Cerebellar and frontal hypometabolism in alcoholic cerebellar degeneration studied with positron emission tomography

Abstract

Local cerebral metabolic rate for glucose was studied utilizing 18F-2-fluoro-2-deoxy-D-glucose and positron emission tomography (PET) in 14 chronically alcohol-dependent patients and 8 normal control subjects of similar age and sex. Nine of the 14 patients (Group A) had clinical signs of alcoholic cerebellar degeneration, and the remaining 5 (Group B) did not have signs of alcoholic cerebellar degeneration. PET studies of Group A revealed significantly decreased local cerebral metabolic rates for glucose in the superior cerebellar vermis in comparison with the normal control subjects. Group B did not show decreased rates in the cerebellum. Both Groups A and B showed decreased local cerebral metabolic rates for glucose bilaterally in the medial frontal area of the cerebral cortex in comparison with the normal control subjects. The severity of the clinical neurological impairment was significantly correlated with the degree of hypometabolism in both the superior cerebellar vermis and the medial frontal region of the cerebral cortex. The degree of atrophy detected in computed tomography scans was significantly correlated with local cerebral metabolic rates in the medial frontal area of the cerebral cortex, but not in the cerebellum. The data indicate that hypometabolism in the superior cerebellar vermis closely follows clinical symptomatology in patients with alcoholic cerebellar degeneration, and does not occur in alcohol-dependent patients without clinical evidence of cerebellar dysfunction. Hypometabolism in the medial frontal region of the cerebral cortex is a prominent finding in alcohol-dependent patients with or without alcoholic cerebellar degeneration.

Actividad prefrontal y alcoholismo de fin de semana en jóvenes

“…También con técnicas de neuroimagen funcional se ha observado un mayor efecto del alcohol sobre los lóbulos frontales. Por ejemplo, se ha encontrado una reducción del metabolismo de la glucosa en estas áreas en alcohólicos sin otras patologías neurológicas (Adams, Gilman, Koeppe, Kluin, Brunberg, Dede et al, 1993;Gilman, Adams, Koeppe, Berent, Kluin et al, 1990). Por otro lado, Jaatinen, Riikonen, Riihioja y Kajander (2003) demostraron que el consumo crónico intermitente de alcohol, el equivalente al consumo de fin de semana, ocasiona un descenso del metabolismo energético de las neuronas en la corteza prefrontal que contribuye al proceso de neurodegeneración y al consiguiente deterioro de las funciones cerebrales.…”

Direct voxel-based comparisons between grey matter shrinkage and glucose hypometabolism in chronic alcoholism

“…This finding could suggest that metabolic dysfunction occurs before GM shrinkage, in agreement with a study showing hypometabolism in alcoholic patients without brain atrophy. 12 Other studies reported a relationship between global brain metabolism and volume in alcoholic patients, 1,13 suggesting, according to the authors, a causal relationship between cortical atrophy and brain metabolism or vice versa. 13 Such discrepancies may be explained by several methodological issues.…”

“…[1][2][3] Previous studies have shown alcohol-related grey matter (GM) volume deficits predominantly in the frontal cortices. 3,4 The dorsolateral cortex showed GM shrinkage, reaching up to 20%.…”

Reduced posterior mesofrontal cortex activation by risky rewards in substance-dependent patients

“…Functional magnetic resonance imaging (fMRI) studies consistently reveal frontocortical recruitment by behavior control tasks (Horn et al, 2003;Li et al, 2006a;Li et al, 2006b;Ridderinkhof et al, 2004), such as risk-taking . SUD subjects also show blunted frontocortical glucose utilization (Gilman et al, 1990;Samson et al, 1986) and blood flow (Bolla et al, 2003), that correlate with reaction times (Dao-Castellana et al, 1998) and risky choices (Bolla et al, 2003;Fishbein et al, 2005) in decision-making tasks. These findings suggest a possibility that higher-order cortical regions that maintain or integrate representations of potential penalties for immediately rewarding behavior are impaired in persons with SUD.…”