In patients with basilar artery thrombosis, initial mild hemisensory or hemimotor deficits with dysarthria may predispose them to severe conditions (such as the locked-in state). Since most infarctions in the brainstem region are due to thrombotic occlusive disease of the basilar artery, anticoagulant therapy may be indicated in these patients when the initial deficit is mild.
Five patients aged 56 to 77 years old who presented with a mild but progressing brainstem syndrome were treated with heparin within the first 12 hours of onset. Before heparin was administered, a CT scan was performed to rule out intracranial hemorrhage. An irregularly shaped ischemic lesion in the brainstem was found on CT or MRI scans in each case on the first day or later. An elevated blood pressure was carefully controlled. All of the patients were given an intravenous bolus of 5, 000 units of heparin followed by a constant daily infusion of 15, 000 units for 3 days. At the same time, warfarin (2 mg/day) was started. The desired anticoagulant level was a thrombotest result of 3040% of the control value after heparin was discontinued. Progression of the symptoms stopped immediately after the initiation of heparin, and gradually regressed thereafter. During the follow-up period of 6 months to 2 years, the patients become more independent in their activities of daily living and their prognosis seemed good. Warfarin was changed to an antiplatelet agent after 2 to 6 months in 4 patients. Hemorrhagic complications did not occur in any patient.
The benefits of anticoagulant therapy have been demonstrated in several controlled trials of patients with brainstem stroke in evolution. Our results suggest that anticoagulant therapy may be promising if initiated in the early period of onset when the neurological deficit is mild. A CT scan should be performed to exclude hemorrhagic lesion and blood pressure must be controlled before and during this treatment. Anticoagulant therapy with heparin and warfarin has not been widely used in Japan except in the management of emboli of cardiac origin. However, the method described here caused no complications because heparin was given in a low dose for a short period. Every patient who was given heparin in the initial stage of thrombosis had a good prognosis. For progressing thrombotic stroke, especially in the basilar artery territory, anticoagulant therapy appeares to help prevent further progression.

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We evaluated the effect of treatment with different timings of glycerol solution on survival rate, brain edema and energy metabolism (ATP, lactate, pyruvate) in acute cerebral ischemia using spontaneously hypertensive rat (SHR). Cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL). The rats were devided into seven groups according to the treated methods of glycerol or saline. A : 20 ml/kg glycerol was administered immediately after BLCL for 3 hrs, B : 20 ml/kg glycerol 3 hrs after BLCL for 3 hrs, C : 6.6 ml/kg glycerol for 1 hr three times intermittently, D : 6.6 ml/kg glycerol once immediately after BLCL for 1 hr, E : 20 ml/kg glycerol continuously for 9 hrs, F : 20 ml/kg saline immediately after BLCL for 3 hrs and G : 20 ml/kg saline continuously for 9 hrs. After 12 hrs of ischemia, group C and E showed higher survival rate of all groups. At 9 hrs, group C showed significant decrease of water contents, however other glycerol treated groups had no significant decrease when compared to saline treated controls. Group C also showed higher levels of ATP and reduction of lactate/pyruvate (L/P) ratio compared to saline treated controls. However other glycerol treated groups showed no effect on ATP levels and the L/P ratio. There were no differences in levels of lactate and pyruvate between all the glycerol treated groups and saline treated groups. These results showed that intermittent (C) administration of glycerol was most effective to reduce cerebral ischemic impairment.

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The relationship between the duration of cerebral ischemia and the acute recovery in brain energy metabolism was studied in 18 adult Mongolian gerbils using P-31 magnetic resonance spectroscopy (MRS). Brain pH (=pHi), phosphocreatine (PCr) /inorganic phosphate (Pi) ratio, /3-ATP content (%) and β-ATP/Pi ratio were evaluated.
Transient forebrain ischemia was produced by a clipping of bilateral common carotid arteries for 30 min (n=6), 60 min (n=6), or 90 min (n=6).
The P-31 MRS was measured before clipping and after 30-, 60- and 90-min of reperfusion, respectively.
The pHi recovered rapidly to the level of pre-ischemia following reperfusion without showing significant differences in mean pHi values among the three groups. After reperfusion, PCr/Pi ration, β-ATP content (%), and β-ATP/Pi ratio recovered gradually but never returned to the pre-ischemic level in each groups of ischemia. There were significant differences between 90-min ischemia group and 30- or 60-min one for the extent of the acute recovery in PCr/Pi ratio (p<0.01 and p<0.05, respectively). There were significant differences between 30-min group and 90-min one for the extent of the acute recovery in β-ATP/Pi ratio (p<0.01-0.05), respectively.
The results suggest that β-ATP/Pi ratio is the most sensitive parameter for the evaluation of the acute recovery of brain energy metabolism after reperfusion of the forebrain ischemia in Mongolian gerbils.

