Authors: Andrew Siegal, PhD and Nils. R.Varney, PhD
There is a growing need for clinicians, in a variety of disciplines, to have as strong a background in long-term neuropsychiatrically-related,management skills in traumatic brain injury as they do for acute care and neurorehabilitation issues if acceptable outcomes are to be achieved. Of particular concern are the long-term neuropsychiatric outcomes which constitute a public health problem of considerable proportions for a substantial sub-group of patients with TBI.
Neuropsychiatric sequelae of TBI can include any form of the various psychoses, neuroses, or personality disorders, (Lishman, 1998). There are neuropsychiatric signs and symptoms which are differentially highly prevalent in TBI involving personality, cognitive, and affective-systemic changes which reflect the anatomical vulnerability of the pathophysiologic substrate affected by trauma. Particularly prevalent are those syndromes associated with damage to the frontal and occipital poles, as well as to the temporal poles (Alexander, 1982). Damage at specific "coup" and "contrecoup" sites may produce specific regional syndromes, as well as focal or multi-focal effects of shearing of white matter fibers, injured vascular structures, as well as “miscarried” multi-systemic responses to the presence of injury. Thus, the syndromes, which must receive the greatest attention in terms of constituting diagnostic targets of long term follow up efforts, are:
- The Frontal Lobe Syndromes,
- Temporal Lobe Epilepsy and Related Disorders,
- Catastrophic Emotional Reactions to Selective Cognitive Impairments
- More Enduring Affective Disorders: Related Multi-Organ System Reactions
Frontal Lobe Syndromes
Critical concepts which are currently developing in our understanding of frontal lobe disorders are that the frontal lobes’ “executive functions” usually involve hierarchically organized "plans" of motoric reactivity, basal ganglia/caudate up to dorsolateral frontal cortex. Similarly, anteroposterior-connectivity to and from motoric response posteriorly mediated sensoriperceptual information via extensive white-matter tracts with those various fasiculi now have been visualized using novel functional neuroimaging techniques. With damage done to either frontal inhibitory structures, or to white matter connective tracts, environmental stimuli acquire the ability to directly "elicit" or pull out maladaptive, impulsive responses such as utilization behavior, environmental dependency, and imitation behavior, etc. The level of disordered behavior is dependent, at least in part, by which connections are left relatively intact vs. those which are maximally impaired, e.g. primitive Kluver-Bucy, oral or nasal exploration appears when visual object recognition is impaired. Environmental stimuli, similarly, become more compelling ("stimulus boundedness") since the capacity to attenuate "orienting responses" (Cf. Sokolov) is diminished as the result of frontal lobe inhibitory activity. Thus, common to the descriptions of frontal lobe personality disorder, an individual is "sucked along" by the environment, responding to object after object in his path. This pattern, oppose someone who has set upon a predetermined and well thought-out plan of action in which obstacles and unexpected events are dealt with as they arise in the service of keeping the individual "on track" and actively problem solving in pursuance of his goal. Jochain Fuster (1995) described the frontal lobes’ ability to organize both perceptual experience and memory together to form a "memory of the future" which the individual can use to guide himself using an internal representation of the result of his intended course of action. Absence of the "memory of the future," along with the predisposition to respond to fragmentary, immediate experience, and without adequate delay and reflection, provide the essence of many of the clinically-derived descriptions impulsivity personality alterations sustained by individuals with traumatic brain injury and "frontal lobe personality." The frontal lobe personality disorders are well conceived by the analogy used as early as the 1870s when Hughlings-Jackson likened injury to a “loss of government,” with the resultant behavior as being analogous to the “anarchy of the ungoverned.”
