Smith-Kettlewell Eye Research Institute, Department of Neurology, University of California-San Francisco, 505 Parnassus Ave., San Francisco, CA 94143-0114, USA.
Ann Neurol. 2011 Oct;70(4):574-82. doi: 10.1002/ana.22462. Epub 2011 Jun 27.
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.
特发性全面性癫痫(IGE)的神经兴奋性过高的起源尚不清楚。本研究的目的是确定在精确测量的视觉诱发电位中存在过度兴奋的证据,并了解导致人类 IGE 患者反应改变的兴奋和抑制变化的性质。
使用光谱分析在广泛的刺激对比度下记录对比反转光栅的稳态视觉诱发电位(VEPs)。使用频谱分析在图案反转率下分析 VEPs。10 名 IGE 患者和 13 名健康受试者参与了这项研究。所有受试者的视力正常,且无光诱发癫痫发作或光阵发性脑电图(EEG)活动史。
在组水平上,与对照组相比,患者在高刺激对比度下视觉反应的振幅没有饱和。这反映了神经元增益控制的异常。在个体水平上,VEPs 没有足够的能力可靠地区分患者和对照。使用标准增益控制框架的参数建模表明,异常在于来自相邻神经元的抑制减少,而不是对刺激的兴奋性反应增加。
视觉诱发电位揭示了调节神经元敏感性的基本机制的变化。这些变化可能导致一般性癫痫的过度兴奋。