10
OTHER HEALTH OUTCOMES

Traumatic brain injury (TBI) is an important cause of death worldwide and contributes to a considerable number of deaths and disability in the United States. The Centers for Disease Control and Protection has estimated that about 50,000 of the 1.4 million people who sustain a TBI in the United States will die as a direct consequence (NCIP, 2008). This section examines mortality and premature death in people who have a TBI.

MORTALITY AND TRAUMATIC BRAIN INJURY
PRIMARY STUDIES

Mortality and Traumatic Brain Injury in Military Populations

That head injuries reduce life expectancy has been posited since World War I. Medical records of Bavarian World War I veterans who were patients at a head-injury center were analyzed in 1964–1966 (Walker et al., 1971) (see Chapter 5 for a description of the military cohorts). The head-injury center was established in 1916, and many of the 5,500 men who sustained head injuries in World War I were followed for up to 50 years (Credner, 1930). About 1,000 records were randomly selected, and death certificates were sought from social-welfare offices in Bavaria and West Germany. Vital statistics were obtained for 647 cases and matched with those of 616 uninjured Bavarian World War I decorated veterans, who were able to be traced because they received pensions. Veterans were excluded if they were born before 1880 or died before the age of 35 years, if death dates were unknown, or if records were incomplete. Both penetrating TBI and nonpenetrating TBI were identified; posttraumatic epilepsy was also assessed. Compared with the general population of German men who were at least 35 years old in 1925, those with head injuries had 1.8% more deaths than expected. In 1965, 73% of the veterans with TBI had survived from the age of 35 years to the age of 65 years compared with 80% of those without TBI. Life expectancy of veterans with TBI was about 4 years shorter than that of those without TBI. Posttraumatic epilepsy had the greatest effect on life expectancy after the age of 50 years. Weiss et al. (1982) used data from the same cohort through 1972 to assess life expectancy and correlate it with the severity of injury. By 1972, 77% of TBI veterans (497 of 647) and 78% of control veterans (483 of 616) had died. When TBI was categorized as shallow (nonpenetrating or penetrating less 3 cm; 314 veterans) or deep (penetration greater than 3 cm, perforating wounds, or wounds of ventricle or brainstem; 283 veterans), those with deep wounds



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10 OTHER HEALTH OUTCOMES Traumatic brain injury (TBI) is an important cause of death worldwide and contributes to a considerable number of deaths and disability in the United States. The Centers for Disease Control and Protection has estimated that about 50,000 of the 1.4 million people who sustain a TBI in the United States will die as a direct consequence (NCIP, 2008). This section examines mortality and premature death in people who have a TBI. MORTALITY AND TRAUMATIC BRAIN INJURY PRIMARY STUDIES Mortality and Traumatic Brain Injury in Military Populations That head injuries reduce life expectancy has been posited since World War I. Medical records of Bavarian World War I veterans who were patients at a head-injury center were analyzed in 1964–1966 (Walker et al., 1971) (see Chapter 5 for a description of the military cohorts). The head-injury center was established in 1916, and many of the 5,500 men who sustained head injuries in World War I were followed for up to 50 years (Credner, 1930). About 1,000 records were randomly selected, and death certificates were sought from social-welfare offices in Bavaria and West Germany. Vital statistics were obtained for 647 cases and matched with those of 616 uninjured Bavarian World War I decorated veterans, who were able to be traced because they received pensions. Veterans were excluded if they were born before 1880 or died before the age of 35 years, if death dates were unknown, or if records were incomplete. Both penetrating TBI and nonpenetrating TBI were identified; posttraumatic epilepsy was also assessed. Compared with the general population of German men who were at least 35 years old in 1925, those with head injuries had 1.8% more deaths than expected. In 1965, 73% of the veterans with TBI had survived from the age of 35 years to the age of 65 years compared with 80% of those without TBI. Life expectancy of veterans with TBI was about 4 years shorter than that of those without TBI. Posttraumatic epilepsy had the greatest effect on life expectancy after the age of 50 years. Weiss et al. (1982) used data from the same cohort through 1972 to assess life expectancy and correlate it with the severity of injury. By 1972, 77% of TBI veterans (497 of 647) and 78% of control veterans (483 of 616) had died. When TBI was categorized as shallow (nonpenetrating or penetrating less 3 cm; 314 veterans) or deep (penetration greater than 3 cm, perforating wounds, or wounds of ventricle or brainstem; 283 veterans), those with deep wounds 333

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334 GULF WAR AND HEALTH had slighter higher mortality between the ages of 45 and 60 years, but the difference was not significant (p = 0.6). Similar results were seen when cases were divided by severity of coma (p > 0.6). Confirming the results of Walker et al., Weiss and colleagues (1982) found that mortality was nonsignificantly (p = 0.08) higher in older TBI veterans with posttraumatic epilepsy than in older TBI veterans without posttraumatic epilepsy; moreover, posttraumatic epilepsy had a marked effect in reducing life expectancy (p = 0.01) in veterans with TBI compared with control veterans. Men with TBI were more likely to die of cerebrovascular disease than the controls (19% vs 12%; p = 0.01), particularly men younger than 60 years old (p = 0.015), but that difference did not correlate with the severity of the TBI. Corkin et al. (1984) continued work begun by Teuber and colleagues in 1948 on a cohort of 190 World War II veterans with penetrating TBI. Corkin et al. (1984) compared those veterans with a control group of 106 veterans who had peripheral nerve injury, matched for age at injury, years of formal education, and preinjury intelligence-test scores. As of 1983, 28.4% of the veterans with penetrating TBI and 17.0% of those with peripheral nerve injury had died—a statistically significant difference (p = 0.03). However, when veterans with head injuries were categorized by whether they had posttraumatic epilepsy, only those with epilepsy had significantly higher mortality than the controls (p = 0.0002). Such factors as the site of the brain lesion, age at injury, and preinjury and postinjury intelligence scores did not affect survival, although veterans with more education lived longer. Rish and colleagues (1983) followed 1,127 male Vietnam veterans who had penetrating head injuries for 15 years. Over the 15-year period, 90 deaths (8%) had occurred: 46 in the first year after injury, 9 during the second year, and then 1–4 per year. Most deaths occurred early in the first year after trauma and were the result of the injury or coma sequelae. After 3 years, compared mortality in the head-injured Vietnam veteran population approached the norm, according to actuarial projections for North American men 21–35 years old. Length of coma was the best predictor of long-term outcome, and posttraumatic epilepsy was not a significant factor in mortality in the first 15 years, although each seizure event carried its own inherent risk. Mortality and Traumatic Brain Injury in Civilian Populations Mortality in TBI patients can be studied from the time of injury, from the time of discharge from inpatient acute-care hospitals, or from the time of admission into or discharge from inpatient rehabilitation. Rates in cohorts of patients at those different points of entry into a study will be different. For example, rates in patients from the time of injury will be greatest because they include early deaths. In contrast, survivors of the acute phase who are studied during rehabilitation are likely to have lower mortality. Mortality in Patients from Time of Injury or Admission into Acute-Care Hospitals Brown et al. (2004) carried out a study to determine whether mortality from TBI was affected by the severity of the injury. Their population-based retrospective cohort study identified all Olmsted County, Minnesota, residents who had a diagnosis indicative of a potential TBI, and they reviewed the medical records from the Rochester Epidemiology Project for 1985– 1999 (see Chapter 5). The review confirmed 1,448 cases of TBI—164 (11%) moderate to severe and 1,284 (80%) mild. There were 68 deaths in the moderate-to-severe TBI group. The Kaplan–

