Postconcussional Disorder and Loss of Consciousness

Stephen D. Anderson, MD, FRCP(C)

Postconcussional disorder (PCD) has been described in the psychiatric, neuro- logical, neuropsychological, and rehabilitation medicine literature for many years. PCD has recently been introduced into DSM-IV, appearing in an appendix that contains a number of proposals for new categories and axes that were suggested for possible inclusion in DSM-IV. There are some major difficulties with the proposed criteria for PCD. This article explores some of these difficulties, partic- ularly focusing on the criteria of loss of consciousness (LOC). A review of the literature demonstrates that LOC is not necessary for PCD to occur. The major difficulty with the DSM-IV criteria is the definition of concussion. The article suggests that, instead, the criteria for mild traumatic brain injury, as defined by the American Congress of Rehabilitation Medicine, may be more appropriate.

Postconcussional disorder (PCD) has been symptoms include headache pain, nausea. described in the medical literature for dizziness or vertigo. unsteadiness or poor over a century. The telm Post-concussion coordination, tinnitus, hearing loss. blurred syndrome was coined by Strauss and vision, diplopia, convergence insufficiency. Savitsky in 1934.' PCD is the most preva- light and noise sensitivity, and altered sense lent and yet controversial neuropsychiat~ic of taste and smell. The cognitive deficits diagnosis following brain injury. PCD is include memory difticulties, decreased at- linked most commonly to minor brain in- tention and concentration, decreased speed jury. because the symptoms are unobscured of information processing, communication by the myriad of findings that accompany a difficulties, difficulties with executive fin- more severe brain injuly. The constellation tioning (including initiation and planning, of symptoms includes physical symptoms. judgment and perception). and an increased cognitive deficits, and emotional sequelae. sensitivity to lack of sleep. fatigue, stress. PCD is described in the neurological, neu- drugs, and alcohol. Emotional symptoms ropsychological. psychiatric. and rehabilita- include emotional lability, irritability and tion medicine literature. Common physical aggression, a change in personality. fatigue and decreased energy, anxiety, depression, Dr. Anderson is clinical assistant PI-ofessor,Univcl-sity apathy, disordered sleep, loss of libido. and of British Colunlbia Faculty of Medicine, Department of poor appetite.' Psychiatry, Vancouver, Canada. Addl-ess cot-respon- dence to: Stephen I). Anderson, MD, University ol Although the underlying pathology of BI-itish Columbia Faculty of Medicine, Department ol PCD is uncertain, a generally accepted Psychiatry, 204-2775 Heathel- St., Vancouver, BC, Can- ada V5Z 1M9. theory is that it is caused by rotational

