Abnormalities of frontal system functioning are most apparent in alcoholics with Korsakoff's syndrome. In non-Korsakoff alcoholics, factors contributing to cognitive performance are age, duration of abstinence, duration of alcoholism, and amount of alcohol consumed.
Alcoholism and antisocial personality disorder (ASPD) often are comorbid conditions. Alcoholics, as well as nonalcoholic individuals with ASPD, exhibit behaviors associated with prefrontal brain dysfunction such as increased impulsivity and emotional dysregulation. These behaviors can influence drinking motives and patterns of consumption. Because few studies have investigated the combined association between ASPD and alcoholism on neuropsychological functioning, this study examined the influence of ASPD symptoms and alcoholism on tests sensitive to frontal brain deficits. The participants were 345 men and women. Of them, 144 were abstinent alcoholics (66 with ASPD symptoms), and 201 were nonalcoholic control participants (24 with ASPD symptoms). Performances among the groups were examined with Trails A and B tests, the Wisconsin Card Sorting Test, the Controlled Oral Word Association Test, the Ruff Figural Fluency Test, and Performance subtests of the Wechsler Adult Intelligence Scale. Measures of affect also were obtained. Multiple regression analyses showed that alcoholism, specific drinking variables (amount and duration of heavy drinking), and ASPD were significant predictors of frontal system and affective abnormalities. These effects were different for men and women. The findings suggested that the combination of alcoholism and ASPD leads to greater deficits than the sum of each.
A 45-year-old white, college-educated, right-handed woman was referred to the Boston University Neurology Associates Neuropsychology Service by her neurologist. She was reportedly exposed to carbon monoxide while at work in a restaurant and suffered from subsequent changes in behavior and cognition. She was referred for an evaluation to rule out CO-associated central nervous system (CNS) dysfunction. She was initially seen on 15 April 1998.According to the patient, she discovered that she had been exposed to CO in November 1996, when she came to work early, noticed the smell of gas, and called the gas company. She said that the gas company employee informed her that there were extremely high levels of CO in the kitchen where she worked as a restaurant cook. The patient went to the hospital approximately 6 hr after leaving her workplace on the day she called for help, but, at that time, her carboxyhemoglobin was reportedly not elevated and no focal neurologic signs were noted. She explained that she had been off work for 5 days and, immediately upon arriving at work the morning the leak was detected, she sought fresh air and did not have further exposure. The restaurant was then closed for 2 weeks so the furnace, which was the source of the CO fumes, could be replaced. The patient believed that CO had been leaking into her workplace for at least a year, given the duration of her symptoms.We were unable to obtain a copy of the gas company reports on levels taken on the day that the leak was identified
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