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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury 5 MAJOR COHORT STUDIES This chapter provides an overview of the major cohort studies identified by the committee that examined long-term health outcomes related to traumatic brain injury (TBI). The studies are categorized by population, including military and veteran populations, general population, and people who sustained sports-related TBIs. Most major cohorts, once established, led to additional health outcome studies, which the committee refers to as derivative studies. Table 5.1, at the end of this chapter, provides information on each original cohort study, including the study design, the recruitment method, the eligible population, the study population, and the percentage of subjects who were enrolled. Information on the derivative studies appears in the table under the information on the original cohort studies from which they drew their populations and includes purpose, design, enrollment of subjects, sample size, response rates, and other characteristics if provided by the study authors. The information on derivative studies helped the committee to identify the populations that have been studied frequently and to understand which studies were independent of each other so that it could avoid evaluating studies of health outcomes in the same population repeatedly. Studies discussed below might not be included as primary studies in Chapters 6 through 10, because they did not meet the committee’s strict criteria for primary studies. However, many of those not included as primary studies have been included as secondary studies and informed the committee’ decisions about the long-term consequences of TBI. GENERAL LIMITATIONS OF COHORT STUDIES A number of limitations were encountered when the committee was reviewing the studies that are detailed below. Among them are self-reporting of exposure and health outcomes, lack of representativeness, selection bias, and failure to include a reference or control population. Many of the cohort studies relied on self-reporting of exposure (such as TBI, concussion, and loss of consciousness) and outcomes (such as headache and memory problems) rather than clinical evaluation or medical-record review. Self-reporting of exposure in retrospective cohort studies introduces the possibility of recall bias, the tendency for participants who have an outcome to overestimate (or underestimate) their exposure. That can limit the usefulness of study findings because outcomes may not necessarily be attributable to the exposure in question (TBI).
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Self-reporting of outcomes can introduce reporting bias. Reporting bias, which occurs when the group being studied reports more frequently what it remembers than a comparison group, can potentially lead to an overestimation of the incidence or prevalence of symptoms or diagnoses in the exposed populations. Self-reporting of outcomes based solely on symptoms might also introduce misclassification bias, in which there are errors in how symptoms are classified into outcomes. Low participation rates, which can introduce selection bias, can severely limit the ability to generalize study results because the study population may not be representative of the larger population to which the results are meant to be generalized. A related issue is the use of inappropriate controls, such as comparison of military populations with civilian populations; military personnel may be healthier than the general population, so the two populations may be noncomparable. That is referred to as the healthy-warrior effect; there may have been nonrandom assignment of those selected and not selected for participation in the military. It is possible to measure the potential for such biases and to adjust for them in the analysis. Another important limitation of some of the cohort studies is that they lack unexposed control groups. An unexposed group is a necessary component of a well-designed cohort study because it permits comparisons of rates of disease between exposed and unexposed populations and understanding of how an exposure affects the incidence of an outcome. Some of the studies discussed below are registries of participants who presented for care. These studies are not intended to be representative of the symptoms and diagnoses of an entire population. Although this is not necessarily a limitation, many studies discussed below were not designed with the committee’s research question in mind. It was therefore difficult to use their findings to assess the broader question of the relation of long-term health outcomes to TBI. ORGANIZATION OF THE CHAPTER This chapter has sections on military cohort studies, population-based studies, other cohort studies, and sports-related studies. For each major cohort study, the methods for selecting the study population, the outcomes assessed, and the general findings are discussed. The committee was most interested in studies of long-term health outcomes related to TBI in military and veteran populations, so this group of studies is given primary consideration below. MILITARY STUDIES Studies of TBI have been conducted in nearly all the major conflicts of the 20th century, including World Wars I and II, the Korean War, and the Vietnam War; many of the studies evaluated seizure as the outcome of interest. Meirowsky (1982) noted that studying military populations “offers the advantage of similarity in age and general health of the subjects at the time of injury and the relative ease with which they can be followed in subsequent years.” The committee paid particular attention to studies that assessed TBI in military populations because these were generally long-term prospective assessments of the population of interest.
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury E. A. Walker’s Studies of Head-Injured Bavarian World War I Veterans Walker and Erculei (1970) examined a cohort of head-injured Bavarian World War I veterans. The veterans were patients at a medical center established in Munich in 1916 for head injuries. Medical records, including field medical records and neurology reports on 5,500 men who had sustained head injuries, were reviewed in 1964–1966. The records also included information on the men for up to 50 years after injury. About 1,000 records were randomly selected from the 5,500, and death certificates were sought from social-welfare offices in Bavaria and West Germany. Vital statistics were obtained for about 600 of the 1,000 men; the remainder could not be located. Controls were about 600 uninjured Bavarian World War I veterans. Men who were born before 1880, who died before the age of 35 years, or whose dates of death were not known were excluded. Head injuries were diagnosed on the basis of demonstration of immediate posttraumatic neurologic disturbance or evidence of a contusion, laceration, or compound wound injury of the scalp. Posttraumatic epilepsy was diagnosed on the basis of absence of preinjury seizures and the occurrence of seizures at some time after injury. Seizures were verified by a physician, nurse, or family member; if no outside party could verify the seizure occurred, this was noted. The authors noted that most of the patients had their first seizure within a year after the injury and others many years after the injury (Walker et al., 1971). Walker and colleagues (1971) compared life expectancy of those with injuries and unwounded Bavarian veterans of World War I who had been awarded service medals carrying small pensions. The injured group had 1.8% more deaths than expected in the general male population, and a 4-year shorter life expectancy than the control group. In 1965, 73% of men at least 65 years old with TBI and 80% of those at least 65 years old without TBI were alive. Weiss et al. (1982) used the same data and found that in 1972, 497 (76.8%) of 647 TBI veterans and 483 (78.4%) of 616 of the control group had died. E. A. Walker’s Studies of Head-Injured World War II Veterans Walker and Ercluei (1969) also conducted a cohort study of 364 severely head-injured World War II veterans 15 years after injury. Of these, 241 were originally studied at the Army Posttraumatic Epilepsy Center at Cushing General Hospital in Framingham, Massachusetts, in 1945–1946; these patients experienced at least one posttraumatic seizure. A battery of medical, psychologic, and electroencephalographic (EEG) tests were administered 1–3 years after injury; a 10-year followup consisted of examination, phone interview, or questionnaire. The authors reported that annual contact was made with nearly all subjects. The other 123, unselected head-injured men were studied as part of a followup in Baltimore from 1950 to 1954 and identified through Army and Veterans’ Administration (VA) pension rosters; the population was comparable with the Cushing General Hospital group in severity of injury. Medical records were not as detailed and complete as those on the group described previously. Neurologic, social, psychometric, and EEG tests were administered 6–9 years after injury. In general, the study participants had more severe brain wounds than would typically be seen in civilian or military hospitals. Dural penetrating frontal wounds tended to be included in the series although occipital and temporal injuries tended to be excluded (Walker and Erculei, 1969); dural penetration was found in 87% of the Cushing General Hospital group and in 71% of the Baltimore group (Walker and Erculei, 1970).
