Study on pathological changes of the cerebral arteries of malignant

2001 Fiscal Year Final Research Report Summary

• Project/Area Number: 12670155
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Human pathology
• Research Institution: Tokyo Medical & Dental University
• Principal Investigator: OKEDA Riki Tokyo Medical & Dental University, Medical Research Institute, Neuropathology, Prof., 難治疾患研究所, 教授 (70013977)
• Project Period (FY): 2000 – 2001
• Keywords: malignant hypertension / malignant nephrosclerosis / Binswanger's encephalopathy / cerebral artery / 脳動脈

Research Abstract

It is proposed that hypertension (HT) induces stiffening of the cerebral medullary arteries resulting in diffuse atrophy of the cerebral white matter in Binswanger's disease (BE). In order to clarify whether hypertension is the sole cause of BE, and if HT is severe, whether it can induce arterial and parenchymal changes similar to BE, the cerebral arteries in the frontal lobe of five autopsy cases of malignant hypertension (MH) were investigated by reconstruction of serial sections and morphometry of the medial thickness. The total duration of hypertension ranged clinically from one week to 31 years. The heart Weight was 380g to 900g. Morphometry of medial thickness of the arachnoidal arteries presented significant medial hypertrophy in four cases of MH, but in the medullary arteries in only two cases with marked cardiomegaly of 700 and 900g. Seven to twelve medullary arteries per case could be recostructed segmentally or completely. In four cases of MH, only a few arteries showed adventitial fiborosis or short segments of medial smooth Muscle cell (SMC) loss or intimal fibrosis. But, in the another case with cardiomegaly of 900g, all ten arteries showed multiple segments of atheroma and medial SMC loss, and prominent dilatation ; no luminal obstruction was present, and the both arachnoidal and medullary arteries showed significant medial hypertrophy. Although the white matter of this case presented diffuse myelin pallor, atrophy of the white matter was absent.
In conclusion, (1) in respect of the medial hypertrophy, HT influences lesser on the cerebral medullary arteries than on the arachnoidal arteries, (2) extent of the pathological changes of the cerebral arteries of MH is various between the MH-patients, and (3) hypertension, if so severe to induce marked cardiomegaly of 900g can induce severe pathological changes of the cerebral medullary arteries, yet does not instantaneously induce the diffuse atrophy of the cerebral white matter comparable to BE.