors in the Second Decade: Comparison with Unexposed and Non-Litigant Groups, 20 J. Applied Soc. Psychology 1033-50 (1990).
S. M. Southwick et al., Trauma-Related Symptoms in Veterans of Operation Desert Storm: A Preliminary Report, 150 Am. J. Psychiatry 1524-28 (1993).
S. M. Southwick et al., Trauma-Related Symptoms in Veterans of Operation Desert Storm: A 2-Year Follow-Up, 152 Am. J. Psychiatry 1150-55 (1995) (the overall severity of PTSD symptoms as measured by the Mississippi scale and the DSM-III-R-based PTSD scale increased in severity over two years, with the greatest change occurring between one month and six months; it should be noted that 22 of the 84 participants who initially completed assessments dropped out in the two-year follow-up).
R. J. Ursano et al., Acute and Chronic Post-Traumatic Stress Disorder in Motor Vehicle Accident Victims, 156 Am. J. Psychiatry 589-95 (1999).
73 C. Van Dyke et al., Posttraumatic Stress Disorder: A Thirty-Year Delay in a World War II Veteran, 142 Am. J. Psychiatry 1070-73 (1985) (reporting that a decorated WWII veteran developed PTSD 30 years after the WWII-related combat stressor).
74 A. Ehlers et al., Psychological Predictors of Chronic Post-Traumatic Stress Disorder After Motor Vehicle Accidents, 107 J. Abnormal Psychology 508-19 (1998).
75 Judith L. Herman, Trauma and Recovery 9, 28, 30 (1992).
Dr. Herman’s less articulate but equally destructive comrades include Ellen Bass and Laura Davis, whose book, The Courage to Heal: A Guide for Women Survivors of Child Sexual Abuse (3d ed. 1994), has become the bible of the repressed-memory movement.
Daniel A. Furber & Suzanna Sherry, Beyond All Reason, The Radical Assault on Truth in American Law 95-117 (1997); Glen O. Gabbard, Patients Who Hate, 52 Psychiatry 96-106 (1989).
76 The suggested criteria of Complex PTSD are as follows:
(1) A history of subjection to totalitarian control over a prolonged period (months to years). Examples include hostages, prisoners of war, concentration-camp survivors, and survivors of some religious cults. Examples also include those subjected to totalitarian systems in sexual and domestic life, including survivors of domestic battering, child physical or sexual abuse, and organized sexual exploitation.
(2) Alterations in affect regulation, including
persistent dysphoria
chronic suicidal preoccupation
self-injury
explosive or extremely inhibited anger (may alternate)
compulsive or extremely inhibited sexuality (may alternate)
(3) Alterations in consciousness, including
amnesia or hyperamnesia for traumatic events
transient dissociative episodes
depersonalization/derealization
reliving experiences, either in the form of intrusive posttraumatic stress disorder symptoms or in the form of reminative preoccupation
(4) Alterations in self-perception, including
sense of helplessness or paralysis of initiative
shame, guilt, and self-blame
sense of defilement or stigma
sense of complete difference from others (may include sense of specialness, utter aloneness, belief no other person can understand, or nonhuman identity)
(5) Alterations in perception of perpetrator, including
preoccupation with relationship with perpetrator (includes preoccupation with revenge)
unrealistic attribution of total power to perpetrator (caution: victim’s assessment of power realities may be more realistic than clinician’s)
idealization of paradoxical gratitude
sense of special or supernatural relationship
acceptance of belief system or rationalization of perpetrator
(6) Alterations in relations with others, including
isolation with withdrawal
disruption in intimate relationships
repeated search for rescuer (may alternate with isolation and withdrawal)
persistent distrust
repeated failures of self-protection
(7) Alterations in systems of meaning
loss of sustaining faith
sense of hopelessness and despair
77 L. E. Walker, The Battered Woman Syndrome (1984); Donald G. Dutton & Susan Painter, The Battered Woman Syndrome: Effects of Severity and Intermittency of Abuse, 63 Am. J. Orthopsychiatry 614-22 (1993).
78 R. A. Schuller & N. Micmar, Battered Woman Syndrome Evidence in the Courtroom, 16 Law & Hum. Behav. 273-91 (1992).
79 State v. Stevens, 970 P.2d 215 (Or. 1998) (testimony that the battered-woman syndrome is a variety of posttraumatic stress disorder); Millie C. Astin et al., Posttraumatic Stress Disorder and Childhood Abuse in Battered Women: Comparisons With Maritally Distressed Women, 63 J. Consulting & Clinical Psychology 308-12 (1995).
80 Diana M. Elliot & John Briere, Posttraumatic Stress Associated With Delayed Recall of Sexual Abuse: A General Population Study, 8 J. Traumatic Stress 629-47 (1995); Linda M. Williams, Recovered Memories of Abuse in Women With Documented Child Sexual Victimization Histories, 8 J. Traumatic Stress 649-73 (1995); R. Joseph, The Neurology of Traumatic “Dissociative” Amnesia: Commentary and Literature Review, 23 Child Abuse & Neglect 715-27 (1999); Bessel A. van der Kolk & Rita Fisler, Dissociation and the Fragmentary Nature of Traumatic Memories: An Overview and Exploratory Study, 8 J. Traumatic Stress 505-25 (1995); Harrison G. Pope et al., Questionable Validity of “Dissociative Amnesia” in Trauma Victims, 172 Brit. J. Psychiatry 210-15 (1998); Cathy Spatz Widom & Robin L. Shepard, Accuracy of Adult Recollections of Childhood Victimization: Part 1. Childhood Physical Abuse, 8 Psychological Assessment 412-21 (1996); Cathy Spatz Widom & Suzanne Morris, Accuracy of Adult Recollections of Childhood Victimization: Part 2. Childhood Sexual Abuse, 9 Psychological Assessment 34-46 (1997); S. Brandon J. Boakes et al., Recovered Memories of Childhood Sexual Abuse, 172 Brit. J. Psychiatry 296-307 (1998); Scott P. Orr et al., Psychophysiologic Assessment of Women With Posttraumatic Stress Disorder Resulting From Childhood Sexual Abuse, 66 J. Consulting & Clinical Psychology 906-13 (1998); Jonathan W. Schooler et al., “Taking the Middle Line: Can We Accommodate Both Fabricated and Recovered Memories of Sexual Abuse?,” in Recovered Memories and False Memories (Martin A. Conway ed., 1997); Naomi Breslau et al., Previous Exposure to Trauma and PTSD Effects of Subsequent Trauma: Results From the Detroit Area Survey of Trauma, 156 Am. J. Psychiatry 902-07 (1999); Judith Lewis Herman & Emily Schatzow (Women’s Mental Health Collective), Recovery and Verification of Memories of Childhood Sexual Trauma, 4 Psychoanalytic Psychology 1-14 (1987); John Briere & Jon Conte, Self-Reported Amnesia for Abuse in Adults Molested as Children, 6 J. Traumatic Stress 21-31 (1993); Linda Meyer Williams, Recall of Childhood Trauma: A Prospective Study of Women’s Memories of Child Sexual Abuse, 62 J. Consulting & Clinical Psychology 1167-76 (1994).
81 E.g., Daniel L. Schacter, Searching for Memory ch. 9 (1996); Paul R. McHugh, Psychotherapy Awry, American Scholar, Winter 1994; Fred H. Frankel, Discovering New Memories in Psychotherapy—Childhood Revisited, Fantasy, or Both?, 333 New Eng. J. Med. 591-94 (1995); William H. Anderson, Letter to Editor, 334 New Eng. J. Med. 274 (1996).
82 Elizabeth Bass & Laura Davis, The Courage to Heal (1988).
83 Kenneth S. Pope, Memory, Abuse & Science: Questioning Claims About the False Memory Epidemic, 51 Am. Psychologist 957-74 (1996); Alan W. Scheflin & David Spiegel, From Courtroom to Couch, Working With Repressed Memory & Avoiding Lawsuits, 21 Psychiatric Clinics N. Am. 847-67 (1998).
84 John F. Kihlstrom, Memory, Abuse, and Science, Am. Psychologist 994-95 (Sept. 1997); Kenneth S. Pope, Science as Careful Questioning: Are Claims of a False Memory Syndrome Epidemic Based on Empirical Evidence?, Am. Psychologist 997-1006 (Sept. 1997); Frederick Crews, The Memory Wars, Freud’s Legacy in Dispute (1995).
85 Elizabeth Loftus & Katherine Ketcham, The Myth of Repressed Memory: False Memories and Allegations of Sexual Abuse (1994); Daniel L. Schacter, Searching for Memory, The Brain, the Mind, and the Past ch. 9 (1996); Elizabeth F. Loftus, The Price of Bad Memories, Skeptical Inquirer, Mar./Apr. 1998, at 23-24; Daniel L. Schacter, Implicit Memory: History and Current Status, 13 J. Experimental Psychology: Learning, Memory & Cognition 501-18 (1987); Ethel Spector Person & Howard Klar, Establishing Trauma: The Difficulty Distinguishing Between Memories & Fantasies, 42 J. Am. Psychoanalytic Ass’n 1055-81 (1994); Elizabeth F. Loftus et al., Forgetting Sexual Trauma: What Does It Mean When 38% Forget?, 62 J. Consulting & Clinical Psychology 1177-81 (1994); Elizabeth F. Loftus et al., Memories of Childhood Sexual Abuse, Remembering & Repressing, 18 Psychology of Women Q. 67-84 (1994); Patricia J. Bauer, What Do Infants Recall of Their Lives? Memory for Specific Events by One- to Two-Year-Olds, 51 Am. Psychologist 29-41 (1996); Daniel Schacter, Memory Wars, 272 Scientific Am. 135-39 (1995).
86 J. K. Briere, Methodological Issues in the Study of Sexual Abuse Effects, 60 J. Consulting & Clinical Psychology 196-203 (1992).
D. O. Femina et al., Child Abuse: Adolescent Records vs. Adult Recall, 145 Child Abuse & Neglect 227-31 (1990) (69 adults with documented histories of childhood physical abuse were interviewed about their childhood abuse. 26 responded in ways not reflecting their histories. When 8 of these subjects were re-interviewed, they acknowledged their abuse and admitted withholding information about their abuse in their first interview.).
S. N. Gold et al., Degrees of Repression of Sexual Abuse Memories, 49 Am. Psychologist 441-42 (1994).
P. M. Coons et al., “Repressed Memories in Patients with Dissociative Disorder: Literature Review, Controlled Study and Treatment Recommendations,” in 16 Review of Psychiatry 11: 153 to 11: 172 (L. J. Dickstein et al. eds., 1997).
L. M. Williams, Recall of Childhood Trauma. A Prospective Study of Women’s Memories of Child Sexual Abuse, 62 J. Consulting & Clinical Psychology 1167-76 (1994).
J. Briere & J. Conte, Self-Reported Amnesia for Abuse in Adults Molested as Children, 6 J. Traumatic Stress 21-31 (1993) (267 of 450 subjects said there was a time between the forced sexual experience and their 18th birthday when they could not remember the forced sexual experience. The subjects were recruited by their therapists (selection bias). None of the abuse was corroborated. The subject’s response was ambiguous. Did they merely forget? Did they repress the experience? Some subjects may have been influenced by suggestion because all were in therapy with therapists who were part of an informal sexual abuse treatment referral network.).
