Special Articles

A Neuropsychological Hypothesis Explaining

Posttraumatic Stress Disorders

Lawrence C. Koib, M.D.

minants or early traumatic experiences? In short, are

The author reports findings from recent the phenomena of the stress disorders only reflections
psychophysiological and biochemical research on of psychological processing of information signifying
Vietnam combat veterans with chronic posttraumatic existential threat, or are they representative of other
stress disorder. Applying these data and the analogy (possibly preceding) psychopathological and/or neural
of the known functional and structural defects in the changes?
peripheral (cranial) sensory system consequent to
high-intensity stimulation, he hypothesizes that
cortical neuronal and synaptic changes occur in RECENT CLINICAL OBSERVATIONS
posttraumatic stress disorder as the consequence of
excessive and prolonged sensitizing stimulation It is my work over the past 9 years with men who
leading to depression of habituating learning. He have come to suffer the severe forms of chronic
postulates that the “constant” symptoms of the posttraumatic stress disorder that I shall report in this
disorder are due to the changes in the agonistic paper. Due to my World War II clinical experiences in
neuronal system which impair cortical control of diagnosis and treatment of patients with acute combat-
hindbrain structures concerned with aggressive induced posttraumatic stress disorders, it was possible
expression and the sleep-dream cycle. for me to quickly recognize the chronic and delayed
(Am J Psychiatry 1987; 144:989-995) forms of these disorders in many hospitalized men.
The data to be reported here come from personal
examination and engagement in treatment of more
C ontroversy continues to rage over the posttrau- than 300 Vietnam veterans with chronic or delayed
matic stress disorders. Are the symptoms evidence posttraumatic stress disorder, 10 prisoners of war of
only of a consistent process set in motion following World War II, and a sizable number of patients whose
any major threat to one’s security? Does the condition chronic and delayed posttraumatic stress disorder
merit consideration as a clinical entity to be classified from the Korean and World War II conflicts had been
separately in our diagnostic scheme? Are the stress missed-as well as many noncombatant Vietnam-era
disorders merely variants of other personality disor- veterans without posttraumatic stress disorder in hos-
ders? Is massive psychological trauma the etiologic pital in- and outpatient services. The majority of these
agent? May the condition be induced in adulthood patients had experienced long and high-level combat
without preceding genetic and/or constitutional deter- exposure. My impression is that the more disabled
patients, with predominantly dissociative, “catete-
noid,” or psychosomatic symptoms, have come or
Presented in part at the 138th annual meeting of the American
Psychiatric Association, Dallas, May 18-24, 1985. Received July 22,
have been brought to the hospital services for years.
1985; revised June 6 and Sept. 8, 1986; accepted Nov. 3, 1986. Among the earlier and more severely disturbed
From the Department of Psychiatry, Veterans Administration Mcd- patients were a number of men with socially impairing
ical Center, and the Department of Psychiatry, Albany Medical
dissociative states (flashbacks) or panic attacks. Many
College, Albany, N.Y. Address reprint requests to Dr. Kolb, Depart-
indicated the persistence of a startle reaction with
ment of Psychiatry, VA Medical Center, 1 13 Holland Ave., Albany,
NY 12208. associated physiological arousal on exposure to sharp
Supported by NIMH grant MH-37839. sounds produced by helicopters or other explosive

