Types, location and risk factors of recurrent stroke were assessed retrospectively. In a consecutive series of 2, 342 patients of cerebral infarction (CI) and 1, 014 patients of intracerebral hemorrhage (ICH) who were admitted to our hospital between April 1, 1977 and March 31, 1987, 111 patients with recurrent stroke (CI and ICH) were identified on CT findings and clinical informations. In this study, 80 male and 31 female were included. The mean age at the initial stroke was 62.6 years while the mean age at the recurrence was 64.8 years. The mean interval between two episodes was 26.3 months. Seventy-nine patients (71.2%) repeated CI twice and 12 patients (10.8%) repeated ICH twice. CI were followed by ICH in nine patients (8.1%) and ICH were followed by CI in 11 patients (9.9%). In CI-repeated group, 54 patients repeated atherothrombotic infarction and 22 patients repeated cerebral embolism. 90% of recurrences were CI in patients with CI as the initial stroke, whereas only 52% of recurrences were ICH in patients with ICH as the initial stroke. In patients who had both CI and ICH alternatively, many patients had combination of basal-ganglionic infarction and putaminal or thalamic hemorrhage. This suggests basal-ganglionic infarction and putaminal or thalamic hemorrhage have some common ethilogical background in spite of different types of stroke. From the view point of stroke recurrence, hypertension was the most important and modifiable risk factor. Especially, it is important to get good control of blood pressure after ICH, because only 33% of ICH-repeated group got good control of blood pressure after the initial stroke.

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In order to clarify the pathophysiology of Binswanger-type dementia, we investigated regional cerebral blood flow (rCBF) using single photon emission computed tomography with ¹²³I-IMP. The subjects consisted of 9 patients with Binswanger-type dementia (mean age 80.8 ± 5.1 years), diagnosed on the basis of clinical and neuroradiological examinations, and healthy controls (mean age 77.9 ± 5.7 years). rCBF was measured quantitatively using a method based on the microsphere model proposed by Kuhl et al.
With the exception of the occipital visual cortex, rCBF was widely and significantly reduced in patients with Binswanger-type dementia when compared with the healthy controls. There was an especially marked decrease in rCBF in the deep white matter. There was also a uniform approximately 20% reduction in rCBF in the frontal, temporal, parietal cortices. The degree of dementia (Hasegawa Dementia Rating Scale) was correlated with rCBF, but not with brain atrophy (bifrontal cerebroventricular index and cella media index). The decreased rCBF in widespread cortical regions is likely to be mediated by neuronal mechanisms via projection fiber connections as a result of the subcortical lesions, namely disconnection between the cerebral cortex and subcortical structures.
We must take into account widespread functional depression of the cerebral cortex as well as morphological damage in the deep white matter in understanding the pathophysiology of patients with Binswanger-type dementia.

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Regional cerebral blood flow (rCBF) by ¹²³I-IMP SPECT was measured before and 2.8, 10.3 months during medication of bifemelane hydrochloride in 10 patients with cerebrovascular diseases and compared with 5 control patients without medication. Semiquantitative rCBF indices of asymmetry and redistribution (AI, RI) were calculated from mean regional counts/pixel of each region of interest (ROI) in the early and delayed images of IMP SPECT. Before medication, no significant differences of RI and AI were observed between patients with and without medication of bifemelane hydrochloride. Significantly (p<0.05) higher RI was observed in the second measurement 2.8 months in mean during medication of bifemelane hydrochloride, while AI was less in patients medicated with bifemelane hydrochloride. In the third measurement 10.3 months in mean during medication of bifemelane hydrochloride, RI was kept to be higher than that in the second measurement of the control patients without medication. The ratio of the number of ROI, where the redistribution being observed, was significantly (p<0.05) higher in patients medicated than in control patients. From the results, medication of bifemelane hydrochloride might keep the redistribution phenomenon, which may indicate reversible cerebral ischemia, more persistently and intensively in patients with cerebrovascular diseases.

