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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury 7 NEUROLOGIC OUTCOMES This chapter discusses neurologic outcomes, such as seizure disorders, postconcussion symptoms, ocular and visual motor degeneration, neuroendocrine disorders, and the neurodegenerative diseases dementia of the Alzheimer type, dementia pugilistica, parkinsonism, multiple sclerosis, and amyotrophic lateral sclerosis. SEIZURE DISORDERS The onset of seizures has been linked to an excessive electric discharge in the brain, cortical disruption, scarring, irritability, and the release of various endogenous neurotoxins (Silver et al., 2005). Seizures can cause a wide variety of symptoms, including loss of consciousness, shaking, and changes in vision, hearing, taste, mood, and mental function. There are two main types of seizures: generalized and focal. Generalized seizures result from abnormal electric activity on both sides of the brain, and focal, or partial, seizures result from localized excessive electric activity in one portion of the brain. A number of studies have noted the presence of seizures after traumatic brain injury (TBI). Seizures that occur within the first 7 days after TBI are termed acute symptomatic or provoked. Seizures that occur more than 7 days after injury are termed remote symptomatic or unprovoked. If unprovoked posttraumatic seizures are recurrent, they are called posttraumatic epilepsy. A 5% incidence of posttraumatic seizures has been found after closed head injury and a 30–50% incidence after open head injury (Silver et al., 2005). The overall risk of seizures caused by penetrating TBI related to war injuries is as high as 53%; in civilian populations, the overall risk of seizures after closed head trauma of any severity ranges from 0.5% to 8% (Jennett, 1975; Salazar et al., 1985). The prevalence of epilepsy in the general population as estimated by the Centers for Disease Control and Prevention during the period 1986–1990 was 4.7 cases per 1,000 persons (CDC, 1994). Garga and Lowenstein (2006) note that TBI “accounts for 20% of symptomatic epilepsy in the general population and 5% of all epilepsy.” Primary Studies The committee identified 10 primary studies that examined the association of TBI with seizures: six studies of military populations with penetrating head injuries and four of civilian cohorts with closed head injuries. See Table 7.1 for a summary of the primary studies.
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury The six primary studies lack the controls that were a key part of the Rochester Epidemiology Project (discussed below), but the rate of seizures in this group was generally higher than the rate in the general population. Furthermore, in most studies it is not possible to determine how many subjects had only a single seizure within 6 months of injury and none later. Thus, the overall proportion of those classified as having post-TBI seizures, ostensibly lasting more than 6 months, might be slightly inflated. In general, the risk of unprovoked seizures after penetrating TBI is higher than the risk after even the most severe forms of closed TBI. Caveness et al. (1962) compared the number of seizures reported by others in soldiers who sustained both penetrating and nonpenetrating head injuries during World War I (WWI; Credner, 1930; Ascroft, 1941), World War II (WWII; Russell, 1951; Walker and Jablon, 1961), and the Korean War (Caveness and Liss, 1961). They found that seizures were more likely to occur after penetrating head injury (34–43%) than after blunt and blast head injury (12–24%). Of the 317 cases in the WWI cohort, 34.8% reported having seizures compared with 28% of those in the WWII cohort and 24.1% of those in the Korean War cohort. The proportion of patients who had penetrating TBI that later had seizures ranged from 42% in the Korean War cohort (Caveness and Liss, 1961) to 47% in the WWI cohort (Ascroft, 1941). A followup study was conducted by Caveness (1963) 8–11 years after initial injury. During the followup period, 356 of the original Korean War subjects participated (76.2% of the total and 87.2% of those suitable for followup). Information was collected through mailed questionnaires, physical examinations, interviews with the American Red Cross, and a review of Veterans Administration (VA) records. During the period 1957–1958, additional VA information was available on 84.6% of the participants. Questionnaires were obtained in 1961–1962 from 90.5% of the participants, personal letters from 21.6%, and telephone replies from 9.6% (Caveness, 1963). Caveness (1963) found that of the 356 men, 109 (30.6%) had postinjury seizures; 30 patients had seizures that did not persist beyond 6 months, so 79 (22%) apparently had seizures more than 6 months after injury. Of those with penetrating head wounds, 42% suffered seizures, and 16.4% of those with blunt head wounds had seizures. The authors noted that there was no significant difference in the number of seizures between the total original group and those who were followed for 8–11 years. Evans (1962) assessed the prevalence of seizures in the same 422 head-injured Korean War veterans at 3–11 years after injury. The overall prevalence was 19.7%. The prevalence was 32% in those with penetrating head injuries, 2% in those with blast wounds, and 8% in those with blunt head injuries. Phillips (1954) conducted a conditional cohort study of 500 head-injured men admitted within 3 days of injury into the Military Hospital for Head Injuries, Oxford. Information was collected on amnesia, electroencephalographic findings, personal and family history, cerebrospinal fluid (CSF) pressure, epilepsy, intracranial hemorrhage, CSF leak, infection, mental-health changes, condition on discharge, and followup after rehabilitation. The author found that 31 men (6%) developed seizures after injury; 24 had generalized seizures, 5 focal seizures, and 2 mixed seizures. Seven with seizures had focal signs after injury, of whom 5 had focal seizures and 2 had generalized seizures. All the focal seizures occurred within the first 6 days after injury, whereas generalized seizures typically did not typically for several months. It is unclear whether the head injuries were combat-related, and the time between injury and seizure
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury is ambiguous. Thus, it was not possible to determine from the report the number of patients who had their only seizure within 6 months of injury. Russell (1968) conducted a conditional cohort study of the prevalence of epilepsy after penetrating head injury in 185 patients injured in WWII. The men were followed for 10–20 years after injury. Of the 185, 77 (41.6%) had posttraumatic grand mal epilepsy, and 40 (21.6%) were still having seizures 10 years or more after injury. The study was limited in that it did not include a control population and the cohort was not described in terms of age, sex, and nationality. It also is not clear who may have had only one seizure in the first 6 months after injury. Weiss et al. (1983) studied 1,221 head-injured Vietnam veterans enrolled in the Vietnam Head Injury Study (VHIS). Although the focus of the study was on prognostic factors in the occurrence of epilepsy, they reported that 31% of the cohort had seizures more than a week after injury. A followup study of this cohort was reported by Salazar et al. (1985) and by Rish et al. (1983). The four studies of closed TBI and seizure risk in civilians come from the Rochester Epidemiology Project (see Chapter 5). Annegers et al. (1980) reported the risk of unprovoked seizures in a cohort of 2,747 patients (1,132 children and 1,615 adults) in Olmsted County, Minnesota, who had sustained TBI in 1935–1974. An additional 4,541 patients who sustained TBI in 1975–1984 were added later (Annegers et al., 1998). As part of the Rochester Epidemiology Project, medical records containing physician diagnoses of TBI were linked to later medical records documenting unprovoked seizures in the study interval and compared with records of those who did not sustain TBI. The authors found the overall risk of unprovoked seizures after TBI to be 3.6 times (95% CI, 2.7–4.8) that in the noninjured population. That risk, also known as the standardized incidence ratio (SIR), was highest among those with severe TBI (SIR, 17.0; 95% CI, 12.3–23.6), followed by those with moderate TBI (SIR, 2.9; 95% CI, 1.9–4.1) and mild TBI resulting in loss of consciousness (LOC) or posttraumatic amnesia (PTA; SIR, 1.5; 95% CI, 1.0–2.2). The overall unprovoked-seizure risk was found to be highest in the first year after injury (SIR, 12.7) and to fall (to 4.4) 1–4 years after injury and fall further (to 1.4) 5 years or more after injury. That pattern of seizure risk over time was also found in each TBI-severity group. Although the risk of unprovoked seizures after mild TBI was increased at all times after injury, it was significantly different from the risk in the uninjured population only during in the period 1–4 years after injury. A limitation of both Annegers et al. studies (1980, 1998) is that the authors included children in the study and in the risk estimates. It is not possible with the available data to calculate rates for adults only, and reported rates may be misleading inasmuch as seizures occur more frequently in children than adults. Therefore, the generalizability to the veteran population is unclear. Two additional published analyses of the Rochester Epidemiology Project included children but presented the post-TBI incidence of seizures in adults separately. Annegers and colleagues (1995) reported that the age-adjusted incidence of post-TBI seizures in adults ranged from 2.0/100,000 person-years in 25- to 34-year-olds to 14.0/100,000 person-years in those over 74 years old. In addition, the age-adjusted incidence of post-TBI seizures was higher in males at all ages (8.6/100,000 person-years in males and 4.8/100,000 person-years in females). Singer (2001) used data from the Rochester Epidemiology Project to compare the incidence of post-TBI seizures with the incidence of idiopathic epilepsy previously determined for Olmsted County.