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OTHER HEALTH OUTCOMES 335 Meier estimated 30-day case-fatality rate was 29.3% (95% CI, 22.0–35.9). The 68 deaths, compared with mortality in the 1990 Minnesota white population, were significantly more than the 12.8 expected (relative risk [RR], 5.29; 95% confidence interval [CI], 4.11–6.17); but the 14 deaths in those with moderate or severe TBI who survived for the first 6 months after injury did not differ significantly from the 12.7 expected (RR, 1.10; 95% CI, 0.60–1.85; p = 0.72). There were 78 deaths in the mild-TBI group, and the Kaplan–Meier estimated 30-day case-fatality rate was 0.2% (95% CI, 0.0–0.4). Over the full followup period, the 78 deaths were significantly greater than the 58.8 expected (RR, 1.33; 95% CI, 1.05–1.65; p = 0.012); but the 69 deaths in the people with mild cases who survived 6 months after injury were not significantly different from the 58.6 expected (RR, 1.18; 95% CI, 0.92–1.49; p = 0.173). Mortality in Patients Discharged from Acute-Care Hospitals Selassie et al. (2005) studied a representative sample of 3,679 TBI patients within a year of their discharge from any of 62 acute-care hospitals in South Carolina in 1999–2000 to document mortality within 15 months of discharge. Patients were stratified on the basis of TBI severity and hospital size. Of the sample, 3,371 (91.6%) were alive, and 308 (8.4%) had died within about 15 months of their discharge. Deaths were confirmed by using the Social Security Death Index (SSDI) and were classified as TBI-related or not. Of the 308 deaths, 17% were classified as TBI-related, and 63% of them occurred within the first 3 months after discharge, compared with 47% of the non-injury-related deaths. Findings indicate that the older the person, the higher the likelihood of early death. Males were more likely than females to die after TBI hospitalization if they were younger than 35 years old or older than 54 years old, but mortality was higher in females in the age range of 35–54 years. The authors also report that the severity of the TBI influenced mortality, as did the place of treatment. Patients who were treated in hospitals with trauma centers were less likely to die within 15 months after hospital discharge than patients treated in hospitals without trauma centers. Mortality in Patients Admitted into or Discharged from Rehabilitation Centers In a retrospective cohort study, Baguley et al. (2000) assessed mortality in 476 people who had sustained severe TBI over a 10-year period compared with an age- and sex-matched sample of the general Australian population. Patients with TBI, resulting primarily from closed head trauma due to motor-vehicle collisions, were admitted into a rehabilitation hospital 1986– 1996. Twenty-seven of the 476 patients with TBI had died by August 1997, for a mortality rate of 5.7%. The median interval between injury and death was 17 months (range, 45 days–108 months after injury). Mortality in the TBI group was significantly associated with a lower level of functional independence on the basis of the Functional Assessment Measure (p < 0.001) slightly significantly with male sex (p < 0.078), with greater age (38 vs 32 years of age; p < 0.055), and with a premorbid psychiatric history (p < 0.064), but not significantly with a history of premorbid substance abuse (p < 0.308). In the general-population sample, the mortality rate was 1.5%. A Fisher’s exact test indicated that significantly more people (p < 0.001) with TBI died (compared with the general population), with most deaths occurring in the first 12 months after injury. The leading causes of deaths were cardiorespiratory events (8 of 27) and infection (6 of 27). The study is limited by the short followup period of about 5 years, the use of data from only one state in Australia, and the lack of functional assessment of and preinjury data on 52% of the deceased and 22% of the living TBI patients.

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336 GULF WAR AND HEALTH Harrison-Felix et al. (2004) studied 2,178 patients with moderate to severe TBI identified in the Traumatic Brain Injury Model Systems (TBIMS) national database, which covers 15 TBIMS rehabilitation centers. Most of the TBIs resulted from motor-vehicle crashes (62%) or acts of violence (20%). The study participants had a mean age of 37 years, 76% were men, 60% were white, and 37% had severe TBI on the basis of 24-hour postinjury Glasgow Coma Scale (GCS) scores. Using vital-status information obtained from the SSDI the authors identified 161 deaths in 2,178 people with TBI who were followed for 17 days–12.8 years after injury for a mortality rate of 7.4%. Compared with age-, sex-, and race-specific mortality rates for the general population, the authors found that individuals with TBI were at twice greater risk of death than those in the general population (95% CI, 1.69–2.31). The median interval between injury and death was 2 years; 38 of the 161 deaths occurred between rehabilitation discharge and 1 year after injury. Life expectancy was reduced by 5–9 years (average, 7 years), depending on age at injury, race, and sex. Long-term survival of severely injured TBI patients was also studied by Ratcliff and colleagues (2005), who reviewed medical records of 640 TBI patients discharged from a rehabilitation hospital in Pennsylvania during 1974–1984 and during 1988–1989. Most of the injuries resulted from motor-vehicle crashes (66.6%), and falls were next most common cause (16.4%). There were 464 males and 176 females in the TBI population, and their mean age was 37 years. Vital status as of 1997 was determined by using the SSDI. There were 126 deaths, for a standardized mortality ratio (SMR), relative to the expected mortality in the Pennsylvania population, of 2.78 (p = 0.0001). An increased risk of early death was associated with a known history of alcohol abuse (SMR, 6.10; p = 0.0001), substance abuse (SMR, 8.00; p = 0.0264), and other personal or social problems (SMR, 7.03; p = 0.0001). A criminal record or history of psychiatric disorder and years of followup did not modify mortality. The studies by Brown et al. (2004) and Ratcliff et al. (2005) indicate that functional status at time of discharge from rehabilitation is a leading indicator of later survival time, although severity of injury and other demographic variables, such as age at time of injury, are not. Shavelle and Strauss (2000) published two mortality studies of people with TBI who received services from the California Department of Developmental Services and survived at least 12 months after injury. The department serves the severely disabled, including those with developmental disabilities and those with long-term cognitive deficits. In nonambulatory patients, observed mortality exceeded expected mortality by a factor of 16.6 in 15- to 29-year- olds and 7.3 in 30- to 44-year-olds. In patients who were more ambulatory, the SMR was 2.5 for 15- to 29-year-olds who could walk with support or could walk unsteadily for at least 10 feet and 2.7 for those who could walk well alone for at least 20 feet. SECONDARY STUDIES The committee identified 12 secondary studies, as discussed below. Several studies used cohort designs to examine mortality in people who have TBI. The people studied have been only patients with TBI; that is, there have been no external comparison groups. The best of the studies have followed patients from the time of TBI. Others have examined subsets of the universe of patients with TBI, such as those admitted into rehabilitation hospitals, in which case the more selective nature of the population (survivors of the acute period who enter rehabilitation) may