Temporal Lobe Epilepsy and Related Disorders
The development of post-traumatic epilepsy most often assumes the form of "temporal lobe epilepsy," so named because the seizures either emanate from or at least secondarily involve epileptiform discharges within the temporal lobes. In more recent classifications of seizure types the distinction has been emphasized between simple and complex "partial seizures," with the term "partial seizures" serving to differentiate the two aforementioned seizure types from "generalized seizures such as "grand mal" or "tonic clonic" convulsive seizures, and from "petit mal" seizures, with the latter presenting as brief arrests of activity, often with fluttering of the eyelids and lasting only seconds. "Partial seizures" may involve confusion, amnesia, or other "clouding of consciousness" whereas in "simple partial seizures" awareness of the transient abnormal experience of the seizure is maintained, i.e. the person remains in contact with surrounding events. In complex partial seizures, hereafter referred to, incorrectly and conveniently, as "temporal lobe seizures," there is often partial recall of some portion of events during especially the earliest portions of seizures, and the rule of thumb is that patients are more likely to recall sensory events and to be amnesic for motoric events during temporal lobe seizures. The reader is referred to encyclopedic classics by Penfield and Jasper (1954) and by Gastaut and Broughton (1970) for magnificently detailed descriptions of the variegated seizure symptoms, which an individual can experience.
The confusion or "mental clouding" of temporal lobe seizures seldom involves complete amnesia, and may include the various "dreamy states" first described by Hughlings Jackson ( Critchley & Critchley, 1998), distortions of the sense of reality, illusions of enhanced brilliance and clarity, or feelings of intense and uncanny deja vu/entendu or jamais vu/entendu. Along with mental clouding there may be specific disturbances of memory, such as when Jackson’s physician patient carried out an entire physical examination and wrote a chart note during a seizure with no recall afterward to far less extensive memory fragmentation. Memory may also be augmented with the appearance of unusually vivid memories, which recur only during seizures.
Jackson drew distinctions between "negative symptoms," "positive symptoms," and "complex positive symptoms." Negative symptoms involve an absence, arrest, or diminution of a function with should normally be present, e.g. if visual object recognition is impaired during a seizure a transient visual agnosia is an example of a "negative symptom." "Positive Symptoms" involve a pathological amplification or exaggeration or distortion of a normal function. Within the visual modality, a visual object, which is actually present, appears larger or smaller than its actual size (macropsia/micropsia). A "complex positive symptom" is the appearance, di novo, of a stimulus which is not physically present in the environment, but which experienced as present, for example a formed visual hallucination. That hallucination constitutes a "complex positive symptom" irrespective of whether or not the individual accepts the image as hallucinatory or as uncritically accepting his experience as veridical, and in temporal lobe seizures either assessment can occur.
In temporal lobe epilepsy negative, positive, or complex positive symptoms can occur in any sensoriperceptual modality, within the motoric systems, within affective/autonomic systems, and within cognitive systems. With such a dazzlingly rich array of symptomatology, and one which can include hallucinosis, distortions of the sense of familiarity, and reality, forced thoughts, intrusive memories, to include only a few of the types of seizures which can occur during seizures differentiation of an "ictal," i.e occurring during a seizure versus a "functional psychopathologic" basis can be confusing for the clinician. There are in fact so many symptoms of temporal lobe epilepsy and schizophrenia which overlap that epileptologist, Michael Trimble stated that when Schneider’s First Rank Symptoms of Schizophrenia are present, they should instead serve as diagnostic clues to the presence of temporal lobe dysfunction, rather than of schizophrenia. Several rules of thumb are useful in generating diagnostic hypotheses of an ictal basis for patient’s symptomatology, and it is crucial to keep in mind that exceptions occur to most rules of thumb and few are absolute criteria in and of themselves. The issue is more one of how many of the rules of thumb begin to form a syndromal constellation. The picture is not black or white, but several grey sketches, which may or may not when taken together, form a more consistent picture. Temporal lobe seizures, for example, tend to be relatively brief, lasting seconds or minutes rather than days or months. They tend to begin and end precipitously and abruptly, are often experienced as coming from without and as overcoming the patient. Typically the experiences of the "ictus" or seizure proper are stereotyped in their presentation, and occur either along, or in a small number of phenomena, and if occurring in series, the serial order tends to be relatively fixed. The presence of automatic movements, i.e. "automatism" such as "pill rolling," purposeless fumbling with clothing or buttons, oromotor and masticatory movements or adversive movements of the head are more likely to be seen in seizures than in functional hallucinosis. Periods of confusion, fatigue, exhaustion tend to follow temporal lobe seizures and, as mentioned, there will characteristically be dysmnesia for at least some portion of the events of the episode. It is noteworthy that in addition to the ictal autonomic manifestations of temporal lobe epilepsy, which may involved paroxysmal (burst-like) rage, sadness, and most often fear, there is often marked irritabililty and inability to tolerate stimuli following temporal lobe seizures.
