The purpose of the present investigation was to study the effect of carteolol on blood pressure, regional cerebral blood flow and cardiac output in experimental middle cerebral artery (MCA) occlusion.
Nine rabbits were anesthetized with nitrous oxide, underwent 3 hours of right MCA occlusion. Five rabbits were untreated. Four rabbits were given carteolol (300 μg/ml saline) 30 μg/kg through the auricular vein immediately after MCA occlusion. The rCBF was measured by a laser doppler flowmeter, cardiac output was measured by thermodilution (1 ml bolus of iced water) and blood pressure with a transducer through the catheter introduced into the auricular artery.
Arterial blood pressure was significantly reduced at 2 hours after the occlusion and administration of carteolol, and had decreased about 15% at 3 hours, in the treated group. Cardiac output remained the same in both the treated and untreated groups. The rCBF decreased 5070% at 1 hour after MCA occlusion in both groups and recovered slightly in the treated group at 3 hours.
These results indicate that mean arterial pressure is reduced, but the rCBF is not reduced, by a pharmacological beta adrenergic blockade with carteolol in the acute stage of cerebral ischemia.

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Specific problems for patients on prolonged hemodialysis who suffered from cerebrovascular diseases are bleeding tendency due to either systemic heparinization or potential platelet dysfunction, and progressive brain edema as a result of dialysis dysequilibrium syndrome. We report ten patients on hemodialysis who developed intracerebral hemorrhage or subarachnoid hemorrhage. Mortality was very high in cases with intracerebral hemorrhage. Immediate initiation of hemodialysis with slow blood flow, and use of DDAVP, blood transfusion or administration of hyperosmotic dehydrating agents are recommended for treatment of such patients.

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Nine patients with lesions in the territory of the anterior cerebral artery (ACA) and 18 patients with other cerebral lesions were examined. All of the patients were usually writing with their right hands. They were requested to write replies to verbal questions, to take dictation or to copy with their left hand and to perform bimanual coordination tasks. Four patients out of 9 with ACA lesions presented pathologic left-handed mirror writing and mirror movements during bimanual coordination. None was accompanied by left-handed apraxia or agraphia, and one patient presented a grasping reflex in his left hand. Copying characters was done without difficulty with either hand without evidence of mirroring. Their corresponding lesions on CT scan involved the right supplementary motor are a and partially the anterior cingulate gyrus. Left-handed mirror writing ceased within several months in 3 patients, but in one patient whose CT lesion contained the entire right 6 Brodmann's area it continued for more than two years. In contrast, only one patient out of 18 who had a single cerebral lesion other than ACA territory showed left-handed mirror writing, and the symptomatology of his mirror writing presented no difference from that of the ACA lesions. Five patients with ACA lesions didn't present any mirror writing. Four of these patients had left-sided lesions and one was a right-sided lesion containing corpus callosum.
When the right supplementary motor area is destroyed and if a motor program such as writing or praxis to verbal commands that is organized predominantly by the left hemisphere is executed by the right primary motor area without non-mirror transformation, then mirror movements of the left hand will occur. Similarly in bimanual coordination tasks, the left hand will behave in a mirror fashion to the right because the right primary motor area receives only untransformed motor programs originating from the intact left supplementary motor area.

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We report results of B-mode ultrasonic and doppler flowmetric studies on patients with various forms of cerebral infarction. The subjects of this study consist of 49 patients with cerebral infarction (thrombosis; 38 and embolism; 11) and 15 control patients without cerebral infarction or risk factors for cerebrovascular accidents. Atherosclerotic lesions in the extracranial carotid arteries were found in 77% of the patients with large artery thrombosis, in 58% of those with lacunar infarction, in 11% with Binswanger-type infarction, 12% with infarction in the vertebrobasilar territory, and 18% of those with cerebral embolism.
Incidence of these atherosclerotic lesions among the patients with cerebral thrombosis was much higher than that among those with cerebral embolism. The sensitivity of the B-mode ultrasonography in detecting these atherosclerotic changes was much higher than that of intravenous disital subtraction carotid angiography. In addition, the magnitude of carotid stenosis and occlusion was more precisely evaluated by the doppler flowmetry than angiography. The velocity of the carotid blood flow was significantly increased in the stenotic portion as compared with the contralateral side. On the other hand, the end-diastolic blood flow velocity was decreased in the acute stage of the patients with cerebral embolism. In contrast, that of those with cerebral thrombosis was unchanged. Thus, this may be used as an indicator to differentiate embolism from thrombosis. In conclusion, B-mode ultrasonic and doppler flowmetric evaluation of extracranial carotid arteries is an useful and noninvasive method for patients with cerebral infarction.

