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Memory and the evolving psychobiology of post traumatic stress

by Bessel van der Kolk

Bessel A. van der Kolk, MD.
Harvard Medical School
HRI Trauma Center
227 Babcock Street
Boston, MA 02146

The author wishes to thank Rita Fisler, Ed.M. for her editorial assistance.


For more than a century, ever since people's responses to overwhelming experiences were first systematically explored, it has been noted that the psychological effects of trauma are expressed as changes in the biological stress response. In 1889, Pierre Janet (1), postulated that intense emotional reactions make events traumatic by interfering with the integration of the experience into existing memory schemes. Intense emotions, Janet thought, cause memories of particular events to be dissociated from consciousness, and to be stored, instead, as visceral sensations (anxiety and panic), or as visual images (nightmares and flashbacks). Janet also observed that traumatized patients seemed to react to reminders of the trauma with emergency responses that had been relevant to the original threat, but that had no bearing on current experience. He noted that victims had trouble learning from experience: unable to put the trauma behind them, their energies were absorbed by keeping their emotions under control at the expense of paying attention to current exigencies. They became fixated upon the past, in some cases by being obsessed with the trauma, but more often by behaving and feeling like they were traumatized over and over again without being able to locate the origins of these feelings (2,3).

Freud also considered the tendency to stay fixated on the trauma to be biologically based: "After severe shock.. the dream life continually takes the patient back to the situation of his disaster from which he awakens with renewed terror.. the patient has undergone a physical fixation to the trauma"(4). Pavlov's investigations continued the tradition of explaining the effects of trauma as the result of lasting physiological alterations. He, and others employing his paradigm, coined the term "defensive reaction" for a cluster of innate reflexive responses to environmental threat (5). Many studies have shown how the response to potent environmental stimuli (unconditional stimuli-US) becomes a conditioned reaction. After repeated aversive stimulation, intrinsically non-threatening cues associated with the trauma (conditional stimuli-CS) become capable of eliciting the defensive reaction by themselves (conditional response-CR). A rape victim may respond to conditioned stimuli, such as the approach by an unknown man, as if she were about to be raped again, and experience panic. Pavlov also pointed out that individual differences in temperament accounted for the diversity of long term adaptations to trauma.

Abraham Kardiner(6), who first systematically defined posttraumatic stress for American audiences, noted that sufferers from "traumatic neuroses" develop an enduring vigilance for and sensitivity to environmental threat, and stated that "the nucleus of the neurosis is a physioneurosis. This is present on the battlefield and during the entire process of organization; it outlives every intermediary accommodative device, and persists in the chronic forms. The traumatic syndrome is ever present and unchanged". In "Men under Stress", Grinker and Spiegel (7) catalogue the physical symptoms of soldiers in acute posttraumatic states: flexor changes in posture, hyperkinesis, "violently propulsive gait", tremor at rest, masklike facies, cogwheel rigidity, gastric distress, urinary incontinence, mutism, and a violent startle reflex. They noted the similarity between many of these symptoms and those of diseases of the extrapyramidal motor system. Today we can understand them as the result of stimulation of biological systems, particularly of ascending amine projections. Contemporary research on the biology of PTSD, generally uninformed by this earlier research, confirms that there are persistent and profound alterations in stress hormones secretion and memory processing in people with PTSD.


Starting with Kardiner(6), and closely followed by Lindemann (8), a vast literature on combat trauma, crimes, rape, kidnapping, natural disasters, accidents and imprisonment have shown that the trauma response is bimodal: hypermnesia, hyper-reactivity to stimuli and traumatic reexperiencing coexist with psychic numbing, avoidance, amnesia and anhedonia (9,10,11,12). These responses to extreme experiences are so consistent across traumatic stimuli that this biphasic reaction appears to be the normative response to any overwhelming and uncontrollable experience. In many people who have undergone severe stress, the post-traumatic response fades over time, while it persists in others. Much work remains to be done to spell out issues of resilience and vulnerability, but magnitude of exposure, prior trauma, and social support appear to be the three most significant predictors for developing chronic PTSD (13,14).