Bull Am Acad Psychiatry Law, Vol. 24, No. 4, 1996 493 Anderson sheer strains and corresponding diffuse surgery Update Series, ~lexander' in- axonal injury throughout the brain. Stud- cluded a computed tomography (CT) scan ies of primates have confirmed that ac- of a 59-yeat--old man who never lost con- celeration of the head without impact can sciousness, but developed amnesia and a cause severe diffuse destruction of brain personality change. His CT scan clearly substance. Gennarelli et al.' produced demonstrated hemorrhagic lesions in an- traumatic coma in 45 monkeys by accel- terior and inferior frontal regions. erating their heads without impact. At Patients suffering from PCD usually autopsy, the principal abnormality seen have a reduction in the overall speed, was best appreciated microscopically and efficiency, execution, and integration of consisted of diffuse axonal injury (DAI), mental processes. This has been de- which manifest as axonal retsaction balls scribed as "reduced information process- or abnosmalities of axonal morphology in ing capacity" by Gronwall.' Following the white matter of the brain. Axonal mild brain injury, patients have difficul- damage was not confined to focal areas, ties in areas that require them to analyze but rather was scattered widely through- complex information. and they therefore out the white matter of the cerebral hemi- present as slower. more distractible. and spheres. 0ppenheimer4 found damaged forgetful. When patients are concentrat- axons with neuropathological changes ing on point A. they are unable to also similar to more severe injury in five pa- process point B simultaneously. and they tients with mild traumatic brain injury therefore present as inattentive because who had died from other injuries. One of they are unable to process a normal the patients had been knocked down by a stream of information. motor scooter, had no loss of conscious- Often there are few if any findings on ness. and was described only as physical examination, and the micro- "stunned" following his accident. scopic bsain damage is usually not de- In addition to DAI, focal in.juries may tected with conventional imaging tech- occur following head injury. For exam- niques such as CT or magnetic resonance ple, contusions may appear on the under- imaging (MRI) scanning. Neuropsycho- surface of the temporal and frontal lobes logical assessment is often undertaken, and the anterior pole of the temporal but tends to err in the direction of under- lobes due to contact with rough bony estimating disorders. Many valid prob- surfaces. The orbital frontal cortex is par- lems are not registered on neuropsycho- ticitlarly sensitive to damage during ac- logical testing. Orbital-frontal deficits are celeration/deceleration injuries because difficult to detect with standard neuropsy- of its proximity to the bony structures of chological testing. Subtle changes in at- the skull. This area is sometimes irrever- tention and concentration, new learning ently referred to as the "dashboard" of the ability, word retrieval. and judgment of- brain.%any patients even with severe ten do not register in the testing. Tradi- focal contusions never lose conscious- tional IQ tests are often insensitive. Al- ness. In the 1984 Neurology LII~Neuro- though no single test is diagnostic of

494 Bull Am Acad Psychiatry Law, Vol. 24, No. 4, 1996 Postconcussional Disorder frontal lobe functioning, the tinker toy deficits may be temporary, this does not test has been shown to have some predic- mean that brain damage is reversible. tive value with regard to future employ- Brain tissue does not regenerate. The cu- ment.8 mulative effect of subsequent head injury, Most available tests of memory assess causing ongoing cognitive deficits. is an verbal memory and learning and do not example of the ongoing residual effects of involve high level processing of complex brain in.jury. As discussed by ~ronwell,' information. Patients, however-, often there may be persistent "cognitive fragil- complain of difficulties with episodic ity" to central nervous system (CNS) memory (for day to day activities) or with stressors. Ewing rt al.'" compared perfor- procedural memory (the learning and re- mance under conditions of mild hypoxia call process). It is important, therefore, to in a group of imiversity students who had carefully interview patients and obtain made a "full recovery" from mild head collateral information from family, injury between one and three years before fsiends. and employers. Psychiatric and the study was done with a matched group neuropsychological assessments are per- of control students who had never had a formed in quiet, controlled environments head injury. The mild head injury group that do not include the distractions and perfommd, when mildly hypoxic. at a sig- frustrations of everyday living. and these- nificantly lower level than control sib fore difficulties may be undesestimated. jects on a memory and vigilance task. Testing of a patient within a few Although the students who had suffered months of the injury with repeated tcsting previously fsom mild head injury had re- a year 01- more later may provide more turned to their previous level of function- useful information then an examination ing and had engaged in full-time univer- given at only one point in time. Testing sity work, the mild head injury may have that revealx improvement oves time helps left a residual effect that impaired their confirm that the disorder began at the ability to withstand another CNS stressor. time of the brain il~.jur~." Psychological factors may also intlu- Fortunately. the majority of studies ence late symptoms. This often occurs suggest that although PCD is seen in the when primary deficits are undiagnosed, majority of patients within the first month resulting in a dysfunctional cycle. Pa- following mild traumatic brain injury. the tients are frequently bewildered and over- incidence of PCD is reduced significantly whelmed by their symptoms. Despite by three to six months following the in- having relatively mild injuries, they may jury." However, at one year after inj~~ry. continue to be plagued by problems such approximately 15 percent of patients still as headaches. lack of enesgy. dizziness. have disabling symptoms.' '. I* Patients at and an inability to concentrate on or cope high risk of having pessistent PCD symp- with life's stressors. It is not surprising. toms include those with a history of head therefore. that patients become frustrated. injury and older patients (probably above angry, and depressed. ~a~"described 40 years of age).13 Although the cognitive how a person's sense of predictability and