Complicating diagnostic issues further in the establishment of an "ictal" basis for transient, paroxysmal changes in mood, behavior, or cognition seen in survivors of brain injury is the fact that especially early in the course of TLE, neuropsychological testing may show an absence or paucity of abnormalities, as may the electroencephalogram (EEG). Thus, the neurobehavioral clinician must rely upon clinical acumen to raise the diagnostic hypothesis of a seizure disorder and often empirical treatment with anti-epileptic medication yields additional support for a diagnosis of epilepsy. While controversy exists, medications which are helpful in the treatment of depression and functional psychoses may lower seizure thresholds, if prescribed without prior appropriate antiepileptic treatment, and set off a vicious cycle of worsening neuropsychopathology which are actually ictal and inter-ictal disturbances and progressively increasing dosages of medications with iatrogenic effects.
Other hazards in patient management which ensue when the diagnosis of post-traumatic temporal lobe epilepsy are missed include deterioration of cognitive functions, as well as increasing the likelihood that the patient will develop various forms of neuropsychopathology, among which the "epileptic personality" or "Geschwind Syndrome," and epileptic psychoses are of particular interest. Similarly, the presence of affective disorder in the wake of uncontrolled seizures has been recognized literally since Hippocrates observed and reported that phenomenon which current prevalence estimates of depression in temporal lobe epilepsy reaching 50%.
As noted, it can take up to seven years from the time of a brain injury for post-traumatic epilepsy to occur, and it has been reported that psychoses secondary to epilepsy may not occur until fourteen years after the onset of seizures. Thus, the presence of cerebral insult may not even be suspected given the extensive delay between the initial insult and the onset of observable neuropsychopathology. Tucker (1998) also points out that many of the precipitants of functional psychopathology also act to lower seizure thresholds, thus adding further confusion to the diagnostic picture. Such factors include alcohol or drug use and withdrawal, stress, missed sleep, over-stimulation, etc.
Epileptic psychoses can take the form of paranoid, schizophreniform, or of affective psychoses and more characteristically follow frequent or extended bouts of uncontrolled temporal lobe seizures. In about ten per cent of patients, psychosis appears following aggressive treatment of the seizures with apparent control having been achieved to the point of "forced normalization" of the EEG. It is thought that the epileptic psychoses are at least in part representative of a breakdown in the sense of reality which is attendant upon the intrusive hallucinosis and distortions in the sense of reality experienced during the ictus, as well as by the severity of the cognitive deficits present inter-ictally.
A less severe alteration of personality was described by Geschwind and his students and colleagues, and while controversy exists over the specificity of the syndrome to TLE, or to epilepsy in general, the constellation usually includes traits of extreme pre-occupations with philosophical issues, hyper-religiosity, and hyper-graphia. These individuals often have a pedantic quality to their speech, feeling that they have not been understood and reiterating obsessively, and there is a generalized obsessive quality, along with a "viscosity" in which topics, objects, and issues seem impossible for the person to move on from and to move to the next event, topic or experience. "Deepening of emotions," rage, fear, and depression are all characteristically present, as well as either hypo-sexuality or the development of paraphiliae.
