Central conduction time in primate brain ischemia -- a study in baboons.
The relationship between central conduction time (CCT) and levels of regional blood flow were studied in 9 primates. Flows were recorded in both hemispheres using the method of hydrogen (2 min) clearance. The somatosensory evoked potentials were recorded over the contralateral cortex and the dorsal columns, following median nerve stimulation. The CCT, a measure of the brain's electrical conduction, was determined by the difference in latencies between N10, (the arrival of the afferent volley at the sensory cortex) and N7 (its arrival at the dorsal column). Ischemia was produced by transorbital occlusion of the right middle cerebral artery. In the acute ischemic phase within 5 minute of occlusion, there was a significant correlation between the change in CCT and the decrease in flow. In the later occlusive phase, the CCT was unaltered with flows above 15 ml/100g/min. Below that level smaller decreases in flow resulted in progressively larger changes in CCT until a flow was reached where the N10 disappeared or the entire cortex was electrically silent. Focal ischemia had no effect on the first positive deflection recorded from the cortex (P8) or the first negative peak response from the cervical region (N7). However, the latency of P8 was increased or it was absent with the introduction of hypotension, while N8 was unaltered. From our measurements, it appears that prolongation of CCT can be related to developing ischemia, and that the thresholds for change are not dissimilar to those already recorded for somatosensory evoked responses to the basis of amplitude alterations in the cortex. Below these levels, prolongation of CCT appears to bear a parametric relationship to alteration in blood flow. While the measurement displays only one of the many alterations which are induced by ischemia in the brain, its attraction lies in its simplicity and in the fact that it may be applied with relative ease in the clinical situation. Under these circumstances, it appears to be an adequately sensitive monitor of developing brain ischemia, and deserves further study.
D000208:Acute Disease; D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D004553:Electric Conductivity; D005071:Evoked Potentials; D006801:Humans; D009333:Neck; D010215:Papio; D012039:Regional Blood Flow; D012535:Scalp; D013003:Somatosensory Cortex / Q000503:physiopathology*