Am ] Psychiatry 1 44:8, August 1987 989

NEUROPSYCHOLOGICAL HYPOTHESIS

noises. When pushed to describe their combat experi- with and four without psychiatric disorders), 1 1 same-
ence, these men often provided sketchy accounts with- aged university students, and 14 civilians with other
out associated affect. anxiety disorders. Since that study, Blanchard et al. (3)
For 18 of these patients, treatment using a modified have examined a total of 91 combat veterans-57 with
form of narcosynthesis directed at verifying the exist- and 34 without posttraumatic stress disorder.
ence of repressed emotion was initiated to provide All participants took the following psychological
emotional “de-repression.” An audiovisual recording tests: State-Trait Anxiety Inventory, Beck Depression
of these patients’ behavior during the treatment was Inventory, and Buss-Durkee Hostility Scale (2). The
made to be used as confrontation in later psychother- veterans scored significantly (p<.OO1) higher than
apy. The narcosynthetic technique was also modified control subjects on all measures, indicating more pa-
to test the existence of a conditioned emotional re- thology.
sponse. Rather than verbal suggestion, which was used The physiological data analyzed to date have yielded
in treatment of severely, acutely disturbed patients the most interesting findings. Analyses of the six
during World War II, each patient was exposed to a physiological responses revealed three statistically sig-
brief train of combat sounds as the initiating stimulus nificant (p<.OO1) differences between the veterans
for abreaction. with posttraumatic stress disorder and the control
Fourteen of the 1 8 men exposed to a moderate- subjects: heart rate, systolic blood pressure, and dias-
intensity combat sound stimulus of 30 seconds while in tolic blood pressure. In each instance the veterans with
arousable pentobarbital anesthesia immediately re- posttraumatic stress disorder showed more arousal in
sponded with time regression and reenacted a Vietnam response to the combat sounds than did the control
combat experience with intense emotional abreaction subjects. The arousal of many men was so distressing
of the affects of fear, rage, indignation, sadness, and personally that they terminated the experiment at low
guilt. No responses were elicited by musical stimuli or levels of sound intensity. The later study (3), using a
by silence, and two noncombat veterans exposed to the single cutoff rate for highest heart rate response fol-
sound train also failed to abreact. The characteristics lowing exposure to combat sounds, found that heart
of this group of men and their responses have been rate response alone accurately identified 40 (70.2%) of
described in some detail elsewhere (1). The emotion- the 57 combat veterans with posttraumatic stress
ality was so evident during abreaction that an effort disorder and 30 (88.2%) of the 34 combat veterans
was made to monitor various physiological systems. without posttraumatic stress disorder. Using this cutoff
No clear-cut abnormalities were discovered in the resulted in only six false-positives among the 34 vet-
subnarcotic state, presumably because the injected erans without the disorder. Four of these false-posi-
drug obscured related organ responses during the tives would have met the diagnostic criteria for
emotional storm. posttraumatic stress disorder in the past and were
therefore considered clinically remitted. Further anal-
ysis using the other physiological measures is now
RECENT PSYCHOPHYSIOLOGICAL RESEARCH underway in this group of veterans.
There are two other reports of psychophysiological
To examine the hypothesis that autonomic arousal assessment of combat veterans with chronic posttrau-
did indeed occur following the startle reactions on matic stress disorder. Dobbs and Wilson (4) compared
exposure to a meaningful sound stimulus reminiscent the psychophysiological responsivity to audiovisual
of combat, I initiated a collaborative study with Prof. stimuli of two groups of World War II veterans with
Edward Blanchard of the Stress Laboratory of the the chronic posttraumatic stress disorder of combat
State University of New York at Albany. Initially, he (13 men considered socially compensated and eight
and his colleagues, Thomas Pallmeyer and Robert men considered socially decompensated some 10 years
Gerardi, exposed 12 combat veterans who met the after their war experiences) with that of a group of 10
operational criteria of DSM-III for posttraumatic noncombatant university students. Increases in pulse
stress disorder to a train of combat sounds of varying and respiratory rate as well as a decrease in alpha
intensity given at varying times and interspersed with rhythm occurred in the vast majority of the combat
periods of music and silence (2). The veterans were in veterans when exposed to the audiovisual stimuli but
a fully conscious state, and their diastolic and systolic not in the control group. Many of the men in the
blood pressure, heart rate, finger-tip skin temperature, socially decompensated group were unable to corn-
and galvanic skin reflex were monitored. In addition to plete the test, leaving the experimental setting before
the combat sounds, the subjects were also exposed to the sound stimulation was completed.
an arousal sound. They were also given an intellectual Malloy et a!. (5) compared the physiological re-
stress test and a variety of standardized psychological sponses of 10 Vietnam combat veterans with posttrau-
tests. Their responses to these instruments were corn- matic stress disorder, 10 noncombat veteran control
pared with those of control subjects tested in precisely subjects, and 10 psychiatric inpatients without post-
the same manner. The control groups consisted of 10 traumatic stress disorder. As stimuli they presented
Vietnam combat veterans without posttraumatic stress both combat-related and noncombat audiovisual
disorder, 16 Vietnam-era noncombat veterans (12 scenes.