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An effect of local intraarterial fibrinolytic therapy with urokinase was evaluated in 15 patients with acute cerebral arterial occlusion (16 times). CT scans on admission demonstrated no low density lesions in all patients. Urokinase (UK) was infused nearly to the occlusion site through 3F Tracker-18 catheter 3.5-9.0 hours (mean 5.8 hours) after the onset of symptoms. The amount of UK ranged from 240, 000 to 1, 500, 000 units in each procedure. The sites of arterial occlusion were on the middle cerebral artery in 13 patients, on the basilar artery in 2 and on the internal carotid artery in one. Recanalization of the occluded arteries occurred immediately after the infusion on therapy in 12 of 16 procedures. Clinical symptoms recovered immediately after the infusion in 11 cases and gradually disappeared at the time of discharge in 7 cases. CT scans following the infusion therapy revealed hemorrhagic infarction in 3 patients who had received the therapy more than 6 hours after onset, but these lesions did not cause further deterioration of symptoms.
It has been suggested that superselective intraarterial UK infusion through 3F Tracker-18 catheter may be effective for patients with acute cerebral arterial occlusion, if the indication for the therapy is strictly, made.

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It is well known that the acute phase response to tissue injury is manifested by increased synthesis of acute phase reactant proteins (APRPs) at the liver, which is mediated by cytokines. APRPs in subarachnoid hemorrhage (SAH) have not been thoroughly studied. We investigated the chronological changes of serum APRPs in 70 patients with SAH in order to determine how much APRPs correlate with the severity of initial clinical findings and hemorrhage on CT, and with the clinical outcome. None of the patients had steroid therapy, liver dysfunction, infections, malnutrition, or immune disease in the past and during the course of the study. Blood samples were taken on the 1st, 4th, 7th, 14th and 21st day after the catastrophe. APRPs examined were serum total protein (TP), albumin (Alb), alpha 1-acid glycoprotein (α1-AG), alpha 1-antitrypsin (α1-AT), alpha 2-macroglobulin (α2-MG), immunosuppressive acidic protein (IAP), interleukin-1 alpha (IL-1α) and tumor necrosis factor-alpha (TNF-α). As results, TP, Alb and α2-MG were depressed, and α1-AG, α1-AT, IAP and CRP were elevated throughout the study. Patients could be considered to be immunosuppressed from the early phase of SAH, because immunosuppressive agents like α1-AG, α1-AT and IAP were raised soon after the catastrophe. Further, α1-AG, α1-AT, IAP and CRP tended to be higher in patients with Hunt & Kosnik (H & K) III, IV, V grades, Fisher III, IV groups or dead outcome than in those with H & K I, II grades, Fisher I, II groups or good recovery. In other words, patients with bad clinical and CT findings or dead outcome tended to have high APRP levels. The acute phase response remained at least for 3 weeks. There was no any relationship of APRP changes with age, site of aneurysm, and presence or abscence of vasospasm and operative intervention. Neither IL-1α nor TNF-α was detected in any patient, presumably because of a short half-life time or very low undetectable circulating amounts. These results suggest that a follow-up study of serum APRPs is useful laboratory marker reflecting the degree of acute phase response after SAH, and becomes new adjunct data to understand the nature of SAH.

