抄録
The mechanism of the production of the intracerebral hematoma in cerebrovascular moyamoya disease is still being debated. The authors experienced a case, whose intracerebral hematoma was evacuated 18 hours after the ictus. During the operation, a hematoma ball near the bleeding point in the hematoma cavity was extirpated and used for preparing pathologic specimens. Four hundred serial specimens, 4 μm in thickness, showed abnormal perforating arteries, the diameter of which was around 300 μm. The wall of these vessels presented variable intimal elastofibrosis and tortuosity of internal elastic laminae, resulting in irregular narrowing or dilata-tion of vessels. In addition, many disrupted arterioles, the size of which ranged from 50 to 150 μm in diameter, were found. The walls of these smaller vessels were not accompanied by the fibrinoid necrosis change and presented almost the same changes as were seen in the larger ones, but to a smaller extent. These arteriolar changes were considered to evolve during the formation of the hematoma. So long as there is production of intracerebral hematoma, these findings indicate that the pathologic mechanisms in moyamoya disease are similar to those in hypertensives, especially in the massive type.