990 Am J Psychiatry 144:8, August 1987

 LAWRENCE C. KOLB

Physiologically, during exposure to the combat intensities), none was able to do so without arousing
stress scenes the veterans with posttraumatic stress somatic responses. One, angered at his failures, played
disorder showed an increase in heart rate and skin the tape at high intensity on his sound system, disso-
resistance; these increases did not occur in either group ciated cognitively, and in a violent rage tore apart his
of control subjects. Multivariate analyses of the van- workroom. Beyond that, the long-term follow-up of
ous physiological, behavioral, and self-report observa- patients in continuing treatment has demonstrated
tions successfully discriminated all of the Vietnam time and again the recrudescence of the constant
combat veterans with posttraumatic stress disorder symptoms of the condition, as defined by Kardiner and
from all of the control subjects. Spiegel (9). These symptoms arise in the face of either
To summarize, three entirely independent and unre- a current stressful life event involving threat or loss-
lated studies of American combat veterans from two arousing once again emotions of terror, sadness, or
wars with the clinical symptoms of posttraumatic anger-or a threat to the individual’s own body by acute
stress disorder exhibited more abnormal behavioral illness or an accident. On exposure to such stimuli,
and physiological arousal than control subjects from a patients with posttraumatic stress disorder respond
variety of groups when exposed to meaningful stimuli with immediate and excessive physiological arousal,
reminiscent of combat (6). Thus, psychophysiological particularly in their cardiovascular and neuromuscular
assessment offers strong potential not only for diag- systems, and are at risk for cognitive dissociation.
nostic identification of a special subgroup of patients We have, then, a clinical condition induced by either
with war-induced posttraumatic stress disorder but a single massive psychological assault or by recurrent
also for assessment of the severity of the disorder. The or continued exposure to experiences associated with
total number of subjects with posttraumatic stress violent death, destruction, and/or mutilation of others,
disorder now tested from the three studies equals 88, which induce high-intensity emotional arousal. The
and the number of control subjects is now 64. emotions of fear, terror, and helpless despair are
followed by a number of constant yet repetitive behav-
ioral, cognitive, and physiological processes. In many,
SIGNIFICANCE OF FINDINGS withdrawal from exposure, nonrecurrence of expo-
sure, or avoidance of memory-arousing experiences
These findings define a subgroup of combat veterans similar to the initial stressing events is followed by
with chronic, delayed, or remitted forms of posttrau- extinction of these phenomena. In some the extinction
matic stress disorder who have a persisting condi- is only partial; somatic arousal still may be observed
tioned emotional response to stimuli reminiscent of when the gross clinical symptoms have remitted. Other
battle. We may postulate that in such men there exists patients go on to suffer delayed, recurrent, or persist-
not only an ongoing perceptual abnormality (impair- ent display of the consequences of the overwhelming
ment of the ability to discriminate specific sensory emotional assault. I emphasize “emotional” and not
inputs associated with the traumatic event) but also “psychological.” Emotion implies stimulus facilita-
excessive autonomic arousal of central adrenergic or- tion. Depending on the intensity of stimulation, it may
igin. facilitate or destroy cognitive processing. Among those
Two other research studies suggested abnormal who fail to recover from the initial assault are a group
physiological functioning in posttraumatic stress dis- who suffer recurrent or persistent clinical symptoms
order. Wenger (7) carried out extensive psychophysi- and demonstrate evidence of a conditioned emotional
ological testing to examine the assumption that differ- response.
ences in autonomic balance existed between 298
World War II combat flyers convalescing from what
was then designated in the Air Force as “operational CONDITIONED FEAR IN ANIMALS
fatigue” and 482 aviation students in training who had
not yet been to combat. He recorded without stimula- Much has been learned about conditioned fear in
tion 20 different tests of autonomic function and found animals that seems directly relevant here. Directly
that nine attained differential statistical significance pertinent to chronic posttraumatic stress disorder are
and supported his hypothesis that excessive sympa- the studies of Anderson and Parmenter (10) of the
thetic function is characteristic of operational fatigue. long-term effects of experimentally induced neurosis in
Mason et a!. (8) reported on separating out neuro- animals. These researchers followed both sheep and
chemically a group of nine men with posttraumatic dogs over 12 years after induction of experimental
stress disorder and depression from 10 others with neuroses in which electric shock was used as the
major depressive disorders. The former had unusually unconditional stimulus and the sound of a metronome
high urine levels of norepinephnine as well as a dis- was used as the conditioning stimulus. The long-term
criminating norepinephrine-cortisol ratio. behavioral and physiological hyperactivity of these
Pertinent here are some clinical observations re- animals was remarkably similar to that noted in the
ported in a paper cited earlier (6). Of seven men whom chronic posttraumatic stress disorder of combat veter-
I had instructed to use a tape of combat sounds for ans with conditioned emotional response. This hyper-
desensitization (initially to be played at subliminal activity included hyperalertness to touch, the startle

