Although non-specific complaints (e.g., mild to moderate headache and dizziness) are considered to relate to silent cerebrovascular disease (CVD), the prevalence of abnormal findings on computed tomographic (CT) scans in patients with such symptoms has not been reported. The purpose of our study was to assess prospectively the characteristics of CT images in patients with headache, dizziness or vertigo. From August 1993 to May 1994, we examined 70 consecutive outpatients with headache, dizziness or vertigo who were 40 years of age or older (27 men and 43 women; age range, 40 to 87 years; mean age 67 ± 12 years) at Kaita Hospital. The patient's own description of their headache, dizziness or vertigo was first elicited in an open-ended fashion, and then a structured interview was conducted to characterize specific aspects of the complaints, according to a standardized protocol before undertaking radiological assessments. A CT scan of the brain was performed, basically, on the day of referral.
Among 62 CT scans in the 70 patients, brain infarction was demonstrated in 19 cases (18 with small infarction and one with moderate-sized borderzone infarction). A history of CVD was present in 6 cases, so that the prevalence of silent CVD was 21% (13/62). White matter lesions were found in 4 cases, and of these, 3 showed extensive lesions, and were diagnosed as vascular dementia of the Binswanger type. The prevalence of hypertension was 67% in lesion-positive patients with a history of CVD and 77% in those with silent CVD, respectively, and these values were significantly higher than the 37% in patients without infarction on CT (p <0.05, X² test).
Patients with silent CVD were significantly older than those without infarction (p < 0.008, ANOVA and an unpaired t-test).
In summary, we found CT evidence of silent stroke in 21% of cases who visited our outpatient clinic because of headache, dizziness or vertigo. Age and hypertension appear to be major factors for such silent infarction in patients with headache, dizziness or vertigo.

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To detect cervical carotid stenosis as a candidate for carotid endarterectomy (CEA), the authors attempted a prospective trial by exploring stenosis for one year in a rural district with a population of 20, 000, employing helical CT angiography which apparently displayed three-dimensional reconstructed images of the carotid bifurcation. Thirty-three patients, 24 males and 9 females, with a mean age of 71.8 years, suffering from TIA, RIND or stroke were investigated for their carotid systems. The clinical symptoms of the patients were briefly as follows : motor weakness in 30 cases, dysarthria in 8 cases and aphasia in 4 cases; and 6 of 22 (27%) stroke cases had previously suffered an episode of TIA. The risk factors of the whole group of patients were hypertension in 13 cases, diabetes mellitus in 6, heart disease in 17, and hypercholesteremia in 4. Helical CT angiography was performed in 11 cases of TIA, 2 cases of RIND, and 16 cases of stroke. Only 3 cases of the TIA group and 3 cases of the stroke group were found to have extracranial carotid stenosis of more than 50%, which subsequently required conventional angiography. For the detection of stenosis, CT angiography was beneficial as well as conventional angiography. Finally, CEA was performed in 2 of 3 cases with severe carotid stonosis in the TIA group, while such cases in the stroke group were only observed. The above results meant that the occurrence of extracranial carotid stenosis was 6 out of 6, 589 elderly inhabitants (over 60 years old), although the possible detection rate of candidates for CEA was 2 out of 20, 000 population per year.

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TIA has mainly been explained by microembolism from a major cerebral artery. However, it is still unresolved as to whether this mechanism is applicable to Japanese cases or not, because of the low frequency and mild degree of cerebral arterial lesions in Japanese cases as compared to those in Whites. To examine the mechanisms of TIA in Japanese cases, we classified the patients, whose neurological deficits seemed to be caused by supratentorial lesions, into perforator TIA (the P group) with classical lacunar syndrome, and cortical TIA (the C group) with cortical signs such as monoparesis and aphasia. Cerebral angiographic findings in which major arteries were occluded or were stenosed by over 50% of the vessel diameter or had ulcerative plaque, were diagnosed as abnormal.
Thirty-eight patients were included in the present study. The respective numbers of patients in the P and C groups were 21 (55%) and 12 (34). The remaining 5 cases (13%) could not be classified into the P or C group because of nonspecific neurologic findings. Among the risk factors of TIA, hypertension was frequently observed in the P group, but arrythmia and heart disease were not. Cardiogenic embolism (CE) was suspected only in 4 cases of the C group. On angiography, half of all cases revealed normal findings; 62% of the cases in the P group and all the CE cases in the C group showed normal findings, but 87% of the cases in the C group (except for the CE cases) showed abnormal findings. The underlying mechanism of TIA in the P group was thus suspected to be mainly in-situ perforating arterial lesions, such as lipohyalinosis, and in part, microembolism. In the C group, on the other hand, the mechanism appeared to be mainly microembolism, and partially CE and cerebral blood flow insufficiency.
The present data suggest that there are many cases who exhibit lacunar syndrome and whose mechanism seems to be perforating arterial lesion. Also, to classify TIA caused by supratentorial lesions into perforator and cortical types is evidently useful for predicting cerebral vascular lesions and the mechanism of TIA.