Interestingly, within the neurobehavioral community opinion seems to vary from doubting the existence of an "epileptic personality," per se, to one clinician’s having stated that he could diagnose epileptic personality while getting off the elevator on the neurology floor from a patient’s conversation at the nursing station.
In many cases the diagnostic process for patients with previously undiagnosed neurobehavioral disorders does not begin until there has been some untoward event in which the patient has behaved violently or otherwise out of character and an explanation for the aberrant behavior is absent or seems incomplete. Similarly, those charged with the management of identified neurobehavioral patients are familiar with the occurrence of explosive outbursts and the role of ictal disorganization is a routine part of the management process in sophisticated rehabilitational and neuropsychiatric facilities. The relationships between violence, aggression, or angry outbursts and the presence and nature of the role of seizure disorder have been a source of controversy since the time of English Common Law. A corollary issue is what set of signs, symptoms, and course are necessary to qualify for a diagnosis of epilepsy, per se, and a variety of disorders which stand at "the borderland of psychiatry and neurology" have been described under rubrics which include, "episodic behavior disorders," "episodic dyscontrol syndrome" (Monroe, 1970), "Limbic? Psychotic Trigger Reaction" (Pontius & Wieser, 2004 ), and "Seizure-Like Symptoms (Varney and Roberts, 1999). Again, as rough rules of thumb, if violence occurs in an individual with a diagnosable seizure disorder, the violent or aggressive episode is more likely to have occurred in a situation in which the patient was physically restrained during a seizure, and the actions tend to be poorly planned and poorly executed with largely fragmentary actions. It is less likely that a highly pre-meditated plan requiring great behavioral sophistication and flexibility is carried out during a seizure. Violent, aggressive or explosive anger is more likely to eventuate during a post-ictal confusional state following bouts of prolonged or repeated temporal lobe seizures. It is of note, however, that in studies of both adult and juvenile death row inmates, the prevalence of seizure disorders, head injuries, mental subnormality, and school failure was ubiquitous, whether or not that information was used in the criminal defense of those individuals (Lewis, et. al., 1988). Similarly, studies of implanted electrodes and brain stimulation produced violent outbursts in patients with violence and epilepsy, which could then be treated with antiepileptic medications (Monroe, 1970) and the relationships between violent behavior and epilepsy have remained controversial and clinically challenging.
Catastrophic affect and cognitive deficits
While the frontal and temporal poles are particularly vulnerable to injury in traumatic brain injury (TBI) as noted, both coup and contrecoup injuries are anticipated as primary causes of brain damage, and forces such as shearing, vascular damage, edema etc focal and multi-focal brain damage may also occur. . While there is some oversimplification involved in making an exact point to point correlation between site of lesion and the specific nature of the cognitive deficit associated with that lesion site, it is fair to say that there is more order than chaos which ensues using that clinicoanatomic correlation as an operating principal in examining patients. The various lesion sites in TBI may produce any known type of aphasia, agnosia, apraxia, or dysmnesia.
Progressively more attention is also being paid to the study of the various conative and motivational disorders. “Athymohormia,” one of the motivational aspects of "executive functions," which involve the initiation, maintenance and direction of behavior, and the timing of when to cease a behavioral plan and to switch to another course of action underlie the deficits in initiation (apathy), maintenance, and termination (perseveration) which are seen clinically.
Other classes of cognitive functions involve the study of "categorical cognition," for example being able to identify whether a patient’s ability to identify objects visually is specific to animate versus inanimate objects. Other patients can name tools but not foods. All of the classical disorders of language, action, or perception can each show selective impairment of specific categories of information.
Yet another class of cognitive functions now known to show impairment in the wake of TBI are disorders of "social communication" which include the ability to accurately perceive the speaker’s emotional message in tone of voice, facial expression, or gesture, and to be able to express one’s self via those same modalities. Lastly, the ability of the individual to synthesize all of this information into a coherent and accurate construction of what the thoughts, intentions, and feelings of the other, "theory of mind") are have been studied in detail and have been noted to show impairment in the wake of TBI. Similarly, the individual who has sustained brain injury may have difficulty in identifying, remaining aware of, or in describing even their own feelings, i.e., "alexithymia".