Am ] Psychiatry 1 44:8, August 1987 991

NEUROPSYCHOLOGICAL HYPOTHESIS

reaction to sound (crouching, trembling, running, and out gross neunoanatomical rearrangement. Kandel’s
even defecation), a “set” toward overreaction, gener- sensitization experiments have not been carried to the
alization of the reaction to other stimuli, and restless- point of excessive stimulation oven long periods of
ness. Some animals later developed a state of immo- time.
bility when placed in the experimental room, as Reiser (14) recognized the relationship between the
though they were afraid to move. Also noted in these new neurobiological understandings and psychological
animals over a period of years was continued cardiac processing and illustrated this in an analysis of a
and respiratory dysfunctions. Tachycardia occurred typical case of social stress. My clinical and research
when the animals were brought to the laboratory. data derive from the consequence of overwhelming,
In their work on traumatic avoidance learning in often repeated catastrophic stress. Such stress requires
animals, Solomon and Wynne (11) stated, “In the case that we go beyond the ordinary learning experiences or
of intense anxiety established with the support of an their absence and examine the consequences of exces-
initial pain-fear reaction, we believe that the classically sive sensitizing stimulation on the neural structure.
conditioned responses have become incapable of corn-
plete extinction.” Further, they postulated a relatively
permanent “decreased threshold phenomenon or sen- NEURONAL EFFECTS OF HIGH-INTENSITY
sitization phenomenon,” which leads to “an increase STIMULATION
in probability of occurrence.”
That environmental experiences provide the sensory That excessive external stimulation might affect
stimulation on which both functional and anatomical neuronal structure has been postulated in the past.
development of the brain depends is now cleanly Freud (15) described a “stimulus barrier” consisting of
evident from neurobiological research. These findings a series of neunoanatomical structures-including the
became possible only through the advances in electro- skin, the peripheral sense organs, and an internalized
physiological, neurochemical, and imaging techniques. neuronal layer-developed to protect organisms from
For instance, Hubel and Wiesel (12) demonstrated that excessive and destructive external stimulation. Miller
the visual cortex (area 17) of both cats and macaque (16) brought together the physiological and psycholog-
monkeys fails to develop physiologically if they are ical data pertaining to excessive stimulation under the
deprived of monocular vision at critical periods of rubric of overload of information processing. In gen-
early life. Neurons from the opposite geniculate nu- era!, the data indicate that as information input in-
cleus tend to grow into visually deprived and undevel- creases, information output initially increases but
oped columns of cortical dominance. These findings gradually falls behind at the level of channel capacity.
suggested to the researchers that a form of competitive With further increases in input, output decreases to
interaction takes place between the neuronal growth of complete nonfunction and psychological confusional
the two opposing visual pathways. Stimuli from the states occur. Before that, a variety of efforts at adap-
eye not deprived of vision induce electrophysiological tation to overload take place; these are evident in
activity in the maldeveloped area. These maldevelop- obvious errors, omissions, etc. Possible central neuno-
ments were confirmed neuroanatomically by autora- nal structural (neuroanatomical) change as the result
diographic techniques. of such overload has not been studied.
Studies of learning processes in the simple nervous Nevertheless, both clinical and laboratory data exist
system of the snail Aplysia californica by Kandel (13) that demonstrate both functional and structural
have made it clear that synaptic function changes change following high-intensity stimulation of the
depending on the nature of the learning process. Thus, peripheral nervous system. The known consequences
during habituation of the gill reflex of Aplysia, when of such stimulation for the acoustic system provide an
the animal learns “to recognize and ignore a particular excellent model to conceptualize central neunonal
stimulus because its consequences are trivial” (a prim- change. Clinical observations (17, 18) have established
itive form of perception), many synaptic connections that such stimulation-either remittent on of long
become inactive without the intervention of revenber- duration-causes deafness of varying types and duna-
ating circuits as in a closed set of neurons. Kandel’s tion. Clinically, such loss of function may occur
studies on sensitization learning are particularly rele- acutely, may be temporary, or may be permanent;
vant to questions related to posttraumatic stress disor- these outcomes relate to both the intensity and the
den. Sensitization enhances the animal’s attention to duration of the sound stimulation. Thus, volunteers
threatening stimuli. It involves postsynaptic facilita- exposed to 1 10 to 130 decibels for periods of 1 to 64
tion mediated by axo-axonic synapses. If habituation minutes consistently develop temporary high-tone
has been achieved, sensitization reverses the presynap- hearing loss. In animal experimental studies of induced
tic and behavioral depression produced by either noise deafness after excessive sound stimulation, light
short- on long-term learning. Although change is evi- microscopy has demonstrated initial changes in the
dent electrophysiologically, it is not now fully under- external hair cells in the form of deformation of
stood what occurs at the synaptic terminals during the swelling of the cell body. With more severe injuries,
learning process. Kandel suggested that neurochemi- other cells (pillar, Deitens’ and Hensen’s), including the
cal changes must occur at synaptic connections with- internal hair cells, are damaged, and eventual cochlean

