Early component changes in corticomotor evoked potentials following experimental stroke
Corticomotor evoked potentials have recently been used in experimental animals and patients as a measure of neurologic function after stroke. However, little is known about the fundamental electrophysiologic properties contributing to the formation of these potentials. To define some of these properties, corticomotor evoked potentials were recorded from the contralateral hindlimb in response to transcortical stimulation in cats anesthetized with halothane. These potentials were obtained hourly for 6 hours after middle cerebral artery occlusion. Four major identifiable components were recorded in control responses. Immediately after infarction, all component amplitudes were significantly attenuated. However, after approximately 5 hours, the early latency components exceeded control values; late latency components were also increased. Corresponding somatosensory evoked potentials were abolished and did not return throughout the recording session. Based on classic neurophysiologic studies, the amplitude increment can be explained as combined activation of low-threshold brainstem facilitatory centers and/or direct activation of subcortical axonal pathways. With further study, corticomotor evoked potentials may be a valuable adjunct to current electrophysiologic monitoring techniques, particularly with regard to defining the extent and location of an infarct, as well as to assessing functional recovery.