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury The authors contacted participants by mail, and information was obtained through interviews and examination. They collected data on time from injury to examination, socioeconomic and work status, clinical symptoms, state of cranium and scalp, neurologic examination, epileptic status, EEG examinations, and psychometric testing (Wechsler-Bellevue, Minnesota Multiphasic Personality Inventory, Goddard Form Board, and McGill Picture Anomaly Test). Information was obtained on 343 (94%) of the 364 men originally identified; 31 died, leaving 313 living patients.2 Of the 313, 243 (78%) were examined in person (Walker and Erculei, 1969). The authors assessed a variety of outcomes related to head injury, including neurologic symptoms (nervousness, headache, and other posttraumatic symptoms, such as nervousness and headache), posttraumatic epilepsy, employment status and other social-function outcomes, and psychologic outcomes. Of the 313 men, 212 (68%) reported some form of nervousness, from mild to severe, and 200 (64%) reported that they had experienced headaches. The authors also assessed posttraumatic syndrome, defined as a complex of symptoms that follow a minor head injury, including dizziness, nervousness, anxiety, and emotional instability. Of the 306 veterans on whom information was available, 34 (11%) reported no complaints, 65 (21%) had isolated symptoms, and 207 (68%) had posttraumatic syndrome (Walker and Erculei, 1969). Walker and Erculei (1969) also studied the prevalence of posttraumatic epilepsy. Two primary groups were defined for the analysis: 199 posttraumatic epileptic men from Cushing General Hospital and 114 men with posttraumatic encephalopathy from the Baltimore group who were matched by class of injury. Clinical examinations were conducted on 154 of those with epilepsy and 95 of those with encephalopathy. The authors found a statistically significantly lower survival rate in those with posttraumatic epilepsy. Patients with posttraumatic epilepsy were more likely to be unemployed (57%) than those with posttraumatic encephalopathy (14%). Similarly, neurologic deficits were more likely in the group with epilepsy than in the group with encephalopathy. Hemiplegia, for example, was found in 64% of the men with epilepsy and 40% of those with encephalopathy. Increased mental impairment was also noted in the epileptic group; in the memory tests, two errors or fewer were recorded by 85% of the posttraumatic-encephalopathy group and 66% of the epilepsy group. Walker and Erculei (1970) also assessed posttraumatic epilepsy and found that 15 years postinjury, 40% (n = 92) had no seizures of any time between the 5th and 15th year; 3% had no seizures from the 10th to 15th year. Twenty-three percent or 52 men continued to have 1 to 6 episodes annually; 68 had more than 6 episodes per year. In another analysis, Walker and colleagues (1969) assessed employment status after head injury in 303 subjects (nine were omitted because they were hospitalized during the followup assessment) and found that 182 (60%) men were regularly employed and 121 (40%) were unemployed or working irregularly. Neurologic deficits were also assessed (Walker and Erculei, 1969). Of the 249 men examined, 199 (80%) exhibited abnormality of neurologic function. Of those with abnormal neurologic function, hemiplegia was present alone or in combination with other findings in 118 (59%), hemianesthesia in 121 (61%), hemianopsia in 43 (22%), aphasia in 36 (18%), mental impairment in 13 (7%), and cranial nerve defect in 137 (69%). 2 Numbers as reported in study.
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Walker and Erculei (1969) found that few of the patients who had psychologic conditions in the early posttraumatic years recovered, 19 men developed mental abnormalities 10–15 years after injury, and severe mental disturbances occurred in only a small percentage of the patients. Finnish Studies Since 1948, the treatment, rehabilitation, and study of all head-injured Finnish war veterans have been monitored by one central institution, the Rehabilitation Institute for Brain-Injured Veterans. Achte and colleagues (1969), in an uncontrolled series, followed 3,552 men who suffered head injury in the Finnish wars of 1939–1945 to identify the prevalence of posttraumatic psychoses that developed up to 22–26 years after injury. On admission, mild injuries accounted for 19%, moderately severe for 59%, and severe for 22% of the sample; open head injuries were present in 42% of patients. Patients’ initial medical records and examination and treatment records were reviewed to ensure the presence of a brain injury; questionable cases were excluded. In addition, moderate and severe injuries may have been overrepresented inasmuch as patients with mild traumas were often left untreated. Most patients were examined personally by the authors; otherwise, records of psychiatric treatment were obtained in addition to personal communication with the patients. Between the time of injury and 1966, 317 (8.9%) of the original population experienced at least one psychotic episode; schizophrenic psychosis was the most prevalent at 21.1% of the 317 (it appeared to be more frequent in the mildly injured and those under 20 years old), followed by paranoid psychosis (17.6%), epileptic psychosis (14.6%), and concussion psychosis (13.7%). Psychosis began in 24.0% of the cases less than 1 year, in 16.0% 1–5 years, in 17.7% 5–10 years, and in 42.3% over 10 years after injury. In a more inclusive series by Achte and colleagues (1991), roughly 10,000 Finnish veterans were followed for 50 years after brain injury. Of them, 2,907 suffered some type of psychiatric disturbance throughout their lives, 26% (762) of which were classified as psychotic. At the time of study publication, 251 of those veterans were assigned a detailed diagnosis with the following distribution: delusional psychosis, 28%; major depression, 21%; delirium, 18%; and paranoid schizophrenia, 14%. Delusional psychosis tended to develop 15–19 years after injury and persisted for over 5 years in 40% of cases; paranoid schizophrenia and schizophreniform generally had a shorter latency—less than a year in 23% of cases—and persisted for over 5 years in 63% of cases. Teuber’s Cohort In the late 1940s and 1950s, Teuber and colleagues at the New York University–Bellevue Medical Center recruited and examined over 300 World War II veterans (and some from World War I and the Korean War) who lived near New York City and had sustained penetrating injuries of the brain or the peripheral nervous system (Weinstein, 1954). All the veterans in this longitudinal cohort study, originally identified from rosters maintained by the VA, incurred traumatic lesions in the service. Sensory, motor, and cognitive tests were administered to the veterans, first in Teuber’s New York laboratory and later by investigators at the Massachusetts Institute of Technology. In one early study by Teuber and Weinstein (1954), 35 brain-injured veterans and 12 controls with arm or leg peripheral nerve injury were selected for assessment of performance on a modified Seguin-Goddard formboard task by area of brain injury. The brain-injured veterans