J. L. Herman & E. Schatzow, Recovery and Verification of Memories of Childhood Sexual Trauma, 4 Psychoanalytic Psychology 1-14 (1987) (This was a case series of 53 women treated by the authors in time-limited group therapy for “incest survivors.” Fourteen had severe amnesia; but some had this during the period of normal childhood amnesia. Only 21 of the 53 obtained corroborating evidence of the incest, but it is unclear whether any of the 21 had severe amnesia.).
L. M. Williams, Recall of Childhood Trauma. A Prospective Study of Women’s Memories of Child Sexual Abuse, 62 J. Consulting & Clinical Psychology 1167-76 (1994) (129 women who had been brought as children (10 months old to 12 years old) to a hospital emergency room for treatment after reported sexual abuse were interviewed as adults and asked whether they had been sexually abused. 49 did not report the abuse. These 49 were considered to have amnesia. 25 of these 49 experienced the abuse at age 6 or younger. These 25 may represent normal childhood amnesia. The remaining nonreporters may merely have forgotten or may not want to discuss the issue with the researchers.).
J. W. Schooler et al., “Taking the Middle Line: Can We Accommodate Both Fabricated and Recovered Memories of Sexual Abuse?,” in Recovered Memories and False Memories (M. A. Conway ed., 1997).
D. M. Elliot & J. Briere, Posttraumatic Stress Associated with Delayed Recall of Sexual Abuse: A General Population-Study, 8 J. Trauma Stress 629-47 (1995).
D. M. Elliot, Trauma to Events: Prevalence and Delayed Recall in the General Population, 65 J. Consulting & Clinical Psychology 811-20 (1997).
C. S. Widom & S. Morris, Accuracy of Adult Recollections of Childhood Victimization: Part 2. Childhood Sexual Abuse, 8 Psychological Assessment 412-21 (1997).
C. Bagley, Validity of a Short Measure of Child Sexual Abuse, 66 Psychological Rep. 449-50 (1990).
B. A. Van der Kolk & R. Fisler, Dissociation and the Fragmentary Nature of Traumatic Memories: Overview and Exploratory Study, 8 J. Trauma Stress 505-25 (1995).
Shirley Feldman-Summers & Kenneth S. Pope, The Experience of “Forgetting” Childhood Abuse: A National Survey of Psychologists, 62 J. Consulting & Clinical Psychology 636-39 (1994).
Elizabeth F. Loftus, The Reality of Repressed Memories, 48 Am. Psychologist 518-37 (1993).
David S. Holmes, “The Evidence of Repression: An Examination of Sixty Years of Research,” in Repression and Dissociation ch. 4 (Jerome L. Singer ed., 1990).
87 Harrison G. Pope, Jr. & James I. Hudson, Can Memories of Childhood Sexual Abuse Be Repressed?, 25 Psychological Med. 121-26 (1995).
Harrison G. Pope, Jr. & James I. Hudson, Can Individuals “Repress” Memories of Childhood Sexual Abuse? An Examination of the Evidence, 25 Psychiatric Annals 715-25 (1995).
John Briere, Methodological Issues in the Study of Sexual Abuse Effects, 60 J. Consulting & Clinical Psychology 196-203 (1992).
“To demonstrate dissociative amnesia, investigators should interview and follow-up people who experience a well-documented trauma. These people must be at least six years old at the time of the trauma and free of neurological problems such as head injury or drug intoxication. The traumatic event must be too important to the individual to plausibly be lost by ordinary forgetfulness. If some of the victims do not report memories on an initial interview, they must participate in a clarification interview in which they should be asked whether they remember the specific event that they are known to have experienced. Although this last step might be criticized as over-cueing, data show that any lesser approach risks mis-classifying many people who actually remember. . . .[U]ntil studies meeting these criteria appear, dissociative amnesia remains unproven.”
88 L. C. Terr, Chowchilla Revisited: The Effects of Psychic Trauma Four Years After a School-bus Kidnapping, 140 Am. J. Psychiatry 1543-50 (1983).
L. C. Terr et al., Children’s Memories in the Wake of Challenger, 153 Am. J. Psychiatry 618-25 (1996).
W. A. Wagenaar & J. Groeneweg, The Memory of Concentration Camp Survivors, 4 Applied Cognitive Psychology 77-87 (1990).
C. S. Widom & R. L. Shepard, Accuracy of Adult Recollection of Childhood Victimization. Part 1: Childhood Physical Abuse, 8 Psychological Assessment 412-21 (1996).
C. S. Widom & S. Morris, Accuracy of Adult Recollections of Childhood Victimization. Part 2: Childhood Sexual Abuse, 9 Psychological Assessment 34-46 (1997).
L. M. Williams, Recall Childhood Trauma. A Prospective Study of Women’s Memories of Child Sexual Abuse, 62 J. Consulting & Clinical Psychology 1167-76 (1994).
C. Bagley, Child Sexual Abuse and Mental Health in Adolescents and Adults: British and Canadian Perspectives (1995).
A. W. Burgess et al., Memory Presentations of Childhood Sexual Abuse, 33 J. Psychosocial Nursing 9-16.
D. D. Femina et al., Child Abuse: Adolescent Recovers v. Adult Recall, 145 Child Abuse & Neglect 227-31 (1990).
R. L. Leopold & H. Dillon, Psycho-anatomy of a Disaster: A Long Term Study of Post-traumatic Neuroses in Survivors of a Marine Explosion, 119 Am. J. Psychiatry 913-21 (1963).
U. Malt, The Long-term Psychiatric Consequences of Accidental Injury: A Longitudinal Study of 107 Adults, 153 Brit. J. Psychiatry 810-18 (1988).
C. Peterson & M. Bell, Children’s Memory for Trauma Injury, 67 Child Development 3045-70 (1996).
L. C. Terr, Children of Chowchilla: A Study of Psychic Trauma, 34 Psychoanalytic Study of the Child 552-623 (1979).
Chris R. Brewin et al., Psychopathology and Early Experience: A Reappraisal of Retrospective Reports, 113 Psychological Bull. 82-98 (1993).
89 H. G. Pope et al., Questionable Validity of ‘Dissociative Amnesia’ in Trauma Victims, 172 Brit. J. Psychiatry 210-15 (1998).
90 K. A. Kendall-Tackett et al., Impact of Sexual Abuse on Children: A Review and Synthesis of Recent Empirical Studies, 113 Psychological Bull. 164-80 (1993).
91 Elizabeth A. Feigon & Joseph deRivera, “Recovered Memory” Therapy: Profession at a Turning Point, 39 Comprehensive Psychiatry 338-44 (1998).
Scott P. Orr et al., Psychophysiologic Assessment of Women With Posttraumatic Stress Disorder Resulting From Childhood Sexual Abuse, 66 J. Consulting & Clinical Psychology 909-13 (1998).
Christine A. Courtois, “Delayed Memories of Child Sexual Abuse: Critique of the Controversy and Clinical Guidelines,” in Recovered Memories and False Memories (Martin A. Conway ed., 1997).
Fred H. Frankel, Discovering New Memories in Psychotherapy—Childhood Revisited, Fantasy, or Both?, 333 New Eng. J. Med. 591-94 (1995).
Elizabeth F. Loftus & Jacqueline E. Pickrell, The Formation of False Memories, 25 Psychiatric Annals 720-25 (1995).
Daniel L. Schacter, Searching for Memory, The Brain, the Mind, and the Past ch. 9 (1996).
92 John F. Kihlstrom, Memory, Abuse, and Science, Am. Psychologist 994-95 (Sept. 1997).
93 The AMA has issued a statement on RMS with these recommendations.:
“1. That the AMA recognize that few cases in which adults make accusations of childhood sexual abuse based on recovered memories can be proved or disproved and it is not yet known how to distinguish true memories from imagined events in these cases.
“2. That the AMA encourage physicians to address the therapeutic needs of patients who report memories of childhood sexual abuse and that these needs exist quite apart from the truth or falsity of any claims.
“3. The AMA considers recovered memories of childhood sexual abuse to be of uncertain authenticity, which should be subject to external verification. The use of recovered memories is fraught with problems of potential misapplication.
“4. That the AMA encourage physicians treating possible adult victims of childhood abuse to subscribe to the Principles of Medical Ethics when treating the patients and that psychiatrists pay particular attention to the Principles of Medical Ethics with Annotations Especially Applicable to Psychiatry.”
This last recommendation concerns, as the AMA noted,
“[T]he role of the therapist in developing new memories. It is well-established for example that a trusted person such as a therapist can influence an individual’s reports, which would include memories of abuse. Indeed, as the issue of repressed memories has grown, there have been reports of therapists advising patients that their symptoms are indicative—not merely suggestive—of having been abused, even when the patient denies having been abused. Other research has shown that repeated questioning may lead individuals to report events that in fact never occurred. Unfortunately, the dynamics that underlie an individual’s suggestibility are only beginning to be understood.”
An article by Fred Frankel of the Harvard Medical School in the New England Journal of Medicine accurately surveys the issues involved in RMS:
“The new-found confidence in the accuracy of long-delayed recall may have been engendered by . . . the influence of the feminist movement. . . . Women in distress, with a wide range of symptoms from anxiety and depression to sexual dysfunction, came to be regarded as victims of trauma even in the absence of memories of the events themselves.”
“[P]roof of the existence of dissociation or repression is weak . . .. The question is whether we can accept as valid, without corroboration, stories that emerge for the very first time in therapy, totally unsuspected until then by patients now in their 30s and 40s.”
“[A] number of parents . . . reported being denied access to a family meeting with the therapist who had validated their adult child’s memories, unless the parents admitted in advance that they were guilty . . .. I was [also] familiar with a series of reports by authors with academic appointments that appeared to be methodologically unpersuasive.”
“The paper cited by Herman and Schatzow, although widely cited as providing evidence corroborating reports of long-forgotten trauma, has been criticized largely on two grounds: the suggestive context in which the memories were elicited and insufficient data. The women were reported to have confirmed their memories of trauma by checking with relatives, perpetrators, and available records. Except for the few illustrative case histories at the end of their article, however, Herman and Schatzow did not discuss the nature and the extent of the corroboration in any detail. Nor was it clear that the women who reported confirmation of their memories included any of those who had been unaware of the trauma before their group experience. The paper thus does not provide persuasive examples of accurate memories totally unsuspected until their discovery in therapy.”
“We thus see that even if dissociation or repression exists, the case for it at this stage rests largely on anecdotes and case reports.”
Bowman & Mertz, A Dangerous Direction: Legal Intervention and Sexual Abuse Survivor Therapy, 109 Harv. L. Rev. 551-639 (1996) (This article is a plea to plaintiffs’ lawyers to desist in suing therapists for malpractice who specialize in the repressed memory syndrome, citing all the highly suspect research by that cult of memory therapists. Characteristically, the authors do not suggest that plaintiffs’ attorneys desist in suing the alleged perpetrators of sexual abuse, even though the incidence of false positive diagnoses is extremely high.).