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OTHER HEALTH OUTCOMES 337 lead to death rates different from that in the whole universe of TBI patients who survive the acute period. Six population-based studies were identified; most found consistent results regarding TBI and increased mortality (Harris et al., 2003; Hukkelhoven et al., 2003; Engberg and Teasdale, 2004; Lu et al., 2005; Flaada et al., 2007; Winqvist et al., 2007;). Using data from the Rochester Epidemiology Project (see Chapter 5), Flaada and colleagues (2007) compared the observed number of deaths after TBI with the expected number of deaths. Mortality within 6 months increased with age in both moderate and severe TBI cases. Mortality in moderate and severe cases was 40 times that in mild cases independently of age. Among those surviving at least 6 months, 10-year mortality differed from expected only in the adult cases. Lu et al. (2005) studied mortality associated with TBI in 1984–1996 to determine whether mortality had been decreasing. The study population consisted of 1,839 severely head- injured patients, whose data were extracted retrospectively from the Traumatic Brain Injury Data Bank (635 patients), the Medical College of Virginia (382), and clinical-trial databases in the United States (822). People with penetrating head injuries and treatment groups in the clinical- trial databases were excluded. Of the 1,839 patients with severe TBI, 526 died, for a mortality rate of 28.6%. Over the period 1984–1996, mortality from severe TBI fell from 39% to 27%. After adjustment for a variety of factors—including age, admission motor score, and pupillary response—the difference remained significant (p < 0.05). Engberg and Teasdale (2004) conducted a population-based study of 389 patients identified in the national hospital register in Denmark who had cranial fractures or traumatic cerebral lesions. The mortality rate was assessed 15 years or more after injury. The acute and subacute mortality rate was 27% in those who sustained cerebral lesions and 4% in those who sustained cranial fracture. Harris et al. (2003) assessed mortality after head injury in 13,908 people identified through the New York State Trauma Registry from January 1, 1994, to December 31, 1995. The overall mortality rate in all age groups was 14.7% (range, 5.6–30.2%). The authors found an increased mortality rate with increased age: 10.9% at ages 0–30 years, 12.4% at ages 31–50 years, and 21.3% at age above 50 years. Winqvist et al. (2007) assessed mortality related to TBI by using the Northern Finland Birth Cohorts. One cohort is made up of people born in 1966 in two provinces in Finland and followed over a 34-year period. The authors identified 457 subjects who sustained their first ever TBI during 1966–2000, 78.1% of whom had sustained mild TBIs, including concussions and skull fractures. Nearly 10% had sustained moderate to severe TBIs, including brain contusions, intracranial hematomas, and diffuse traumatic axonal injuries. The authors found that the annual mortality in people with TBI was 14 per 100,000. Mortality related to TBI accounted for 12% of the total mortality in this group. Hukkelhoven et al. (2003) analyzed individual patient data from four prospective studies (three multicenter randomized clinical trials and one prospective series with closed TBI) to assess mortality and outcome related to TBI. The mean mortality rate ranged from 23% to 40% in the four studies; the mean proportion with an unfavorable outcome ranged from 43% to 60%.

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338 GULF WAR AND HEALTH The authors found that mortality increased with age from 21% in those 35 years old and younger to 72% in those 65 years old and older. Five secondary studies assessed mortality related to TBI in hospitalized patients (Miller and Jennett, 1968; Fearnside et al., 1993; Lai et al., 1998; Gomez et al., 2000; Pentland et al., 2005). Many of the study populations consisted of consecutive series of patients admitted to hospitals with TBI. The studies found consistent results regarding TBI and increased mortality. Fearnside et al. (1993) conducted a prospective study of 315 consecutive patients with severe TBI admitted to Westmead Hospital in Sydney, Australia. Severe TBI was defined as a GCS of no more than 8 within 6 hours after injury or deterioration to this level within 48 hours after injury. The authors found that GCS was inversely related to mortality. The correlation coefficient between mortality and GCS was 0.418 (t = 8.14; p < 0.005). Gomez and colleagues (2000) studied outcomes in a cohort of 810 patients with severe closed head injuries who were consecutively admitted to a hospital in Spain in 1987–1996. Severe head injury was defined as a GCS at admission of no more than 8 or deterioration to this level 48 hours after injury. At 6 months after injury, the overall mortality rate was 50.3%. In general, older patients had worse outcomes: the mortality rate reached 77% in the subgroup of 142 patients over 55 years old, but it was 37.5% in patients 46–55 years old. Miller and Jennett (1968) evaluated mortality in a consecutive series of 400 patients with depressed fracture of the skull who were treated in the neurosurgical division of the Institute of Neurological Sciences in Glasgow during 1956–1967. The authors found that the cases were associated with a significant increase in mortality (p < 0.005). Lai et al. (1998) conducted a retrospective study to evaluate long-term outcomes related to severe TBI in 70 patients admitted to a surgical intensive-care unit over a 29-month period. At 1 year after injury, the overall mortality was 50%. Pentland (Pentland et al., 2005) assessed mortality in a cohort of 1,871 patients with mild, moderate, and severe TBI admitted to a regional head-injury unit in Scotland between 1981 and mid-2002. Of the 1,871, 93 had severe TBI, 205 moderate, and 1,573 mild. Fifty-seven patients died during the initial admission into the unit (42 with severe TBI, 8 with moderate, and 7 with mild). During subsequent years, 340 patients died (six had severe TBI, 33 moderate, and 301 mild). Studies in the Sports-Injury Literature To study the influence of intense physical training on life expectancy, Bianco et al. (2007) examined male athletes born in 1860–1930 who had been inducted into various halls of fame: baseball (154), ice hockey (130), tennis (83), football (81), boxing (81), track and field (59), basketball (58), swimming (37), and wrestling (32). Because boxing is characterized by repetitive blows to the head, numbers of bouts and rounds were scrutinized. Median life expectancy of all the samples was 76.0 years; boxers had the lowest median life expectancy (73.0 years), and no differences were found by number of rounds or bouts.

