A monoclonal antibody, termed AD11/8, reactive to microglial cells, was produced by immunization of mice with partially purified amyloid fibrils of senile (neuritic) plaques. With immunoperoxidase staining on human tissues, AD11/8 also recognized macrophages in the red pulp of the spleen, Kupffer cells in the liver, and macrophages in the bone marrow. The results show that AD11/8 recognizes the antigens associated with mononuclear phagocytes lineage. In normal brains a few resting microglial cells were stained in gray matter, and less frequently in white matter. In senile dementia of the Alzheimer type numerous microglial cells were stained intensively and they often formed clusters in gray matter. By double immunostaining with AD11/8 and a polyclonal antibody against synthetic amyloid beta-protein, clustered microglial cells were observed in and around senile plaques with amyloid deposits. Some amyloid plaque cores were surrounded by microglial cell processes. These results indicate that microglial cells may play an important role in senile plaque formation.
Three cases of moyamoya phenomenon associated with an aneurysm in the periphery of a lateral ventricle presenting with intracranial haemorrhage are reported. In case 1 the aneurysm was located in the right basal ganglia, and the patient improved under conservative management. The aneurysm had increased in size on the second angiogram, and disappeared on the third angiogram obtained nine months after the attack. In Case 2 the aneurysm was located in the peripheral portion of the left posterior cerebral artery, and was surgically excised. Pathological examination on surgical material revealed collagenous tissue and laminae only in part of the aneurysmal wall. In Case 3 the aneurysm was located in the peripheral portion of the right anterior choroidal artery. This patient died, and the autopsy revealed an angiomatous lesion in the choroid plexus of the right lateral ventricle, but the aneurysm itself could not be identified. These findings indicate that an aneurysm has formed in a portion of a weakened vascular group represented by an abnormally dilated collateral pathway, and that the most likely reason for this would be haemodynamic stress.
The pathological changes in the brains of seven patients who had been clinically diagnosed as normal pressure hydrocephalus (NPH) are described and the possible etiological mechanisms are discussed. The pathological findings in all cases consisted of demyelination akin to Binswanger's type of encephalopathy, especially in the frontal lobes. Arteriosclerosis accompanied by occasional organized thrombi and scattered microinfarcts in the periventricular white matter were seen. Focal leptomeningeal fibrosis, diminution of arachnoidal granulations, and non‐specific aging processes were noted. Among the above of particular interest, was the degeneration of both periventricular and deep white matters with microinfarcts, and moderate to severe arteriosclerosis. On the basis of these observations, we assume that the degeneration in the white matter is not merely a secondary change due to the result of enlargement of ventricle, but plays an important role in the development of NPH. The development of NPH requires not only the disturbance of cerebrospinal fluid, but also the pre‐or coexisting vulnerability in the white matter caused by variables such as ischemia, hypoxia, and trauma.
Free amino acids were estimated quantitatively in the motor cortex from 3 patients with amyotrophic lateral sclerosis (ALS) and 11 control subjects. Among 7 amino acids which showed statistically significant changes, taurine was the only one which was increased constantly and most markedly in the motor cortex of all the 3 ALS cases. It was suggested that the metabolism of sulfur amino acids might be affected in comparatively early stages of ALS.
Both the Moyamoya Phenomenon and occlusion of the internal carotid fork are essential radiological findings in true Moyamoya Disease of unknown aetiology. However, the Moyamoya Phenomenon is often observed in occlusive diseases of the internal carotid bifurcation of known aetiology. The authors recently observed acute development of the unilateral Moyamoya Phenomenon following severe vasospasm of the anterior and middle cerebral arteries due to rupture of an anterior communicating aneurysm. The following four factors have been suspected of contributing to development of the Moyamoya Phenomenon: 1. The chronology of arterial occlusion. 2. Extent and location of occlusion. 3. The cause of occlusion. 4. Anatomical and functional disposition of the basal circulation. As regards the chronology, chronic or slowly progressive arterial stenosis has been thought to be a mandatory factor in development of a Moyamoya network, which plays an important role in the form of collateral channels. However, based on the findings outlined in this paper, the congenital factor may be the most important of the four factors.
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