The Neuropsychological Basis of Potential Co-occurrence of Mild Traumatic Brain Injury with Post-Traumatic Stress Disorder
Robert B. Sica, Ph.D., B.C.E.T.S.


The impact of traumatic brain injury (TBI) is enormous. The effect at the individual level is seen in the changed life of each person who incurs the TBI.

In the United States, an overall rough estimate of TBI incidents in 1990 is about 2 million cases. This includes about 51,600 deaths plus 202,000 (220,000 hospital admissions minus 18,000 deaths occurring after admission) hospitalized patients who survive, plus 1.74m cases that only involved physician consultation or at least one day of disability. These latter two figures are extrapolated from 1991 and 1977-1981 national data. (Fife, 1987).

To begin with, TBI technically, (cranio-cerebral trauma) is defined either:

  1. as an occurrence of injury to the head that is documented in a medical record with one or more of the following conditions (injuries to the head may arise from blunt or penetrating trauma or from acceleration-deceleration forces):
    • Observed or self reported decreased level of consciousness, that is, a transient alteration of consciousness including partial or complete loss of consciousness, obtundation, stupor or coma.
    • Amnesia, including the time preceding, during, and subsequent to the injury.
    • Skull fracture.
    • Objective neurological or neuropsychological abnormality.
    • Diagnosed intracranial lesion.
  2. or as an occurrence of death resulting from trauma, with head injury listed on the death certificate, autopsy report, or medical examiners report in the sequence of conditions that resulted in death.

Virtually all of these above changes have been noted with moderate to severe head injury unequivocally, that is, where there was a serious injury, often life threatening, with obvious disability and the need for specialized treatment. However, over a number of years a new population is increasing namely that of the minor head injury. These are injuries where patients spent a brief time (if any) in the hospital, made quick medical recoveries, and were discharged directly (and often prematurely) from the ER to home without any perceived need for formal neuropsychological assistance. What followed was, though appearing fine, they attempted to return to their former responsibilities at home, work, or school. When they did so, a significant number experience great difficulty. They complained of inability to remember, concentrate, organize, handle a number of tasks at once, or be as efficient as before. The relationship with family, peers, and bosses often suffered, and they developed secondary psychological problems. Their doctors were unable to find anything wrong with them, and they were thought to have psychiatric problems - or worse yet, to be malingering. They became the outcasts of neurologists, psychologists, psychiatrists, or vocational counselors all of whose unusual techniques did not produce positive results.

In such cases the unique problem if minor TBI readily became apparent despite swift and complete physical recoveries, and despite no obvious neurological basis for their problems, these persons experienced significant cognitive, emotional, and behavioral deficits that seriously interfered with their functional lives.

The trauma itself may have involved a fall, a blow to the head, or (most commonly) the head striking a stationary object as in a motor vehicle accident. Minor TBI may also occur after a severe whiplash injury, even if the head is not struck, especially (it appears) if the whiplash involves some rotation of the head in addition to linear movement.

The alteration of consciousness usually, but not always, involves some brief loss of consciousness. With moderate to severe head injury, there is a rough correlation between length of coma and severity of injury (as measured by outcome). Within the group of minor TBI, however, when loss of consciousness lasts less than an hour, there is no demonstrable relationship between length or alteration of consciousness and severity of problems. Severe functional deficits can occur even with transient loss of consciousness. Those patients have already "awaken" by the time they arrive at the hospital after minor TBI, although they might not recall the events for some period of time after the accident, despite being awake and communicating (post-traumatic amnesia).

It is also possible that significant, long term deficits can occur in the absence of any documentable loss of consciousness. In such cases, the alteration of consciousness may take the form of the patient feeling dazed, confused or agitated for some period of time even though consciousness was never lost. The neuroanatomical sequelae to minor TBI can be of diffuse or focal nature. The secondary cognitive deficits in terms of the former are that of reduced speed and compacity of information processing, complex attention, learning and memory, and integrative abstract thinking. In terms of the latter such deficits may run the gamut of (but not limited to) word finding difficulties, perception, (neglect) sensory functions (especially) ansomia, motor functions, sensory motor integration, and arithmetic calculations.

