The effects of calcium antagonists in relation to cerebral vessels and circulation were widely reviewed throughout the literature. Their effectiveness in stroke and migraine patients were also discussed.
Calcium antagonists usually inhibit cerebral vasoconstriction induced by various agents in vivo. They seem to dilate pial and basilar arteries in vitro, and increase cerebral blood flow in normal animals. Cerebral vasospasms, produced experimentally or in patients, are readily reversed by calcium antagonists. Clinical trials of these drugs on patients with subarachnoid hemorrhage are now under way, with some favorable preliminary outcomes. There are a number of investigations on the effects of calcium antagonists on cerebral circulation following experimental cerebral ischemia, but the results are not uniform, probably due to the various experimental conditions used. The therapeutic effects of calcium antagonists on ischemic stroke patients are mostly demonstrated in their chronic stage, and studies on patients with acute strokes are scarce. Calcium antagonists are also shown to be beneficial in the prophylaxis of migraine attacks.
Although there are yet many problems to be investigated, the usefulness of calcium antagonists on medical practice may be promising.

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The authors encountered 300 cases of intracranial aneurysm in the past 10 years. Among them a giant intracranial aneurysm was present in 15 cases (5%). The giant aneurysm was located in the internal carotid artery in 11 cases, anterior communicating artery in 1 case, middle cerebral artery in 1 case, and basilar artery in 2 cases. Its symptoms were cavernous syndrome in 9 cases, and bleeding from the nose, hydrocephalus and paresis of lower cranial nerves each in 1 case. It was incidentally discovered in 2 cases, while manifesting itself with subarachnoid hemorrhage only in 1 case. Direct operation (clipping) was done wherever it was feasible, with 3 cases treated so far by this method. The next best surgical procedures were ST-MC anastomosis + internal carotid ligation, these were done in 3 cases, and common carotid ligation was performed in 4 cases. In cases treated by non-surgical mean, death due to rupture oc-curred in as many as 3 cases. CT scan performed an important role in dignosis. Histopathologic findings suggested that an intracranial aneurysm gradually enlarges to attain a huge size through repeated clot-formation within aneurysm, organization of the clot and fresh bleeding into aneurysm.

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The location of a hematoma in the internal capsule (IC) was diagnosed using CT scan. However, the changes in the function of the nervous system caused by the hematoma are hard to evaluated even by using CT scan.
Somatosensory evoked potential (SEP) have been used for the evaluation of the functions of diseases of the central nervous system.
The following experiments are designed to examine the changes in the nervous function caused by types of lateral hematomas in the IC. Eleven adult mongrel dogs were used in this series of experiments. An intracerbral hematoma was made laterally to the internal capsule by an injection of 2 ml of homologous blood in each animal. The SEP and intracranial pressure (ICP) were monitored before and for six experimental hours after making the lesion. Systemic blood pressure and respiratory movements were also simultaneously monitored. The location of the hematoma in each dog was examined in detail by continuous coronal sections of the brain.
The types of hematomas were classified into three groups according to the degree of their invasion into the IC : Group I; a hematoma situated laterally to the IC with some brain tissue remaining between them, Group II; a hematoma invading partially into the IC and Group III; the same as Group I except accompanied by petechial hemorrhages. Significant P₁ waves of SEP with their peak latency at ca 22 ms were observed during the control stage and were considered to be indicators of the nervous function. In Group I, P₁ was largely within the normal range except at five hours where a significant prolongation of the peak latency occurred. ICPs were normal or slightly increased in this group. The frequency of the disappearences of P₁ was the highest in Grouo II. However, the wave appeared again transiently throughout the six experimental hours in spite of a gradual increment of ICP which was the highest in this group. In Group III, P₁ suddenly disappeared after four to five experimental hours. ICP increased moderately.
The function of the nervous system seemed to be impaired by the degree of the invasion of the IC by the hematoma. Three representative types appeared with changes of SEP. A recovery of P₁ generally within six hours. This was independent of increases in ICPs. From this, it appear that disappearences of P₁ were probably caused by ischemia rather than by compression at the IC. Pressure waves appeared frequently with the invasion of a hematoma into the IC in Group II, without relation to the appearence of P₁·SEP was very useful in the evaluation of the function of nervous system by the lateral type hematoma in the IC.