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OTHER HEALTH OUTCOMES 339 SUMMARY AND CONCLUSIONS There is clear evidence of increased mortality in the acute phase after TBI and for some time afterward in both military and civilian populations with moderate to severe TBI. In the military literature, posttraumatic epilepsy in patients who initially survive penetrating head injuries is associated with an increased risk of death and about a 5-year decrease in life expectancy. In the civilian literature, studies in Minnesota suggest that although there is clear evidence of increased mortality in the first 6 months after injury, there is no evidence of increased mortality in patients with TBI beyond 6 months, regardless of severity. Studies of the subset of more severely injured patients who survive initial hospitalization and require inpatient rehabilitation demonstrate a worse prognosis, consistent with the greater degree of residual compromise: mortality some 2–7 times higher than in age- and sex-matched comparison populations. The committee has reviewed 10 primary studies and 12 secondary studies of TBI and mortality and has found consistent results. The committee concludes, on the basis of its evaluation, that there is sufficient evidence of a causal relationship between penetrating TBI and premature mortality in survivors of the acute injury. The committee concludes, on the basis of its evaluation, that there is sufficient evidence of an association between moderate or severe TBI and premature mortality in the subset of patients who are admitted into or discharged from rehabilitation centers or receive disability services. The committee concludes, on the basis of its evaluation, that there is inadequate/insufficient evidence to determine whether an association exists between surviving 6 months or more after sustaining a mild, moderate, or severe TBI and premature mortality.

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340 TABLE 10.1 TBI and Mortality Health Outcomes or Outcome Comments or Reference Study Design Population Type of TBI Measures Results Adjustments Limitations Baguley et Cohort Patients with TBI None Missing FAM, Severe; 97% Mortality by 476 patients, mean al., 2000 composed of admitted to Brain preinjury closed, August 1997 duration of followup clinical case Injury information on 3% penetrating (mean, 5 years 64 mo; 97% closed series Rehabilitation substance abuse, after trauma; head injury, 3% Service, Westmead psychiatric range, 8 mo–11 penetrating head Hospital, New history from years after injury; 62% MVC, South Wales, patients admitted trauma); 21% falls or hit by Australia, 1986– before 1990 on ascertained by object, 12% assault, 1996; cases had 52% of the New South Wales 4% sports-related survived through deceased, 22% vital-statistics admission into of the living; no search 27 of 476 (5.7%; 95% rehabilitation multivariate CI, 0.037–0.083) dead facility; analysis (median, 17 mo after comparison group: trauma; range, 45 day– expected mortality 9 years 2 mo after in age- and sex- trauma); expected matched Australian mortality rate, 1.5% population in 1997 (CI, 0.006–0.03) (p<0.001 by Fisher’s exact test) Contributing factors: low FAM on discharge (p < 0.001), being male (p = 0.078), greater age (p = 0.055), prior psychiatric morbidity (p = 0.064), but not prior substance abuse (p = 0.308) by x2 or t test Cause of death: cardiorespiratory arrest

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Health Outcomes or Outcome Comments or Reference Study Design Population Type of TBI Measures Results Adjustments Limitations (30%), infection (22%) Brown et Population- Any Olmsted Documented Vital status Age 35.3 years for Age, sex for Unique database al., 2004 based County, MN, concussion with through 2002 moderate–severe, 26.8 mortality on medical care retrospective resident with LOC; PTA; from medical years for mild; mean analysis; of county’s cohort from medically attended neurologic records, state followup, 7.4 years age, sex, year entire Rochester TBI, 1985–1999 (N signs of brain death tapes of TBI with population; Epidemiology = 45,831); random injury and/or Mortality in moderate– Cox cohort not Project 15.7% sample of intracerebral, severe: proportional- generalizable TBI patients (N = subdural, or 68 deaths in 164 cases; hazards beyond Olmsted 7,175) reviewed; epidural overall risk of death model for County—few 1,448 met inclusion hematoma; increased compared comparison minority-group criteria; cerebral with expected, RR, of moderate– members (96% comparison group: hemorrhage or 5.29 (95% CI, 4.11– severe vs white), all care age- and sex- contusion; brain 6.71) by long-rank mild in only 2 specific 1990 white stem injury; statistic; institutions Minnesotans penetrating 30-day CFR, 29.3% by head injury; Kaplan–Meier, risk skull fracture; increased compared or with expected, RR, postconcussive 5.29 (95% CI, 4.11– syndrome 6.71); 14 deaths in those Moderate or surviving 6 mo, no severe (11%): increase in risk, RR skull fracture, 1.10 (95% CI, 0.60– intracranial 1.85) hematoma, brain contusion, Mortality in mild: penetrating 78 deaths in 1,284 head injury, cases; overall risk of brain stem death increased injury, or compared with severe expected, RR, 1.33 complications (95% CI, 1.05–1.65); 9 (neurosurgery, deaths in first 6 mo CNS infection, (CFR, 0.2%), no 341

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342 Health Outcomes or Outcome Comments or Reference Study Design Population Type of TBI Measures Results Adjustments Limitations subarachnoid difference from hemorrhage, expected hydrocephaly, 69 deaths in those CSF leak) surviving 6 mo; risk of death not increased Mild (89%): compared with LOC, PTA, expected, RR, 1.18 postconcussive (95% CI, 0.92–1.49) symptoms, focal Comparison of neurologic moderate–severe with signs mild: risk of death increased in first 6 mo, RH, 5.18 (95% CI, 3.65–7.30) by Cox proportional-hazards model; no difference 6 mo, RH, 1.04 (95% CI, 0.57–1.88) Corkin et Prospective All WWII veterans Penetrating, at Mortality to Mortality: 54 of 190 Cox Vital status al., 1984 cohort (World with penetrating least 3 years 5/1/1983 as (28.4%) with proportional could not be War II head injury from after trauma function of penetrating head injury regression determined on veterans Teuber series (n = various factors dead vs 18 of 106 adjusted for only one subject assembled at 190); excludes few (17.0%), significant age at injury, (treated as alive); NYU by with difference by Kaplan– years of no cause-of- Teuber in nonpenetrating Meier (p = 0.03); those education, death data 1948) head injury; 106 with PT epilepsy (n = difference in collected WWII controls 82) more likely to be AGCT with peripheral dead than those (preinjury vs nerve injuries without (n = 91) or 10 years after matched for age, controls (p = 0.0002); trauma) education, PT epilepsy (p = preinjury AGCT 0.003), lower (85% of controls in education (p = 0.02) Teuber series with associated with death such injuries) by Cox

