Posttraumatic bilateral middle cerebral artery occlusion

1975 ◽  
Vol 42 (2) ◽  
pp. 217-221 ◽  
Author(s):  
Skip Jacques ◽  
C. Hunter Shelden ◽  
D. Thomas Rogers ◽  
Anthony C. Trippi
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Content Type ◽  
Pathophysiological Mechanisms ◽  
Cerebral Artery Occlusion ◽  
Fine Print

✓ The authors report a case of bilateral posttraumatic middle cerebral artery occlusion. Previously reported unilateral cases are reviewed and possible pathophysiological mechanisms disscussed.

Indomethacin-mediated improvement following middle cerebral artery occlusion in cats

1985 ◽  
Vol 62 (6) ◽  
pp. 874-881 ◽  
Author(s):  
Robert J. Dempsey ◽  
Mark W. Roy ◽  
Kathleen L. Meyer ◽  
David L. Donaldson
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Focal Cerebral Ischemia ◽  
Artery Occlusion ◽  
Opposite Hemisphere ◽  
Content Type ◽  
Beneficial Effects ◽  
Cerebral Artery Occlusion ◽  
Fine Print

✓ Focal cerebral ischemia initiates multiple detrimental effects in the brain. Chief among these are the regional development of ischemic edema, decreased local perfusion, altered neuronal function, and eventual infarction. To determine if pretreatment with the cyclo-oxygenase inhibitor, indomethacin, would result in improvement in these parameters, adult cats were given indomethacin or control solvent (4 mg/kg intraperitoneally twice daily) and were studied for periods up to 24 hours after right middle cerebral artery occlusion. The interaction of anesthetic agents with indomethacin was also examined in separate groups of experimental animals using pentobarbital and ketamine. In cats allowed to recover from pentobarbital anesthesia, indomethacin reduced gray and white matter edema at 6 and 24 hours after occlusion (p < 0.05). This was noted in densely ischemic areas (indomethacin = 84.3%, control = 87.5%), in “penumbra” regions (indomethacin = 82.5%, control = 85.3%), and in nonischemic zones (indomethacin = 81.5%, control = 82.3%) at 24 hours. Somatosensory evoked potential amplitude and central latency were also improved in the indomethacin group (p < 0.05), as was cerebral perfusion (p < 0.05). In animals anesthetized with continuous ketamine administration, cerebral edema and perfusion as well as evoked potentials were not significantly improved in any region by indomethacin. Regional cerebral blood flow in the group was increased by indomethacin in the nonischemic opposite hemisphere (indomethacin = 64.7 cc/100 gm/min, control = 48.5 cc/100 gm/min, p < 0.05), but not in the penumbra region of the ischemic hemisphere (indomethacin = 15.0 cc/100 gm/min, control = 18.6 cc/100 gm/min, p < 0.05), when measured 4 hours after occlusion. This suggested a steal phenomenon. Beneficial effects of indomethacin were evident in the presence of pentobarbital, but not after ketamine anesthesia. This suggests a synergism dependent on decreased arachidonic acid production from pentobarbitalstabilized membranes coupled with diminished production of cyclic endoperoxides from available arachidonate due to inhibition of cyclo-oxygenase with indomethacin.

Pathophysiology and treatment of focal cerebral ischemia

1992 ◽  
Vol 77 (3) ◽  
pp. 337-354 ◽  
Author(s):  
Bo K. Siesjö
Keyword(s):  
Free Radicals ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Ischemic Lesion ◽  
Glutamate Antagonists ◽  
Content Type ◽  
Cerebral Artery Occlusion ◽  
Fine Print