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Singer (2001) found that the incidence was highest in the first year after head injury. Compared with the expected seizure rate in idiopathic epilepsy, seizures were 3.1 times more likely to occur during the first year after mild head injury, 6.7 times more likely after moderate head injury, and 95 times more likely after severe head injury. Overall, mild head injury resulted in 0.4 excess seizure per 1,000 per year, whereas severe head injury resulted in 10 per 1,000 per year. Secondary Studies The committee identified 19 secondary studies of the relationship between TBI and the onset of seizures. The major limitation of the studies is lack of a control or comparison population. Two secondary studies were drawn from the VHIS registry, which is described in more detail in Chapter 5. Both studies found an increase in epilepsy 15 years after injury. Rish and colleagues (1983) studied male Vietnam veterans who had had penetrating craniocerebral injuries and had survived for 1 week after injury. Of 1,127 veterans, 378 had a diagnosis of posttraumatic epilepsy (34%). Similarly, Salazar and colleagues (1985) studied the first 421 head-injured veterans to followup as part of phase II of the VHIS and found that 53% had posttraumatic epilepsy. The relative risk of epilepsy in the head-injured veterans was 580 times that in the general age-matched population in the first 6 months and fell to 25 times higher after 10 years. About 57% of patients with seizures had attacks within a year after injury; in about 18%, the first seizure occurred more than 5 years after injury; and in 7%, the first seizure came 10 years or more after injury. At 15 years after injury, 28% of all those who sustained head injuries had persistent seizures. Jennett and Lewin (1960) and Jennett (1962, 1969, 1973, 1975) conducted a number of studies of posttraumatic epilepsy in head-injured patients admitted into hospitals in Oxford, Glasgow, and Rotterdam. (A detailed description of the cohort is included in Chapter 5.) Jennett and Lewin (1960) studied 1,000 patients who sustained nonmissile head injuries and were consecutively admitted to the Radcliffe Infirmary, Oxford, in 1948–1952. In the first month after injury, 4.6% of the cohort experienced seizures. Four years after the last case was admitted, the authors followed up the series to determine the rate of seizures and found that 28 (10%) of the 275 patients who were able to be followed had one or more seizures. Jennett (1962) assessed the incidence of epilepsy in 315 patients of the above cohort. The 315 patients included 75 who were in the inclusive series with early epilepsy and 240 from the original 1,000 who did not have early epilepsy. Some 58 cases of late epilepsy were observed in this population. Jennett (1969) expanded on the original Oxford series of patients by including additional cases and cases from a hospital in Glasgow, Scotland. Seizure risk was assessed in 600 patients who had blunt head injury and depressed skull fracture. After 1 year, 9.5% of the 333 patients able to be followed up had developed seizures. Jennett (1973) studied the Oxford and Glasgow population and included an additional 250 head-injured patients from Rotterdam who had depressed fractures. The incidence of late epilepsy in the unselected series of injuries was calculated to be about 5% and about 45% in those who sustained missile injuries. Jennett (1975) provided a summary of the seizure cases identified in the Oxford, Glasgow, and Rotterdam cohorts. Several other authors reported on head-injured patients admitted into the Radcliff Infirmary. Roberts (1979) studied the subset of head-injured patients admitted with severe TBI
