We investigated the incidence of intracranial ruptured aneurysms in Yamagata city during the period of 1987 to 1989. This series included 148 cases of this disorder. The diagnosis was confirmed by angiography or surgery in 123 cases, and by clinical course and CT in 25 cases. Yamagata city has a population of approximately 250, 000. The annual incidence was 19.9 per 100, 000 population. The annual incidence increased with increasing age, and had its peak (82.2 per 100, 000 population) at the eighth decade. The ages ranged from 23 to 85 years with a mean age of 58.9. The ratio of men to women was 1 : 1.6; for cases over 70 years of age it was 1 : 2.7. The Hunt & Kosnik's grades on admission were Grades 1 or 2, 62 cases (41.8%); Grade 3, 32 cases (21.6%); Grade 4, 13 cases (8.8%), and Grade 5, 41 cases (27.7%). Fourteen cases (9.4%) were dead on arrival at the receiving medical facility. This data shows that once aneurysms have ruptured, nearly 30 percent of such patients are of poor grades and untreatable.

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Six dialyzed neurosurgical patients were presented. All these patients had craniotomy for intracranial diseases, three for intracerebral hemorrhage and the others for ruptured aneurysms. The causes for dialysis were chronic glomerulonephritis in four patients, polycystic kidneys in two. One patient was treated with continuous peritoneal dialysis (CPD) and the others were with hemodialysis (HD). The patients treated with CPD and two hemodialyzed patients died. The mortality rate was 50%. Dialysis disequilibrium syndrome (DDS) occurred in two patients on HD, one of which died for irreversible cerebral hemiation. The management of the neurosurgical patients requiring dialysis in perioperative period was discussed and reviewed in the literature. It was proposed that CPD is superior to HD at least in perioperative period to prevent bleeding tendency and DDS. Slow dialysis and maintenance of a high osmolality in plasma with intravenous mannitol or glycerol injection were effective to prevent intracranial pressure (ICP) change during HD. Continuous ventricular drainage and ICP monitoring were simple and essential methods to prevent irreversible cerebrel herniation during HD especially in comatose patients.

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We examined the relation of aging to the localization of hematomas in 644 consecutive patients with spontaneous intracerebral hemorrhage (ICH), who were admitted to Kitasato University Hospital.
The ages of the 644 patients varied from 16 to 92 years, with a mean of 58.9 ± 12.4 years. Although the highest incidence of ICH was found to occur in patients aged 50-59 years of either sex, ICH was more common in men than in women up to the age of 69 years. Among the patients aged >70 years, there was no difference in incidence of ICH between the sexes.
In the patients with ICH, the location of the hematomas was classified on the basis of the CT findings into the putamen (n=233, mean age of 55.6 ± 11.3 years), thalamus (n=167, 61.3 ± 10.9 years), pons (n=69, 53.9 ± 9.4 years), cerebellum (n=61, 67.6 ± 9.9 years), subcortex (n=78, 60.6 ± 16.7 years), or other locations. The mean ages of the patients with putaminal hemorrhage and with pontine hemorrhage were significantly lower than those of the patients with cerebellar hemorrhage and with subcortical hemorrhage. The group aged <40 years more commonly had putaminal hemorrhage (60%). Pontine hemorrhage was also common in the group aged <50 years, while in the group aged >60 years, cerebellar hemorrhage occurred more frequently.
The presence of hypertension was found to be related to the localization of the hematomas. Thus, 213 of 233 patients with putaminal hemorrhage (91%) and 63 of 69 with pontine hemorrhage (91%) revealed hypertension in their history, while 44 of 61 patients with cerebellar hemorrhage (72%) and 46 of 78 with subcortical hemorrhage (59%) had hypertension.
These results suggest that putaminal hemorrhage and pontine hemorrhage occur more commonly in patients of relatively young age, and that persistent hypertension may be more closely related to the pathogenesis of bleeding in these locations.

