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Brain, Vol. 116, No. 5, 1191-1199, 1993
© 1993 Guarantors of Brain

research-article

Striatal (18F)dopa uptake in familial idiopathic dystonia

E. D. Playford1, N. A. Fletcher2, G. V. Sawle1, C. D. Marsden2 and D. J. Brooks1,2

1MRC Cyclotron Unit, Clinical Sciences Section, Hammersmith Hospital London, UK 2Department of Clinical Neurology, Institute of Neurology, National Hospitals for Neurology and Neurosurgery London, UK

Correspondence to: Correspondence to Dr E. D Playford, MRC Cyclotron Unit, Hammersmith Hospital, DuCane Road, London W12OHS, UK

It is known that most cases of idiopathic torsion dystonia (ITD) are inherited in an autosomal dominant fashion. Despite clarification of the underlying genetic defect, no consistent structural lesion has been identified in ITD, and it is probable that a biochemical disturbance is the basis of the disorder.

To determine whether there is impaired function of the nigro-striatal dopaminergic terminals in ITD we studied 11 subjects with generalized ITD and a positive family history using (18F)dopa and PET scanning. Of these 11 patients, eight had putamen (18F)dopa uptake within the lower half of the normal range, while three had uptake reduced by >2 SDs below the normal mean. The lowest putamen [18F]dopa influx constants were found in the most disabled patients. As these reductions were mild it is unlikely that abnormalities of the nigro-striatal dopaminergic pathway are the primary determinant of either the nature or the severity of dystonic symptoms.

In addition, we studied three presumed carriers of the ITD gene. These subjects all had normal striatal (18F)dopa influx constants suggesting that (18F)dopa PET is unsuitable as a screening tool for JTD.

Received October 5, 1992. Revised April 22, 1993. Accepted June 15, 1993.


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