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Anticardiolipin antibodies (ACA) are recently recognized to be enhanced risk of thrombosis including cerebral infarction. However, there are no available data concerning the profile of clinical and laboratory findings in patients without evidence of collagen disease who suffered cerebral infraction with positive ACA. The purpose of this study was to clarify the clinical and laboratory features of these patients. ACA was measured by enzyme linked immunosorbent assay (ELISA) in 72 consecutive patients affected by cerebral infarction without collagen diseases.
Among 72 patients, ACA was positive in 15 (21%), including 9 males and 6 females. These 15 patients had at least one risk factor for cerebral infarction, such as hypertension, diabetes, hyperlipidemia, smoking history, atrial fibrillation, valvular heart disease, but none of them showed thrombocytopenia. The mean age of ACA-positive patients when they had the first attack of stroke was significantly younger than that of ACA-negative patients (55 ± 15 years versus 66 ± 12 years, p<0.05). In 15 ACA-positive patients, 8 (53%) had a history of recurrent cerebral infarcts, and that was more frequent than patients without ACA (13/57, 23%) (p<0.05). Hypertension was rarer in patients with ACA (3/15, 20%) than in those without ACA (37/57, 65%) (p<0.05), while the prevalence of atrial fibrillation and/or valvular heart diseases was significantly higher in ACA-positive patients (8/15, 53%) than in ACA-negative patients (12/57, 20%) (p<0.05). In platelet function tests, platelet factor 4 was significantly higher in patients with ACA than patients without ACA (54.6 ± 32.0 ng/ml versus 22.3 ± 23.6 ng/ml, p<0.05). In the molecular markers of coagulation and fibrinolysis system, D-dimer, fibrinopeptide Bβ_15-42, thrombin-antithrombin III complex were significantly higher in patients with ACA than in controls, but not than in patients without ACA.
In conclusion, the presence of ACA in patients with cerebral infarcts without collagen diseases, is associated with early and/or recurrent onset of cerebral infarction and higher prevalence of heart diseases. Platelet activation was suggested to contribute the pathogenesis of cerebral infarction in ACA-positive patients.

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The authors has experienced 3 cases of moyamoya disease with sudden onset of intraventricular hemorrhage, which showed the focal neurological signs as hemiparesis or aphasia without the evidence of hemorrhage or infarction in the area of responsible cerebral lesion. In case 1, hypertensive hydrocephalus was recognized at the time of developing the focal neurological signs, and these signs were disappeared along with the improvement of hypertensive hydrocephalus by cerebrospinal fluid drainage and shunt surgery. The focal neurological signs may be produced by the decrease of perfusion pressure in the area, where has been threatened from chronic ischemic condition in moyamoya disease.
In case 2 and 3, although we could not deny the hypertensive hydrocephalic stage, we could followed up these cases without the treatment of hydrocephalus. However, at the time when the focal neurological signs developed, EEG and single photon emission computerized tomography (SPECT) demonstrated the electro-physiological dysfunction and the decrease of cerebral blood flow in the responsible cerebral lesion.
In these cases, the focal neurological signs may be produced by the compression of casting like intraventricular hematoma itself, to the area of circulatory vulnerable condition in moyamoya disease.

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The purpose of this study is to examine histological and behavioral changes following the bilateral carotid ligation in normotensive rats. Using male Sprague-Dawley rat, the bilateral common carotid arteries were permanently ligated under halothane anesthesia. One, 2 weeks, 1 month and 3 months after the carotid ligation, serial coronal sections of formalin-fixed brain were stained with H-E or Kluver-Barrela method and microscopically examined. For behavioral study, place navigation taks (Morris's water maze) and step-through type dark avoidance task were performed 1, 2 weeks, 1 month and 3 months after the ischemia. The survival rate within 48 hours after the carotid ligation was above 90% throughout the experiment. Among 46 survivors examined, 31 (67%) showed the development of ischemic lesions. The caudo-putamen was the most frequent site where ischemic lesion was observed in 26 rats (57%). The incidence of ischemic lesion in hippocampus, cerebral cortex or thalamus was 30%, 17% or 13% respectively. Post-operative place navigation taks showed transient impairment of spatial leaning/ memory, whereas pre-operative spatial memory was well preserved. Step-through type dark avoidance task revealed persistent impairment of acquisition and retention of dark avoidance reaction in the ischemic rats. These results indicate that bilateral carotid occlusion can cause considerable neuropathological and behavioral changes and thus may be a useful model for the study of mild global ischemia, particularly in its chronic stage.