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We examined the relationship between presenile, senile depressive states and silent cerebral infarction (SCI) using magnetic resonance imaging (MRI).
The diagnostic criteria of major depression according to DSM-III-R was used to diagnose. Patients in whom stroke had occurred or who had local neurologic symptoms were not included.
About half of the patients with depressive states of presenile onset and most of the patients with those of senile onset had SCI, were considered to be organic-depressive states complicated with SCI.
Because patients with depressive states with SCI are at high risk of occurrence of stroke, we designated this condition “pre-stroke depression”, and classified it with endogene depression. At this time, it is important to begin therapy for cerebrovascular disease.

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To clarify the role of platelets in cardiogenic embolism (CE), the authors studied plasma β-thromboglobulin (BTG) levels and computed tomographic (CT) findings in 31 patients with both CE and atrial fibrillation (Af). There were 11 males and 20 females, and their mean age was 77.5 ± 10.3 years. Fifty-three paired blood samples were simultaneously obtained from the internal jugular vein (A) and the antecubital vein (B) for measurement of BTG. The ΔBTG value was defined as A-B/B, which indicates activated platelets in the cerebral circulation, and the BTG (B) level denotes those in the systemic circulation. The data obtained from the 31 patients with CE and Af (CE/Af group) were compared with those of the following four groups; age-matched, healthy volunteers (control group, n=24); non-stroke patients with Af (Af group; n=25); patients with other than stroke (non-stroke group; n=25); and patients with chronic-phase cerebral thrombosis (Th group; n=44). Blood sampling was performed in the early acute phase (<3 days post-ictus), late acute phase (4-7 days post-ictus) or non-acute phase (>8 days post-ictus). The site and extent of infarction were determined by CT. The mean BTG (B) level (± SD) of the CE/Af group (78.7 ± 65.9 ng/ml) was significantly higher than that of the control group (39.9 ± 19.4 ng/ml), although considerable variability was observed. Even in the chronic phase of CE, the BTG (B) level was elevated 75.5 ± 66.3 ng/ml as it was in the Af group (65.7 ± 56.7 ng/ml). These findings suggest that the elevation of BTG (B) in the CE/Af group was due to the presence of Af. The mean ΔBTG values (± SD) in patients were 0.42 ± 0.70 (n=14), 0.14 ± 0.49 (n=7) and 0.22 ± 0.75 (n=28) in the early, late, and non-acute phases, respectively. Only in the early acute phase was the Δ BTG value higher than that of the non-stroke group (-0.04± 0.42), although it was lower than that of the Th group (2.20 ± 4.54). The majority of patients in the early acute phase and those with hemorrhagic infarction had temporarily increased ΔBTG values. No correlation between ΔBTG values and CT findings was observed in any phase of infarction. These findings suggest that in cardiogenic embolism, platelet activation occurs mainly in the heart, but that platelets can be activated in the cerebral circulation when there is a secondary thrombosis in the early acute phase or repair of damaged blood vessels at the site of hemorrhagic infarction is in progress. Therefore, it appears that the pathophysiological role of platelets differs in cardiogenic embolism and cerebral thrombosis.

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We measured the values of hemorheological parameters of blood viscosity, plasma viscosity, hematocrit, serum protein, albumin and plasma fibrinogen in 12 patients with acute cerebral infarction (mean age : 69.1 Y.O.) within 3 days and at 1 month after onset, respectively, 30 patients with chronic cerebral infarction (mean age : 66.2 Y.O.) at 12.5 months (mean) after onset, 14 patients with hypertension (mean age : 63.4 Y.O.), 12 patients with hyperlipemia (mean age : 62.9 Y.O.), and 15 elderly controls (mean age : 65.8 Y.O.), respectively. The corrected blood viscosity at the hematocrit level of 45%, yield shear stress index, and fibrinogen/albumin ratio were calculated at the same time.
The values of corrected blood viscosity, plasma fibrinogen level, yield shear stress index and fibrinogen/ albumin ratio in patients with acute cerebral infarction within 3 days after onset were significantly higher while those of serum albumin were lower as compared to those in elderly controls (p<0.00050.05). These differences persisted to be significant until 1 month after onset. The significant differences of the values of hemorheological parameters were observed as well in patients with chronic cerebral infarction (12.5 months after onset) as compared with those in elderly controls (p<0.00010.05). In patients with hypertension, the values of hematocrit, corrected blood viscosity, and yield shear stress index were significantly higher than in elderly controls (p<0.0050.05). In patients with hyperlipemia, the values of plasma viscosity, corrected blood viscosity, and yield shear stress index were higher than those in elderly controls (p<0.010.05).
Blood viscosity already increased in patients with hypertension and hyperlipemia higher than in elderly controls. After onset of cerebral infarction, blood viscosity increased further due to elevated plasma fibrinogen levels and subsequent increases of yield shear stress index, which might cause a persistent vicious cycle of cerebral circulation until the chronic stage of cerebral infarction.

