Eighty-six patients with primary pontine hemorrhage were evaluated from October 1980 through September 1989. The sixty-nine of 86 patients were male and 17 female, and the average age was 53.1 years. Thirty-one patients had good or moderate recovery (ADL 1-3), 18 severe disability, and 14 vegetative state. Twenty-nine patients died within 3 weeks and 8 from 1 to 6 months.
Amongst various factors for predicting outcome, over 100 points of Japan Coma Scale, diminished oculocephalic reflex and unreactive pupil were significantly related to death. Hematoma extending into upper midbrain and/or into the 4th ventricle also indicated poor outcome. Amongst 60 patients whose hematomas were more than 26 mm in diameter, 30 patients died and remaining 30 were severely disabled or vegetated.
For the cumulative cases from 1980 through 1985, the mortality rate was 60.5%. This came down to 29.1% from 1986 through 1989. Prevention of systemic complication and respiratory management seems to be the largest contributing factor. On the other hand, the rate of severely disabled or vegetative patients was increased from 13.2% to 56.3%.
The results clearly indicate that various mode of intensive care is useful for decreasing early mortality for primary pontine hemorrhage, although long term result is not yet satisfactory.
Further effort for more vigorous therapies, along with the preventive medicine such as antihypertensive treatment seems to be required.

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On November 5 1989, a 51-year-old man suddenly experienced a sever throbbing headache follows shortly by the sensation of weakness in the right limbs. He was admitted to our hospital on the same day. Neurological examination showed lethargy, right hemiparesis predominating in the lower limb and urinary incontinence.
A CT scan revealed a low density area in the territory of the left anterior cerebral artery, and a left common carotid angiogram demonstrated a dissecting aneurysm at the A₂ and A₃ segments of the anterior cerebral artery.
In the literature, it is very rare that dissecting aneurysm involves solely the anterior cerebral artery, and we consider that such a case should be included in the differential diagnosis of the etiology of cerebral infarction.

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Between May 1976 and October 1989, 246 patients with primary cerebellar hemorrhage were admitted to our university hospital and affiliated hospitals.
The patients were classified into four categories; benign type, moderate type, severe type and fulminant type, according to the grading of hypertensive cerebellar hemorrhage proposed by Matsumoto in 1982. We then decided the most appropriate therapy according to this grading, i.e., conservative treatment for benign type, either conservative treatment or ventricular drainage, or hematoma evacuation for moderate type, hematoma evacuation by suboccipital craniectomy or stereotactic aspiration surgery for severe type, and urgent surgical treatment for fulminant type if possible.
There were 76 patients (30.9%) with benign type, 51 (20.7%) with moderate type, 65 (26.4%) with severe type, and 54 (22.0%) with fulminant type.
One hundred and twelve patients (45.5%) underwent conservative treatment, 37 (15.1%) were given ventricular drainage, 59 (24.0%) underwent suboccipital craniectomy and 38 (15.4%) underwent stereotactic aspiration surgery.
The age of the patients at onset showed a peak in the seventh decade, the mean age being 67.2 years. The mean age of patients with fulminant type was significantly lower than that of patients with other types.
Patients with past history of hypertension numbered 132 (53.7%), those with cerebral infarction 28 (11.4%), and those with cerebral hemorrhage 11 (4.5%).
Nausea and vomiting were the most common initial symptoms of benign type hemorrhage followed by vertigo and dizziness. However, in patients with the fulminant type, disturbance of consciousness was most common.
Hematoma in the benign type was mostly located in the cerebellar hemisphere, but in most cases of the severe type and fulminant type it had invaded the vermis or was located within it.
Among patients given conservative therapy, the proportion with benign type showing a good outcome (ADL1 or 2) was 84, 7%, the corresponding figure for moderate type was 56.3%, but all patients with severe and fulminant type died except one.
Among patients given ventricular drainage, the proportion showing a good outcome for moderate type was better than that for those given conservative therapy. However proportion of cases of severe and fulminant type with poor outcome were 75.0% and 100% in each.
Among patients given surgical treatment, the proportion of patients with moderate, severe and fulminant types showing a good outcome were 70.8%, 39.2%, and 20.0%, respectively. In other words, the outcome for these types with surgical treatment was better than those with conservative therapy. However, the outcome in fulminant type cases was poor with any treatment.
Thus it appears that patients with benign type hemorrhage can be controlled with conservative therapy only. Patients with moderate type who do not have hydrocephalus and have hematoma less than 3 cm in diameter can be treated by ventricular drainage only, and those who have hematoma more than 3 cm in diameter must be undergone surgical removal of the hematoma. Patients with severe type should also be undergone surgical removal of the hematoma. If patients with the fulminant type hemorrhage are not in a deep coma, stereotactic aspiration may be indicative.