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The effect of S-adenosyl-L-methionine (SAM) on ischemic changes in cerebral energy metabolism was studied. Male dd-mice weighing 25-28 g were used. The animals were injected with 100 mg/kg of SAM intravenously. After 30 min, they were decapitated and at interval of 10 or 30 sec the heads were frozen in liquid nitrogen. The cerebral concentrations of phosphocreatine, ATP, glucose, glycogen and lactate were determined with the enzymatic fluorometric methods described by Lowry et al. from the changes in the concentrations of phosphocreatine, ATP, glucose and glycogen, the rate of cerebral high energy phosphate utilization was calculated. In control, decapitation produced immediate decrease in the levels of phosphocreatine, ATP, glucose and glycogen and increase in lactate level. In SAM-treated mice, the cerebral glucose level was significantly higher than in control at the time of decapitation, while there was no change in the other metabolites. After decapitation the cerebral levels of phosphocreatine, ATP, glucose and glycogen were higher than in control. The rate of cerebral high energy phosphate utillization during 10 sec after decapitation in SAM-treated mice fell to 77.1% of that in control. It is suggested that SAM improved the cerebral energy metabolism on ischemia and that SAM may be of clinical use in the treatment of stroke.

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Local cerebral blood flow (LCBF) was quantitated by a method of xenon enhanced computer assisted tomography (Xe-CT) and its methodological problems were assessed. The materials consisted of 7 healthy controls and 9 patients with cerebral infarctions. The optimal concentration of xenon gas was found to be approximately 50% derived from data on xenon enhanced rate, signal to noise ratio and known anesthetic effects of xenon gas. A method of inhalation technique of short duration was designed for making it less traumatic. Scan interval was set every 1 minute in early phase of inhalation following by every 5 minutes thereafter. The scan data were treated by exponential curve fittings as modified from the autoradiography method. The results disclosed that measurements of LCBF in basal ganglia and thalamus were reasonably accurate by 6 minutes inhalation. By this method a mean value of LCBF of basal ganglia in healthy controls was 85.7 + 19.3 ml/100 g/min correlating well to a mean value of 94.8 + 17.4 ml/100 g/min as derived from actual saturation curves. The calculation of LCBF was considered most reliable from the aspects of effciency of scanner and of radiation dose when xenon built-up curves were selected for calculations of in vivo autoradiography.

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Cerebral apoplexy sometimes recurs in patients who have previous history of hypertensive cerebral hemorrhage. However, the recurrent attacks include not only cerebral hemorrhage, but also considerable number of cerebral infarction. There are few clinical reports of recurrent hypertensive cerebral hemorrhage.
Authors experienced two rare cases of recurrent hypertensive cerebral hemorrhage in the same basal ganglia. Cases were presented and clinical characteristics, CT findings and pathophysiology of this condition were discussed.
Case 1
A 61-year-old male with hypertension and diabetes mellitus was admitted to our clinic because of right hemiparesis and speech disturbance. CT scans showed hypertensive cerebral hemorrhage in the left basal ganglia. An emergency operation was performed and his neurological deficits improved postoperativly. He was readmitted 5 years later with exacerbation of the right hemiparesis and speech disturbance. CT scans and cerebral angiogram revealed hypertensive hemorrhage in the same basal ganglia. He was medically treated with marked improvement of hemiparesis and speech disturbance.
Case 2
A 60-year-old female with heart disease was admitted to Ube Kosan Central Hospital because of left hemiparesis and perioral sensory disturbance. CT scans and cerebral angiogram showed hypertensive cerebral hemorrhage in the right basal ganglia. She was medically treated with good recovery of hemiparesis. She was readmitted 5 years later with exacerbation of left hemiparesis. CT scans revealed hypertensive cerebral hemorrhage which recurred in the same basal ganglia. She was medically treated with left residual hemiparesis.