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Health Outcomes or Outcome Comments or Reference Study Design Population Type of TBI Measures Results Adjustments Limitations Harrison- Retrospective 2,178 TBI patients Age 37.4 years, Mortality from Mortality: 123 of Age, sex, Maximum Felix et al., cohort from 15 16 years old 76% male, 60% SSA Death Index 2,140; median, 2 race in followup only 13 2004 TBIMS completing white through 2001 years; overall, SMR, determining years, average centers inpatient 2.00 (95% CI, 1.69– SMRs from 3.1 years from 1 rehabilitation in Cause of injury: 2.31); <1 year after federal year after 1988–2000; sample MVC, 62%; trauma, 38 deaths; 1 statistics for trauma; 38% loss is 2,140 who violence, 20%; year after trauma, 123 2000; to followup; two survived >1 year falls, 16%; deaths, SMR, 1.95 Cox of 17 centers did after trauma; other, 2% (95% CI, 1.61–2.29); proportional not participate, comparison group: life expectancy, hazards for so sample less US age- and sex- Severity: 37% average reduction, 7 those representative specific mortality severe (24-h years, depending on surviving >1 in 1994 max GCS 8) age at injury, sex, race, year with range 5–9 years ALOS: 21 days acute care, 30 Risk factors: higher days acute age, unemployment at rehabilitation time of injury, higher DRS score at discharge Lewin et Retrospective 7,000 consecutive Severe in large Vital status; for Overall mortality, 178 Age, Only 2% loss to al., 1979 cohort head injured part closed, but 178 (consecutive of 469 (38%) maximum followup; patients admitted complicated by series), 28 central neural developed model (same into John Radcliffe compression or (selected series) Life expectancy for disability for predicting population Infirmary, Oxford, penetration who died, cause four neurophysical- score, long-term studied in 10–24 years earlier (traumatic or of death; for 331 disability patterns— maximum outcome on basis book by AH (1955–1969); of surgical for survivors, “decerebrate mental of age at injury, Robert, 1979, these, 479 amnesic internal neurologic dementia”: most <1 disability worst category with same or unconscious >1 decompression) examination (all), year, one >10 years; score, of mental and results, but week; additional for 77 and 14, test of cognitive “athetoid duration of neurophysical also mentioned selected series: 64 respectively, of function (217) pseudobulbar”: PTA for disability, length suicide as cases unconscious 331 survivors reduced only by model of PT amnesia in cause of >1 mo admitted to epilepsy, drowning, selected series increased this or other facility inhalation of food, deaths) 3–25 year earlier suicide; 343

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356 TABLE 10.2 TBI and Brain Tumors Health Outcomes or Outcome Study Comments or Reference Design Population Type of TBI Measures Results Adjustments Limitations Annegers et Double All TBI in Head injury with Brain tumors Four brain tumors observed None TBI that did not al., 1979 cohort Olmsted County, LOC, PTA, or skull (three astrocytomas, one reach medical care MN, 1935–1974 fracture meningioma); RR uncounted survived initial (observed/expected) not trauma; no significant overall or for two Expected numbers known pre- tumor types of tumors not existing tumor; adjusted for age or comparator data sex to match study from previous population incidence study of brain tumors in Olmsted County Burch et Case– All brain tumors Accidents, injuries Brain tumors 215 matched pairs analyzed; Matching on Excluded al., 1987 control in Toronto and that involved head more cases than controls basis of sex, area spongioblastomas, southern Ontario (not further reported injuries involving of residence, ependymomas, diagnosed in specified) head (RR, 2.51; p 0.0001), marital status, ±5 meningiomas, 1977–1981 and but difference not years of birth, neuroepitheliomas, still resident in significant if head injury date of pituitary adenomas, 1979–1982; of required medical attention diagnosis, date neurilemmomas. 328 eligible, 247 (RR, 1.2; p = 0.65) of death (if death (75%) occurred) Recall bias, participated; nonparticipation comparator, bias noted by matched hospital authors controls; of 410 controls asked to participate, 228 (56%) interviewed Carpenter Nested Workers at two Head injury, self- Fatal primary 82 primary brain Matched by race, Misclassification of et al., 1987 case–control nuclear facilities reported on malignancy of malignancies: OR, 0.9 (95% sex, work site, exposures in Oak Ridge, occupational- brain CI, 0.2–4.2); for tumors of year of birth, TN, in 1943– medicine pre- glial origin: OR, 1.4 (95% year of hire Outcome assessed 1977; cases employment CI, 0.3–7.2) by death certificate,

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Health Outcomes or Outcome Study Comments or Reference Population Type of TBI Measures Results Adjustments Design Limitations determined by assessments excluding those death certificate; who had not died four controls per of primary brain case malignancy Hochberg Case– Cases with Severe: resulted in Glioblasatoma, Unmatched analysis on 160 Stratification by Participation bias, et al., 1984 control glioblastomas skull fracture or histologically cases and 128 controls: age; RR adjusted recall bias from three concussion, confirmed overall RR, 2.1 (95% CI, (unknown for Boston, one followed by 1.1–4.0); severe RR, 3.8 what) Providence, one complications (95% CI, 1.3–11.0); mild Baltimore (such as coma, RR, 1.5 (95% CI, 0.7–3.3) hospitals; 15 intracranial years old; 160 of hemorrhage, Risk increased with age: 231 (69%) of epilepsy, shock, or RR, 10.6 (95% CI, 2.1– eligibles long-lasting 53.3) for 15 years old at participated; impairment of time of TBI 125 friend memory, hearing, controls matched or vision; mild: by 5-year age well-described group concussion or brief LOC without other complications Hu et al., Case– Cases from six History of head Histologically 34 of 218 cases vs 10 of 416 Matching on age Alcohol and skull 1998 control major hospitals trauma by self- confirmed controls reported head (±5 years), sex, x-rays also found in Heilongjiang report primary trauma; adjusted OR, 4.85 area of residence as risk factors Province, China, gliomas (95% CI, 2.52–9.44) in 1989–1995; requiring controls from surgery same hospitals with nonneurologic and nonneoplastic disease Inskip et Double All Danish Concussion, Intracranial Overall SIR, 1.36 (95% CI, None al., 1998 cohort; residents fractured skull, or tumors of CNS 1.20–1.53); 1 year PT 357

