Showing papers on "Middle cerebral artery published in 1993"
TL;DR: New protein synthesis appears to contribute to ischemic cell death in which endonucleolytic DNA degradation is apparent and may open unique therapeutic approaches for the preservation of neurons in stroke.
Abstract: Cells die by one of two mechanisms, necrosis or programmed cell death. Necrosis has been implicated in stroke and occurs when the cytoplasmic membrane is compromised. Programmed cell death requires protein synthesis and often involves endonucleolytic cleavage of the cellular DNA. We assessed the potential contribution of programmed cell death to ischemia-induced neuronal death.Cycloheximide (protein synthesis inhibitor; 1 mg/kg per 24 hours) or vehicle (1 mL/kg per 24 hours) was continuously infused into the right cerebral ventricle of spontaneously hypertensive rats. Neocortical focal ischemia was produced by tandem occlusion of the right common carotid artery and the ipsilateral middle cerebral artery. After 24 hours the brain was stained with 2% 2,3,5-triphenyltetrazolium and the ischemic zone quantitated. Protein synthesis was determined by [3H]methionine incorporation into acid-precipitated protein. DNA integrity was determined in isolated DNA by gel electrophoresis and in whole cells by flow cytomet...
719 citations
TL;DR: Traditional direct measurement of infarct volume is associated with an overestimation of infArct volume during the development of brain edema in the first 3 days after ischemia, which can be reduced with indirect measurement, which is based on noninfarcted cortex volume.
Abstract: Infarct volume is one of the common indexes for assessing the extent of ischemic brain injury following focal cerebral ischemia. Accuracy in the measurement of infarct volume is compounded by postischemic brain edema that may increase brain volume in the infarcted region. We evaluated the effect of brain edema on infarct volume determined by triphenyltetrazolium chloride and hematoxylin and eosin stains in a focal cerebral ischemia model in rats.In a middle cerebral artery occlusion model in rats, infarction is confined to the cerebral cortex. The infarct was delineated by triphenyltetrazolium chloride stain and, in selected samples, by hematoxylin and eosin stain. We determined infarct size at different times after the ischemic insult (6 hours to 7 days) in relation to the evolution of brain edema by the direct measurement of infarct volume. Indirect measurement to reduce the effect of edema on infarct volume was also conducted in the same brain samples.Direct measurement showed that infarct volume fluct...
702 citations
TL;DR: Data suggest that at the time of craniotomy, diameters of the large cerebral vessels do not significantly change during moderate variations in blood pressure and CO2, but that larger changes may occur in smaller vessels.
Abstract: Forty-five measurements of diameters of 12 human cerebral arteries were performed during 10 craniotomies under moderate changes in mean blood pressure and end tidal CO2. The mean change in blood pressure was 30 +/- 16 mm Hg (standard deviation) and that of end tidal CO2 was 14 +/- 6 mm Hg (standard deviation). These changes were induced with nitroprusside, phenylephrine, and adjustment of ventilator rate. Measurements were made through the operating microscope focused at the highest power, with meticulous attention to constant angle and distance from the artery. The mean diameter change in the large cerebral arteries (carotid, middle cerebral artery, vertebral artery) was less than 4%, but the smaller arteries (anterior cerebral artery, M2 segment of middle cerebral artery) showed diameter changes as large as 29% and 21% to end tidal CO2 and blood pressure changes, respectively. These data suggest that at the time of craniotomy, diameters of the large cerebral vessels do not significantly change during moderate variations in blood pressure and CO2, but that larger changes may occur in smaller vessels. This constancy of diameter suggests that the transcranial Doppler velocities obtained during intraoperative monitoring of craniotomies may closely reflect blood flow through the insonated artery.
698 citations
Journal Article•
TL;DR: Emergency cerebral angiography adds important information about the nature and extent of the arterial occlusions, and the recanalization efficacy of fibrinolytic therapy for patients with acute stroke.
