Benzodiazepine receptor binding in cerebellar degenerations
studied with positron emission tomography
Citation
Gilman, S., Koeppe, R.A., Junck, L., Kluin, K.J., Lohman, M., & St. Laurent, R.T. (1995). Benzodiazepine receptor binding in cerebellar degenerations
studied with positron emission tomography. Annals of Neurology 38: 176-185.
Abstract
We used positron emission tomography with [11C]
flumazenil to study gamma-aminobutyric acid type A / benzodiazepine receptor
binding quantitatively in the cerebral hemispheres, basal ganglia, thalamus,
cerebellum, and brainstem of 72 subjects, including 14 with multiple system
atrophy of the ataxic (olivopontocerebellar atrophy) type, 5 with multiple
system atrophy of the extrapyramidal / autonomic (Shy-Drager syndrome) type,
18 with sporadic olivopontocerebellar atrophy, 15 with dominantly inherited
olivopontocerebellar atrophy, and 20 normal control subjects with
similar age and sex distributions.   In comparison with data obtained from
the normal control subjects, we found significantly decreased ligand influx
in the cerebellum and brainstem of multiple system atrophy
patients of the olivopontocerebellar atrophy type and in patients with
sporadic olivopontocerebellar atrophy, but not in patients with multiple
system atrophy of the Shy-Drager syndrome type.   Despite these differences
in ligand influx, benzodiazepine binding was largely preserved in the cerebral
hemispheres, basal ganglia, thalamus, cerebellum, and brainstem in patients
with multiple system atrophy of both types as well as those with sporadic or
dominantly inherited olivopontocerebellar atrophy as compared with normal
control subjects.   The finding of relative preservation of
benzodiazepine receptors indicates that these sites are available for
pharmacological therapy in these disorders.