Alcoholic neurobiology: Changes in dependence and recovery

This article presents the proceedings of a symposium held at the meeting of the International Society for Biomedical Research on Alcoholism (ISBRA) in Mannheim, Germany, in October, 2004. Chronic alcoholism follows a fluctuating course, which provides a naturalistic experiment in vulnerability, resilience, and recovery of human neural systems in response to presence, absence, and history of the neurotoxic effects of alcoholism. Alcohol dependence is a progressive chronic disease that is associated with changes in neuroanatomy, neurophysiology, neural gene expression, psychology, and behavior. Specifically, alcohol dependence is characterized by a neuropsychological profile of mild to moderate impairment in executive functions, visuospatial abilities, and postural stability, together with relative sparing of declarative memory, language skills, and primary motor and perceptual abilities. Recovery from alcoholism is associated with a partial reversal of CNS deficits that occur in alcoholism. The reversal of deficits during recovery from alcoholism indicates that brain structure is capable of repair and restructuring in response to insult in adulthood. Indirect support of this repair model derives from studies of selective neuropsychological processes, structural and functional neuroimaging studies, and preclinical studies on degeneration and regeneration during the development of alcohol dependence and recovery from dependence. Genetics and brain regional specificity contribute to unique changes in neuropsychology and neuroanatomy in alcoholism and recovery. This symposium includes state-of-the-art presentations on changes that occur during active alcoholism as well as those that may occur during recovery-abstinence from alcohol dependence. Included are human neuroimaging and neuropsychological assessments, changes in human brain gene expression, allelic combinations of genes associated with alcohol dependence and preclinical studies investigating mechanisms of alcohol induced neurotoxicity, and neuroprogenetor cell expansion during recovery from alcohol dependence.

Remembrance of things past: Amnesic syndrome with partial preservation of professional skills

J.L., then a 25-year-old physiotherapist, became densely amnesic following herpes simplex encephalitis. She displayed severe retrograde amnesia, category-specific semantic memory loss, and a profound anterograde amnesia affecting both verbal and visual memory. Her working memory systems were relatively spared as were most of her cognitive problem-solving abilities, but her social functioning was grossly impaired. She was able to demonstrate several previously learned physiotherapy skills, but was unable to modify her application of these procedures in accordance with patient response. She showed no memory of theoretical or propositional knowledge, and could neither plan treatment or reason clinically. Three years later, J.L. had profound impairment of anterograde and retrograde declarative memory, with relative sparing of working memory for problem solving and long-term memory of procedural skills. The theoretical and practical implications of her amnesic syndrome are discussed.