The medical records of 567 patients with aneurysmal subarachnold hemorrhage (SAH) were reviewed, and the circumstances and physical activities in which they had been involved immediately before the onset of SAH were analyzed. SAH was most frequent in the winter and occurred least in the autumn. Its peak incidence was observed during 6-9 A.M. and 6-9 P.M., with the lowest incidence during 0-6 A. M. These differences were statistically significant. SAH occurred most frequently while chatting, watching TV or relaxing at home without any strenuous physical activity. When considering the time spent, the highest incidence was found to be related to defecation or micturition. Other daily life activities such as eating/drinking, taking a bath, washing/brushing teeth and (un) dressing carried relatively high incidences. These daily routines tend to be concentrated during the two periods of the day when the peak incidence was observed. Many patients developed SAH while working at their work place or working in the household. When these two categories were combined together as working, they accounted for the highest number of patients, but the incidence itself was lower than average considering the working hours. There was no evidence that aneurysmal SAH was prone to occur during physical work. Hypertension was the most common preexisting disease, and its association was significantly high in patients younger than 70 years of age as compared to control patients. Hypertension was considered to be a risk factor of SAH, particularly for younger patients.

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In an ischemia-hypoxia model (I-H) employing neonatal rats, preconditioning by whole-body hyperthermia or hypoxia was induced at 24 hours prior to I-H. The numbers of animals that developed ishemia were 79 of 23 rats in the control group, 4 of 21 in the hyperthermia group, and 0 of 8 in the hypoxia group. The proportions of the ischemic area that survived the ischemia in striatal and hippocampal coronal sections were 54.6 ± 5.2% and 49.3 ± 5.6%, 90.6 ± 4.8% and 92.5 ± 3.8%, and 100 ± 0% and 100 ± 0% in the three groups, respectively (mean ± SE). The stress of hyperthermia induced an ischemic tolerance phenomenon (cross tolerance) during subsequent I-H in the immature rat brain.

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We investigated the cognitive functions and relevant factors in patients with diffuse white matter lesions. Out of 408 patients with asymptomatic cerebral infarction admitted during the period 1988-1996, we studied 15 patients who revealed diffuse white matter hyperintensities on T₂-weighted magnetic resonance imaging. These patients were further divided into demented and nondemented subgroups on the basis of the results of the Hasegawa Dementia Scale Revised and Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV). All patients in the demented group also satisfied the diagnostic criteria of probable vascular dementia proposed by the National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et Enseignemant en Neurosciences (NINDS-AIREN). The control group consisted of 25 age-matched subjects with asymptomatic T₂ hyperintensities. Patients in the nondemented and asymptomatic groups were also evaluated cognitively by the use of the “Kana-Hiroi” (Letter pick out) Test, Stroop test, Wisconsin Card Sorting Test, Raven Coloured Progressive Matrices and Kohs Block Design Test in addition to the Hasegawa Dementia Scale Revised. The demographic characteristics, amount and distribution of T₂ hyperintensities larger than 3 mm on magnetic resonance imaging, thicknees of the corpus callosum, and ventricular indices were evaluated in the demented and nondemented patients. Subsequently, we addressed the following issues; 1) the differences in cognitive functions in the nondemented and control groups; 2) the factors relevant to cognitive functions in the nondemented patients; and 3) the lesion distributions in the demented and nondemented patients and factors discriminating these two groups. The results showed that : 1) the nondemented patients made more perseverative errors in the Wisconsin Card Sorting Test than did the control patients; 2) the amount of lesions in the frontal white matter and thalamus/posterior internal capsule, thickness of the corpus callosus, and educational level were related to cognition in the nondemented patients; and 3) the demenented patients had a significantly higher lesion distribution in the left thalamus/posterior internal capsule, which was the only factor significantly related to the presence of dementia. We concluded that cognitive function in the nondemented patients was characterized by more prominent frontal system dysfunction than in the control patients, and was influenced by multiple factors as well as the presence of white matter lesions. We also postulate that diffuse white matter lesions may predispose a patient to dementia by causing frontal system dysfunction, but not dementia per se unless additional lesions appear in the left thalamus which is closely associated with verbal memory.