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury (PTA of over a week or LOC of over a month). Of the 291 patients in this series examined 10–24 years after head injury, 25.5% developed seizures (Roberts, 1979). Lewin et al. (1979) reported that posttraumatic epilepsy was diagnosed in 28% of 479 patients admitted into the John Radcliffe Infirmary in Oxford in 1955–1969 with a head injury resulting in PTA or LOC of a week or more. Three secondary studies assessed seizure rates in veterans or military personnel who had sustained penetrating head injury. Wagstaffe (1928) studied the prevalence of epilepsy in 377 WWI veterans who had sustained a penetrating gunshot wound of the head and found that 37 had seizures and that “traumatic epilepsy is nearly ten times more common with penetrating wounds of the dura than with other injuries to the head.” Watson (1947) studied the prevalence of epilepsy in 279 patients admitted with penetrating head injury sustained during WWII and found that 101 (36.2%) had had seizures at the 2-year followup. Russell and Davies-Jones (1969) conducted a conditional cohort study of the occurrence of epilepsy after penetrating head injury in WWII soldiers and found that 42% of 562 soldiers had had epilepsy by 5 years after the penetrating TBI. Four secondary studies assessed seizure rates in head-injured patients admitted into hospitals. Miller and Jennett (1968) studied seizure rates in 400 patients who had penetrating or puncture head wounds. Over half had brief or no LOC and PTA less than 1 hour, and late posttraumatic epilepsy occurred in 9.5%. Stevenson (1931) assessed the occurrence of epilepsy in 84 patients who sustained gunshot wounds of the head; 74% of those with penetrating and 23% of those with superficial wounds of the head had epilepsy. Sargent (1921) found that 800 of 18,000 people who had sustained gunshot wounds of the head had seizures (4.5%). And Penfield and Shaver (1945) assessed epilepsy in patients admitted into a hospital because of a head injury in 1929–1941; of the 407 patients assessed, 11 developed epilepsy, for an incidence of 2.7%. Two secondary studies assessed risk factors for posttraumatic epilepsy. Angeleri et al. (1999) conducted a prospective study of risk factors for posttraumatic epilepsy in 137 consecutively enrolled patients up to 1 year after injury. They found that the posttraumatic epilepsy group included 18 who had at least two seizures at 2–12 months; risk factors included a low score on the Glasgow Coma Scale (GCS), early seizures, and single brain lesions seen with computed tomography (CT). Englander et al. (2003) also studied risk factors for late posttraumatic epilepsy in 647 patients who had moderate or severe TBI and were admitted into trauma centers within 24 hours of injury. The patients were followed for up to 2 years, until death, or until their first late posttraumatic seizure. Sixty-six had late posttraumatic seizures, 337 had no late posttraumatic seizures during the full 24-month followup, 167 had no late posttraumatic seizures during the time they were followed, and 54 patients were given anticonvulsants and did not have late posttraumatic seizures. The authors found that the highest cumulative probabilities of late posttraumatic seizures were associated with biparietal contusions (66%), dural penetration with bone and metal fragments (62.5%), multiple intracranial operations (36.5%), multiple subcortical contusions (33.4%), subdural hematoma with evacuation (27.8%), midline shift greater than 5 mm (25.8%), and multiple or bilateral cortical contusions (25%). In addition, initial GCS score was associated with the cumulative probabilities of late posttraumatic seizures at the 24-month followup (GCS score of 3–8, 16.8%; score of 9–12, 24.3%; and score of 13–15, 8.0%).
