A dynamic concept of middle cerebral artery occlusion and cerebral infarction in the acute state based on interpreting severe hyperemia as a sign of embolic migration.

Abstract

SUMMARY The present study investigates the pathogenesis of focal cerebral hyperemia, its effect on brain tissue and discusses its pathophysiological and therapeutic importance in the light of interpreting severe hyperemia as a sign of arterial reopening probably due to embolic migration. Cerebral angiography, serial CT-scans and serial TC"-scans were performed in a consecutive group of 73 patients with completed stroke all admitted to hospital within 3 days after stroke onset. When possible the regional cerebral blood flow (rCBF) was studied with the intracarotid Xe" J injection method. Twenty-nine patients had evidence of middle cerebral artery (MCA) occlusion; rCBF was investigated in 24. Fourteen patients had either occlusion or severe internal carotid artery (ICA) stenosis; rCBF was not measured in these patients. Thirty patients had no angiographical evidence of MCA occlusion, ICA occlusion or severe ICA stenosis; rCBF was investigated in 24.Focal hyperemia was observed in 21 patients but exclusively in the group with evidence of MCA occlusion. Hence, these 21 patients are typical and representative for the group of patients with evidence of MCA occlusion. Hyperemia was found in infarcted as well as in non-infarcted tissue. Apparently, it is the severity of the initial ischemic episode and not the hyperemia that determines whether or not tissue necrosis develops. Interpreting severe hyperemia as a sign of arterial reopening and embolic migration (evidenced by partial reopening affecting only some MCA branches) reopening had occurred in about 'A of the patients with MCA occlusion before they were examined 1 to 4 days after stroke onset. Autopsy studies performed in 8 of the patients with MCA occlusion indicate that arterial reopening also takes place in many patients later on (7 of 8). According to this interpretation, hypothetical as it is, the changing position of the embolus is associated with partial or complete reperfusion leading to hyperemia in the initially ischemic brain tissue. The hemodynamic basis for appropriate therapy therefore may change from one day to the next in the acute state of stroke due to MCA occlusion. Stroke Vol 15, No 3, 1984 FOCAL CEREBRAL ISCHEMIA is the initial blood flow derangement after occlusion of a cerebral artery. When seen clinically on admission to hospital most infarcts are consequently thought to be low flow areas, perhaps with a rim of moderate hyperemia in the surrounding intact brain tissue due to diffusion of vasoactive substances to the borderzone. Spontaneous reopening of the occluded artery, in the first hours or days, allowing early reperfusion of the ischemic area with a resultant high flow, is thought to be a fairly rare event.Ischemia is thus considered to be the major blood flow abnormality in acute stroke when seen clinically. Nevertheless, focal hyperemia is an outstanding feature in the early stages after cerebral infarction.'" 9 In a recent report of rCBF in acute stroke patients, all well visualized cortical infarcts were consistently associated w...

Reperfusion after thrombolytic therapy in ischemic stroke measured by single-photon emission computed tomography.

“…In one study using planar ( l33 Xe) imaging focal hyperemias were seen in 8 of 21 patients with MCA occlusion within 4 days of stroke onset. 15 A PET study of 12 patients studied within 48 hours of stroke onset demonstrated that at least some reperfusion had occurred in 4 of 12 patients. 16 A more recent PET study of 18 patients found hyperperfusion in 6 of 18 patients studied between 5 and 18 hours after stroke onset.…”

The Effects of Delayed Reduction of Tonic Inhibition on Ischemic Lesion and Sensorimotor Function

“…[11][12][13][14][15][16] In contrast to Clarkson et al, we implanted the L-655,708 tablets subcutaneously and used a dosing regimen, following Atack et al, 17 that results in a steady-state plasma drug concentration that is low enough to produce selective α5-subunit-containing GABA A receptor occupancy during the course of treatment. We thereby assessed drug effects following a clinically relevant delivery method at a dose that minimizes side effects by preserving receptor subtype specificity.…”

In vivo Binding of Nimodipine in the Brain: I. The Effect of Focal Cerebral Ischemia

“…These concepts have limited practical application because postischemic CBP, at least in the acute phase, is an unreliable index of tissue viability: it can be extremely low as in "no-reflow" (Ginsberg et aI., 1978;Hossmann, 1982;Kagstrom et aI., 1983) or it can be unneces sarily high in lUXury perfusion when CBP exceeds the metabolic needs of the tissue (Traupe et aI., 1982;Olsen and Lassen, 1984). Therefore, it has increasingly become necessary to characterize isch emic severity and predict tissue survival not only on the basis of perfusion but as a function of changes in basic membrane properties.…”