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Decreased striatal monoaminergic terminals in multiple system atrophy detected with positron emission tomography
Author(s) -
Gilman Sid,
Koeppe Robert A.,
Junck Larry,
Little Roderick,
Kluin Karen J.,
Heumann Mary,
Martorello Susan,
Johanns Jewel
Publication year - 1999
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/1531-8249(199906)45:6<769::aid-ana11>3.0.co;2-g
Subject(s) - monoaminergic , putamen , atrophy , positron emission tomography , cerebellum , pathology , magnetic resonance imaging , medicine , olivopontocerebellar atrophy , psychology , neuroscience , endocrinology , degenerative disease , central nervous system disease , radiology , receptor , serotonin
Abstract We examined the density of striatal presynaptic monoaminergic terminals, using a ligand for the type 2 vesicular monoamine transporter, (+)‐[ 11 C]dihydrotetrabenazine, with positron emission tomography in 7 normal control subjects, 8 multiple system atrophy (MSA) patients with predominantly parkinsonian features (MSA‐P), 8 MSA patients with principally cerebellar dysfunction (MSA‐C), and 6 sporadic olivopontocerebellar atrophy (sOPCA) patients. The findings were correlated with the results of neurological evaluations and magnetic resonance imaging studies. Specific binding was significantly reduced in the putamen of all patient groups in the order MSA‐P < MSA‐C < sOPCA, compared with controls. Mean blood‐to‐brain ligand transport (K 1 ) was significantly decreased in the putamen of all patient groups and in the cerebellar hemispheres of MSA‐C and sOPCA but not MSA‐P groups, compared with controls. Significant negative correlations were found between striatal binding and the intensity of parkinsonian features and between cerebellar K 1 and the intensity of cerebellar dysfunction. The results suggest fundamental differences between MSA‐P and MSA‐C groups reflecting differential severity of degeneration of nigrostriatal and cerebellar systems in these two forms of MSA. The findings also show that some sOPCA patients have subclinical nigrostriatal dysfunction and are at risk of developing MSA with disease progression. Ann Neurol 1999;45:769–777