Bull Am Acad Psychiatry Law, Vol. 24, No. 4, 1996 495 Anderson

Table 1 DSM IV Research Criteria for PCDa A. A history of head trauma that has caused significant cerebral concussion. B. Evidence from neuropsychological testings or quantified cognitive assessment of difficulty in attention or memory. C. Three or more of the following occur shortly after the trauma and last at least three months: 1. becoming fatigued easily; 2. disordered sleep; 3. headache; 4. vertigo or dizziness; 5. irritability or aggression on little or no provocation; 6. anxiety, depression, or affective lability; 7. changes in personality; 8. apathy or lack of spontaneity. D. The symptoms in criteria B and C have their onset following head trauma or else represent a substantial worsening of preexisting symptoms. E. The disturbance causes significant impairment in social or occupational functioning and represents a significant decline from a previous level of functioning. F. The symptoms do not meet the criteria for dementia due to head trauma and are not better accounted for bv another mental disorder. aSee Reference 17 stability may be disrupted. especially in cific criteria are suggested as including the absence of external validation of two of the following: (1) a period of un- symptoms: a cycle of "failure, fear, consciousness lasting more than five min- avoidance. anxiety, depression, loss of utes; (2) a period of posttraumatic amne- self-esteem, isolation, and alienation" sia that lasts more than 12 hours after may result. Personality changes and psy- closed head injury: or (3) a new onset of chiatric symptoms such as irritability may seizures (or marked worsening of a pre- occur as a direct result of mild traumatic existing seizure disorder) that occurs brain injury. but depressive symptoms within the first six months after the closed tend not to occur until at least six months head injury. after the injury. '" There are several difficulties with the definition of PCD provided in DSM IV. DSM IV Criteria for PCD The bulk of this article will focus on the The research criteria for PCD, as de- csiteria of loss of consciousness (LOC). scribed in DSM IV, is given in Table 1. Other apparent difficulties include the PCD is listed in Appendix B of DSM-IV, DSM-IV description of how PCD occurs which provides criteria sets and axes for as a consequence of closed head injury. further study.I7 In the text of DSM-IV, it However, "head injury" does not need to is noted that there is insufficient evidence occur in order for brain damage to occur. to establish a definite threshold for the Head injury is a poorly defined term that severity of closed head injury, but spe- refers to an injury to the head. face. and

