Topographical analysis of epileptiform potentials in rat somatosensory cortex: the interictal to ictal transition.
Topographical analysis of epileptiform potentials in rat somatosensory cortex: the interictal to ictal transition.
复制标题
大鼠体感皮层癫痫样电位的地形分析：发作间期到发作期的转变。
DOI：
10.1016/0006-8993(92)90975-f
复制
发表时间：
1992
期刊：
影响因子：
2.9
通讯作者：
Di,S
中科院分区：
文献类型：
--
作者：
Barth,DS;Di,S
Large quantities of penicillin were applied to the face and forelimb region of rat somatosensory cortex, producing an epileptic focus with both electrographic and behavioral signs of seizures that regularly repeated over a period of several minutes. Epicortical potentials were recorded simultaneously from a 64 chabnel micro-electrode array (8×8 platinum elec3rodes) with inter-electrode distance of 0.5 mm, covering a 3.5×3.5 mm2area centered on the penicillin injection site. Cluster analysis was used to classify successivv epileptiform discharges into interichal, transitional, and ictal groups. Principal components analysis (PCA) was used to extract fundamental waveforms producing the spike complex in each group, and to estimate the locations and spatial extent of neuronal populations participating in epileptiform discharge, During all states of epileptic excitability, it was possible to account for over 90% of the variance in the epicortical potential waveforms using a model with only two spatially overlapping populations of cells. The location and spatial extent of the populations remained unchanged by the transition to seizures; the interictal and ictal states were distinguished only by changes in the timing and amplitude of potentials in the two putative neuronal populations. The present model, using only two stationary neuronal populations to reproduce all spatiotemporal patterns in the neocortical epileptogenic focus, is compared to models proposed by others in which epileptic discharge is thought to propagate sequentially through adjacent cortex. It is concluded that the initiation, maintenance, and termination of seizures in neocortex relies on mechanisms that are not necessarily reflected in changes in spatiotemporal interactions among epicortically recorded cell groups within the focus. These mechanisms may be distinguished from those responsible for the spread of seizures within neocortex.
