Etiopathogenesis of a pathological state called subcortical arteriosclerotic encephalopathy (Binswanger's type) (abbreviated as ESCP), which was at first described by Binswanger in 1894 as one to be differentiated from progressive paralysis, was discussed on the basis of review of the literature and a typical autopsy case.
It is now reasonable that ESCP is caused by hypertension-related vascular changes including atherosclerosis of the cerebral medullary arteries, which are more prominent than those of the subarachnoidal arteries of the same case and those of cases of hypertensive cerebral bleeding or cerebral infarct. ESCP, therefore, is considered to be a special form of cerebral diseases caused by systemic hypertension, and should not be lumped together as arteriosclerotic brain diseases.
ESCP of the aged seems to be pathologically identical with the so-called
“classical” type initiating at presenile age. Moreover, other diseases which present severe demyelination and atrophy of the cerebral white matter due to vascular changes, but etiologically different from ESCP, were also discussed.

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Histamine is a mediator of cerebrovascular response; however, it has not yet been confirmed as a modulator for cerebral vascular responses either in physiological or pathological states. In this paper, an experimental study on the reactivity of the cerebral artery to histamine was performed as a preliminary study to evaluate alterations in the reactivity of histamine receptors of the cerebral artery in cerebral vasospasm. The bovine basilar arteries were isolated from the brain stem immediately after the animals were slaughtered. Arterial strips (2 × 20 mm) were prepared and the isometric tension development of the vascular response to histamine and related agents was measured in a heated tissue bath (37°C) containing aerated modified Krebs-Ringer solution.
Histamine and 2, 2-pyridylethylamine (PEA, H₁ receptor agonist) produced dose-dependent vasoconstriction of the cerebral artery, whereas dimaprit (H₂ receptor agonist) did not induce any vascular response. With pretreatment of tripelennamine (H₁ receptor antagonist), the dose-response curves of the bovine basilar arteries to histamine were shifted parallel to the right. The slope of the regression line in Schild's plot for tripelennamine on the response of histamine was 0.904 and pA₂ value was 8.76. The antagonistic effect of tripelennamine on the vascular response to histamine was competitive. The histamine-induced vasoconstriction of cerebral arteries was not influenced by cimetidine, α- or β-blockers; however, it was influenced by the phospholipase C inhibitor. No significant differences were found in histamine-induced vasoconstriction of cerebral arteries either with or without removal of endothelium.
The results indicate that the contractile response of the cerebral artery to histamine is induced by activation of H₁ receptors. In the bovine basilar artery, H₂ receptors are few or entirely absent. It is also suggested that histamine-induced vasoconstriction is mediated by an increase of intracellular Ca²⁺ through the activation of phospholipase C after direct action of histamine on H₁ receptors of the cerebral artery. Further study will be carried out to examine alterations in the reactivity of the histamine receptor of the cerebral arteries in experimental cerebral vasospasm.

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Recently, several reports suggest the abnormalities of cerebral venous system in Struge-Weber syndrome. We present a case of Sturge-Weber syndrome in a 13 year old female with convulsion, right hemiparesis and motor aphasia, in association with rectal sinus thrombosis. In the acute stage, carotid angiography revealed cerebral venous anomalies and disappearance of rectal sinus. Enhanced CT represented particular gyral enhancement on damaged hemisphere. Two weeks after the onset, the second carotid angiography indicated the recanalization of rectal sinus and gyral enhancement on repeat CT was diminished. The clinical course was septic. She was treated by antibiotics, anticonvulsants and antiplatelet agents. The inflammation of otolaryngeal lesion was supposed to be the cause of sinus thrombosis. After the recanalization of rectal sinus, she was rapidly improved.

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A 58-years-old woman with hypertension admitted to the hospital because of left leg paresis which occurred the day before. On admission, neurological examinations revealed mild left crural paresis (4/5) and ataxia in the left side. Finger-nose test showed dysmetry and intentional tremor in the left. Cranial nerves were normal. Slight hypesthesia in the left leg was observed. The CT scan showed right parasagittal subcortical hematoma. Right carotid angiogram showed mild atherosclerotic changes. There were no tumor stain nor arteriovenous malformation. Ataxic hemiparesis disappeared about 3 weeks after the admission. Enhanced CT scan showed no abnormal enhancement in the parasagittal region 3 months after the onset. Fisher had reported homolateral ataxia and crural paresis (Ataxic hemiparesis) from pontine lesion. However, it has been known that ataxic hemiparesis also occurred by the small lesion of internal capsule or corona radiata. There were few case reports of ataxic hemiparesis from parasagittal hematoma. In our case, damage of cortico-ponto-cerebellar tract at frontal subcortical region may cause homolateral ataxia.

