We report an attempt to obtain the image of the basilar artery and to measure the absolute mean-flow velocity in basilar artery by the real-time color flow Doppler ultrasonography.
In 16 healthy volunteers (range 20-59 : mean 30 ± 9 years old), basilar artery could be recorded from a nuchal position via the posterior bone and/or the foramen magnun. The basilar artery was clealy delineated as a red stream. The absolute mean-flow velocity was calculated by dividing the measured velocity by the cosine of the incident angle. The corrected mean-flow velocity of the basilar artery was 41.2 ± 12.6 cm/sec.
Real-teim color flow Doppler ultrasonography permits more accurate noninvasive quantification of basilar hemodynamic consequences than TCD.

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A comparative study was conducted for clinical symptoms and MRI findings in 8 cases of cortical central facial monoparesis, and the somatotopy in the precentral motor gyrus was discussed. Six cases with cortical infarction and one case each with subcortical hemorrhage and metastatic brain tumor were included in this study. The precentral gyrus was arbitrarily divided into 3 segments, the upper, middle and lower one-third, between the longitudinal cerebral fissure and Sylvian fissure on a coronal MRI scan through the precentral gyrus. The lesions in all cases were situated in the middle segment of the precentral gyrus, and none extended into the upper one-third. Two cases with complicated facial palsy had localized lesions in the middle segment, three cases with dysphagia, dysarthria, and lingual paresis had more extensive lesions in the middle and lower one-third, and the remaining three cases with lesions involving the deep white matter also exhibited unilateral spatial neglect or aphasia. None of the 8 cases showed a discrepancy between voluntary and emotional facial movements, and it was inferred that the neural pathways for these two different types of motor control of the facial muscles run adjacent to each other in the vicinity of the precentral gyrus.

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The possible role of leukocytes in tissue ischemia has attracted recent interest. In this paper, the rheologic behavior of leukocytes and erythrocytes in cerebral vascular disease was studied. This study aimed at quanitifying the filtrability through a milipore membrane of leukocyte and erythrocyte subpopulations in 31 stroke patients in the acute and chronic stages compared with 33 age-matched patient controls using the St. George's Filtrometer. Leukocyte filtrability was reduced in 11 stroke patients in the acute stage and 20 stroke patients in the chronic stage compared with controls (p<0.05). No significant differences existed in erythrocyte filtrability between three groups. Leukocyte filtrability was significantly reduced in 24 patients with thrombotic stroke but not in 7 patients with cardioembolic stroke. Leukocyte filtrability was significantly reduced in 14 patients with small infarct than in 11 patients with large infarct (p<0.01). Those results suggest that the reduction in leukocyte filtrability may contribute to the insufficiency of microcirculation in thrombotic stroke, particularly in the small foci of cerebral infarct.

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In 47 patients with infarction of the cerebellum and/or cerebellar peduncle (CP), outcome of ataxia and functional localization in the cerebellum were studied with analysis of clinical signs and magnetic resonance imaging (MRI). Cerebellar ataxia disappeared in 81% of the patients within 12 months from the stroke. Total involvement of the middle CP or combined involvement of the superior CP and dentate nucleus showed markedly poor recovery of limb ataxia, whereas ataxia in patients with lesion of the cerebellar cortex or inferior CP recovered well.
Although no difference was observed between ataxia due to cerebellar afferent system (middle and inferior CP) and efferent system (superior CP) lesions, intention tremor or rhythmic skeletal myoclonus appeared later in the patients with the latter lesion.
Ataxic dysarthria in upper cerebellar hemisphere lesion and ocular dysmetria in lower vermis or hemisphere lesion were frequently shown, whereas limb ataxia had no obvious correlation with the site of lesion. These results suggest that, in the cerebellum, somatotopic localization exists at least in coordination of arthria and eye movement.