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury made significantly more errors, recalled fewer forms, and had greater variability in the time it took to place the correct form in the correct opening. The investigators did not observe greater impairment in those with frontal lobe injuries than in those with lesions in the parietal, temporal, or occipital lobes. In another study, Weinstein and Teuber (1957a) obtained preinjury scores on the Army General Classification Test (AGCT) for 62 men who subsequently sustained penetrating brain injuries and 50 controls who incurred nerve injuries of the arm or leg. Both groups of men were retested with a comparable form of the AGCT (First Civilian Edition). The preinjury scores of the two groups were similar: the mean score was 106.4 in the controls and 105.0 in the brain-injured group. Scores on the postinjury test showed some gains in the controls (48 of the 50 controls increased their mean scores to 119.4) while there was little or no change in the brain-injured men’s test scores. In the same sample of veterans, Weinstein and Teuber (1957b) reported that the findings were independent of any effects for differences in preinjury education and preinjury AGCT score. A study of roughness discrimination was also conducted with Teuber’s cohort (Weinstein et al., 1958), in which 43 veterans with brain injury were compared with 20 controls with leg peripheral nerve injuries. The study participants’ task was to touch a patch of sandpaper and then attempt to find in a comparison array of 18 patches the one that was identical in roughness. Four sets of experiments were conducted: unilateral-successive for ipsilateral hand, unilateral-successive for contralateral hand, bilateral-successive, and bilateral-simultaneous. In all groups, there was a significantly lower average error in the unilateral experiments. However, there was a deficit in roughness discrimination in veterans who had sustained a penetrating brain injury. Under unilateral testing conditions, the left hand appeared to be more vulnerable to error than the right hand, regardless of the location of the brain injury. In more recent studies by Corkin et al. (1984, 1989), the investigators examined whether life expectancy or cognitive decline late in life is associated with having survived a penetrating brain injury. To study factors that might influence life expectancy, the authors evaluated 190 men who had sustained a brain injury during World War II and 106 men who had sustained peripheral nerve injuries during the war. Survival information was obtained from the VA, and the Kaplan–Meier method was used to estimate cumulative survival distributions for the two groups. Although sustaining a penetrating head injury alone did not shorten life expectancy, the risk of death increased when it was coupled with posttraumatic epilepsy. As of May 1, 1983, mortality was 3.6 times higher in veterans with brain injury and epilepsy than in veterans with peripheral nerve injury. Corkin et al. (1989) also evaluated the interaction between aging and effects of brain injury in a similar series of veterans. To study whether head injury exacerbates cognitive decline in later years, the authors evaluated 57 World War II veterans with head injury and 27 with peripheral nerve injury matched on age, premorbid intelligence, and education. The participants received two timed cognitive tests: the ACGT (Total, Vocabulary, Arithmetic, and Block Counting) and the Hidden Figures Test, in which participants trace a simple geometric figure embedded in another geometric figure. On all five cognitive measures, the group with brain injury was statistically significantly inferior to the control group 10 years after injury. Over another 30-year period (that is, 40 years after injury), cognitive decline was observed in the brain-injury group on every AGCT measure except Vocabulary as compared to the control group (Corkin et al., 1989).
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury W. F. Caveness Studies of Korean War Veterans In 1951, W. F. Caveness, then chief of the neurologic service in the US Naval Hospital, in Yokusaka, Japan, initiated a study of craniocerebral injuries in male military personnel wounded during or immediately after the Korean War. The participants were seen at Yokusaka or in the US Navy hospital ships off the coast of Korea. The investigators identified 467 cases in 1951–1954, many of them in Navy or Marine Corps personnel. During the initial period, investigators conducted a review of medical records, gave periodic physical examinations, distributed supplemental questionnaires and personal letters, and conducted interviews. The head injuries were categorized as related to missiles (resulting from contact with small-arms fire, grenades, land-mine mortar, or heavy artillery) or not related to missiles (resulting from blunt or sharp objects or vehicle accidents or secondary to blast); missile-related injuries accounted for more than half the injuries in the cohort (Caveness, 1963). A followup study was conducted 8–11 years after the initial injury. During the followup period, 356 of the original cases participated (76% of the total and 87% of those eligible for followup). Information was collected with a mailed questionnaire, a physical examination, interviews with the American Red Cross, and review of VA records. During the period 1957–1958, additional VA information was available on 85% of the participants. Questionnaires were obtained in 1961–1962 from 91% of the participants, personal letters from 22%, and telephone replies from 10% (Caveness, 1963). Additional studies of this cohort evaluated the prevalence of posttraumatic epilepsy as diagnosed by EEG. Seizures were diagnosed if they fulfilled the criteria for focal somatomotor, somatosensory, special sensory, or adversive seizures. Other less well-defined focal events, such as patterns attributed to the temporal lobe, were included if accompanied by other overt phenomena of seizures (Caveness, 1963). The investigators noted that generalized seizures, characterized by a loss in consciousness with or without bilateral motor expression, “were recognized either as a progression from a focal onset, in conjunction with focal seizures, or as a principal expression of the convulsive disorder.” Evans (1962) evaluated the prevalence of seizures in 422 of the head-injured Korean War veterans 3–11 years after injury. The authors found the overall prevalence of seizures to be 19.7%. Those with penetrating head injuries had a prevalence of seizures of 32%, those with blunt head injuries 8%, and those with blast wounds 2%. Caveness and colleagues (1962) assessed the prevalence of seizures in five retrospective cohorts from three wars (World War I, World War II, and the Korean War). In a random sample of 407 cases from the Korean War 5 years after injury, 24.1% had seizures—35.1% of those with missile head wounds and 12.2% with blunt or blast wounds. Caveness (1963) also found that 8–9% of the 467 men initially included in the study population had seizures within the first 2 weeks. Of the 356 men followed up 8–11 years after injury, 109 (30.6%) had seizures. Forty-two percent of those with penetrating head wounds and 16.4% with blunt head wounds had seizures. There was no significant difference in seizure incidence between the total original group and those followed for 8–11 years.
