OBJECTIVE: To investigate the etiology, pathology, and mechanism of pathogenesis of @entity7025 . METHODS: A total of 15 @entity1 autopsies were analyzed. In addition, in order to create an animal model of the disease, 21 Japanese @entity95 were divided randomly into two groups and subjected to injections of horse serum either intravenously or locally in the area of the sympathetic ganglia. Pathological and immunohistochemical characteristics were observed. RESULTS: The pathological features of the autopsies and the animal models both involved @entity1373 and @entity850 or even occlusion of the lumen in the terminal ends of the internal carotid artery and the anterior and middle cerebral arteries. Disconnections or even breakages of the inner layer of the lumen were also observed, without an obvious inflammatory response. Hyperplasic smooth muscle cells of the medial membrane had extended inward through broken portions of the internal elastic lamina, with @entity1373 resulting in lumen @entity850 . The hyperplastic vascular walls were positive for IgG and IgM. CONCLUSIONS: The etiology of @entity7025 may involve @entity56 . A possible mechanism is that proximal portions of the circle of Willis first develop chronic @entity850 or occlusion, leading to compensatory small vessel proliferation, which perforates into the cerebral parenchyma.

Clinical and experimental pathology of XXXX .

@entity1 :: ('9606', 'Species') :: ['human'] @entity1373 :: ('MESH:D006965', 'Disease') :: ['intima hyperplasia', 'intima cell hyperplasia'] @entity95 :: ('9986', 'Species') :: ['rabbits'] @entity7025 :: ('MESH:D009072', 'Disease') :: ['Moyamoya disease'] @entity56 :: ('MESH:D004342', 'Disease') :: ['allergic angiitis'] @entity850 :: ('MESH:D003251', 'Disease') :: ['stenosis']
@entity7025 :: (MESH:D009072,Disease) :: ['Moyamoya disease']