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In vivo brain dialysis was applied to investigate the effects of cerebral ischemia on striatal dopaminergic neurons. Cerebral ischemia was induced in spontaneously hypertensive rats (SHR) by bilateral carotid artery ligation. Extracellular dopamine and 3.4-dihydroxyphenylacetic acid (DOPAC) were determined in the striatum of SHR during 20 min ischemia and 60 min recirculation. Striatal tissue contents of dopamine and DOPAC were also determined in sham-operated, 20 min ischemia and 20 min recirculation groups.
Dopamine in the perfusates increased remarkably to 241 times at 20 min ischemia and returned to the control level after 30 min recirculation. DOPAC decreased to 50% of the control at 20 min ischemia and increased to 211% after 40 min recirculation. Dopamine content in 20 min recirculation group increased by 9% compared with sham-operated group (p<0.05), although DOPAC was not different among the three groups.
These results indicate massive release of striatal dopamine in the acutely induced ischemic brain.

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Stroke models with the acute and chronic infarction were made in 54 rabbits after injection of 0.06-0.15 ml of sephadex G-75 (SG-75) suspension (1 : 1) into the carotid artery. All rabbits were males, about 2 months old. Hourly pathological changes of cerebral tissues were examined at certain time. No change appeared at 10 minutes. At 30 minutes, mitochondria of the nerve cells increased. At 3 hours, swelling of the astocyte process and shrinkage of the nerve cells occurred. Electron density of nucleus and cytoplasma increased. At 6 hours, Nissl's body change of interstitial substances could also be observed. At 24 hours, inflammatory cells infiltrated and disruption of the nerve cells appeared. At 48 hours, axonal disruption could be seen. In addition, from the third and the fourth day, the gitter cells inside the lesion and around the capillary were observed, and they increased more remarkably at one week. Hyperplastic astrocytes could also be observed. At 5 weeks, fibrillary gliosis around infarction could be seen. Seven weeks later, glial network with the fibrillary gliosis was produced. Haemorrhagic infarction could be observed in 40% of these animals from 12 hours to 7 days after SG-75 injection.

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Haemorrhagic infarction was studied in rabbits brain with stroke model. In this study, to clarify the mechanism of hemorrhagic infarction, following experiments were used to make stroke models. They were divided into 3 groups : 20 of them were treated by clipping left common carotid artery (group A); 20 of them were not down (group A); and the rest were used a control (group C).
All groups were subjected to injection into left internal carotid artery. 0.06 ml of sephadex (SG-75) suspension was used for group A and group B, whereas normal saline solution was used for group C. The histological lesions of rabbits brain were examined with light and electron microscope. Furthermore, carbon mixture was perfused to investigate the dynamic capillary circulation. (1) Haemorrhagic infarction easily developed in the left cerebral cortex as well as in the basic ganglia; (2) In group A, it was more frequently seen than in group B; (3) perfused carbon particles could be seen in capillary bed of group C. However, they could not be seen in the occlusive lesions of A and B groups injected with SG-75. Yet, it was remarkably observed in haemorrhagic infarction area; (4) The blood vessels surrounding the haemorrhagic infarction showed marked degeneration by light and electron microscopy.
These results show that the mechanism of haemorrhagic infarction may be due to bleeding from collateral circulation.

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Two cases presenting with subarachnod hemorrhage in pregnancy were reported, and verified ruptured intracranial aneurysms and arteriovenous malformations (AVM's) during pregnancy were reviewed in the Japanese literature. Case 1 : a primipara 27-year-old woman at 13 weeks of gestation was referred to the hospital after suddenly developed occipitalgia, nausea and vomiting. On admission the patient was stuporous, with stiffness of her neck and a dilated pupil on the right. There was also a left flaccid hemiparesis. A CT scan demonstrated evidences of subarachnoid hemorrhage associated with intracerebral as well as subdural hematomas at the right fronto-temporal region. Ventricular shift and deformity were prominent. Angiography revealed an arteriovenous malformation fed by the right anterior temporal artery and drained into the sphenoparietal sinus. In view of neurological signs indicative of impending herniation, an emergency operation was performed and the AVM was totally exstirpated with complete hematoma evacuation. Vital sings of the patient and the fetus were carefully monitored and found stable during surgery. The postoperative course was uneventful and the patient was discharged without neurological deficits. The fetus was, however, eventually aborted in three weeks after discharge. Case 2; a multipara 28-year-old woman was admitted to the hospital after the onset of a subarachnoid hemorrhage. No abnormality was disclosed on neurological examination except for nuchal rigidity. A CT scan showed areas of high density within the basal subarachnoid cisterns, consistent with the finding of subarachnoid hemorrhage. Angiography revealed a saccular aneurysm approximately 7 mm in diameter projecting inferiorly at the junction of the right internal carotid and posterior communicating arteries. Immediately after a 2900 g female was delivered by cesarean section, the patient underwent a right fronto-temporal cranitomy and the aneurysm was successfully clipped within 24 hours of onset. The patient was discharged without neurological deficits.

