The accessory middle cerebral artery as a collateral blood supply

We describe two cases of acute embolic occlusion of the internal carotid artery and the middle cerebral artery in association with a patent accessory middle cerebral artery. Because of the presence of the accessory middle cerebral artery, the frontal lobe was salvaged to some extent, but it did not provide sufficient collateral blood supply to the middle cerebral artery territory to spare the rest of the frontal lobe, the temporal lobe, and the basal ganglia.     

Cerebral revascularization by omental free flap using contralateral superficial temporal vessels as recipient vessels: case report

BACKGROUND: Although the most common technique of cerebral revascularization is superficial temporal artery to middle cerebral artery bypass, we occasionally encounter a situation in which the ipsilateral superficial temporal artery is not available. Treatment may require several techniques including long vein graft bypass. METHODS: A 54-year-old man experienced transient ischemic attacks, and cerebral angiography revealed occlusion of the right common carotid artery. Cerebral blood flow study revealed reduced perfusion reserve capacity of the right cerebral hemisphere. We applied an omental free flap to the brain surface using the contralateral superficial temporal vessels as recipient vessels. RESULTS: Cerebral blood flow study revealed improvement of perfusion reserve capacity. Cerebral angiography revealed good collateral circulation from the omentum to the brain. The patient has not experienced a transient ischemic attack, following additional ligation of the occipital artery 13 months after the first operation. CONCLUSIONS: Because an omental flap has a long pedicle and its circulation can be monitored easily, this method is safe and as effective as a long bypass graft in a patient such as ours in whom the ipsilateral superficial temporal artery is not available for anastomoses.     

Transient osteoporosis of the hip: a densitometric study

A 62-year-old man was admitted to our hospital with abrupt onset of monoballism in the left arm. Brain MRI showed a hemorrhagic lesion in the right subthalamic nucleus. MRA demonstrated occlusion of the right internal carotid artery occlusion. Cerebral angiogram indicated a leptomeningeal anastomosis to the right middle cerebral artery from the right posterior cerebral artery. SPECT with 99mTc-HMPAO demonstrated the reduction of cerebral blood flow in the right frontotemporal region. Right superficial temporal artery-middle cerebral artery anastomosis was performed 7 months after onset. Monoballism disappeared after surgery and the patient had a good clinical course during the postoperative period. Monoballism associated with internal carotid artery occlusion is rare, and we were able to show the subthalamic nucleus lesion with MRI soon after onset. We considered that the reason for this hemorrhage in the subthalamic nucleus was the hemodynamic stress to the posterior cerebral artery area caused by the ipsilateral occlusion of the internal carotid artery.     

Predicting the effect of carotid artery occlusion during carotid endarterectomy: comparing transcranial doppler measurements and cerebral angiography

BACKGROUND and PURPOSE: We correlated the mean transcranial Doppler blood flow velocity (FVm) during carotid endarterectomy with the functional collateral pathway(s) documented by angiography. METHODS: Three patient groups were established: group 1 was dependent on the anterior communicating artery, group 2 on the anterior communicating artery and ipsilateral posterior communicating artery, and group 3 on the ipsilateral posterior communicating artery. Continuous middle cerebral artery FVm and electroencephalographic monitoring were performed in 45 patients during carotid endarterectomy. RESULTS: Clamped FVm was lowest in group 3 at 17+/-9 cm/s versus 36+/-16 and 33+/-11 cm/s for groups 1 and 2 (P<0.01). FVm values in groups 1 and 2 were similar. There was significant cerebral arterial vasodilation in group 3 patients on the basis of a pulsatility index of 0.38+/-0.15. The maximum FVm after clamp release was similar among the 3 groups. Normalized blood flow velocity 1 minute before release of the clamp was increased from the minimum flow velocity after clamping only in group 1 and 2 patients. CONCLUSIONS: The ipsilateral posterior communicating artery is a minor collateral pathway during acute carotid occlusion that contributes little to the collateral flow if there is a functional anterior communicating artery. Collateral flow through the middle cerebral artery is not recruited during occlusion in group 3 patients. The reperfusion FVm transient is independent of the primary collateral pathway. Documentation of functional collateral pathways on the basis of Doppler or angiographic examination may be advantageous in future studies since it can provide the basis for comparison among studies.     