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Table 2 confused. Patients need to be carefully Definition of Mild Traumatic Brain Injurya questioned, because approximately one- - - A patient with MTBI is a person who has had third of patients who are questioned fol- traumatically induced physiological disruption lowing MTBI give a history of an island of brain function, as manifested by at least one of the following: of recall well before memories become 1. any period of loss consciousness; continuous. resulting in a potential error 2. any loss of memory for events of underestimating the total duration of immediately before or after the accident; PTA.'~Patients with MTBI are often dis- 3. any alteration in mental state at the time of the accident (e.g., feeling dazed, charged from the hospital while still suf- disoriented, or confused); and fering PTA. When patients are inter- 4. focal neurological deficit(s) that may or viewed retrospectively. it cannot be may not be transient; but where the severity of the injury does not exceed the assumed that their memory is reliable. following: especially if they have had repeated brief- 1. loss of consciousness of ings by family members and others. Pro- approximately 30 minutes or less; spective assessment that commences 2. after 30 minutes, an initial Glasgow Coma Scale (GCS) of 13-1 5; and prior to the resolution of PTA overcomes 3. posttraumatic amnesia (PTA) not the possible errors inherent in assessing greater than 24 hours. PTA retrospectively by clinical interview. a From the Mild Traumatic Brain Injury Committee of but this is not always pos~ible.'~ the Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation The duration of PTA has been used as Medi~ine.~~ an indicator of the severity of injury. In 1932. Russell proposed mild head illjury neck area, which does not necessarily as causing PTA lasting up to 1 hour. cause injury to the brain. Instead. a more moderate head injury as causing PTA appropriate term would be "brain in.jury." lasting longer than 1 hour but less than 24 The definition of mild traun~atic brain hours, and severe head injury as causing illjury (MTBI) is fully defined later in this PTA lasting longer than 24 hours.'" Us- article (see Table 2). ing a duration of 12 hours of PTA as a Because seizures, rarely occur follow- cut-off for PCD would thesefore rule out ing MTBI. the proposed DSM-IV thresh- a number of patients who are suffering old criteria for concussion would essen- from moderate head injury. who have tially require both a period of LOC longer PTA less than 12 hours. and would by than five minutes as well as posttraumatic definition exclude all patients with mild amnesia (PTA) lasting longer than 12 head injury. hours. One difficulty is that PTA is not Another difficulty with the DSM-IV adequately defined. A generally accepted criteria is the stipulation that symptoms definition of PTA is the interval between need to be present for at least three the injury and the time when the patient months following the trauma. Evidence in begins to lay down continuous memory of the literature has suggested that for most ongoing events. PTA includes the time patients PCD symptoms are reduced sig- during which the patient was awake. but nificantly by three months posttrauma.

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One study conducted at three different ing, which includes setting goals. assess- locations showed that at one month after ing strengths and weaknesses, planning the injury most patients demonstrated at- and directing activity, initiating and in- tentional deficits and reduced visual nlo- hibiting behavior, monitoring activity. tor speed. These problems, and associated and evaluating results. There may also be complaints of headache, fatigue, and diz- difficulties with communication. includ- ziness. diminished significantly during ing inefficient word retrieval. tangential- the next two months. However, at three ity of thought and speech. overtalkative- months almost all of the patients still ness, use of peculiar words and phrases. complained of headaches and many of and uninhibited choice of words. There them complained of fatigue and dizzi- may also be disorders of judgment and ness.-7 I Some patients may only have perception, including misinterpretation of marked impairment in their ability to actions or intentions of others. a tendency function at work for a few weeks follow- to bc socially inappropriate in verbal ing mild traumatic brain injury, and it is communications. and unrealistic ap- unclear why the DSM IV criteria requires praisal of onesself and one's strengths a duration of symptoms for at least three and weaknesses. Finally, there may be months. increased sensitivity to lack of sleep. fa- Concerning the symptoms themselves, tigue, stress. drugs, and alcoh~l.~It is DSM-IV includes a number of physical, iunclear why the DSM-IV criteria include cognitive. and emotional symptoms. only memory, attention. and concentra- Physical symptoms such as difficulties tion difficulties and do not include these with headaches, dizziness and vertigo, other cognitive deficits that commonly hearing loss. visual problems, and dimin- occur following MTBI. ished taste and smell are discussed. How- According to the DSM-IV criteria. if a ever, it is unclear why other physical patient has difficulties with memory func- symptoms such as nausea, tinnitus. im- tioning and executive functioning follow- paired coordination and balance, and light ing mild traumatic brain injury. he or she and noise sensitivity are not included. should be given a diagnosis of dementia. These physical symptoms co~nmonlyoc- not a diagnosis of PCD.~~In many ways. cur following MTBI. and some of them a diagnosis of dementia is easier to make may cause a marked impairment in the than a diagnosis of PCD, which is coun- ability to return to work. It is also unclear terintuitive to what one would expect. why the DSM-IV criteria only include the Following MTBI, a patient need only cognitive deficits of memory and atten- demonstrate problems with executive tion and concentration. Most patients also functioning and memory to be given a have impairment in their speed of infor- diagnosis of dementia. There is no need mation processing as represented with for the patient to experience a period of testing such as the paced auditory serial LOC or PTA to be given a diagnosis of addition task PASA AT).^' Patients also dementia. have difficulties with executive function- One of the major difficulties with the