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To determine the clinical significance of the extracranial carotid atherosclerosis in silent brain infarction (SBI), we studied serial 117 neurologically-free subjects (62.0 ± 9.4 yo. : mean ± S.D.) with at least one of the following risk factors for stroke; hypertension, diabetes mellitus, hypercholesterolemia and ischemic heart disease. All subjects underwent B-mode ultrasonography and were divided into four groups of patients with no, mild, moderate and severe carotid atherosclerosis based on the severity of plaque score (Stroke 1990; 21 : 1567-1572). Maximum percent stenosis and the existence of ulcerated lesions in each vessel were also evaluated. SBI lesions were detected by 0.1 T MRI and were investigated for their number, size, and localization.
The incidence of SBI was 42% in all subjects and significantly increased with advancing age. Most of the SBI lesions were smaller than 1 cm in diameter, and were localized in the subcortical white matter and in the basal ganglia. The incidence of subjects with no, mild, moderate or severe carotid atherosclerosis was 36%, 38%, 15% or 11%, respectively.
Though the incidence of subjects with plaques did not increase significantly with advancing age, those with moderate or severe atherosclerosis increased significantly. Subjects with severe stenosis (≥50%) orulcerated lesions were chiefly belonged to severe atherosclerosis group.
Although there were no significant differences in the SBI incidence between the subjects with plaques (47%) and those without (33%), SBI incidence increased significantly as the severity of plaque score increased (p<0.05) or when subjects had severe stenosis (p<0.05) or ulcerated lesions (p<0.01). These relationships were also noted in each decade of age (50s, 60s, and 70s). Especially in the subjects with severe stenosis or ulcerated lesions, higher incidence of larger lesions (>1 cm) was found in the brain hemisphere ipsilateral to the carotid lesions. As for the remaining risk factors, only hypertension was significantly related with the appearance of SBI.
Both the severity and characteristics of carotid atherosclerosis estimated by B-mode ultrasonography were closely related to the appearance of SBI. These results demonstrated that noninvasive assessment of carotid atherosclerosis was quite useful to predict the appearance of SBI.

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Patients with cardiogenic cerebral embolism are often treated with diuretics because of underlying cardiac disease. Although extracellular fluid volume depletion is a common complication of diuretic use, particularly when the potent loop-acting diuretics are employed.
To investigate the influence of dehydration at the time of onset of stroke, the data obtained from 44 patients with acute cardiogenic cerebral embolism (27 males and 17 females, mean age of 59, ranged 21 to 82 years) were analysed. On admission and 4 weeks later, hematocrit (Ht), serum total protein, sodium, urea nitrogen and creatinine were measured and the degrees of extracellular fluid volume depletion were calculated from them. In addition, blood viscosity and sizes of the low density areas on brain CT were measured.
Results showed that the patients with cardiogenic cerebral embolism were complicated extracellular fluid volume depletion and blood hyperviscosity at the time of onset. In particular, diuretics-use group had higher degree of extracellular fluid volume depletion (p<0.001) and higher blood viscosity (p<0.01) than non-diuretics-use group. In addition, blood viscosity was higher (p<0.05) in the group of patients who had a recurrent embolism than in the group of patients without recurrence. The sizes of infarction on CT was not correlated with Alit calculated from the ratio of Ht at onset and 4 weeks after onset. Therefore, the increase in Ht and blood viscosity was not regarded as a result of acute brain tissue injury. The results suggest that dehydration is one of the important triggers for inducing cardiogenic cerebral embolism.