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This study deals with the metabolism of neutral lipids in experimentally produced cerebral infarcts in rats. A biochemical analysis of the lesions was carried out chronologically at various stages of the lesions in order to know what constituents of the neutral lipids are present and also to know where and how the neutral lipids are metabolized in the pathological conditions.
The results lead us to the following conclusions;
1. Neutral lipids that were increased in the lesions were made up of cholesterol esters (ChE), free fatty acids (FFA) and triglycerides (TG). The accumulation of ChE was most prominent at 14 days old infarcts, occupying up to 14% of the total amounts of the lipids. Further, both ChE and FFA remained in considerably high amounts at 40 and 100 days old infarcts, when the lesions were well healed.
2. Lipid analysis in macrophages isolated from the lesions suggested that the neutral lipids were mainly metabolized in these cells especially at the early stage of the infarcts, and also suggested that the increase of the neutral lipids in pathological condition depends upon the metabolic activity of macrophages.
3. There was a considerable difference in fatty acid composition of ChE between recent and old infarcts. ChE in old infarcts had a relative high ratio of longer chained fatty acids ranging from C22 to C28 as compared with the recent ones. It might be therefore concluded that the variations of fatty acid composition of ChE are related to the stage of the injury; namely, the older the lesions the higher the ratio of longer chained fatty acids to the total amounts of fatty acids of ChE is obtained.
4. Increased neutral lipids appear to have an important effect on the evolution and healing process of cerebral infarcts.

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The difference in the values of cerebral blood flow (CBF) as determined by two nonivasive methods, i.e., the 133-xenon inhalation method and the 133-xenon intravenous injection method (IV method), was analyzed in 12 subjects with the mean age of 58 years (range 36-84). Two serial measurements were done on the same day with an interval of 12 to 25 minutes in 11 subjects. The blood flow of the fast compartment (gray matter) of the brain (F₁) was calculated as well as the initial slope index (ISI), the relative weight (W₁) and the fractional flow (FF₁ ) of the fast compartment.
The mean value of the hemispheric F₁ in the IV method (71.5±10.8ml/100g brain/min) was significantly higher than that in the inhalation method (64.3±7.3), whereas the mena value of the hemispheric W₁ in the IV method (39.3±4.2%) was significantly lower than that in the inhalation method (41.3±3.9). In order to clarify whether differences are due to the unreliability in estimating the arterial concentration curve from the exhaled air curve, direct arterial sampling as well as exhaled air counting after the introduction of 133-xenon was done in 4 other subjects with normal arterial gas values. A distinct difference between the two curves was found in 4 out of 4 in the inhalation method and in 3 out of 4 in the IV method. It is concluded that (1) there is a difference between the concentration curves in the arterial blood and in the expired air after 133-xenon inhalation as well as after 133-xenon intravenous injection, even if there is no obvious pulmonary function disturbance and no abnormality in the arterial gas tensions, and (2) the differences in F₁ and W₁ as determined by the two noninvasive methods may be explained by the observed difference of the two concentration curves.

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B-mode real-time ultrasonsgraphy using a linear array electronic scanner with 5 MHz transducer was employed to image atheromatous plaque in the carotid bifurcations of one hundred and eighty three patients with cerebral infarctions, transient ischemic attacks (TIA), diabetes mellitus (DM), hyperlipidemia, and hypertension. In twenty nine patients with cerebrovascular diseases, forty nine carotid arteriographies were performed. The quality of the carotid sonograms were classified to eight categories, i.e., type 0; normal, type I; tiny plaque (diameter below 2 mm), type IIa; bow shaped plaque with smooth surface, type IIb; bow shaped plaque with irregular surface, type IIIa; flat and rectangular plaque with smooth surface, type IIIb; flat and rectangular plaque with irregular surface, type IV; nodular plaque and type V; obstruction.
In comparison with arteriography, for detection of normal vessels, stenotic lesions and obstructions, sonographic accuracy was 80%, 100% and 67% respectively. The detection rate of carotid plaque in each disease was as follows; 67% in cerebral infarction, 73% in TIA, 50% in DM, 45% in hyperlipidemia, 32% in hypertension and in 7% in healthy controls. In healthy controls and patients with hypertension, carotid plaques consited of type 0 and type IIa. In patients with DM and hyperlipidemia, type IIIa and type IIa was the most noticeable respectively. In cotrast to findings in subjects who had no strokes, carotid arteries perfusing diseased hemispheres in patients with cerebral infarction and TIA had plaques of type V and IV and plaques with irregular surfaces predominantly.
These data suggested that non-invasive detection of morphological characteristics of carotid plaques could be of considerable value in the assessment of severity of macroangiopathy in patients with stroke prone diseases and in the management of patients with cerebrovascular diseases.