Alpha-ketoglutarate dehydrogenase in Alzheimer brains bearing the APP670/671 mutation

The authors describe the use of a microanastomotic device to perform intracranial end-to-end vascular anastomoses. Direct end-to-end anastomosis was performed between the superficial temporal artery and branches of the middle cerebral artery (MCA) in three patients. Two patients had moyamoya disease, with severe proximal MCA disease, and one suffered an internal carotid artery occlusion with poor collateral flow. All patients reported a history of recent ischemic symptoms. Each anastomosis was accomplished in less than 15 minutes with technically satisfactory results. Postoperative angiographic studies demonstrated patency of the bypasses in all patients.     

Fastigial stimulation increases ischemic blood flow and reduces brain damage after focal ischemia

Electrical stimulation of the cerebellar fastigial nucleus (FN) increases CBF and reduces brain damage after focal ischemia. We studied whether FN stimulation "protects" the brain from ischemic damage by increasing blood flow to the ischemic territory. Sprague-Dawley rats were anesthetized (halothane 1-3%) and artificially ventilated through a tracheal cannula inserted transorally. CBF was monitored by a laser-Doppler probe placed over the convexity at a site corresponding to the area spared from infarction by FN stimulation. Arterial pressure (AP), blood gases, and body temperature were controlled, and the electroencephalogram (EEG) was monitored. The stem of the middle cerebral artery (MCA) was occluded. After occlusion, the FN was stimulated for 60 min (100 microA; 50 Hz; 1 s on-1 s off) while AP was maintained at 97 +/- 11 mm Hg (mean +/- SD) by controlled hemorrhage. Rats were then allowed to recover, and infarct volume was determined 24 h later in thionin-stained sections. In unstimulated rats (n = 7), proximal MCA occlusion reduced CBF and the amplitude of the EEG. One day later, these rats had infarcts involving neocortex and striatum. FN stimulation after MCA occlusion (n = 12) enhanced CBF and EEG recovery [61 +/- 34 and 73 +/- 43%, respectively at 60 min; p < 0.05 vs. unstimulated group; analysis of variance (ANOVA)] and reduced the volume of the cortical infarct by 48% (p < 0.05). In contrast, hypercapnia (PCO2 = 64 +/- 4; n = 7) did not affect CBF and EEG recovery or infarct volume (p > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebral blood flow response pattern during balloon test occlusion of the internal carotid artery

PURPOSE: To evaluate the risk of temporary or permanent internal carotid artery occlusion. METHODS: In 156 patients intraarterial balloon test occlusion in combination with a stable xenon-enhanced CT cerebral blood flow study was performed before radiologic or surgical treatment. All 156 patients passed the clinical balloon test occlusion and underwent a xenon study in combination with a second balloon test. Quantitative flow data were analyzed for absolute changes as well as changes in symmetry. RESULTS: Fourteen patients exhibited reduced flow values between 20 and 30 mL/100 g per minute, an absolute decrease in flow, and significant asymmetry in the middle cerebral artery territory during balloon test occlusion. These patients would be considered at high risk for cerebral infarction if internal carotid artery occlusion were to be performed. With one exception they belonged to a group (class I) of 61 patients who showed bilateral or ipsilateral flow decrease and significant asymmetry with lower flow on the side of occlusion. The other 95 patients, who showed a variety of cerebral blood flow response patterns including ipsilateral or bilateral flow increase, were at moderate (class II) or low (class III) stroke risk. In contrast to these findings, exclusively qualitative flow analysis failed to identify the patients at high risk: a threshold with an asymmetry index of 10% revealed only 16% specificity whereas an asymmetry index of 45% showed only 61% sensitivity for detection of low flow areas (< 30 mL/100 g per minute). CONCLUSION: For achieving a minimal hemodynamic related-stroke rate associated with permanent clinical internal carotid artery occlusion we suggest integration of a thorough analysis of quantitative cerebral blood flow data before and during balloon test occlusion.     