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The effects of tissue-type plasminogen activator (t-PA) on the local cerebral microcirculation was examined after occlusion of the middle cerebral artery (MCA) in rats.
Female Sprague-Dawley rats were divided into two groups, 4 in the therapeutic group (A), and 5 in the control group (B). Cerebral ischemia was produced by occlusion of the MCA under ketamine anesthesia. The t-PA (1.6 × 10⁵ IU/kg/hr) was administrated from 30 minutes after MCA occlusion in group A, whereas normal saline was administrated in group B. Three hours after MCA occlusion, dichliorotriazinil aminofluorescein-labelled plasma (DTAF plasma) was injected. Each rat was decapitated, and the brain was fixed in ethanol. We calculated the microvascular DTAF plasma perfusion at 25 μm-thick slice.
The total length of perfused microvessels at the ischemic area were 68.8 ± 0.6% of the contralateral corresponding area in group A, and 38.4 ± 6.9% in group B (p<0.01). The area of histological change was 24.8 ± 2.6% of the ipsilateral hemisphere in group A, and 38.7% ± 3.6% in group B (p<0.05).
These results suggest that t-PA is effective in improving the local microcirculation and in ameliorating the histological damage in the acute stage of focal cerebral ischemia.

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A noninvasive 3D-TOF MRA was compared with conventional angiography in evaluating the ability to detect abnormalities in intracranial arteries. A comparison was made to detect the presence of the variation of the circle of Willis in 12 patients without occlusion. The presence of collateral circulations was sought using MRA in 7 patients with internal carotid artery occlusion. Then MRA was employed to determine the site of occlusion in patients known to have middle or posterior cerebral artery occlusion.
MRA was capable to demonstrate the patency of posterior communicating artery in 10 out of 12 patients. However the patency of the anterior communicating artery was only seen in 5 of 12 patients. MRA could show the collateral circulations through the circle of Willis (anterior communicating artery and/or posterior communicating artery) and the leptomeningeal collateral circulation from the posterior cerebral artery in all patients with internal carotid artery occlusion. MRA was capable to demonstrate the site of occlusion in patients with middle or posterior artery occlusion.
Thus, the 3D-TOF MRA is a useful noninvasive technique compared with conventional angiography to demonstrate the variation of the circle of Willis and collateral circulations in patients with intracranial artery occlusion, particularly internal carotid artery occlusion.

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The effects of hyperbaric oxygenation (HBO) therapy were reported in 39 patients with acute cerebral infarction.
The neurological scores (N.S.) and X-ray CT were evaluated before and after HBO treatment and compared with non-treated patients (51 cases) as a control. HBO was applied under spontaneous respiration of oxygen at a pressure of 2.0 ATA and a period of exposure of 60 minutes in a one-person chamber. Initial HBO treatment was done within 24 hours after cerebral ischemic insult. As a result, neurological improvement was significantly better in HBO treated group than in control one, particularly the patients who had good recovery showed small or medium-sized low density area on X-ray CT. However, HBO treatment was less effective for patients who had lower consciousness level and severe neurological deficits, and showed a presence of large low density area on X-ray CT. Four patients (10%) in HBO treated group coursed downhill, who had lower conciousness level below 11-20 (J.C.S.), polyfocal ventricular premature contraction, atrial fibrillation, congestive heart failure, renal failure or arteriosclerotic obliterans (ASO), while six patients (12%) in control group were also coursed downhill, its difference being not significant. HBO therapy is effective and safety for acute cerebral infarction.

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Case 1 is a 45-year-old female with a left lateral type cerebral hemorrhage.
Case 2 is a 41-year-old female who also had myocardial infarction and a cerebral thrombosis in the left middle cerebral artery, following a cerebral thrombosis in the right middle cerebral artery. A literature study of Turner's syndrome and cerebrovascular disorders was done. This research revealed that the cerebrovascular disorder in Turner's syndrome is most likely due to the fragility of the arterial wall resulting from abnormal metabolism of collagen and mucopolysaccharide.
These facts suggest that the occurrence of the cerebrovascular disorder must always be considered when diagnosing a Turner's syndrome.