✓ The mechanisms that give rise to ischemic brain damage have not been definitively determined, but considerable evidence exists that three major factors are involved: increases in the intercellular cytosolic calcium concentration (Ca++i), acidosis, and production of free radicals. A nonphysiological rise in Ca++i due to a disturbed pump/leak relationship for calcium is believed to cause cell damage by overactivation of lipases and proteases and possibly also of endonucleases, and by alterations of protein phosphorylation, which secondarily affects protein synthesis and genome expression. The severity of this disturbance depends on the density of ischemia. In complete or near-complete ischemia of the cardiac arrest type, pump activity has ceased and the calcium leak is enhanced by the massive release of excitatory amino acids. As a result, multiple calcium channels are opened. This is probably the scenario in the focus of an ischemic lesion due to middle cerebral artery occlusion. Such ischemic tissues can be salvaged only by recirculation, and any brain damage incurred is delayed, suggesting that the calcium transient gives rise to sustained changes in membrane function and metabolism. If the ischemia is less dense, as in the penumbral zone of a focal ischemic lesion, pump failure may be moderate and the leak may be only slightly or intermittently enhanced. These differences in the pump/leak relationship for calcium explain why calcium and glutamate antagonists may lack effect on the cardiac arrest type of ischemia, while decreasing infarct size in focal ischemia. The adverse effects of acidosis may be exerted by several mechanisms. When the ischemia is sustained, acidosis may promote edema formation by inducing Na+ and Cl− accumulation via coupled Na+/H+ and Cl−/HCO3− exchange; however, it may also prevent recovery of mitochondrial metabolism and resumption of H+ extrusion. If the ischemia is transient, pronounced intraischemic acidosis triggers delayed damage characterized by gross edema and seizures. Possibly, this is a result of free-radical formation. If the ischemia is moderate, as in the penumbral zone of a focal ischemic lesion, the effect of acidosis is controversial. In fact, enhanced glucolysis may then be beneficial. Although free radicals have long been assumed to be mediators of ischemic cell death, it is only recently that more substantial evidence of their participation has been produced. It now seems likely that one major target of free radicals is the microvasculature, and that free radicals and other mediators of inflammatory reactions (such as platelet-activating factor) aggravate the ischemic lesion by causing microvascular dysfunction and blood-brain barrier disruption. Solid experimental evidence exists that the infarct resulting from middle cerebral artery occlusion can be reduced by glutamate antagonists, by several calcium antagonists, and by some drugs acting on Ca++ and Na+ influx. In addition, published reports hint that qualitatively similar results are obtained with drugs whose sole or main effect is to scavenge free radicals. Thus, there is substantial experimental evidence that the ischemic lesions due to middle cerebral artery occlusion can be ameliorated by drugs, sometimes dramatically; however, the therapeutic window seems small, maximally 3 to 6 hours. This suggests that if these therapeutic principles are to be successfully applied to the clinical situation, patient management must change.

Treatment of intraoperative middle cerebral artery occlusion with pentobarbital and extracranial-intracranial bypass

1979 ◽  
Vol 51 (5) ◽  
pp. 710-712 ◽  
Author(s):  
Pablo M. Lawner ◽  
Frederick A. Simeone
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Neurological Deficit ◽  
Artery Occlusion ◽  
Content Type ◽  
Cerebral Artery Occlusion ◽  
Fine Print

✓ A patient with a meningioma of the medial sphenoid wing underwent inadvertent intraoperative occlusion of the middle cerebral artery. Neurological deficit and infarction were presumably prevented by immediate administration of pentobarbital followed by extracranial-intracranial bypass.

Histochemical studies in the zone of ischemia following middle cerebral artery occlusion in cats

1972 ◽  
Vol 37 (1) ◽  
pp. 45-54 ◽  
Author(s):  
Vance D. MacDonald ◽  
Thoralf M. Sundt ◽  
R. K. Winkelmann
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Enzyme System ◽  
Artery Occlusion ◽  
Tissue Reaction ◽  
Specific Enzyme ◽  
Content Type ◽  
Cerebral Artery Occlusion ◽  
Enzyme Changes

✓ Representative enzymes in brain were studied by histochemical techniques at intervals varying between 6 hours and 8 weeks after permanent middle cerebral artery occlusion in 18 cats. Unequivocal enzyme changes did not develop until 12 hours after occlusion, and no specific enzyme system was demonstrated to fail prior to others. That the ischemia of the first 6 hours is reversible in the cat was further substantiated by histological studies in a separate group of animals subjected to temporary middle cerebral artery occlusion for 6 hours. This study demonstrated progressive axonal changes, after the period of reversibility, bordering the core area of ischemia and resembling neural tissue reaction to injury in the spinal cord. Correlation of this study with previous biochemical determinations suggests that a self-induced and self-perpetuated toxicity might explain, in part, progressive changes in ischemic areas.