Kurt Goldstein (1942) developed the foundational concept of "catastrophic emotions" to describe the experience of panic, rage or depression which besets the individual with brain damage when he or she suddenly encounters a situation which they are no longer able to master, which they could previously have done given their full complement of cognitive skills. "Catastrophic reactions" may, indeed, be relatively transient, and may even respond to distracting patients over to tasks which they are familiar, have mastered and can perform immediately. Catastrophic emotional reactions are by definition “reactive”, can be contrasted with more predictable and usually more enduring types of affective syndromes, which occur in predictable patterns following insult to specific regions of brain. The presence of "catastrophic emotional reactions" and observations of precipitating circumstances can serve as guides to understanding the nature of a hitherto undiagnosed specific cognitive deficit. That same understanding of the deficit may then be used in designing compensatory strategies and in providing supportive counseling and or psychoeducational interventions to patient, family, or significant others from the patient’s "ecosystem." Thus the monitoring of catastrophic affect can serve as a barometer of the efficacy of rehabilitative efforts due to its "reactive" nature. Treatment breakthroughs occur when the presence and nature of categorical cognitive deficits are identified and communicated to the patient. If not recognized, even though “rare” it may be wrongly regarded as malingering, exaggeration, or attention seeking, and the patient becomes alienated from treatment as the result of misdiagnosis.
Affective Disorders Associated with Regional Cerebral Pathology
In contradistinction to the aforementioned "catastrophic emotional reactions", there are more enduring affective disorders which appear to be related to damage to particular brain regions. Left frontal lobe lesions, for example, are more likely to produce unipolar depression; right frontotemporal lesions are more likely to elicit mania or bipolar syndromes.
Affective symptomatology also can develop over time, rather than becoming fully evident in the immediate injury period. Epilepsy, and consequent epileptic psychoses or personality disorders, are similar to the more enduring affective disorders in that these affective disorders may not become manifest until considerable time has passed from the actual impact. Typically neuropsychiatric symptoms occur following the time at which medical and rehabilitation treatment efforts have plateuaed. Multi-systemic, psychoneuroimmunologic disorders also build to a crescendo over time. Psychosocial factors often intercede between cessation of treatment and the development of later psychopathologic manifestations. They may include repeated failures at vocational or educational pursuits, estrangement from spouses, parents, and peer supports, and either or both medication non-compliance and substance abuse. This complement of pathophysiologic mechanisms operates synergistically to move individuals with TBI toward either recovery or to neuropsychiatric morbidity.
The aforementioned scenarios apply to those patients who have been identified at least at some point as having sustained clinically significant TBI. There is another sector of the population who have simply never had the presence of brain injury identified. T heir injuries were fallaciously considered to be benign, e.g., sports injuries , emergency room visit after a "fender bender," assured that they were "fine, treated for facial injuries.” These patients then appear with neuropsychopathologic presentations in settings in which there is no record of the patients having sustained craniocerebral trauma. Interventions are, thus, made solely on the basis of the presenting picture of the individual at that point in time, changes in behavior are attributed to what appears to be the most likely “situational issue ” ( e.g. "Patient had argument with wife leading to.... etc") rather than to clinicians’ attending to the true underlying disorder. Conditions that need to be considered include endocrine disorders, post -traumatic epilepsy, frontal lobe personality changes or cognitive and dysexecutive deficits which have eventuated in job loss secondary to dysexecutive and or cognitive deficits, family strife secondary to the identified patient’s frontal lobe personality changes, or legal involvements from financial mismanagement or impulsive action.