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We conducted a clinical study of 155 cases that were confirmed to have brainstem infarctions on MRI (T₁-weighted image showed a low signal and T₂-weighted image showed a high signal, measuring in excess of 2 × 2 mm). The majority of the brainstem infarction were located in the pontine base in 132 cases (85.2%). Of these, 19 cases had double lesions including infarctions in the pontine base. Second infarctions frequently occurred in the cerebral peduncle or medical medulla oblongata, unilateral to the pontine infarctions. In addition to 98 symptomatic cases, there were 57 cases of “asymptomatic” brainstem infarction. They comprized 24 cases accompanying other symptomatic cerebrovascular diseases in the supratentorium and 33 cases with transient subjective complaints such as headache or vertigo-dizziness. Complication by supratentorial infarctions was significantly frequent in cases of brainstem infarctions (p<0.001), 122 of 155 cases (78.7%), especially in the pontine base (88.6%); while in the control cases (without brainstem infarction) only 65 of 221 cases (29.4%). These findings are considered to show the widespread progress of arteriosclerosis in brainstem infarctions, especially in ones in the pontine base.

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Small pial and intraparenchymal vessels are innervated by ascending serotonergic fibers, and it has been demonstrated that the ascending serotonergic pathways containe the fibers not only from rostral raphe nuclei but also from nucleus raphe pontis and nucleus raphe magnus which located within the lower pons. The participation of lower pontine raphe nuclei in cerebral hemodynamics and vasomotor responses, however, has not been clarified. The present study was aimed at elucidating the role of lower pontine raphe nuclei in these themes using chronic monkey model.
Studies were performed on 14 monkeys (macaca fuscata) weighing 5.3 ± 1.2 kg. An electrode was stereotaxically inserted into the nucleus raphe pontis or nucleus raphe magnus and lesion was made by electrical coagulation in 8 monkeys, and non-lesioned was done in 6. Seven days later, the animals were anesthetized with α-chloralose and urethane. PaCO₂ and body temperature were maintained within a physiological range. Bilateral internal carotid blood flow (ICBF) was continuously measured by electromagnetic flowmeters with blood pressure and pulse rate. Cerebral vasomotor responses were quantitatively analyzed by means of chemical vasomotor index (%CVI=ΔICBF/ΔPaCO₂/steady state ICBF × 100, %/mmHg) and autoregulation index (%AI=ΔICBF/ΔMABP/ steady state ICBF × 100, %/mmHg). Cerebral oxygen consumption (CMRO₂) was calculated from multiplying the differences of arterio-sagittal sinus O₂ content by ICBF.
I Blood pressure and pulse rate : Significant changes were not observed between lesioned and non-lesioned groups in the steady state.
II Cerebral blood flow : ICBF showed no significant differences between lesioned and non-lesioned groups.
III Cerebral metabolism : CMRO₂ in the lesion group had significant increase as compared with that in the non-lesioned group (p<0.05).
IV CBF chemical regulation : %CVI to induced hypercapnia in the left side of lesioned group had a tendency to be higher as compared with that in the non-lesioned group. The response to induced hypocapnia in the right side of lesioned group was significantly lower as compared with that in the non-lesioned group (p<0.02) and had a tendency to be lower as compared with that in the non-lesioned group.
V CBF autoregulation : %AI to changes in blood pressure had no significant differences between lesioned and non-lesioned groups.
These data suggest that the lower pontine raphe nuclei modulate cerebrovascular tone in the carotid vascular system through the ascending serotonergic pathway and have an important role in the CBF chemical regulation.

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A 57-year-old woman was admitted due to acute onset of gait disturbance. On admission, she presented with bilateral internuclear ophthalmoplegia (INO) and cerebellar ataxia. Brain CT and MRI showed a focal infarct in the paramedian midbrain tegmentum, extending to the left cerebral peduncle. Vertebral angiogram disclosed complete occlusion of the left vertebral artery without stenosis in the basilar and posterior cerebral arteries. The patient's neurological symptoms remained unchanged for five weeks, and thereafter rhythmic tremor appeared in the head and limbs on both sides. The focal infarct might be ascribed to artery to aretry embolism in the paramedian mesencephalic artery, presumably arising from the occluded vertebral artery. The present case suggests that a focal infarct in the paramedian midbrain tegmentum involves bilateral ocular motor, cerebellar and extrapyramidal systems.

