The relation between brain atrophy and P300 latency studied by computed tomography was evaluated in 19 nondemented patients with cerebral infarcts in the territory of the deep perforators of the internal carotid artery system. Brain atrophy was quantitatively measured on CT images by two-dimensional measurement of brain areas as shown in Figure 1, and ventricular area index (VAI) and brain atrophy index (BAI) were calculated. VAI increased and BAI decreased significantly with advancing age (Figure 2). It clearly demonstrated that P300 latency significantly increased with advancing age (Figure 3). There was a significant correlation between brain atrophy and P300 latency (Figure 4).
These results indicate that there is a close correlation between brain atrophy and mild intellectual impairment in the nondemented lacunar stroke patients.

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A 59-year-old male patient was described who, despite major cerebellar infarction due to occlusion of the perimedullary segment of the posterior inferior cerebellar artery (PICA), had only vertigo, nausea, vomiting, and nystagmus without any other neurological symptoms and who achieved a recovery in 4 days. It has been found that some patients with cerebellar infarction show mainly vertigo, nausea and gait disterbance without neocerebellar syndrome and present a clinical picture very similar to labyrinthine disorders. Beside the case described in this paper, only two mild cases with even no gait disturbance have been reported in the literature. Responsible lesions were found in the cerebellar PICA area in all these cases. It is therefore necessary to suspect cerebellar infarction in the PICA area in treating vertigo patients with no cerebellar symptom.

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CBM 36-733 (2-methyl-alpha-ergocryptin) is known to have central dopaminergic, serotoninergic and cholinergic activities. In this study, we examined the protective actions of CBM 36-733 on experimental cerebral ischemia in spontaneously hypertensive rats (SHR). SHR aged 6 months were divided into 4 groups; control (vehicle-treated), CBM 36-733 0.01, 0.1 or 1.0 mg/kg, i.v.. After anesthesia, bilateral common carotid artery was ligated (BCL) to produce cerebral ischemia for one hour. Cerebral blood flow to the parietal cortex was repeatedly measured by H₂ clearance technique. Brain tissue lactate, ATP and pyruvate were determined by enzymatic method. By BCL, cortical blood flow decreased to 919% of resting value at 30 min and further to 511% at 60 min. Blood flow reduction was not altered by CBM 36-733 administration. At 1 hour ischemia, brain lactate greatly increased to 27.5±2.6 mmol/kg in control SHR, while it less increased to 7.5 ± 1.4 in CBM 36-733 0.1 mg/kg group. Brain ATP decreased to 1.31 ± 0.05 mmol/kg in control SHR after BCL, but it changed little, being almost normal level (2.60 ± 0.19) by 0.1 mg/kg of CEM 36-733, suggesting beneficial effects of CBM 36-733 on the ischemic cerebral metabolism.
In conclusion, CBM 36-733 seems to have protective effects on the brain against ischemia by improving metabolism but not affecting homodynamics. Further study is desired to clarify the details of the mechanisms.

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We studied the association between mental ability as rated by Hasegawa's scale, the severity of hypertension, the severity of brain atrophy, and the severity of lesions in the cerebral white matter on magnetic resonance imaging in 34 patients with multiple cerebral infarcts but without obvious cortical lesions. Data were analyzed using multiple regression analysis. The patients having both marked brain atrophy and severe white matter lesions showed an impairment of mental ability. Brain atrophy was correlated with aging and the severity of white matter lesions. There was a significant positive correlation between the diastolic blood pressure and the severity of white matter lesions. These findings suggest that the white matter lesions in patients with multiple cerebral infarcts are correlated with brain atrophy and mental deterioration, and that uncontrolled hypertension is an important risk factor in exacerbating the lesions in the cerebral white matter.

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A series of 1422 patients underwent CT examination over the last 12 years at the Higashi Nagoya National Hospital and Nagoya National Hospital, and a low density area in the region of the posterior cerebral artery was found in 167 cases (11.7%). Among the 167 cases, 120 (71.8%) were males and 39 (23.3%) had cerebral embolism.
The cases of posterior cerebral artery infarcts (PCAI) were classified according to the site of lesion as shown by CT, as well as by the left-right distribution and presence or absence of medial temporal lobe lesions (MTL), i.e. 20 cases Lt-PCAIcMTL, 24 cases Lt-PCAIsMTL, 16 cases Rt-PCAIcMTL, 19 cases Rt-PCAIsMTL, 7 cases Bil-PCAIcMTL, 4 cases Bil-PCAIsMTL, 12 cases Lt-thalamic lesion, 18 cases Rt-thalamic lesion and 3 cases Bil-thalamic lesion.
Excluding 44 cases in which an adequate evaluation could not be obtained, we studied neuropsychological examinations in 123 cases. The incidence of amnestic syndrome was high in cases associated with MTL, especially in cases with left-sided lesions. Hemianopsia was found in 46 of 123 cases (37%). Amnestic syndrome was also observed in cases with left-sided and bilateral anteromedial thalamic lesions. Pure alexia and color agnosia were observed frequently in cases with bilateral and left-sided lesions accompanied by MTL. Many cases of watershed area infarct with amnestic syndrome had lesion of MTL.

