the prefrontal cortex are the ones associated with aggression and violence and especially with verbal confrontations. That demonstration of an association between a localized frontal lobe injury and TBI is especially important in light of the considerable literature documenting loss of inhibition and greater aggressive behavior after frontal lobe injury. They hypothesized that lesions to the prefrontal cortex impair the ability to sustain “managerial knowledge” and bias behavior away from plans and social rules toward aggressive and violent behavior.

DRUG AND ALCOHOL ABUSE DISORDERS

Secondary Studies

Many studies have shown a relationship between drug and alcohol use and TBI, and it is generally accepted that drug and alcohol use precedes the TBI and increases the risk of head injury. Therefore, studies have examined post-TBI alcohol use only in the context of previous drug and alcohol use estimated as closely as possible. Horner et al. (2005) focused on the assessment of alcohol abuse and dependence (AA/D) in a 1-year period in a sample of 1,606 TBI patients, randomly sampled from a large state-wide sample of all TBI patients discharged from South Carolina hospitals in 1999–2002 and fully assessed at the time of the incident. A telephone interview a year after TBI was used to obtain information on alcohol use for the month preceding assessment. Overall, 15.4% were heavy drinkers, 14.3% moderate drinkers, and 70.3% infrequent drinkers or abstainers. Almost all interviewed (99.8%) reported drinking the same or less than a year before; half the current heavy and moderate drinkers were consuming less than they were a year before. Risk factors for heavy drinking were male sex, lower age, substance abuse before TBI, and a diagnosis of depression since TBI.


Jorge et al. (2005) studied 158 Level I TBI patients of whom 24.1% were alcohol-dependent and 10.8% were alcohol abusers; alcohol use during the year before TBI was 34.8%. Of the 55 TBI patients with premorbid AA/D, 30 completed 1 year of followup and 60% of the group followed up resumed their alcohol use; of those 55, 60% developed a mood disorder during the post-TBI year compared with 36.9% of the non-AA/D group. Patients with pre-existing AA/D had reduced cerebral grey matter (GM) volumes compared with patients without AA/D, and post-TBI relapsers had even greater reductions in GM volumes. Moreover, vocational outcome was lower in those with AA/D, especially if it coexisted with mood disorders.


Bombardier et al. (2003) followed a group of consecutively admitted TBI patients over the course of a year. They showed that drinking decreased considerably from before injury to 1 year after TBI: abstinence rates increased from 14% to 36%; people without substantial alcohol-related problems increased from 64% to 84%; and remission of substantial alcohol problems ranged from 30.8% to 56%. However, there was a subset of survivors (about 25%) who drank heavily at 1 year after TBI, and the level of pre-TBI alcohol use predicted who would be in the post-TBI heavy-drinking group. That suggests that drug and alcohol use should still be monitored after TBI.



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