Abstract: PURPOSE 1) To describe the effectiveness and safety of thrombolytic therapy in patients with acute atherothrombotic and embolic stroke and 2) to study the variables of the occlusion site as seen on the angiograms, the CT signs of early ischemia, the hyperdense middle cerebral artery sign (HMCAS), and the size of the infarcts as seen on the 24-hour CT scan.
METHODS Ninety-three of 139 patients with acute stroke were treated with intravenous tissue plasminogen activator (rt-PA). The initial disease and the effects of treatment were assessed with both CT and cerebral angiography.
RESULTS Recanalization of occluded arteries occurred in 32 patients and was more frequent in distal occlusions. In general, patients displaying recanalization tended to develop small infarcts and patients with a HMCAS tended to develop large infarcts. Patients with signs of early ischemia developed large infarcts. The presence of a HMCAS was 100% fic for an occluded artery, but only 27% sensitive. Hemorrhagic transformations occurred in the distribution of the occluded arteries in 32 patients.
CONCLUSIONS Emergency cerebral angiography, which can be carried out relatively safely, adds important information about the nature and extent of the arterial occlusions, and the recanalization efficacy of fibrinolytic therapy for patients with acute stroke. Fibrinolytic therapy can be carried out with a relatively low complication rate that still needs to be correlated with the clinical benefits of the treatment. Fibrinolytic therapy in the doses utilized in this study, is more effective with distal than with proximal carotid territory occlusions.
424 citations
TL;DR: Local intra-arterial fibrinolysis was capable of improving clinical outcome in acute vertebrobasilar artery occlusion, reducing mortality to 50% in patients fulfilling inclusion criteria and in the carotid territory multiple occlusions had a poor prognosis while good clinical results could be achieved.
Abstract: A group of 59 patients with stroke due to acute vertebrobasilar or carotid territory occlusion have been treated by local intra-arterial fibrinolysis (LIF). A high recanalisation rate was accomplished with either urokinase or recombinant tissue plasminogen activator (r-TPA). However, with either substance, even if a high dose was used, recanalisation was a time-consuming process which usually took 120 min. A reasonable explanation for the lack of effectiveness of these plasminogen-activating substances might be a deficit of substrate, e.g. plasminogen, in aged thrombus. LIF was capable of improving clinical outcome in acute vertebrobasilar artery occlusion, reducing mortality to 50% in patients fulfilling inclusion criteria. In the carotid territory multiple occlusions had a poor prognosis while good clinical results could be achieved in occlusions of the proximal middle cerebral artery or single branches.
321 citations
TL;DR: Differing patterns of swallowing in 40 patients with their first ischemic middle cerebral artery (MCA) stroke are reported and changes in the consistency of foods and other modifications for safe nutrition should be considered during the first month of recovery for unilateral stroke patients with swallowing difficulty.
255 citations
TL;DR: It is demonstrated that endothelin-1 is capable of reducing blood flow to pathologically low levels and provide a new model of controlled focal ischaemia followed by reperfusion.
Abstract: The capacity of endothelin-1 to induce severe reductions in cerebral blood flow and ischaemic neuronal damage was assessed in anaesthetised rats. Endothelin-1 (25 microliters of 10(-7)-10(-4) M) was applied to the adventitial surface of an exposed middle cerebral artery and striatal blood flow assessed by the hydrogen clearance technique. Endothelin-1 induced severe dose-dependent reductions in cerebral blood flow (e.g., minimum CBF at 10(-5) M of 9 +/- 11 ml 100 g-1 min-1 compared to 104 +/- 22 ml 100 g-1 min-1 with vehicle, p < 0.05), which persisted for at least 60 min at each concentration of endothelin-1. Application of endothelin-1 to the middle cerebral artery produced dose-dependent ischaemic brain damage (e.g., volume of damage of 65 +/- 34 mm3 at 10(-5) M compared to 0.22 +/- 0.57 mm3 for vehicle, p < 0.01). These data demonstrate that endothelin-1 is capable of reducing blood flow to pathologically low levels and provide a new model of controlled focal ischaemia followed by reperfusion.
