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Regional cerebral glucose metabolism in SLE chorea: Further evidence that striatal hypometabolism is not a correlate of chorea†
Article first published online: 12 OCT 2004
Copyright © 1987 Movement Disorder Society
Volume 2, Issue 3, pages 201–210, 1987
How to Cite
Guttman, M., Lang, A. E., Garnett, E. S., Nahmias, C., Firnau, G., Tyndel, F. J. and Gordon, A. S. (1987), Regional cerebral glucose metabolism in SLE chorea: Further evidence that striatal hypometabolism is not a correlate of chorea. Mov. Disord., 2: 201–210. doi: 10.1002/mds.870020307
- Issue published online: 12 OCT 2004
- Article first published online: 12 OCT 2004
- Positron tomography;
- Glucose metabolism;
- Systemic lupus erythematosus
The pathophysiology of chorea in systemic lupus erythematosus (SLE) is uncertain. Pathologic examination has not identified a specific localtion for the causative lesions (s) and immunologic mechanisms have been suggested in its etiology. In other choreic disorders, such as Huntigton's disease and benign hereditary chorea, glucose hypometabolism in the striatum has been domonstrated by positron computed tomography (PCT) using [18F] deoxyglucose. With this technique we have studied four patients with chorea secondary to SLE. In these patients the regional distribution of cerebral glucose metabolism was normal. In particular, striatal glucose metabolism was within the normal range, even though the ratio of striatal to cortical glucose metabolism was increased. Our results show that striatal hypometabolism, as seen in other disorders manifesting chorea, is not the PCT correlate of the dyskinesia.