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Vietnam Head Injury Study The Vietnam Head Injury Study (VHIS) is a long-term, prospective followup study of head-injured Vietnam veterans, originally organized by William Caveness at the National Institutes of Health (NIH). The ultimate goal of the study is to evaluate the long-term neuropsychologic and other health outcomes of patients with penetrating head injury to learn about the role of head injury in the etiology of dementia and posttraumatic epilepsy, mechanisms of motor and cognitive recovery, and functions of various regions of the brain. The initial registry phase, conducted during the Vietnam War, consisted of military physicians’ entering demographic, injury, and outcome data on registry forms for about 2,000 head-injured soldiers who had survived the first week after sustaining injury. Data were entered during 1967–1970. Over 95% of the patients enrolled were male, had penetrating head injuries, and were 18–25 years old (Grafman, 2007). Phase I of the study was a detailed medical-records review conducted some 5 years after injury. At that time, the VHIS cohort consisted of 1,200 men who had either closed or penetrating head injuries. Field records and records of acute hospitalization, rehabilitation, and followup were available for all subjects. The VHIS cohort allowed tracking over long followup periods and included preinjury vocational and intelligence testing (National Naval Medical Center, 2008). Phase II, conducted primarily by Grafman and Salazar, was a collaborative effort of the VA, NIH, and the American Red Cross and consisted of a comprehensive inpatient evaluation at the Walter Reed Army Medical Center of 520 head-injured subjects from the original cohort of 1,200 and 85 matched normal controls who were evaluated in 1981–1984 (12–15 years after injury) (National Naval Medical Center, 2008). The controls were recruited from the VA files of non-head-injured soldiers who had served in Vietnam in the same years and were within the same age range as the head-injured soldiers. Many patients were lost to followup and were no longer receiving medical care or were not honorably discharged, because of behavioral changes related to their head injuries. Phase II was also used to identify these patients and refer them for appropriate medical care. During phase II, researchers conducted a number of tests of neurologic, motor, speech and language, and neuropsychologic outcomes. Phase II also identified veterans with specific lesions (such as orbitofrontal and dorsal frontal) or with particular cognitive or neurobehavioral deficits and studied the prevalence of posttraumatic epilepsy and cognitive function after head injury (National Naval Medical Center, 2008). Two such studies in phase II assessed seizures after head injury (Salazar et al., 1985; Swanson et al., 1995). Swanson and colleagues (1995) assessed interictal personality traits in 238 veterans who had developed seizure disorders and compared them with personality traits in 229 veterans with penetrating head injuries but without seizures and 84 uninjured controls. Of the 238 with seizure disorders, 39 had simple partial seizures, 59 had complex partial seizures, 76 had partial seizures with secondary generalization, and 64 had generalized seizures. The authors assessed history of psychiatric treatment, preinjury intelligence, brain-volume loss, seizure frequency, and duration of epilepsy. Statistically significant increases in interictal psychopathology were observed in the groups with complex partial seizures, partial seizures with secondary generalization, and generalized seizures (but not simple partial seizures) compared with controls. No group differences between groups with seizure types were found.
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury In an evaluation of 421 veterans from the VHIS cohort, Salazar and colleagues (1985) found that 53% had posttraumatic epilepsy. The relative risk of epilepsy in the head-injured veterans was 580 times higher than that in the general age-matched population in the first 6 months after injury and fell to 25 times higher after 10 years. Hemiparesis (p = 0.03), organic mental disorder (p = 0.015), aphasia (p = 0.009), headache (p = 0.001), and visual-field loss (p = 0.015) were associated with seizures. The authors found that the incidence of posttraumatic epilepsy was 86% in patients who had residual aphasia. Of patients with seizures, 57% had attacks within a year and 25% 1–5 years after injury; in about 18%, the first seizure occurred more than 5 years after injury; and in 7%, the first seizure occurred 10 years or more after injury. Patients with frequent seizures in the first year after injury were more likely to have a longer duration of epilepsy (p < 0.001). Of all those who sustained head injuries, 28% had persistent seizures 15 years after injury. The major limitations of the study include its lack of a reference group. It is also unclear whether seizures occurred before head injury. Phase III, conducted from 2004 to 2006, examined the role of head injury in cognitive neuroplasticity of the aging brain, memory and amnesia, such neurologic disorders as epilepsy, and social functioning. Phase III testing included elective neuroimaging, such as positron-emission tomography, and quantitative EEG. Of the 520 patients in phase II, 182 (35%) participated in phase III, and 17 were newly recruited. Of the 85 controls in phase II, 32 (38%) participated in phase III, and 23 were newly recruited (Grafman, 2007). Two studies from phase III have been published: TBI and cognitive outcomes and TBI and posttraumatic stress disorder (PTSD). Raymont and colleagues (2008) studied the relationship of preinjury intelligence, brain-tissue volume loss, lesion location, demographic variables, and the role of genetic markers in long-term cognitive decline. They found that subjects with penetrating head injury had a greater degree of overall cognitive decline than controls. Preinjury intelligence was the most consistent predictor of cognitive outcomes. Koenigs and colleagues (2007) studied the relationship between TBI and PTSD and found a “reduced occurrence of post traumatic stress disorder … following ventromedial prefrontal cortex damage and the complete absence of PTSD following amygdala damage.” Phase IV will begin in 2015, about 45 years after injury. The VHIS will provide baseline premorbid and injury information that can be used to asses the effects of penetrating head injury on the development of a variety of neurologic disorders in old age, the rate of physical and cognitive decline, and the effects of various variables on performance data. The investigators will re-examine the patients on some of the tasks (including standardized tests and the Armed Forces Qualification Test) administered during the phase II evaluation to assess cognitive, mood, personality, and neurologic functions. Vietnam Experience Study The Vietnam Experience Study (VES) was a multidimensional health assessment that began with data collection from Vietnam-era veterans in the middle 1980s, about 16 years after discharge (Luis et al., 2003). The VES included four components: medical and psychologic examinations, mortality assessments, telephone interviews, and reproductive-outcome assessments (CDC, 1989). The eligible population consisted of male US Army veterans who first entered the military during the period January 1965–December 1971, served at least 4 months on active duty, served only one tour of duty, obtained a military occupational specialty, and