246 citations
TL;DR: The results suggest that within 5-18 h of stroke onset, PET is a good predictor of outcome in patterns I and III, for which therapy seems limited, and may have important implications for acute MCA stroke management and for patients' selection for therapeutic trials.
228 citations
TL;DR: It is suggested that perivascular microapplication of Et-1 may provide a useful model for the study of the functional disturbances associated with focal cerebral ischaemia in the conscious rat.
Abstract: In the present study, we describe the effects of perivascular microapplication of the potent vasoconstrictor peptide endothelin-1 (ET-1; (120 pmol in 3 microliters), delivered via a guide cannula stereotaxically positioned above the left cerebral artery (MCA) of the conscious male Sprague-Dawley rat. Ten minutes after the administration of Et-1, mean arterial blood pressure had increased by 20% and profound reductions in local cerebral blood flow (up to 93%) were observed within those brain areas supplied by the MCA. In addition, significant increases in local cerebral blood flow were observed within the globus pallidus (100%), substantia nigra pars reticulata (48%), ventrolateral thalamus (65%), and dorsal hippocampus (74%) ipsilateral to the insult. Twenty-four hours following the insult, the pattern of ischaemic damage was similar to that reported previously following permanent occlusion of the rat MCA. It is suggested that perivascular microapplication of Et-1 may provide a useful model for the study of the functional disturbances associated with focal cerebral ischaemia in the conscious rat.
228 citations
TL;DR: It is shown that during temporary MCA occlusion, penumbral levels of amino acid neurotransmitter initially rise but subsequently decline to baseline despite ongoing ischemia and that moderate extracellular glutamate release and massive release of GABA and glycine occur at a CBF threshold of 48%.
Abstract: We simultaneously measured neurotransmitter amino acids by the microdialysis technique and cortical CBF by laser-Doppler flowmetry in the ischemic penumbral cortex of rats subjected to 2-h normothermic (36.5-37.5 degrees C) transient middle cerebral artery (MCA) clip-occlusion. Brains were perfusion-fixed 3 days later and infarct volume measured. CBF (% of preischemic values) fell to 32 +/- 2% (mean +/- SD) during ischemia and rose to 157 +/- 68% during recirculation. Extracellular glutamate levels increased from a baseline value of 7 +/- 3 microM to a peak value of 180 +/- 247 microM 20-30 min following onset of ischemia but subsequently returned to near baseline levels after 70 min of ischemia despite ongoing MCA occlusion. The threshold CBF for moderate glutamate release was 48%. Massive glutamate release was seen during the first 60 min of MCA occlusion in the two animals showing the largest infarcts and occurred at CBF values < or = 20% of control levels. Mean CBF during ischemia exhibited an inverse relationship with infarct volume, and the magnitude of glutamate release during ischemia was positively correlated with infarct volume. Extracellular gamma-aminobutyrate and glycine changes were similar to those of glutamate but showed no significant correlation with infarct volume. These results suggest that (a) accumulation of extracellular glutamate is an important determinant of injury in the setting of reversible MCA occlusion and (b) reuptake systems for neurotransmitter amino acids may be functional in the penumbra during transient focal ischemia.
217 citations
TL;DR: It is proposed that brief ischemia induces hsp70 mRNA and HSP70 protein in the cells most vulnerable to ischemIA—the neurons.
