Somatosensory evoked potentials in rat cerebral cortex before and after middle cerebral artery occlusion.

Abstract

We recorded somatosensory evoked potentials in pentobarbital-anesthetized rats before and after middle cerebral artery occlusion. Trigeminal (vibrissae), median (forelimb), and sciatic (bind limb) nerve stimuli produced consistent, robust, and sharply localized responses in the trigeminal, forelimb, and hind limb regions of the somatosensory cortex of 18 rats. These regions are situated at sequentially greater distances from the center of infarcts produced by middle cerebral artery occlusion. In eight rats, occlusion 1-2 mm below the rhinal fissure abolished somatosensory evoked potentials in all three cortical region within minutes. Positive wavelets preceding the primary cortical response were also diminished by the occlusion, suggesting that ischemia affected the thalamocortical white matter. Four of these eight rats did not show histologically apparent ischemic involvement of the hind limb cortical region at 3 hours after occlusion; sciatic nerve evoked potentials recovered substantially in all four rats, and the amplitudes exceeded baseline (129±30% at 1 hour, 173±33% at 3 hours) in three of the four rats. Three of the eight rats did not have gross ischemic involvement of the forelimb cortical region; median nerve evoked potentials recovered fully in all eight rats, but the amplitudes did not exceed baseline. All eight rats had evidence of ischemic damage in the trigeminal cortex; no rat showed full recovery in this region, and all but one had trigeminal evoked potentials that were <20% of baseline amplitudes by 3 hours after occlusion. Two rats had large infarcts involving the hind limb and forelimb cortical regions and were studied for 24 hours; these rats did not recover evoked potentials in the three regions at 24 hours, although one rat transiently recovered hind limb evoked potentials to 83% of baseline amplitude at 3 hours. Amplitude of the hind limb somatosensory evoked potentials recorded in the contralateral hemisphere doubled after occlusion. Thus, middle cerebral artery occlusion causes widespread loss of somatosensory evoked potentials in the hind limb, forelimb, and trigeminal cortical regions of the ischemic hemisphere of rats. These regions show distinctly different temporal patterns of recovery. Our findings suggest that cortical evoked potentials may be useful for monitoring ischemic damage in these cortical regions after middle cerebral artery occlusion (Stroke 1990^1 89 and causes infarcts largely localized to the cerebral cortex.:The rat primary somatosensory cortex has three anatomically and physiologically distinct regions: the hind limb area (HL), the forelimb area (FL), and the parietal 1 area (Parl).1112 Parl is situated most laterally and receives projections mainly from the cutaneous mechanoreceptors of the mystacial vibrissae, the head, and the neck. HL is located most medially, and FL lies between HL and Parl. Peripheral nerve stimulation produces localized field potentials in the somatosensory cortex. The typical ischemic infarct produced by MCAO encroaches on these regions....

Early Prediction of Functional Recovery after Experimental Stroke: Functional Magnetic Resonance Imaging, Electrophysiology, and Behavioral Testing in Rats

“…SSEP recording of the primary somatosensory cortex in healthy animals revealed a typical waveform with a first positive peak (P1) followed by a first negative (N1) and a second positive peak, similar to the SSEP signals recorded from intracranially or transcranially implanted electrodes (Sakatani et al, 1990;Ogawa et al, 2000;Gsell et al, 2006). No significant interhemispheric differences for latency of P1 (mean Ϯ SD; P1 left , 12.4 Ϯ 0.6 ms; P1 right , 12.3 Ϯ 0.5 ms; p ϭ 0.62), for N1 latency (N1 left , 18.3 Ϯ 0.8 ms; N1 right , 18.2 Ϯ 1.3 ms; p ϭ 0.71), or for the amplitude between these two peaks (amplitude left , 31 Ϯ 9.3 V; amplitude right , 33.8 Ϯ 9.7 V; p ϭ 0.21) were observed.…”

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%.…”

Selective cortical neuronal damage after middle cerebral artery occlusion in rats.

“…2 ' 24 We recently observed that MCAo transiently abolished evoked potentials in the forelimb and hindlimb somatosensory cortex even though the infarct did not involve these areas. 25 These findings suggest that MCAo causes widespread physiologic disruption of the cortex beyond the infarct site.…”