The question arises, now what are the psychological/behavioral consequences of minor TBI? There are a number if functional scenarios that arise following premature discharge from the ER and limited follow-up medical intervention at best. First, the patient is assumed to have completely recovered. However, even in this "complete recovery" scenario it is in a modified form. That is, a person may notice minor problems with memory or problem solving, but not to the extent they seriously interfere with functioning or require any conscious adaptation. It is this population that physicians and attorneys often describe as completely recovered with no permanent neuropsychosocial sequelae. However, this person may experience changes in cognitive processing abilities, but only rarely and only at certain times _ such as under extreme stress, anxiety, fatigue, or after even mild use of alcohol or drugs. In addition, even after "complete recovery" the occurrence of cumulative effect is established. That is, the occurrence of any subsequent minor head injury (especially, in sports) eventually produces noticeable deficits, even though none is any worse than the first - implying that the initial "complete recovery" was really a decrement in nervous system integrity too small to notice behaviorally.

Next is the spontaneous accommodation. In this case the individual does, as a result of a minor TBI, experience long term cognitive impairment but succeeds in adapting successfully to his cognitive and behavioral changes. His life and work is disrupted by the impairment. Finally, the person compensates for the deficits by making changes in their environment.

On the other hand, there are a number of dysfunctional scenarios that result from minor TBI of which the posttraumatic stress reaction will be the focus. It is precisely this phenomenon that has caused considerable controversy in terms of its legitimacy. The psychological sequelae of minor TBI are typically conceptualized in terms of organic impairment with the aforementioned cognitive deficits as well as emotional functioning. Collectively these are known as primary psychological reactions where as Posttraumatic Stress Disorder (PTSD) is typically a secondary psychological reaction. However, the minor TBI is a frightening experience, and the circumstances of the injury may range from the moderately distressful to the horrific. While brain injured patients are usually thoroughly worked up from a medically and neuropsychological point of view, clinicians have paid rather less attention to the emotional sequelae of minor TBI. Thus the importance of recognizing the potential association of PTSD with minor TBI.

PTSD is a psychological condition estimated to occur in about 2-20% of civilians exposed to life-threatening experiences in which there is no injury to the brain. PTSD is characterized by 3 "symptom clusters": 1) persistent and painful re-experiencing of the trauma such as flashbacks, nightmares, or obsessive thoughts: 2) emotional numbing or societal withdrawal in attempts to avoid stimuli associated with the events; 3) increased arousal as manifested by symptoms such as irritability, poor concentration, and disturbed sleep. These symptoms require duration of at least one month to meet the DSM-IV diagnostic criteria.

With litigation burgeoning, PTSD have come into prominence. Traditionally, PTSD has been applied to personal injury claims based upon the psychological consequences of automobile, home, industrial accidents and mass disasters.

A brief history of PTSD reveals that, in an earlier definition, it was diagnosed as railway spine in the 19th century. Such injuries were particularly common with the growth of railroads. It was thought that concussion of the spine was a concomitant injury to the sympathetic nervous system causing the observed traumatic neurosis (Trimble, 1981). In World Wars I & II, traumatic stress disorders were called variously shell shock, battle fatigue, traumatic neurosis and concentration camp syndrome.

On the surface, logic dictates that an emotional disturbance caused by a specific experience must be dependent on the ability of the person to recall that experience. However, when an event such as an automobile accident, fall or assault results in a blunt traumatic brain injury, the individual typically cannot remember the traumatic experience, nor the events that surround its occurrence. This inability to recall events immediately preceding the event (retrograde amnesia) and following it (post-traumatic amnesia) is caused by physical disruption of brain mechanisms involved in memory function described earlier. This differs from memory loss due to emotional (psychogenic/functional) factors such as a "need to forget" a life threatening experience. It is at this juncture the interface between neurological insult and subsequent cognitive and behavioral stress-related symptoms in the form of PTSD is questioned. Because trauma can occur under a broad range of external conditions, PTSD occurs with minor TBI in some cases. These instances make the examination of cognitive status especially critical. Thus an individual suffering a minor TBI may incur neurological damage and secondary cognitive dysfunction; these may produce isolated performance deficits or a combination of psychological and behavioral alterations in the form of PTSD. Thus a number of situations can arise on which physical and psychological components exert distinct effects on performance or where they combine to influence diagnostic presentation.

Therefore this raises the question how is it possible that an individual with minor TBI can be suffering PTSD, an emotional disturbance that is dependent on memory for the event that has caused it? Many clinicians by virtue of PTSD criteria recheck the notion of the co-occurrence e.g. Sbordone, 1992. On the other hand studies by Horton, 1993, Layton and Zonna, 1995 and Rattok and Ross, 1993 have clearly demonstrated the possibilities. At the 1993 European meeting of the International Neuropsychological Society, Rattok and Ross reported 20% of 40 patients who suffered TBI with coma of at least one hour could be diagnosed with PTSD used in modified criteria for the disorder.