Abstract: Induction of the 70-kDa heat shock protein (HSP70) was demonstrated immunocytochemically in adult rats 4 h to 7 days following temporary middle cerebral artery (MCA) occlusions lasting 30, 60, or 90 min. Maximal HSP70 induction occurred approximately 24 h following ischemia. Thirty minutes of ischemia induced HSP70 in neurons throughout the cortex in the MCA distribution, whereas 90 min of ischemia induced HSP70 in neurons in the penumbra. HSP70 protein was induced in endothelial cells in infarcted neocortex following 60-90 min of MCA occlusion, and HSP70 was induced in endothelial cells in infarcted regions of lateral striatum following 30-90 min of MCA occlusion. hsp70 mRNA was induced in the MCA distribution in cortex and to a lesser extent in striatum at 2 h to 3 days following 60 min of ischemia. It is proposed that brief ischemia induces hsp70 mRNA and HSP70 protein in the cells most vulnerable to ischemia--the neurons. HSP70 protein is not induced in most neurons and glia following 60-90 min of ischemia in areas destined to infarct, whereas it is induced in vascular endothelial cells.
TL;DR: The sensitivity to nitroglycerin-induced dilatation of large intracranial arteries was studied and support that NO supersensitivity may be an important molecular mechanism of migraine pain.
Abstract: The sensitivity to nitroglycerin-induced dilatation of large intracranial arteries was studied in 17 patients with migraine without aura, 17 age and sex-matched healthy subjects and 9 patients with episodic tension-type headache. Nitroglycerin in the doses of 0.015, 0.03, 0.25 and 0.5 μg/kg/min was successively infused for 15 min per dose. Blood velocity (Vmean) in the middle cerebral artery (MCA) was recorded with transcranial Doppler before and at the end of every infusion period, and 30 and 60 min after end of the last infusion. In all three groups Vmean decreased with increasing doses (p < 0.001). The response was more pronounced in migraine patients at the two higher doses (p < 0.05). Since nitroglycerin acts as an exogenous source of nitric oxide (NO), these data support that NO supersensitivity may be an important molecular mechanism of migraine pain.
TL;DR: Transcranial doppler measurements of blood flow velocity in the middle cerebral artery were made during treatment of raised intracranial pressure (ICP) in 22 patients with severe brain injury, suggesting that autoregulation became a factor above this CPP threshold.
Abstract: Transcranial doppler measurements of blood flow velocity in the middle cerebral artery were made during treatment of raised intracranial pressure (ICP) in 22 patients with severe brain injury. Twenty patients also had continuous measurement of arterial and jugular bulb venous oxygen saturation (SJO2). The transcranial Doppler parameters studied included both mean flow velocity and pulsatility index (PI). Successful treatment was defined as a reduction of ICP to less than 20 mm Hg with improvement or preservation of cerebral perfusion pressure (CPP) above 60 mm Hg. Successful therapy was associated with a significant rise in SJO2 and reduction of cerebral arteriovenous oxygen content difference (AVDO2) and PI only when the pretreatment CPP was less than 60 mm Hg. An increase in CPP beyond 70 mm Hg did not further improve cerebral oxygen delivery and PI, suggesting that autoregulation became a factor above this CPP threshold. Treatment failure during administration of hypnotic drugs resulted in a reduction in arterial pressure, CPP, SJO2, and mean velocity and in an increase in PI and AVDO2, despite a decrease in ICP. CPP is the most important parameter to monitor during ICP therapy. It should be maintained above 70 mm Hg in patients with severe brain injury.
TL;DR: It is suggested that the stenosed arterial segment is the main source of cerebral embolism detectable with ultrasound in symptomatic patients with high-grade internal carotid stenosis, and thatcarotid endarterectomy substantially reduces the rate of these events.