94 Harrison G. Pope, Jr. & James I. Hudson, Can Memories of Childhood Sexual Abuse Be Repressed?, 25 Psychological Med. 121-26 (1995).
95 B. S. Everitt, The Cambridge Dictionary of Statistics 283 (1998).
96 L. Wittgenstein provided this analogy in one of his notebooks.
97 Steven N. Allen, Psychological Assessment of Post-Traumatic Stress Disorder, Psychometrics, Current Trends, and Future Directions, 17 Psychiatric Clinics N. Am. 327-49 (1994).
Jessica Wolfe & Terence M. Keane, “Diagnostic Validity of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder 52 (Marion E. Wolf & Aron D. Mosnaim eds., 1990); Terence Keane et al., Post-Traumatic Stress Disorder: Evidence for Diagnostic Validity and Methods of Psychological Assessment, 43 J. Clinical Psychology 32-43 (1987).
98 Lee J. Cronbach, Coefficient Alpha and the Internal Structure of Tests, 16 Psychometrika 297-334 (1951).
George A. Ferguson, On the Theory of Test Discrimination, 14 Psychometrika 61-68 (1949).
99 Richard A. Kulka et al., Assessment of Posttraumatic Stress Disorder in the Community: Prospects & Pitfalls From Recent Studies of Vietnam Veterans, 3 Psychological Assessment: J. Consulting & Clinical Psychology 547-60 (1991).
100 E. V. Berk et al., Traumatogenicity: Effects of Self-Reported Noncombat Trauma on MMPIs of Male Vietnam Combat and Non-Combat Veterans Treated for Substance Abuse, 45 J. Clinical Psychology 704-08 (1989).
R. Long et al., Chronicity: Adjustment Differences in Vietnam Combat Veterans Differing in Rates of Psychiatric Hospitalization, 45 J. Clinical Psychology 745-53 (1989).
W. E. Penk et al., Post-Traumatic Stress Disorder (PTSD): Issues of Utility, Traumatogenicity, Co-Morbidity, Teratogenicity vs. Psychogenicity, Ethnicity, “Gendericity” and Chronicity, 45 J. Clinical Psychology 688-90 (1989).
101 Frank W. Weathers et al., “Psychometric Theory in the Development of Posttraumatic Stress Disorder Assessment Tools,” in Assessing Psychological Trauma and PTSD, ch. 4 (John P. Wilson & Terence M. Keane eds., 1997).
Charles G. Watson, Psychometric Posttraumatic Stress Disorder Measurement Techniques: A Review, 2 Psychological Assessment: J. Consulting & Clinical Psychology 460-69 (1990).
Assessing Psychological Trauma and PTSD (John P. Wilson & Terence M. Keane eds., 1997).
102 John Briere, Psychological Assessment of Adult Posttraumatic States 107-12 (1997).
Terence M. Keane et al., Utility of Psychophysiological Measurement in the Diagnosis of Posttraumatic Stress Disorder: Results From a Department of Veterans Affairs Cooperative Study, 66 J. Consulting & Clinical Psychology 914-23 (1998).
Terence M. Keane et al., Post-Traumatic Stress Disorder: Evidence for Diagnostic Validity and Methods of Psychological Assessment, 43 J. Clinical Psychology 32-43 (1987).
103 John Briere, Psychological Assessment of Adult Posttraumatic States 109 (1997).
Brett T. Litz et al., Similarities and Differences Between MMPI & MMPI-2 Applications to the Assessment of Posttraumatic Stress Disorder, 57 J. Personality Assessment 238-53 (1991).
104 Harold R. Miller et al., What’s in a Name? The MMPI-2 PTSD Scales, 51 J. Clinical Psychology 626-61 (1995).
105 John Briere, Psychological Assessment of Adult Posttraumatic States 108 (1997).
106 John Briere, Psychological Assessment of Adult Posttraumatic States 112-17 (1997).
107 John Briere, Psychological Assessment of Adult Posttraumatic States 133-34 (1997).
Terence M. Keane et al., Mississippi Scale for Combat-Related Posttraumatic Stress Disorder: Three Studies in Reliability and Validity, 56 J. Consulting & Clinical Psychology 85-90 (1988).
Miles E. McFall et al., Reliability and Validity of Mississippi Scale for Combat-Related Posttraumatic Stress Disorder, 2 J. Consulting & Clinical Psychiatry 114-21 (1990).
108 Dawn L. Vreven et al., The Civilian Version of the Mississippi PTSD Scale: A Psychometric Evaluation, 8 J. Traumatic Stress 91-109 (1995).
John Briere, Psychological Assessment of Adult Posttraumatic States 134-35 (1997).
Dean Lauterbach et al., Psychometric Properties of the Civilian Version of the Mississippi PTSD Scale, 10 J. Traumatic Stress 499-513 (1997).
109 Fran H. Norris & Julia L. Perilla, The Revised Civilian Mississippi Scale for PTSD: Reliability, Validity, and Cross-Language Stability, 9 J. Traumatic Stress 285-98 (1996).
John Briere, Psychological Assessment of Adult Posttraumatic States 135 (1997).
110 John Briere, Psychological Assessment of Adult Posttraumatic States 130-32 (1997).
111 John Briere, Psychological Assessment of Adult Posttraumatic States 131 (1997).
112 John Briere, Psychological Assessment of Adult Posttraumatic States 131 (1997).
D. S. Weiss et al., Predicting Symptomatic Distress in Emergency Services Personnel, 63 J. Consulting & Clinical Psychology 361-68 (1995).
C. R. Marmar et al., Characteristics of Emergency Services Personnel Related to Peritraumatic Dissociation During Critical Incident Exposure, 153 Am. J. Psychiatry 94-102 (1996).
113 John Briere, Psychological Assessment of Adult Posttraumatic States 138 (1997).
Melvyn Hammarberg, Penn Inventory for Posttraumatic Stress Disorder: Psychometric Properties, 4 Psychological Assessment 67-76 (1992).
114 John Briere, Psychological Assessment of Adult Posttraumatic States 118-19 (1997).
115 John Briere, Psychological Assessment of Adult Posttraumatic States 132-33 (1997).
116 John Briere, Psychological Assessment of Adult Posttraumatic States 135-36 (1997).
117 S. A. Falsetti, The Modified PTSD Symptom Scale: A Brief Self-Report Measure of Post-traumatic Stress Disorder, 17 Behavior Therapist 66-67 (1993).
John Briere, Psychological Assessment of Adult Posttraumatic States 136 (1997).
118 John Briere, Psychological Assessment of Adult Posttraumatic States 136-37 (1997).
119 John Briere, Psychological Assessment of Adult Posttraumatic States 137-38 (1997).
120 D. Lauterbach & S. Vranna, Three Studies on the Reliability and Validity of a Self-Report Measure of Posttraumatic Stress, 3 Assessment 17-5 (1996).
John Briere, Psychological Assessment of Adult Posttraumatic States 137-38 (1997).
121 John Briere, Psychological Assessment of Adult Posttraumatic States 96-98 (1997).
Charles G. Watson et al., The PTSD Interview: Rationale, Description, Reliability, and Concurrent Validity of a DSM-III-Based Technique, 47 J. Clinical Psychology 179-88 (1991).
Daniel S. Weiss, “Structured Clinical Interview Techniques,” in International Handbook of Traumatic Stress Syndromes 179-87 (John P. Wilson & Beverley Raphael eds., 1993).
Jessica Wolfe & Terence M. Keane, “Diagnostic Validity of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder 54 (Marion E. Wolfe & Aron D. Mosnaim eds., 1990).
122 John Briere, Psychological Assessment of Adult Posttraumatic States 98 (1997).
123 John Briere, Psychological Assessment of Adult Posttraumatic States 101-02 (1997).
Dudley David Blake et al., The Development of a Clinician-Administered PTSD Scale, 8 J. Traumatic Stress 75-89 (1995).
124 Daniel S. Weiss, “Structured Clinical Interview Techniques,” in Assessing Psychological Trauma and PTSD 506-07 (John P. Wilson & Terence M. Keane eds., 1997).
125 Daniel S. Weiss, “Structured Clinical Interview Techniques,” in Assessing Psychological Trauma and PTSD 505 (John P. Wilson & Terence M. Keane eds., 1997).
John Briere, Psychological Assessment of Adult Posttraumatic States 99 (1997).
126 John Briere, Psychological Assessment of Adult Posttraumatic States 100 (1997).
Daniel S. Weiss, “Structured Clinical Interview Techniques,” in Assessing Psychological Trauma and PTSD 506 (John P. Wilson & Terence M. Keane eds., 1997).
127 Daniel S. Weiss, “Structured Clinical Interview Techniques,” in Assessing Psychological Trauma and PTSD 506 (John P. Wilson & Terence M. Keane eds., 1997).
John Briere, Psychological Assessment of Adult Posttraumatic States 99-100 (1997).
128 Patti Levin, “Assessing Posttraumatic Stress Disorder With the Rorschach Projective Technique,” in International Handbook of Traumatic Stress Syndromes 189-200 (John P. Wilson & Beverley Raphael eds., 1993).
129 J. M. Wood et al., The Comprehensive System for the Rorschach: A Critical Examination, 7 Psychological Sci. 3-10 (1996); L. R. Aiken, Personality Assessment: Methods and Practice (1996).
John Briere, Psychological Assessment of Adult Posttraumatic States 120-26 (1997).
Patti Levin & Bruce Reis, “Use of the Rorschach in Assessing Trauma,” in Assessing Psychological Trauma and PTSD ch. 9 (John P. Wilson & Terence M. Keane eds., 1997).
Scott O. Lilienfeld, Projective Measures of Personality and Psychopathology, How Well Do They Work?, Skeptical Inquirer, Sept./Oct. 1999, at 32-39.
Irving B. Weiner, Some Observations on the Validity of the Rorschach Inkblot Method, 8 Psychological Assessment 206-13 (1996).
130 Jeffrey A. Knight, “Neuropsychological Assessment in Posttraumatic Stress Disorder, in Assessing Psychological Trauma and PTSD 475-76 (John P. Wilson & Terence M. Keane eds., 1997).
131 John Briere, Psychological Assessment of Adult Posttraumatic States 83 (1997).
132 John Briere, Psychological Assessment of Adult Posttraumatic States 83-84 (1997).
133 John Briere, Psychological Assessment of Adult Posttraumatic States 84-85 (1997).
134 John Briere, Psychological Assessment of Adult Posttraumatic States 85 (1997).
135 David Faust & Jay Ziskin, The Expert Witness in Psychology and Psychiatry, 241 Science 31 (1988); Steven N. Allen, Psychological Assessment of Post-Traumatic Stress Disorder, 17 Psychiatric Clinics of N. Am. 327 (1994).
136 1 The Official ABMS Directory of Board Certified Medical Specialists (31st ed. 1999).