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A 42-year-old right-handed woman with a 7-year history of high blood pressure had a sudden onset of hemiparesis and hemihypesthesia on her right side. These symptoms were predominant in the lower extrimity. A CT scan which was examined on the following day showed multiple low density areas in the territory of the left anterior cerebral artery (ACA), which suggested cerebral infarctions. Cerebral angiography revealed changes of so-called “string of beads” appearance in the cerevical portion of the left internal carotid artery (ICA), the A2 portion of the left ACA and the foramen magnum portion of the left vertebral artery (VA), which are known as characteristic findings of fibromuscular dysplasia (FMD). Her ischemic attack was attributed to the lesion of FMD in the left ACA. In addition, the appearance of “tubular stenosis with aneurysmal dilatation” and “diverticulum-like outpouching” were found in the cervical portion of the left VA, and multiple fusiform aneurysm were confirmed in the cervical portion of the left ICA, the cervical portion of the right VA, and the right superior cerebellar artery (SCA). However occlusion or stenosis of the branches of left ACA were absent. Treated conservatively, symptoms had gradually improved. One month after admission she returned to her duties as a housewife without neurological deficit.
This patient had interesting rare lesions, namely FMD of the ACA and fusiform aneurysm of the SCA, and coexistence of both lesions hasn't been reported in the literature thus far. We are discussing intracranial FMD, and the relationship between FMD and fusiform aneurysm in review of the literatures.

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We conducted clinical and neuroradiological studies on 3 cases of Gasperini syndrome, Case 1 (a 42-year-old female) and case 2 (a 70-year-old male) were pontine infarction. Case 3 (a 42-year-old male) was pontine hemorrhage. The main symptoms included 5th, 6th, 7th and 8th cranial nerve palsy, cerebellar ataxia on the ipsilateral side, and sensory disturbance on the contralateral body in all 3 cases. We found Horner syndrome and lateral gaze palsy in 1 case and contralateral muscle weakness in 2 cases. The cerebral angiographic findings in two cases with the pontine infarctions showed occlusion of the bilateral vertebral arteries and stenosis of the basilar arteries. MRI showed the lesion at the lateral tegmentum of lower pons in all cases. The pathogenesis of the Gasperini syndrome caused by brainstem infarction is thought to be the terminal zone infarction of three branches from basilar artery (paramedian, short circumferential, long circumferential branches).

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A 50-year-old man a continuous headache, vertigo, gait disterbance, nausea and vomiting. He was diagnosed as left side lateral medullary syndrome by vertigo, left blephaloptosis, nystagmus, dysphagia, left side discoordination, right hemisensory disturbance. Computed tomography findings had no definite abnormal region, but magnetic resonanced image had abnormal region in left lateral side of medulla oblongata. His symptoms became stable by 15 days, but 18th day from onset, he died suddenly from subarachnoid hemorrhage, due to ruptured intracranial vertebral dissecting aneurysm. Serial MRI findings were obtained during the course of his illness and the progression of the dissecting aneurysm was shown. In this case, we speculate that MRIs are useful for early diagnosis and evaluation of the intracranial vertebral artery dissecting aneurysm.

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A case of infective endocarditis complicated with subarachnoid hemorrhage and bleeding from brain abscess was reported.
A 43-year-old male with hypertrophic obstructive cardiomyopathy suffered from high fever for one month. He developed subarachnoid hemorrhage 1.5 month after he became feverish. He was diagnosed as infective endocarditis caused by streptococcus viridans (α-hemolytic streptococcus). Penicillin G and Amikacin were started to effectively administer. Two weeks after subarachnoid hemorrhage he suddenly developed right hemiplegia with impairment of consciousness. Computed tomography showed brain abscess with hemorrhage, which ruptured into the ventricle, in the left hemisphere.
We emphasize the importance of early diagnosis and adequate treatment in acute stage of infective endocarditis for the protection against intracranial hemorrhage.

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