Abstract: Fourteen symptomatic patients with severe extracranial internal carotid artery stenosis (> or = 70% of luminal narrowing) were monitored using long-term transcranial Doppler ultrasonography to determine the rate of clinically silent embolism of the ipsilateral middle cerebral artery. Before carotid endarterectomy (all patients being treated with intravenous heparin), 462 such events occurred during a total monitoring time of 45 h. Statistical analyses of the inter-event intervals and of the relationship between events and cardiac cycle revealed random occurrence. While the ipsilateral events were found in each subject, silent embolism of the contralateral middle cerebral artery occurred in only four patients each of whom had angiographically proven intracranial cross-flow from the symptomatic carotid territory (39 embolic events during 7 h monitoring time). The other 10 patients showed no contralateral embolism (10 h monitoring time). Five or more days (median 10 days) after surgery and cessation of intravenous anticoagulation the ipsilateral event rate had dropped to 13 in 33 h (P < 0.001) and the contralateral rate to zero. This suggests that the stenosed arterial segment is the main source of cerebral embolism detectable with ultrasound in symptomatic patients with high-grade internal carotid stenosis, and that carotid endarterectomy substantially reduces the rate of these events. Since reduction of ipsilateral stroke risk by successful endarterectomy is known to be of a similar degree in patients as those studied here, transcranially detected embolism may represent a new marker of disease activity of extracranial carotid artery stenosis.
TL;DR: It is indicated that NO improves blood flow and reduces tissue damage after focal cerebral ischemia and could have an important role in the management of acute ischemic stroke.
Abstract: We used the nitric oxide (NO) donor sodium nitroprusside (SNP) and the NO synthase inhibitor nitro-L-arginine methyl ester (L-NAME) to study the role of NO in the ischemic damage produced by occlusion of the rat middle cerebral artery (MCA). After MCA occlusion, intracarotid administration of SNP (2.5 mg kg h-2 for 1 h) enhanced the recovery of neocortical cerebral blood flow and of the EEG and reduced cortical infarct size by 76 +/- 2% (p < 0.01; n = 5). In contrast, administration of L-NAME (10 mg kg h-2) worsened the recovery of CBF and EEG and increased infarct size (+ 60 +/- 16%; p < 0.05; n = 5). The findings indicate that NO improves blood flow and reduces tissue damage after focal cerebral ischemia. Thus, NO donors could have an important role in the management of acute ischemic stroke.
TL;DR: High-dose intravenous nicardipine reduces the incidence and severity of delayed cerebral arterial narrowing in patients following aneurysmal SAH, and a balance of prognostic factors for vasospasm is found.
Abstract: ✓ Calcium antagonist drugs were proposed for use in patients with recent aneurysmal subarachnoid hemorrhage (SAH) because of their ability to block the effects of a wide variety of vasoconstrictor substances on cerebral arteries in vitro. It was suggested that these agents might, therefore, be useful in ameliorating cerebral vasospasm and its ischemic consequences which frequently complicate SAH. This hypothesis was tested in an arm of a randomized double-blind placebo-controlled trial of high-dose intravenous nicardipine in patients with recently ruptured aneurysms. Participating investigators were required to send selected copies of all admission and follow-up angiograms obtained between Days 7 and 11 following hemorrhage (the peak period of risk for vasospasm) to the Central Registry of the Cooperative Aneurysm Study for blinded interpretation and review for the presence and severity of angiographic vasospasm. In centers with transcranial Doppler ultrasound (TCD) capabilities, middle cerebral artery (M...
TL;DR: The depth of ischemia is more profound, occlusion is achieved in a much higher proportion of cases, and the incidence of perforation of the intracranial internal carotid is much less frequent than by Longa's method.
Abstract: Our purpose was to assess the effectiveness of middle cerebral artery occlusion in producing acute focal ischemia in the rat by the use of Koizumi9s and Longa9s methods, in which occlusion is achieved by passing a nylon thread into the internal carotid artery. Cerebral blood flow was measured by using the hydrogen clearance method, and the brains were examined histologically to assess ischemic damage. By Koizumi9s method profound reduction in cerebral blood flow was achieved in 28 of 30 rats (93%). The mean cerebral blood flow in the middle cerebral artery territory was 10.7 (95% confidence interval, 9.9-11.5) ml/100 g per minute. By Longa9s method reduction in cerebral blood flow was achieved in only 29 of 52 rats (56%), and in these animals mean cerebral blood flow was 33 (95% confidence interval, 28.3-33.7) ml/100 g per minute (p By Koizumi9s method the depth of ischemia is more profound, occlusion is achieved in a much higher proportion of cases, and the incidence of perforation of the intracranial internal carotid is much less frequent than by Longa9s method.