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358 Health Outcomes or Outcome Study Comments or Reference Population Type of TBI Measures Results Adjustments Design Limitations Danish hospitalized with other head injury SIR, 1.15 (95% CI, 0.99– population TBI, 1977–1992 1.32); no difference by cell with TBI (n = 228,955); type compared comparator, with Danish Danish population population without TBI without history of TBI Monteiro et Hospital- 231 patients 30– Head injury >1year New diagnosis Association with prior head Age, sex, Only 80% of cases al., 2006 based case– 65 years old before diagnosis of of primary injury: adjusted OR, 1.49 education, confirmed control newly diagnosed brain neoplasm brain (95% CI, 1.03–2.15) epilepsy, alcohol histopathologically, with primary (cases) or neoplasm, consumption but brain tumors in hospitalization including By histologic type: glioma nonhistopathologic 1999–2002, (controls) by self- cerebral (n = 31), OR, 1.30 (95% CI, findings most admitted into 10 report; meningiomas, 0.71–2.35); meningioma (n suggestive; hospitals in Rio hospitalization, brain cancer, = 38), OR, 1.63 (95% CI, participation rate de Janeiro, amnesia, LOC used cranial nerve 0.96–2.75); 94% for cases and Brazil; as indicators of tumors, benign other with histopathology (n 90% for controls; 261 controls trauma severity and = 15), OR, 1.07 (95% CI, reason for matched by age, unspecified 0.52–2.21); other without hospitalization for sex, region of brain tumors histopathology (n = 23), 37.4% of controls residence from OR, 1.92 (95% CI, 0.99– was trauma; recall inpatients for 3.73) bias cannot be conditions other ruled out; than brain cancer As function of severity: information on hospitalized (n = 15), OR, head injury based 0.78 (95% CI, 0.37–1.64); on self-reports lost consciousness (n = 22), OR, 1.03 (95% CI, 0.55– 1.94); amnesia (n = 5), OR, 1.48 (95% CI, 0.38–5.83); any of these (n = 31), OR, 0.93 (95% CI, 0.54–1.60) As function of number of head injuries: 1 (n = 74),

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Health Outcomes or Outcome Study Comments or Reference Population Type of TBI Measures Results Adjustments Design Limitations OR, 1.29 (95% CI, 0.85– 1.96); >1 (n = 28), OR, 3.14 (95% CI, 1.50–6.61; (p trend = 0.004) As function of years since head injury: 1–9 (n = 19), OR, 1.18 (95% CI, 0.73– 1.89); 10–19 (n = 27), OR, 1.31 (95% CI, 1.06–1.64); 20–29 (n = 23), OR, 1.07 (95% CI, 0.91–1.27); 30–39 (n = 20), OR, 1.09 (95% CI, 0.94–1.26); 40 (n = 18), OR, 1.09 (95% CI, 0.96– 1.24) Nygren et Retrospec- 311,006 patients Skull trauma that Primary brain 281 cases of brain tumors Stratification by Record-linkage al., 2001 tive hospitalized for survived tumors (55 meningiomas, age at injury, design permits population- TBI in 1965– hospitalization occurring >1 161 primary brain tumors, sex, years after assembly of large based cohort 1994 from (ICD-7 801, 853– year after 65 others) observed in TBI trauma, severity sample, but limited Swedish 855; ICD-8 801, trauma subjects (SIR, 1.0; 95% CI, of injury information Inpatient 850–854; ICD-9 through 1995 0.9–1.2); no relationship for available on other Register (of 801, 850–854); found by individual types of brain risk factors; discharges) considered in three linkage with tumor or severity radiation only without current severity groups: Swedish Suggestion of increase in likely confounder cancer vs age-, concussion, severe Cancer group 30–44 years old at for brain tumors, sex- and year- without Register, time of TBI: overall, SIR, but no apparent specific neurosurgery, Cause of 1.3 (95% CI, 1.0–1.7); problem in these incidence rates severe with Death benign meningiomas, SIR, negative findings; for Swedish neurosurgery Register, 1.0 (95% CI, 0.5–1.8); design adopted population Emigration primary brain tumors, SIR, because of question Register 1.4 (95% CI, 1.0–1.8); of reliability of other, SIR, 1.7 (95% CI, exposure recall in 0.8–3.2) case–control studies of brain- No suggestion of trend with tumor patients; 359

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360 Health Outcomes or Outcome Study Comments or Reference Population Type of TBI Measures Results Adjustments Design Limitations time since trauma (p = 0.69) completeness of or increasing age (p = 0.25) ascertainment of meningiomas in registry of malignant diagnoses unknown Phillips et Population- 200 cases newly History of head Newly 99 cases, 142 controls with Age at diagnosis, Participation 84% al., 2002 based case– diagnosed in trauma by self- diagnosed any head trauma: OR, 1.83 sex, skull in cases, 55% control January 1995– report; considered meningiomas (95% CI, 1.28–2.62); mild, radiography, CT random-digit June 1998, 18 “serious” if LOC, (intracranial); OR, 3.23 (95% CI, 1.82– scanning of dialing controls, years old, went to ED, or exposures 5.71); severe, OR, 1.27 head; race, 67% in Medicare histologic hospitalized before (95% CI, 0.82–1.98); single, education left out controls confirmation by diagnosis (case OR, 1.51 (95% CI, 0.99– of model when Cancer applied to two 2.29); multiple, OR, 2.75 shown to have Lack of blinding of Surveillance controls) (95% CI, 1.48–5.08) had no effect interviewers to System at Fred gathered by in- case or control Hutchinson; 400 person Time before diagnosis: status might controls, two per interviews <10 years, OR, 1.39 (95% increase potential case matched on CI, 0.72–2.68;) 10–19 years, for recall bias age ± 5 years, OR, 4.33 (95% CI, 1.28– sex by RDD or 2.62); 20 years, OR, 1.59 Cases arising less Medicare (95% CI, 1.09–2.31) than 1 year after eligibility lists; trauma not all English- excluded, so tumor speaking might have been residents of three cause of injuries or counties in found incidentally western during workup for Washington state TBI with telephone Conditional logistic analysis with information on medical, dental exposures to radiation

