The atherosclerotic changes in the carotid bifurcation were examined in 70 Japanese and 73 German cadavers. Initially, a fatty streak or dot appeared in the carotid sinus and/or on the anterior side of the common carotid artery. Further progression occurred predominantly in the carotid sinus, resulting in a localized atheromatous plaque. Finally an atheromatous plaque was formed all around the bifurcation. The following speculation was made from observations of many carotid bifurcations; the accumulation of fatty streaks on the anterior surface of the common carotid artery results in an atheromatous plaque in the carotid sinus analogous to accumulation of sand on a sandbank in a river. This concept may be useful in understanding the progression of atheromatous plaques.

We report the third case of intracerebral neurinoma in a patient with von Recklinghausen's disease, who died of recurrent subdural hematomas after head injury. A total of ten tumors were found in the brain. Both by histological and ultrastructural standards the multiple tumors resembled neurinomas. The pattern of positivity for S-100 and myelin basic protein indicated the Schwann cell origin of the tumors. The ultrastructural findings indicated Schwann cells and numerous areas showing a well defined basement membrane surrounding spindle-shaped neoplastic cells and other areas lacking basement membrane with Schwann cells embedded in collagen. The present case may be categorized as a mixed form of peripheral and central neurofibromatosis. It seems safe to assume that perivascular nerves are the site of origin of the tumors.

Sixty-three patients with lacunar-type of acute capsular infarction were treated in our service during the last 2 years. Their lesions were identified by computed tomography (CT) and classified into six types according to their locations: anterior, lateral, posterior, superior, inferior and multiple. The lesions were thought to be in the watershed areas of the regional arterial supplies, and the areas were considered to be prone to ischemia. The clinical course of each type showed characteristic features of ischemic strokes. In the majority of the patients with the lateral type, reversible ischemic neurological deficit (RIND) was seen as the predominant symptom, transient ischemic attack (TIA) was noted in the patients with the superior type, and major completed stroke was observed in those with posterior type.

Adult identical twins with Moyamoya disease are reported. Laboratory examinations such as blood types, AB, Rh(+), HLA (human leucocytic antigen) analysis [AW26(9), A26(10), BW62(15), BW61(40), CW3], and finger prints, and hairs confirmed that two patients were identical twins. Both had normal serum immunoglobulin levels and no anti-DNA antibodies. Patient No. 1, a 39-year-old female, was admitted to our service with chief complaints of nausea, vomiting and left hemiparesis with sudden onset on Oct 31, 1981. The patient had an episode of tetraplegia that occurred suddenly at 4 years of her age and lasted about a week. Motor weakness had completely disappeared but moderate mental retardation remained. She had been employed just prior to this attack. CT and angiographic examinations revealed ventricular hemorrhage with Moyamoya disease, which had miliary aneurysm in the branch of the right posterior choroidal artery. The operation of encephalomyosynangiosis was performed on her left hemisphere. The postoperative course was uneventful. Patient No. 2, the twin sister of patient No. 1, was in good health and mental state until 19 years of her age, when she suddenly lost consciousness and developed hemiparesis. After this attack, her motor function had recovered well. However, mental ability gradually deteriorated and she was admitted to a psychiatric ward. CT examination and angiographic studies were performed on Oct 12, 1982, and she was diagnosed as having Moyamoya disease.(ABSTRACT TRUNCATED AT 250 WORDS)

A 45-year-old female had sudden onset of severe headache, nausea and vomiting without any inducing moments and was transferred to our hospital by an ambulance car. On admission the patient was alert and showed only signs of meningeal irritation. There were no other neurological deficits at all. Immediate CT examination revealed a small high density spot in the area of the right basal ganglia, and a large high density in the frontal horns of both lateral ventricles. Right carotid angiogram showed completely patent carotid siphon with Moyamoya vessels. A small round aneurysmal shadow of 3 mm in diameter was seen in the area of these Moyamoya vessels of the right basal ganglia, and it was thought to be corresponding to the high density spot in the CT examination. Left carotid angiogram showed stenosis of C portion with typical Moyamoya vessels. Therefore, diagnosis of atypical Moyamoya disease with a ruptured aneurysm and ventricular penetration of hematoma was made. The patient was placed on conservative treatment. On 25th day from onset, repeated angiogram showed enlargement of the aneurysmal shadow from 3 mm to 5 mm in diameter. So, on 33rd day, right STA-MCA anastomosis and encephalomyosynangiosis were carried out. Angiogram on 12th day after surgery revealed no aneurysmal shadow. The patient was discharged without any neurological deficit at all. Previous paper, which reported cases of Moyamoya disease with aneurysm, were reviewed. According to the location of the aneurysm, these cases were classified into 3 types angiographically; type I: aneurysm in the area of Moyamoya vessels, type II: aneurysm of cerebral-peripheral artery, and type III: aneurysm of the circle of Willis. It has been generally believed that the Moyamoya disease may be associated with either a true or a pseudoaneurysm in the case of type I. However, pseudoaneurysm in the area of Moyamoya vessels has not been found in postmortem examination but true aneurysms so far. Therefore it may not be denied that the aneurysm of this case was true aneurysm although it showed an enlarging tendency and disappeared rather spontaneously.