Typically these undiagnosed patients never become included in epidemiological studies of TBI and their situation then erroneously becomes thought of as "rare." Once a condition is thought to occur only "rarely," it is then regarded as "unlikely" when encountered in future patients. Then, when "base rates” are considered in formulating differential diagnosis the diagnosis is thus relegated to "improbability" dismissed as “functional psychiatric disorder,” "hysteria," or worse, to "malingering." While not universally accepted, there is one large-scale study showing that physical illness will be found to be present in 75% of the patients who were initially diagnosed as having “conversion disorders” or “hysteria.”
If undiagnosed or under-diagnosed, patient care decisions are often treated only on the basis of their presenting symptoms. These patients consequently find their ways to the correctional and judicial system, the medical health care delivery system for non-neurologic disorders, and to psychiatric and community mental health service delivery systems. One example is the frequently encountered state hospital patient whose Axis I diagnosis is schizophrenia and an Axis III diagnosis of Seizure Disorder appears almost parenthetically as though it is simply unfortunate that one individual, by chance is afflicted with two disorders, rather than having a psychosis secondary to temporal lobe epilepsy diagnosed and aggressively treated.
The types of diagnostic errors, which occur in both clinical and forensic situations, and the key error in each case inherent in the clinicians’ bias toward "functional" misdiagnoses is the fact that psychiatric disorders attributable to systemic medical disorders, or to primary disease (i.e. brain damage are not considered in the context of the differential diagnosis. Once the set toward functional diagnosis is assumed, the acquisition of relevant information, as well as the recognition of the neurobehavioral issues becomes less likely.
Gary Tucker (1998) emphasized that there are a finite number of ways in which perturbation of brain function can express itself, and therefore neurobehavioral syndromes and functional psychiatric disorders often share a superficial similarity of presenting symptoms. The limited number of symptoms of brain dysfunction contrasts starkly with a vastly greater number of causes of brain dysfunction. Tucker emphasized study of the "clinical course" of the disorder in guiding the diagnostic process to neurobehavioral etiologies. For example, auditory and visual hallucinations which are present almost constantly over a period of years are often seen in schizophrenia. When hallucinations begin and end abruptly, are occasioned by nearly identical environmental circumstances, occur in fixed sequence with three other unusual experiences including feelings of unreality and are followed by sudden fatigue, then the astute clinician should consider that the primary clinical problem is one of and not schizophrenia.
Patients tend to express their condition in experiential terms that all persons can understand in terms of how their own lives would be affected by such a symptom as that of which the patient complains. This directs the examiner’s attention to the patient’s emotions, interpersonal situation, or subjective feelings about themselves, and their "human" situation. Unfortunately, attention to situational and existential issues too early in the diagnostic process diverts the examiner’s attention away from accurately identifying the relevant neurobehavioral, signs, symptoms and course, and their significance in pointing to a specific region of compromised brain tissue. The patient may feel better understood but will remain ill.
Psychiatric researcher, Robert Spitzer described two paths leading toward misdiagnoses among the various "functional" psychiatric disorders, 1) " informational errors" vs. " criterion errors." Informational errors were defined as diagnostic errors, which resulted from the failure to gather those clinical and historical data requisite to making the correct diagnosis. Criterion errors, in contradistinction occurred when the full complement of information requisite to making the correct diagnosis had been collected, but in which the significance of those data as indicating the presence of the correct or criterion diagnosis was not evident to the clinician, i.e. the clinician did not recognize the illness. Neurologist, Norman Geschwind’s efforts were directed toward the differential diagnosis of neurologic disorders from functional psychiatric disorders and basically used the same conceptual framework for analyzing diagnostic errors. Geschwind drew upon his detailed understanding of clinicoanatomical correlations which had been developing explosively during the 1960s and 1970s and upon his knowledge of classical, European behavioral neurologic literature. Geschwind, too, emphasized incomplete history taking, and failure to fully query a sufficiently wide range of symptomatology, e.g. olfactory hallucinations in a temporal lobe epileptic, and failures to delineate the clinical course of illness during patient interviews, as all being among the most salient factors leading to misdiagnosis of neurologic disorders as "functional." Informational errors resulting from incomplete or superficial objective mental status examination were similarly addressed systematically (Cf. Strub and Black, 1977).