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Platelet aggregation (PA) was measured for 2 μM ADP in 130 patients with acute stage-cerebral infarction. In 86 of them, antithrombin III (AT III) and α₂-plasmin inhibitor (APL) were also measured. They were classified by type and sex as follows : Lacunar group (L group), Atherothrombotic group (T group), Cardioembolic group (E group) and Male group (M group) and Female group (F group). The examinations were made in six groups of ML, MT, ME, FL, FT and FE. The control group comprizes ambulatory patients with some risk factors of arteriosclerosis. Compared with the controls, the patient group showed decreased PA, AT III and APL. Values of PA and AT III were lower in E group than in L and T groups, but there was no difference in APL. M group showed lower values than F group in PA, AT III and APL, which might stem mainly from the difference between ML and FL groups. In patients with acute stage-cerebral infarction, PA was generally and significantly lower in males than in females, especially in those having lacune.

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A 67-year-old woman, who complained of paralysis of right eye movement and ataxia was described. Neurological examination showed complete palsy of right oculomotor nerve, paralysis of upward movement of the left eye. conjugate gaze was possible, and doll's head eye phenomenon and Bell's phenomenon were not elicited; bilateral cerebellar ataxia which was predominantly on the left side more than on the right side; mild consciousness disturbance, disorientation and hallucinations; mild paralysis of the left upper extremity in the first stage. CT and MRI studies revealed infarction in the midbrain tegmentum extended to the right side of the medial thalamus.
The association of unilateral oculomotor palsy, and bilateral ataxia and disturbed upward gaze of contralateral side referred to as Nothnagel syndrome. And clinical features of our case was consistent with those of Nothnagel syndrome.
We concluded that these neurological findings were caused by the vascular lesion of the right oculomotor nucleus, the decussation of the superior cerebellar peduncle, reticular formation of the midbrain, and thalamus.

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A 43-year-old man with medial medullary infarction associated with interesting angiographic findings is reported. He suffered from contralateral hemiplegia and motor paresis of the tongue. But disturbance of deep sensation was absent. MRI (T2 weighted image) revealed a lesion in the left medial portion of medulla oblongata. Cerebral angiography revealed that the left vertebral artery was obstructed in the cervical region. The contrast medium passed through the anterior spinal artery and reached the left vertebral artery and posterior inferior cerebellar artery. The right vertebral artery was obstructed distal to the origin of the posterior inferior cerebellar artery. We suspected that the left medial medullary infarction occurred in this case because ischemia was most likely to occur at the basilar artery or at the vertebral artery.

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Described are 5 patients presenting acute onset global aphasia with slight hemiparesis due to cerebral infarction. Magnetic resonance imaging (MRI) and computed tomography (CT) of the brain revealed left frontal cerebral infarctions without the involvement of primary motor cortex in two patients, and scattered infarction in the left frontal and periventricular white matter and the basal ganglia in three. Additionally conventional angiography or magnetic resonance angiography (MRA) were utilized. They revealed the occlusion of the left middle cerebral artery in two patients, and the questionable occlusion of the left middle cerebral artery in one. The occlusion of the left internal carotid artery was observed in one, and the bilateral occlusion of the middle cerebral arteries with moyamoya vessels was seen in the last patient. Also, single photon emission computed tomography (SPECT) showed hypoperfusion in the diffuse left hemisphere in two of the cases. And left frontal hypoperfusion with mild hypoperfusion in the left temporal or temporo-occipital region in two cases.
Therefore, global aphasia with slight hemiparesis may depend on more extensive areas of hypoperfusion and dysfunction than the lesions demonstrated by brain CT and MRI.