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Finally, Ryan et al. (2006) assessed seizure symptoms in 127 college undergraduates who reported a history of head injury. Participants were divided into three categories on the basis of their self-reported head-injury status: students who sustained head injury with brief LOC, students who had head injury with brief alteration of consciousness (AOC), and students who had no head injury. The authors found that those in the LOC group reported a greater frequency of seizure symptoms and a greater number of clinically significant seizure symptoms (p < 0.015) than the no-head-injury group and had more clinically significant seizure symptoms than the AOC group (p < 0.09). There was no significant difference between the AOC and no-head-injury groups in frequency of seizure symptoms or number of clinically significant seizure symptoms. Summary and Conclusion The committee reviewed 10 primary studies and 19 secondary studies of TBI and seizures. The secondary studies are largely supportive of the primary studies that indicate that brain injury is associated with seizure activity. Unprovoked seizures were strongly associated with most types of TBI. The highest risk of unprovoked seizures occurred in those suffering penetrating head injury (which usually occurred during military combat): 32–53% had seizures. After blunt trauma, seizure risk varied with initial injury severity. Compared with the healthy, uninjured population, the risk of unprovoked seizures was about 17–95 times higher after severe TBI and 2.9–6.6 times higher after moderate TBI. The seizure risk after mild TBI that resulted in LOC or PTA was about 1.5 times that in the healthy, uninjured population. The risk of seizure after a blast is not clear, although one study of Korean War veterans reported that 2% suffered a seizure within 11 years of injury. In general, the seizure risk after all forms of TBI appears to be highest within the first year after trauma and to decline thereafter. Animal models confirm the presence of seizures after both penetrating and blunt TBI. Using a lateral fluid percussion model of TBI in adult rats, several authors have demonstrated both provoked and unprovoked seizures (Golarai et al., 2001; Santhakumar et al., 2001; D’Ambrosio et al., 2004; Kharatishvili et al., 2006). A single episode of severe fluid percussion injury can cause a spontaneous seizure and recurrent seizures that become chronic and become worse with time (D’Ambrosio et al., 2004). Seizures have also been demonstrated after TBI induced in rats in a penetrating–ballistic-injury model (Williams et al., 2005). The committee concludes, on the basis of its evaluation, that there is sufficient evidence of a causal relationship between sustaining a penetrating TBI and the development of unprovoked seizures. The committee concludes, on the basis of its evaluation, that there is sufficient evidence of a causal relationship between sustaining a severe TBI and the development of unprovoked seizures. The committee concludes, on the basis of its evaluation, that there is sufficient evidence of a causal relationship between sustaining a moderate TBI and the development of unprovoked seizures. The committee concludes, on the basis of its evaluation, that there is limited/suggestive evidence of an association between sustaining a mild TBI
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury resulting in loss of consciousness or amnesia and the development of unprovoked seizures.
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury TABLE 7.1 Seizure Disorders and TBI Reference Study Design Population Type of TBI: Mild, Moderate, Severe; Blunt, Penetrating, Blast Health Outcomes or Outcome Measures Results Adjustments Comments or Limitations Annegers et al., 1980 Retrospective cohort 2,747 patients of Olmsted County, MN, with head injuries sustained 1935–1974 compared with age-, sex-specific rates in general population; followed for 28,176 person-years Excluded deaths within 1 mo, seizures before TBI, prior epilepsy, second head injury, prior TBI, seizure within 1 week of TBI, febrile seizures 1,132 of 2,747 patients (41%) were children less than 15 years old TBI determined by health-care provider, documented in medical record 195 severe head injuries: documented brain contusion (diagnosed by observation during surgery, or from focal neurologic abnormalities), intracranial hematoma, or at least 24 h of unconsciousness or PTA Seizures determined from medical records SIR; seizures in adults, children: < 1 year after trauma, SIR, 12.7 (95% CI, 7.7–20); 1–4 years after trauma, SIR, 4.4 (95% CI, 2.7–6.9); 5+ years after trauma, RR, 1.4 (95% CI, 0.7–2.5); overall SIR, 3.6 (95% CI, 2.7–4.8) Age- and sex-matched controls Children included in risk estimate; results include children, whose rates of seizures may be different from adults’ rates 912 moderate head injuries: skull fractures or head injuries, causing at least 0.5 h of unconsciousness or PTA 1,640 mild head injuries: no fracture but unconsciousness or PTA for less than 30 min Annegers et al., 1998 Retrospective cohort Same as above, but new cases added (4,541) for Mild: LOC or amnesia for less than 30 min Seizures determined from medical records Including children, adults: Mild: SIR, 1.5 (95% Cumulative probability of unprovoked Children included in risk estimate; results include children,
