Functional impairment due to white matter ischemia after middle cerebral artery occlusion in cats.

Abstract

We recorded regional cerebral blood flow, somatosensory evoked potentials, and auditory evoked potentials in the thalamic relay nuclei (ventral posterior lateral nucleus and medial geniculate body) and in the somatosensory and auditory cortices during and after 1 hour of transient left middle cerebral artery occlusion in nine cats. Regional cerebral blood flow was also measured in the thalamocortical tracts of five of these cats. Additionally, the integrity of thalamocortical connections was tested by retrograde labeling of the thalamic nuclei with horseradish peroxidase in eight cats (three of which experienced no ischemia). Regional cerebral blood flow was severely reduced during middle cerebral artery occlusion in the left primary auditory cortex (8.5 ml/100 g/min) and in white matter pathways (6.4-7.6 ml/100 g/min). In contrast, regional cerebral blood flow did not change significantly in the somatosensory cortex or in either thalamic nucleus. Evoked potentials were abolished in both cortices but remained unchanged in the thalamic nuclei. Cortical somatosensory evoked potentials disappeared 5-8 minutes later than auditory evoked potentials. Recirculation after 1 hour of ischemia resulted in rapid and almost complete recovery (94%) of somatosensory evoked potentials and little recovery (18.4%) of auditory evoked potentials. We conclude that in the auditory pathway both cortical and fiber tract ischemia are (perhaps synergistically) responsible for dysfunction, while in the somatosensory cortex evoked potentials are abolished due to white matter ischemia. The delayed disappearance and better recovery of somatosensory than of auditory evoked potentials indicate that ischemic tolerance is higher in fiber tracts than in cortex. (Stroke 1990^1:923-928) N umerous experimental studies have concentrated on the effect of ischemia on the functional and morphologic integrity of the cerebral cortex.1 -6 In many investigations, evoked potentials (EPs) recorded from specific cortical areas have served as the paradigm of function, and disturbances of EPs were usually interpreted as indicating cortical disorder. 1 -36 -9 In many clinical cases, however, strokes cause capsular or supracapsular lesions in the white matter, resulting in neurologic deficits not related to cortical destruction. As demonstrated by x-ray computed tomography and even better by magnetic resonance imaging, ischemic damage can be confined in such cases to the white matter or can From the

The Existence and Evolution of Diffusion–Perfusion Mismatched Tissue in White and Gray Matter After Acute Stroke

“…The median NIHSS score on admission was 12 (range 2 to 27). All patients had 3 (37 to 100 cm 3 ). Diffusion-perfusion mismatch was able to be identified in both gray and white compartments of brain.…”

“…2 The importance of ischemic injury to cerebral white matter is that this may be a major contributor to the functional disability experienced after stroke. 3 Hence, the failure of some neuroprotection trials may be explained by ineffectiveness of the neuroprotective agents in protecting against white matter axonal damage. This may, in part, be the result of differing cellular constituents and ischemic neurochemical cascades in gray and white matter compartments which, in turn, may confer a differential vulnerability to ischemia.…”

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

“…Second, in some experimental models of global and focal ischemia in mature brain, loss of SEP correlated with reduction in blood :flow, high energy phosphates and edema in subcortical white matter tracts rather than in gray matter (7)(8)(9)(10)(11). Perinatal models of asphyxia often show histologic changes in white matter (41,42).…”

“…With moderate forebrain ischemia, decreases in white matter blood flow and energy metabolism can precede those in gray matter and affect SEP (7,8). With focal cerebral ischemia, some regions of somatosensory cortex can have near-normal levels of blood flow but have depressed SEP associated with subcortical white matter ischemi a (9)(10)(11). During reperfusion and reoxygenation, recovery of SEP depends on the severity , duration, and location of reduced blood flow (12)(13)(14).…”

Experimental evidence of ischemic thresholds and functional recovery.

“…Differences between cortical and white matter ischemia were studied in greater depth, using simultaneous recordings of flow and electrophysiological activity in thalamic relay nuclei, cerebral white matter, and primary cortex. 13 During the ischemic period, the EPs were abolished both in auditory and in somatosensory cortex. After 1-hour ischemia at a local flow rate of 8.5 ml/100 g per minute, the amplitude of auditory cortical EPs attained only 18% of its preischemic level during reperfusion.…”