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We diagnosed patent formen ovale by contrast transesophageal echocardiography with the Valsalva maneuver in cardioembolic stroke and cerebral embolism with unknown embolic sources. Patent foramen ovale was diagnosed in 4 (12%) of 33 cases with cardioembolic stroke, and in 6 (67%) of 9 cases. with cerebral embolism with unknown embolic sources. The prevalence of patent foramen ovale was thus higher in the cases with cerebral embolism with unknown embolic sources. Cryptogenic stroke with patent foramen ovale was considered to represent paradoxical cerebral embolism. Paradoxical embolism through a patent foramen ovale arose in younger and elder patients (aged from 33 to 70). Regardless of patient age contrast transesophageal echocardiography should be considered for the detection of patent foramen ovale in cases of cryptogenic stroke, especially cerebral embolism with unknown embolic sources.

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We evaluated carotid endarterectomy (CEA) for use in patients with asymoptomatic carotid stenosis (As-CS). Among 287 cases of CEA, 90 were performed for As-CS. We divided the 90 patients concerned into three groups : Group A, CEA performed for As-CS after CEA for symptomatic carotid stenosis : Group B, CEAs performed for bilateral As-CS; and Group C, CEA performed for single As-CS. Coronary angiography was carried out in 39 of these patiets, and coronary stenosis was evaluated by Gensini's scoring systom (GS). The overall mortality and morbidy was 3.1%, with the values for Groups A, B and C being 5.9%, 8.3% and 1.5%, respectively. Twenty-one of the above 39 patients showed values of more than 6 for GS, and 10 patients among them underwent coronary artery reconstruction before or after CEA. Eighty-two patients (91.1%) were discharged without neurological deficis. Among 80 patients who could be followed up for a long period (mean, 68.2 months) 15 patients died. Six of them died of cardiovascular disease. In conclusion it can be said that although the overall results of CEA for As-CS were generally good, care most be taken in cases of bibateral CEA (Groups A and B). Since coronary lesions tend to be associated with As-CS, it is important to check and treat such lesions in order to reduce the mortality and morbidity of CEA.

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We investigated the clinical characteristics of progressive stroke on admission. The subjects comprised 300 patients who were admitted on the day of onset of cerebral infarction in the territory of the internal carotid arteries and who showed a low density area on CT images within 5 days. These patients were treated with sodium ozagrel. Of the total of 300 patients, 221 had cerebral infarction in the territory of the deep perforate arteries, 56 had cerebral infarction in the territory of the cortical branch of the middle cerebral artery (MCA), and the remaining 23 demonstrated cerebral infarction throughout the MCA territory. The results obtained may be summarized as follows :
1) Progressive stroke was observed in a total or 29 (9.7%) of the patients, including 9 (4.1%) of the patients with infarction of the deep perforate arteries. 9 (14.8%) of the patients with infarction of the cortical branch of the MCA, and 11 (47.8%) of the patients with cerebral infarction throughout the MCA territory. Progressive stroke was seen significantly more frequently in patients with cerebral infarction throughout the MCA territory than in those with cerebral infarction of the deep perforate arteries (p<0.001; χ² test). Similarly, progresive stroke was significantly more frequent in patients with cerebral infarction of the cortical branch of the MCA than in those with cerebral infarction of the deep perforate arteries (p<0.005; χ² test).
2) All patients with progressive stroke demonstrated initial evidence of deterioration of their nearlogical deficits within 5 days after onset, with 13 patients showing deterioration on day 2 and patients showing deterioration on day 3. The maximal period from the beginning to end of such deterioration was 7 days.
3) progressive stroke was seen in only 29 (29.8%) of the 97 patients who were admitted with motor distrubances and unilateral negiect.
4) There was no significant incidence of progressive stroke among patients with atrial fibrillation (Af) on ECG.
5) Hemorrhagic infarction was observed in 14 (4.7%) of the patients, and there was no significant incidence of progressive stroke among these patients with hemorrhagic infarction.
6) Twenty-three (79.3%) of the 28 patients with progressive stroke showed severe motor impairment in the upper limbs.
In order to diagnose progressive stroke, therefore, it is useful to assess the motor disturbances and unilateral negleat.