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3-Methoxy-4-hydroxyphenylglycol (MHPG) is known to be a major metabolite of brain norepinephrine, and the central noradrenergic activities are presumed to be reflected in plasma and cerebrospinal fluid (CSF) levels of MHPG. We measured plasma and CSF levels of MHPG as well as plasma levels of norepinephrine in patients with acute stroke in order to investigate whether or not the activation of the central noradrenergic system was associated with the increase in activities of the peripheral noradrenergic system. Investigations were made on 42 patients with brain hemorrhage, 35 with brain thrombosis, and 15 with brain embolism. A significant correlation existed between norepinephrine and MHPG in the plasma during the subacute stage (14-28 days after onset). However, during the acute stage (within 72 hours of onset), no correlation was noted except in patients with brain embolism. In 27 patients with brain infarction in whom CSF MHPG was measured, a similar relationship was also observed between the CSF MHPG and plasma norepinephrine levels. These results suggest that in some types of stroke changes in central noradrenergic activities may not always be accompanied by a corresponding degree of changes in the peripheral noradrenergic activities.

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A 46-year-old right-handed man with a 28-year history of hypertension suffered from intracerebral hemorrhage in the right parietal lobe followed by aphasia without other neurological findings. Radiological examinations including positron emission tomography (PET) served valuable information suggesting that this case had crossed aphasia.
In the morning on May 29th, 1989, the patient found himself unable to read numbers and Japanese “kana”. He had no difficulty in reading “katakana” nor “kanji” (Chinese characters), but his repetition and digit span were impaired. Head CT on the next day revealed intracerebral hemorrhage approximately 3 cm in diameter at the right parietal lobe. Magnetic resonance imaging on the 85th day after the onset showed several old small infarcts in the bilateral deep white matter regions. In PET study, cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO₂) in the right parietal lobe decreased by 56% and 60%, respectively, compared to those in the left parietal lobe. There were no other significant lateralities in CBF and CMRO₂ between the two hemispheres. A PET study is an useful tool to detect functional abnormalities, and the measurements of CBF and CMRO₂ gave valuable informations in considering about responsible lesion for crossed aphasia.

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Two cases of multiple hypertensive intracerebral hematomas which occurred simultaneously are presented. The first case is 89-year-old with 10 years history of hypertension. He suddenly suffered from disturbance of consciousness and was admitted with comatose state. A CT scan taken within 4 hours after the onset revealed a large high density area in the right putaminal region and a small high density area in the left putamen with massive ventricular hemorrhage. Considering his age and neurological grading, he was not indicated for direct surgery. However his family asked for surgery, so the aspiration surgery was performed, but 4 days after the onset he died due to acute cardiac failure. The other case is 66-year-old-man with history of hypertension. He was transfered with comatose state. A CT scan taken within 2 hours after the onset disclosed high density areas in the left thalamus, in the right cerebellum and in the brain stem with intraventricular hemorrhage. Bilateral ventricular drainages were performed and he was treated conservatively. However, 11 days after the onset he died.
The incidence of bilateral hypertensive intracerebral hematomas is reported as 1.5% and 9.5%. The advent of CT scan has made it easy to diagnose multiple hypertensive intracerebral hematomas, however, its simultaneous occurrence is still rate.
We collected 27 cases of simultaneously occurring multiple intracerebral hematomas. Twelve cases were male and 15 were female. The age of the patients ranged from 42 to 89 years. Fifty-five hematomas of 27 cases distributed to 26 in putamen, 12 in thalamus and 17 in other regions. The clinical symptoms of multiple hypertensive intracerebral hematomas are severe and prognosis of these patients is poor. The mechanism and indication for surgery of multiple hypertensive intracerebral hematomas were discussed.

