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J Neurophysiol (February 9, 2005). doi:10.1152/jn.00971.2004
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Submitted on September 17, 2004
Accepted on February 3, 2005

Spontaneous pallidal neuronal activity in human dystonia: Comparison with Parkinson's disease and normal macaque

Philip A. Starr1*, Geoff M. Rau1, Valerie Davis1, William J. Marks1, Jill L. Ostrem1, Donn Simmons1, Nadja Lindsey1, and Robert S. Turner1

1 Neurological Surgery, University of California, San Francisco, San Francisco, CA, USA

* To whom correspondence should be addressed. E-mail: starrp{at}itsa.ucsf.edu.

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, respectively) of 22 patients with dystonia, 140 neurons from eleven patients with Parkinsons disease (PD), and 157 neurons from two normal nonhuman primates (NHPs) (Macacca mulatta). All recordings were performed without systemic sedation. Mean GPi discharge rate (+/- SEM) in dystonia was 55.3+/- 1.3 Hz. This was significantly lower than in the normal NHP (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 NHP (69.7 +/- 3.3 Hz) and was indistinguishable from that in PD (56.6 +/- 3.5 Hz). Mean GPi discharge rate was inversely correlated with dystonia severity. GPi showed increased oscillatory activity in the 2-10 Hz range and increased bursting activity in both dystonia and PD as compared with the normal NHP. Since 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, while 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.




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