137 Id.
138 Ethical Principles of Psychologists and Code of Conduct, 47 Am. Psychologist 1597 (1992); American Academy of Psychiatry & the Law: Ethical Guidelines for the Practice of Forensic Psychiatry (1991); Robert I. Simon, “Toward the Development of Guidelines in the Forensic Psychiatric Examination of Posttraumatic Stress Disorder in Claimants,” in Posttraumatic Stress Disorder in Litigation 63-66 (Robert I. Simon ed., 1995).
139 DSM-IV-TR, Use of Clinical Judgment, at xxxii.
140 Id.
A differential diagnosis means different things to different people. To some it may mean an exhaustive list, not probabilistically ordered, of diagnoses that could explain a set of clinical findings. To others, it may mean a short list of diagnoses remaining after a large bulk of clinical data has been evaluated. To others, it may mean a probabilistically ordered list of potential diagnoses.
141 Arthur S. Blank, Jr., Clinical Detection, Diagnosis, and Differential Diagnosis of Post-Traumatic Stress Disorder, 17 Psychiatric Clinics of N. Am. 351-83 (1994).
Deborah A. Zarin & Felton Earls, Diagnostic Decision Making in Psychiatry, 150 Am. J. Psychiatry 197-206 (1993).
David Faust & Jay Ziskin, The Expert Witness in Psychology and Psychiatry, 241 Science 31-35 (1988).
142 John G. Gunderson & Alex N. Sabo, The Phenomenological and Conceptual Interface Between Borderline Personality Disorder and PTSD, 150 Am. J. Psychiatry 19-27 (1993).
Steven L. Shearer et al., Frequency and Correlates of Childhood Sexual and Physical Abuse Histories in Adult Female Borderline Inpatients, 147 Am. J. Psychiatry 214-16 (1990).
Susan N. Ogata et al., Childhood Sexual and Physical Abuse in Adult Patients With Borderline Personality Disorder, 147 Am. J. Psychiatry 1008-13 (1990).
Bessel A. van der Kolk & Onno van der Hart, Pierre Janet and the Breakdown of Adaptation in Psychological Trauma, 146 Am. J. Psychiatry 1530-40 (1989).
143 David Malakoff, Bayes Offers a “New” Way to Make Sense of Numbers, 286 Science 1460-64 (1999); Colin Howson & Peter Urbach, Bayesian Reasoning in Science, 350 Science 371-74 (1991).
144 J. R. T. Davidson et al., Posttraumatic Stress Disorder in the Community: An Epidemiological Study, 21 Psychological Medicine 713-21 (1991) (the lifetime prevalence of PTSD in the Piedmont region of North Carolina (using the criteria of the DSM-III measured by the Diagnostic Interview Scale) was 1.3 percent).
J. E. Helzer et al., Post-Traumatic Stress Disorder in the General Population: Findings of the Epidemiologic Catchment Area Study, 317 New Eng. J. Medicine 630-34 (1987) (the lifetime prevalence of PTSD in the St. Louis area (using the criteria of the DSM-III measured by the Diagnostic Interview Scale) was 1.0 percent).
J. H. Shore et al., Community Patterns of Posttraumatic Stress Disorders, 177 J. Nervous & Mental Disease 681-85 (1989) (the lifetime prevalence of PTSD (using the criteria of the DSM-III measured by Diagnostic Interview Schedule, criticized as lacking sensitivity to traumatic stress) was for men 2.9 percent (including combat-induced PTSD) and for women 3.3 percent).
R. S. Pynoos et al., Life Threat and Posttraumatic Stress in School-Age Children, 44 Archives Gen. Psychiatry 1057-63 (1987).
R. C. Kessler et al., Posttraumatic Stress Disorder in the National Comorbidity Survey, 52 Archives Gen. Psychiatry 1048-60 (1995) (The lifetime prevalence of PTSD (using the criteria of the DSM-III-R, measured by a modified version of the Composite International Diagnostic Interview and a modified version of the Revised Diagnostic Interview Schedule) was 7.8 percent (10.45 percent in women and 5.0 percent in men). Lifetime prevalence of exposure to trauma for men was 60.7 percent and for women 51.2 percent.).
F. H. Norris, Epidemiology of Trauma: Frequency and Impact of Different Potentially Traumatic Events on Different Demographic Groups, 60 J. Consulting & Clinical Psychology 409-18 (1992) (the prevalence of current not lifetime PTSD in 250 persons (not drawn randomly) from four southern cities (using the criteria of the DSM-III-R, measured by “The Traumatic Stress Schedule,” denied by the author) was 7.4 percent: 6.0 percent for men and 8.8 percent for women).
N. Breslau et al., Traumatic Events and Posttraumatic Stress Disorder in an Urban Population of Young Adults, 48 Archives Gen. Psychiatry 216-22 (1991) (The lifetime prevalence of PTSD (using the criteria of the DSM-III-R measured by NIMH Diagnostic Interview Schedule Version III-Revised to be more sensitive to traumatic stress) was 9.55 percent (11.3 percent in women and 5.6 percent in men). The lifetime prevalence of exposure to traumatic events qualifying for the DSM-III-R stressor criterion in this sample of young adults was 39.1 percent. The lifetime prevalence of DSM-III-R PTSD was 9.2 percent.).
Ronald C. Kessler et al., Posttraumatic Stress Disorder in the National Comorbidity Survey, 52 Archives Gen. Psychiatry 1048-60 (1995).
Jonathan R. T. Davidson & John A. Fairbank, “The Epidemiology of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder, DSM-IV and Beyond ch. 8 (J. R. T. Davidson & Edna B. Foa eds., 1993).
J. R. T. Davidson et al., Post Traumatic Stress Disorder in the Community: An Epidemiological Study, 21 Psychological Med. 1-9 (1991).
J. E. Helzer et al., Post Traumatic Stress Disorder in the General Population, 317 New Eng. J. Med. 1630-34 (1987).
DSM-IV-TR at 466.
145 Rachel Yehuda et al., Impact of Cumulative Lifetime Trauma and Recent Stress on Current Posttraumatic Stress Disorder Symptoms in Holocaust Survivors, 152 Am. J. Psychiatry 1815-18 (1995).
Rachel Yehuda et al., Vulnerability to Posttraumatic Stress Disorder in Adult Offspring of Holocaust Survivors, 155 Am. J. Psychiatry 1163-71 (1998).
Bonnie L. Green et al., Buffalo Creek Survivors in the Second Decade: Stability of Stress Symptoms, 60 Am. J. Orthopsychiatry 43-54 (1990).
Bonnie L. Green et al., Identifying Survivors at Risk: Long-Term Impairment Following the Beverly Hills Supper Club Fire, 53 J. Consulting & Clinical Psychology 672-78 (1985).
Bonnie L. Green et al., Buffalo Creek Survivors in the Second Decade: Comparison With Unexposed and Nonlitigant Groups, 20 J. Applied Soc. Psychology 1033-50 (1990).
Bonnie L. Green, “Disasters and Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder, DSM-IV and Beyond ch. 5 (J. R. T. Davidson & Edna B. Foa eds., 1993).
146 Bonnie L. Green, “Disasters and Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder, DSM-IV and Beyond ch. 5 (J. R. T. Davidson & Edna B. Foa eds., 1993).
Penny Dixon et al., Peripheral Victims of the Herald of Free Enterprise Disaster, 66 Brit. J. Med. Psychology 193-202 (1993).
147 A. C. McFarlane, The Aetiology of Post Traumatic Morbidity: Predisposing, Precipitating and Perpetuating Factors, 154 Brit. J. Psychiatry 221-28 (1989).
Dieter Wagner et al., Prevalence of Symptoms of Posttraumatic Stress Disorder in German Professional Firefighters, 155 Am. J. Psychiatry 1727-32 (1998).
Robert J. Ursano et al., Posttraumatic Stress Disorder and Identification in Disaster Workers, 156 Am. J. Psychiatry 353-59 (1999).
148 Bonnie L. Green, “Recent Research Findings on the Diagnosis of Posttraumatic Stress Disorder, Prevalence, Course, Comorbidity, and Risk,” in Posttraumatic Stress Disorder in Litigation ch. 2 (Robert L. Simon ed., 1995).
Dean G. Kilpatrick & Heidi S. Resnick, “Posttraumatic Stress Disorder Associated With Exposure to Criminal Victimization in Clinical and Community Populations,” in Posttraumatic Stress Disorder, DSM-IV and Beyond ch. 7 (J. R. T. Davidson & Edna B. Foa eds., 1993).
I. Winfield et al., Sexual Assault and Psychiatric Disorders Among Women in a Community Population, 147 Am. J. Psychiatry 335-41 (1990).
B. O. Rothbaum et al., A Prospective Examination of Post-Traumatic Stress Disorder in Rape Victims, 5 J. Traumatic Stress 455-75 (1992).
F. H. Norris, Epidemiology of Trauma: Frequency and Impact of Different Potentially Traumatic Events on Different Demographic Groups, 60 J. Consulting & Clinical Psychology 409-18 (1992).
Idee Winfield et al., Sexual Assault and Psychiatric Disorders Among a Community—Sample of Women, 147 Am. J. Psychiatry 335-41 (1990).
Glenn Craig Davis & Naomi Breslau, Post-Traumatic Stress Disorder in Victims of Civilian Trauma and Criminal Violence, 17 Psychiatric Clinics of N. Am. 289-99 (1994).
Chris R. Brewin et al., Acute Stress Disorder and Posttraumatic Stress Disorder in Victims of Violent Crime, 156 Am. J. Psychiatry 360-66 (1999).
Ned Rodriguez et al., Posttraumatic Stress Disorder in Adult Female Survivors of Childhood Sexual Abuse: A Comparison Study, 65 J. Consulting & Clinical Psychology 53-59 (1997).
149 F. H. Norris, Epidemiology of Trauma: Frequency and Impact of Different Potentially Traumatic Events on Different Demographic Groups, 60 J. Consulting & Clinical Psychology 409-18 (1992).
150 Lenore M. Williams, Recall of Childhood Trauma: A Prospective Study of Women’s Memories of Child Sexual Abuse, 62 J. Consulting & Clinical Psychology 1167-76 (1994); D. E. Russell, Sexual Exploitation: Rape, Child Sexual Abuse, and Sexual Harassment (1984); D. Finkelhor, Sexually Victimized Children (1979); S. D. Peters et al., “Prevalence,” in A Sourcebook on Child Sexual Abuse 15-59 (D. Finkelhor et al. eds., 1986); M. H. Stinson & S. S. Hendrick, Reported Childhood Sexual Abuse in University Counseling Center Clients, 39 J. Counseling Psychology 370-74 (1992); G. E. Wyatt, The Sexual Abuse of Afro-American and White-American Women in Childhood, 9 Child Abuse & Neglect 507-19 (1985); D. Stephen Lindsay & J. Don Read, Psychotherapy and Memories of Childhood Sexual Abuse: A Cognitive Perspective, 8 Applied Cognitive Psychology 281-338 (1994).
151 Dean G. Kilpatrick & Heidi S. Resnick, “Posttraumatic Stress Disorder Associated With Exposure to Criminal Victimization in Clinical and Community Populations,” in Posttraumatic Stress Disorder, DSM-IV and Beyond ch. 7 (J. R. T. Davidson & Edna B. Foa eds., 1993).