The problem with critics of this potential co-occurrence of PTSD with minor TBI is the continual reliance on unitary memory theory. This position is most represented by Sbordone's argument that PTSD and retrograde amnesia seen with legitimate head injury may not be diagnosed concurrently since memory (or psychologically repressed memory) for the trauma is assumed to be a necessary condition for PTSD. Understanding how there may be coexistence of minor TBI and PTSD requires a brief introduction and some information on memory theory.

To begin with it is important to understand the distinction between explicit (declarative) vs. implicit (non-declarative) memory. Explicit memory represents the ability to recollect consciously earlier experiences: implicit memory on the other hand, refers to the retrieval of such information without conscious attention of the awareness on the part of the subject. Explicit memory can be assessed using traditional tests of recall and recognition, where as implicit memory requires testing under conditions that obviate the subjects awareness of the topic or stimulus being investigated.

Recent studies on functional amnesias also indicate that similar patterns of memory dysfunction exist in psychologically distressed patients who have experienced traumatized events. In these patients, implicit memory abilities appear to be strikingly preserved despite the presence of explicit memory deficits (Kaszniak et. al. 1988).

Such findings suggest a possibility of a disassociation between these two memory systems in patients without neurological lesions. On the basis of this work, some authors (Schacter and Kihlstrom 1989) have proposed that similar memory assessment paradigms be used to search for disassociations between explicit and implicit memory systems in disorders such as PTSD, in which recall, processing, and retrieval of certain types of information are purportedly disrupted.

Thus from the point of view of minor TBI and PTSD, two features about multiple memory system theory are essential. First, one category of implicit memory is sensitization, defined as increased reactivity to a previously neutral stimulus as a result of exposure to an extreme stimulus (the traumatic event and PTSD). Second, an individual event may have both explicit and implicit properties and be stored simultaneously in both systems. This is the concept of dual storage. For example, an experience that causes physical trauma may be registered consciously and later be recalled. The same trauma also may change the person in a manner that is independent of conscious memory, that is, implicit, for example, by altering responsiveness to events (such as driving through intersections) which previously had no notable effect on arousal.

The recent appreciation that memory is diverse rather than unitary and that memory systems are autonomous is theoretically compatible with the position that PTSD may occur in the absence of recall for the traumatic event. Hence, sensitizing stimuli in the form of MVAs and assaults are stored simultaneously in both implicit and explicit systems and the effect on behavior of these sensitizing situations are a result of the combined effects of registration of both systems. This argument is consistent with DSM-IV description of the effects of PTSD in terms of changes in cognition, behavior and autonomic responsiveness. Thus accidents or assaults that result in minor TBI, and compromise functioning of the neural systems that normally would mediate the ability consciously to recall the event (that is operation of the explicit system) is nonetheless stored in the implicit memory systems with sensitizing aspects of the event operationally causing the symptoms of PTSD (Layton and Zonna 1995).

The position can be further buttressed by the work of Parker 1990, and Deitz 1992 regarding autonomic arousal as defined in DSM-IV. In addition to the immediate, direct effects of the minor TBI to brain tissue, a host of complex acute and delayed biochemical effects are activated in terms of attendant stress effects according to Parker. The head injury is accompanied by a tremendous catecholamine surge which precipitates electrocardiographic changes, depression of thyroid function and hypoxia. In addition there is an outpouring of other neurotransmitters, neuropeptides, and hormones. The person's ongoing stress is accompanied by heightened catecholamine endorphin secretion with eventual depletion. The behavioral consequences include anxiety, irritability, explosive outbursts, insomnia, hyperalertness, and emotional ability. Thus, some multiple afferent signals through sensory and emotional pathways induce the secretion of corticotrophin releasing hormone (CRH) from the hypothalamus which stimulates the pituitary gland to produce adrenocorticotrophic hormone (ACTH). This, in turn, stimulates the secretion of glucocorticoid hormones such as cortisol (the classic stress hormone) from the adrenal cortex.

High levels of this cortisol appears to depress brain cell function. The hippocampus, which plays an important role in memory, contributes to feedback to the adrenal cortex to modulate the stress response, together with input from the pituitary, amygdala, septum, and reticular formation. The hippocampus possesses receptor sites for vasopressin and glucocorticoids (example, cortisol), and circulating glucocorticoids exert feedback effects via the hippocampus.