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Reference Study Design Population Type of TBI: Mild, Moderate, Severe; Blunt, Penetrating, Blast Health Outcomes or Outcome Measures Results Adjustments Comments or Limitations additional 10-year period (1975–1984) and followup of original cases (followup of 53,222 person-years) Moderate: LOC for 30 min–24 h or skull fracture Severe: LOC or amnesia for more than 24 h, subdural hematoma, or brain contusion CI, 1.0–2.2); moderate, SIR, 2.9 (95% CI, 1.9–4.1); severe, SIR, 17.0 (95% CI, 12.3–23.6) Mild: < 1 year, SIR, 3.1 (95% CI, 1.0–7.2); 1–4 years, SIR, 2.1 (95% CI, 1.1–3.8); 5–9 years, SIR, 0.9 (95% CI, 0.3–2.6); ≥ 10 years, SIR, 1.1 (95% CI, 0.5–2.1) Moderate: < 1 year, SIR, 6.7 (95% CI, 2.4–14.1); 1–4 years, SIR, 3.1 (95% CI, 1.4–6.0); 5–9 years, SIR, 3.0 (95% CI, 1.2–6.2); ≥ 10 years, SIR, 1.8 (95% CI, 0.8–3.6) Severe: < 1 year, SIR, 95.0 (95% CI, 58.4–151.2); 1–4 years, SIR, 16.7 (95% CI, 8.4–32.0); 5–9 years, SIR, 12.0 (95% CI, 4.5–26.6); ≥ 10 years, SIR, 4.0 (95% CI, 1.1–10.2) seizure after TBI estimated with Kaplan-Meier method Importance of prognostic factors determined with Cox proportional hazards analysis whose rates of seizures may be different from adults’ rates Singer, 2001 Retrospective cohort Same population as above (4,541 patients) with TBI Mild head injury: LOC or amnesia for less than 30 min Seizures determined from medical records 97 of 4,541 TBI cases had at least one seizure in 50-year Included children and adults
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Reference Study Design Population Type of TBI: Mild, Moderate, Severe; Blunt, Penetrating, Blast Health Outcomes or Outcome Measures Results Adjustments Comments or Limitations diagnosed in Olmsted County, MN, 1935–1984 Post-TBI seizure incidence rates compared with expected idiopathic seizure rate as ratio (comparative incidence rate) and absolute difference (excess event rate) per 1,000 of population per year Moderate head injury: LOC for 30 min–24 h or skull fracture Severe head injury: LOC or amnesia for more than 24 h, subdural hematoma, or brain contusion period Mild head injury: comparative incidence rate, 1.52 (3.1 in first PT year, 2.1 in years 1–5); excess event rate, 0.3 Moderate head injury: comparative incidence rate, 2.85 (6.65 in first PT year, 3.1 in years 1–5); excess event rate, 1.1 Severe head injury: comparative incidence rate, 17.0 (95 in first PT year, 16.7 in years 1–5); excess event rate, 10 Annegers et al., 1995 Retrospective cohort 692 patients in Olmsted County, MN, who developed acute symptomatic post-TBI seizures in 1955–1984 Head trauma Seizures determined from medical records; acute symptomatic seizures defined as occurring within 7 days of brain trauma or during period of recovery from such an insult Age-adjusted incidence rates of acute symptomatic post-TBI seizures, 2.0 per 100,000 person-years (25- to 34-year-olds) to 14.0 per 100,000 person-years (> 74-year-olds); incidence higher in males than females at all ages (overall age-adjusted rate, 8.6 in males vs 4.8 in females) Age Included children and adults Caveness et Five WWI: 1,990 Blunt and penetrating Seizures 38.2% had seizures None No referent group;
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Reference Study Design Population Type of TBI: Mild, Moderate, Severe; Blunt, Penetrating, Blast Health Outcomes or Outcome Measures Results Adjustments Comments or Limitations al., 1962 retrospective cohorts from WWI, WWII, Korean War German war injuries; head trauma examined 1914–1928 (> 50% were > 5 years after trauma) determined at Hechsler Institution undetermined whether there were preinjury seizures; inability to determine number who may have had their one and only seizure within first 6 mo after TBI WWI: 317 GSW of head, 7–20 years after trauma Penetrating Seizures determined at British Ministry of Pensions 34% WWII: 820 GSWs within 5 years after trauma; Dural penetration Seizure determined by postal inquiry 43% WWII: 739 head injured selected from Army and VA 7–8 years after trauma Blunt, blast, penetrating Seizures 28% (missile, 33.9%; blunt, blast, 24.1%) Korean War: 407 random sample 5 years after trauma “Craniocerebral injury in combat” Seizures determined by record review or interviews 24.1% (missile, 35%; blunt, blast: 12.2%) 214 missile, 52 blast, 141 blunt 135 with dura matter rupture Caveness, 1963 Conditional cohort 356 Korean War veterans with head injuries treated by study author or two other NS and assessed 7–8 years after injury Penetrating (52%), blunt (48%) Six categories: I, head blow without MS change; II, transient LOC; III, focal brain injury Seizures determined with postal questionnaire Prevalence of seizures: overall, 30.6%; seizures lasting > 6 mo, 22%; penetrating, 42.1%; blunt, 16.4%; I, 7.1%; II, 10.4%; III, No reference group; no screening for preinjury seizure disorder Cohort may overlap with Evans 13526