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A 22-year-old woman was admitted to the hospital because of acute neurological abnormalities of eclampsia. She suddenly complained of severe headache and bilindness during prolonged delivery, became proggresively confused, and presented with generalized tonic convulsion. Neurological examination revealed quadriparesis, exaggerated tendon reflexes and bilateral Babinski signs in the lower extermities. She did not have toxemia, and her blood pressure was 150/100 mmHg.
Cranial CT scans showed symmetrical low density areas in the striatum and the cerebral white matter. A SPECT study demonstrated decreased up-take areas in basal gray and cortical borderzone regions. Cerebral angiography showed vasospasm in the M₁ portion of the right middle cerebral artery and C₁ portion of the internal carotid artery. Neurological symptoms gradually disappeared after immediate delivery. Follow-up CT scans, MRI and angiography became normal. Her neurological symptoms of eclampsia may have been caused by transient stagnant hypoxia due to vasospasm.

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Occlusion of vertebrobasilar system in young adult is rare. A 18-year-old man presented with disturbance of consciousness. While the level of consciousness fluctuated in the acute stage, eventually he regained consciousness. Neurological examination disclosed hypesthesia of the right half including the right face, right facial palsy, dysarthria and right hemiplegia. CT and MRI showed ischemic lesions in the pons and superomedial region of the cerebellum on the left side. Initial VAG demonstrated the occlusion of left superior cerebellar artery (SCA) and bead-like stenosis of basilar artery (BA).
Transient neurological deterioration correlated with the extension of ischemia or edema into the left inferior colliculus. Left posterior cerebral artery (PCA) as well as left SCA became occluded on the second VAG 3 weeks later.
Neurological symptoms gradually improved. The 3rd VAG which was carried out 1 month from the onset confirmed the recanalization of left PCA and SCA, and almost normal posterior circulation was demonstrated in the 4th VAG another 1 month later. The latest MRI showed the ischemic lesions in the territories of left lateral pontine branch of BA and left SCA. Residual neurological deficits on discharge were mild cerebellar ataxia, dysarthria and right hemiparesis.
The pathogenesis of this lesion was possibly attributable to idiopathic angiitis.

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Hospital records and CT films of 108 patients with putaminal hematoma were reviewed in order to evaluate factors influencing the outcome. Univariate analyses using λ² test were first employed to find relationships between clinical and CT factors relative to patients' outcome. Factors contributing significantly to the determination of outcome were found to be-level of consciousness estimated by the Edinburgh 2 Coma Scale (E2CS), volume of hematoma, pupillary reaction, abnormality in respiration, midline shift, degree of paresis, ventricular rupture, time from onset to admission, alcohol intake, and past history of hypertension.
Using these factors, we attempted to find an important factor influencing patients' outcome by multivariate analysis (discriminating analysis by Hayashi's categorical quantitative method, type 2).
Correct discrimination rates by the 1st and 2nd synthetic variate of clinical factors alone (i.e. without CT factors) were 83 and 63%, and correlation ratios of them were 0.84 and 0.44 respectively. Factors showing high correlation coefficient were level of consciousness by the E2CS, degree of paresis, and pupillary reaction. Correct discrimination rates and correlation ratios of CT factors were noted to be lower than those of clinical factors. Combination of both clinical and CT factors did not improve the above statistical parameters.
This study showed that addition of CT factors to the clinical ones does not necessarily improve discrimination of the outcome in patients with putaminal hematoma. Close observation of clinical conditions, particularly the level of consciousness by the E2CS, is important in estimating the prognosis of the patients.

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