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From the Departments of Psychiatry (Dr. Black), Radiology (Drs. Black and Perlmutter), Neurology and Neurological Surgery (Drs. Black and Perlmutter), and Anatomy and Neurobiology (Dr. Öngür), Washington University School of Medicine; and Mallinckrodt Institute of Radiology (Drs. Black and Perlmutter), St. Louis, MO.
Address correspondence and reprint requests to Dr. Kevin Black, Campus Box 8225, 4525 Scott Avenue, St. Louis, MO 63110-1093.
Objective: To determine whether the volume of the putamen is abnormal in patients with idiopathic focal dystonia.
Background: The cause of adult-onset focal cystonia is unknown, but substantial evidence suggests that the putamen may be abnormal in this condition. Cell loss and gliosis have been suggested. We hypothesized that this might be reflected as abnormal putamen volume on MRI.
Design and methods: A high-resolution MRI was acquired in 13 adults with cranial or hand dystonia and 13 normal individuals matched for age and sex. Putamen volume was measured using a stereologic method (Study 1). In a replication study, another rater measured putamen volume using manual tracing and direct voxel count (Study 2). Neither rater was aware of the diagnosis, and the order of measurement was random in each study.
Results: In Study 1, putamen measurements were reasonably accurate (coefficient of error, 
6%). The putamen was 13% larger in patients, both in absolute terms (p = 0.03) and after covarying total brain volume(p = 0.02). In Study 2, putamen volumes correlated with those measured in Study 1 (intraclass correlation coefficient, 0.68 to 0.83). The putamen was 8% larger in patients (p = 0.06) and was larger in the patient than in the matched control subject in 10 of 13 pairs (p = 0.046).
Conclusion: We find no evidence of putaminal atrophy or degeneration in adult-onset idiopathic focal dystonia. In fact, in this group, the putamen is about 10% larger in patients than in matched control subjects. This finding may reflect a response to the dystonia or may relate to its cause.
Supported by National Institutes of Health grants NS01898, NS32318, and NS31001; the Charles A. Dana Foundation (The Dana Clinical Hypotheses Research Program); the American Parkinson Disease Association; the National Alliance for Research on Schizophrenia and Depression; the McDonnell Center for Higher Brain Function; the generosity of Mr. and Mrs. Jefferson Miller; and the Sam and Barbara Murphy Fund.
Received December 8, 1997. Accepted in final form May 15, 1998.
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