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From the Program in Physical Therapy (Dr. Zackowski) and Departments of Anatomy and Neurobiology (Drs. Hakimian and Thach), Neurology and Neurological Surgery (Dr. Thach), and Neurology (Dr. Perlmutter), Washington University School of Medicine, St. Louis, MO; Kennedy Krieger Institute, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD (Dr. Bastian); Department of Neurology (Dr. Mink), University of Rochester School of Medicine, NY; and Department of Neurology (Dr. Koller), University of Miami School of Medicine, FL.
Address correspondence and reprint requests to Dr. W.T. Thach, Jr., Washington University School of Medicine, Department of Anatomy and Neurobiology, Box 8108,660 South Euclid, St. Louis, MO 63110; e-mail: thachw{at}pcg.wustl.edu
Background: Electrical stimulation of the thalamus dramatically reduces essential tremor (ET). It has been hypothesized that the cerebellum and inferior olive are involved in the generation of ET, and thalamic stimulation is presumed to dampen ET through interactions with cerebellar output to the thalamus. Evidence suggests that abnormal timing of agonist and antagonist muscle responses contribute to cerebellar tremor (CbT); however, this relationship has not been investigated for ET. The mechanisms of the tremor and improvement are unknown.
Objective: To measure the effect of ventral intermediate thalamic stimulation in controlling the ET response to sudden stretch of an agonist muscle and to determine whether, in ET, the timing relationships between the initial agonist and antagonist electromyography (EMG) responses show abnormalities similar to those seen in CbT.
Methods: The authors studied ET subjects (with implanted thalamic stimulators turned off and on) and normal controls as they responded to mechanical torque pulses given at the wrist joint. The wrist joint angle, wrist agonist, and antagonist EMG were recorded.
Results: Like CbT, patients with ET showed delayed onsets of antagonist EMG and excessive rebound. Thalamic stimulation reduced the tremor but did not alter the antagonist delay or the rebound.
Conclusions: In ET, antagonist muscle responses to a torque pulse are similar to that in CbT. However, benefit from thalamic stimulation did not alter these EMG responses; therefore, suppression of tremor must be caused by mechanisms other than the re-establishment of normal agonist–antagonist timing.
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