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We studied 20 patients with subarachnoid hemorrhage of unknown etiology who admitted to our clinic during the last 10 years from 1980 to 1989. Aneurysms were detected in 14 patients by either repeat angiography or exploratory surgery. The most frequent causes of unvisualized aneurysms on the initial angiography were small in size and/or protrusion at the wall unrelated to the arterial division. Most cases with diffuse subarachnoid clots or localized Sylvian clots on CT had their aneurysms revealed by repeat angiography and/or exploratory surgery. None of cases with localized perimesencephalic clots on CT had aneurysms detected by angiography and/or exploratory surgery. Repeat angiography revealed aneurysms in 54% (7/13) of the cases. The timing of repeat angiographies was plotted with respect to positive and negative visualization : the average times were 12 days in patients without visualization, and 22 days in patients with visualization. Seven patients had early exploratory surgery without repeat angiographies, five of them were detected ruptured aneurysms by the surgeries.
At least, we believe, angiography should be reexamined at about three weeks after the onset. Sometimes, exploratory surgery is indicated in the case with probable ruptured aneurysm even in early stage.

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One hundred and seventy-nine patients with hypertensive intracerebral hemorrhage (ICH) were studied to reevaluate the clinical significance of the Fisher's table for local diagnosis of ICH. Subjects consisted of 39 thalamic, 60 putaminal, 30 combined type, 21 subcortical, 13 cerebellar and 16 brain stem hemorrhages. They fulfilled the following conditions, that is, 1st episode of ICH, admission within 3 days of the onset and detailed evaluation by neurologists and by CT. Medical history and the presenting manifestations in the acute stage were investigated, including 17 items listed as of importance for differentiation by Fisher.
The results of the present study were not consistent with the Fisher's well-accepted belief. The important results were as follows :
1) In thalamic hemorrhage, miotic pupil, anisocoria and absent light reflex were noted only in 23%, 36% and 26% respectively, and not so different from those in putaminal hemorrhage, suggesting that they are not characteristic of thalamic hemorrhage.
2) Downward deviation of the eyes (DDE) were observed only in 21% of thalamic hemorrhage, but none in other types of ICH except for combined type ICH, that is, highly suggestive for thalamic lesion.
3) Recurrent severe vomiting without consciousness disturbance at onset, suggests cerebellar or subcortical hemorrhages.
4) Even in brain stem hemorrhage, consciousness disturbance at onset, quadriplegia and miotic pupil were observed only in 50%, 44% and 43%, respectively.
These results probably reflect the current trends in the clinical picture of ICH. Based on these observations, it is strongly suggested that Fisher's table should be reappreciated in many points, especially in thalamic, brain stem and cerebellar hemorrhages. These changes in the clinical pictures of ICH seem to be due to the relative increase of the mild cases as a result of improvement of the medical management especially for hypertension, while Fisher's table was based on the diagnosis by autopsy findings of the patients who may had large and severe hematomas.

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To investigate a participation of atherosclerosis of basilar artery (BA) in vertebrobasilar insufficiency (VBI), the deviation, elongation and mural thrombi of BA were studied in 17 patients with VBI and 30 controls by magnetic resonance imaging (MRI). We measured the maximum deviation of BA from midline of pons on the horizontal section of MRI using a vernier scale. Based on Smoker's classification the height of BA bifurcation was classified. On the sagittal section of T1 weighted MRI, mural thrombi were detected as high signal intensities. The deviation and elongation of BA in VBI patients were more remarkable than those in controls. The deviation of BA on MRI significantly correlated with those demonstrated on cerebral angiography. Furthermore, the mural thrombi of BA were frequently observed on MRI in VBI patients. Hypertensive patients had significantly greater deviation and elongation of BA than did normotensive patients. An increase in hematocrit was correlated with BA deviation. These results indicated that deviation, elongation and mural of BA revealed on MRI are useful indicators for the diagnosis of VBI, and also that MRI is superior in detecting mural thrombi to cerebral angiography.