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DSM-IV criteria is not only that LOC of of these patients are oriented by the time longer than five minutes is suggested, but they are first assessed and therefore score also that the term "loss of consciousness" at the top of the Glasgow Scale. Yet some (or LOC) has not been adequately de- of these patients have had a period of fined. Consciousness is not an "all or altered consciousness, either witnessed or nothing" phenomenon. Instead, there are evidenced by their being amnesic for levels of consciousness. For example, if events immediately following injury. The an accident victim is able to respond to impairment of consciousness is indicative painful stimuli but not verbal stimuli, are of diffuse brain damage, but there can they then labeled as being unconscious or also be marked local damage without ei- conscious? The answer is unclear. Defi- ther alteration in consciousness or amne- nitions of consciousness include vigi- ~ia."~' lance. the ability to react to the environ- ment. and awareness of facts and the Research on LOC and PCD content of mental phenomenon.24 Certain Despite the difficulties in defining terms have been used to describe degrees LOC, following are summaries of a few of consciousness including "alert wake- studies that explore the issue of LOC and fulness. lethargy. obtundation. stupor, PCD. and coma." However. these terms have Yarnell and ~ossie~~investigated 27 not been adequately defined, and it is patients who suffered apparent whiplash unclear from the DSM IV criteria whether injuries in motor vehicle accidents. The LOC refers. for example. to "obtunda- patients were assessed at least one year tion" or to "stupor," to both or to neither. following their injuries. None of the pa- There are difficulties, therefore, in defin- tients were more than initially dazed from ing consciousness or loss of conscious- their accidents, and periods of PTA were ness. It is assumed that others use the brief. All of the patients had been em- same definition of LOC. but this may not ployed prior to their accidents. The pa- be the case. tients suffered from the classical symp- The Glasgow Coma Scale (GCS), often toms of PCD. Neurological examination used by paramedics as well as physicians, and neurodiagnostic testing (MRI, elec- may provide a more accurate. objective troencephalogram. and brain stem audi- tool for measuring levels of conscious- tory response testing) results were ness. It should be noted, however, that the essentially normal. However. neuropsy- GCS was designed to classify severe chological evaluation showed impair- brain injuries and may be of little rele- ments on tests of vigilance. selective at- vance for patients suffering from mild tention, memory, mental stamina, and traumatic brain injury. Brian enn nett,^' cognitive flexibility. At 18 months the originator of the GCS, described how postinjury, none of the patients tested had the GCS was not intended to be a means returned to their previous level of occu- of distinguishing among different types of pational functioning. Fifty percent of milder injuries. Jennett wrote that "many them were unemployed and the other 50