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We examined the effects of age on the blood flow volumes, blood flow velocities, mean vessel diameters, and vessel elasticities in common carotid arteries using a quantitative ultrasonic measurement system. This device consisted of an improved ultrasonic Doppler velocimeter and an echotracking system controlled by a microprocessor (QFM-2000XA, NIHON KOHDEN), which were used to measure the vessel diameter and wall motion. The subjects comprised 37 healthy volunteers (19 males and 18 females, mean age = 50.5 years, range= 44 to 79 years, in 1995) without hypertension, diabetes mellitus or hyperlipidemia. The measurements were made in 1991 and 1995. The blood flow volumes did not change between 1991 and 1995. However, the blood flow velocities were significantly decreased ('91, 21.6 ± 3.4 cm/sec; '95, 19.8 ± 3.4 cm/sec) (p<0.05). The mean vessel diameters were significantly increased ('91, 7.4 ± 0.6 mm; '95, 7.7 ± 0.7 mm) (p<0.05), and the vessel elasticities were significantly decreased ('91, 4.7 ± 1.2%; '95, 3.9 ± 1.1%) (p<0.005). No differences in results for males and females, or for subjects younger and older than 60 years of age, were obtained. These findings suggest that the flow velocities, mean vessel diameters and changes in ratio of vessel diameters for the mean vessel diameters of the common carotid arteries underwent significant change through aging over a period of only 4 years in healthy volunteers who had no atherothrombotic risk factors.

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The clinical usefulness of so-called cerebral vasodilators and metabolic activators for patients in the chronic stage of CVD is now in question, and the regulatory authorities in Japan have requeasted further information. There have been many parallel-comparison, randomized, placebo-controlled trials of metabolic activators in Japan, and after an exhaustive search, 14 were selected. Most of them had adopted an 8-week treatment period. To quantify the average treatment effect, meta-analysis was conducted. The primary endopint was the clinical global outcome assessed at the end of 8 weeks of treatment by using a 5-point Likert scale. Secondary endpoints included the subjective, psychiatric, and neurological symptoms, and ADL, which were assessed in the same manner as the clinical glabal outcome. The upper two categories in each scale were considered as “effective” outcomes. The odds ratios in terms of the efficacy were 1.59 (p<0.0001) for the clinical global outcome, 1.77 for the subjective symptoms, and 1.85 for the psychiatric symptoms. However, the odde ratios for the nourological symptoms and ADL were relatively low. Efficacy appeared to be greater in patients with ischemic stroke than in those with cerebral hemorrhage. The pooled control efficacy rate in the placebo group was estimated to be 18.1%, with an absolute difference of 8.4% from active drugs. In conclusion, cerebral vasodilators and metabotic activators were shown to be 1.6 times more effective than a placebo in terms of the relative global efficacy, based on a meta-analysis of 14 selected, randomized, placebo-controlled drug trials conducted in Japan from 1972 to 1992.

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We encountered a case of progressive stroke caused by vertebral artery occlusion and severe basilar artery stenosis. The patient was treated emergently by a combination of local intra-arterial thrombolytic therapy and percutaneous transluminal angioplasty (PTA), with satisfactory results. A 61-year-old man was admitted with consciousness disturbance and tetraparesis. An emergent angiogram revealed occlusion at the V4 portion of the left vertebral artery and the PICA end of the right vertebral artery. Thrombolysis with tissue plasminogen activator was performed, and a slender recanalization was recognized for both the left vertebral artery and basilar artery. PTA was subsequently performed using a balloon catheter, and sufficient dilatation of both stenotic lesions was accomplished at 7.5 hours after onset. The patient was discharged with left hemiparesis. PTA for basilar artery stenosis involves high risk on occlusion of perforating branches. Nevertheless, thrombolytic therapy and PTA for acute progressive stroke would rather be first-choice therapy than medical therapy or bypass surgery.

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We report a patient with MRI-proven isolated infarction in the left lateral geniculate body (LGB) who demonstrated unusual homonymous defects in the lower right visual field. A 72-year-old man with hypertension and diabetes mellius developed incongruous lower right wedge-shaped defects without macular sparing. The pattern of the visual field defects reported in this case was different from that in previous cases of LGB infarction. This probably arose becaause of individual differences in vascular anastomoses between the anterior and the lateral posterior choroidal arteries which suppy the LGB or in anastomoses betewen the perforating arteries within the LGB.

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