Sequential measurement of somatosensory evoked potentials in a canine model of hemispheric ischaemia.

We have previously shown that occlusion of 6 canine intracranial vessels produces profound hemispheric ischaemia and abolishes the ipsilateral SSEP. In the present study, this work was extended to ascertain the differential contributions of 6 intracranial vessels to SSEP function. Five dogs underwent craniotomy, brain retractions, and ipsilateral arterial microdissection, and were prepared for SSEP recordings. Stimulation-recording sequences were performed firstly prior to craniotomy, secondly following craniotomy and microdissection and thirdly following sequential occlusion of each of 6 vessels: (a) anterior cerebral (A2), (b) ethmoidal, (c) ophthalmic, (d) middle cerebral (MCA), (e) posterior communicating (PCoA), and (f) posterior cerebral artery. Individual SSEP amplitudes and latencies were measured and averaged and values for each wave were compared statistically to baseline values and to the immediately preceding value. Two thalamocortical potential components were identified: an early wave (6-10 ms) and a late wave (10-15 ms). No significant amplitude declines between waves occurred with A2, ethmoidal, and ophthalmic occlusions. Following MCA occlusion, amplitude decreased to 49.1% and 34.5% of baseline in the early and late waves respectively; a significant decrease (p less than 0.05) both from baseline and from post-ophthalmic occlusion. Further occlusions (PCoA and posterior cerebral) produced progressive declines in amplitude to a nadir of 12.5% (early) and 2.1% (late) of baseline. Although latency did increase slightly from baseline with each occlusion (5-7% total), no consistent and significant latency changes were identified.(ABSTRACT TRUNCATED AT 250 WORDS)