Bull Am Acad Psychiatry Law, Vol. 24, No. 4, 1996 499 Anderson percent were working at a reduced capac- emission tomography (PET). PET scan- ity in terms of hours or income level. ning is a computerized technique that pro- Active involvement in a lawsuit did not duces a picture showing the distribution correlate with return to work. of radioactivity in the brain, after the in- In a commonly quoted study, Lenniger jection of a radioactive isotope. Whereas et examined 53 patients who had a CT or MRI scan provides a static pic- experienced PCD symptoms for at least ture of brain structure. the PET scan re- one month following motor vehicle acci- flects brain function by showing blood dents. Thirty-one patients had sustained a flow and metabolic activity in different brief LOC (concussion group). Twenty- areas of the brain. It provides an illustra- two were only dazed, with no LOC (mild tion of disruptions in brain metabolism by concussion group). Eight neuropsycho- monitoring the amount of glucose that logical tests were selected for their ability brain cells consume. Humayun et to measure brain dysfunction. The results studied regional glucose utilization with demonstrated that mild head injury pa- PET in three patients with mild head in- tients compared with control subjects ex- jury and persisting cognitive deficits. All perienced deficits on test of reasoning three patients had normal MRI and CT (category test), information processing scans. Compared with three control sub- (PASAT-revised), verbal learning (audi- jects. the patients had abnormal glucose tory verbal learning test), and attention utilization in several frontal and temporal and organization (complex figure-copy). regions and the left caudate nucleus. There was no evidence that illjuries asso- In a recent study by Ruff et nine ciated with LOC were more debilitating MTBI cases were examined. Four of the than injuries that resulted in "dazing" but nine patients reported no LOC. A control no LOC. In other words, as far as minor group of 24 right-handed volunteers was head injuries are concerned, the study used. All nine patients had negative CT or showed that the occurrence of LOC did MRI findings, but had positive neuropsy- not distinguish people as being at greater chological results. Patients had impair- risk for neuropsychological conse- ment on tests of sensory-motor function- quences. In addition, the authors found no ing, attention, memory and learning, evidence of differences between the liti- language, spacial abilities, as well as gating and the nonlitigating patients in problem-solving. All subjects received their study. the continuous performance test (CPT). One difficulty with such studies is that for which they were instructed during up- neuropsychological testing is not com- take. The PET findings validated the neu- pletely objective. Any examination that robehavioral sequelae on an objective ba- allows a patient to give at least two pos- sis not only for those with. but also for sible answers is not completely objective. those without, LOC. The patients were However. in recent years there have been examined at an average of 18 months objective studies of brain functioning us- postaccident. Neither the neuropsycho- ing imaging techniques such as positron logical findings nor PET findings were

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substantially different between mildly in- ~attok~'described how LOC does not jured patients with or without LOC. The always occur with concussion, and direct PET procedures documented neuropa- blows to the head are not necessary to thology, which was frequently pro- cause concussions. Instead, concussive nounced in the frontal and anteriotempo- effects may be associated with a whiplash ral regions. injury if the acceleration and deceleration Although further study is needed, it is are sufficiently rapid." ~ezak,~~in her clear that both PET and neuropsychological recent textbook. wrote that diffuse axonal test results provide converging evidence injury can occur without any direct im- that even mild traumatic brain injury with- pact on the head, as it.requires only the out LOC may lead to neuropathology in the condition of rapid acceleration/deceleration absence of evidence from MRI or CT scan- such as takes place in whiplash injuries. ning. Functional imaging techniques such Lezak also noted that the neuropsycholog- as functional MRI, PET, and single pho- ical sequelae of concussion without LOC ton emission computerized tomography do not differ in severity from those occur- (SPECT) are, however, rnainly research ring when there is a brief comatose period. tools at the present time and further studies Lezak described how patients whose inju- are needed to determine their validity. ries seem mild, as measured by most ac- General Literature on LOC cepted methods, may have relatively poor and PCD outcomes, both cognitively and socially. In the recent psychiatric textbook Neu- In addition to clinical research. it has ropsyclziatq of Traunzatic Brain Itzju q, generally been accepted in the scientific literature that LOC is not necessary for ~c~llister~~defined mild brain injury as postconcussional disorder to occur. Text- including injury with brief (less than 20 books and review articles in the neurolog- minutes) or no loss of consciousness and ical, neuropsychological, psychiatric, and with GCS scores, when available, of 13 to rehabilitation medicine literature have 15. McAllister described how "mild" generally adopted the opinion that MTBI brain injury is a misnomer. because the or PCD may occur without LOC. For sequelae may be anything but a minor example. in Prognosis qf Nei~rological problem. Instead, the constellation of Disorders, ~vans" wrote that LOC does symptoms that make up postconcussive not have to occur for the postconcussion syndrome leads to a surprisingly high rate syndrome to develop. In Current Therapy of disability. in Neurological Disease. ord don^' de- Finally. ~lexander'\ecentl~reviewed scribed how no LOC or temporary lapse the pathophysiology. natural history. and of cerebral function was necessary. Gor- clinical management of mild traumatic don wrote that "Any sufficient blow, fall, brain injury. He describes how MTBI in- or acceleration-deceleration movement of cludes cases in which there is no LOC. the head (such as whiplash) can cause but simply a brief period of dazed con- postconcussional syndrome." Binder and sciousness.

