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BACKGROUND:Studies have shown that latency changes of some elements in a somatosensory evoked potential (SEP) and motor evoked potential (MEP) can reflect electrical activity of cerebral cortical neurons and conduction of white matter nerve fibers. However, there is a paucity of information regarding the dynamic observation of SEP and MEP following cerebral ischemic injury. OBJECTIVE:To explore SEP and MEP changes following acute ischemic stroke, and investigate the role of evoked potentials in monitoring brain function in stroke. DESIGN, TIME AND SETTING:A randomized, controlled, animal experiment was performed at the Chongqing Key Laboratory of Neurology, Affiliated Hospital of Chongqing Medical University from September 2007 to August 2008.MATERIALS:Hydrogen blood flow detector was purchased from Soochow University Medical Instrument Co., China, and Power lab system was purchased from AD Instruments, Inc., USA. METHODS:A total of 36 healthy, adult, male, Sprague Dawley rats were randomly assigned to four groups (n = 9), including three ischemia groups (12, 24 and 72 hours of ischemia) and a sham-surgery group. The rat model of acute ischemic stroke was established by middle cerebral artery occlusion (MCAO) in the left hemisphere.MAIN OUTCOME MEASURES:SEP and MEP of the left limbs were detected, and cerebral blood flow was measured by the hydrogen cleaning method.RESULTS:The latency of positive wave 1 (P1), negative wave 1 (N1) and positive wave 2 (P2) waves in SEP, and latency of negative wave 1, 2 (N1, N2) waves in MEP were significantly prolonged with increasing ischemic duration following MCAO (P < 0.01), but cerebral blood flow was significantly decreased (P < 0.05, or P < 0.01).CONLUSION:Ischemic stroke prolongs the latency of SEP waves (P1, N1, P2) and MEP waves (N1, N2), and cerebral cortical evoked potential may correlate with cerebral blood flow changes. This indicates that SEP and MEP can be used to evaluate brain function following acute ischemic stroke.