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The occurrence of intracranial aneurysm in Nagasaki Prefecture has been studied since 1979 when subarachnoid hemorrhage started to be diagnosed correctly by computed tomographic scan. The incidence of aneurysmal patient was 8 per 100 thousands habitants in the first three years when neurosurgical survices were avairable only in major hospital. The incidence dramatically increased following years when another 7 hospitals began to serve for neurosurgical clinic, which considered to be covered all over the prefecture. The incidence increased to 16.6 per 100 thousands habitants in the end of 1990.
The unruptured aneurysm which was not related to another ruptured aneurysm, arteriovenous malformation and Moyamoya disease increased to be detected in recent years. The incidence of unruptured aneurysm was about 10% of all intracranial aneurysm in the end of 1990, however, most of them were detected as to be symptomatic aneurysm. Since the operative result in the unruptured aneurysm has been better than that in the ruptured aneurysm, we need further effort to detect the asymptomatic unruptured aneurysm by using computerized angiotomography and/or magnetic resonance angiography.

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To clarify the vascular lesions with pathophysiological changes in the corona radiata infarcts adjacent to the body of the lateral ventricle (CRILV), 17 patients with CRILV were studied clinically with neuroradiological images. Based on the MRI findings in coronal images obtained between the anterior and posterior commissures, patients were divided into a PER group and a COR group. The PER group was defined as having infarcts localized bellow a line (IC-CC line) extending from the upper edge of the insular cistern (IC) to the external angle of the lateral ventricle adjacent to the corpus callosum (CC), while the COR group had lesions located above this line towards the centrum semiovale. The 11 patients in the PER group were mostly hypertensive men, as well as 6 patients in the COR group.
In both groups, the stepwise deterioration of symptoms and the completion of stroke in a morning was frequent, though the time from onset to completion was longer in the COR group. Comparing the clinical manifestations of the PER and COR groups, pure motor hemiparesis was seen in 5 and 3 patients, and sensorimotor stroke in 2 and 1 patients, respectively. Drowsiness was found in 2 patients of the PER group, while aphasia was occurred in 2 of the COR group. Furthermore, one patient had pseudobulbar palsy and another was asymptomatic in the PER group. The outcome in both groups was good, except that the 2 drowsy patients died of aspiration pneumonia. Eleven of 13 infarcts in the PER group were small well-defined lesions less than 15 mm in diameter on CT scans, and angiography showed sclerotic changes of the main arteries without obstruction. In contrast, the COR group demonstrated ill-defined and rather large low-density areas on CT and main trunk obstructions of the internal carotid or middle cerebral arteries was found on angiography. ¹²³I-IMP single photon emmission computed tomography (SPECT) showed diffuse defects in the COR group, though the SPECT images of the PER group varied from normal to having diffuse or multiple defects.
These findings suggest that the PER group had lacunar lesions caused by ischemia of the perforators, while the COR group had terminal zone infarcts in the territory of the cortical branches or watershed infarcts induced by main trunk obstruction. In conclusion, a demarcating line (IC-CC line) on coronal MRI was a useful diagnostic technique for differentiating CRILV due to two different types of vascular lesions.

