CHANGES IN THE SOMATOSENSORY EVOKED-POTENTIAL DURING AND IMMEDIATELY FOLLOWING TEMPORARY MIDDLE CEREBRAL-ARTERY OCCLUSION PREDICT SOMATOSENSORY CORTEX ISCHEMIC LESIONS IN MONKEYS

被引:5
作者
DOWMAN, R
BOISVERT, DP
GELB, AW
TANG, C
LAM, AM
MEILKE, B
机构
[1] Department of Surgery, University of Alberta, Edmonton, AB
[2] Department of Anesthesia, University Hospital, University of Western Ontario, London, ON
[3] Department of Anesthesia, University of Alberta, Edmonton, AB
[4] Department of Pathology, University of Alberta, Edmonton, AB
关键词
Cerebral infarction; Hypotension; Middle cerebral artery occlusion; Somatosensory evoked potential;
D O I
10.1097/00004691-199004000-00008
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Somatosensory evoked potentials (SEP) were recorded during and immediately following temporary middle cerebral artery (MCA) occlusion to determine whether they can be used to predict ischemic lesions to the somato-sensory cortex (SI). Twenty-one cynomolgous female monkeys were subjected to four different MCA occlusion durations (15–60 min) during hypotension (45–50 mm Hg mean arterial blood pressure). The amplitude and central conduction time (CCT) of the median nerve SEP were recorded preceding, during, and following occlusion. Two groups were established based on the development of SI ischemic lesions: animals developing SI lesions formed the Si-lesion group (n = 9), and animals without ischemic lesions or with lesions outside the SI cortex formed the Si-spared group (n = 12). Changes in the SEP during and following MCA occlusion under conditions of hypotension were similar to those reported by others. The SEP disappeared in all animals within 15 min of occlusion and reappeared 5 min following reperfusion. Several differences were observed between the Si-lesion and Si-spared groups. The Si-lesion group had a more rapid decrease in SEP amplitude during the first 5 min of occlusion and had smaller SEP amplitudes and longer CCTs during reperfusion. These results suggest that changes in SEP amplitude and latency during and immediately following temporary MCA occlusion predict development of SI ischemic lesions. © 1990 American Electroencephalographic Society.
引用
收藏
页码:269 / 281
页数:13
相关论文
共 32 条
[1]  
Allison T., Hume A.L., A comparative analysis of short latency somatosensory evoked potentials in man, monkey, cat and rat, Exp Neurol, 72, pp. 592-611, (1981)
[2]  
Arezzo J., Legatt A.D., Vaughn H.G., Topography and intracranial sources of somatosensory evoked potentials in the monkey. I. Early components, Electroencephalogr Clin Neurophysiol, 46, pp. 155-172, (1979)
[3]  
Arezzo J., Vaughn H.G., Legatt A.D., Topography and intracranial sources of somatosensory evoked potentials in the monkey. II. Cortical components, Electroencephalogr Clin Neurophysiol, 51, pp. 1-18, (1981)
[4]  
Balestrino M., Somjen G.G., Chlorpromazine protects brain tissue in hypoxia by delaying spreading depression-mediated calcium influx, Brain Res, 385, pp. 219-226, (1986)
[5]  
Boisvert D.P., Gelb A.W., Tang C., Lam A.M., Mielke B., Dowman R., Brain tolerance to middle cerebral artery occlusion during hypotension in primates, Neurol Surg, 31, pp. 6-13, (1989)
[6]  
Branston H.M., Symon L., Crockard H.A., Pasztor E., Relationship between cortical evoked potential and local cortical blood flow following acute middle cerebral artery occulusion in the baboon, Exp Neurol, 45, pp. 195-208, (1974)
[7]  
Desmedt J.E., Generator sources ofthe SEP in man, Evoked potentials, frontiers in clinical neuroscience, 3, pp. 235-245, (1986)
[8]  
Dowman R., Wolpaw J.R., Diurnal rhythms in primate spinal reflexes and accompanying cortical somatosensory evoked potentials, Electroencephalogr Clin Neurophysiol, 72, pp. 69-80, (1989)
[9]  
Fox J.E., Williams B., Central conduction time following surgery for cerebral aneurysm, J Neurol Neurosurg Psychiatry, 47, pp. 873-875, (1984)
[10]  
Friedman W.A., Kaplan B.L., Day A.L., Sypert G.W., Curran M.T., Evoked potential monitoring during aneurysm operations: Observations after fifty cases, Neurosurgery, 20, pp. 678-687, (1987)