Geschwind also stated that criterion errors resulted from the failure to recognize regional syndromes, i.e., inability to relate the syndrome to an understanding of what neuroanatomical pathophysiology would be necessary to produce such a syndromal constellation. Geschwind also emphatically cautioned against over-emphasizing test results and the results of special diagnostic procedures. Geschwind specifically discussed the problem of abdication of diagnostic hypothesis generation and testing based upon history, review of systems, and mental status examination in favor of over-reliance upon special diagnostic procedures including the electroencephalogram and neuropsychological testing taken in isolation.
Long Term Follow-up of TBI Survivors
Intensive training both in the “neuropsychopathology” of those disorders most likely to be seen in survivors of TBI are required both for individuals enrolled in clinical training programs in mental health and in rehabilitational disciplines. In-service education for staff in neuropsychopathology not only of rehabilitiation facilities is essential, but also for the staffs of “the wrong systems” in which persons with TBI can be expected to find themselves, i.e., correction al, mental health, psychiatric facilities, and non-neurologic medical treatment settings. Structured approaches to history taking and clinical interviewing which are sensitive to a wide range of neurobehavioral symptoms and clinical courses have been developed to minimize “informational errors” which can be used by appropriately trained and supervised mental health and rehabilitational staffs. Special purpose interview formats with research-validated criteria have been developed for at least two of the most frequently encountered neurobehavioral disorders encountered in individuals who have developed neuropsychiatric sequelae of TBI i.e. frontal lobe syndromes and temporolimbic epilepsy) and address informational errors selectively as well as act to minimize “criterion errors” toward pattern recognition levels of diagnostic hypothesis generation. The basic wisdom of grounding diagnostic work upon the “anamnesis,” (i.e. history, symptom reviews, and examination in this case the mental status examination, is an accepted bulwark in clinical medicine including neurology and psychiatry, is cost effective, and addresses the widest range of management concerns.
Current issues confronting health care delivery systems have led to the acceptance of the strategy of "delegating to the appropriate level of care," i.e. either turning professional responsibilities over to another discipline, or to practitioners at less highly credentialed levels within a discipline. The history and clinical interview is not only the most cost effective system for long-term follow up but probably is sensitive to the broadest range of posttraumatic disorders. Given the impaired awareness of deficits and of personality change which so frequently follows TBI interviews with family members must be carried out at follow up intervals for cross comparison with patient reports. Staff training in the use of structured interview techniques for case identification and case management constitute a training priority.
Suggested Readings
Alexander, M.P. Traumatic brain injury. In D.F. Benson & D. Blumer (eds) Psychiatric aspects of neurological disease Vol II pp 219-251 New York: Grune & Stratton.
Blumer, D. & Benson, D.F. (1975) Personality changes with frontal and temporal lobe lesions. In D.F. Benson & D. Blumer Psychiatric aspects of neurologic disease. New York: Grune & Stratton.
Benson, D.F. ( 1991) The Geschwind syndrome. Advances in neurology. 55: 411-421.
Dantzer, R. (2005) Somatization: a psychoneuroimmune perspective. Psychoneuroendocrinology. 30: 947-952.
Feinberg, T. & Farah, M. (2003) BehavioralNeurology & Clinical Neuropsychology. New York: McGraw Hill.
Fuster, J. (1995) Memory and planning: Two temporal perspectives of frontal lobe functioning.Epilepsy and the Functional Anatomy of the frontal lobe. (Ed) H.H. Jasper & P.S. Goldman-Rakic. New York: Raven Press.9-20.
Gastaut, H. & Broughton, R. (1970) Epileptic seizures: clinical and electrographic features. Springfield, IL: CC Thomas Geschwind, N. (1975) The borderland of psychiatry and neurology: some common misconceptions. In D.F. Benson & D. Blumer Psychiatric Aspects of Neurologic Disease.(pp.1-9). New York : Grune & Stratton.