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Pseudoxanthoma elasticum (PXE) is a hereditary disorder with an autosomal dominant or recessive mode of transmission. PXE is now generally believed to be a disease which is mainly characterized with a genetically determined degeneration of the elastic tissue throughout the body, with secondary calcium deposition. The disease presents clinically three major manifestations : (1) skin lesion, characterized by yellowish papules, (2) angioid streakes of the retina, (3) cardiovascular changes which include symptoms of vascular insufficiency and hemorrhage involving different organs.
In this report, a case of PXE associated with middle cerebral artery occlusion is described. A 52-year-old woman was complicated by dysarthria and left hemiparesis. Angiography showed right middle cerebral artery occlusion. The ischemic attack was presumably due to cerebrovascular involvement of PXE which was confirmed by skin biopsy. Thirty-three cases of PXE with the involvement of the central nervous system reported in the literature were analyzed for characteristics of this disease.

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There are many studies concerning cerebral blood flow (CBF) and cerebral atrophy in cerebrovascular disease (CVD), but few longitudinal studies of the relationship between CBF and cerebral atrophy have been reported.
We investigated the relationship between the changes in CBF and cerebral atrophy in 14 patients with CVD (11 lacunar stroke, 3 TIA). They showed no neurological symptoms and no new CT lesions during 13 years of our observation.
Cerebral atrophy was estimated by Brain atrophy index (one of area measurement methods) on CT films and CBF was measured using ¹³³Xe inhalation method. The significant pogression of cerebral atrophy was observed, but there was no significant changes in CBF during 13 years of the observation.
We concluded that, in our patients with chronic CVD, the progression of cerebral atrophy preceeded the changes in CBF without new neurological symptoms. Chonic CVD might accelerate cerebral atrophy.

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A 58-year-old man presented with a pure sensory deficit involving the spinothalamic modalities in the right half of the body excluding the face. Magnetic resonance imaging (MRI) demonstrated a lacune in the left marginal portion of the medulla oblongata, corresponding to the location of the spinothalamic tract, although there was no evidence for ischemic lesion on serial computed tomograms. The usefulness of MRI in the topographic delineation of lacunar infarcts in the posterior fossa is stressed.

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Among the total cases of 480 subarachnoid hemorrhage (SAH), aneurysms were not found in 64 who had SAH at an initial cerebral angiogram (CAG) (group IUE) during period from 1975 to 1989. In those patients, aneurysms were found in 23 cases at subsequent angiograms, but not in 41 cases (group AUE).
In group AUE, CT scans revealed intraventricular hemorrhage and acute hydrocephalus in 9 cases (30%) and 6 cases (20%), respectively. Fifty percent of patients were grade 12 and others were grade 34 according to Fisher CT grading scale. Symptomatic vasospasms (SV), rebleeding and normal pressure hydrocephalus (NPH) were developed in 6 cases (15%), 4 cases (10%) and 4 cases (10%), respectively. Outcome was excellent or good in 34 cases (83%), and rebleeding was not observed in 37 cases after discharge in medium to long-term follow up. In patients in group IUE, the location of the aneurysm with the highest incidence were the anterior communicating (35%), and middle cerebral arteries (22%). In most of the cases (20 out of 23), aneurysm found on repeated angiography was small and less than 5 mm in diameter. Diagnosis was more easily made when angiography showed vasospasm of parent artery (39%). Postulated that repeated CAG was indicated in the patient who had evidence of any grade 34 of Fisher, IVH, hydrocephalus on CT scan on admission, SV, rebleeding or NPH when initial CAG after SAH was negative, false negative rate in group IUE was 17%, whose aneurysms were overlooked. False positive rate in group AUE was 39%.
It was suggested that subsequent CAG should be performed repeatedly even there is no aneurysm at an initial CAG in any clinical features.

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The effects of chronic tobacco smoking on regional cerebral blood flow (rCBF) were studied in 26 normal male volunteers over a 6 year period.
They were divided into two groups of 13 smokers (mean age of 68.3 years) and 13 non-smokers (mean age of 69.9 years). The rCBF was measured twice by ¹³³Xe inhalation method using a 16-ch-NOVO-cerebrograph, and an initial measurement followed by a subsequent measurement 6 years later.
There was no correlation between the rCBF changes and age. The rCBF in the smoking group was significantly decreased over 6 years, while that in the non-smoking group was not. There was no significant difference in rCBF between the two groups at the first measurement, but rCBF values in the smoking group tended to be lower than that in the non-smoking group at the second measurement. There was no correlation between the rCBF changes and the smoking index. There was no significant difference in FEV_1.0%, %VC, V₅₀, V₂₅ and PeCO₂ between the two groups. There was also no significant difference in the history of hypertension between the two groups, but at the second measurement the smoking group had a higher mean arterial blood pressure than the non-smoking group. There were no significant changes of 6 years and difference in hematocrit, total cholesterol and HDL-cholesterol between the two groups over 6 years.
These results suggest that chronic tobacco smoking might be a factor in accelerating a reduction in rCBF in normal subjects.