Therefore, hippocampal damage or depletion of hippocampal glucocorticoid receptors after chronic stress leads to an increase in adrenal secretion via hypersecretion of ACTH. This is followed by eventual glucocorticoid depletion. Parker (1990) goes on to sight experimental evidence showing that impaired adrenocorticial secretion leads to loss of granule cells in the dentate gyrus of the hippocampus, which could account for deficits in cognition. Additionally, severely disturbing or emotionally arousing events can result in the release of endogenous benzodiazepines, which alters hippocampal functioning.

Thus, Parker's (1990) stress theory of head injury can easily explain the seemly obverse clinical phenomenon of post-traumatic stress reaction: intrusive thoughts or memories. After a biologically important event (physical or emotional), recently active neuronal circuits may be "primed" by neurotransmitters or neurohormonal substances. This produces sensitization to dangerous stimuli, or generalized stimuli that resemble them, repeating the trauma and creating new synaptic connections fixating it.

Next, Deitz's 1992 theory of brain functions in the post head injury stress response interim, places location of the sight of the disorder in the temproalamygdaloid area consistent with neuroanatomical and neurophysiological data. This suggests that sensory stimuli and their subsequent cortical projections follow two main routes: 1) a broad pathway between information transmitted to Broca's and Wernicke's areas concerned with language, and 2) another pathway where different aspects of the same information is transmitted to the temporal lobe, arriving at the amygdalar nuclei.

According to this model, both Wernicke's area (receptive language) and the amygdala are connected to the hypothalamus at the core of the brain where hormonal control and visceral/emotional reactions are regulated, but via very different routes. Wernicke's area is connected to language association cortices and to the speech center in the motor cortex (Broca's). From language association cortices, information penetrates into the hippocampal formation concerned with the registration of memory, which is connected to the hypothalamus by way of the fornix.

The amygdala, which consists of several densely populated and clearly differentiated nuclei deep in the temporal lobe, is directly connected to the hypothalamus. Information processed through amygdalar pathways can reach the hypothalamus without higher cortical processing (conscious awareness). The amygdala splits the sensory formation it receives into positive and negative emotional values, relaying this information to different locations in the hypothalamus (Fonberg 1986). Thus, the hypothalamus receives the amygdalar output, a distillation of the positive or negative affective tone associated with the sensory data, independent of higher thinking processing concerned with abstract meaning or rational analysis.

For survival purposes, it is critical that the amygdalar process positive/negative discrimination be made as fast possible to allow for appropriate fight/fight or approach/avoid responses. In order to link the affective turn to higher processing - the feelings and meanings connected to language and complicated thought processes - the second, phylogenetically newer pathway is need. It is also likely that both pathways influence each other, the amygdalar affective tone facilitating the receptivity of the hypothalamic system reached by neuronal projections originating in neocortical pathways.

In summary, traumatic learning experiences be they minor TBI or PTSD are believed to be the origins in most anxiety disorders. During traumatic experiences, learning occurs through these two separate memory systems. The individual forms conscious, explicit/declarative memories through the temporal lobe memory system involving the hippocampus and related cortical areas, but also forms implicit/nondeclarative emotional memories through our memory system centered around the amygdala that most likely operates unconsciously. The neural pathways through which the amygdala participates in the acquisition and expression of implicit traumatic learning demonstrates that malfunctions in the prefrontal cortex can make implicit emotional memories especially resistant to extinction. Stressful experiences can interfere with hippocampal and facilitate amygdala memory functions, thereby forming especially potent and difficult to eliminate implicit emotional memories, sometimes in the absence of a well formed explicit memory of the experience as seen with retrograde amnesia in the minor TBI case.

This finally brings us to an elegant model presented by McLaurin and Titchener (1982). These researchers observed that the traditional disputes in the professional community regarding whether the syndrome arises "principally from mental and emotional reactions to head trauma or from disordered neurophysiological mechanisms and brain damage" go on to point out that such conflicts can be avoided by recognizing that complex casual change are involved in minor TBI, including neurophysiological, psychological, and probably unknown factors. This conceptual framework, in turn, leads McLaurin and Titchener to discuss the syndrome in terms of "organic and psychic" causes.