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury AMYOTROPHIC LATERAL SCLEROSIS Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, is a neuromuscular disease that causes degeneration of motor neurons in the cerebral motor cortex, the brainstem, and the spinal cord, which leads to muscle weakness and atrophy. In the final stages of the disease, the muscles responsible for breathing are disrupted; patients often die from respiratory failure. It is estimated that 5–10% of ALS cases are inherited, and the causes of the remaining cases are unknown. ALS affects 20,000–30,000 people in the United States and is more prevalent in men than in women. The risk of the disease increases with age (IOM, 2006). The committee identified no primary studies and few secondary studies of the relationship between TBI and ALS, but it recognized the importance of evaluating the literature for this outcome because there has been a concern about a relationship of the disease to military service (IOM, 2006). Secondary Studies The committee identified two secondary studies related to ALS. Chen et al. (2007) conducted a case–control study of 110 ALS cases at two major referral centers in New England. The patients, recruited in 1993–1996, received a diagnosis of ALS according to the standard criteria of the World Federation of Neurology and met the following criteria: received the diagnosis within the previous 2 years, lived in New England for half the year, spoke English, and were mentally competent. The control population consisted of 270 people without a diagnosis of dementia, parkinsonism, neuropathy, postpoliomyelitis syndrome, ALS, or other motor neuron diseases. Controls were frequency-matched to cases on age, sex, and telephone area code. Information on subjects and controls was collected by using a structured questionnaire administered by trained interviewers. To determine whether people had TBI, they were asked whether they had ever been injured so severely that they required medical attention and, if so, were then asked for details about the injury to identify TBI. The authors found that a history of TBI was associated with a higher risk of ALS. Compared with those who did not have TBI, there were significantly higher odds of ALS in patients with more than one TBI (OR, 3.1; 95% CI, 1.2–8.1) and in patients who had TBI during the preceding 10 years (OR, 3.2; 95% CI, 1.0–10.2). In patients who had multiple TBIs in the preceding 10 years, the risk of ALS was more than 11 (95% CI, 1.1–114.3), but the number of cases was small. Kurtzke and Beebe (1980) conducted a case–control study to assess risk factors for ALS. They identified 504 WWII veterans whose deaths were attributed to ALS during 1963–1967. The control population consisted of 504 men matched to subjects on age, entry into military service, and branch of service. To assess the validity of the ALS diagnosis, the authors reviewed hospital records and identified 37 representative deaths attributed to ALS; 36 were found to have definite ALS. The records were also reviewed for information about physical condition on entry into the service and other medical issues, including diseases and injuries. There were eight intracranial injuries in ALS subjects compared with two in controls. The authors found that “men dying of ALS more often had a history of injury 15 or more years before death than did the controls during the same period.”
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Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury Summary and Conclusion The committee did not find any studies that met the criteria for a primary study of TBI and ALS (see Chapter 4); however, it did identify two secondary studies. Chen and colleagues (2007) found that ever having experienced a TBI was not significantly associated with a higher ALS risk. However, compared with those who did not have TBI, there were significantly higher odds of ALS risk for patients with more than one TBI (OR, 3.1; 95% CI, 1.2–8.1) and patients who had TBI during the preceding 10 years (OR, 3.2; 95% CI, 1.0–10.2). For patients with multiple head injuries in the preceding 10 years, the risk of ALS was more than 11-fold. Kurtzke and Beebe (1980) found a higher frequency of intracranial injury in ALS subjects than in controls and stated that “men dying of ALS more often had a history of injury 15 or more years before death than did the controls during the same period.” The secondary studies generally found higher rates of ALS in the head-injured, but no studies that met the criteria of a primary study were identified. The committee concludes, on the basis of its evaluation, that there is inadequate/insufficient evidence to determine whether an association exists TBI and the development of ALS.
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