region of the brain affected and the volume of brain tissue lost. That evidence was consistently found in veterans of World War II and Vietnam. With regard to closed head injuries, the committee found sufficient evidence of an association between severe TBI and neurocognitive deficits, limited but suggestive evidence of an association between moderate TBI and neurocognitive deficits, and inadequate and insufficient evidence of an association between mild TBI and neurocognitive deficits.


With regard to neurologic effects, the studies reviewed had numerous findings, including a strong association between brain injury and unprovoked seizures. For example, there is a causal association between penetrating TBI or severe closed TBI and unprovoked seizures, whereas the risk of unprovoked seizures after mild TBI is limited but suggestive of an association. In general, the risk of seizures after all types of TBI severity appears to be highest in the first year after trauma and declines thereafter. Some of the literature reviewed supports an association between TBI and neurodegenerative diseases—for example, studies that demonstrated a sufficient association between moderate or severe TBI and dementia of the Alzheimer type or parkinsonism, although sufficient evidence of an association with dementia pugilistica could be supported only in professional boxers. Other studies reviewed did not support a relationship between TBI and multiple sclerosis or amyotrophic lateral sclerosis and were categorized as inadequate and insufficient to determine whether an association exists. There were endocrine outcomes, such as sufficient evidence of an association between moderate to severe TBI and growth hormone insufficiency and hypopituitarism; however, the studies only supported a finding of limited and suggestive evidence of an association between moderate to severe TBI and diabetes insipidus.


Psychiatric outcomes have been discussed by the committee, and there is some uncertainty regarding the mechanisms linking TBI and psychiatric diagnoses. For example, it is not clear whether psychopathologic conditions after TBI are biologic consequences of the injury, reactions to the person’s cognitive and social dysfunction after TBI, or a continuation of preexisting conditions. The committee has chosen, however, to use the terminology of primary psychiatric disorders, as has been the custom in the TBI literature. The committee notes that the predominance of studies indicated that groups with TBI (mild, moderate, or severe) had higher rates of major depression 6 months or more after TBI than did appropriate comparison groups. The committee concluded that there is sufficient evidence of an association between TBI and depression and aggressive behaviors. The association between mild TBI and posttraumatic stress disorder (PTSD) appears to be different between military and civilian populations. Studies conducted in military personnel who served in the Gulf War led the committee to conclude that there is limited but suggestive evidence of an association between TBI and PTSD. In contrast, studies conducted in civilian populations led the committee to conclude that there is inadequate and insufficient evidence to determine whether an association exists between TBI and PTSD. With regard to aggressive behaviors, the studies support a conclusion of sufficient evidence of an association, but TBI is not associated with increased drug and alcohol use as there is limited but suggestive evidence of an association between TBI and decreased alcohol and drug use. Finally, the literature supported a finding of limited but suggestive evidence of an association between moderate to severe TBI and psychoses generally appearing in the second and third years after TBI.


Social functioning is often severely hampered after TBI, especially if it is severe. Social function in those hospitalized with TBI is adversely affected, relative to those with no injury, for



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