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Health Outcomes or Outcome Study Comments or Reference Population Type of TBI Measures Results Adjustments Design Limitations Dose–response relationship for number of head traumas but not expected direction with “severity” of head injury (as defined) Preston- Case– Cases, women Head injury >2 Meningioma, 185 matched pairs analyzed: Matched by sex, 189 of 218 (87%) Martin et control 65 years old years before histologically OR for head injury treated race or ethnicity, eligible cases al., 1980 with intracranial interview that was confirmed medically, 2.0 (95% CI, year of birth (±5 interviewed; meningiomas medically treated 1.2–3.5) years); by interviewers not identified by history selecting blinded to case– through cancer controls from control status registry living in neighborhood, Los Angeles also matched by Differential recall County; one socioeconomic bias matched control status; per case from multivariate neighborhood logistic regression Preston- Case– Cases, men 65 Head injury >2 Meningiomas, 105 matched pairs analyzed Matched by sex, One-sided tests of Martin et control years old with years before histologically with exact binomial test: race or ethnicity, significance; al., 1983 intracranial diagnosis by confirmed serious head injury not year of birth (±5 differential recall meningiomas history; severe related to boxing, OR, 1.9 (p years); by bias identified head injury defined = 0.01); boxed as sport, OR, selecting through cancer as LOC or 2.0 (p = 0.03); either boxed controls from registry living in permanent scar or had severe head injury neighborhood, Los Angeles unrelated to boxing, OR, 1.8 also matched by County; one (95% CI, 1.1–3.2) SES; matched control multivariate per case from logistic neighborhood regression Preston- Case– Cases, men 25– Serious head injury Gliomas and 272 matched pairs (202 Matched by sex, 277 of 478 (58%) eligible cases Martin et control 69 years old with >2 years before meningiomas, glioma, 70 meningiomas) race or ethnicity, 361

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362 Health Outcomes or Outcome Study Comments or Reference Population Type of TBI Measures Results Adjustments Design Limitations al., 1989 glioma or diagnosis of case histologically analyzed with exact year of birth (±5 interviewed; meningioma that resulted in confirmed binomial test years); by differential recall identified LOC, dizziness, or selecting bias less likely with through cancer medical For history of serious head controls from different findings registry, consultation trauma 20 years before neighborhood, for meningioma diagnosed in diagnosis: glioma, also matched by and glioma 1980–1984 in OR 0.8 (95% CI, 0.5–1.3); SES; Los Angeles meningioma, OR 2.1 (95% multivariate County; one CI, 1.1–5.4) logistic matched regression neighborhood For meningiomas only, control per case number of serious head injuries, p for trend = 0.01 Preston- Case– Cases from eight Medically treated Gliomas and 297 gliomas, 59 Individual and Subject to recall Martin et control centers in six head injuries; meningiomas meningiomas frequency bias; different al., 1998 countries subgroup of serious matching by age methods used for (Adelaide, TBI: medically Glioma: any TBI, males, and sex; some matching at Melbourne, treated injuries that OR, 1.18 (95% CI, 0.94– centers matched different centers Australia; resulted in LOC, 1.48), females, OR, 1.03 on race or Grenoble, PTA, or (95% CI, 0.42–2.55); any geographic France; hospitalization; serious TBI, males, OR, region; ORs Heidelberg, also recorded 1.13 (95% CI, 0.87–1.48), computed by Germany; participation in females, OR, 1.07 (95% CI, maximal- Toronto, sports (differed by 0.74–1.56) likelihood Winnipeg, region) that could estimates by Canada; result in TBI; Meningioma: any TBI, using both Stockholm, proxy respondents males, OR, 1.49 (95% CI, conditional, Sweden; Los could be used if 0.86–2.57), females, OR, unconditional Angeles, US; case or control 0.83 (95% CI, 0.54–1.28); logistic men, women 20 unavailable any serious TBI, males, OR, regression years old with 1.15 (95% CI, 0.57–2.34), diagnosed females, OR, 0.79 (95% CI, glioma or 0.45–1.39) meningioma Borderline increase in risk

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Health Outcomes or Outcome Study Comments or Reference Population Type of TBI Measures Results Adjustments Design Limitations for >1 TBI in men with glioma (OR, 1.52; 95% CI, .00–2.32) but not seen in women or men with meningioma No correlation with sports participation Risk of meningioma in men higher 15-24 years after trauma (OR, 5.35; 95% CI, 1.72–16.62) Schlehofer Population- 226 cases in Self-reported Primary brain For all tumor types: 46 of Age-, sex- 418 of 521 (72%) et al., 1992. based case– Rhein-Neckar- history of head tumors (ICD-9 226 (20%) vs 113 of 418 matching for potential controls control Odenwald area injury requiring 191, 191.1, (27%); RR, 0.71 (95% CI, controls participated; self- of Germany with medical attention; 192.0), 0.5–1.1) reports of head primary brain obtained by restricted to trauma; no tumors interview gliomas (115), For gliomas: 27 cases vs 66 comparisons by diagnosed 1987– meningiomas controls; RR, 0.70 (95% CI, severity or number 1988; controls, (81), acoustic 0.4–1.2) of injuries 418 randomly neuromas (30) selected from For meningiomas: 13 cases residential vs 39 controls; RR, 0.52 registers (95% CI, 0.3–1.0) NOTE: CI = confidence interval, CNS = central nervous system, CT = computed tomography, ED = emergency department, ICD = International Classification of Diseases, LOC = loss of consciousness, OR = odds ratio, PT = posttrauma, PTA = posttraumatic amnesia, RDD = random-digit dialing, RR = relative risk, SES = socioeconomic status, SIR = standardized incidence ratio, TBI = traumatic brain injury. 363

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364 GULF WAR AND HEALTH REFERENCES 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. Baguley, I., S. Slewa-Younan, R. Lazarus, and A. Green. 2000. Long-term mortality trends in patients with traumatic brain injury. Brain Injury 14(6):505–512. Bianco, M., C. Fabbricatore, N. Sanna, C. Fabiano, V. Palmieri, and P. Zeppilli. 2007. Elite athletes: Is survival shortened in boxers? International Journal of Sports Medicine 28(8):697–702. 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. Burch, J. D., K. J. Craib, B. C. Choi, A. B. Miller, H. A. Risch, and G. R. Howe. 1987. An exploratory case-control study of brain tumors in adults. Journal of the National Cancer Institute 78(4):601–609. Carpenter, A. V., W. D. Flanders, E. L. Frome, P. Cole, and S. A. Fry. 1987. Brain cancer and nonoccupational risk factors: A case-control study among workers at two nuclear facilities. American Journal of Public Health 77(9):1180–1182. Choi, N. W., L. M. Schuman, and W. H. Gullen. 1970. Epidemiology of primary central nervous system neoplasms. II. Case-control study. American Journal of Epidemiology 91(5):467–485. 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. Credner, L. 1930. Klinische und soziale auswirkungen von hirnsschädigungen. Z. Gesamte Neurologie et Psychiatrie 126:721–757. Engberg, A. W., and T. Teasdale. 2004. A population-based study of survival and discharge status for survivors after head injury. Acta Neurologica Scandinavica 110(5):281–290. Fearnside, M. R., R. J. Cook, P. McDougall, and R. J. McNeil. 1993. The Westmead Head Injury Project outcome in severe head injury. A comparative analysis of pre-hospital, clinical and CT variables. British Journal of Neurosurgery 7(3):267–279. 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. Gomez, P. A., R. D. Lobato, G. R. Boto, A. De la Lama, P. J. Gonzalez, and J. de la Cruz. 2000. Age and outcome after severe head injury. Acta Neurochirurgica 142(4):373–380. Harris, C., S. DiRusso, T. Sullivan, and D. L. Benzil. 2003. Mortality risk after head injury increases at 30 years. Journal of the American College of Surgeons 197(5):711–716. 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. Hochberg, F., P. Toniolo, and P. Cole. 1984. Head trauma and seizures as risk factors of glioblastoma. Neurology 34(11):1511–1514.

