AN EXPERIMENTAL STUDY OF THE TRANSITION FROM NORMAL TO CONVULSOID CORTICAL ACTIVITY

Abstract

The transition from normal to convulsoid activity was studied in 20 rabbits (minimal anesthesia). Paroxysms of slow development were initiated in the visual cortex by 11/sec. or slower repetitive stimuli to the homolateral lateral geniculate nucleus. The intensity of a single stimulus was sufficient to produce about a half maximal visual response. 60[mu] needle electrodes insulated to the tip were used to follow the development of paroxysm in the cortex. One lead was placed on the surface. Three other leads were thrust obliquely into the brain so that they were positioned beneath the surface lead at successive depths. The most deeply placed electrode was in the white matter. The leads divided the cortex into several strata and records were obtained from superficial, middle, deep and the entire cortex. An ink-writing electro-encephalograph and a cathode ray oscilloscope were used for recording. Prior to the appearance of paroxysm a progressive decline often occurred in amplitude of the responses to successive stimuli; this is called the low period. When the stimulus was broken during it, paroxysm usually developed slowly in the cortex. Isolated clonic discharges, surface-positive in polarity, were the first overt evidence of paroxysm. These were followed by a period of fast tonic discharge which preceded build-up to the high-voltage paroxysmal pattern of the rodent. In rapidly developing paroxysm any or all of the above mentioned phases can be missing. Paroxysm occasioned by stimuli of quite slow frequency may demonstrate increasing prominence of the early negative phase as a prelude to paroxysm. This relates the preparoxysmal status of the prepn. to the sequence of events leading to the appearance of spontaneous strychnine spikes in other studies. Most often paroxysm initiated in the cortex by repetitive thalamic stimulation was observed first in middle or superficial cortical fractions. Paroxysms activated by intraperitoneal Metrazol, or appearing spontaneously, may also commence locally in the middle and superficial cortex as well as by developing simultaneously throughout. The thalamic radiation from the lateral geniculate nucleus establishes a synaptic zone in the III and IV layer of the cortex. The placement of the cortical electrodes confined these layers to the stratum designated as middle cortex. Since paroxysm first developed in the superficial as well as the middle cortex, it is not felt justified to relate the origin of paroxysm to neurones in layers III and IV. From the present work, the only inference drawn in this respect is that the upper cortex has more innate lability than the lower.