Naomi Breslau et al., Posttraumatic Events and Posttraumatic Stress Disorder in an Urban Population of Young Adults, 48 Archives Gen. Psychiatry 216-22 (1991).
152 F. H. Norris, Epidemiology of Trauma: Frequency and Impact of Different Potentially Traumatic Events on Different Demographic Groups, 60 J. Consulting & Clinical Psychology 409-18 (1992).
Edward B. Blanchard & Edward J. Hickling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors 16-19, 21-34 (1997).
153 Alan Fontana & Robert Rosenbeck, Effects of Compensation-Seeking on Treatment Outcomes Among Veterans With Posttraumatic Stress Disorder, 186 J. Nervous & Mental Disease 223-30 (“Among inpatients in programs designed programmatically to provide an extremely long length of stay (100 days on average), the motivation to apply for or to maintain compensation status appeared to inhibit improvement.”).
Paul Ekman & Maureen O’Sullivan, Who Can Catch a Liar?, 46 Am. Psychologist 921-30 (1991).
154 David Faust, The Detection of Deception, 13 Neurologic Clinics 255-65 (1995).
155 Phillip J. Resnick, “Guidelines for the Evaluation of Malingering in Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder in Litigation ch. 6 (Robert L. Simon ed., 1995).
156 John A. Fairbank et al., Psychometric Detection of Fabricated Symptoms of Posttraumatic Stress Disorder, 142 Am. J. Psychiatry 501-03 (1985).
Stephen T. Perconte & Anthony J. Goreczny, Failure to Detect Fabricated Posttraumatic Stress Disorder With the Use of the MMPI in a Clinical Population, 147 Am. J. Psychiatry 1057-60 (1990).
Paul R. Lees-Haley, Efficacy of MMPI-2 Validity Scales and MCMI-II Modifier Scales for Detecting Spurious PTSD Claims: F, F-K, Fake Bad Scale, Ego Strength, Subtle-Obvious Subscales DIS, and DEB, 48 J. Clinical Psychology 681-89 (1992).
157 Roger L. Greene, The MMPI-2/MMPI, An Interpretive Manual 50 (1991).
158 Id. at 68.
159 R. S. Epstein, Avoidant Symptoms Cloaking the Diagnosis of PTSD in Patients With Severe Accidental Injury, J. Traumatic Stress 451-58 (1993) (15 motor vehicle accident victims were followed who had been admitted to a regional trauma center. (They were interviewed periodically over nine months.) Four individuals initially met diagnostic criteria for PTSD; two others, who had partial PTSD, went on to meet delayed-onset criteria during the follow-up interval. Thus, it appears that PTSD secondary to motor vehicle accidents can have a delayed onset.).
M. M. Green et al., Undiagnosed Post-Traumatic Stress Disorder Following Motor Vehicle Accidents, 159 Med. J. Australia 529-34 (1993) (24 motor vehicle accident victims were followed over an 18-month period. Between the initial and 18th month assessments, five individuals who were not initially diagnosed with PTSD had developed symptoms severe enough to warrant a diagnosis of PTSD. It should be noted that these five participants with delayed-onset PTSD were diagnosed with borderline PTSD at the initial interview (none of those who were initially symptom-free went on to develop delayed-onset PTSD in this study). The participants were interviewed at only these two time points, making it impossible to determine whether they would have met criteria for delayed-onset PTSD by DSM-III-R standards. These five individuals were delayed in their development of the disorder in the sense that they did not meet criteria in the month after the trauma.).
R. Mayou et al., Psychiatrist Consequences of Road Traffic Accidents, 307 Brit. Med. J. 647-51 (1993) (a consecutive series of accident victims were followed who had sought medical attention after their accidents (N = 188). These accident victims were prospectively followed over a one-year period. Five individuals met criteria for PTSD three months post-trauma, eight met criteria at both the 3- and 12-month interviews, and six met criteria at the 12-month interview only. At least 6 of the 19 participants with PTSD would have met criteria for delayed-onset PTSD. It was found that poor social, medical, and occupational outcome was associated with increased psychological morbidity at one year.).
B. L. Green et al., Buffalo Creek Survivors in the Second Decade: Stability of Stress Symptoms, 60 Am. J. Orthopsychiatry 43-54 (1990) (This study reported 14-year follow-up data on a sample of individuals exposed to the devastating Buffalo Creek Dam collapse of 1972. Of those who participated in the follow-up portion of the study, 11 percent had delayed-onset PTSD. The only differentiating characteristic in the delayed-onset group in this sample was ethnicity. Caucasians were more likely than African-Americans to meet the diagnostic criteria shortly after the trauma; however, being African-American put participants at a higher risk for developing delayed-onset PTSD. Attempting to draw inferences about the nature of delayed-onset PTSD from this study would be difficult given the long interval between initial assessment and follow-up, as well as potential problems with retrospective bias.).
A. C. McFarlane, The Longitudinal Course of Posttraumatic Morbidity: The Range of Outcomes and Their Predictors, 176 J. Nervous & Medical Disease 30-39 (1988) (This study reported prospective questionnaire data on a sample of 469 Australian firefighters over a 29-month period. Of the final 315 firefighters who participated in a follow-up, 62 showed delayed onset of PTSD (20 percent). There was a statistically significant effect for the delayed-onset group to avoid thinking about their trauma shortly after the fire. Discriminate function analyses revealed that neuroticism and the impact of attending debriefing meetings were the best predictors of delayed-onset PTSD.).
T. C. Buckley et al., A Prospective Examination of Delayed Onset PTSD Secondary to Motor Vehicle Accidents, 105 J. Abnormal Psychology 617-25 (1996) (This study, another “salami” publication by this group, used 158 victims of motor vehicle accidents. Of 158 motor vehicle accident victims who had sought medical treatment within three days of the accident, on initial evaluation of PTSD one to four months post-accident, 62 met the criteria of PTSD under the DSM-III-R as measured by CAPS and 96 did not. Of the 96, seven developed PTSD during the one-year follow-up interval, with the average interval from accident to development of PTSD being 8.5 months. All of the seven had “subsyndromal PTSD” at initial evaluation (meeting clusters B and D but not C). 71 percent (five of those who developed delayed-onset PTSD] were involved in litigation.).
160 Paul R. Lees-Haley, Efficacy of MMPI-2 Validity Scales & MCMI-II Modifier Scales for Detecting Spurious PTSD Claims: F, F-K, Fake Bad Scale, Ego Strength, Subtle-Obvious Subscales, DIS & DEB, 48 J. Clinical Psychology 681-89 (1992); Paul R. Lees-Haley et al., A Fake Bad Scale on the MMPI-2 for Personal Injury Claimants, 68 Psychological Rep. 203-10 (1991).
161 Otfried Spreen & Esther Strauss, A Compendium of Neuropsychological Tests 625 (1998); P. A. Abrisi & J. S. Ben-Porath, An MMPI-2 Infrequent Response Scale for Use With Psychopathological Populations: The Infrequency—Psychopathology Scale F(p), 7 Psychological Assessment 424-31 (1995); P. A. Abrisi & J. S. Ben-Porath, Characteristics of the MMPI-2 F(p) Scale as a Function of Diagnosis in an Inpatient Sample of Veterans, 9 Psychological Assessment 102-05 (1997).
162 Landy Sparr & Loren D. Pankratz, Factitious Posttraumatic Stress Disorder, 140 Am. J. Psychiatry 1016-19 (1983); Loren Pankratz, Patients Who Deceive 169 (1998); J. A. Fairbank et al., Psychometric Detection of Fabricated Symptoms of PTSD, 142 Am. J. Psychiatry 501-03 (1985); J. E. Lynn & M. Belza, Factitious Posttraumatic Stress Disorder: The Veteran Who Never Got to Vietnam, 35 Hosp. & Community Psychiatry 697-701 (1984).
163 R. S. Epstein, Avoidant Symptoms Cloaking the Diagnosis of PTSD in Patients With Severe Accidental Injury, J. Traumatic Stress 451-58 (1993) (15 motor vehicle accident victims were followed who had been admitted to a regional trauma center. (They were interviewed periodically over nine months.) Four individuals initially met diagnostic criteria for PTSD; two others, who had partial PTSD, went on to meet delayed-onset criteria during the follow-up interval. Thus, it appears that PTSD secondary to motor vehicle accidents can have a delayed onset.).
M. M. Green et al., Undiagnosed Post-Traumatic Stress Disorder Following Motor Vehicle Accidents, 159 Med. J. Australia 529-34 (1993) (24 motor vehicle accident victims were followed over an 18-month period. Between the initial and 18th month assessments, five individuals who were not initially diagnosed with PTSD had developed symptoms severe enough to warrant a diagnosis of PTSD. It should be noted that these five participants with delayed-onset PTSD were diagnosed with borderline PTSD at the initial interview (none of those who were initially symptom-free went on to develop delayed-onset PTSD in this study). The participants were interviewed at only these two time points, making it impossible to determine whether they would have met criteria for delayed-onset PTSD by DSM-III-R standards. These five individuals were delayed in their development of the disorder in the sense that they did not meet criteria in the month after the trauma.).
R. Mayou et al., Psychiatrist Consequences of Road Traffic Accidents, 307 Brit. Med. J. 647-51 (1993) (A consecutive series of accident victims were followed who had sought medical attention after their accidents (N = 188). These accident victims were prospectively followed over a one-year period. Five individuals met criteria for PTSD three months post-trauma, eight met criteria at both the 3- and 12-month interviews, and six met criteria at the 12-month interview only. At least 6 of the 19 participants with PTSD would have met criteria for delayed-onset PTSD. It was found that poor social, medical, and occupational outcome was associated with increased psychological morbidity at one year.).
B. L. Green et al., Buffalo Creek Survivors in the Second Decade: Stability of Stress Symptoms, 60 Am. J. Orthopsychiatry 43-54 (1990) (This study reported 14-year follow-up data on a sample of individuals exposed to the devastating Buffalo Creek Dam collapse of 1972. Of those who participated in the follow-up portion of the study, 11 percent had delayed-onset PTSD. The only differentiating characteristic in the delayed-onset group in this sample was ethnicity. Caucasians were more likely than African-Americans to meet the diagnostic criteria shortly after the trauma; however, being African-American put participants at a higher risk for developing delayed-onset PTSD. Attempting to draw inferences about the nature of delayed-onset PTSD from this study would be difficult given the long interval between initial assessment and follow-up, as well as potential problems with retrospective bias.).
A. C. McFarlane, The Longitudinal Course of Posttraumatic Morbidity: The Range of Outcomes and Their Predictors, 176 J. Nervous & Medical Disease 30-39 (1988) (This study reported prospective questionnaire data on a sample of 469 Australian firefighters over a 29-month period. Of the final 315 firefighters who participated in a follow-up, 62 showed delayed onset of PTSD (20 percent). There was a statistically significant effect for the delayed-onset group to avoid thinking about their trauma shortly after the fire. Discriminate function analyses revealed that neuroticism and the impact of attending debriefing meetings were the best predictors of delayed-onset PTSD.).
