Brain, Vol. 118, No. 6, 1473-1484, 1995
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The metabolic topography of idiopathic torsion dystonia
1Department of Neurology, North Shore University Hospital, Manhasset and Cornell University Medical College New York, USA 2Department of Psychiatry, New York State Psychiatric Institute, Columbia College of Physicians and Surgeons New York, USA 3Department of Neurology, Neurological Institute, Columbia College of Physicians and Surgeons New York, USA
Correspondence to:
Correspondence to: Dr Eidelberg, Department of Neurology, North Shore University Hospital, 300 Community Drive, Manhasset, NY 11030, USA
We used [18F]fluorodeoxyglucose (FDG) and PET with a statistical model of regional metabolic covariation to study brain topographic organization in idiopathic torsion dystonia (ITD). We studied 11 patients with predominantly right-sided ITD and 11 age-matched controls, and measured global, regional cerebral and normalized metabolic rates for glucose (GMR, rCMRGlc, rCMRGlc/GMR). The Scaled Subprofile Model was applied to the combined rCMRGlc dataset to identify topographic covariance profiles associated with ITD. We found that global and regional metabolic rates were normal in ITD. The SSM analysis of the combined groups of ITD patients and normals revealed a significant topographic profile characterized by relative bilateral increases in the metabolic activity of the lateral frontal and paracentral cortices, associated with relative covariate hypermetabolism of the contralateral lentiform nucleus, pons and midbrain. Subject scores for this profile correlated significantly with Fahn-Marsden disease severity ratings (r= 0.67, P<0.02). In contrast to parkinsonism, lentiform and thalamic metabolism were dissociated in dystonia. We conclude that ITD is characterized by relative metabolic overactivity of the lentiform nucleus and premotor cortices. The presence of lentiform thalamic metabolic dissociation suggests that in this disorder hyperkinetic movements may arise through excessive activity of the direct putameno-pallidal inhibitory pathway
torsion dystonia; glucose metablism; PET
Received April 10, 1995. Revised June 12, 1995. Accepted July 22, 1995.
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