Somatosensory evoked potentials as a measure of experimental cerebral ischemia

Abstract

Somatosensory evoked potentials (SEP's) reflect the integrity of the central neuronal pathway, and as such may be used to assess function that remains during a variety of cerebral insults. To evaluate the natural history and utility of SEP's during experimental cerebral ischemia and infarction, SEP's were measured in 17 adult cats at 24 hours and 1 hour prior to right middle cerebral artery (MCA) occlusion, and again immediately afterward and at either 6 hours (five cats) or 24 hours (six cats) post-occlusion. Before occlusion of the right MCA, the SEP's were identical in the right and left hemispheres. After occlusion, there was a significant slowing of the interpeak latency of the first positive peak (P1) in the right hemisphere (3.53 +/- 0.6 msec before compared to 3.99 +/- 0.6 msec after occlusion, p less than 0.001). Maximal slowing in right hemisphere P1 latency was seen in those animals in which the stroke extended into the thalamus (4.38 +/- 0.1 msec). This was significantly slower than left hemisphere values (3.92 +/- 0.32 msec, p less than 0.01). The ipsilateral cortical components of the SEP's, the second positive peak (P2), and the major negative deflection (MN) were slowed in all cats immediately after right MCA occlusion compared to preocclusion measurements (p less than 0.001). Severe infarcts in the mid-suprasylvian and posterior ectosylvian gyri (including the somatosensory cortex) resulted in a greater slowing of the latency of MN compared to less severe infarcts in that region (20.6 +/- 3.9 msec versus 16.4 +/- 1.1 msec, p less than 0.05). There was a precipitous decrease in the amplitude or voltage of the ipsilateral P2-MN complex immediately after occlusion (5.32 +/- 0.4 microV before compared to 0.98 +/- 0.3 microV after occlusion, p less than 0.001). Therefore, the central latencies and cortical amplitudes of the SEP's are sensitive experimental tools as indicators of the onset and extent of a cerebral ischemic insult.

Transhemispheric diaschisis. A review and comment.

“…However, somatosensory evoked potential (SEP) amplitude increased to 124% and 132%, respectively, during the hyperacute and acute periods. Meyer et al 29 also found an increase in contralateral SEP amplitude during both the hyperacute and acute periods, as did Sakatani et al 30 for contralateral hind limb SEP. Andrews and Muto (unpublished data, 1990), during the hyperacute period in a miniature swine unilateral brain retraction ischemia model, noted an average increase in contralateral auditory evoked potential or SEP amplitude to 121%.…”

Correlation between somatosensory evoked potentials and neuronal ischemic changes following middle cerebral artery occlusion.

“…5 " 8 In an attempt to explore the relationship between evoked potentials and histologicai focal cerebral ischemia, we examined SEP's and ischemic neuronal changes in cats following unilateral middle cerebral artery occlusion.…”

“…This section includes part of the somatosensory cortex. 8 ' l0 Photographic prints were made of each histological slide. Without knowledge of the post-occlusion SEP's, the left hemisphere was microscopically examined.…”

“…All these cats had ischemic areas of less than 15% (mean 9 ± 3%) of the total ipsilateral cortex. These results demonstrate that the disappearance of the SEP and their failure to recover correlate with the extent and degree of histologicai cerebral ischemia.Stroke 4 Recently, SEP's have been applied to canine and feline models to study cerebral ischemia.5 " 8 In an attempt to explore the relationship between evoked potentials and histologicai focal cerebral ischemia, we examined SEP's and ischemic neuronal changes in cats following unilateral middle cerebral artery occlusion. …”

Anesthetic modulation of cerebral hemodynamic and evoked responses to transient middle cerebral artery occlusion in cats.

“…19 We used the forepaw somatosensory evoked potential as a noninvasive indicator that MCA occlusion reduced CBF.…”