Cortical Branch Of Middle Cerebral Artery Research Articles

Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique.

Ischemic stroke remains the predominant cause of mortality and functional impairment among the adult populations globally. Only a minority of ischemic stroke patients are eligible to receive intravascular thrombolysis or mechanical thrombectomy therapy within the optimal time window. Among those stroke survivors, around two-thirds suffer neurological dysfunctions over an extended period. Establishing a stable and repeatable experimental ischemic stroke model is extremely significant for further investigating the pathophysiological mechanisms and developing effective therapeutic strategies for ischemic stroke. The middle cerebral artery (MCA) represents the predominant location of ischemic stroke in humans, with the MCA occlusion serving as the frequently employed model of focal cerebral ischemia. In this protocol, we describe the methodology of establishing the distal MCA occlusion (dMCAO) model through transcranial electrocoagulation in C57BL/6 mice. Since the occlusion site is located at the cortical branch of MCA, this model generates a moderate infarcted lesion restricted to the cortex. Neurological behavioral and histopathological characterization have demonstrated visible motor dysfunction, neuron degeneration, and pronounced activation of microglia and astrocytes in this model. Thus, this dMCAO mouse model provides a valuable tool for investigating the ischemiastroke and worth of popularization.

Shoulder Palsy due to Middle Cerebral Artery Embolism

An 80-year-old Japanese woman with paroxysmal atrial fibrillation suddenly developed sensory aphasia, with moderate weakness restricted to the right shoulder with normal muscle strength in the elbow, wrist and fingers. There were no other neurological abnormalities. Diffusion-weighted cranial magnetic resonance imaging demonstrated scattered infarct lesions in the territory of the left middle cerebral artery (MCA), probably due to cardiogenic embolism. Right-sided shoulder palsy might have been caused by a localized infarct lesion in the precentral gyrus on the left side, and resolved within 10 days. Because the area corresponding to the shoulder is small in the primary motor cortex, isolated shoulder palsy due to cortical infarction is very rare. Its etiology remains controversial, but borderzone ischemia between the anterior cerebral artery and MCA, and atherothrombosis of the cortical branch of MCA are proposed. Our case shows that the area corresponding to the shoulder receives blood from the cortical branch of MCA. J Med Cases. 2013;4(2):86-88 doi: https://doi.org/10.4021/jmc936w

中大脳動脈M1部塞栓症に対する局所線溶療法施行後のレンズ核線条体動脈領域病巣の検討

Middle cerebral artery (MCA) occlusion can be treated successfully with local intraarterial infusion of tissue-type plasminogen activator (t-PA). If the M1 segment of MCA is occluded, the ischemia of lenticulostriate territory occurs. The lenticulostriate arteries are end-arteries, whereas the cortical branches of MCA have leptomeningeal anastomoses. The pathophysiological effect on the lentriculostriate arterial territory after quick reperfusion of the M1 by fibrinolytic therapy is, however, not yet well understood. We investigated changes in neuroradiological findings for the lenticulostriate arterial territory following fibrinolytic therapy for embolic M1 occlusion.The clinical and neuroradiological findings in nine patients treated with intra-arterial infusion of t-PA were reviewed. All patients had had computerized tomographic (CT) scans before and after fibrinolysis. Six (66.7%) had areas of increased attenuation on immediate postperfusion CT scans in the lenticulostriate arterial territory. Three patterns were categorized according to the changes in neuroradiological findings in the lenticulostriate arterial territory following sequential CT scans. In three cases (Group 1), the high density lesions as seen in the immediate postperfusion CT scans disappeared within 24 hours; they subsequently became low density areas. In three cases (Group 2), the high density lesions as seen in the immediate postperfusion CT scans persisted for several days. Only one of them was symptomatic. Three cases (Group 3) had normal findings on immediate postperfusion CT scans; all showed low density areas on the next day. All patients were observed to show hemorrhagic transformation within seven days.In Group 1, the rapid clearance of the high attenuation represented contrast that had entered into the disrupted blood-brain barrier (BBB). In Group 2, hemorrhagic extravasation had occurred in the lenticulostriate arterial territory since the vessel walls were damaged so badly that they no longer could resist the pressure of reperfusion. In Group 3, recirculation caused oligemia due to the no-reflow phenomenon.