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The purpose of the stereotactic aspiration for hypertensive intracerebral hemorrhage is to regain patient's motor function as early as possible, and lead to good outcome. We studied the results of the stereotactic aspiration by comparing the changes in muscle strength of affected extremities before and 1 week after the operation in patients with hypertensive intracerebral hemorrhage. Preoperative neurological grading (NG) and computed tomography (CT) classification were evaluated by the Japanese Ad Hoc Commitee proposed in 1978.
Among various factors such as age, NG, CT classification, hematoma volume, and timing of operation, we selected the important ones which could influence the early postoperative improvement of motor function.
Stereotactic aspiration of hematoma was performed in 65 patients with putaminal hemorrhage (PH), and 43 patients with thalamic hemorrhage (TH). The mean timing of operation was 3.9 days after the onset of hemorrhage, and the mean ratio of aspirated hematoma was 77% (80% for PH and 72% for TH).
The marked improvement of motor function was observed in following cases. (a) Age was less than 70 years old in the case of TH. (b) NG was better than III in PH, and II in TH. (c) CT classification was better than IIIa in PH, and IIa in TH. (d) Volume of hematoma was less than 60 ml in PH, and 20 ml in TH. (e) Timing of the operation was not related to the post-operative results.
Somatosensory evoked potential (SEP) was recorded in 32 patients with PH before and after the operation. The N₂₀ of SEP was recognized pre- and post-operatively, or reappeared post-operatively in 8 of 9 patients who showed marked improvement of motor functions. Cerebral blood flow (CBF) was measured using ¹²³I-IMP SPECT in 8 patients before and after the operation. Increase in CBF was recognized postoperatively in all 3 patients who showed marked improvement of motor function.

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Clinical features and magnetic resonance imaging (MRI) of infarction in the territory of the superior cerebellar artery (SCA) were studied in eight patients. The study included also eight patients with anterior inferior cerebellar artery (AICA) infarcts and sixteen patients with posterior inferior cerebellar artery (PICA) infarcts. Ataxic dysarthria was frequent (75%) in the SCA group, compared to the AICA (25%) and PICA (13%) groups. In three patients with SCA infarct, limb ataxia was more predominant in the lower limb than in the upper limb. Patients with AICA and PICA infarct showed no predominancy between upper and lower limb ataxia. Vertigo and nystagmus were less frequent in the SCA group (13%) than in the AICA (75%) and PICA (86%) groups. MRI showed that 75% of the SCA infarcts were localized within the territory of its cortical branches, whereas 92% of the AICA and PICA infarcts involved the territory of their main-stems or circumferential branches. These results suggest that the SCA infarct has some special features compared to the AICA and PICA infarct. (1) ataxic dysarthria and lower limb ataxia are frequent, (2) vestibular symptoms are rare, (3) cortical infarcts without brain-stem lesion are frequent.

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In order to classify the pathophysiology in patients with multi-infarct dementia (MID) and dementia of Alzheimer type (DAT), cerebral blood flow (CBF) was measured and relationship between CBF and the severity of dementia was examined in 22 patients with MID (15 male, 7 female, age from 50 to 88 years, mean ± S.D. 68 ± 10), and 12 patients with DAT (7 male, 5 female, age from 45 to 82 years, mean μ S.D. 65 ± 11). The diagnosis of dementia was based on DSM-IIIR criteria, as well as the clinical symptoms. To differentiate MID and DAT exactly, Hachinski's ischemic score was calculated and magnetic resonance imaging was performed in all subjects. Paients with large or medium-sized infarction in the cortical regions were excluded from this study, so that the MID patients were those with cerebral infarctions located only in the basal ganglia or deep white matter. The Suzuki Binet intelligence test was performed in all patients to classify the severity of dementia. CBF studies were performed on all patients by the ¹³³Xe intravenous injection method, and mean hemispheric and regional gray matter flow (F₁) and initial slope index (ISI) were calculated. The mean F₁ values were 59.1 ± 9.6 ml/100 g/min and 59.3 ± 16.5 ml/100 g/min in the patients with MID and DAT, respectively. There were significant positive correlations between mean hemispheric CBF and IQ in both groups (MID; F₁ r=0.37, ISI r=0.41, DAT; F₁ r=0.60, ISI r=0.78). The tendency of decline in CBF with increasing severity of dementia was larger in the DAT group than in the MID group. In the mildly demented subgroups (IQ>56), the mean CBF in MID (N=8, F₁ 62.5 ± 10.3 ml/100 g/min, ISI 48.7 ± 7.8) was lower than in DAT (N=5, F1 73.9 ± 5.0 ml/100 g/min, ISI 57.4 ± 2.8) with statistical significance (F₁ p<0.05 ISI p<0.01), whereas in severely demented subgroups, the mean CBF in MID (N=5, F₁ 53.6 ± 5.0 ml/100 g/min, ISI 41.7 ± 3.9) was higher than in DAT (N=3, F₁ 49.5 ± 8.2 ml/100 g/min, ISI 33.4 ± 1.6).
In DAT group, regional CBF in severely demented subgroups was lower than CBF in mildly demented subgroups in all regions examined with tendency of larger decrease in the parietal regions. In MID group, there were no difference in the decrease in regional CBF over the all regions examined.
It is possible that the decrease in CBF precede the appearance of dementia in the MID group, whereas CBF decreases in proportion to the progress of dementia in the DAT group.