TL;DR: The rate of successful recording of blood flow signals in Japanese subjects decreases with advancing age, especially in females, and increasing the emitted power markedly improves the successful recording rate.
Abstract: To assess the usefulness of transcranial Doppler sonography, we investigated the rate of blood flow signal recording failure in the middle cerebral artery in Japanese subjects. Furthermore, we studied the effect of increased emitted power on the rate of successful recording in some of the patients in whom recording failure had been detected at the standard transducer power of 100 mW/cm2.To evaluate the rate of successful recording, we measured blood flow signals in 597 patients (age range, 16 to 89 years) for screening of cerebrovascular disease by using a 2-MHz range-gated, pulsed-wave Doppler instrument at the standard transducer power. In 18 elderly patients with recording failure at the standard power, we assessed the effect of increased emitted power of 400 mW/cm2 on flow signal recording.Blood flow signals were recorded in 920 (77.1%) of the 1194 middle cerebral arteries of the 597 patients studied. The rate of successful recording of bilateral middle cerebral artery flow signals (70.9%; 423 of 597 ...
TL;DR: The Kety-Schmidt technique was applied to measure the global average levels of CBF and cerebral metabolic rate of oxygen (CMRO2) during rest and dynamic exercise and found that the exercise-induced increase in MCA Vmean is not a reflection of a proportional increase in CBF.
Abstract: Results obtained by the 133Xe clearance method with external detectors and by transcranial Doppler sonography (TCD) suggest that dynamic exercise causes an increase of global average cerebral blood flow (CBF). These data are contradicted by earlier data obtained during less-well-defined conditions. To investigate this controversy, we applied the Kety-Schmidt technique to measure the global average levels of CBF and cerebral metabolic rate of oxygen (CMRO2) during rest and dynamic exercise. Simultaneously with the determination of CBF and CMRO2, we used TCD to determine mean maximal flow velocity in the middle cerebral artery (MCA Vmean). For values of CBF and MCA Vmean a correction for an observed small drop in arterial PCO2 was carried out. Baseline values for global CBF and CMRO2 were 50.7 and 3.63 ml.100 g-1.min-1, respectively. The same values were found during dynamic exercise, whereas a 22% (P < 0.0001) increase in MCA Vmean was observed. Hence, the exercise-induced increase in MCA Vmean is not a reflection of a proportional increase in CBF.
TL;DR: Trans transcranial Doppler was used to determine mean arterial flow velocity of the middle cerebral artery in 95 patients before and after carotid endarterectomy, demonstrating an immediate cessation of symptoms with reduction of arterial pressure even in normotensive patients.
TL;DR: Despite deficits appropriate to the area of infarction, prompt management of life-threatening postinfarction swelling by surgical decompression by xenon-enhanced computed tomographic studies of cerebral blood flow can yield favorable outcome.
Abstract: Objective: We report favorable outcome after surgical decompression, or strokectomy, guided by xenonenhanced computed tomographic studies of cerebral blood flow in the setting of potentially fatal swelling from massive cerebral infarction. Design: Retrospective analysis with 3 months to 3 years of follow-up. Setting: University of Pittsburgh (Pa) Medical Center, a tertiary care university referral center. Patients: Four patients, aged 14 to 46 years, presented with focal neurologic deficits appropriate for a massive middle cerebral artery infarction (two dominant and two nondominant). In spite of medical therapy, all patients deteriorated to at least a decreased level of consciousness. Intervention: Using xenon-enhanced computed tomographic studies of cerebral blood flow in three patients, areas of severely ischemic (blood flow, Outcome Measure: Outcome was measured by survival and ability to perform activities of daily living. Results: Postoperatively, all patients recovered rapidly ( Conclusion: Despite deficits appropriate to the area of infarction, prompt management of life-threatening postinfarction swelling by surgical decompression can yield favorable outcome.