T. C. Buckley et al., A Prospective Examination of Delayed Onset PTSD Secondary to Motor Vehicle Accidents, 105 J. Abnormal Psychology 617-25 (1996) (This study, another “salami” publication by this group, used 158 victims of motor vehicle accidents. Of 158 motor vehicle accident victims who had sought medical treatment within three days of the accident, on initial evaluation of PTSD one to four months post-accident, 62 met the criteria of PTSD under the DSM-III-R as measured by CAPS and 96 did not. Of the 96, seven developed PTSD during the one-year follow-up interval, with the average interval from accident to development of PTSD being 8.5 months. All of the seven had “subsyndromal PTSD” at initial evaluation (meeting clusters B and D but not C). 71 percent (five of those who developed delayed-onset PTSD) were involved in litigation.).
164 See endnote 150.
165 Rachel Yehuda et al., Conflict Between Current Knowledge About Posttraumatic Stress Disorder and Its Original Conceptual Basis, 152 Am. J. Psychiatry 1705-13 (1995); Chris R. Brewin et al., Meta-Analysis of Risk Factors for Posttraumatic Stress Disorder in Trauma-Exposed Adults, 68 J. Consulting & Clinical Psychology 748-66 (2000).
166 Arieh Y. Shaleu et al., Predictors of PTSD in Injured Trauma Survivors: A Prospective Study, 153 Am. J. Psychiatry 219-25 (1996).
Naomi Breslau et al., Risk Factors for PTSD-Related Traumatic Events: A Prospective Analysis, 152 Am. J. Psychiatry 529-35 (1995).
Sara A. Freedman et al., Predictors of Chronic Post-Traumatic Stress Disorder, 174 Brit. J. Psychiatry 353-59 (1999).
167 DSM-IV-TR at 466; 2 DSM-IV Sourcebook 588-90 (1996); Edward B. Blanchard & Edward J. Hickling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors ch. 7 (1997); Arthur S. Blank, Jr., “The Longitudinal Course of Posttraumatic Stress,” in Posttraumatic Stress Disorder DSM-IV & Beyond 3-22 (Jonathan R. T. Davidson & Edna B. Foa eds., 1993); Bonnie L. Green, “Recent Research Findings on the Diagnosis of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder in Litigation ch. 2 (Robert I. Simon ed., 1995).
168 DSM-IV-TR at 466; 2 DSM-IV Sourcebook 588-90 (1996); Edward B. Blanchard & Edward J. Hickling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors ch. 7 (1997); Arthur S. Blank, Jr., “The Longitudinal Course of Posttraumatic Stress,” in Posttraumatic Stress Disorder DSM-IV & Beyond 3-22 (Jonathan R. T. Davidson & Edna B. Foa eds., 1993); Bonnie L. Green, “Recent Research Findings on the Diagnosis of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder in Litigation ch. 2 (Robert I. Simon ed., 1995).
169 S. D. Solomon et al., Efficacy of Treatment for Post-Traumatic Stress Disorder, 268 J. Am. Med. Ass’n 633-38 (1992).
Jeffrey J. Sherman, Effects of Psychotherapeutic Treatments for PTSD: A Meta-Analysis of Controlled Clinical Trials, 11 J. Traumatic Stress 413-35 (1998).
170 S. D. Solomon et al., Efficacy of Treatment for Post-Traumatic Stress Disorder, 268 J. Am. Med. Ass’n 633-38 (1992).
171 D. Brom et al., Brief Psychotherapy for Post-Traumatic Stress Disorder, 57 J. Consulting & Clinical Psychology 607-12 (1989).
E. B. Foa & N. J. Kozak, Emotional Processing of Fear: Exposure to Corrective Information, 99 Psychological Bull. 20-35 (1986).
E. G. Peniston, EMG Biofeedback-Assisted Desensitization Treatment for Vietnam Combat Veterans’ Post-Traumatic Stress Disorder, 9 Clinical Biofeedback & Health 35-41 (1986).
172 K. Kuch, Treatment of PTSD Following Automobile Accidents, 10 Behavior Therapist 224-42 (1987).
K. Kuch et al., Post-Traumatic Stress Disorder After Car Accidents, 30 Can. J. Psychiatry 426-27 (1985).
173 Edward B. Blanchard & Edward J. Hickling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors 211-20 (1997); S. D. Solomon et al., Efficacy of Treatment for Post-Traumatic Stress Disorder, 268 J. Am. Med. Ass’n 633-38 (1992); Edna B. Foa et al., “Posttraumatic Stress Disorder,” in 2 Treatment of Psychiatric Disorders 1499-1519 (Glen O. Gabbard ed., 1995).
174 S. D. Solomon et al., Efficacy of Treatment for Post-Traumatic Stress Disorder, 268 J. Am. Med. Ass’n 633-38 (1992).
L. J. Veronen & D. G. Kilpatrick, “Stress Management for Rape Victims,” in Stress Reduction and Prevention 341-74 (D. Meichenbaum & M. E. Jaremko eds., 1983).
Edna Foa & N. J. Kozak, Emotional Processing of Fear: Exposure to Corrective Information, 99 Psychological Bull. 20-35 (1986).
Edna B. Foa et al., “Posttraumatic Stress Disorder,” in 2 Treatment of Psychiatric Disorders 1499-1519 (Glen O. Gabbard ed., 1995).
175 Julia B. Frank et al., “Antidepressants in the Treatment of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder, Etiology, Phenomenology & Treatment ch. 14 (Marion E. Wolf & Aron D. Mosnaim eds., 1990).
176 J. Davidson et al., Treatment of Posttraumatic Stress Disorder With Amitriptyline and Placebo, 47 Archives Gen. Psychiatry 259-66 (1990); C. Reist et al., Controlled Trial of Desipramine in 18 Men With Posttraumatic Stress Disorder, 146 Am. J. Psychiatry 513-16 (1976).
177 J. B. Frank et al., A Randomized Clinical Trial of Phenelzine and Imipramine for Posttraumatic Stress Disorder, 1145 Am. J. Psychiatry 1289-91 (1988).
T. R. Kosten et al., Pharmacotherapy for Posttraumatic Stress Disorder Using Phenelzine or Imipramine, 179 J. Nervous & Mental Disease 366-70 (1988).
178 Edna B. Foa et al., “Posttraumatic Stress Disorder,” in 2 Treatment of Psychiatric Disorders 1499-1519 (Glen O. Gabbard ed., 1995).
179 Matthew J. Friedman, “Interrelationships Between Biological Mechanisms and Pharmacotherapy of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder 215-17 (Marion E. Wolf & Aron D. Mosnaim eds., 1990).
180 A. Steven Lipper, “Carbamazepine in the Treatment of Posttraumatic Stress Disorder: Implications for the Kindling Hypothesis,” in Posttraumatic Stress Disorder, Etiology, Phenomenology, and Treatment ch. 15 (Marion E. Wolf & Aron D. Mosnaim eds., 1990).
181 Matthew J. Friedman, “Interrelationships Between Biological Mechanisms and Pharmacotherapy of Posttraumatic Stress Disorder,” in Posttraumatic Stress Disorder 215-17 (Marion E. Wolf & Aron D. Mosnaim eds., 1990).
182 A well-known psychiatrist has remarked that:
“This report, which brings into doubt not only the treatment but the nature of the underlying ‘disease,’ has produced many agonized debates within the VA. Enthusiasts for PTSD argue that the investigators somehow missed the patients’ ‘real’ states of mind while at the same time over-looking subtle but nonetheless positive responses to treatment. They have also stepped up the search for biological evidence of brain changes produced by the emotional trauma of combat—changes that might validate chronic PTSD as a distinct condition and justify characterizing certain patients as its victims regardless of whether a successful treatment yet exists for it. In the psychiatric journals, reports of such a ‘biological marker’ come and go.
“Yet while we await final word on chronic PTSD, the skeptics—both within and without the VA system—would appear to hold much the stronger hand. They have pointed, for example, to analogous research on war veterans in Israel. According to Israeli psychiatrists, long-term treatment in hospitals has the unfortunate tendency of making battle-trauma victims hypersensitive to their symptoms and, by encouraging them to concentrate on the psychological wounds of combat, distracts their attention from the ‘here-and-now’ problems of adjusting to peace-time demands and responsibilities.
. . . .
“When a patient’s reaction does not follow this standard course, one need hardly leap to conclude he is suffering from an ‘abnormal’ or ‘chronic’ or ‘delayed’ form of PTSD. More likely, the culprit will be a separate and complicating condition like (most commonly) major depression, with its cardinal symptoms of misery, despair, and self-recrimination. In this condition, memories of past losses, defeats, or traumas are reawakened, giving content and justification to diminished attitudes about oneself. But such memories should hardly be confused with the cause of the depression itself, which can and should be treated for what it is. America’s war veterans, who are entitled to our respect and support, surely deserve better than to be maintained in a state of chronic invalidism.” Paul R. McHugh, How Psychiatry Lost Its Way, Commentary 35 (Dec. 1999).
183 Carl P. Malmquist, The Use and Misuse of Psychiatry in Sexual Harassment Cases, 26 Psychiatric Annals 149-56 (1996).
184 Edward B. Blanchard & Edward J. Hinkling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors 16-19, 21-34 (1997).
185 Margaret M. Green et al., Undiagnosed Post-traumatic Stress Disorder Following Motor Vehicle Accidents, 159 Med. J. Australia 529-34 (1993); A. Feinstein & R. Dolan, Predictors of Post-traumatic Stress Disorder Following Physical Trauma: An Examination of the Stressor Criterion, 21 Psychological Med. 85-91 (1991); R. Mayo et al., Psychiatric Consequences of Road Traffic Accidents, 307 Brit. Med. J. 647-51 (1993); A. Burstein, Posttraumatic Stress Disorder (letter), 46 J. Clinical Psychiatry 554 (1985).
186 Danny Koren et al., Acute Stress Response and Posttraumatic Stress Disorder in Traffic Accident Victims: A One-Year Prospective; Follow-Up Study, 156 Am. J. Psychiatry 367-73 (1999) (“injured victims of traumatic events, traffic accidents in our case, are at considerable risk for development of PTSD even when they are only mildly injured”).
A problem with studies assessing the correlation between the severity of motor vehicle accidents and PTSD is that no adequate measure of “severity” exists. Edward B. Blanchard & Edward J. Hinkling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors 15 (1997) (“there are no validated scales of accident severity”).
187 Edward B. Blanchard, Psychiatric Morbidity Associated With Motor Vehicle Accidents, 183 J. Nervous & Mental Disease 495-504 (1995).
Klaus Kuch et al., Posttraumatic Stress Disorder and Motor Vehicle Accidents: A Multidisciplinary Overview, 41 Can. J. Psychiatry 429-34 (1996).
Douglas L. Delahanty et al., Acute and Chronic Distress and Posttraumatic Stress Disorder as a Function of Responsibility for Serious Motor Vehicle Accidents, 65 J. Consulting & Clinical Psychology 560-67 (1997).