Effects of etomidate administration on cerebral collateral flow

OBJECTIVE: Augmentation of blood flow to collateral-dependent tissue (CDT) as a result of selective vasodilation of collateral vessels has been shown to occur with various stimuli after middle cerebral artery occlusion. Etomidate, a carboxylated imidazole derivative, is a nonbarbiturate anesthetic that is used clinically both as an anesthetic and as a neuroprotective agent. The effect etomidate has on collateral cerebral vessels is unknown. The purpose of our studies was to test whether etomidate selectively augmented cerebral blood flow (CBF) to CDT during ischemia as an additional mechanism of neuroprotection. METHODS: A left craniotomy was performed in each of 14 dogs, with the animals under halothane anesthesia. A branch of the middle cerebral artery was occluded and cannulated distally for determination of CDT using a "shadow flow" technique. CBF and vascular pressures were measured and used to calculate vascular resistance. An etomidate infusion (0.1 mg/kg of body weight/min administered intravenously) was started, and CBF and vascular pressures were measured at 10 and 40 minutes. Hypotension was then induced, and CBF and pressures were again measured. RESULTS: CBF was significantly reduced in all regions of the brain, including CDT, when etomidate was infused. CDT showed a 53.7% reduction in flow, whereas normal CBF was reduced by at least 63.4%. During hypotension, blood flow to CDT was reduced by an additional 42.7%, whereas normal cerebrum was reduced by at least 22.7%. Vascular resistance was increased in all vessels during etomidate infusion. CONCLUSION: The neuroprotective effects of etomidate do not seem to be through the augmentation of collateral or global CBF.     

The hemodynamics and anatomy of the circle of Willis. The technic and clinical value of selective MR angiography

This study evaluates the usefulness of MR angiography in analysing the individual collateral flow dynamics and anatomy of the circle of Willis in 56 patients with high-grade extracranial carotid stenosis or occlusion. Selective MRA of the carotid or vertebrobasilar area was performed by means of presaturation up to the brain-supplying arteries at the level of the middle neck (angled presaturation slabs). Results obtained with selective and non-selective MRA in 56 consecutive patients were compared with the findings at transcranial Doppler ultrasonography and arterial angiography. Ischaemic cerebral infarctions were classified by computerized tomography and correlated with the results of collateral flow analysis: Sensitivity of selective MRA in detecting intracranial collateral flow via anterior or posterior communicating artery was 96 and 97%, respectively; sensitivity in depicting extracranial transorbital flow was lower (71%). Non-selective MRA was 100% sensitive in detecting a non-filling of the horizontal (A1) segment of the anterior cerebral artery and in identifying an origin of the posterior cerebral artery from the intracranial carotid artery. Slow flow infarctions occurred more frequently in patients with transorbital and posterior-to-anterior collateral flow than in patients with collateral flow via anterior communicating artery.     

Mydriatic pupil as the presenting sign of common carotid artery dissection

BACKGROUND: Ipsilateral mydriasis is known to accompany signs of cerebral ischemia in unilaterally compromised carotid blood flow. Mydriasis as the presenting sign of common carotid artery (CCA) dissection has not been reported thus far. CASE DESCRIPTION: We report the case of a patient who presented with a mydriatic pupil after intraoperative injury of the ipsilateral CCA. Mydriasis preceded complete third-nerve palsy and symptoms of cerebral ischemia for 12 hours. Cerebral angiography revealed occlusion of the CCA with slow collateral flow to the internal carotid artery and fetal origin of the posterior cerebral artery, suggesting a hemodynamic mechanism causing ischemia of the oculomotor nerve. Signs of cerebral ischemia and third-nerve palsy resolved completely after reconstructive surgery of the occluded vessel. CONCLUSIONS: A mydriatic pupil may be the unusual first sign of compromised carotid blood flow and impending cerebral ischemia.     

Ministrokes in rat barrel cortex

BACKGROUND AND PURPOSE: Many stroke models in rats are based on occlusion of the middle cerebral artery, which supplies a significant portion of multifunctional cortical and deep structures in the cerebral hemisphere. The purpose of this study was to develop a model for direct observation in real time of blood flow in and around focal ischemic regions of the cortex of known function. METHODS: Cranial windows were placed over the parietal cortex of adult Wistar and Sprague-Dawley rats anesthetized with ketamine and xylazine. Whisker barrel cortex responding to stimulation of the contralateral whiskers was identified by an intrinsic optical signal. Transits of vital dyes were recorded by videomicroscopy before and after ligation of three to six branches and major collaterals of the middle cerebral artery through the dura. Infarcts were demonstrated with triphenyl-tetrazolium chloride staining; their relation to barrel cortex was determined by Nissl and cytochrome oxidase histology. RESULTS: Reduced blood flow in small ischemic regions was outlined by patient blue violet in the surrounding nonischemic area; arteriovenous latencies increased more than four times in ischemic cortex. Infarcts,typically 3 mm or less, were seen at 24 hours in 8 of 16 Wistar and 9 of 9 Sprague-Dawley rats. The ministrokes were confirmed by histology to be in the somatosensory cortex. CONCLUSIONS: This model of local ischemia, produced deliberately in the functionally defined barrel cortex in rats, leads to ministrokes. Changes can be followed by videomicroscopy as they develop, and processes of recovery can potentially be monitored. Infarcts are confirmed by histology for their location and extent in the somatic representation.     