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A case of a 70-year-old male with anteromedial thalamic infarction on the non-dominant side presenting as Korsakoff syndrome was reported. The case was charactarized by anterograde and retrograde amnesia, disorientation, confabulation, and lack of insight into his own disability. In this case CT and MRI revealed an infarct on the right dorsomedial nucleus of his non-dominant thalamus. Cerebral blood flow scintigram using ^99mTc-IIMPAO showed a reduction in blood flow to the right thalamus and right occipital lobe where the infarction was observed, and also, a tendency for a reduction in the blood flow to the right frontal and temporal lobe. Thus it was thought that damage of the right dorsomedial nucleus in the non-dominant thalamus can give rise to Korsakoff syndrome because of blockage of Yakovlev's circuit.

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The patient, a 47-year-old male had a long history of hypertension, first noted pain in the back of his head on July 14, 1991. On July 17, he suddenly lost consciousness and was admitted. Upon admission the patient was semicomatose, his right eye deviated to the left, the “doll's head eye phenomenon” was absent, his pupils were constricted bilaterally, and the reaction to light and the corneal reflex were absent. His both upper extremities were atonic and his both lower extremities were spastic. Deep tendon reflexes were normal in both upper extremities and hyperactive in both lower extremities. The Babinski sign was positive biliaterally. A head CT scan examined immediately after admission was normal. Cerebral angiography which was done 2 hours after the onset revealed irregular narrowed segment with tapering from the V3 portion of both vertebral arteries (VA) to their transition into the basilar artery and an existence of embolus shadow defect at the top of the basilar artery. There were no atherosclerotic changes of internal carotid arteries. On the second day, a CT scan and MRI revealed infarctions of the cerebellum, pons, midbrain, the bilateral thalamus, and the left occipital lobe. He was suggested that his symptoms were due to vertebral arteries dissection.
This is the first reported case about the top of the basilar syndrome due to vertebral artery dissection.

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A case of idiopathic normal pressure hydrocephalus (NPH) was reported. A 75-year-old woman with gait disturbance and dementia was admitted to Kyushu university hospital on June 18, 1990. Brain computed tomography revealed fronto-parietal cortical atrophy, dilatation of the ventricular system and marked perivenTricular lucency. Isotope cisternography showed a delay of the radioisotope absorption. She was diagnosed as NPH and underwent operation of ventricular-peritoneal shunt. One month after the operation, she got a slight improvement in her cognitive function, but no change in gait disturbance. We measured cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRO₂) and oxygen extraction fraction (OEF) by means of position emission tomography (PET) before and after the operation. Preoperative PET study revealed reduction in CBF and CMRO₂ especially in the basal ganglia, white matter and fronto-temporal cortex, whereas OEF was rather elevated (misery perfusion). One month after the shunt operation, repeated PET study showed a slight elevation in CBF and normalization in OEF, with little change in CMRO₂. In this case, cerebral hemodynamic was improved by shunting, whilst there still existed a residual and irreversible disturbance in cerebral metabolism. It is important to examine not only cerebral hemodynamics but also metabolic state of the brain in NPH patients to clarify the mechanism (s) in detail.

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The authors experienced a rare case of a fusiform aneurysm of the vertebrobasilar artery which presented with massive hemorrhage in the brainstem. A 56-year-old woman admitted complaining of dysarthria, dysphagia, hoarsness and left side hemiparesis and hypoesthesia. Vertebral angiography revealed a fusiformal dilatation of right vertebral and basilar artery with elongation. CT scan and MR image demonstrated the brainstem compressed by the fusiform aneurysm. She was followed up with the medication of aspirin 100 mg/day. Four months after discharge, she sustained severe headache and rapidly lapsed into coma. She died twelve hours later. Autopsy revealed rupture of a giant fusiform aneurysm of vertebrobasilar artery and massive hemorrhage extending from the pons to the medulla oblongata as well as in subarachnoid space. The aneurysmal wall adjacent to the rupture site was involved by intramural hemorrhage and plasma insudate with fibrinoid substance. Dissection by intramural hemorrhage and histolysis by plasma insudate might be factors for the rupture. In hemorrhagic lesion of the brainstem, congestion, diapedetic hemorrhage and rhexis with fibrinoid degeneration were observed mainly in capillaries, venules and arterioles. These vascular changes are similar to those resulted from increased vascular permeability in ischemic brain tissue. Serial sections of the brainstem failed to demonstrate rupture of microaneurysms and vascular malformations attributable to the hemorrhage. The brainstem hemorrhage in the present case might be caused by diapedesis from small vessels and rhexis of small vessel walls in the brainstem following ischemia after massive subarachnoid hemorrhage, and/or by the bleeding directly from the ruptured aneurysm.