Their model of the post-traumatic event be it the concussion, post-traumatic reaction or ongoing symptom complaint persistent beyond 3 months after the injury (post-concussion syndrome) started with a "massively threatening situation" represented by injury to the head. Incidentally this specific type of severe anxiety was noted many years earlier by Schilder (1934). This model begins with the trauma, resulting alteration of consciousness, gradual recovery during a period of confusion, possible amnesia for the injury and signs of PTSD. At this time the patient's intellectual functions are disorganized. From a biological point of view, the person is essentially helpless.

McLaurin and Titchener postulate that the problem moves from this biological stage of helplessness to its psychological counterpart as a result of "actual flooding of the psychic apparatus with the terror of the moment." The individual attempts to recover from this condition by "mastering the traumatic event"; the victim relives the accident in dreams as well as in the waking state and maintains an intense vigilance to protect himself against any further stimuli which might overwhelm his adaptive apparatus. The next step in this process is found in those persons in which the disorder becomes severe and chronic and results in sematization of the traumatic anxiety. The post-traumatic reactions then become more generalized and integrated with any pre-existing anxiety tendencies that the individual may have had. For example, depression will blend with elements of the post-traumatic reaction and become intensified.

All these factors lead to increased feelings of defensiveness, limitation of interest, and change of relations with the outside world, collectively identified in the post-traumatic reaction. Thus, McLaurin and Titchener identified these changes as representing personality constriction in which the individual is principally interested in protecting himself against a restorative change, resisting novel experiences and narrowing his range of experience. At this stage the person begins to view all aspects of his life in terms of his injury. He may relate every personal inadequacy to the head injury or traumatic event. Any personal professional difficulty may automatically attributed to the accident.

There appears to be a distinct interaction, however, between the customary neurological and psychological effects of head injury and this situation almost certainly would represent the basis for expecting discrepancies among individual experts with respect to assessment of ideology, especially among patients with minor TBI. This is clearly represented by the different positions of Sbordone vs. Layton & Zonna already discussed on co-occurrence of minor TBI and post-traumatic reaction. However, there are other factors that can be identified that contribute to such discrepancies. First, investigators often compare their samples of patients from various populations. Some samples may include disproportionate numbers of persons who were anxious and emotionally disturbed before the injury. Much, for instance, has been written in the literature to the effect that these subjects tend to exaggerate their symptoms and are even malingering. However, these claims are grossly exaggerated. Second, as with recovery from any injury considerable variability would be expected among patients, either in terms of residual deficits or the time scale for recovery. Thirdly, premorbid emotional status of the patient is important. Head injury and PTSD victims have a great range of personalities and often include persons with deviant or even unstable characteristics. Although post-traumatic stress reaction may occur in someone who previously had not the slightest psychiatric difficulty, it usually strikes the emotionally predisposed. That is, the man or woman whose pre-trauma personality was characterized by hyperconscientiousness, obsessive perfectionism, militant self-reliance, overachievement, denial and displacement onto others of emotional conflicts and disappointment, and great emphasis on physical appearance, activity and stamina, coupled with an intolerance of weakness or impairment. Thus a psychologically fragile person can develop a post-traumatic stress disorder after minimal stress while a psychologically strong, healthy person has little predisposition to this diagnosis and will develop one only if confronted with enormous stress - and is more likely to make a rapid and complete recovery. Hence, the severity of the underlying emotional predisposition inversely determines that of the precipitating stress (or proximate cause).

Finally, the customary clinical methods for evaluating residual effects of head injury are rather gross and insensitive. Many persons do not demonstrate any abnormalities on neurological examination, EEG, or CT of the brain. In these cases, there may be a natural tendency to conclude that no neurological deficits were sustained as a result of the injury and the person's complaints are therefore concluded to be PTSD and minimized at that.

Obviously, the presence of emotional difficulties in the form of the PTSD have important clinical ramifications. In most cases a complete neuropsychosocial examination (NPE) can differentiate between psychological and neuropsychosocial deficits in the minor TBI. The NPE can offer the opportunity to investigate conditions under which the cognitive deficits are effected by extreme emotional experience if it is PTSD, and the way in which these changes mediate subsequent behavioral response.

