Abstracts

Stimulation-Induced Inhibition of Epileptogenic Cerebral Cortex

Abstract number : 2.327
Submission category :
Year : 2001
Submission ID : 427
Source : www.aesnet.org
Presentation date : 12/1/2001 12:00:00 AM
Published date : Dec 1, 2001, 06:00 AM

Authors :
K.A. Jenrow, Ph.D., Neurosurgery, Henry Ford Hospital, Detroit, MI; B.J. Smith, M.D., Neurology, Henry Ford Hospital, Detriot, MI; K.V. Elisevich, M.D., Ph.D., Neurosurgery, Henry Ford Hospital, Detroit, MI

RATIONALE: Epilepsy is a prevalent neurological disorder that affects about 1% of the US population. Twenty-five percent of this population are uncontrolled by medication or have unacceptable side effects. Surgical resection is an option for a defined focus in noneloquent cortex, although morbidity such as memory deficiency, visual, motor or sensory deficits are possible. Novel therapeutic options are being explored including stereotactically focused radiation and electrical stimulation. Neural stimulation is relatively free from side effects and is reversible. Moreover, the possibility of acceptable seizure control while maintaining the functional integrity of the brain makes neural stimulation an appealing prospect.
METHODS: Extraoperative electrocorticography was performed on two patients. JL is a 44 year old patient with a 40 year history of focal epilepsy with virtually continuous clonic activity of the left arm and hand that occasionally progress to tonic clenching, followed by a secondary convulsive state. LJ is a 29 year old patient with a 21 year history of focal epilepsy with motor seizures involving left facial twitching that occasionally progress to tonic-clonic seizures involving the left side. Prior to removal of the subdural electrodes, pairs of these electrodes were stimulated in several different orientations in the vicinity of the putative epileptic focus at subthreshold currents to determine the effect upon periodic cortical discharges.
RESULTS: For patient JL, frequent periodic focal discharges were identified at a discrete locus in the primary motor area. Monophasic stimulation for three minutes (2 mA, 50 Hz) of electrode pairs oriented along the gyral axis in this region resulted in a 10 minute interval of diminished interictal spike frequency from a baseline of 148.3 Hz to 11.6 Hz. A gradual crescendo-like recurrence of the discharge followed. For patient LJ, periodic focal discharges were identified regionally in the anterior temporal area with a frequency of approximately 2 Hz. Monophasic stimulation for 3 minutes at multiple orientations (1-3.5 mA, 50 Hz) had no effect on spike amplitude or frequency; however, stimulation at 2 and 5 Hz reproducibly diminished spike amplitude by approximately 30 %.
CONCLUSIONS: The demonstration that subthreshold stimulation diminishes interictal activity raises the possibility of subduing the epileptogenic potential of a given region. The efficacy of this approach may depend on both the nature/location of the epileptic focus and the amplitude/frequency characteristics of stimulation. Focal stimulation as a means of exerting an inhibitory effect upon epilepsy holds considerable promise as a therapeutic modality that is relatively safe, nondestructive, and adjustable over time.