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A 57-year-old woman was admitted to our hospital for the further evaluation of intraventricular hemorrhage, which had been developed with hydrocephalus two years ago. On admission, upward gaze palsy and downbeat nystagmus were observed. Brain magnetic resonance imaging revealed old hemorrhage between the thalamus and the lateral ventricle on the right side. She had no history of hypertension or evidence of vascular anomaly, such as aneurysm or arteriovenous malformation, and we diagnosed her as a primary intraventricular hemorrhage. Although the intraventricular hemorrhage is known as one of specific forms of brain hemorrhage, being uncommon in adults, its pathophysiological aspects of oculomotor dysfunction have not been fully understood.
In our case, upward gaze palsy was though to be attributed to destruction of rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) by intraventricular hemorrhage.

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We reported 2 cases of anomia for proper names caused by cerebrovascular disease. Case 1 was a 69-year-old man of left temporo-occipital subcortical hemorrhage and case 2 is a 53-year-old woman of infarction in the territory of the insular branch of the left middle cerebral artery. Both cases were alert and right-handed with normal visual field and acuity. Naming of common names were normal. However naming of proper names were disturbed, especially naming of persons and places. They spoke fluently. Auditory comprehension and repetition were normal. Case 1 presented alexia with agraphia simultaneously. There was no lesion in the classical memorial circuit. There have been few reports of cases presenting anomia for proper names. The opposite phenomenon, a selective sparing of naming of proper names, has also been reported. We concluded that anomia selectively for proper names might appear in the patients with focal cerebral damage of the dominant hemisphere under some special condition. Proper and common names might be separately registered, retained or recalled in the brain.

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A case of the vertebral artery (VA) aneurysm located extradurally at the origin of the posterior inferior cerebellar artery (PICA) and associated with a ruptured anterior communicating artery (AcomA) aneurysm is presented. This 34-year-old man was referred to our hospital with sudden onset of severe headache. On admission, CT scan demonstrated high density in the interhemispheric fissure. Cerebral angiography revealed saccular aneurysms at the AcomA and the origin of the right PICA which was originated from the extracranial part of the vertebral artery. Nine days after the onset, neck of the AcomA aneurysm was successfully clipped without any postoperative deficit. One month after the first craniotomy, the second operation was performed to explore the PICA aneurysm. Right suboccipital approach was employed. Initially, the right VA and PICA were identified in the intradural space. Both arteries were followed proximally, and they were found to have penetrated the dura mater separately. Therefore, the VA aneurysm was confirmed to locate in the extradural space. No further exploration was performed. Such an extradural VA-PICA aneurysm has not been reported in the literature.

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Despite the advent of recent neuroradiological techniques, subarachnoid hemorrhage (SAH) of unknown cause represents approximately 10% of all SAH. Since the prognosis is considered good, SAH of unknown cause has received less attention than aneurysmal SAH. The specific treatment of SAH of unknown cause has not been determined.
A 50-year-old man was admitted to our hospital presenting severe headache and vomiting. CT scans showed SAH. The initial cerebral pan-angiogram demonstrated no responsible lesions. Then conservative therapy was initiated. On 18th day after the onset, he suddenly complained of severe headache followed by deterioriation of consciousness level. CT scans showed intraventricular hemorrhage and acute hydrocephalus. The second cerebral angiogram revealed a large saccular aneurysm arising from right A1-A2 junction. He underwent emergent craniotomy and neck clipping of the aneurysm. He died on 52nd day after the onset. The need for repeat panangiogram and careful follow-up were emphasized.

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