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Internal carotid artery (ICA) occlusion presents a broad spectrum of clinical manifestations ranging from death due to extensive infarction to absence of neurological deficit and infarction.
In order to evaluate the relationship between the obstructive mechanism of ICA occlusion and the effect of this phenomenon on cerebral parenchyma, both CT scans and angiograms of forty-eight cases of ICA occlusion (eighteen cases of embolism and thirty of thrombosis) were reviewed. The size and location of low density areas (LDA), the presence of mass effect and the responce to contrast enhancement demonstrated on CT scans were analysed in relation to angiographic findings. About 90% of these cases demonstrated various sizes of LDA on CT. In this study, a large infarction was defined as LDA larger than 2/3 of the hemispheric area and a small infarction as LDA smaller than 1/3 of the hemispheric area. 61% of patients with embolism presented with large infarctions, with many being total infarctions of the cerebral hemisphere or middle cerebral artery (MCA) territory. On the contrary, small infarctions accounted for 67% of thrombotic cases. Most of them were partial infarctions of MCA territory; other small infarctions were distributed in various regions including watershed infarctions (27% of thrombotic cases). The frequency of mass signs was higher in embolism (78%) than in thrombosis (17%). Contrast enhancement was seen in 97% of embolic cases and 44% of thrombosis.
Angiograms, mostly performed within one week after the onset of attack, revealed that collateral circulation (CC), which was derived from three major routes, was present in various combinations, i.e.
1) CC via the circle of Willis (CW) was present in 66.7% of the thrombotic cases. Good filling of both the anterior and middle cerebral arteries from the contralateral ICA was seen in 16 cases. Embolism had the same percentage, although good filling was seen in only half of the cases.
2) CC via the ophthalmic anastomoses was present in 36.7% of the thrombotic cases and 11.1% of the embolic cases.
3) CC via the leptomeningeal anastomoses was present in 53.4% of the thrombotic cases and 44.4% of the embolic cases.
The analysis of the CT scans correlated with the angiograms, leading to the conclusion that the size of the infarcted area depended on the degree of collateral flow and that the CC of embolism mainly relied on CW. Therefore, cases with sufficient collateral flow developed either no or minimal infarction. In contrast, absent or insuffcient collateral flow through the CW resulted in a large infarction in spite of the presence of collateral flow from the other routes.
In thrombosis, the role of collateral flow from the CW seemed not to be as important as in embolism. Six cases failing to show collateral flow through the CW developed small infarctions with the presence of collateral flow from other routes.
A higher frequency of intracranial occlusio-supra-occlusioneum and propagation of secondary thrombosis distal to the occlusion in embolism may be attributed to the extension of infarction due to reduced collateral flow.

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A new form for differential diagnosis between cerebral hemorrhage and cerebral infarction was developed by application of the quantification theory group 2.
Clinical histories, symptoms and signs within 72 hours after stroke were analyzed in 43 cases of cerebral hemorrhage and 78 cases of cerebral infarction whose diagnoses were established by CT scan. Other 36 cases of cerebral hemorrhage and 63 cases of cerebral infarction were used for external check.
The analysis of the data using a personal computer revealed that the following 12 items were most contributory to the diagnosis; age, past history of TIA and/or RIND, past history of cerebral hemorrhage and/or cerebral infarction, past history of heart disease, vomiting, bladder disturbance, diastolic blood pressure, convulsion, stiff neck and/or Kernig's sign, extraocular movement, and light reflex. The weight of each category in these items was computed, and the sum of the weights was calculated as a score in each case to determine the discriminant point between cerebral hemorrhage and cerebral infarction. The form was made to simplify the calculation of the sample scores. The differential diagnosis was determined by comparing the sample score to the discriminant point.
The rates of correct diagnosis in internal check were 90.7% (39/43) for cerebral hemorrhage and 87.2% (68/78) for cerebral infarction. Those in external check were 80.6% (29/36) for cerebral hemorrhage and 79.4% (50/63) for cerebral infarction.
The result indicates that the present method seems to be superior to previous ones with respect to the accuracy of diagnosis.