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Plasma atrial natriuretic peptide (ANP) and antidiuretic hormone (ADH) levels were determined in patients with hypertensive intracerebral hemorrhage (HIH) and in those with cerebral infarction (CI), and their effects on hyponatremia were studied. The subjects were 19 cases of HIH and 11 cases of CI who were admitted to our hospital from March 1989 to March 1990. Serum electrolytes and plasma ANP and ADH were determined in acute stage on Day 1 to 4, in hyponatremia stage on Day 5 to 14, and in chronic stage on Day 15 and after. The serum sodium level of less than 130 mEq/l was taken as hyponatremia. The plasma ANP level in normal controls (n=20), who were admitted to the hospital for a close checkup, was 26.5 ± 11.6 pg/ml (10-50) and therefore, plasma ANP levels exceeding 50 pg/ml were regarded as abnormally high level. Four HIH cases showed hyponatremia, while none of CI had hyponatremia. Sites of the lesion in these HIH cases were putamen in 2 cases and subcortical area in 2 cases. Hyponatremia in HIH developed at average 7.7 hospital day and lasted for 4.9 days. The minimum serum sodium level was 129.3 mEq/1. The plasma ADH level increased in acute stage of HIH regardless of hyponatremia, decreased gradually thereafter, and became normal in hyponatremia stage. ADH level in CI cases remained unchanged during each stage. There was no significant difference in plasma ANP levels between HIH cases with and without hyponatremia. But ANP level in acute stage tended to persist to hyponatremia stage in cases with hyponatremia. In contrast, ANP level of CI in each stage was significantly higher than that in control cases. These were some cases having abnormally high level of ANP exceeding 50 pg/ml. Heart diseases were found in 6 out of 11 CI cases, and renal diseases were complicated in 2 cases. Plasma ANP levels in CI were thought to be high because of these complications. The results above suggest that it is difficult to predict the development of hyponatremia from plasma ADH and ANP levels in acute stage, and plasma ADH and ANP levels are not always abnormally high even at the onset of hyponatremia.

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We studied the relationship between white matter changes and P300 latency, regional cerebral blood flow (rCBF), and cerebral atrophy in patients with cerebral infarction in the territory of the deep perforators.
Thirty-two nondemented patients (27 males, 5 females, mean age 62.8 years) with chronic cerebral infarction in the territory of the deep perforators were divided into three groups by the severity of their white matter changes on MRI. Group I had either no or mild white matter lesions, group II had moderate white matter lesions and group III had severe white matter lesions. Although there were no significant differences among the three groups in the Hasegawa's intelligence scale, P300 latency in group III was significantly longer than that in groups I and II. There were no significant differences among the three groups in rCBF. The severity of brain atrophy was greater in group III than in groups I and II.
It is concluded that white matter lesions are related to cognitive functions and cerebral atrophy in nondemented patients with cerebral infarction in the territory of the deep perforators.

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We report 28 cases of bilateral symmetrical aneurysms, which comprise 6.5% of all aneurysms found in our clinic between April 1979 and March 1990, and compare their features with those of the previous reports. The most common locations are the internal carotid artery (57%) and the middle cerebral artery (36%). Bilaterally symmetrical internal carotid artery aneurysms are much more common in women, with the female to male ratio of 15 : 1. Five to 10% of aneurysms at the internal carotid artery, middle cerebral artery or the distal anterior cerebral artery are bilaterally symmetrical. Based on the focal signs, laterality of subarachnoid hemorrhage found on CT, and angiographic size and shape of the aneurysm (including irregularity of its contour), we could accurately predict the side of the ruptured aneurysms in 92.3% of cases. It has been reported that both ruptured and non-ruptured aneurysms should be treated in one-stage. In our series, however, most cases were treated by two-stage operations without any adverse effects.

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We reported a 31-year-old woman with the spontaneous intracranial carotid dissection. She suffered from sudden onset severe headache and transient left homonymous hemianopsia. Angiography demonstrated the tapering of right internal carotid artery at the supraclinoid portion. About 24 hours later she developed progressing left weakness. Sequential angiography demonstrated the occlusion of right internal carotid artery at the same site. Thrombotic embolus caused transient hemianopsia at the onset, and thrombotic occlusion caused progressig hemiparesis. Anticoagulation treatment was effective and her prognosis was good. We think that thrombotic embolism and thrombotic hypoperfusion were two main important pathogenesis of the intracranial internal carotid dissection.

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Intracranial aneurysms may rupture to cause an acute subdural haematoma, but intracranial arteriovenous malformations (AVMs) hardly cause it. A case is described in which bilateral internal carotid artery aneurysms and a small temporal arteriovenous malformation (AVM) were found following an episode of unconsciouness. CT scan and MRI revealed an acute subdural haematoma in the posterior fossa and over the left supratentorial convexity. The right irregular-shaped aneurysm was attributed to cause the subdural haematoma and was first clipped three weeks following the episode. The other aneurysm and AVM were later treated on the second stage. None of three could be confirmed to be the source of subdural haematoma.
Larger aneurysms, either ruptured or unruptured, are apt to bleed giving a high mortality rate in comparison with AVMs. If the source of intracranial haemorrhage is uncertain in cases with aneurysms associated with AVMs, aneurysms must be planned for the first radical surgery.

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Geisböck's syndrome, which manifests hypertension and polycythemia, is important as a representative high risk group of CVD, especially cerebral thrombosis. We investigated the clinical pictures of the patients with Geisböck's syndrome in the outpatient clinic of Yufuin-Kosei-Nenkin Hospital. We chose patients having a hematocrit value over 50% in males and 45% in females and hypertension over 160/95 mmHg. There were 82 cases of Geisböck's syndrome, and 43 cases among them were associated with CVD, mainly with mild cerebral thrombosis. In the majority of the cases, the CT showed multiple small lesions. Most of them had stress polycythemia, and sympathetic nerve hyperfunction was strongly suggested as the cause based on life history, QTc prolongation, etc.

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