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The recurrence rate of hemorrhagic and ischemic stroke in patients with intracerebral hemorrhage was assessed during a mean follow-up period of 25 months. Subjects were 194 consecutive patients with hypertensive intracerebral hemorrhage confirmed by brain CT scan who admitted to our hospital within one week after onset.
Among 194 patients, 25 died with one month after the onset without any recurrent attacks. Nine of 169 patients survived, had recurrence of cerebral hemorrhage (10 attacks in 9 cases), resulted in the annual recurrence rate of 2.9%. Seven patients (8 episodes; 2.4%/year) developed cerebral infarction, six of which were lacunar stroke. One had TIA and two cases had bilateral intracerebral hematomas at the same time.
Twenty-eight of 194 patients had a history of stroke, five of which were definite cerebral hemorrhage and 18 (22 episodes) were definite cerebral infarction. Six of 11 patients in whom blood pressure before recurrent hemorrhage were known had been hypertensive without appropriate control.

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We have evaluated the effects of treatment with three different doses of 10% glycerol solution on ischemic brain edema, metabolism and cerebral blood flow (r-CBF). Furthermore, pathological study was investigated. Sixteen week old spontaneously hypertensive rats (SHR) were used to induce cerebral ischemia. The rats underwent an operation were divided into four groups. The each group was given 3 ml/kg/hr, 6 ml/kg/hr or 20 ml/kg/hr of the solution of glycerol or 20 ml/kg/hr saline, respectively immediately after ischemia for 1 hr. At 3 hrs after ischemia, increase of the brain water content was suppressed in a dose response manner by glycerol treatment. At 6 hrs after ischemia, the brain water content was significantly lower only in 6 ml/kg glycerol administered group than in salie group. Until 3 hrs of ischemia, all glycerol treated groups showed improvement of brain metabolic disturbance as compared to saline group. During 3-6 hrs of ischemia, 6 ml/kg glycerol treated group was more effective in improving disruption of brain metabolism compared to the 3 ml/kg and 20 ml/kg treated group. On the other bands, 20 ml/kg administered group had rather higher lactate concentration than saline group. At 2 and 3 hrs after ischemia, decrease of r-CBF was suppressed in 6 ml/kg glycerol administered group. The pathological observation of middle cerebral artery (MCA) area showed a minimal edematous change in 6 ml/kg glycerol administered group. In this experiment, it is suggested that the most suitable dose of glycerol for treatment of ischemic injury in rats could be 6 ml/kg, and excessive administration of glycerol might aggravate brain injury.

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We studied silent cerebrovascular lesions (infarct and hemorrhage) in 76 patients with symptomatic brain hemorrhage (41 male and 35 female, mean 62 years) by high-field magnetic resonance imaging (MRI). Of the patients, 65 were diagnosed as hypertensive brain hemorrhage and the remaining 11 were as non-hypertensive brain hemorrhage. Silent brain infarct on MRI was detected more frequently in patients with hypertensive brain hemorrhage (88%) than in those with non-hypertensive brain hemorrhage (55%) (p<0.05). Silent brain hemorrhage was found in the former (23%) but not in the latter. Ten (20%) of the 51 patients who developed first attack of hypertensive brain hemorrhage were complicated with silent brain hemorrhage, mainly in putamen and thalamus. They tended to have long lasting hypertension or receive antihypertensive therapy. The incidence of silent brain hemorrhage seems to be higher than ever considered in patients with hypertensive brain hemorrhage. Further studies need to elucidate the clinical significance of these silent cerebrovascular lesions.