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Lobar intracerbral hemorrhage with speical reference to amyloid angiopathy was investigated clinicopathologically in 2181 consecutive autopsied cases above 60 years of age (aged 60 to 106 years, with a mean of 77.4 years).
The result were as follows;
1) Spontaneous intracerebral hemorrhages were observed in 230 cases (10.5%) with 35 cases of multiple hemorrhage. The lobar type was found in 39 cases (17.0%) of intracerebral hemorrhage.
2) The causes of lobar hemorrhage consisted of hypertension in 14 (35.8%), amyloid angiopathy in 8 (20.5%), neoplasm in 6 (15.4%), hemorrhagic diathesis in 4 (10.3%), rupture of aneurysm in 3 (7.7%), vascular malformation in 1 (2.6%), and unknown etiology in 3 cases (7.7%).
3) Among 8 cases with lobar hemorrhage due to amyloid angiopathy, aged 71 to 92 years, 3 male and 5 female, dementia was present in 5 cases, and hypertension in 3 cases. Neuropathologically, hemorrhages involved the cortex to the white matter, with dissection into the subarachnoid space. Multiple lobar hemorrhages were found in 4 cases, and small cortical infarction in association with amyloid angiopathy, frequently multiple, was observed in 5 cases. Amyloid angiopathy was seen in small arteries and atrerioles of the meninges and cortex of the cerebrum, occasionally of the cerebellum, but was not entirely seen in subcortical white matter. Additionally, amyloid angiopathy in the basal ganglia and brain stem was observed only in 1 case. Five cases with dementia were pathologically classified in 3 types; that is, vascular dementia in 3, mixed type in 1, and Alzheimer type in 1 case.
In conclusion, amyloid angiopathy is an important etiological consideration for lobar intracerebral hemorrhage in the aged. Cerebral hemorrhage due to amyloid angiopathy is characterized by the lobar type involving the cortex, with direct extension into the subarachnoid space, frequently multiple hemorrhages and complicated with cortical infarctions, in elderly patients without risk factors. dementia is not necessary present, and if present, dementia of the vascular type shoud be taken into consideration.

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The effects of blood glucose on brain tissue metabolism and blood flow were studied in 3-hour incomplete cerebral ischemia induced by bilateral carotid ligation in spontaneously hypertensive rats (SHR). Prior to cerebral ischemia, blood glucose levels were varied by intraperitoneal injections of 50% glucose (hyperglycemia), 8% NaCl (normoglycemia) or insulin + 8% NaCl (hypoglycemia). Lactate, pyruvate and adenosine triphosphate (ATP) concentrations in the supratentorial brain frozen in situ were measured by the enzymatic method. Local cerebral blood flows (CBF) in the parietal cortex and thalamus were measured by the hydrogen clearance method before and after carotid ligation. Brain metabolites and blood flows were also determined in sham-operated, non-ligated SHR with various blood glucose levels.
Supratentorial lactate in ischemic brain increased more greatly in hyperglycemia (34.97±1.29 mmol/kg) than normoglycemia (23.43±3.13 mmol/kg) (p<0.005), although cerebral ATP decreased to a similar extent in both groups. In contrast, cerebral lactate as well as pyruvate was less markedly increased in hypoglycemia (7.20±1.54 mmol/kg) as compared with those in normoglycemia (p<0.001), but reduction of ATP was greater in the former (0.45±0.05 mmol/kg) than the latter (1.04±0.25 mmol/kg), of its difference being significant (p<0.05). In non-ischemic brains, there were no differences of cerebral metabolites among three glycemic groups of animals. Cortical CBF was pronouncedly decreased to approximately 10% of a pre-ligated value immediately after, and further to less than 1% at 3 hours after carotid ligation, nevertheless blood glucose levels. Thalamic CBF was similarly but less markedly reduced during cerebral ischemia in all animals.
It has been reported that hyperglycemia is vulnerable to brain metabolism in complete cerebral ischemia, presumably due to hyperglycemia-induced lactic acidosis of the brain. In complete ischemia as demonstrated in the present study, however, brain energy metabolism was maintained in hyperglycemia as much as normoglycemia, although an increase in lactate was significantly greater in the former. It was indicated that increased blood glucose level might be beneficial rather than vulnerable to brain metabolism in incomplete ischemia. On the other hand, hypoglycemia of even moderate degree caused more severely impaired energy metabolism of the brain because of an insufficinet supply of substrate to ischemic brain.