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury achieved a pay grade no higher than E-5 (sergeant) on discharge. On the basis of those requirements, random sampling of military records found 9,324 men who had been members of the US Army and served a single tour in Vietnam and 8,989 who served elsewhere (CDC, 1989). From the total eligible population, 4,462 veterans were randomly selected. A comprehensive 3-day medical and psychologic evaluation was administered to ascertain what health-related events occurred from time of military discharge to the study date (Luis et al., 2003). Numerous studies were published on the basis of extracted data on the cohort; the three described below evaluate the effects of mild TBI. Luis and colleagues (2003) compared the prevalence of persistent postconcussion symptom complex (PPCSC) in veterans with and without a history of mild TBI. Of the 4,462 randomly selected veterans, 329 were excluded because they met criteria for PPCSC in the 10th edition of the International Classification of Diseases (ICD-10) or in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) but not both; 55 were excluded because of hospitalization, and 121 were excluded because data on them were incomplete. The remaining 3,957 were categorized as follows: 2,937 with no history of motor-vehicle accident (MVA) and no history of TBI, 488 with a history of MVA but no history of TBI, 323 with a history of TBI unaccompanied by loss of consciousness (LOC), and 209 with a history of TBI accompanied by LOC. Results indicated that the group that had had TBI with LOC had significantly greater odds of having PPCSC than the unexposed control group (odds ratio [OR], 2.84; 95% confidence interval [CI], 2.12–3.80). No significant difference was found between the group with a history of an MVA but no TBI and the group with TBI but no LOC. Multiple factors (demographic, psychiatric, and social support) accounted for 33% of the variance in PPCSC in participants with TBI (history of TBI with or without LOC), but significantly less variance was found in the no-TBI group (23.9%). Vanderploeg and colleagues (2007) used a cross-sectional cohort sample to examine the long-term psychiatric, neurologic, and psychosocial outcomes resulting from self-reported mild TBI. A subsample of 4,384 veterans (excluding 40 who were hospitalized after injury and 38 on whom data were incomplete) were categorized into three groups: no history of MVA and no history of TBI (normal control, 3,214, 73%), injured in an MVA but no history of TBI (MVA control, 539, 12.3%), and TBI with altered consciousness (mild TBI, 254, 5.8%); those who reported a TBI without LOC were excluded (n = 377, 8.6%). Age, education, enlistment General Technical Test scores, and medical and psychiatric conditions varied among the three groups and were statistically controlled for in later analyses. The mild-TBI group had higher odds of having depression than the normal control group (OR, 1.77; 95% CI, 1.13–2.78). Antisocial personality disorder was twice as prevalent in the veterans with mild TBI as in the normal control group, but this outcome probably reflects a risk factor for obtaining an injury, given the similar rates of preinjury conduct disorder. The odds of postconcussion symptoms (PCSs) were about doubled in patients with a history of mild TBI by both DSM-IV and ICD-10 criteria (OR, 2.00 and 1.80, respectively; 95% CI, 1.49–2.69 and 1.33–2.43, respectively). The odds of peripheral visual imperceptions were twice as high (OR, 1.98; 95% CI, 1.21–3.24) and of impaired tandem gait were about three times as high (OR, 2.93; 95% CI, 1.34–6.38). People with TBI had higher odds of being unmarried (OR, 2.01; 95% CI, 1.57–2.75) and higher odds of employment issues (OR, 1.89; 95% CI, 1.36–2.64), low income (OR, 1.88; 95% CI, 1.29–2.74), and self-reported disability (OR, 2.90; 95% CI, 1.63–5.15).
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Vanderploeg and colleagues (2005) used the same cohort to conduct a cross-sectional study of neuropsychologic outcomes. A full 15-measure neuropsychologic battery with neurologic measures of tandem gait and peripheral visual attention was administered. Results revealed no statistically significant difference in any of the measures among the three groups. In examining more subtle differences in attention, concentration, and memory, it was found that the mild-TBI group had significantly higher odds of being unable to continue the Paced Auditory Serial Addition Test (PASAT) than either of the two control groups (comparison with normal control group: OR, 1.32; 95% CI, 1.00–1.73; comparison MVA control, OR, 1.53; 95% CI 1.10–2.13). With respect to working memory, the mild-TBI group had excessive proactive interference (comparison with normal control group: OR, 1.66; 95% CI, 1.11–2.47). PASAT continuation problems were associated with left-side visual imperceptions, and excessive proactive interference was associated with impaired tandem gait in the mild-TBI group. In another study of the VES cohort, Vanderploeg and colleagues (2003) conducted logistic regression analyses to survey long-term outcomes of work and marital status in people who had mild TBI and any pre-existing factors that may perpetuate the symptoms of the injury. The author notes that the subsample (after exclusion of 53 people because they were hospitalized and 87 because data on them were incomplete) consisted of 4,322 people: 626 (14%) who had a mild TBI (373 without LOC, and 253 with LOC) and 3,896 (86%) who did not have a TBI. Psychiatric disorders were assessed with the Diagnostic Interview Schedule (DIS-II-A), and psychosocial outcomes were gathered by trained examiners. Results indicate that the outcome of a mild TBI may be influenced by the presence of any pre-existing demographic, medical, or psychiatric factors. Factors associated with work and marital status accounted for 23% and 17%, respectively, of the variance in those with head injury. Variance was significantly lower in those without head injury: 13.6% and 9.4%, respectively. POPULATION-BASED STUDIES Rochester Epidemiology Project The Rochester Epidemiology Project is a medical-records-linkage system that encompasses detailed health-care information on residents of the City of Rochester and Olmsted County, Minnesota. Funded initially in 1966 with medical records dating back to 1910, the project was designed to link all medical data and clinical information developed by the Mayo Clinic with data obtained by community health providers, including Olmsted Medical Group, the Olmsted Community Hospital, the University of Minnesota Hospital, and the Minneapolis VA Medical Center. Each patient was assigned a unique identifier, and information on all medical visits has been recorded for each patient. The database includes thorough medical histories, clinical assessments, consultation reports, surgical procedures, laboratory and radiology results, death certificates, and autopsy reports (Flaada et al., 2007). The medical information is continuously updated into an electronic format. By maintaining complete medical histories, the Rochester Epidemiology Project provides the capability to conduct population-based studies of disease risk factors and health outcomes and can be used to study long-term secular trends in disease incidence (Melton, 1996). As of 1996, the project included medical records on a population with more than 3.6 million person-years of experience in 1950–1995 (Melton, 1996). The demographic characteristics of Olmsted County residents largely resemble those of the US white population (Melton, 1996). Over 1,500 publications have resulted from the project,