Cell density-dependent mitogenic effect and -independent cellular handling of epidermal growth factor in primary cultured rat hepatocytes

Brain swelling is a serious complication associated with focal ischemia in stroke and severe head injury. Experimentally, reperfusion following focal cerebral ischemia exacerbates the level of brain swelling. In this study, the permeability of the blood-brain barrier has been investigated as a possible cause of reperfusion-related acute brain swelling. Blood-brain barrier disruption was investigated using Evans Blue dye and [14C]aminoisobutyric acid autoradiography in a rodent model of reversible middle cerebral artery (MCA) occlusion. Acute brain swelling and cerebral blood flow (CBF) during ischemia and reperfusion were analyzed from double-label CBF autoradiograms after application of the potent vasoconstrictor peptide endothelin-1 to the MCA. Ischemia was apparent within ipsilateral MCA territory, 5 min after endothelin-1 application to the exposed artery. Reperfusion, examined at 30 min and 1, 2, and 4 h, was gradual but incomplete within this time frame in the core of middle cerebral artery territory and associated with significant brain swelling. Ipsilateral hemispheric swelling increased over time to a maximum (>5%) at 1-2 h after endothelin-1 but was not associated with a significant increase in the ipsilateral transfer constant for [14C]aminoisobutyric acid over this time frame. These results indicate that endothelin-1 induced focal cerebral ischemia is associated with an acute but reversible hemispheric swelling during the early phase of reperfusion which is not associated with a disruption of the blood-brain barrier.     

Acute coeliac artery occlusion: initial collateral blood flow from the superior mesenteric artery. An experimental study

The collateral blood flow from the superior mesenteric artery after acute occlusion of the coeliac truck was measured in experiments in dogs. Immediately after clamping of the coeliac axis the collateral flow was about 30 % of the original coeliac blood flow. During an observation time of three hours the collateral flow increased, the corresponding value at the end of experiment being about 50 %. At the same time the blood pressure in the coeliac artery rose from a mean value of 20 mmHg to 35 mmHg. The initial collateral blood flow was evidently not sufficient, since after this short occlusion period ischaemic changes, even necrosis, were observed in the liver and stomach in some of the test animals.     

Augmentation of blood flow through cerebral collaterals by inhibition of nitric oxide synthase

We examined the influence of nitric oxide (NO) on normal and collateral cerebral blood flow after occlusion of the middle cerebral artery (MCA). Effects of NG-nitro-L-arginine (nitroarginine), an inhibitor of NO synthase, were examined during normotension and hypotension (arterial pressure, 50 mm Hg) in 49 anesthetized dogs. Following a craniotomy, a branch of the MCA was cannulated, and collateral-dependent tissue was identified using the shadow-flow technique. Regional cerebral blood flow was measured with microspheres, and pial artery pressure was measured with a micropipette. Intravenous nitroarginine reduced blood flow to normal cerebrum by approximately 40% (p < 0.05) during normotension and hypotension, with aortic pressure maintained constant after nitroarginine administration. Injection of nitroarginine during hypotension, without control of pressor effects, increased aortic and pial artery pressure approximately twofold. Concurrently, blood flow to normal cerebrum decreased (p < 0.05), while flow to collateral-dependent cerebrum increased (p < 0.05). Phenylephrine was infused during hypotension to increase arterial pressure to values similar to those achieved following nitroarginine. Blood flow to collateral-dependent cerebrum increased (p < 0.05), but flow to normal cerebrum was not altered during infusion of phenylephrine. Thus, inhibition of NO synthase during hypotension increases arterial pressure, decreases blood flow to normal cerebrum, and increases blood flow to collateral-dependent cerebrum. Phenylephrine also increases perfusion pressure and blood flow to collateral-dependent cerebrum, but in contrast to nitroarginine, it does not redistribute blood flow from normal cerebrum.     

