Visual and auditory evoked responses during penicillin-induced generalized spike-and-wave activity in cats

In 13 healthy adult cats chronically implanted with parasagittal electrodes applied to the dural surface, curarization was performed and baseline recordings of the visual evoked response (VER), auditory evoked response (AER), and brainstem auditory evoked response (BAER) were made. Following the procedure of Prince and Farrell (1969), the animals were then given intramuscular doses of 300,000 to 500,000 U/kg of penicillin with the subsequent development of diffuse, bilaterally symmetrical, photosensitive spike-and-wave discharges in the EEG from 1 to 1 1/2 hr later and concomitant facial myoclonus, arrest of movement, and "absence-like" staring in non-curarized animals. The VER, AER, and BAER were monitored at 15-min intervals for several hours during which time the VER consistently decreased in amplitude up to the time at which the first spike-and wave bursts could be elicited by photic stimulation, approximately 1 hr after injection, after which all early components (0-200 msec) of the VER were progressively increased from 150 to 300% until spontaneous spike-and-wave bursts were consistently recorded (1 1/2-2 hr). Coincident with this change, a marked increase in late components (200-500 msec) was also observed. Both th early diminution and later augmentation of the VER were equally observable in visual and nonvisual cortex. Changes in the AER were also recorded with the development of this model, and were similar to those of the VER but of a lesser degree. The amplitudes of waves I through V of the BAER were found to increase from 28 to 88% maximal at 1 1/2 hr following penicillin injection. These data and the similarity of this model to human petit mal epilepsy argue against increased inhibitory impulses to the visual system during the ictal discharge being responsible for the subjective loss of visual information during petit mal absence. If the amplitude of the evoked response is directly related to the functional integrity of a sensory system, this suggests that the impairment of sensory input, or absence, during spike-and-wave paroxysm is due to interference with sensory processing rostral to the brainstem ascending auditory pathway, and probably does not occur in primary sensory cortex but rather in cortical or subcortical association tracts.