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The influence of blood glucose levels on the light (LM)- and electron-microscopic (EM) changes of the cerebral cortex was studied in 3-hour incomplete cerebral ischemia in spontaneously hypertensive rats (SHR). Prior to cerebral ischemia, blood glucose levels were varied by intraperitoneal injections of 50% glucose (hyperglycemia), 8% NaCl (normoglycemia) or insulin + 8% NaCl (hypoglycemia). The brains were fixed by perfusion with formaldehydeglutaraldehyde mixture at 3 hours of cerebral ischemia rendered by bilateral carotid artery occlusion (ischemic group) and of sham operation (non-ischemic group).
There were no abnormal LM and EM findings of the cerebral cortex of non-ischemic animals with various glucose levels. In contrast, LM examinations of the ischemic brain of various glucose levels showed cellular shrinkage and cytoplasmic vacuoles of the neurons, empty perineuronal spaces and rough appearance of neuropils. Electronmicroscopically, ischemic tissue revealed shrunken neurons with swelling of rough endoplasmic reticulum and ballooning of perineuronal astrocytes. These deleterious changes of the cerebral cortex were most strikingly exaggerated in hypoglycemic animals as compared to hyper- and normoglycemic ones.
It is concluded that hypoglycemia exaggerated structural alterations of ischemic brain, and that hyperglycemia never worsen structural alterations of the brain than those observed in normoglycemic animals in this animal model of cerebral ischemia.

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A 77-year-old woman with a history of valvular heart disease, atrial fibrillation and a massive infarction in the right cerebral hemisphere developed contralateral infarction due to occlusion of the internal carotid artery. A string-like structure with higher density than normal brain was demonstrated on non-enhanced computed tomography that was performed in the acute stage. This abnormal structure seen in the left hemisphere was thought to be consistent with the middle cerebral artery trunk of the affected side. Seventeen days after the onset, the abnormal structure was no more visuslized on non-enhanced CT.
These findings suggested that the abnormal structure with increased density was compatible with thromboembolus or intraluminal clot formed in the distal part of the occluded internal carotid artery. An importance of this finding as a diagnostic sign of the cerebral arterial occlusion was discussed.

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The mechanism responsible for the reduction of contralateral cerebral blood flow (CBF) and metabolism in early stage of unilateral hemispheric infarction in man has not been fully understood.
In order to investigate the above mechanism influences of unilateral global ischemia in 107 gerbils on contralateral CBF, water content, electrolytes and glucose metabolism were investigated.
Thirty minutes after ligation of the right common carotid artery, ipsilateral CBF decreased to less than 20ml/100g brain/min. Both water content and Na : K ratio increased and these changes were significantly correlated with the reduction of CBF.
In the contralateral hemisphere, CBF decreased from 51.0±7.9 to 42.3±11.4ml/100g br./min and water content increased significantly as early as thirty minutes after the ligation, but the Na : K ratio did not change during this period. Since the degree of the reduction of contralateral CBF was not large enough to produce brain edema by ionic disturbance, the increased water content of the contralateral hemisphere must be attributed to factors other than ionic disturbances.
Semiquantitative measurements of contralateral glucose utilization rate (GUR) by ¹⁴C-deoxyglucose showed two different patterns depending on severity of the ischemic symptoms.
In the animals with the mild or moderate symptoms, contralateral cerebral GUR did not change as compared with the control animals. On the contrary, in the animals with the severe symptoms, regions with an increase of GUR was observed in the contralateral hemisphere.
In conclusion, the contralateral reduction of CBF observed in the early phase of the unilateral ischemia was not always accompanied by the suppression of glucose matabolism. The above data are inconsistent with the “diaschisis” hypothesis where the transneural inhibition of metabolism is considered to be prerequisite to the reduction of contralateral CBF.

