[Experimental study of brain stem infarction in dogs--effect on BAEP, SSEP, blink reflex and EEG of perforator occlusion]

Assessment of the lesion in the brain stem by evoked potentials has not been well established. We have already developed a model of brain stem ischemia by occluding the perforators of the posterior cerebral arteries of the dog. The ischemic lesions locates mainly in the ventral side of the midbrain. Using this model, we assessed brain stem function by brain stem auditory evoked potential (BAEP), surface- and depth-recorded (in medial lemniscus) short latency somatosensory evoked potential (SSEP), blink reflex (BR) and electroencephalography (EEG), and investigated the correlation between the electrophysiological abnormalities and the lesion in the brain stem. The studies were performed for 6 hours after perforator occlusion. Furthermore, depth-recorded SSEP and regional cerebral blood flow (rCBF) were measured under induced hypotension by withdrawal of arterial blood. BAEP did not change in 13 of 16 animals. Surface-recorded SSEP remained unchanged in all 6 animals. The results are probably due to the fact that the lesion does not involve the auditory and somatosensory pathways and the accompanying events such as edema does not affect the both pathways. Depth-recorded SSEP remained unchanged after occlusion and did not disappear even when rCBF fell below 10 ml/100 g/min. It may be suggested that the threshold for electrical failure in the brain stem is much lower than that in the cortex. In BR, R1 did not change but ipsilateral R2 became nearly invisible immediately after perforator occlusion in all animals. The fact that the ischemic lesion did not involve the pons and disturbed reticular formation in the midbrain may probably account for the remaining of R1 and the disappearance of ipsilateral R2.(ABSTRACT TRUNCATED AT 250 WORDS)