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Neurology 2001;56:1576-1579
© 2001 American Academy of Neurology
Brief Communications

Lesion of thalamic centromedian– parafascicular complex after chronic deep brain stimulation

J. M. Henderson, PhD;, D. J. O’Sullivan, FRACP;, M. Pell, FRACS;, V. S. C. Fung, MBBS;, M. A. Hely, MBBS;, J. G. L. Morris, DM; and G. M. Halliday, PhD

From the Neuropathology Laboratory, Prince of Wales Medical Research Institute (Drs. Henderson and Halliday), Departments of Neurology (Dr. O’Sullivan) and Neurosurgery (Dr. Pell), St. Vincent’s Hospital, and Department of Neurology, Westmead Hospital (Drs. Fung, Hely, and Morris), Sydney, Australia.

Address correspondence and reprint requests to Dr. J.M. Henderson, Prince of Wales Medical Research Institute, Barker St., Randwick, N.S.W. 2031, Australia; e-mail: j.henderson{at}unsw.edu.au

A patient with PD who exhibited disabling tremor and prominent dyskinesia underwent deep brain stimulation (DBS) of the left thalamic ventral intermediate nucleus. The electrode migrated and was replaced but with suboptimal clinical response. Two years later, postmortem analysis found the second electrode tip had entered the thalamic centromedian–parafascicular complex. There was a small thalamotomy and cell loss exceeding that found in PD. Thalamic damage may occur in association with DBS for PD.




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