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We encountered a patient with cryptococcal meningitis who developed superior sagital sinus occlusion during his clinical course.
A 50-year-old male with diabetes who developed a headche, neck stiffness, followed by fever and conciousness disturbance was admitted to our department. On admission, neurogical examinations showed slight disorientation, meningeal irritating signs, hypesthesia in the periphery of 4 limbs, and anisocoria. The cerebrospinal fluid obtained under an initial pressure of 160 mmH₂O showed a cell count of 136/mm³, a protein level of 400 mg/dl, and a glucose level of 16 mg/dl (blood sugar 240 mg/dl). India ink staining demonstrated cryptococcus neoformans.
The symptoms slightly improved after treatment with Amphotericine B and 5-FC. About 3 months after the initiation of treatment, however, right hemiparesis suddenly developed. Brain CT showed multiple low density areas, the empty triangle sign, and gyral enhancement, while angiography showed no abnormality in the arterial phase but delayed enhancement in the cortical vein and poor enhancement of the posterior 1/3 portion of the superior sagittal sinus in the venous phase. Cryptococcosis is considered to be less frequently complicated by vascular damages than mucomycosis or aspergillosis. This case may be the first in which sperior sagittal sinus occlusion as a complication was radiologically demonstrated.

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We report a case of subclavian steal syndrome in which recanalization of the left subclavian artery by percutaneous transluminal angioplasty (PTA) resulted in global improvement of cerebral blood flow (CBF).
A 57-year-old diabetic male was admitted to our neurologic ward due to right homonymous hemianopsia and word amnesia. Coarse bruit was audible in the left supraclavian fossa and blood pressure measured in the left upper limb was lower by 39 mmHg than that in the opposite side. Digital subtraction angiogram revealed 90% stenosis of the left proximal subclavian artery, back flow in the left vertebral artery, and severe stenosis of the left internal carotid artery, as well. Left hemisphere was mainly perfused from the contralateral internal carotid artery and vertebral artery via the circle of Willis. CT scan showed low attenuated area in the territories of left posterior and middle cerebral arteries. Stenosis of the left subclavian artery was released by PTA with a balloon catheter so that flow direction in the left vertebral artery returned to forward. SPECT ^99mTc-HMPAO) performed before and after the PTA demonstrated a significant recovery of CBF in the territories of both posterior and middle cerebral arteries. The flow improvement persisted in the follow-up SPECT performed 4 months later. Neurological abnormalities such as visual field defect and word amnesia are gradually improved after the PTA.
Subclavian steal syndrome is frequently accompanied with arteriosclerotic stenosis of the other major cerebral arteries. The present case suggests that normalization of vertebral flow can cause global CBF improvement by raising perfusion pressure at the Willis ring. Percutaneous transluminal angioplasty can be a first choice of treatment in cases of subclavian syndrome with ischemic events.