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We report on a patient who had intractable partial seizures caused by a cerebral infarction due to embolic occlusion of the right middle cerebral artery. This 74-year-old woman was admitted to our hospital because of a hemiclonic convulsion on the left side. On admission, she was stuporous, and was unable to follow simple commands. There was a conjugate ocular deviation to the left. She had focal clonic convulsions involving the proximal part of the left arm and the left side of the neck and face. An X-ray CT revealed an inhomogeneous low density area in the right frontoparietal, posterior parietal, and occipital regions. Although a cerebral angiography showed no steno-occlusive lesions, findings showing a localized capillary brush and an early venous filling were noted in a territory of the cortical branches of the right middle cerebral artery. These findings suggested recanalization of the once occluded arteries of embolic origin. EEG findings showed background activity during the interictal state consisting of theta or delta activities of 2-5 Hz in frequency, and an amplitude of 20-40 μV. There was a prominent slowing of the background activity over the right hemisphere. Both ictal and interictal EEGs revealed epileptogenic foci in the right frontocentral area. A SPECT scan during a somatomotor seizure demonstrated focal hyperperfusion of the right perirolandic area, with extensive hypoperfusion of the right parietal and occipital areas. Hyperperfusion in the right perirolandic area corresponded to the epileptogenic lesion that was confirmed by the ictal EEG study. Thus, this patient was diagnosed as having status epilepticus of the somatomotor type during the course of a hemorrhagic infarction caused by embolic occlusion of the right middle cerebral artery. Treatment with diphenylhydantoin, diazepam and clonazepam slightly decreased the frequency of seizures. In spite of high doses of medication, her seizures continued to be poorly controlled. Two weeks after the onset of the seizures, they changed from the somatomotor to the psychomotor type, and were accompanied with perioral automatism. During the psychomotor seizures, the patient was stuporous but mumbled continuously without responding to commands. An ictal EEG during the psychomotor seizure revealed the right temporal epileptogenic focus. Ictal SEPCT scans obtained during the psychomotor seizures demonstrated focal hyperperfusion of the right temporal area. According to both EEG and SPECT findings, it was concluded that the right perirolandic focus during the somatomotor seizure shifted to the right temporal area during the psychomotor seizure. In this case, the increase of the local cerebral blood flow and the disruption of the blood brain barrier may have caused the hemorrhagic change that induced the epileptogenic discharge. It is speculated that a persistent increase of the cerebral blood flow might be the secondary phenomenon that was accompanied with status epilepticus. Icatal SPECT scans revealed more exactly the localization of the epileptogenic focus that corresponded with the EEG. SPECT may be suitable for evaluating the localization of the seizure focus in order to confirm surface EEG findings.

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We reported a case of cerebral arteriovenous maliformation (AVM) draining into the primitive callosal vein. A six-year-old man admitted to our hospital for the purpose of treatment of cerebral AVM, after operation of AVM of the lung. His mother was also operated due to cerebral AVM 14 years ago. Cerebral angiography revealed a large aneurysmal dilatation in the left frontal lobe draining into a dilated vein running along the corpus callosum, which were corresponding to the primitive callosal vein. A nidus adjacent to the aneurysmal dilatation was recognized. Other two small AVMs were also seen in the right frontal lobe. This case had multiple cerebral AVMs, and AVMs of the lung. Futhermore, his mother was operated due to cerebral AVMs. It was likely that this case was corresponding to Rendu-Osler-Weber disease.
AVMs draining into the primitive callosal vein seen in this case confirmed that AVMs develop during embryonic life.

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We described a case of Avellis syndrome due to a small lateral medullary infarction demonstrated by magnetic resonance imaging (MRI).
A 59-year-old male presented with sudden onset dysphagia and hoarseness, slight occipitalgia. Neurological examination revealed weakness of left soft palate and vocal cord, mild dysesthesia of right distal upper limb. There was no weakness, definite sensory disturbance, cerebellar ataxia, nystagmus, dizziness, Horner's syndrome, or pathological reflex. MRI showed a small infarction in the left lateral medulla, nearly corresponding to the left ambiguus nucleus and vagus nerve.
Although Avellis syndrome is very rare and used to be diagnosed by clinical and neurological findings, MRI is very useful for revealing the small lateral medullary lesion.

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