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Plasma levels of 3-methoxy-4-hydroxy-phenylethyleneglycol (MHPG) were measured in 101 patients with acute stroke, admitted within 72 hours of onset. Plasma MHPG was determined by the use of high-performance liquid chromatograph with electrochemical detection.
The mean value of plasma MHPG in patients with cerebral hemorrhage (7.3±0.5 ng/ml, N=47) was significantly higher than that in healthy subjects (3.7±0.3 ng/ml, N=15) (p<0.001). An increase in the levels of plasma MHPG was also noted in patients with cerebral infarction (6.8±0.5 ng/ml, N=54). Within the group of cerebral infarction, plasma MHPG in patients with cerebral embolism increased significantly as compared with cerebral thrombosis.
Plasma levels of MHPG were markedly elevated in patients with massive hemorrhage and with large infarction, and these levels well reflected the prognosis. In 16 of 23 patients, levels of MHPG in the cerebral venous blood were higher than those in the arterial blood, which was suggestive of the release of MHPG from the brain into the circulating blood.
These results suggest that following the onset of the stroke, an increase in the activity of the noradrenergic neurons may occur in the central nervous system, and noradrenaline and its metabolites may be massively released into the blood.

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The protective effect of thromboxane synthetase inhibitor, OKY-046, on brain ischemia was studied in spontaneously hypertensive rats. Cerebral ischemia was produced by bilateral carotid artery ligation (BCL) for 1 or 3 hours and reopened for 15 minutes. OKY-046, 5 or 30 mg/kg, was administered before BCL.
Blood pressure and blood gases were not altered by OKY-046 injection. During BCL, cerebral cortical blood flow was reduced below 10% of the resting value (55 ml/100 g/min), and in rats with OKY-046, 30 mg/kg, blood flow was better preserved, 10-16% of the resting value at 1 to 2 hours ischemia, than control rats. After 15 min reopen, supratentorial lactate was lower and ATP was higher in rats with OKY-046 treatment than control rats. Increase in plasma thromboxane B₂ was almost completely inhibited and 6-keto-PGF_1α, was elevated by 8.7 fold after 1 hour ischemia in rats with OKY-046, 30 mg/kg.
OKY-046 seems to have an antiischemic effect on acutely induced cerebral ischemia. Selective inhibition of thromboxane A₂ production may protect microcirculation during ischemia and preserve ischemic cerebral metabolism.

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Time-related changes in cerebrovascular (stroke) mortality were studied based on data from both death certificate and autopsy examination in Hisayama town, Fukuoka, Japan. From 1962 to 1985, 139 men and 132 women were certified to death by stroke, of which 46 men and 25 women were diagnosed as intracerebral hemorrhage (ICH), while 43 men and 53 women as cerebral infarction (CI). Mortality figures from type-specific strokes (ICH or CI) obtained from death-certificate data were corrected by the proportion of congruity or incongruity between deathcertificate and autopsy diagnoses (estimated death rate). Statistics based on death certificates revealed that the mortalities from all types of stroke for both sexes and from ICH for men decreased, showing a similar pattern of those from the nation-wide statistics during the observation period. The mortality from CI for both sexes turned from increase to decrease between 1962 and 1974, being also similar to figures of the whole Japan. However, its figures from 1962 to 1969 were assumed to be underestimated compared to those calculated by autopsy data. Meanwhile, the mortality from ICH for women tended to decrease during the period, although the rate was markedly lower than that of the nation-wide figures. These were also verified by estimated death rates. Analyzing the results from autopsy studies, nation-wide mortality statistics of ICH for women were considered to be partially biased by misdiagnosis on subarachnoid hemorrhage. On the other hand, an increasing trend of CI for both sexes during the period since 1962 to 1969 was partially resulted from the fact that more CIs could be selected as the cause of death on the death certificate than those actually occurred.

