BODY KEEPS THE SCORE:
and the evolving psychobiology of post traumatic stress
Bessel van der Kolk
A. van der Kolk, MD.
Harvard Medical School
HRI Trauma Center
227 Babcock Street
Boston, MA 02146
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.
THE SYMPTOMATOLOGY OF 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
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
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
The failure to habituate to acoustic startle suggests that traumatized
people have difficulty evaluating sensory stimuli, and mobilizing...
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