992 Am J Psychiatry 144:8, August 1987

 LAWRENCE C. KOLB

neuronal atrophy ensues. A variety of neunonal bio- ogy to explain posttraumatic stness disorder psychopa-
chemical changes have also been identified as follow- thology. Their two-factor theory relies both on symp-
ing the stimulus trauma. From these studies it has been tom explanation through classical conditioning
suggested that moderate intensities of acoustic stimu- (through association a fear response is learned) as well
lation lead to increased metabolic activity. If excessive, as on instrumental learning principles (individuals
the changes proceed to exhaustion of enzymes and learn to avoid cues that arouse emotion). This hypoth-
glycogen stones, diminished oxygen tension, decreased esis accounts for the startle reaction in posttnaumatic
energy output, irreversible anatomical change, and stress disorder as well as its arousal by a variety of
permanent deafness. stimuli that the individual has associated with the
The emerging evidence of the existence of psycho- traumatic event-sounds, smells, and a wide variety of
physiological, neuroendocnine, and neunochemical ab- visual perceptions, including people. Keane et a!. nec-
nonmalities in chronic posttraumatic stress disorder ognized that posttraumatic stress disorder victims dis-
outruns the potential of the current psychological play a much widen range of symptoms in that they
explanations derived from psychoanalytic on learning respond to other crises not associated with the event.
theories. Confronted with the phenomenology of acute To explain this phenomenon, they invoked higher-
cases of wan neuroses, Freud (19) stated, “The wan onden conditioning and generalization for those symp-
neuroses insofar as they ane distinguished from the toms not definable by their two-factor theory. I have
ordinary neuroses of peacetime by special chanactenis- discussed and critiqued these various explanations in a
tics are to be regarded as traumatic neuroses whose paper presented during a National Institute of Mental
occurrence has been made possible by a conflict in the Health workshop on delayed effects of posttraumatic
ego.” The conflict was perceived as occurring between stress disorders held in April 1986.
the individual’s striving to maintain his moral integrity
as a soldier against the drive for self-preservation. The
breakdown was perceived as due to the overwhelming A NEUROPSYCHOLOGICAL HYPOTHESIS
of the psychological defensive structure of the exposed.
Plagued by the challenge to both dream and libido Using the analogy of the effect of excessive stimula-
theory in the face of the repetitive dreams and night- tion on the contact barrier leading to change in
mares of combat, psychoanalysts later offered the drive neunonal function and/on structure, we can easily
for mastery through repetition as an explanation for accommodate the symptoms and signs of posttraumat-
these symptoms as well as for related neurotic and ic stress disorder within traditional neunopsychological
chanacterological changes (20). theory (22). The primary result of excessive emotional
From their examination of many patients with stimulation is its effect on the function and perhaps the
chronic war neurosis from World Wan I, Kandiner and structure of the cortical neunonal barrier, particularly
Spiegel (9) came to the conclusion that the condition as it concerns control of aggnessivity. Such stimulus
was a “physioneunosis.” They suggested that the star- overload occurs when the human organism’s capacity
tie reaction seen in the patients with chronic neurosis to process information signaling threat to life oven-
was due to “conditioning” and that the existence of whelms the cortical defensive structural processes con-
this pattern was central to understanding patients with cenned with perceptual discrimination and effective
chronic disorders as the cause of the irritability and the adaptive responses for survival. Such stimulation may
psychosomatic symptoms. To them, the chronic war be thought to first lead to synaptic changes related to
neurosis was different from social neurosis in that the the process of neunophysiological sensitization, as de-
central focus of distress in the former nested in the scnibed by Kandel (13). If continued at high intensity
individual’s difficulty with his body image-his so- and repeated frequently over time, the processes may
matic functioning-and not with social conflict. The lead to depnession of those synaptic processes which
personality reactions were considered secondary and permit habituation and thus discriminative perception
reactive to the physioneurosis. This hypothesis more and learning. As Kandel has suggested, subtle
satisfactorily covers most of the criteria needed to neunochemical changes may occur in synaptic func-
explain the observed symptoms than do others. tions that currently defy detection by available meth-
Dobbs and Wilson (4) concluded that there existed ods. We cannot exclude the potential of actual
“remarkable similarity of the behavioral and physio- neuronal death. Sapolsky et a!. (23) reported hip-
logical responses of the war neuroses to those pro- pocampal neunonal death in cells with high glucocon-
duced experimentally in animals through condition- ticoid receptors-interpreted as the result of response
ing.” They suggested that sounds and sights simulating to stress oven time.
those of combat serve as conditioned stimuli to induce The neunonal synaptic structures affected are prob-
the self-preservative emotional responses of fight, ably located in the temponal-amygdaloid complex con-
flight, or paralysis, which become the conditioned cenned with agonistic behavior; these structures are
responses. They did not attempt to explain the coex- stressed by necunnent intensive stimulation. They may
isting personality reactions of their patients. recover, be temporarily impaired, or undergo perma-
Elaborating on this hypothesis, Keane et a!. (21) nent change, which is known to occur in the peripheral
offered a two-factor learning theory of psychopathol- (acoustic) sensory system.