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Reference Purpose Study Design Population (Where Appropriate) Comments Eligible Located Enrolled (Response Rate) Dikmen et al., 1995c Global outcome, independent living, employment, income, Sickness Impact Profile Prospective cohort 466 subjects with TBI selected from 3 prospective, longitudinal studies (Behavioral Outcome in Head Injury, Patient Characteristics and Head Injury Outcome, and Dilantin Prophylaxis of Post-Traumatic Seizures) 91% of 514 subjects followed to 1 year after injury Results presented as weighted averages to adjust for differences in eligibility criteria between studies 374 of 418 (89%) followed to 1 year after injury 124 trauma controls who had bodily injury other than to head 88 friend controls, friends of TBI patients, with no pre-existing conditions Doctor et al., 2005 Employment status Prospective cohort 418 TBI working before injury from 4 longitudinal investigations enrolled 1980–1994 (Behavioral Outcome in Head Injury, Patient Characteristics and Head Injury Outcome, Dilantin Prophylaxis of Post-Traumatic Seizures, Valproate Prophylaxis of Post-Traumatic Seizures) Reference Eligible Population Type of Study or Methods Date(s) of Enrollment Subgroup (n= Eligible Subjects) Contacted or Located (% of Eligible) Responded or Enrolled (Response Rate) Comments Roberts (Radcliffe, UK) Studies Roberts, 1979 548 people (from total population of 7,000) 5–83 years old who sustained TBI and remained unconscious or amnestic > 1 week admitted to Radcliffe Infirmary, Oxford: 479 admitted directly of accident (consecutive series), 69 transfers from Addenbrook Hospital, Cambridge Prospective 1948–1961 11 lost to followup, 206 died, leaving 331 surviving patients (291 from consecutive series, 40 from selected series)
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Reference Purpose Study Design Population (Where Appropriate) Comments Eligible Located Enrolled (Response Rate) Roberts, 1979 Hypothalamic, pituitary dysfunction Prospective 291 patients from consecutive series Roberts, 1979 Positional vertigo, headaches Prospective 291 patients from consecutive series Roberts, 1979 Epilepsy Prospective 291 patients from consecutive series Lewin et al., 1979 Epilepsy, mortality Prospective, retrospective 291 patients from consecutive series, 75 patients in whom cause of death was determined Reference Eligible Population Type of Study or Methods Date(s) of Enrollment Subgroup (n= Eligible Subjects) Contacted or Located (% of Eligible) Responded or Enrolled (Response Rate) Comments Jennett (Oxford, Rotterdam, Cardiff, and Manchester) Studies Jennett and Lewin, 1960 Oxford series: 1,000 head-injured patients with at least brief period of unconsciousness Prospective, retrospective November 1948–February 1952 821 unselected patients admitted directly from accident site; 179 selected patients transferred from other hospitals—these cases were considered more severe and complicated
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Reference Purpose Study Design Population (Where Appropriate) Comments Eligible Located Enrolled (Response Rate) Jennett, 1969 Epilepsy Prospective 189 patients from Oxford series, cases from Lewin; 150 patients from Glasgow series epileptic within 8 weeks after injury; 73 patients with missile injuries as comparison group; 333 patients 1 year after injury, 219 patients 4 years after injury with depressed fractures from Oxford and Glasgow series Jennett, 1962 Epilepsy Prospective 381 patients who had blunt head injuries followed by early epilepsy (n = 139), late epilepsy (n = 282) drawn from Oxford series (additional patients captured outside study dates), Manchester and Cardiff, England Jennett, 1973 Epilepsy Prospective Patients with known risk factors for late epilepsy—early epilepsy, intracranial hematoma (evacuation within 14 days of injury), depressed fracture—drawn from Oxford series, Glasgow series; 250 patients with depressed fractures from Rotterdam Jennett, 1975 Epilepsy Prospective Summary of previous data and findings Reference Eligible Population Type of Study or Methods Date(s) of Enrollment Subgroup (n= Eligible Subjects) Contacted or Located (% of Eligible) Responded or Enrolled (Response Rate) Comments Football Players: Guskiewicz et al. 2005, 2007 Guskiewicz et al., 2005 All 3,683 living members of National Football League Retired Players Association Retrospective cohort 2001–2002 3,683 2,552 2,552 Reference Purpose Study Design Population (Where Appropriate) Comments Eligible Located Enrolled (Response Rate) Guskiewicz et al., 2007 Depression Retrospective cohort 2,552 (69%) responded to questionnaires
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Reference Eligible Population Type of Study or Methods Date(s) of Enrollment Subgroup (n= Eligible Subjects) Contacted or Located (% of Eligible) Responded or Enrolled (Response Rate) Comments Boxing Studies: Porter et al., 1996, 2003 Porter and Fricker, 1996 Male boxers in amateur boxing clubs in Ireland 16–25 years old; subjects had to complete minimum of 40 bouts Prospective, observational 1991–1992 53 53 20 selected randomly (38%) Many lost because of strict exclusion criteria; study of boxing, not brain injury; flawed comparison group in that controls also had concussion; differentiation in rate of concussion in cases, controls Exclusion criteria: excess alcohol consumption (> 20 standard drinks/week or > 4 drinks/day) Reference Purpose Study Design Population (Where Appropriate) Comments Eligible Located Enrolled (Response Rate) Porter, 2003 Neuropsychologic impairment Prospective, observational 20 male boxers from amateur boxing clubs in Ireland 16–25 years old; subjects had to complete a minimum of 40 bouts See comments above 1 case and 2 controls lost to followup NOTE: ALS = amyotrophic lateral sclerosis, CHSA = Canadian Study of Health and Aging, CT = computed tomography, DSM-IV = Diagnostic and Statistical Manual of Mental Disorders, 4th ed., ED = emergency department, GCS = Glasgow Coma Scale, GSW = gunshot wound, ICD-10 = International Statistical Classification of Diseases and Health Related Problems, 10th revision, LLI = lower-limb injury, LOC = loss of consciousness, MA = Massachusetts, MN = Minnesota, MS = multiple sclerosis, MTBI = mild traumatic brain injury, MVA = motor vehicle accident, PCS = postconcussion syndrome, PD = Parkinson disease, PPCSC = predictors of postconcussion symptom complex, PTA = posttraumatic amnesia, PTSD = posttraumatic stress disorder, TBI = traumatic brain injury, TCDB = Traumatic Coma Databank, UK = United Kingdom, US = United States, VA = Veterans Affairs, VHIS = Vietnam Head Injury Study, WA = Washington.
