The Effects of Electroconvulsive Shock on the Superior Colliculus Visual Evoked Potential

Electroconvulsive therapy (ECT) remains an effective somatic treatment for a variety of psychiatric disorders. Despite its introduction almost a century ago, its site and mode of action remains elusive. One method of obtaining relevant information is by the recording of sensory evoked potentials from patients undergoing ECT. However, such human data is plagued with problems of methodology and interpretation. These limitations are not an impediment when employing an animal model of electroconvulsive shock (ECS). In the present experiment, the effects of ECS were studied on the superior colliculus visual evoked potential (SCVEP) in the non-medicated rat. The SCVEP was used as a measure of activity in the subcortical visual system as, in the rodent, the SC lies directly below the visual cortex. Immediately after the induction of generalised seizure activity (GSA) by ECS, all the components of the SCVEP were still preserved, basically intact. There was, however, a marked but very transient attenuation in its waveform not associated with any increase in the latency of the primary component. These findings are compared to a previous study where the cortical VEP was found to be completely abolished for up to two minutes following ECS. Judging solely by these and related neurophysiological data recorded from other exteroceptive sensory systems, it is concluded that the seat of ECT’s mode of action may lie quite discretely at the cortical level. Nevertheless, ECT has a profusion of effects on cerebral structure and function. Therefore, at the present time, this putative insight may be most applicable to an understanding of the negative or adverse (usually cognitive) side-effects which accompany ECT rather than to its positive (therapeutic) benefits. The acute loss of amplitude in the SCVEP waveform may not necessarily indicate that GSA impacts SC function, even momentarily. Instead, it is suggested that the interference more likely reflects a deficit in retinal processing which has been transferred to the SC.