Am J Psychiatry 144:8, August 1987 993

NEUROPSYCHOLOGICAL HYPOTHESIS

In terms of clinical expression in behavior, the cal expressions of the startle reaction or conditioned
individual reverts (regresses) to a state of hypensensi- emotional response-expressed subjectively as palpita-
tivity in which a multitude of stimuli, both internal and tions, panic attacks, and other pains, including head-
external, lead to arousal. Recurrent intensive emo- ache, nausea, vomiting, and diarrhea.
tional arousal both sensitizes further and simulta- “Delay,” intensification of symptoms, and dissocia-
neously disrupts those processes related to learning tion may be recognized as expressions of primary
and habituation. This leads to reappearance or inten- cortical functional impairment. Each successive anous-
sification of existing symptoms. al of aggressive emotion by exposure to external
With excessive cortical sensitization and diminished stimuli or social incidents arousing the traumatic com-
capacity for habituation of the agonistic neunonal plex, if intense enough to overwhelm the central
system, lower brainstem structures, such as the medial controls, leads to activation of the lower centers,
hypothalamic nuclei and the locus ceruleus, activated which in turn reactivates the cortical areas related to
by the neurotransmitter norepinephnine (24), escape emotions and memory. Highly intense arousal, as in
from inhibitory cortical control. Through their exten- terror, widely disrupts cognitive functioning and pro-
sive cortical and subcortical connections, they, in turn, duces dissociative behaviors.
repeatedly reactivate the perceptual, cognitive, affec- It is the inescapable recurrence of the physiological
tive, and somatic clinical expressions related to the disturbance that affects personality organization and
original traumata. Thus, in the face of perceived stability. The repeated reminders of the traumatic
threats there occurs excessive sympathetic arousal- event associated with somatic symptoms disrupt the
including neuroendocrine disturbances as well as be- sufferer’s body image and self-concept. Subsequent
havioral expressions of rage and irritability and repet- cognitive processing induces the reactive symptoms,
itive cortical reactivation of memories related to the which present as various avoidance behaviors and a
traumatic events. The latter are projected in the day- chronic dysphonic-anxious state. Thus, one sees avoid-
time as intrusive thoughts and at nighttime in the ance behaviors such as social withdrawal, distancing
recurrent traumatic nightmares of posttraumatic stress from others, alcohol and drug abuse, or compulsive
disorder in all forms. The “constant symptoms” of activities (including work) and affective disturbances
posttraumatic stress disorder, then, are explainable as (depression, survival guilt, and shame with suicidal
expressive of cortical synaptic change related to those ideation). These symptoms cause diagnostic difficulty
processes which underlie sensitization, learning, and only when examiners fail to probe for the primary
habituation. symptoms mentioned heretofore in this paper.
It may well be that other central neuronal changes Additional intrapsychic attempts lead to restitutive
occur that underlie certain other features of chronic symptoms and behaviors as the individual recognizes
posttraumatic stress disorder. Hoppe and Bogen (25) his deficiencies in social relations due to loss or fear of
have likened the alexithymia of commissurotomized loss of control of aggressive behavior. In conflict, he
patients to that of survivors of the Nazi concentration musters up whatever personality resources and psy-
camps (chronic posttraumatic stress disorder) and chological defenses are available to him. The sufferers
psychosomatic patients. are often thought to have a personality disorder. Lindy
The hypothesis presented here of functional change and Titchenen (26) emphasized that character change
in neuronal and synaptic cortical processing of intense is to be expected after exposure to overwhelming
memories of aversive stimulation allows an under- personal disasters.
standing of the variegated symptom expressions of the As for predisposition to develop the chronic form of
condition. We may define the symptoms of posttrau- posttraumatic stress disorder and its variable impair-
matic stress disorder as 1) impaired perceptual, cogni- ment of psychosocial functioning, I now classify all
tive, and affective functions, 2) release of functions, 3) patients as having severe, moderate, on mild forms of
reactive affective states and avoidance behaviors, and the disorder. These classifications depend on the num-
4) restitutive symptoms and behaviors. ben of symptoms, their expression, and evidence of the
The primary symptoms, due to cortical neuronal conditioned emotional response as well as the poten-
change, are those of impairment of perceptual discnim- tial for later intensification of symptom expression on
ination, lessened capacity to control agonistic im- re-exposure to emotional stress. If change has occurred
pulses, and, perhaps, affective blunting. Discnimina- through excessive stimulation, future processing of
tion of threatening stimuli is less accurate, as such messages will vary according to the extent of
demonstrated in the increased sensitivity to a multi- sensitizing change brought about by the excessive
tude of external cues associated by conditioning to the traumatic stimulation as well as the number of acti-
threatening traumatic incident or incidents. vated neurons available.
The symptoms of release, due to excessive activation Younger persons are said to be more susceptible to
of hindbrain centers, are the “constant” symptoms of the development of posttnaumatic stress disorder. They
the condition. These are the startle reaction (condi- have had less experience and therefore, perhaps, less
tioned emotional response), irritability, hypenalertness, neunonal activation. Olden persons, who are also more
intrusive thinking, repetitive fearful nightmares and susceptible, are already undergoing neuronal inactiva-
dreams of the event, and the various psychophysiologi- tion. As for the reported greater resistance of military