Goldstein, K. (1942) After-effects of brain injuries in war. New York: Grune & Stratton.
Habib, M. Athymohormia and disorders of motivation in basal ganglia disease. Journal of neuropsychiatry and clinical neuroscience. 16: 509-524.
Hecaen, H. & Albert, M. (1975) Disorders of mental functioning related to frontal lobe pathology. In D.F. Benson & D. Blumer (eds) Psychiatric Aspects of Neurological Disease. Vol I. New York: Grune & Stratton.
L’Hermitte, F. (1986) Human autonomy and the frontal lobes: part II: patient behavior in complex and social situations: the "environmental dependency syndrome." Annals of Neurology 4: 335-343.
Lewis, D.O., Pincus, J.D., Bard, B.,Richardson, E., Prichepp, L.,Feldman, M. Yeager, C., (1988) Neuropsychiatric, Psychoeducational, and family characteristics of 14 juveniles condemned to death in the United States. American Journal of Psychiatry. 145.
Lishman, W.A.(1998) Organic psychiatry: the psychological consequences of cerebral disease.(3rd ed) London: Blackwell Scientific
Makris, N., Worth, A.J., Sorensen, A.G., Papadimitriou, G.M., Wu. O.,Reese, T.G., Reese, T.G.,Wedeen, V.J.,, Davis, T.L., Stakes, J.W., Caviness, V.S., Kaplan, E. Rosen, B.R., Pandya, D.N.Kennedy, D.N. (1007) Morphometry of in vivo white matter association pathways with diffusion-weighted magnetic resonance imaging. Annals of Neurology. 42: 951-962.
Monroe, R.R. (1970) Episodic behavior disorders: a psychodynamic and neurophysiologic analysis. Cambridge, MA: Harvard University Press.
Ovsiew, F. (1999) Neuropsychiatry and mental health services. Washington, CD: American Psychiatric Press.
Penfield, W. & Jasper, H. (1954) Epilepsy and the functional anatomy of the human brain. Boston, MA Little, Brown.
Pontius, A.A. & Weiser, H.G. (2004) Can memories kindle non-convulsive seizures in humans? Case report exemplifying the "limbic psychotic trigger reaction." Epilepsy and behavior. 5: 775-783
Siegal, A.W. (1996) Historical, phenomenological, and observational data: the context for neuropsychological test findings. In R.J. Sbordone & C.L. Long Ecological Validity of Neuropsychological Testing. (pp 43-75) Boca Raton: CRC Press.
Siegal, A.W., Schechter, M.D., & Diamond, S.P. (1981/1996) Neurobehavioral assessment format .In R.J. Sbordone & C.L. Long Ecological Validity of Neuropsychological Testing. (p 429-505) Boca Raton: CRC Press.
Stuss, D.T., Murphy, K.J., Binns, M.A. & Alexander, M.P. (2003) Variability in Job Performance:. Brain. 126: 1-18.
Thayer, J.F. & Brosschot, J.F., (2005) Psychosomatics and psychopathology: looking up anddown from the brain. Psychoneuroendocrinology. 30: 1050-1058.
Trimble, M.R. (1990) First rank symptoms of Schneider: a new perspective? British Journal ofPsychiatry. 156. 195-200.
Tucker, G. J. (1998) Seizure disorders presenting with psychiatric symptomatology. Psychiatric Clinics of North America. 21: 625-635.
Varney, N.R. (1999) Postraumatic anosmia and orbital frontal injury. In N.R. Varney & R. Roberts The evaluation and treatment of mild traumatic brain injury. (pp 115-133) Mahwah: Laurence Erlbaum.
Vuilleumier, P., Staub, F. & Assai, G. (1997) Sniffing behavior: recognizing a lily by smell but not recognizing a sock on sight. Cortex. 33: 571-577
Appendix: Iowa collateral head injury interview 128-130