Corticomotor evoked potentials have recently been used in experimental animals and @entity1 as a measure of neurologic function after @entity64 . 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 @entity468 anesthetized with @entity1508 . These potentials were obtained hourly for 6 hours after @entity2500 . Four major identifiable components were recorded in control responses. Immediately after @entity1188 , 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 @entity1188 , as well as to assessing functional recovery.

Early component changes in corticomotor evoked potentials following experimental XXXX .

@entity1 :: ('9606', 'Species') :: ['patients'] @entity64 :: ('MESH:D020521', 'Disease') :: ['stroke'] @entity1508 :: ('MESH:D006221', 'Chemical') :: ['halothane'] @entity2500 :: ('MESH:D020244', 'Disease') :: ['middle cerebral artery occlusion'] @entity1188 :: ('MESH:D007238', 'Disease') :: ['infarct', 'infarction'] @entity468 :: ('9685', 'Species') :: ['cats']
@entity64 :: (MESH:D020521,Disease) :: ['stroke']