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We have reported that red blood cell aggregability (RBC-A) is enhanced in patients with cerebral infarction (Stroke 1989; 20 : 1202-1207). Diabetes mellitus is one of the risk factors for cerebral infarction and is known to be associated with various hemorheological abnormalities. The purpose of the present study is to investigate if there is any difference in RBC-A values between patients with cerebral infarction with diabetes mellitus and those without diabetes mellitus. The subjects comprized 94 patients at the chronic phase (more than 1 month after onset) of cerebral infarction and 52 age-matched healthy human volunteers. The patients were divided into two groups; Group A, non diabetic patients with cerebral infarction, N=70, 59 ± 9 YO, and group B, diabetic patients with cerebral infarction, N=24, 61 ± 10 YO. RBC-A was measured using the whole blood RBC aggregometer developed by us (Am J Physiol 251 : H1205H1210, 1986) with concomitant measurement of the hematocrit, albumin-globulin ratio (A/G ratio) and fibrinogen. The RBC-A values in group A and group B were 0.147 ± 0.026/sec and 0.159 ± 0.023/sec, respectively. These values were statistically significantly (p<0.01, p<0.01) higher than that of the control group (0.122 ± 0.027/sec). There was a statistically significant difference (p<0.05) in RBC-A between group A and group B. Although the values of hematocrit and A/G ratio did not differ between group A and group B, there was a tendency for the fibrinogen level to be higher in group B (341 ± 89 mg/dl) as compared to group A (313 ± 63 mg/dl). The above data suggested that diabetes mellitus had deleterious effect on the patients with cerebral infarction from the hemorheological point of view.

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A deep cerebral venous thrombosis in puerperium is reported for a 36-year-old woman who delivered her first child by a Caesarean operation. Disorientation and speech disturbance were noted as initial signs three days after childbirth. Plain X-ray CT revealed a high density lesion of the deep cerebral veins itself and a low density lesion of the bilateral thalamus and basal ganglia. Deficiency of shadow was observed in the most part of the Galenic vein on the contrasted X-ray CT. A cerebral angiogram showed an evidence for occlusion in the internal cerebral vein. the Galenic vein and straight sinus. Hypercoagulability, detected as increased blood platelet count, increased platelet aggregation and shortened activated partial thromboplastin time (APTT) in the patient, was suspected to be a factor causing the venous thrombosis. Though hemiparesis and pathognomonic mental signs of thalamic disorder were noted, the patient recovered with no neurological deficit following conservative treatment. Three years later, she delivered a second child without any problems. Solitary obstruction of the deep cerebral veins, which is rare in the cerebral venous/venous sinus thrombosis in adults, is regarded as serious, however its prognosis is good after going through the acute phase of the disease as is the case with the superficial venous/venous sinus thrombosis.

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The lower threshold of blood pressure (BP) in cerebral circulatory autoregulation was investigated by stepwise lowering of blood pressure with head-up tilting and/or with infusion of trimetaphan camsilate in patients with chronic cerebral infarction; group A with no vascular occlusion in the major cerebral arteries (n=37) and group B with middle cerebral artery (MCA) occlusion (n=17). Cerebral blood flow (CBF) was monitored by the arteriovenous oxygen difference technique.
Although age, size of infarction, grade of neurological deficits and hypertension severity in two groups were almost the same, the autoregulatory responses exhibited a large difference. In most cases of group A, CBF remained unchanged over a wide range of BP changes, while in group B, majority of cases showed a pressure dependent CBF reduction. In group B, however, normal autoregulatory response was recovered after the bypass surgery anastomosing superficial temporal artery to MCA.
The present study has demonstrated impairment of pressure-flow relationship in cases of MCA occlusion and its restoration after bypass surgery which improved local pressure drop. It can be concluded that the impaired pressure-flow relationship in cases of MCA occlusion does not necessarily indicate a true dysautoregulation.

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We evaluated the intracardiac thrombus in patients with potential source of cardiac embolism by means of ultrafast CT scan (UFCT). Cardiac UFCT was performed in 66 patients with various cardiac diseases; 33 patients with nonvalvular atrial fibrillation, 19 patients with rheumatic heart disease, 5 patients with myocardial infarction, 6 patients with cardiomyopathy and 3 patients with sick sinus syndrome.
We used an Imatron C-100 ultrafast CT scanner. Cardiac ultrafast CT scans were obtained by flow-mode after iodinated contrast material was injected into a peripheral vein. The scanning time was 100 msec, and the slice thickness was 6 mm. Advantages of cardiac UFCT are its rapid scan aquisition time and the absence of motion artifacts, resulting in clear images of excellent spatial resolution. The abnormal filling defect in the cardiac chamber was diagnosed as a thrombus. As a result of our study, 31 patients (47%) out of 66 had intracardiac thrombi. All of them were present in the left atrium; 55% in nonvalvular atrial fibrillation, 53% in rheumatic heart disease, 20% in myocardial infarction, 33% in cardiomyopathy and 0% in sick sinus syndrome.
Our preliminary study suggests that UFCT appears to be sensitive and useful for detection of intracardiac thrombus, especially in the left atrium.

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