In an apparent attempt to compensate for chronic hyperarousal, traumatized people seem to shut down: on a behavioral level, by avoiding stimuli reminiscent of the trauma; on a psychobiological level, by emotional numbing, which extends to both trauma-related, and everyday experience (15). Thus, people with chronic PTSD tend to suffer from numbing of responsiveness to the environment, punctuated by intermittent hyperarousal in response to conditional traumatic stimuli. However, as Pitman has pointed out (16), in PTSD, the stimuli that precipitate emergency responses may not be conditional enough: many triggers not directly related to the traumatic experience may precipitate extreme reactions. Thus, people with PTSD suffer both from generalized hyperarousal and from physiological emergency reactions to specific reminders(9,10) The loss of affective modulation that is so central in PTSD mayhelp explain the observation that traumatized people lose the capacity to utilize affect states as signals (18). Instead of using feelings as cues to attend to incoming information, in people with PTSD arousal is likely to precipitate flight or fight reactions (19). Thus, they are prone to go immediately from stimulus to response without making the necessary psychological assessment of the meaning of what is going on. This makes them prone to freeze, or, alternatively, to overreact and intimidate others in response to minor provocations (12,20).


Abnormal psychophysiological responses in PTSD have been demonstrated on two different levels: 1) in response to specific reminders of the trauma and 2) in response to intense, but neutral stimuli, such as acoustic startle. The first paradigm implies heightened physiological arousal to sounds, images, and thoughts related to specific traumatic incidents. A large number of studies have confirmed that traumatized individuals respond to such stimuli with significant conditioned autonomic reactions, such as heart rate, skin conductance and blood pressure (20,21,22,23, 24,25). The highly elevated physiological responses that accompany the recall of traumatic experiences that happened years, and sometimes decades before, illustrate the intensity and timelessness with which traumatic memories continue to affect current experience (3,16). This phenomenon has generally been understood in the light of Peter Lang's work (26) which shows that emotionally laden imagery correlates with measurable autonomic responses. Lang has proposed that emotional memories are stored as "associative networks", that are activated when a person is confronted with situations that stimulate a sufficient number of elements that make up these networks. One significant measure of treatment outcome that has become widely accepted in recent years is a decrease in physiological arousal in response to imagery related to the trauma (27). However, Shalev et al (28) have shown that desensitization to specific trauma-related mental images does not necessarily generalize to recollections of other traumatic events, as well.

Kolb (29) was the first to propose that excessive stimulation of the CNS at the time of the trauma may result in permanent neuronal changes that have a negative effect on learning, habituation, and stimulus discrimination. These neuronal changes would not depend on actual exposure to reminders of the trauma for expression. The abnormal startle response characteristic of PTSD (10) exemplifies such neuronal changes.

Despite the fact that an abnormal acoustic startle response (ASR) has been seen as a cardinal feature of the trauma response for over half a century, systematic explorations of the ASR in PTSD have just begun. The ASR consists of a characteristic sequence of muscular and autonomic responses elicited by sudden and intense stimuli (30,31). The neuronal pathways involved consist of only a small number of mediating synapses between the receptor and effector and a large projection to brain areas responsible for CNS activation and stimulus evaluation (31). The ASR is mediated by excitatory amino acids such as glutamate and aspartate and is modulated by a variety of neurotransmitters and second messengers at both the spinal and supraspinal level (32). Habituation of the ASR in normals occurs after 3 to 5 presentations (30).

Several studies have demonstrated abnormalities in habituation to the ASR in PTSD (33,34,35,36). Shalev et al (33) found a failure to habituate both to CNS and ANS-mediated responses to ASR in 93% of the PTSD group, compared with 22% of the control subjects. Interestingly, people who previously met criteria for PTSD, but no longer do so now, continue to show failure of habituation of the ASR (van der Kolk et al, unpublished data; Pitman et al, unpublished data), which raises the question whether abnormal habituation to acoustic startle is a marker of, or a vulnerability factor for developing PTSD.

The failure to habituate to acoustic startle suggests that traumatized people have difficulty evaluating sensory stimuli, and mobilizing...


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