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Mild Traumatic Brain lnjury would most appropriately provide the Criteria minimum criteria for diagnosing a con- Because cognitive impairment may oc- cussion. PCD may also occur in patients cur without LOC, a more accurate defi- with more severe brain injury, but the nition for "concussion" needs to be given patients should at least have fulfilled the than that provided in DSM-IV for PCD. criteria for MTBI to be given a diagnosis Also, instead of the term "head injury," a of PCD. Using this definition of concus- more appropriate term would be "brain sion would be most consistent with the injury." because it has been shown that present literature. which clearly adopts brain injury may occur without actual the opinion that LOC does not need to darnage to the head (e.g., severe whip- occur, but the patient should at least have lash). A definition of MTBI has been experienced an alteration in mental state such as feeling dazed. disoriented. or con- developed by the Mild Traumatic Brain fused at the time of the accident. Head Injury Committee of the Head lnjury In- injury itself or a lengthy period of PTA terdisciplinary Special Interest Group of should not be a requirement for PCD. the American Congress of Rehabilitation ~edicine~~(see Table 2). The definition Conclusion of MTBI also includes the brain undergo- This article has examined some of the ing an acceleration/deceleration move- literature on MTBI and PCD. Although ment (i.e.. whiplash) without direct exter- PCD is listed only in an appendix of nal trauma to the head. The subsequent DSM-IV as a diagnosis that requires fur- symptoms include physical symptoms of ther study, the fact that it has been in- brain injury (e.g., nausea, vomiting, diz- cluded in DSM-IV is significant. Because ziness, headaches, blurred vision), cogni- it has now been defined in DSM-IV, cli- tive deficits (involving memory, attention nicians may use these listed criteria as the and concentration, and executive function- basis for making the diagnosis of PCD ing), and behavioral changes (including ir- and providing medicolegal opinions. ritability, disinhibition, and emotional labil- However, a more appropriate definition ity). The authors also described how of concussion has been suggested in this symptoms of brain injury may persist for article. It is clear that LOC is not neces- varying lengths of time after such a neuro- sary for PCD to occur. Similarly. a logical event, and how some patients may lengthy period of PTA is not required. In not become aware of, or admit, the extent of the future. precise definitions of terms their symptoms until they attempt to return such as LOC and PTA will be required to normal functioning. In such cases, the for diagnosis, research. and communica- evidence for MTBI must be reconstructed. tion. The cognitive sequelae of PCD MTBI may be overlooked in the face of should be expanded to include difficulties more dramatic physical injury (e.g., ortho- with executive functioning and other cog- pedic or spinal cord inju~y).'~ nitive deficits, and the duration of symp- I suggest that the definition of MTBI toms may be less than three months.