Allison G. Harvey et al., The Relationship Between Acute Stress Disorder and Posttraumatic Stress Disorder: A Prospective Evaluation of Motor Vehicle Accident Survivors, 66 J. Consulting & Clinical Psychology 507-12 (1998).
Paul Stallard et al., Prospective Study of Post-Traumatic Stress Disorder in Children Involved in Road Traffic Accidents, 317 Brit. Med. J. 1619-23 (1998).
Margaret M. Green et al., Undiagnosed Post-Traumatic Stress Disorder Following Motor Vehicle Accidents, 159 Med. J. Australia 529-34 (1993).
Edward B. Blanchard et al., Psychological Morbidity Associated With Motor Vehicle Accidents, 32 Behav. Res. & Therapy 283-90 (1994).
Allan Burstein, Posttraumatic Stress Disorder in Victims of Motor Vehicle Accidents, 40 Hosp. & Community Psychiatry 295-97 (1989).
Edward B. Blanchard et al., Psychophysiology of Posttraumatic Stress Disorder Related to Motor Vehicle Accidents: Replication and Extension, 64 J. Consulting & Clinical Psychology 742-51 (1996).
Danny Koren et al., Acute Stress Response and Posttraumatic Stress Disorder in Traffic Accident Victims: A One-Year Prospective, Follow-Up Study, 156 Am. J. Psychiatry 367-73 (1999).
Todd C. Buckley et al., A Prospective Examination of Delayed Onset PTSD Secondary to Motor Vehicle Accidents, 105 J. Abnormal Psychology 617-25 (1996).
Edward B. Blanchard et al., Effects of Litigation Settlements on Posttraumatic Stress Symptoms in Motor Vehicle Accidents, 11 J. Traumatic Stress 337-54 (1998).
Edward B. Blanchard et al., Prediction of Remission of Acute Posttraumatic Stress Disorder in Motor Vehicle Accident Victims, 10 J. Traumatic Stress 215-34 (1997).
Edward B. Blanchard & Edward J. Hickling, After the Crash, Assessment and Treatment of Motor Vehicle Accident Survivors (1997).
188 A. Blaszczynski et al., Psychiatric Morbidity Following Motor Vehicle Accidents: A Review of Methodological Issues, 39 Comprehensive Psychiatry 111-21 (1998) (a review of the studies on the relationship between motor vehicle accidents and psychiatric illness, criticizing the studies for a variety of significant methodological shortcomings, such as (1) failure to provide ratings of the severity of injury; (2) failure to use randomly selected subjects, using a disproportionate number of women and using subjects referred for medicolegal assessment; (3) failure to control for involvement in litigation; and (4) failure to specify well-defined diagnostic endpoints).
K. Kuch et al., Post-Traumatic Stress Disorder After Car Accidents, 30 Can. J. Psychiatry 426-27 (1985) (Thirty subjects involved in motor vehicle accidents were referred to a “behavioral medicine service” for a medicolegal opinion or for treatment. (The study group is the product of obvious selection bias.) There were no controls. The severity of the motor vehicle accidents was not clearly described or quantified. These subjects were evaluated under the criteria of the DSM-III, and all were found to have PTSD. Behavioral treatment was considered very successful for these subjects.).
A. Burstein, Posttraumatic Stress Disorder in Victims of Motor Vehicle Accidents, 40 Hosp. & Community Psychiatry 95-297 (1989) (The author reports his experience with 70 of his patients involved in motor vehicle accidents who were diagnosed with PTSD under the criteria of the DSM-III. There were no controls. Nor is the severity of the motor vehicle accidents described. The author remarks that it is difficult to identify those with PTSD from motor vehicle accidents for a variety of reasons: (1) the individuals are too embarrassed to report psychiatric symptoms; (2) physicians overlook psychiatric symptoms; (3) post-concussion symptoms are similar to the symptoms of PTSD and so may mask the PTSD. Subgroups of PTSD patients may be difficult to manage: those with intense feelings of re-experiencing the accident and who have poor impulse control (e.g., alcoholics, antisocial personalities, and the demented).).
E. J. Hickling et al., Motor Vehicle Accidents, Headaches, and Post-traumatic Stress Disorder: Assessment Findings in a Consecutive Series, 32 Headache 147-51 (1992) (Twenty individuals with “post-traumatic” headaches from motor vehicle accidents with suspected psychological problems were referred to a psychologist for treatment of their headaches. (A substantial likelihood of selection bias exists as a result.) Nineteen of these individuals were given psychiatric diagnoses. Of those, 15 had PTSD; 14 had a mood disorder, including 10 with major depression. For all but one, neurological exams were normal.).
E. J. Hickling, Post-traumatic Stress Disorder and Motor Vehicle Accidents, 6 J. Anxiety Disorders 83-304 (1992).
D. Brom et al., Victims of Traffic Accidents: Incidence and Prevention of Posttraumatic Stress Disorders, 49 J. Clinical Psychiatry 131-40 (1993) (Eighty-three individuals in the monitoring group (reflecting a response rate of 36 percent and with a subsequent dropout rate of 24 percent) and sixty-eight in the intervention group (reflecting a response rate of 13 percent with a subsequent dropout rate of 16 percent) involved in moderately serious to serious motor vehicle accidents in the Netherlands. These individuals were examined one and six months after the accident. After one month, 50 percent in the monitoring group and 75 percent in the intervention group showed no or hardly any symptoms, 28 percent in the monitoring group and 17 percent in the intervention group had moderate symptoms, and the remaining 22 percent in the monitoring group and 8 percent in the intervention group had reasonably severe symptoms of intrusion and avoidance. After six months, 82 percent had no symptoms; 10 percent had moderate symptoms and 8 percent had severe symptoms.).
R. Mayou et al., Psychiatric Consequences of Road Traffic Accidents, 307 Brit. Med. J. 647-51 (1993) (All subjects aged 18-70 living in Oxfordshire who had been traffic accident victims seen at the emergency room (188 subjects) were categorized into three categories: (1) multiple-injury victims who had been occupants of motor vehicles in accidents; (2) multiple-injury victims who had been motorcycle drivers or passengers; (3) whiplash-injury victims who had no other physical injury. These subjects were interviewed soon after the accident, at three months, and at six months. At the first assessment, 41 percent had elevated anxiety or depression. Eighteen percent had acute distress syndrome with horrific intrusive memories of the accident. Most subjects reported good psychological outcome at one year. Nineteen people (11 percent) satisfied the DSM-III-R criteria for PTSD. Eight individuals had PTSD at 3 and 12 months, five at 3 months only and six at 12 months only.).
M. M. Green et al., Undiagnosed Posttraumatic Stress Disorder Following Motor Vehicle Accidents, 159 Med. J. Australia 529-34 (1993) (Sixty-nine Australian adults hospitalized after motor vehicle accidents were evaluated four weeks and 18 months after the accident. The sample was biased toward people with more severe injuries who required prolonged hospitalization. At four weeks, of the 24 subjects evaluated, two were diagnosed with PTSD. At 18 months, of these subjects, one still had PTSD and the other could not be contacted. Five other individuals now were diagnosed with PTSD. Those at risk for PTSD were not predicted by the severity of their injuries or the nature of the accident but only by the perceived threat to their lives. No consideration was given to the efforts of seeking financial compensation; the rate of recruitment was low (52 percent), and the measure of disability may have been inadequate.).
E. B. Blanchard et al., Effects of Litigation Settlements on Posttraumatic Stress Symptoms in Motor Vehicle Accident Victims, 11 J. Trauma Stress 337-54 (1998) (50 motor vehicle accident victims who sought medical treatment were referred or self-referred for the study. A control group of non-motor vehicle accident subjects was constituted (40 people). Forty-six percent had PTSD and 20 percent had sub-syndromal PTSD. Previous major depression seemed to predispose the formerly depressed individual to develop PTSD. The high rate of PTSD is probably the result of selection (referral bias). The authors instructed referral sources to refer all motor vehicle accident victims rather than just those evaluated as having psychological difficulties.).
E. B. Blanchard et al., The Impact of Severity of Physical Injury and Perception of Life Threat in the Development of Post-traumatic Stress Disorder in Motor Vehicle Accident Victims, 33 Behavior Res. & Therapy 529-34 (1995) (98 motor vehicle accident victims sought medical help within a week of the accident and were referred to the authors for evaluation by local doctors or through ads in the newspaper. The subjects were evaluated with a structured clinical interview (CAPS). Only the measure of life threat or fear of death significantly predicted PTSD. The extent of the injury is a significant predictor of PTSD, but it lacks specificity.).
E. B. Blanchard et al., Psychiatric Morbidity Associated with Motor Vehicle Accidents, 183 J. Nervous & Mental Disease 495-504 (1995) (This study used 158 adults who had been in a recent motor vehicle accident and sought medical attention within a week of the accident. Subjects were evaluated one to four months after the motor vehicle accident. Sixty-one percent of the sample did not have PTSD. Of the remainder, four variables significantly predicted PTSD: (1) a prior major depressive episode; (2) fear of dying in the motor vehicle accident; (3) the extent of injury, and (4) whether the motor vehicle accident victims had contacted a lawyer, but the direction of casualty is not known.).
R. A. Bryant et al., Initial Posttraumatic Stress Responses Following Motor Vehicle Accidents, 9 J. Trauma Stress 3-234 (1996) (This study used 114 subjects involved in motor vehicle accidents (82 men and 32 women) in whom posttraumatic responses were assessed using the Impact of Event Scale (which cannot diagnose PTSD over an eight-month period after the motor vehicle accident). 25 percent and 18 percent reported extreme and moderate intrusive symptoms, respectively, and 18 percent and 32 percent reported extreme and moderate avoidance symptoms, respectively. The severity of the accident was not disclosed or quantified.).
A. Y. Shalev et al., Predictors of PTSD in Injured Trauma Survivors: A Prospective Study, 153 Am. J. Psychiatry, 219-25 (1996) (61 individuals subjected to traumatic stressors participated in a prospective study on PTSD. 51 completed the study. Of the 51, 27 had been involved in recent motor vehicle accidents. The severity of the motor vehicle accidents was not specified. Of the 51, 13 (25.5 percent) developed PTSD (DSM-III-R) at six-month assessment. (The number of motor vehicle accident victims who developed PTSD was not identified.) The authors noted that trauma severity did not predict PTSD.).
E. B. Blanchard et al., Who Develops PTSD From Motor Vehicle Accidents?, 34 Behav. Res. & Therapy 1-10 (1996) (158 recent motor vehicle accident victims seeking medical attention (but not from the authors) were compared with 93 nonaccident controls. Structured clinical interviews were used by trained clinicians to assess psychiatric status. 62 individuals (39.2 percent) had PTSD (DSM-III-R) and 45 (28.5 percent) had subsyndromal PTSD. 51 (32.3 percent) had no psychological problems. A major limitation of this study is likely selection bias.).