TL;DR: The data suggest that, after 2 h of MCA occlusion, brain tissue progresses from isolated neuronal injury to infarct with a time course dependent on anatomical site; and astrocytic reactivity, expressed by GFAP staining, reflects the outcome of the ischemic injury.
TL;DR: T2*-sensitive echo-planar magnetic resonance imaging was used with first-pass magnetic susceptibility contrast enhancement in a cat model of acute regional stroke to evaluate the relationship between cerebral hypoperfusion and ischemic brain damage.
Abstract: T2*-sensitive echo-planar magnetic resonance imaging was used with first-pass magnetic susceptibility contrast enhancement in a cat model of acute regional stroke to evaluate the relationship between cerebral hypoperfusion and ischemic brain damage. In normal brain, dose-dependent decreases in signal intensity were observed after intravenous injection of 0.15-0.50 mmol/kg dysprosium-diethylenetriaminepentaacetic acid bismethylamide or gadodiamide injection. Shortly after unilateral occlusion of the middle cerebral artery, foci of signal hyperintensity on diffusion-weighted images were observed in the ipsilateral basal ganglia. Sixty minutes after occlusion, perfusion deficits in the ipsilateral parietal and temporal cortical gray matter were observed to be spatially correlated with areas of hyperintensity on diffusion-weighted images. When reflow was attempted after 60 minutes, delayed contrast agent transit suggestive of partial ischemic tissue injury was demonstrated. Attempts to produce reflow after 2 ...
TL;DR: The "brain-sparing" effect is a mechanism to prevent fetal brain hypoxia rather than a sign of impending brain damage.
TL;DR: The carotid arteries are probably the most common sources of intra-arterial emboli to the brain, but emboli also frequently arise from the aorta and the vertebral arteries, and potential embolic materials probably frequently enter the circulation but rarely cause strokes.
Abstract: Treatment of brain embolism should depend on the nature of the embolic material, if discoverable or predictable, not on whether the source was cardiac or intra-arterial. The middle cerebral artery territory is the most common recipient site for emboli, but many emboli do go to the carotid arteries and the posterior circulation. Cardiac and intra-arterial embolism probably each account for about one in five posterior circulation infarcts. Paradoxical embolism is much more common than formerly appreciated. The carotid arteries are probably the most common sources of intra-arterial emboli to the brain, but emboli also frequently arise from the aorta and the vertebral arteries. Potential embolic materials probably frequently enter the circulation but rarely cause strokes.
TL;DR: During carotid endarterectomy, transcranial Doppler immediately provides information about thromboembolism and hemodynamic changes that are not detected by electroencephalography alone.
Abstract: We report the results of combined recording of hemodynamic and thromboembolic phenomena during carotid endarterectomy by means of computerized electroencephalography as well as transcranial Doppler ultrasonography. The study focuses on the additional value of transcranial Doppler to detect ischemia during surgery.
Combined monitoring was performed in 130 consecutive operations, using standard anesthesiological, surgical, and neurophysiological procedures.
A reduction of > or = 70% of blood flow velocities in the middle cerebral artery during cross-clamping was measured in 16 patients. In seven of these cases there were no severe electroencephalographic changes and a shunt was not used, but one of the patients developed a subcortical infarct with slight disability. In 55 patients, 75 episodes of embolization were detected by transcranial Doppler. In one of these, with massive embolization after release of the clamp, an intraoperative stroke occurred without changes on cranial computerized tomography or neurological disability on follow-up. In the other 54 patients, intraoperative embolization did not cause clinical or neuroradiological symptoms. Electroencephalographic changes occurred in only two of the 75 episodes. In addition to the two nondisabling strokes during surgery (1.5%), six strokes occurred within 5 days of operation, including one hemorrhage. There was no significant relation between contralateral carotid occlusion and stroke (p = 0.6).
