Contrast gain control abnormalities in idiopathic generalized epilepsy
Article first published online: 27 JUN 2011
Copyright © 2011 American Neurological Association
Annals of Neurology
Volume 70, Issue 4, pages 574–582, October 2011
How to Cite
Tsai, J. J., Norcia, A. M., Ales, J. M. and Wade, A. R. (2011), Contrast gain control abnormalities in idiopathic generalized epilepsy. Ann Neurol., 70: 574–582. doi: 10.1002/ana.22462
- Issue published online: 25 OCT 2011
- Article first published online: 27 JUN 2011
- Accepted manuscript online: 29 APR 2011 12:51PM EST
- Manuscript Accepted: 22 APR 2011
- Manuscript Revised: 19 APR 2011
- Manuscript Received: 4 NOV 2010
The origin of neural hyperexcitability underlying idiopathic generalized epilepsy (IGE) is not known. The objective of this study is to identify evidence of hyperexcitability in precisely measured visual evoked responses and to understand the nature of changes in excitation and inhibition that lead to altered responses in human patients with IGE.
Steady-state visual-evoked potentials (VEPs) to contrast reversing gratings were recorded over a wide range of stimulus contrast. VEPs were analyzed at the pattern reversal rate using spectral analysis. Ten patients with IGE and 13 healthy subjects participated. All subjects had normal visual acuity and had no history of photic-induced seizures or photoparoxysmal electroencephalograph (EEG) activity.
At a group level, the amplitude of visual responses did not saturate at high stimulus contrast in patients, as it did in the control subjects. This reflects an abnormality in neuronal gain control. The VEPs did not have sufficient power to reliably distinguish patients from controls at an individual level. Parametric modeling using a standard gain control framework showed that the abnormality lay in reduced inhibition from neighboring neurons rather than increased excitatory response to the stimulus.
Visual evoked responses reveal changes in a fundamental mechanism regulating neuronal sensitivity. These changes may give rise to hyperexcitability underlying generalized epilepsy. ANN NEUROL 2011;