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A rare case of Abbie's syndrome, or anterior choroidal artery (Ach) syndrome, is reported. The patient was a 61-year-old hypertensive man, who presented with a left motor-hemiplegia and a left homonymous hemianopsia and no sensory disturbance on admission.
Internal carotid angiography disclosed an occlusion of the right Ach at its origin. CT scan and MRI revealed infarctive foci in the posterior two-thirds of the posterior limb of the internal capsule, the lateral half of the lateral geniculate body, the optic radiation and the uncus, all on the right side. However, the posterior end of the posterior limb of the right internal capsule did not appear involved. IMP-SPECT disclosed a diffuse hypoperfusion area in the affected cerebral hemisphere in the early image and re-distribution phenomenon around the basal ganglia including the posterior limb of the right internal capsule in the delayed image. Findings of other examinations such as urinalysis, blood biochemistry, chest X-ray, electrocardiography and echocardiography were all within normal limits. After undergoing medical and physical therapy for one and a half months, the patient was discharged with a mild left hemiparesis and a persistent complete left hemianopsia.
Previous reports of primary Abbie's syndrome, though very few, have implied that both motor and sensory hemipareses corresponding to the vascular distribution are inevitable in case of Ach occlusion. However, our patient did not demonstrate sensory disturbance of any modality. This may be explained by preservation of the posterior end of the posterior limb of the right internal capsule, through which the sensory fibers run. Sparing of this region may be attributed to collateral blood supply from the middle cerebral, the posterior cerebral, or, most likely, from the lateral posterior choroidal, arteries.

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We reported a 64-year-old male with bilateral vertebral artery occlusion who experienced sudden onset bilateral hearing loss and vertigo.
The patient had no history of hearing impairment and no premonitory symptoms; he was receiving medication for hypertension and hypercholesterolemia.
He had been admitted to a local hospital for colonoscopic polypectomy of a colon polyp. The day after this operation, he suffered bilateral hearing loss, preceded by vertigo and vomiting. The following day, he was transferred to Saku Central Hospital for further evaluation and treatment of the sudden deafness. En route to our hospital, he suffered a respiratory arrest, but voluntary breathing was restored shortly after intratracheal intubation was performed.
On physical examination, the patient's blood pressure was 110/80 mmHg. He had corneal rings and palpebral xanthomas. Neurological examination showed clouding of consciousness. Examination of cranial nerves revealed horizontal gazing nystagmus, predominantly on the right. The patient had severe hearing loss in both ears. Cold caloric stimulation showed severe canal paresis in the left ear and moderate paresis in the right. His speech was scanning and slurred. Deep tendon reflexes were generally hyperactive and pathological reflexes were bilaterally positive, although muscle strength was almost normal. Tests of coordination of the patient's extremities revealed adiadochokinesis and dysmetria, predominantly on the left. He showed truncal ataxia in a sitting position and was unable to walk. He also exhibited dysuria. Laboratory data on admission revealed mild hypercholesterolemia and a diabetic pattern on 75 g OGTT.
Although CT scan on admission revealed small low density areas only in the bilateral cerebellar hemispheres, by the fifth day these lesions were enlarged and new low density areas appeared in the paramedian portion of the mid-to-upper pons and middle cerebellar peduncles. Cerebral angiography of both vertebral arteries (VAs) revealed marked stenosis at the origins and occlusion at the 4th segments. Carotid angiography demonstrated retrograde filling of the basilar artery (BA) and both superior cerebellar arteries, mediating collateral circulation from the anterior and the middle cerebral artery; it was unclear how far the occlusion extended in the rostal direction. Neuroradiological findings suggested that thrombosis extended from the bilateral VA to the middle portion of the BA. Brain-stem auditory evoked potentials (BAEPs), recorded on the 8th day, showed absence of all BAEPs including wave I in both ears, which corresponded to the clinical findings of bilateral hearing loss.
After admission, the patient developed progressive stroke with somnolence, left Horner's syndrome, pseudobulbar palsy, and tetraplegia including facial palsy. Following thrombolytic therapy with urokinase, he improved and was discharged, although bilateral hearing impairment, cerebellar ataxia, mild tetraplegia, and dysuria persisted as sequelae.
Bilateral hearing loss is rarely found as early sign in vertebro-basilar or basilar thrombosis. The BAEPs finding in our case suggested that bilateral hearing loss resulted from damage to the cochlear nerve due to ischemia of its feeder, the internal auditory artery. Sudden onset bilateral hearing loss should be considered a medical emergency which requires immediate evaluation and management, because it may be the initial symptom in critical vertebrobasilar thrombosis.

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