994 Am J Psychiatry 144:8, August 1987

 LAWRENCE C. KOLB

officers to developing posttnaumatic stress disorder, we 5. Malloy PF, Fairbank JA, Keane TM: Validation of a
multimethod assessment of post-traumatic stress disorders in
may presume that their neuronal network is numeni-
Vietnam veterans. J Consult Clin Psychol 1983; 51:488-494
cally larger than that of nonofficers and, through
6. Kolb LC: The post traumatic stress disorders of combat: a
education and diverse experiences, better evolved and subgroup with a conditioned emotional response. Milit Med
integrated and therefore more flexible. Persons who 1984; 149:237-243
have been emotionally traumatized early in life may be 7. Wenger MA: Studies in Autonomic Balance in Army-Air Force
thought to be at risk for breakdown, depending on the Personnel: Comparative Psychological Monograph. Berkeley,
intensity and duration of the early life-threatening University of California Press, 1948

experience. My clinical experience is that surviving 8. Mason J, Giller EL, Kosten TR, et al: Elevated norepinephrine/
cortisol ratio in PTSD, in New Research Program and Abstracts,
men who developed symptoms on the combat line and
138th Annual Meeting of the American Psychiatric Association.
were returned to duty only to collapse later have ended Washington, DC, APA, 1985
up with the most severe pathology-the “catetenoid” 9. Kardiner A, Spiegel H: The Traumatic Neuroses of War. New
states. On the other hand, healthy soldiers who have York, Paul Hoeber, 1947
been sensitized to exposure to emotional suffering by 10. Anderson OD, Parmenter R: Long-Term Study of the Experi-
mental Neurosis in the Sheep and Dog: With Nine Case
their near catastrophic experience often develop adap-
Histories. Psychosomatic Medicine Monograph 2(3,4), 1941
tive social behaviors; their capacity for empathic un- 11. Solomon RL, Wynne LC: Traumatic avoidance learning: the
derstanding often seems enlarged. principles of anxiety conservation and partial irreversibility.
This neuropsychological hypothesis contains many Psychol Rev 1954; 61:353-385
implications for and already has influenced treatment 12. Hubel DH, Wiesel TH: Ferrier lecture: functional architecture
ofmacaque monkey visual cortex. Proc R Soc Land [Biol] 1977;
planning and procedures (27). It has led to the trial of
198: 1-59
adrenergic blocking agents to attenuate the cardinal 13. Kandel ER: Environmental determinants of brain architecture
symptoms of the disorder (28). and of behavior: early experience and learning, in Principles of
Neural Science. Edited by Kandel EP, Schwartz JH. New York,
Elsevier/North Holland, 1982
14. Reiser MF: Mind, Brain, Body: Toward a Convergence of
POTENTIAL FUTURE RESEARCH Psychoanalysis and Neurobiology. New York, Basic Books,
1984
Is possible
it through research to discover support 15. Freud 5: Beyond the pleasure principle (1920), in Complete
for the hypothesis put forward? Some immediate Psychological Works, standard ed, vol 20. London, Hogarth
Press, 1959
projects come to mind:
16. Miller JG: Living Systems. New York, McGraw-Hill, 1978
1. Examine with modern imaging techniques the 17. Schuknecht H: Pathology of the Ear. Cambridge, Harvard