Thus the NPE can be used to evaluate (a) how basic mental processes (example, problem-solving, attention, memory) are effected, in PTSD, and (b) whether changes in these functions play a part in the etiology or maintenance of symptoms found in this disorder. Whether the diagnosis is minor TBI or PTSD, the NPE can determine baseline functioning after psychological or physical trauma, or their combination; (c) NPE can determine functioning under conditions of changes in symptompatology (example, heightened arousal); (d) NPE can assess cognitive capacities for certain PTSD treatment (example, imaginal or exposure-based approaches); (e) NPE can validate the patient's subjective complaints regardless if minor TBI or PTSD. For instance, often patients with PTSD claim cognitive deficits in the form of decreased concentration, and memory deficits. These deficits are also noted with minor TBI. The examination can make overt if these deficits have any basis in terms of head injury vs. the post-traumatic reaction.

This information in conjunction with other findings not only aids in better understanding the condition of the patient whether its a minor TBI or PTSD, but functionally expresses how the patient is going about adapting to their world. For all practical intents and purposes whether the adjustment problem is because of minor TBI or PTSD, it is important to understand the format for problematic areas that undermine the person's efficient daily adaptive functioning. The patient's interpretations of their conditions during self-report to the clinician are entitled to be represented with inaccuracies. On the other hand, the clinician through proper history taking and observation on neuropsychological examination can not only qualify and validate the patient's symptom reports, but also establish a treatment plan on how to handle the behavioral and cognitive impairments be they from the minor TBI, post-traumatic stress reaction or a combination of both.

Therefore, neuropsychologists' input into the analysis of the medical, neuropsychological and behavioral data in instances where traumatic exposure has occurred with central nervous system damage or in the psychological arena in the form of PTSD, we can help to distinguish symptoms that are more emotionally based from those that represent sequelae of known brain damage. Assessment of both quantitative and qualitative changes in cognitive performance can aid in the determination of multiple diagnoses and define the need for a variety of rehabilitation services. This ultimately benefits the unfortunate patient whose case brings to mind the legal phrase, "absence of evidence is not evidence of absence" when evaluating the relationship between minor TBI and PTSD.

References

Fife, D., Faich, G., Hollinshead, W., Wenthworth, B., (1986). Incidence and Outcome of Hospital Treated Head Injury in Rhode Island. AM. J. Public Health 76, 773-778.

Trimble, M.R.: Post-traumatic Neurosis: From Railway Spine to the Whiplash. NY, Wiley 1981, pp 5-20.

Horton, A. M., Jr. (1993). Post-traumatic Stress Disorder Mild Head Trauma: Follow-up of a Case Study. Perceptual and Motor Skills, 76, 243-246.

Layton, B. S. and Wardi-Zonna, K. L., (1995) Post-traumatic Stress Disorder with Neurogenic Amnesia for the Traumatic Event. The Clinical Neuropsychologist, 9, 2-10.

Rattok, J. and Ross, B. P. (1993) Post-traumatic Stress Disorder in the Traumatically Head Injured. Journal of Clinical and Experimental Neuropsychology, 15, 403.

Kaszniak, A. W., Nussbaum, P. D., Berren, N. R., Santiago, J. (1988). Amnesia As A Consequence of Male Rape: A Case Report. Journal of Abnormal Psychology, 97, 100-104.

Schacter, D. L. and Kihlstrom, J. F., (1989). Functional Amnesia.

F. Boller and J. Grafman (Eds.), Handbook of Neuropsychology, Amsterdam: Elsevier Publications.

Parker, R. S. Traumatic Brain Injury and Neuropsychological Impairment: Sensory Motor, Cognitive, Emotion and Adaptive Problems of Children and Adults. NY: Springer-Verlag. Deitz, J. (1992). Self-Psychological Approach to Post-Traumatic Stress Disorder: Neurobiological Approach to Transmuting Internalization. Journal of The American Academy of Psychoanalysis, 20, 277-293.

Fornberg, E. Amygdala, Emotions, Motivation and Depressive States. In R. Plutchnik and H. Kellerman (Eds.), Emotion: Theory, Research, and Experience, Volume, 3: Biological Foundations of Emotion (pp. 301-331). NY: Academic Press.

McLaurin, R. L., and Titchener, J. L. Post-Traumatic Syndrome. N.J. R. Youman, (Ed.), Neurological Surgery, Philadelphia: W.B. Saunders & Co.

Flavin, H. S., Benton, A. L., and Grossman, R. G. (1982) Neurobehavioral Consequences of Closed Head Injury. NY: Oxford University Press.

Schilder, P. (1934) Psychic Disturbances After Head Injuries. American Journal of Psychiatry, 91, 155-158.

©1996 by The American Academy of Experts in Traumatic Stress, Inc.



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