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1.
Alcohol Clin Exp Res ; 26(4): 558-64, 2002 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-11981133

RESUMEN

BACKGROUND: Most studies of the impact of alcohol dependence on the brain have examined individuals in treatment. Such samples represent a small proportion of alcoholics in the general population. Such samples may embody a bias (Berkson's fallacy) if the association between variables (for example, alcoholism and cortical gray matter loss) differs between the population of alcoholics in treatment and alcoholics in the general population. Our objective was to determine if treatment-naïve alcoholics show structural brain changes versus controls and to compare our findings with reports evaluating alcoholic samples drawn from treatment populations. METHODS: Structural MRI was used to assess whole brain and regional volumes of cortical gray matter and white matter in 24 young to middle-aged treatment-naïve alcohol-dependent males versus 17 controls. RESULTS: Cortical gray matter volumes in alcohol-dependent individuals were negatively associated with age and lifetime duration of alcohol use (which were highly confounded). These subjects showed reduced whole brain (p < 0.05), prefrontal (p < 0.01), and parietal (p < 0.05) cortical gray matter compared with controls. White matter and temporal cortex, tissues that usually show volume reductions in samples drawn from treatment, did not differ between treatment-naïve alcoholics and controls (all p > 0.40). CONCLUSIONS: Our findings are consistent with the hypothesis that structural brain changes in treatment-naïve alcoholics are less severe than those reported in clinical samples of alcoholics, perhaps due to less concomitant psychopathology and a reduced severity of alcoholism in treatment-naïve alcoholics. However, caution must be taken when comparing our findings with results from clinical samples, as we did not directly compare treatment-naïve alcoholics with treated alcoholics and our treatment-naïve sample tended to be younger than the (clinical) samples reported in the literature. Nevertheless, we suggest that most of the reports of the central nervous system consequences of alcoholism may not accurately describe the majority of alcoholic-dependent individuals.


Asunto(s)
Alcoholismo/patología , Alcoholismo/terapia , Corteza Cerebral/patología , Adulto , Factores de Edad , Análisis de Varianza , Distribución de Chi-Cuadrado , Humanos , Imagen por Resonancia Magnética/métodos , Imagen por Resonancia Magnética/estadística & datos numéricos , Masculino , Persona de Mediana Edad
2.
J Int Neuropsychol Soc ; 4(6): 559-65, 1998 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-10050360

RESUMEN

Studies of Alzheimer's disease patients show that individuals with larger premorbid brains have a later onset of disease, or a lessened severity of cognitive impairment, or both. This may be due to a "functional reserve" associated with the greater number of neurons and synapses available in larger brains. We used magnetic resonance imaging and the MicroCog Assessment of Cognitive Functioning to examine the association between intracranial volume (premorbid brain size) and neuropsychological function in abstinent crack-cocaine and crack-cocaine-alcohol dependent individuals. There were no significant differences between the crack-only and the crack-alcohol dependent participants in neuropsychological performance or in intracranial volume. The abstinent cocaine-dependent individuals (both crack-only and crack-alcohol) were significantly impaired in many neuropsychological domains. Intracranial volume accounted for a significant proportion of the variance in neuropsychological performance. This result is consistent with the finding in the Alzheimer's literature that larger brains can maintain function to a greater degree, or for a longer period of time, in the face of cerebral disease or insult. Functional reserve may be a heretofore little recognized protective mechanism of the brain that has consequences for the severity of expression of cerebral disease or insult throughout life.


Asunto(s)
Trastornos Relacionados con Alcohol , Encéfalo/patología , Encéfalo/fisiopatología , Trastornos Relacionados con Cocaína , Cocaína Crack , Adulto , Trastornos Relacionados con Alcohol/complicaciones , Encefalopatías/diagnóstico , Encefalopatías/etiología , Trastornos Relacionados con Cocaína/complicaciones , Trastornos del Conocimiento/diagnóstico , Trastornos del Conocimiento/etiología , Femenino , Humanos , Imagen por Resonancia Magnética , Masculino , Pruebas Neuropsicológicas , Índice de Severidad de la Enfermedad , Factores de Tiempo
3.
Addict Biol ; 3(3): 261-70, 1998 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-26734920

RESUMEN

We measured hippocampal volumes and cognitive functioning in crack-cocaine and crack-cocaine/alcoholdependent subjects (abstinent approximately 10-12 weeks) compared to age-matched controls. Cognitive function was evaluated using the computerized MicroCog Assessment of Cognitive Functioning (which includes tests of explicit, declarative memory subserved by the hippocampus). The hippocampal volumes were quantified on T1-weighted MRIs and were expressed as a proportion of intracranial vault volume. Both subjects and controls showed the larger right versus left hippocampal volume expected in normal anatomy, but we found no differences in hippocampal volume between any of the groups. However, both abstinent cocaine-dependent subjects and abstinent cocaine/alcohol-dependent subjects showed persistent cognitive impairments, including deficits in explicit memory. Our results suggest that either: (1) the hippocampus is resistant to structural volume loss in young and middle-aged cocaine or cocaine/alcohol-dependent subjects, (2) the hippocampal volume loss suffered by young and middle-aged cocaine or cocaine/alcohol-dependent subjects resolves after approximately 3 months of abstinence, or (3) hippocampal atrophy is obscured by the process of gliosis. Further, the cognitive impairments persisting in these abstinent cocaine and cocaine/alcohol-dependent samples may (1) be unrelated to hippocampal function or (2) be associated with abnormal hippocampal function that is not reflected in MRI measures of overall hippocampal atrophy.

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