Pharmacokinetics of triptorelin after intravenous bolus administration in healthy males and in males with renal or hepatic insufficiency

PURPOSE: The aim of the present study was to validate a simple MRI-procedure for semiquantitative assessment of regional cerebral blood flow. MATERIALS AND METHODS: Unilateral cerebral ischaemia (30 minutes) in the territory of the middle cerebral artery was induced in 14 anesthetised rates. The MRI-experiment consisted in an intravenous bolus injection of gadolinium-DTPA, recording of the cerebral contrast kinetics with a T2*-weighted pulse sequence, and measurement of the maximal concentration change at a chosen reference point of time. To measure perfusion quantitatively, a microsphere technique, an accepted reference technique was used. With both methods a perfusion index related to the contralateral side was calculated. RESULTS: In all cases decreased perfusion was detected by the MRI technique. The perfusion indices correlated with a coefficient of correlation of r = 0.89 (p < 0.001). CONCLUSION: The results demonstrate that contrast-enhanced MRI with bolus injection can be implemented with clinical potential as a semiquantitative instrument for the assessment of cerebral perfusion. Regional cerebral blood volume and collateral blood flow may interfere with the estimate of blood flow.     

Vasoreactive effect of acetazolamide as a function of time with sequential PET 15O-water measurement

The accurate assessment of vascular flow reserve is crucial for the evaluation of risk among patients with cerebrovascular disease. In six patients with unilateral occlusion of the internal carotid artery and one patient with unilateral occlusion of the middle cerebral artery (mean +/- S.D. age = 68 +/- 3 years), we measured cerebral blood flow (CBF) after the administration of 940 MBq 15O-water using a remotely controlled power injector. Studies were performed at rest, after 10 min, and then 10, 20 and 30 min after the administration of 1 mg acetazolamide to evaluate the vasoreactive effect, as reflected by an increase in CBF. Sixteen regions of interest (ROIs) were drawn over the CBF images. These ROIs were as follows in each hemisphere: Area I, four areas in the cortical middle cerebral arterial territory (superior frontal, frontal, temporal and parietal areas); Area II, four areas of the deep middle cerebral and vertebral arterial territory (occipital area, basal ganglia, thalamus and cerebellum). Taking normalized resting CBF to be 100%, the mean CBF measured 10, 20 and 30 min post-injection using sequential positron emission tomography was as follows: Area I, 141.4 +/- 16.3, 127.7 +/- 15.3 and 128.2 +/- 17.4% for non-occluded sites and 116.3 +/- 22.8, 112.7 +/- 16.4 and 114.9 +/- 17.1% for occluded sites; Area II, 143.4 +/- 14.5, 126.2 +/- 10.4 and 125.0 +/- 12.9% for non-occluded sites and 141.9 +/- 28.9, 126.0 +/- 20.5 and 124.1 +/- 17.1% for occluded sites. A significant difference in mean CBF was noted between the non-occluded and occluded sites in Area I, the most marked difference of 25.1% being observed 10 min after the administration of the acetazolamide. We conclude that for an accurate assessment of vascular reserve in patients with cerebrovascular disease, CBF should be measured 10 min post-administration of the acetazolamide.     

Comparison of the effect of etomidate and desflurane on brain tissue gases and pH during prolonged middle cerebral artery occlusion

BACKGROUND: The authors compared the effects of etomidate and desflurane on brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH in patients who had middle cerebral artery occlusion for > 15 min. METHODS: After a craniotomy, a probe that measures PO2, PCO2, and pH was inserted into cortical tissue at risk for ischemia during middle cerebral artery occlusion. A burst suppression pattern of the electroencephalogram was induced with etomidate (n = 6) or 9% end-tidal desflurane (n = 6) started before middle cerebral artery occlusion. Mean blood pressure was supported with phenylephrine to 90-95 mmHg. RESULTS: During baseline conditions, tissue PO2, PCO2, and pH were similar between the two groups (PO2 = 15 mmHg, PCO2 = 60 mmHg, pH = 7.1). During administration of etomidate before middle cerebral artery occlusion, tissue PO2 decreased in five of six patients without a change in PCO2 or pH. During administration of 9% desflurane, tissue PO2 and pH increased before middle cerebral artery clipping. Middle cerebral artery occlusion for an average of 33 min with etomidate and 37 min with desflurane produced a decrease in pH with etomidate (7.09 to 6.63, P < 0.05) but not with desflurane (7.12 to 7.15). CONCLUSION: These results suggest that tissue hypoxia and acidosis are often observed during etomidate treatment and middle cerebral artery occlusion. Treatment with desflurane significantly increases tissue PO2 alone and attenuates acidotic changes to prolonged middle cerebral artery occlusion.     