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To elucidate the role of dehydration in intracardiac thrombus formation in patients with acute cardiogenic brain embolism, result of repeated two-dimensional echocardiography were related to hematocrit and water-balance in 30 consecutive patients admitted within 48 hours after onset. Echocardiographic examination and measurement of hematocrit were performed on admission, and 4, 7, 10, 14, 21 and 28 days after onset.
Intracardiac thrombi were detected in eight of 30 cases (27%); four on admission and remaining four during admission. Enlargement of the intracardiac thrombi were observed in four cases, and systemic embolism recurred in three of them. Most of the cases with newly appeared and/or enlarged intracardiac thrombi showed negative water balance, while a few cases without thrombus formation did so. A reduction of diameter of the inferior vena cava and an increase in hematocrit value were also found in the former.
These data suggest that intracardiac thrombi are more frequently detected than previously reported, if echocardiographic examination is repeated with short intervals, and that dehydration considerably accelerates intracardiac thrombus formation.

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To elucidate pathophysiology of intracardiac thrombus formation, two-dimensional echocardiographic examination were frequentry repeated on thirty consecutive patients with acute cardiogenic cerebral embolism in parellel with measurement of plasma level of fibrinogen and fibrinopeptide A. Repeated echocardiographic examination was done on admission, 4, 7, 10, 14, 21 and 28 days after onset of stroke.
Intracardiac thrombi were detected in eight cases (27%); four on admission and other four after admission. Enlargement of the thrombi was observed in four cases and systemic embolization recurred in three of the eight cases. When the appearance or the enlargement of intracardiac thrombi were detected by echocardiography, a decrease in plasma levels of fibrinogen and an increase in fibrinopeptide A were demonstrated. These data suggest that the decrease in fibrinogen and the increase in fibrinopeptide A indicate enhanced intracardiac thrombosis, and that intracardiac thrombus formation can be predicted by repeated measurements of these parameters.

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A 53-year-old right handed man with hypertension developed stepwise deterioration in memory and calculation associated with right hemiparesis and small steppage gait in the last 7 years. On admission the blood pressure was 170/100 mmHg and neurological examinations revealed left facial and hypoglossal palsy, increased jaw jerk, and impaired memory, abstraction, constraction and calculation. A CT scan showed hypodensity areas, in bilateral basal ganglia, white matter of the left parietal cortex and the left cerebellar hemisphere. In these regions and in the anterior portion of the left thalamus as well, high field magnetic resonance (MR) with T2-weighted images demonstrated hyperintensity areas surrounded by hypointensity rims, indicating old cerebral hemorrhages. Dementia in this case seemed to be due to, multiple cerebral hemorrhage with hypometabolic areas in the hemorrhage sites and in bilateral frontal lobe. MR is useful to differentiate old cerebral hemorrhage from infarction in those with multiple hypodensity areas on CT scan.

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Local cerebral blood flow (1-CBF) and local CO₂ responsiveness (1-CO₂R) were measured by Xe enhanced CT method in 15 adult patients with moyamoya disease (mean age of 39.9±10.0) and in 11 normal volunteers (mean age of 38.5±6.8). The measurement was performed in chronic phase of the disease, at least 1 month after the last episode of stroke, to avoid the effect of acute insult on cerebral hemodynamics.
In moyamoya disease, 1-CBF value in the anterior part of the brain showed relatively lower value as compared with that of normal volunteers, but remained within normal limits, even after bilateral internal carotid arteries had completely occluded. Cerebral vessels in patients with moyamoya disease revealed a lesser response to hypercapnea with the progress of the angiographical stage. Especially in the late stage group judged by the angiographical findings, 1-CO₂R value was significantly reduced in the frontal cortex and in the caudate nucleus. (p<0.05)
These results suggest that in moyamoya disease the collateral vessels are efficiently functioning to maintein the regional cerebral blood flow in the resting state, but these vessels may have a lesser response to hypercapnea.