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Functional imaging techniques such as son P: Persisting effects of minor head injury observable during hypoxic stress. J Clin Neu- PET, SPECT, and MRI may soon shed ropsychol 2: 147-55, 1980 further light on patients who suffer from IS. Kay T: Neuropsychological treatment of mild cognitive deficits following MTBI de- traumatic brain injury. J Head Trauma Reha- bil 8:74-85, 1993 spite having experienced no LOC. 16. Varney NR, Martzke J, Roberts RJ: Major depression in patients with closed head injury. Neuropsychology 1:7-9, 1987 References 17. American Psychiatric Association: Diagnostic and Statistical Manual ol Mental Disorders Strauss I, Savitsky N: Head injury: neurologic (ed 4, App B). Washington, DC: APA, 1994, and psychiatric aspects. Arch Neurol Psychi- pp 704-06 atry 31993, 1934 18. Ewert J, Levin HS, Watson MG, et ul: Proce- Anderson SD: Postconcussional disorder: dural memory during posttraumatic amnesia common result of head injury. Can J Diagn in survivors of severe closed head i~~jury. 12:4:77-86, 1995 Arch Neurol 46:911-16, 1989 Gennarelli TA, Thibault TE, Adams H, et a/: 19. Forrester G, Encel J, Geffen G: Measuring Diffuse axonal injury and traumatic coma in post-traumatic amnesia (PTA): an historical thc primate. Ann Neul-ol l2:564-74, 1982 review. Brain Injury 8: 175-84, 1994 Oppenheimer DR: Microscopic lesions in the 20. Russell WR: Cerebral involvement in head brain following head injury. J Neurol Neuro- injury: a study based on the analysis of 200 surg Psychiatry 3 1:299-306, 1968 cases. Brain 35549-603, 1932 Varney NR, Menefec L: Psychosocial and 21. Levin HS, Mattis S, Ruff RM, et (11: Neurobe- executive deficits following closed head in- havioural outcome of minor head injury: a jury: in~plicationsfor orbital frontal cortex. J three-center study. J Neurosurg 66:234-43, Head Trauma Rehabil 832-44, 1993 1987 Alexandcr MP: Ncurobehavioural conse- 22. Gronwall D: Paced auditory serial addition quences of closed head injury. Neurol Neuro- task: a measure of recovery from concussion. surg (Update Ser) 5: 1-7, 1984 Percept Mot Skills 44:367-73, 1977 Gronwall D: Cumulative and persisting ef- 23. American Psychiatric Association: Diagnostic fects of concussion on attention and cognition, and Statistical Manual of Mental Disorders in Mild Head Illjury. Edited by Levin HS, (ed 4). Washington DC: APA, 1994, pp Eisenberg HM, Benton AL. New York: Ox- 146-52 ford Univel-sity Press, 1989, pp 153-62 24. Campbell RJ: Psychiatric Dictionary (ed 5) Bayless JD, Varney NR, Roberts RJ: Tinker New Yol-k: Oxford University Press, 1981, p toy test performance and vocational outcome 129 in patients with closed head injuries. J Clin 25. Jennett B: Some international comparisons, in Exp Neuropsychol 1 1 :9 13-1 7, 1989 Mild Head Injury. Edited by Levin HS, Eisen- Bell SD: Medico-Legal Assessment of Head berg HM, Benton AL. New York: Oxford Injury. Springfield, IL: Charles C Thomas, University Press, 1989, p 24 1992, p 196 26. Yarnell PR, Rossie GV: Minor whiplash head Levin HS, Mattis S, Ruff RM, et ul: Ncurobe- illjury with major debilitation. Brain Inj havioural outcome following minor head in- 2:255-8, 1988 jury: a three-center study. J Neurosurg 66: 27. Lenninger BE, Gramling SE, Fan-ell AD, et 234-43, 1987 ~11:Neuropsychologicd deficits in symptom- Rutherford WH, Merrett JD, McDonald JR: atic minor head in.jury patients after concus- Symptoms at one year following conc~~ssion sion and niild conc~~ssion.J Neurol Neurosurg from minor head injuries. Injury 10:225-30, Psychiatry 53:293-6, 1990 I978 28. I-lumayun MS, Presty SK, Lafrance ND. er a/: McLean A, Temkin NR, Dikmen S, et d: The Local cerebral glucose abnormalities in mild behavioral sequelae of head injury. J Clin closed head injured patients with cognitive Neuropsychol S:36 1-76, 1983 impairment. Nucl Med Comniun 10:355-44, Alexander MP: Mild traumatic brain in.jul-y: I989 pathophysiology, natural history, and clinical 29. Ruff RM, Crouch JA, Troster AI, et 01: Se- management. Neurology 45: 1253-60, 1995 lected cases of poor outcome following a mi- Ewing R, McCarthy D, Gronwall D, Wright- nor bl-ain trauma: con~paringneuropsycholog-

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