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury REFERENCES Achte, K., L. Jarho, T. Kyykka, and E. Vesterinen. 1991. Paranoid disorders following war brain damage. Preliminary report. Psychopathology 24(5):309–315. Achte, K. A., E. Hillbom, and V. Aalberg. 1969. Psychoses following war brain injuries. Acta Psychiatrica Scandinavica 45(1):1–18. Annegers, J. F., J. D. Grabow, R. V. Groover, E. R. Laws, Jr., L. R. Elveback, and L. T. Kurland. 1980. Seizures after head trauma: A population study. Neurology 30(7 Pt 1):683–689. Annegers, J. F., W. A. Hauser, S. P. Coan, and W. A. Rocca. 1998. A population-based study of seizures after traumatic brain injuries. New England Journal of Medicine 338(1):20–24. Annegers, J. F., W. A. Hauser, J. R. Lee, and W. A. Rocca. 1995. Incidence of acute symptomatic seizures in Rochester, Minnesota, 1935–1984. Epilepsia 36(4):327–333. Annegers, J. F., E. R. Laws, Jr., L. T. Kurland, and J. D. Grabow. 1979. Head trauma and subsequent brain tumors. Neurosurgery 4(3):203–206. Bower, J. H., D. M. Maraganore, B. J. Peterson, S. K. McDonnell, J. E. Ahlskog, and W. A. Rocca. 2003. Head trauma preceding PD: A case-control study. Neurology 60(10):1610–1615. Brown, A. W., C. L. Leibson, J. F. Malec, P. K. Perkins, N. N. Diehl, and D. R. Larson. 2004. Long-term survival after traumatic brain injury: A population-based analysis. Neurorehabilitation 19(1):37–43. Brown, A. W., J. F. Malec, N. N. Diehl, J. Englander, and D. X. Cifu. 2007. Impairment at rehabilitation admission and 1 year after moderate-to-severe traumatic brain injury: A prospective multi-centre analysis. Brain Injury 21(7):673–680. Bryant, R. A., and A. G. Harvey. 1998. Relationship between acute stress disorder and posttraumatic stress disorder following mild traumatic brain injury. American Journal of Psychiatry 155(5):625–629. ———. 1999a. The influence of traumatic brain injury on acute stress disorder and posttraumatic stress disorder following motor vehicle accidents. Brain Injury 13(1):15–22. ———. 1999b. Postconcussive symptoms and posttraumatic stress disorder after mild traumatic brain injury. Journal of Nervous and Mental Disease 187(5):302–305. Caveness, W. F. 1963. Onset and cessation of fits following craniocerebral trauma. Journal of Neurosurgery 20:570–583. ———. 1966. Posttraumatic sequelae: Chapter 17. In Head Injury: Conference Proceedings, edited by W. F. Caveness and A. E. Walker. Philadelphia, PA: Lippincott. Pp. 209–219. ———. 1972. Vietnam Registry of Head and Spinal Cord Injuries. Report to the Surgeon General, USN, USA, and USAF. Caveness, W. F., A. E. Walker, and P. B. Ascroft. 1962. Incidence of posttraumatic epilepsy in Korean veterans as compared with those from World War I and World War II. Journal of Neurosurgery 19:122–129. CDC (Centers for Disease Control and Prevention). 1989. Health Status of Vietnam Veterans: Vol. IV. Psychological and Neuropsychological Evaluation. Atlanta, GA: Centers for Disease Control and Prevention.
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Chandra, V., E. Kokmen, B. S. Schoenberg, and C. Beard. 1989. Head trauma with loss of consciousness as a risk factor for Alzheimer's disease. Neurology 39(12):1576–1578. Chesnut, R. M., S. B. Marshall, J. Piek, B. A. Blunt, M. R. Klauber, and L. F. Marshall. 1993. Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain injury in the traumatic coma data bank. Acta Neurochirurgica—Supplementum 59:121–125. Cifu, D. X., J. S. Kreutzer, J. H. Marwitz, M. Miller, G. M. Hsu, R. T. Seel, J. Englander, W. M. High, Jr., and R. Zafonte. 1999. Etiology and incidence of rehospitalization after traumatic brain injury: A multicenter analysis. Archives of Physical Medicine and Rehabilitation 80(1):85–90. Corkin, S., T. J. Rosen, E. V. Sullivan, and R. A. Clegg. 1989. Penetrating head injury in young adulthood exacerbates cognitive decline in later years. Journal of Neuroscience 9(11):3876–3883. Corkin, S., E. V. Sullivan, and F. A. Carr. 1984. Prognostic factors for life expectancy after penetrating head injury. Archives of Neurology 41(9):975–977. CSHA (The Canadian Study of Health and Aging). 1994. The Canadian Study of Health and Aging: Risk factors for Alzheimer’s disease in Canada. Neurology 44(11):2073–2080. ———. 2008. Canadian Study of Health and Aging. http://www.csha.ca/contact_us.asp. (accessed September 3, 2008). Dacey, R., S. Dikmen, N. Temkin, A. McLean, G. Armsden, and H. R. Winn. 1991. Relative effects of brain and non-brain injuries on neuropsychological and psychosocial outcome. Journal of Trauma-Injury Infection and Critical Care 31(2):217–222. Dikmen, S., J. Machamer, and N. Temkin. 1993. Psychosocial outcome in patients with moderate to severe head injury: 2-year follow-up. Brain Injury 7(2):113–124. Dikmen, S., J. Machamer, N. Temkin, and A. McLean. 1990. Neuropsychological recovery in patients with moderate to severe head injury: 2 year follow-up. Journal of Clinical and Experimental Neuropsychology 12(4):507–519. Dikmen, S., A. McLean, and N. Temkin. 1986. Neuropsychological and psychosocial consequences of minor head injury. Journal of Neurology, Neurosurgery and Psychiatry 49(11):1227–1232. Dikmen, S., N. Temkin, A. McLean, A. Wyler, and J. Machamer. 1987. Memory and head injury severity. Journal of Neurology, Neurosurgery and Psychiatry 50(12):1613–1618. Dikmen, S. S., J. E. Machamer, D. M. Donovan, H. R. Winn, and N. R. Temkin. 1995a. Alcohol use before and after traumatic head injury. Annals of Emergency Medicine 26(2):167–176. Dikmen, S. S., J. E. Machamer, J. M. Powell, and N. R. Temkin. 2003. Outcome 3 to 5 years after moderate to severe traumatic brain injury. Archives of Physical Medicine and Rehabilitation 84(10):1449–1457. Dikmen, S. S., J. E. Machamer, H. Winn, and N. R. Temkin. 1995b. Neuropsychological outcome at 1-year post head injury. Neuropsychology 9(1):80–90. Dikmen, S. S., J. E. Machamer, H. R. Winn, G. D. Anderson, and N. R. Temkin. 2000. Neuropsychological effects of valproate in traumatic brain injury: A randomized trial. Neurology 54(4):895–902.