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The prognosis of 38 patients (31 men and 7 women aged 30-80 years old; mean age, 58.4 years old) with lateral medullary infarction confirmed by magnetic resonance imaging was investigated. A total of 3 deaths (8%) occurred among the patients under study. The causes of death were : 1) methicillin-resistant Staphylococcus aureus (MRSA) pneumonia on the 29th day, 2) stomach cancer after 22 months, and 3) recurrence of breast cancer after 58 months. The complications among the patients included 4 cases of aspiration pneumonia, one case of gastrointestinal hemorrhage, 4 cases of myocardial infarction, one case of arteriosclerosis obliterans (ASO), and one case of ischemic colitis. Recurrent cerebral infarction occurred in 4 patients (supratentorial in 2 and infratentorial in 2). Swallowing disturbance and gait disturbance were transient in all cases, with a generally good functional prognosis. Factors which suggested a poor prognosis included complications related to aspiration in the acute phase, as well as ischemic heart disease in the chronic phase.

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The acute effects of β-blocker include a decrease in cerebral blood flow (CBF). However, few reports have been published on the acute effects of newly developed β-blockers on CBF. We examined the effects of carteorol on CBF in 10 stroke patients with hypertension during the subacute phase. The subjects consisted of 7 patients with cerebral infarction and 3 patients with cerbral hemorrhage with an average age of 58.2 years. CBF was measured before and at 30 min after oral administration of 10 mg carteorol by the stable xenon CT-CBF method. We analyzed the effects on arterial blood pressure and CBF in 9 patients whose plasma levels of carteorol were detectable. At 30 min after carteorol administration, the mean arterial blood pressure was significantly reduced from 126.1 ± 8.1 mmHg to 120.4 ± 8.5 mmHg (p<0.05). The mean CBF values before and after carteorol administration were 37.8 ± 4.3 ml/100 g brain/min and 40.2± 3.2 ml/100 g brain/min, respectively. The degrees of increase in CBF in both the diseased and healthy hemispheres were not significantly different. The changes in CBF were significantly correlated with the basal mean arterial blood pressure (r = 0.72, p <0.05). These findings indicate that carteorol can act as potent antihypertensive agent without deterioration of the cerebral circulation.

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We examined, by microfluorometry, whether or not 3-isobutyryl-2-isopropylpyrazolo [1, 5-a] pyridine (ibudilast) has any effect on in vitro ischemia-induced rises of intracellular Ca²⁺ concentration ([Ca²⁺] _i) in the CA1 field of gerbil hippocampal slices. Transverse hippocampal slices (300 μm-thick) were loaded with rhod-2, a calcium ion-sensitive dye, and then transferred to a flow-through chamber mounted on an inverted fluorescence microscope. The changes in [Ca²⁺] _i were measured using an intracellular calcium ion imaging system. When the slices were exposed to a glucose-free physiological medium equilibrated with a 95% N₂/5% CO₂ gas mixture (standard in vitro ischemic conditions), a large [Ca²⁺] _i elevation was detected about 5 min after the beginning of the standard in vitro ischemic conditions. Howerver, the extent of in vitro ischemia-induced [Ca²⁺] _i increase in the presence of 43 μM ibudilast was significantly depressed in all subregions of the hippocampal slices as compared with that under standard in vitro ischemic conditions. Similar [Ca2²⁺] _i increases in the CA1 field were induced by Ca²⁺-free in vitro ischemic conditions, a high concentration of KCl or each specific agonist for the glutamate receptor subtypes, N-methyl-D-aspartate, (s) -alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate and kainate; and these increases were also depressed in the presence of 43 μM ibudilast in the perfusion medium. The above findings indicate that ibudilast exerts an inhibitory effect on the in vitro ischemia-induced [Ca²⁺] _i elevation and that this inhibitory effect is caused by decreases in Ca²⁺ influx through the agonist-gated Ca²⁺ channels and also the voltage-gated Ca²⁺ channels as well as in Ca²⁺ release from the intracellular Ca²⁺ stores. The present inhibitory effect of ibudilast on Ca²⁺ accumulation may be involved in the mechanisms whereby ibudilast can diminish ischemic injury in hippocampal CA1 neurons.