During carotid endarterectomy, transcranial Doppler immediately provides information about thromboembolism and hemodynamic changes that are not detected by electroencephalography alone. Acoustic feedback from the transcranial Doppler monitoring unit has a direct influence on the surgical technique. Transcranial Doppler ultrasound may be a useful tool in the study and prevention of intraoperative stroke.
TL;DR: The data suggest that postischemic induction of hypothermia significantly reduces ischemic cell damage after 2 hours of middle cerebral artery occlusion in the rat, and that an interval of time of at least 1 hour after ischemia exists in which hypothermic intervention is effective in either salvaging or postponing irreversible neuronal injury.
Abstract: We investigated the effect of hypothermia induced 1 hour after transient (2-hour) middle cerebral artery occlusion on the extent of ischemic cell damage in the rat.
Middle cerebral artery occlusion was induced extracranially by insertion of a nylon filament into the right internal carotid artery. Two groups of rats were investigated: (1) rats (n = 10) subjected to normothermic (37 degrees C) ischemia and normothermic reperfusion; and (2) rats (n = 10) subjected to normothermic ischemia and 1 hour of normothermic reperfusion followed by 3 hours of hypothermia (30 degrees C). All rats were killed 1 week after the experiment, and brain sections were stained with hematoxylin and eosin for evaluation of ischemic cell damage.
Infarct volume in normothermic rats involved 20.9 +/- 4.6% of the hemisphere, whereas hypothermic rats exhibited a significantly smaller (P < .001) infarct volume of 11.1 +/- 2.7%. The numbers of surviving (or structurally intact) neurons within large sections of the cortex and striatum were significantly greater for hypothermic compared with normothermic rats (P < .01).
Our data suggest that postischemic induction of hypothermia significantly reduces ischemic cell damage after 2 hours of middle cerebral artery occlusion in the rat, and that an interval of time of at least 1 hour after ischemia exists in which hypothermic intervention is effective in either salvaging or postponing irreversible neuronal injury.
TL;DR: The carbon dioxide reactivity of cerebral blood flow measured by this transcranial Doppler technique may be useful for characterizing the hemodynamic changes that occur in various types of ischemic cerebrovascular disease.
Abstract: The response of cerebral blood flow to changes in the arterial carbon dioxide partial pressure (i.e., carbon dioxide reactivity) has been evaluated as a parameter of cerebral perfusion reserve in patients with cerebrovascular disease. In this study, variations in this reactivity in various ischemic cerebrovascular diseases were evaluated by a newly established method, a transcranial Doppler technique.Thirty-three patients with symptomatic cerebrovascular disease, 13 patients with asymptomatic cerebral infarction, and 25 age-matched normal control subjects were investigated. The symptomatic patients were divided into three groups; those with unilateral carotid artery obstruction, those with cortical infarction, and those with lacunar infarction. The carbon dioxide reactivity of each subject was determined by simultaneously measuring the mean spatial Doppler frequency in the middle cerebral artery and the end-tidal carbon dioxide partial pressure under normocapnic, hypercapnic, and hypocapnic conditions.In ...
TL;DR: Using a mouse model with intraluminal blockade of the middle cerebral artery, the effect that superoxide radicals have on cerebral infarction, local cerebral blood flow, and neurological deficits after 24 h of permanent focal cerebral ischemia in transgenic mice overexpressing human CuZn-superoxide dismutase was examined.
Abstract: Using a mouse model with intraluminal blockade of the middle cerebral artery (MCA) which produced both cortical and striatal infarction, the effect that superoxide radicals have on cerebral infarction, local cerebral blood flow, and neurological deficits after 24 h of permanent focal cerebral ischemia in transgenic mice (Tg) overexpressing human CuZn-superoxide dismutase (SOD-1) was examined. There were no difference between SOD-1 Tg mice and non-Tg littermates observed in the infarct areas of brain slices, the infarct volume, the local cerebral blood flow, or the neurological deficits. These data suggest that pre-existing high levels of antioxidant enzyme failed to provide neuronal protection against permanent focal cerebral ischemia.