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Changes in motor cortex excitability with stimulation of anterior thalamus in epilepsy

From the Divisions of Neurology (G.F.M., A.S., C.A.G., D.I.C., R.A.W., R.C.) and Neurosurgery (A.M.L.), Krembil Neuroscience Centre and Toronto Western Research Institute, University Health Network, University of Toronto, Ontario, Canada.

Address correspondence and reprint requests to Dr. Robert Chen, Toronto Western Hospital, 399 Bathurst St., Toronto, Ontario, M5T 1S8, Canada; e-mail: Robert.chen{at}uhn.on.ca

Background: Deep brain stimulation (DBS) is an effective treatment for movement disorders and pain. Recently, bilateral DBS of the anterior nucleus of thalamus (AN) was performed for the treatment of intractable epilepsy. This surgery reduced seizure frequency in an initial group of patients. However, its physiologic effects on the cortex and mechanisms of action remain poorly understood. Different classes of antiepileptic drugs (AEDs) have distinct effects on the excitatory and inhibitory circuits in the motor cortex, which can be studied noninvasively by transcranial magnetic stimulation (TMS).

Objective: To examine the effects of bilateral AN DBS on motor cortex excitability in epilepsy and compare these to the known effects of AEDs.

Methods: Cortical excitability was assessed in five medicated epilepsy patients with bilateral stimulators implanted in the anterior thalamus and nine healthy controls. Single and paired TMS were used to examine cortical inhibitory and facilitatory circuits. Electromyography was recorded from the dominant hand, and TMS was applied over the contralateral motor cortex. Patients were studied during DBS turned off (OFF condition), DBS with cycling stimulation mode (1 minute on, 5 minutes off; CYCLE), and DBS with continuous stimulation (CONTINUOUS) in random order on 3 consecutive days.

Results: Motor thresholds were increased in the patients regardless of DBS condition. Active short-interval intracortical inhibition (SICI) was significantly reduced in the OFF and CYCLE conditions but returned toward normal levels in the CONTINUOUS condition. Rest SICI, long interval intracortical inhibition, and silent period duration were unchanged.

Conclusions: Increased short-interval intracortical inhibition with continuous deep brain stimulation (DBS) suggests that thalamic DBS might drive cortical inhibitory circuits, similar to antiepileptic drugs that enhance -aminobutyric acid inhibition.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the February 28 issue to find the title link for this article.

Supported by the Canadian Institutes of Health Research (G.F.M. and R.C.), the Canada Foundation for Innovation, the Ontario Innovation Trust, and the University Health Network Krembil Family Chair in Neurology.

Disclosure: Dr. Lozano received research grant support in excess of $10,000 and honoraria from Medtronic Inc. Dr. Wennberg acted as a consultant for Medtronic Inc.

Received June 8, 2005. Accepted in final form October 26, 2005.