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To demonstrate the presence, or absence, and the nature of the vulnerability differences in hippocampal neurons at early stages of ischemia without recirculation, immunohistochemical study with antiserum to tubulin was performed on the brains of Mongolian gerbils obtained 5 min to 3 hours after unilateral occlusion of the posterior communicating artery. It has been demonstrated by the previous studies that the occlusion of this vessel causes severe and constant ischemia in the hippocampus, and that disappearence in immunoreactivity of tubulin can be a sensitive indicator for neuronal involvement in cerebral ischemia. During the 3-hour period of ischemia alterations in immunoreactivity of tubulin were more readily produced in the pyramidal cells of the sector CA1 than in those of other sectors; in dendrites of strata oriens et radiatum than in those of alveus and strata lacunosum et moleculare; in neurons of the pyramidal layer than in those of strata oriens et radiatum. Additionally, segmental preservation of tubulin immunoractivity along the small vessels was noted in sectors CA1-2 at 3 hours of ischemia.
The present study demonstrated various kinds of selective vulnerability in hippocampal neurons in the acute stage of ischemia. It was supposed that the observed differences in vulnerability may be associated with a number of unconfirmed factors such as regional differences in neuronal characteristics, differences between neuronal types, or inhomogeneity of partially restored tissue blood flow.

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A case of cryptic AVM ruptured during disseminated intravascular coagulation (DIC) was reported.
The patient was 36 years old female, who was suffered from massive sexual bleeding, fever and patchy cutaneous hemorrhage three days after dilatation and curratage. She suddenly complained of severe headache and fell to drowsiness four hours after the treatment of DIC. CT revealed high density area at the left parietooccipital region, and vertebral angiogram showed early venous filling from the left parietooccipital artery. DIC score was 12 points according to the criteria of the Ministry of Health and Walfare. The patient was carefully treated with whole fresh blood, heparin and glycerol. When DIC score was improved to 5 points, left parietoocipital craniotomy was performed for removal of hematoma and AVM without significant bleeding. Postoperative course was uneventful and the patient was discharged without neurological deficits.

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A case of bacterial intracranial aneurysm which was successully treated with only antibiotics therapy is described.
A 49 year-old man was admitted because of sudden onset of weakness in the left arm and foot. During preceding two months, he had fever of unknown origin. Physical and neurological examination on admission revealed diastolic murmur over the aortic area, stuporous consciousness and left hemiplegia. CT-scan showed high density area in the right frontoparietal region. Blood culture yielded Streptococcus faecalis, and he was treated with appropriate antibiotics. A right carotid angiogram showed a saccular aneurysm of a peripheral branch of the right middle cerebral artery. Repeated angiography 11 weeks later showed resolution of the aneurysm.
Review of the literature suggests that resolution of bacterial intracranial aneurysm by antibiotics therapy is more common than previously suspected. The mechanism of resolution of bacterial intracranial aneurysm is discussed.

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A 61-year-old man who had been hypertensive for 10 years, was admitted to the National Cardiovascular Center, because of acute onset of tetraplegia and slight impairment of consciousness. He was diagnosed as wide-spread brain stem infarction with occlusion of the basilar artery, and his neurological manifestations are compatible with those of “locked-in syndrome”. During the course, Cheyne-Stokes respiration of a short cycle, of which period was within thirty seconds, and “sigh and rest” respiration were observed in the acute, and in both acute and chronic stage, respectively. “Sigh and rest” respiration was characterized by a single episodic deep inspiration followed by a respiratory arrest for 10 to 20 seconds during a regular respiration.
The pathogenesis and pathophysiology of these abnormal respirations were investigated by combinations of neurophysiological, neuro-otological and neuro-radiological examinations.
From the present study, it is suggested that Cheyne-Strokes respiration of a short cycle is caused by the extensive damage of bilateral basis and tegmentum of the pons including its lower level close to the medulla oblongata. Partial damage of the pontine tegmentum with extensive destruction of the basis pontis on both sides appears to cause “sigh and rest” respiration.
To recogniz the presence of these abnormal respiratory patterns provides an important information on the local diagnosis in the brain stem infarction.

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A 59-year-old man was admitted to the hospital because of conscinousness disturbance. He was in agitated delirium, and was noted to have spastic tetraparesis, left central facial palsy, cortical blindness, left oculomotor palsy, down and medial deviation of the right eye, and “hyperkinetic mutism”.
CT scan showed extensive infarction in the left temporal lobe including hippocamous and temporal stem, bilateral occipital lobes, whole the left thalamus, and left half of the midbrain. About one month later, these lesions became hemorrhagic. These neurological findings persisted since his death of two years later. Judging from these neurological findings and location of the lesions, this case was regarded as the “Top of the basilar syndrome” of Caplan.
This case had such unusual finding that whole the unilateral thalamus was destructed because of infarction. The relation between the thalamic vascular supply and the mechanism producing total thalamic infarction was discussed.

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