K. Kuch et al., Posttraumatic Stress Disorder and Motor Vehicle Accidents: A Multidisciplinary Overview, 41 Can. J. Psychiatry 429-34 (1996) (This is a literature review of recent studies on prevalence, symptom profile, and outcome of PTSD. The authors remark that “functional complaints may be reinforced inadvertently by clinicians interested in [PTSD].” “A retrospective study of [the] ferry crew after the Herald of Free Enterprise disaster” disclosed that “three years after the accident, same crew members presented with symptoms of PTSD, who had had no direct contact with the disaster, with bereaved relatives, or with rescuers.”).
D. L. Delahanty et al., Acute and Chronic Distress and Posttraumatic Stress Disorder as a Function of Responsibility for Serious Motor Vehicle Accidents, 656 J. Clinical & Consulting Psychology 560-67 (1997) (subjects who felt responsible for the motor vehicle accident had lower rates of PTSD from the accident than did those who believed another was responsible for the accident).
A. G. Harvey & R. A. Bryant, The Relationship Between Acute Stress Disorder and Posttraumatic Stress Disorder: A Prospective Evaluation of Motor Vehicle Accident Survivors, 66 J. Consulting & Clinical Psychology 507-12 (1998) (a study designed to prospectively examine the relationship between acute dissociation, acute stress disorder (ASD), and PTSD in motor vehicle accident victims. 92 subjects involved in motor vehicle accidents who sought treatment at a hospital were assessed between 2 and 26 days post-trauma. Of the 92, 71 had a follow-up assessment six months post-trauma. On initial assessment, 13 percent had ASD and 20 percent had subclinical ASD. At six months, 25 percent had PTSD and 10 percent had subclinical PTSD. 22 percent of those with ASD initially did not have PTSD six months later. Acute dissociative symptoms are important precursors of long-term PTSD, but they are not sufficient to adequately identify those at risk of developing chronic PTSD. The ASD criteria performed better in predicting the absence of PTSD than in predicting its presence.).
A. G. Harvey & R. A. Bryant, The Relationship Between Acute Stress Disorder and Posttraumatic Stress Disorder: A Two-Year Prospective Evaluation, 67 J. Consulting & Clinical Psychology 985-88 (1999) (This is a two-year follow-up of the study described by Harvey et al. in 1998 in which 92 motor vehicle accident “survivors” were assessed within one month post-trauma and 11 were assessed six months post-trauma. In this current study, 56 were assessed two years post-trauma (a 61 percent retention rate). At the two-year follow-up, 63 percent with a diagnosis of ASD met the full criteria for PTSD. Of those participants with neither full nor subsyndromal ASD, 9 percent met the full criteria for PTSD. Symptoms that had a strong positive predictive power for developing chronic PTSD were emotional numbing, depersonalization, a sense of reliving the trauma, and motor restlessness. The authors note that the current ASD criteria are not optimal and not significantly superior to PTSD criteria in predicting chronic PTSD. The authors caution, however, that the conclusions from their findings cannot be generalized to other trauma populations.).
P. Stallard et al., Prospective Study of Post-traumatic Stress Disorder in Children Involved in Road Traffic Accidents, 317 Brit. Med. J. 1619-23 (1998) (119 children involved in motor vehicle accidents who had sought medical treatment were evaluated. 41 (34.5 percent) had PTSD. Neither the type of incident nor the nature and severity of physical injuries were related to the degree of psychological distress. Some of the children with PTSD were involved in minor accidents.).
K. A. H. Mirza et al., Post-traumatic Stress Disorder in Children and Adolescents Following Road Traffic Accidents, 172 Brit. J. Psychiatry 443-47 (1998) (119 children and adolescents between 8 and 16 years of age from emergency department of a hospital were evaluated for symptoms of PTSD at four weeks and six months. No control groups were established. Accident severity was not defined. But the degree of physical injury was measured. At four weeks, 23 percent had severe PTSD, 6 percent had moderate PTSD, and 19 percent had mild PTSD. At six months, 13 had severe PTSD, 2 individuals had moderate PTSD, and 4 had mild PTSD.).
E. B. Blanchard et al., Prediction of Remission of Acute Posttraumatic Stress Disorder in Motor Vehicle Accident Victims, 10 J. Traumatic Stress 215-34 (1997) (This is another “salami” publication using this research group’s 158 victims of motor vehicle accidents. The sample, predominantly women, was not randomly selected. A motor vehicle accident was defined arbitrarily as “serious” if the “victim” sought medical attention. (No well-recognized studies exist for quantifying the seriousness of a MVA.) PTSD was assessed using the criteria of the DSM-III-R measured by Clinician-Administered PTSD scale. On initial assessment, 62 had PTSD, 45 had “sub-syndromal” PTSD, and 51 had “non-PTSD.” Slightly over half with PTSD had remitted completely or partially by six months, or eight to ten months post-motor vehicle accident. Five percent of those with sub-syndromal PTSD developed PTSD at six months. A good proportion of the remission can be predicted with three classes of variables: (1) overall degree of severity of the symptoms at initial assessment; (2) aspects of the extent of physical injury and relative recovery from the injuries; and (3) whether a family member had experienced a new trauma during the six-month follow-up.).
E. B. Blanchard et al., Effects of Litigation Settlements on Posttraumatic Stress Symptoms in Motor Vehicle Accident Victims, 11 J. Trauma Stress 337-54 (1998) (158 victims of motor vehicle accidents (108 women and 50 men) who sought medical attention within 48 hours of the accident were assessed for PTSD one to four months after the accident (using the criteria of the DSM-III-R measured by the structured clinical interview for DSM-III-R) (another in a series of “salami” publications on PTSD by this group of researchers using the same sample of 158 victims of motor vehicle accidents). 132 subjects were followed 6 months and 12 months later. Of these, 67 had filed litigation and 65 had not filed litigation. 18 in the original group were minors, 13 of whom did not file litigation. Litigants had higher PTSD symptom scores measured by CAPS, showed higher levels of subjective distress, and were more impaired than nonlitigants. Litigants who had settled by the 12-month follow-up remained more psychologically distressed than those who never litigated, but did not have statistically significant differences in posttraumatic stress symptoms. Litigants who settled improved significantly on function but continued to have psychological distress. Litigants who settled within the year of follow-up were more severely injured than those who did not settle and those who did not litigate.).
D. Koren et al., Acute Stress Response and Posttraumatic Stress Disorder in Traffic Accident Victims: A One-Year Prospective, Follow-Up Study, 156 Am. J. Psychiatry 367-73 (1999) (99 motor vehicle accident victims and 21 non-motor vehicle accident controls were prospectively followed for one year. The motor vehicle accident group was recruited from orthopedic hospital wards with mild to moderate physical injury requiring hospitalization for at least two days, and the controls from those seeking elective surgery. The dropout rate at one year was 25 percent (25/99) for the motor vehicle accident group. At one year, 32 percent had PTSD. Assessment for PTSD was not made before this time, but assessment of “PTSD symptoms” (but not PTSD) was made one week after hospitalization. From this study, the authors reached several conclusions: (1) the PTSD diagnosis among traffic accident victims was not significantly associated with any of the accident-related characteristics, including severity of injury, objective responsibility, subjective sense of guilt, and initiation of litigation; (2) previous psychiatric morbidity, especially anxiety and affective disorders, was associated with chronic PTSD; (3) no association existed between PTSD and the major characteristics of the traumatic stressor; (4) symptoms stabilized about three months post-motor vehicle accident; so three months rather than one month might be a more appropriate cutoff for the transition from acute stress disorder to PTSD; (5) PTSD appears to be an abnormal response to traumatic events in predisposed individuals; (6) mildly injured individuals in motor vehicle accidents are at considerable risk for PTSD; and (7) DSM-III-R Scale for Severity of PTSD Symptomatology and Impact of Event Scale scores at three months were the best predictors of PTSD at one year.).
R. J. Ursano et al., Acute and Chronic Posttraumatic Stress Disorder in Motor Vehicle Accident Victims, 156 Am. J. Psychiatry 589-95 (1999) (This is purportedly the only systematic long-term prospective study using structured clinical interviews to examine motor vehicle accident-related PTSD in the general population. 122 subjects involved in a motor vehicle accident and 42 controls were followed for 12 months. The motor vehicle accident subjects were recruited from a metropolitan hospital (50 percent participation rate) and from police reports of “serious” motor vehicle accidents (25 percent participation rate). A “serious” motor vehicle accident was not defined. The controls recruited from emergency rooms were treated for minor injuries from non-motor vehicle accidents. Dropout rates were at six months 23 from motor vehicle accident group and at twelve months a total of 36 from the motor vehicle accident group, leaving 86 motor vehicle accident subjects remaining (about a 30 percent dropout rate). From the study, the authors reached several conclusions: (1) PTSD is a common outcome after a serious motor vehicle accident; after one month, 34.4 percent had PTSD; after three months, 25.2 percent had PTSD (defined as chronic PTSD in the DSM-IV); after six months, 18.2 percent had PTSD; after nine months, 17.6 percent had PTSD; and after 12 months, 14 percent had PTSD; (2) previous trauma was not a risk factor but previous PTSD was a risk factor for motor vehicle accident-related PTSD; (3) chronic PTSD may be more accurately diagnosed at six months than at three months; (4) women have nearly a five times greater risk for motor vehicle accident-related PTSD but not a greater risk for chronic PTSD; and (5) individuals with a history of a major anxiety disorder are more at risk for motor vehicle accident-related acute and chronic PTSD. Individuals with a history of major depression are more at risk for acute but not chronic motor vehicle accident-related PTSD.).
A. Ehlers et al., Psychological Predictors of Chronic Posttraumatic Stress Disorder After Motor Vehicle Accidents, 107 J. Abnormal Psychology 508-19 (1998) (967 patients recruited from an emergency room in an English hospital (67.1 percent of the total patients recruited) were assessed initially and at three months or initially at one year or initially at three months and at one year using DSM-IV criteria measured by the Posttraumatic Stress Symptom Scale; at three months 23.1 percent met DSM-IV criteria for PTSD, and at one year 16.5 percent met the criteria. About half the participants met the re-experiencing, hyperarousal, and disability criteria, but far fewer also met the avoidance and numbing criteria. 6.2 percent of those who did not have PTSD at three months had PTSD at one year. Injury severity was not significantly related to PTSD diagnosis; the greatest predictors of chronic or delayed-onset PTSD were persistent health problems and financial problems owing to the accident. Although not proposed by the authors as a reason for this correlation, the reason may be a function of compensation seeking.).
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189 W. Jake Jacobs & Constance Dalenberg, Subtle Presentations of Post-Traumatic Stress Disorder, 21 Psychiatric Clinics N. Am. 835-45 (1998).
190 W. Jake Jacobs & Constance Dalenberg, Subtle Presentations of Post-Traumatic Stress Disorder, 21 Psychiatric Clinics N. Am. 835, 843 (1998).
191 These studies reported a prevalence rate for all sexual abuse at about 28 percent for girls under age 14 and 38 percent for girls under age 18.
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192 Paul R. Silva et al., Stress and Vulnerability to Posttraumatic Stress Disorder in Children and Adolescents, 157 Am. J. Psychiatry 1229-35 (2000).
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