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The clinical spectrum of cerebral infarction of the Binswanger type, accompanied by severe perventricular leukoencephalopathy ranges from ischemic stroke to dementia with focal deficits, pseudobulbar palsy, gait disturbance, urinary incontinence, and extrapyramidal signs. We examined the differences between the clinical and radiological features of patients with cerebral infarction of the Binswanger type with and without dementia.
Of the 33 patients studied (15 males and 17 females; mean age ± SD, 79.8 ± 5.8 [range 69-90] years), 11 were classified as non-demented and the other 21 as demented on the basis of the DSM-III-R criteria and neuropsychological testing. The periventricular hyperintensity (PVH), temporal horn and body of the lateral ventricle, brain parenchyma, subarachnoid space, and temporal lobe were measured planimetrically by MRI, and the white matter hyperintensity (WMH) and infarcts of the basal ganglia/thalamus were assessed on the basis of subjective ratings. There were no significant differences between the non-demented and demented patients in terms of age, sex, and cerebrovascular risk factors. Clinically, extrapyramidal signs were observed more often in demented than in non-demented patients, and the ADL (activities of daily living) showed significantly poorer values in demented patients. MRI studies revealed no significant differences between the non-demented and demented patients in terms of the ratios for the PVH, temporal lobe area and subarachnoid space, or in the degrees of WMH and infarcts in the subcortical gray matter. However, the ratios for the temporal horn and body areas of the lateral ventricle were significantly higher in demented than in non-demented patients, and the brain parenchyma ratio was significantly lower in demented patients. The temporal horn area ratio was significantly higher in mildly and severely demented patients than in non-demented patients and the brain parenchyma ratio was significantly lower in severely demented patients than in non-demented and mildly demented patients.
Thus clinical features such as subcortical cerebral dysfunction and the ADL, and brain atrophy differed between non-demented and demented patients with cerebral infarction of the Binswanger type. Moreover, our data suggest that medial temporal lobe atrophy appears in the early stages of dementia, while generalized atrophy of the cerebral parenchyma follows in the advanced stages.

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This retrospective analysis concerns 206 among 1472 stroke patients who were discharged from 6 medical centers in Fukuoka Prefecture between January 1989 and December 1990. The objective was to estimate the functional outcome and the situation of living at 3.2 years after 4.5 months of hospitalization. The Rankin disability scale averaged 3.2, and the Barthel index averaged 34.2, at admission. These values were significantly lowered to 2.2 and 22.7, respectively, at discharge, and no further improvement of the scale or index was obtained during the period of the present study. Dysphasic cases among 174 patients decreased from 17.2% to 9.2%, despite 25.7% in embolism. A depressive state was noted in 48.7% in this study without differences between males and females or between age groups. A return to work by the time of follow-up was achieved in 36.8% of the patients, although 20.4% remained bedridden or were still suffering from severely limited activities of living. A need for further social as well as medical support should be anticipated, since the case fatality has been decreasing in recent years.

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Cerebral aneurysms associated with arteriovenous malformation (AVM) have often been reported with special reference to the hemodynamic effect of aneurysm formation. We think that many factors including hemodynamic stress play important roles in the etiology of cerebral aneurysms associated with AVM and that all cases should not be discussed under a single mechanism. Therefore in this study we surveyed 23 AVMs with aneurysms and classified these cases by the relation between the aneurysm and the AVM and discussed the clinical characteristics of cases in each group. We summarized them as follows.
1) Group A : Those cases which had cerebral aneurysms located on the feeder of AVM. These patients were older than the other patients and it was suspected that arteriosclerosis was important in the formation of these aneurysms. These AVMs were no larger than AVMs without aneurysm. In those patients, rupture of aneurysm was a major hazard. 2) Group B : Those cases which had aneurysms located on the proximal arteries which were on the same side of AVM. The size of these AVMs tended to be slightly larger than those AVMs without aneurysm and the patients in this group were low risk as far as cerebral bleeding was concerned. 3) Group C : Those cases which had aneurysms which were thought to have no relation with AVM and the combination of the two lesions was thought to be coincidental. In these patients intracranial hemorrhage accounted for almost all the bleeding and the rupture of aneurysms was rare.

