Comparison of the Effects of Ischaemia on Early Components of the Somatosensory Evoked Potential in Brainstem, Thalamus, and Cerebral Cortex

Abstract

In 14 ventilated, normocapnic baboons anaesthetised with alpha-chloralose, local CBF (hydrogen clearance) and the amplitude and latency of local components of the somatosensory evoked potential (SEP, median nerve stimulation) were measured bilaterally in ventrobasal thalamus (VPL), medial lemniscus (ML), and cerebral cortex before and during progressive ischaemia, produced by occlusion of the right middle cerebral artery and subsequent controlled reductions in mean systemic blood pressure (MSBP). The first significant reduction from control of the left cortical SEP amplitude occurred in the range of 30-40 mm Hg MSBP, but those of the VPL and ML responses only below 30 mm Hg; in the range of 20-30 mm Hg, the average SEP amplitudes in cortex, VPL, and ML were 8.6, 72.6, and 90.7% of control, respectively. In terms of local CBF, the cortical SEP threshold was in the range of 15-20 ml/100 g/min (as in previous work), that of VPL in the range of 10-15 ml/100 g/min, but the ML response was only markedly reduced below 10 ml/100 g/min. Thus, the differential ischaemic sensitivity of the SEP between the three regions was clearly demonstrated. These results indicate that as one descends the neuraxis, there is an increasing resistance of electrophysiological function to systemic hypotension, together with a decreasing threshold for local ischaemia.

Cerebral Blood Flow and Cerebral Metabolic Rate of Oxygen Requirements for Cerebral Function and Viability in Humans

“…These findings are remarkably consistent with thresholds for neu ronal function and viability determined by other in vestigators (Leech et aL, 1973;Trojaborg and Boysen, 1973;Sundt et al , 1974;Jones et aL, 198 1;Astrup, 1982;Heiss and Rosner, 1983;Branston et aL, 1984). However, our results are not strictly comparable with these other data for two reasons.…”

Recovery of Monkey Brain after Prolonged Ischemia. I. Electrophysiology and Brain Electrolytes

“…The waveform structure of the preischemic potentials was similar to that described by Branston et al (1984). The main component was a surface positive wave with a latency of 13-15 ms and an amplitude of up to 145 f.L V. This P15 wave is con sidered to be cortical and postsynaptic because it is inversed when an electrode is passed through the cortex.…”

“…The main component consisted of a large surface-positive wave with a peak latency of 13-15 ms and an amplitude between 45 and 170 f.L V. This wave is designated P15. according to Branston et al (1984). After vascular occlusion, evoked poten tials were completely suppressed within <3 min and remained isoelectric throughout ischemia.…”

Somatosensory Evoked Potential and Brain Water Content in Post-Asphyxic Immature Piglets

“…Depressed SEP amplitude may be associated with impaired cortical neuronal generators of evoked potentials. During the onset of ischemia or severe hypoxemia, alterations in SEP occur at criticall y low levels of cerebral blood flow and oxygen delivery (3,4) that correlate with inability to maintain cerebral oxygen consumption (5,6). In addition to being a sensitive indicator of anoxia in somatosensory cortex, SEP is also influenced by subcortical above baseline.…”