Vertigo Induced by Mesial Hemispheral Electricl Stimulation. Implications for Localization of Vertiginous Epilepsy
Abstract number :
1.094
Submission category :
Clinical Neurophysiology-Brain Stimulation
Year :
2006
Submission ID :
6228
Source :
www.aesnet.org
Presentation date :
12/1/2006 12:00:00 AM
Published date :
Nov 30, 2006, 06:00 AM
Authors :
Kostas N. Fountas, and Joseph R. Smith
Vertigo, as a manifestation of partial epileptic seizures, has remained a poorly understood clinical phenomenon. Previous electrophysiologic, neuroimaging and magnetoencephalography studies in humans have shown that posterior insula, superior temporal region, superficial part of temporo-parietal area, sensorimotor cortex, various structures of the frontal, parietal and occipital lobes, and the hippocampus have been implicated in the production of vertigo.In our current communication, we present our experience and observations regarding the occurrence of vertigo after electrically stimulating distinct mesial hemispheral areas via implanted depth electrodes., In two patients among 346 undergoing depth electrode implantation for invasive monitoring in cases of medically refractory epilepsy, vertigo occurred after stimulation of right posterior cingulate and right frontal supplementary somato-sensory areas. In all cases, AdTech (AdTech, Racine, WI, USA) depth electrodes were employed., The cathodal stimulation parameters were: pulse width 0.5 ms and train duration 3s in both cases, while the employed current amplitude was 2.0 mA in the frontal supplementary somato-sensory area and 3.0 mA in the posterior cingulate area. Both patients described a rotary movement of the surroundings after stimulation., Our findings confirm previous observations of electrophysiologic studies and clinical data demonstrating that cingulate and supplemental somato-sensory areas might be implicated in the pathogenesis of vertigo. Further acquiring of stimulation data might identify dominance of one hemisphere over the other in the development of vertigo and vertiginous epilepsy and could further enlighten us on the exact pathogenetic mechanisms involved in rotational vestibular epilepsy.,
Neurophysiology