physiological and neurochemical processing of mean- University Press, 1974, pp 302-303
ingful combat-simulating stimuli and nonmeaningful 18. Miller JD: Effects of noise on people. J Acoust Soc Am 1974;
56:729-740
stimuli in combat-induced posttraumatic stress disor-
19. Freud S: Preface, in Psychoanalysis and the War Neuroses. By
der victims and control groups. Ferenczi S, Abraham K, Simmel E, et al. New York, Inter-
2. Examine particularly the limbic and lower national Psychoanalytic Press, 1921
brainstem structures with modern neuropathological 20. Ferenczi S: Theory and Technique of Psychoanalysis. New
and neurochemical techniques in post-mortem mate- York, Basic Books, 1952
21. Keane TM, Zimmering RT, Caddell JM: A behavioral formu-
rial from combat veterans, concentration camp survi-
lation of post traumatic stress disorder in Vietnam veterans.
vors, and former prisoners of war with posttraumatic Behavior Therapist 1985; 8:9-12
stress disorder. 22. Jackson JH: Selected Writings, vol II: Evolution and Dissolution
3. Examine prospectively psychophysiological, elec- of the.Nervous System. Edited by Taylor J. New York, Basic
trophysiological, and neunochemical responses in both Books, 1958
23. Sapolsky RM, Krey LC, McEwen BS: Glucocorticoid-sensinve
baseline and arousal status in abused and nonabused hippocampal neurons are involved in terminating the
children. adrenocortical stress response. Proc Nail Acad Sci USA 1984;
4. Carry out similar studies in animals with fear- 81:6174-6177
conditioned chronic states. 24. Redmond DE: Alterations in the function of the nucleus locus
coeruleus: a possible model for studies of anxiety, in Animal
Models in Psychiatry and Neurology. Edited by Hanin 1, Usdin
REFERENCES E. Oxford, Penguin Press, 1977
25. Hoppe KD, Bogen JE: Alexithymia in twelve commissurotom-
1. Kolb LC, Mutalipassi LR: The conditioned emotional response: ized patients. Psychother Psychosom 1977; 28:148-155
a sub-class of the chronic and delayed post-traumatic stress 26. Lindy JD, TitchenerJ: Acts of god and man: long term character
disorder. Psychiatr Annals 1982; 12:979-987 change in survivors of disasters and the law. Behavioral Science
2. Blanchard EB, Kolb LC, Pallmeyer TP, et al: A psychophysia- and the Law 1983; 1:85-96
logic study of post traumatic stress disorder in Vietnam veter- 27. Kolb LC: A theoretical model for planning treatment of post
ans. Psychiatr Q 1983; 54:220-228 traumatic stress disorders of combat. Curr Psychiatr Ther I 986;
3. Blanchard EB, Kolb LC, Gerardi RJ, et al: Cardiac response to 23:119-127
relevant stimuli as an adjunctive tool for diagnosing post 28. Kolb LC, Burns BC, Griffiths 5: Propranolol and clonidine in
traumatic stress disorder in Vietnam veterans. Behavior Ther- treatment of post traumatic stress disorders, in Post-Traumatic
apy 1986; 17:592-606 Stress Disorder: Psychological and Biological Sequelae. Edited
4. Dobbs D, Wilson WP: Observations on persistence of war by van der Kolk BA. Washington, DC, American Psychiatric
neurosis. Dis Nerv Syst 1960; 21:686-691 Press, 1984

Am] Psychiatry 144:8, August 1987 995