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J Neurophysiol 93: 3165-3176, 2005. First published February 9, 2005; doi:10.1152/jn.00971.2004
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Spontaneous Pallidal Neuronal Activity in Human Dystonia: Comparison With Parkinson’s Disease and Normal Macaque

Philip A. Starr1,4, Geoff M. Rau1, Valerie Davis1, William J. Marks, Jr.2,4, Jill L. Ostrem2,4, Donn Simmons1, Nadja Lindsey3 and Robert S. Turner1,4

1Departments of Neurological Surgery, 2Neurology, and 3Nursing, University of California, San Francisco; and 4Parkinson’s Disease Research, Education, and Clinical Center at the San Francisco Veterans Affairs Medical Center, San Francisco, California

Submitted 17 September 2004; accepted in final form 3 February 2005

Dystonia is a movement disorder defined by sustained muscle contractions, causing twisting and repetitive movements and abnormal postures. To understand the abnormalities in pallidal discharge in dystonia, we have analyzed the spontaneous activity of 453 neurons sampled from the internal or external pallidum (GPi or GPe) of 22 patients with dystonia, 140 neurons from 11 patients with Parkinson’s disease (PD), and 157 neurons from two normal non-human primates (NHPs; Macacca mulatta). All recordings were performed without systemic sedation. Mean GPi discharge rate in dystonia was 55.3 ± 1.3 (SE) Hz. This was significantly lower than in the normal NHPs (82.5 ±2.5 Hz) and lower than in PD patients (95.2 ± 2.3 Hz). Mean GPe discharge rate in dystonia (54.0 ± 1.9 Hz) was lower than in the normal NHPs (69.7 ± 3.3 Hz) and was indistinguishable from that in PD patients (56.6 ± 3.5 Hz). Mean GPi discharge rate was inversely correlated with dystonia severity. GPi showed increased oscillatory activity in the 2- to 10-Hz range and increased bursting activity in both dystonia and PD as compared with the normal NHPs. Because the abnormalities in discharge patterns were similar in dystonia compared with PD, we suggest that bursting and oscillatory activity superimposed on a high background discharge rate are associated with parkinsonism, whereas similar bursting and oscillations superimposed on a lower discharge rate are associated with dystonia. Our findings are most consistent with a model of dystonia pathophysiology in which the two striatal cell populations contributing to the direct and indirect intrinsic pathways of the basal ganglia both have increased spontaneous activity.

Address for reprint requests and other correspondence: P. A. Starr, Dept. of Neurosurgery, University of California, San Francisco, 505 Parnassus Ave., 779 Moffitt, San Francisco, CA 94143 (E-mail: starrp{at}itsa.ucsf.edu)




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