Peri-infarct depolarizations reveal penumbra-like conditions in striatum.

Spreading depression-like peri-infarct depolarizations not only characterize but also worsen penumbra conditions in cortical border zones of experimental focal ischemia. We intended to investigate the relevance of ischemic depolarization in subcortical regions of ischemic territories. Calomel electrodes measured DC potentials simultaneously in the lateral and medial portions of the caudate nucleus (CN) of 11 anesthetized cats after permanent occlusion of the middle cerebral artery. Additionally, platinum electrodes measured cerebral blood flow (CBF) in the CN, and laser Doppler probes CBF in the cortex. Depolarizations (negative DC shifts >10 mV) were obtained in 10 of 11 cats. Further differentiation revealed that short-lasting spreading depression-like depolarizations (SDs; 5 of 10 cats: 5.24 +/- 1.22 min total duration; 23.3 +/- 4.2 mV amplitude) were predominantly found in medial and longer depolarizations (LDs; 4 of 10 cats: 64.7 +/- 47.5 min; 25.0 +/- 11.3 mV) in the lateral CN. Terminal depolarizations (TDs; 6 of 10 cats; without repolarization) occurred immediately after occlusion or at later stages, being then accompanied by elevations of intracranial pressure presumably inducing secondary CBF reduction. CBF tended to be lower in regions with TDs (33.3 +/- 29.9% of control) and LDs (37.3 +/- 22.8%) than in regions with SDs (51.5 +/- 48.0%). We conclude that in focal ischemia, transient peri-infarct depolarizations emerge not only in cortical but also in striatal gray matter, thereby demonstrating the existence of subcortical zones of ischemic penumbra. The generation of these ischemic depolarizations is a multifocal process possibly linked to brain swelling and intracranial pressure rise in the later course of focal ischemia, and therefore a relevant correlate of progressively worsening conditions.

Hemodynamic and metabolic effects of decompressive hemicraniectomy in normal brain. An experimental PET-study in cats.

Hemicraniectomy is increasingly used as treatment option in stroke and in head trauma, but little is known on the (patho)physiological regional effects of hemicraniectomy in the normal brain. A standard left-sided craniectomy was performed in three cats. Regional cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO(2)) and cerebral metabolic rate of glucose (CMR(glc)) were measured from the brain tissue underneath the craniectomy at 2, 20 and 28 h after hemicraniectomy. CBF significantly decreased (P<0.01) and oxygen extraction fraction (OEF) (P<0.05) significantly increased. CMRO(2) and CMR(glc) decreased only in regions with most severe CBF reduction. These effects remained for at least a day irrespective of corrective sustaining cranioplasty. The authors demonstrated for the first time that decompressive hemicraniectomy in the cat decreases CBF, and to a lesser extent CMR02 and CMR(glc) 2 h after hemicraniectomy in normal brain tissue that last for at least 1 day. Even though the underlying basis of these phenomena are not fully understood, this finding implies that persisting pathophysiological processes are induced by hemicraniectomy and should be taken into consideration for surgical indications.

Hemodynamic changes after occlusion of the posterior superior sagittal sinus: an experimental PET study in cats.

BACKGROUND AND PURPOSE: Occlusion of the anterior third of superior sagittal sinus (SSS) is generally well tolerated because of sufficient collateral venous blood flow. In contrast, the pathophysiologic effects of occlusion of the SSS posterior to the rolandic vein remain controversial. We aimed to identify the specific hemodynamic effects of this subtype of SSS occlusion. METHODS: We ligated the SSS just behind rolandic vein and in the posterior part near the confluens sinus in three anesthetized cats. Regional cerebral blood flow (rCBF) was measured before and at 2 and 24 hours after the SSS occlusion. At around 48 hours, experimental settings were terminated with perfusion fixation with 4% paraformaldehyde solution. Hematoxylin-eosin histologic evaluation was performed. RESULTS: In all three cats with SSS occlusion, rCBF was reduced over the time period of measurement; this finding was observed in areas covering 5-20% of the brain in planes affected by the occlusion. The degree of rCBF reduction and the extension and severity of histologically proved venous infarction were correlated. CONCLUSION: To our knowledge, this is the first demonstration that occlusion of the SSS posterior to the rolandic vein is associated with a significant rCBF reduction to still-viable tissue in the related vascular territory at 24 hours after occlusion. We describe subacute venous infarction in an experimental occlusion of the SSS. Analogous to clinical conditions, occlusion of SSS alone without additional occlusion of bridging veins is adequate for producing a venous circulatory disturbance.