Diagnosis and therapy of kidney traumas

Argatroban, (2R,4R)-4-methyl-1-(N2 [(3-methyl-1,2,3,4-tetrahydro-8-quinolinyl)-sulfonyl]-L-arginyl)-2-pi peridinecarboxylic acid, a selective and competitive thrombin inhibitor, was examined for effectiveness in three different experimental models of cerebral thrombosis in rats, namely, the four-vessel occlusion model, the middle cerebral artery occlusion model, and the distal middle cerebral artery occlusion model. Argatroban was demonstrated to be effective in these experimental models of thrombosis. Among these models, the distal middle cerebral artery occlusion model was the most similar to clinical cerebral thrombosis with respect to restriction of the infarction to the cerebral cortex and the accompanying stable neurologic deficits. In this model, the thrombus was generated at the Y-shaped bifurcation of the middle cerebral artery by green light irradiation through a cranial window after administration of rose bengal. Argatroban given after thrombus formation by intraperitoneal implantation of an osmotic pressure pump was shown to reduce infarct size and neurologic deficits on day 3 and microthrombi generation on day 1, and to raise the regional cerebral blood flow on day 1, at a plasma level of 0.2 to 0.6 microM supporting its clinical usefulness in the treatment of acute-phase cerebral thrombosis. Argatroban was considered to exert its effects by salvaging neuronal cells in the ischemic penumbra and suppressing extension of the infarction into the penumbra by keeping blood vessels patent, mainly through the inhibition of microthrombogenesis.     

Cerebral revascularization using muscle free flap for ischemic cerebrovascular disease in adult patients

The efficacy of encephalo-myo-synangiosis (EMS) using muscle free flap was evaluated for the treatment of ischemic cerebrovascular disease in adult patients. Three patients with adult moyamoya disease and three patients with atherosclerotic ischemic cerebrovascular disease were treated. EMS used four latissimus dorsi muscles and two serratus anterior muscles. Postoperative selective angiography showed collateral circulation from the transferred muscle to the brain in four of the six patients. The other two patients showed patent nutrient artery of the transferred muscle flap. Cerebral blood flow study disclosed postoperative improvement of perfusion reserve capacity in all sides. One patient suffered a perioperative stroke by hemoconcentration due to poor control of diabetes mellitus. The mean follow-up period was 23 months. EMS using muscle free flap is a possible procedure in selected patients with impaired cerebral perfusion reserve capacity due to multiple stenosis or occlusion of cerebral arteries including moyamoya disease or who required cerebral blood flow augmentation in the anterior and/or posterior cerebral artery territories due to internal carotid artery occlusion.     

Induction of ischemic tolerance following brief focal ischemia in rat brain

The objective of this study was to determine whether brief focal ischemia induces ischemic tolerance in rat brain. Focal ischemia was produced in Wistar rats by occluding the middle cerebral artery (MCA) for 20 min at a distal site. Following recovery for 24 h, the animals were subjected to a 10-min episode of forebrain ischemia using a combination of bilateral carotid artery occlusion and systemic hypotension. Histologic injury, assessed after a survival period of 3-4 days, consisted of selective neuronal necrosis bilaterally in cerebral cortex, striatum, hippocampus, and thalamus superimposed upon a small cortical infarct adjacent to the site of MCA occlusion. However, the intensity of neuronal necrosis in the MCA territory of the neocortex ipsilateral to MCA occlusion was markedly less than that in the contralateral MCA cortex. In contrast, the extent of neuronal necrosis in subcortical structures was similar in both hemispheres. Unexpectedly, animals in which the MCA was manipulated, but not occluded, also exhibited a marked reduction of neuronal necrosis in the ipsilateral MCA neocortex following forebrain ischemia. However, in animals with craniotomy alone, forebrain ischemia caused a similar extent of neuronal necrosis in the MCA neocortex of both hemispheres. Transient occlusion of the MCA induced the focal expression of the 72-kDa heat-shock protein (hsp72) in the MCA territory of the neocortex. Limited expression of hsp72 was also detected following sham occlusion, but not after craniotomy alone. These results demonstrate focal induction of ischemic tolerance in rat neocortex that may be related to expression of heat-shock proteins.