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OTHER HEALTH OUTCOMES 365 Hu, J., K. C. Johnson, Y. Mao, L. Guo, X. Zhao, X. Jia, D. Bi, G. Huang, and R. Liu. 1998. Risk factors for glioma in adults: A case-control study in northeast china. Cancer Detection and Prevention 22(2):100–108. Hukkelhoven, C. W. P. M., E. W. Steyerberg, A. J. J. Rampen, E. Farace, J. D. F. Habbema, L. F. Marshall, G. D. Murray, and A. I. R. Maas. 2003. Patient age and outcome following severe traumatic brain injury: An analysis of 5600 patients. Journal of Neurosurgery 99(4):666–673. Inskip, P. D., L. Mellemkjaer, G. Gridley, and J. H. Olsen. 1998. Incidence of intracranial tumors following hospitalization for head injuries (Denmark). Cancer Causes and Control 9(1):109– 116. Lai, Y. C., F. G. Chen, M. H. Goh, and K. F. Koh. 1998. Predictors of long-term outcome in severe head injury. Annals of the Academy of Medicine, Singapore 27(3):326–331. Lewin, W., T. F. Marshall, and A. H. Roberts. 1979. Long-term outcome after severe head injury. British Medical Journal 2(6204):1533–1538. Lu, J., A. Marmarou, S. Choi, A. Maas, G. Murray, and E. W. Steyerberg. 2005. Mortality from traumatic brain injury. Acta Neurochirurgica Suppl 95:281–285. Miller, J. D., and W. B. Jennett. 1968. Complications of depressed skull fracture. Lancet 2(7576):991–995. Monteiro, G. T. R., R. A. Pereira, R. J. Koifman, and S. Koifman. 2006. Head injury and brain tumours in adults: A case-control study in Rio de Janeiro, Brazil. European Journal of Cancer 42(7):917–921. NCI (National Cancer Institute). 2008. Brain Tumor. http://www.cancer.gov/cancertopics/types/brain/ (accessed September 4, 2008). NCIP (National Center for Injury Prevention and Control). 2008. Traumatic Brain Injury. http://www.cdc.gov/ncipc/tbi/TBI.htm (accessed July 31, 2008). Nygren, C., J. Adami, W. Ye, R. Bellocco, J. L. af Geijerstam, J. Borg, and O. Nyren. 2001. Primary brain tumors following traumatic brain injury—a population-based cohort study in Sweden. Cancer Causes and Control 12(8):733–737. Pentland, B., L. S. Hutton, and P. A. Jones. 2005. Late mortality after head injury. Journal of Neurology, Neurosurgery and Psychiatry 76(3):395–400. Phillips, L. E., T. D. Koepsell, G. van Belle, W. A. Kukull, J. A. Gehrels, and W. T. Longstreth, Jr. 2002. History of head trauma and risk of intracranial meningioma: Population-based case- control study. Neurology 58(12):1849–1852. Preston-Martin, S., W. Mack, and B. E. Henderson. 1989. Risk factors for gliomas and meningiomas in males in Los Angeles County. Cancer Research 49(21):6137–6143. Preston-Martin, S., A. Paganini-Hill, B. E. Henderson, M. C. Pike, and C. Wood. 1980. Case- control study of intracranial meningiomas in women in Los Angeles County, California. Journal of the National Cancer Institute 65(1):67–73. Preston-Martin, S., J. M. Pogoda, B. Schlehofer, M. Blettner, G. R. Howe, P. Ryan, F. Menegoz, G. G. Giles, Y. Rodvall, N. W. Choi, J. Little, and A. Arslan. 1998. An international case- control study of adult glioma and meningioma: The role of head trauma. International Journal of Epidemiology 27(4):579–586.

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366 GULF WAR AND HEALTH Preston-Martin, S., M. C. Yu, B. E. Henderson, and C. Roberts. 1983. Risk factors for meningiomas in men in Los Angeles County. Journal of the National Cancer Institute 70(5):863–866. Ratcliff, G., A. Colantonio, M. Escobar, S. Chase, and L. Vernich. 2005. Long-term survival following traumatic brain injury. Disability and Rehabilitation 27(6):305–314. Rish, B. L., J. D. Dillon, and G. H. Weiss. 1983. Mortality following penetrating craniocerebral injuries. An analysis of the deaths in the Vietnam Head Injury Registry population. Journal of Neurosurgery 59(5):775–780. Schlehofer, B., M. Blettner, N. Becker, C. Martinsohn, and J. Wahrendorf. 1992. Medical risk factors and the development of brain tumors. Cancer 69(10):2541–2547. Selassie, A. W., M. L. McCarthy, P. L. Ferguson, J. Tian, and J. A. Langlois. 2005. Risk of post- hospitalization mortality among persons with traumatic brain injury, South Carolina 1999- 2001. Journal of Head Trauma Rehabilitation 20(3):257–269. Shavelle, R., and D. Strauss. 2000. Comparative mortality of adults with traumatic brain injury in California, 1988–97. Journal of Insurance Medicine (Seattle) 32(3):163–166. Walker, A. E., H. K. Leuchs, H. Lechtape-Gruter, W. F. Caveness, and C. Kretschman. 1971. Life expectancy of head injured men with and without epilepsy. Archives of Neurology 24(2):95–100. Weiss, G. H., W. F. Caveness, H. Einsiedel-Lechtape, and M. L. McNeel. 1982. Life expectancy and causes of death in a group of head-injured veterans of World War I. Archives of Neurology 39(12):741–743. Winqvist, S., M. Lehtilahti, J. Jokelainen, H. Luukinen, and M. Hillbom. 2007. Traumatic brain injuries in children and young adults: A birth cohort study from northern Finland. Neuroepidemiology 29(1-2):136–142. Zampieri, P., F. Meneghini, F. Grigoletto, M. Gerosa, C. Licata, L. Casentini, P. L. Longatti, A. Padoan, and S. Mingrino. 1994. Risk factors for cerebral glioma in adults: A case-control study in an Italian population. Journal of Neuro-Oncology 19(1):61–67.