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Dikmen, S. S., B. L. Ross, J. E. Machamer, and N. R. Temkin. 1995c. One year psychosocial outcome in head injury. Journal of the International Neuropsychological Society 1(1):67–77. Dikmen, S. S., N. R. Temkin, J. E. Machamer, A. L. Holubkov, R. T. Fraser, and H. R. Winn. 1994. Employment following traumatic head injuries. Archives of Neurology 51(2):177–186. Dikmen, S. S., N. R. Temkin, B. Miller, J. Machamer, and H. R. Winn. 1991. Neurobehavioral effects of phenytoin prophylaxis of posttraumatic seizures. JAMA 265(10):1271–1277. Doctor, J. N., J. Castro, N. R. Temkin, R. T. Fraser, J. E. Machamer, and S. S. Dikmen. 2005. Workers' risk of unemployment after traumatic brain injury: A normed comparison. Journal of the International Neuropsychological Society 11(6):747–752. Evans, J. H. 1962. Post-traumatic epilepsy. Neurology 12:665–674. Flaada, J. T., C. L. Leibson, J. N. Mandrekar, N. Diehl, P. K. Perkins, A. W. Brown, and J. F. Malec. 2007. Relative risk of mortality after traumatic brain injury: A population-based study of the role of age and injury severity. Journal of Neurotrauma 24(3):435–445. Fraser, R., S. Dikmen, A. McLean, B. Miller, and N. Temkin. 1988. Employability of head injury survivors: First year post-injury. Rehabilitation Counseling Bulletin 31(4):276–288. Grafman, J. 2007. Vietnam Head Injury Study Phase III: A 30-Year Post-Injury Follow-up Study. Rockville, MD: The Henry M. Jackson Foundation for the Advancement of Military Medicine. Grafman, J., A. M. Salazar, H. Weingartner, and D. Amin. 1986. Face memory and discrimination: An analysis of the persistent effects of penetrating brain wounds. International Journal of Neuroscience 29(1-2):125–139. Grafman, J., K. Schwab, D. Warden, A. Pridgen, H. R. Brown, and A. M. Salazar. 1996. Frontal lobe injuries, violence, and aggression: A report of the Vietnam Head Injury Study. Neurology 46(5):1231–1238. Groswasser, Z., G. Reider II, K. Schwab, A. K. Ommaya, A. Pridgen, H. R. Brown, R. Cole, and A. M. Salazar. 2002. Quantitative imaging in late TBI. Part II: Cognition and work after closed and penetrating head injury: A report of the Vietnam Head Injury Study. Brain Injury 16(8):681–690. Guskiewicz, K. M., S. W. Marshall, J. Bailes, M. McCrea, R. C. Cantu, C. Randolph, and B. D. Jordan. 2005. Association between recurrent concussion and late-life cognitive impairment in retired professional football players. Neurosurgery 57(4):719–726. Guskiewicz, K. M., S. W. Marshall, J. Bailes, M. McCrea, H. P. Harding, Jr., A. Matthews, J. R. Mihalik, and R. C. Cantu. 2007. Recurrent concussion and risk of depression in retired professional football players. Medicine and Science in Sports and Exercise 39(6):903–909. Guskiewicz, K. M., S. W. Marshall, S. P. Broglio, R. C. Cantu, and D. T. Kirkendall. 2002. No evidence of impaired neurocognitive performance in collegiate soccer players. American Journal of Sports Medicine 30(2):157–162. Haaland, K. Y., N. Temkin, G. Randahl, and S. Dikmen. 1994. Recovery of simple motor skills after head injury. Journal of Clinical and Experimental Neuropsychology 16(3):448–456. Harrison-Felix, C., G. Whiteneck, M. DeVivo, F. M. Hammond, and A. Jha. 2004. Mortality following rehabilitation in the traumatic brain injury model systems of care. Neurorehabilitation 19(1):45–54.
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Harrison-Felix, C., G. Whiteneck, M. J. Devivo, F. M. Hammond, and A. Jha. 2006. Causes of death following 1 year postinjury among individuals with traumatic brain injury. Journal of Head Trauma Rehabilitation 21(1):22–33. Harvey, A. G., and R. A. Bryant. 2000. Two-year prospective evaluation of the relationship between acute stress disorder and posttraumatic stress disorder following mild traumatic brain injury. American Journal of Psychiatry 157(4):626–628. Jennett, B. 1973. Epilepsy after non-missile head injuries. Scottish Medical Journal 18(1):8–13. Jennett, B. W. 1969. Epilepsy after blunt (nonmissile) head injury: Chapter 22. In The Late Effects of Head Injury, edited by A. E. Walker, W. F. Caveness, and M. Critchley. Springfield, IL: Charles C. Thomas. Pp. 201–214. Jennett, W. B. 1962. Epilepsy after Blunt Head Injury. London: William Heinemann. ———. 1975. Epilepsy after Non-Missle Head Injuries. Chicago: Year Book Medical Publishers. Jennett, W. B., and W. Lewin. 1960. Traumatic epilepsy after closed head injuries. Journal of Neurology, Neurosurgery and Psychiatry 23:295–301. Koenigs, M., E. D. Huey, V. Raymont, B. Cheon, J. Solomon, E. M. Wassermann, and J. Grafman. 2007. Focal brain damage protects against post-traumatic stress disorder in combat veterans. Nature Neuroscience 11(2):232–237. Kraft, J. F., K. A. Schwab, A. M. Salazar, and H. R. Brown. 1993. Occupational and educational achievements of head injured Vietnam veterans at 15-year follow-up. Archives of Physical Medicine and Rehabilitation 74(6):596–601. Kurland, L. T. 1994. Trauma and multiple sclerosis. Annals of Neurology 36 Suppl:S33–S37. Levin, H. S., H. M. Eisenberg, H. E. Gary, A. Marmarou, M. A. Foulkes, J. A. Jane, L. F. Marshall, and S. M. Portman. 1991a. Intracranial hypertension in relation to memory functioning during the first year after severe head injury. Neurosurgery 28(2):196–199. Levin, H. S., C. Saydjari, H. M. Eisenberg, M. Foulkes, L. F. Marshall, R. M. Ruff, J. A. Jane, and A. Marmarou. 1991b. Vegetative state after closed-head injury. A Traumatic Coma Data Bank report. Archives of Neurology 48(6):580–585. Lewin, W., T. F. Marshall, and A. H. Roberts. 1979. Long-term outcome after severe head injury. British Medical Journal 2(6204):1533–1538. Lindsay, J., D. Laurin, R. Verreault, R. Hebert, B. Helliwell, G. B. Hill, and I. McDowell. 2002. Risk factors for Alzheimer's disease: A prospective analysis from the Canadian Study of Health and Aging. American Journal of Epidemiology 156(5):445–453. Lu, J., A. Marmarou, S. Choi, A. Maas, G. Murray, and E. W. Steyerberg. 2005. Mortality from traumatic brain injury. Acta Neurochirurgica—Supplement 95:281–285. Luis, C. A., R. D. Vanderploeg, and G. Curtiss. 2003. Predictors of postconcussion symptom complex in community dwelling male veterans. Journal of the International Neuropsychological Society 9(7):1001–1015. Machamer, J., N. Temkin, and S. Dikmen. 2002. Significant other burden and factors related to it in traumatic brain injury. Journal of Clinical and Experimental Neuropsychology 24(4):420–433.
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