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A case of thrombosis of the left middle cerebral artery was treated by intra-arterial injection of urokinase (UK) by transbrachial superselective catheterization. The patient was a 69-year-old male who had experienced difficulty in speaking from the morning. After he was admitted to our hospital, his clinical condition worsened. Aphasia, right hemiparesis and disturbance of consciousness appeared. Based on the clinical course, atherothrombotic infarction was suspected. Emergency cerebral angiography was performed by right transbrachial approach, and complete left middle cerebral artery occlusion was diagnosed.
We employed a newly devised transbrachial cerebral catheter with which we can carry out superselective catheterization. After diagnosis, 480, 000 units of UK was administered intra-arterially using this highly selective catheterization. The injection produced a recovery of blood flow in the left middle cerebral artery and resulted in rapid amelioration of the clinical symptoms.
Intra-arterial injection of UK by superselective catheterization can be very effective in acute obstruction of the middle cerebral artery. As regards the technique of cerebral angiography, in many respects the transbrachial approach is preferable to the transfemoral approach. However, there have been no reports of transbrachial superselective thrombolytic therapy. We have demonstrated that it is possible to perform superselective catheterization using the transbrachial approach.

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Left pure motor hemiplegia sparing the face occurred in a 54-year-old woman with a history of hypertension. After reduction of her blood pressure which had risen suddenly, right hemiparesis occurred. She had incomplete quadriplegia, but her face and tongue were spared. Although she complained of numbness in the left limbs, sensory examinations were normal for touch, pain, vibration and position sense. MRI demonstrated small infarctions confined to both pyramids of the upper medulla oblongata, that partially extended to the anterior margin of the right medial lemniscus. Cerebral angiography did not reveal significant abnormalities.
Bilateral infarction of the medullary pyramids resulting in pure motor quadriplegia is a rare occurrence. The extension of the deficit noted in this case could have been due to failure of the collateral circulation elicited by lowering of the blood pressure.

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Two cases of unruptured giant vertebro-basilar aneurysm presenting with marked brain-stem compression are reported. The first patient with a partially thrombosed saccular aneurysm of the left vertebral artery underwent aneurysmal trapping through a suboccipital craniectomy. The second patient with a vertebro-basilar fusiform aneurysm was treated with proximal ballon occlusion of the right vertebral artery by intravascular surgery. Preoperative evaluation with balloon test occlusion and intraoperative monitoring of brain stem responses suggested that the parent artery occlusion was safe in both patients. Postoperatively, however, they fatally continued to suffer from progressive brain-stem insufficiency. Postmortem examinations revealed significant atrophy of the brainstem and its distortion by aneurysmal compression. Histopathological studies demonstrated extensive necrosis of the brain stem in both cases, resulting from compression and/or ischemia. The possible factors causing the neurological deterioration in these two cases are speculated to involve the following :
1) ischemia in the territory of the parent artery and its perforators (hemodynamic ischemia);
2) thrombosis and/or embolism from the distal site of the artery occlusion (thromboembolic ischemia);
3) progressive enlargement of the aneurysm even after trapping or parent artery occlusion; and
4) mechanical trauma due to the surgery.
Our experience with these two cases suggests that successful treatment of such glant aneurysms of the posterior circulation with marked brain-stem compression is extremely difficult.

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Caudate head hemorrhage usually causes severe headache just as subarachnoid hemorrhage does, but rarely causes amnesia. We report a case of right caudate head hemorrhage with impairment of recent memory and cuphoric episodes. A 54-year-old man suddenly displayed global amnesia, impairment of recent memory and disorientation whthout headache or any neurological deficit. After admission, he became hyperactive and euphoric. These symotoms gradually subsided after one month. A CT scan revealed a small hemorrhage in the right caudate head (Fig. 1). ¹²³I-IMP SPECT showed a hypoperfusion area in the right temporal base (Fig. 2). The occurrence of such symptoms appears to be associated with caudate head injury and/or hypofunction of the temporal lobe due to remote effects of caudate head injury.

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