Induced seizures as therapy of experimental strokes in dogs

1971 ◽  
Vol 34 (2) ◽  
pp. 178-184 ◽  
Author(s):  
Ronald R. Reed ◽  
Conrad Ciesel ◽  
Guy Owens
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Oxidative Metabolism ◽  
Collateral Circulation ◽  
Seizure Activity ◽  
Artery Occlusion ◽  
Content Type ◽  
Elevated Rate ◽  
Cerebral Artery Occlusion ◽  
Fine Print

✓ Intracerebral pO2, as measured in normal dog brains by a modified mass spectrometer, was found to increase following seizure activity and remain elevated at least 2 hours. These results were found with both drug- and electrically-induced seizures. The pO2 increased to a greater degree in brain tissue rendered ischemic by middle cerebral artery occlusion. A transient reflex hypertension was observed with seizure activity, but hypertension alone failed to produce significant pO2 changes. Since oxidative metabolism has been shown by other investigators to proceed at an elevated rate during seizure activity, the increased pO2 must reflect improved collateral circulation following seizure activity.

Prediction of tissue survival after middle cerebral artery occlusion based on changes in the apparent diffusion of water

2001 ◽  
Vol 95 (3) ◽  
pp. 450-458 ◽  
Author(s):  
Masaharu Sakoh ◽  
Leif Østergaard ◽  
Albert Gjedde ◽  
Lisbeth Røhl ◽  
Peter Vestergaard-Poulsen ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Artery Occlusion ◽  
Adc Value ◽  
Content Type ◽  
Pet Scanning ◽  
Apparent Diffusion ◽  
Adc Values ◽  
Cerebral Artery Occlusion ◽  
Fine Print

Object. In this study the authors tested the hypothesis that the estimate of the apparent diffusion coefficient (ADC) of water is a reliable pathophysiological index of the viability of ischemic brain tissue. Methods. Cerebral blood flow (CBF) and the cerebral metabolic rates of oxygen and glucose (CMRO2 and CMRglc, respectively) were measured using positron emission tomography (PET) scanning before and after permanent middle cerebral artery occlusion (MCAO) or reperfusion in pigs. The ADC value, which was measured using diffusion-weighted magnetic resonance (DW MR) imaging was compared with physiological variables obtained by PET scanning and with histological findings. After both permanent MCAO and reperfusion, the decrease in the ADC was significantly correlated with decrease in the CMRO2 and CMRglc. The infarction coincided with a CMRO2 threshold of 50% of the value measured on the contralateral side. Thus, an ADC value of 80% or 75% of the contralateral value reflected the CMRO2 threshold after permanent MCAO or reperfusion, respectively. On DW MR images, lesions with ADC values above 80% of the contralateral value are potentially reversible until 6 hours after MCAO, whereas lesions with ADC values below 75% of the contralateral value are irreversible as early as 2 hours after MCAO. Conclusions. The ADC of water provides a reliable pathophysiological index for tailoring therapy to the condition of individual stroke patients in clinical practice.

Expression of neurocan after transient middle cerebral artery occlusion in adult rat brain

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S217-S217
Author(s):  
Kentaro Deguchi ◽  
Mikiro Takaishi ◽  
Takeshi Hayashi ◽  
Atsuhiko Oohira ◽  
Shoko Nagotani ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Rat Brain ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Adult Rat ◽  
Adult Rat Brain ◽  
Cerebral Artery Occlusion
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