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We have reported here a case of paramedian thalamic and midbrain infarct presenting bilateral oculomotor nerve palsy and unilateral asterixis. A 68-year-old man with a history of hypertension and WPW syndrome developed paroxysmal atrial flutter on January 11 1988. An electrical cardioversion was done and his electro-cardiogram returned to sinus rhythm. On the next day morning, he suddenly lost his consciousness after he left his bed and was admitted to our hospital. On examination abnormal neurological findings included bilateral oculomotor nerve palsy, right cerebellar ataxia, transient loss of consciousness and transient unilateral ataxia. As CT and MRI studieis revealed left thalamic and midbrain lesion, paramedian thalamic and midbrain infarct was suspected, which was caused by occlusion of paramedian branches of midbrain artery. Bilateral oculomotor nerve palsy due to cerebral infarction is rare and only 17 cases have so far accumulated in the literatures as far as we know. But in case of occlusion of paramedian mesencephalic artery bilateral oculomotor nerve palsy is supposed to occur more frequently than expected. In addition unilateral asterixis due to midbrain origin is also rare. In a reported case, occlusion of the paramedian mesencephalic artery was suggested by the brain CT image. Even in the literatures of unilateral asterixis caused by thalamic lesion, some authers suggested that midbrain lesion played an important role in the genesis of unilateral asterixis. On the basis of these reports plus CT and MRI findings of our patient, we supposed that occlusion of midbrain paramedian branches had potential participation in the occurrence of unilateral asterixis.

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A 63-year-old man who had history of diabetes mellitus and hypertension occasionally experienced dullness and hypesthesia in the right upper extremity since middle of September, 1986. Approximately one month later, weakness of his left upper and lower extremities and mild dysarthria abruptly developed. Neurological examination revealed left unilateral spatial neglect associated with left hemiparesis. Cerebral angiography showed occlusion of the innominate artery and right subclavian steal syndrome. CT examination demonstrated a small low density area in the right anterior thalamus and posterior internal capsule. Positron emission tomography (PET) taken at 26 and 79 days after the onset demonstrated a marked reduction of both cerebral blood flow and oxygen metabolism in the parieto-occipital cortex ipsilateral to the right thalamic infarction. The elevated oxygen extraction fraction found in the same region indicated uncoupling of flow and metabolism, namely misery perfusion. It is suggested that unilateral spatial neglect in this case was directly due to ischemia in the right parieto-occipital cortex, demonstrated by PET rather than thalamic infarct itself shown by CT. PET study seems to be a useful indicator for determining the site of functional lesion of cerebrovascular diseases.

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A case of recurrent cerebral aneurysm after complete clipping of the aneurysmal neck is reported.
A 25-year-old male was admitted to our hospital after an attack of subarachnoid hemorrhage resulting from rupture of an anterior communicating artery aneurys.
Clipping of the aneurysm's neck was successfully performed and postoperative angiography showed it to have disappeared. The postoperative course was uneventful, and the patient was discharged without any neurological deficits other than systolic hypertension of 200 mmHg.
Five years later he was agin admitted to our hospital with subarachnoid hemorrhage and intracerebral hematoma. Carotid angiography showed a recurrent growth between the previously clipped aneurysm and the anterior communicating artery (7×7 mm).
Trapping of the new aneurysm was performed but the patient died 9 days after this second operation.
Histological findings revealed the presence of internal elastic lamina residue at the site of the aneurysmal neck. We therefore assume that hemodynamic stress exerted on this fragile area by uncontrolled hypertension for five years resulted in the recurrence of the aneurysm and its rupturing.

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The clinical significanse of the PVP-cAMP, cGMP levels in patients with cerebro-vascular disorder (CVD) of acute stage were investigated and such parameters were compared with the brain CT findings, the cAMP-, cGMP-PDE activities and β-TG levels in those patients. The PVP-cAMP, cGMP levels in patients with CVD of acute stage were higher than those of the healthy controls. The negative correlation was seen between Frithz's prognostic score and PVP-cGMP levels in patients with acute cerebral infarction and also this negative correlation was seen between Frithz's prognostic score and PVP-cAMP, cGMP levels in patients with acute cerebral bleeding. The positive correlation was seen between the enlargement of the low density area on brain CT findings and PVP-cGMP level in patients with acute cerebral infarction. Documentary, the negative correlation between PVP-cAMP, cGMP levels and cAMP-, cGMP-PDE activities and also the positive correlation between PVP-β-TG level and cAMP-, cGMP-PDE activities were evaluated at the onset of CVD. On the basis of these findings items, it is suggested that PVP-cAMP, cGMP levels in patients with CVD of acute stage were utilized for the sensitive indicator to prognosis and these cyclic nucleotides level fluctuation were mainly regulated by cAMP-, cGMP-PDE activities releasing from the platlet.

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