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Biomedical subjects

Y Saku

Publications and source records attributed to Y Saku.

At least 19 recordsLinked to original sources

Progressive motor deficits in lacunar infarction.

OBJECTIVE: To study the clinical characteristics of the progression of motor deficits in lacunar stroke patients. BACKGROUND: Some patients with lacunar infarction have progression of their neurologic deficits, but it is not known which patients will progress or why they progress. METHODS: The authors evaluated 92 consecutive patients (47 men, 45 women; age, 69.4 +/- 10.9 years [mean +/- SD]) with first-ever stroke due to supratentorial lacunes in the internal capsule or the corona radiata. By defining lacunar infarction in which motor deficits progressed between admission and the day after admission as progressive lacunar infarction, the authors compared progressive lacunar infarction with stable lacunar infarction. RESULTS: Of 92 patients, 25 (27%) had progression of deficits. Diabetes mellitus (p = 0.02) and severity of motor deficit on admission (p = 0.006) were related independently to progression in a logistic multiple regression analysis. Size of the infarct was slightly larger (1.2 +/- 0.4 cm2 versus 0.9 +/- 0.5 cm2; p = 0.01) and functional status at discharge was worse (median Barthel index, 45 versus 100; p < 0.001) in patients with progressive infarction than in those without progression. There were no significant differences between the two groups regarding the site of the infarct or blood pressure or hematocrit levels on or after admission. CONCLUSIONS: The progression of motor deficits is associated with a relatively poor functional outcome. Diabetes mellitus and the severity of motor deficit on admission may predict progression of motor deficits.

Activities of Daily Living↗

Sonographic detection of haemodynamic changes in a case of vertebrobasilar insufficiency.

We present a diagnostically challenging case of vertebrobasilar insufficiency caused by head rotation. The patient was a 58-year-old man complaining of dizziness and faintness with head rotation to the left. Vertebral arteriography with the head turned to the left revealed mechanical compression of the right vertebral artery at the occipitoatlantal joints and an occluded left vertebral artery. Duplex sonography demonstrated disappearance of the end-diastolic flow signal in the right vertebral artery on head rotation, paralleling the appearance of symptoms. Decompression of the vertebral artery by transversectomy of the atlas and hemilaminectomy of the axis completely relieved the symptoms and the Doppler flow signal pattern of the vertebral artery returned to normal: End-diastolic flow in the right vertebral artery did not disappear even when the head was rotated to the left.

Cerebrovascular Circulation↗

Blood pressure control and recurrence of hypertensive brain hemorrhage.

BACKGROUND AND PURPOSE: Recent studies have demonstrated that recurrence of hypertensive brain hemorrhage (HBH) is not uncommon. However, risk factors for the recurrence of HBH have not been evaluated systematically. METHODS: We analyzed 74 patients with HBH who were admitted to our clinic and followed up as outpatients for a mean of 2.8 years. Blood pressure (BP) and other clinical features were compared between the groups of patients with and without rebleeding. We determined the recurrence rate of HBH in relation to BP. RESULTS: Diastolic BP was significantly higher in the recurrence group than in the nonrecurrence group (88+/-8 versus 82+/-7 mm Hg; P=0.04). Systolic BP and other clinical variables were not different between the groups. The recurrence rate was 10.0% per patient-year in patients with diastolic BP >90 mm Hg and <1.5% in those with lower diastolic BP (P<0.001). No patients with diastolic BP <70 mm Hg experienced rebleeding. CONCLUSIONS: Higher diastolic BP was related to an increased rate of rebleeding. Diastolic BP >90 mm Hg may be regarded as a factor predictive of the recurrence of HBH.

Adult↗

Simultaneous multiple brain hemorrhage associated with migraine--a case report.

A fifty-five-year-old woman with a history of migraine suddenly developed an occipital headache and visual disturbance after a typical migrainous attack. On admission, she had a left homonymous hemianopsia, and computed tomography of the brain demonstrated intracranial hematomas in the occipital subcortices bilaterally. Cerebral arteriography revealed diffuse vasospasm of the intracranial arteries attributed to the migraine. The cystatin C concentration in the cerebrospinal fluid was low, which suggested the existence of cerebral amyloid angiopathy. According to the clinical course and angiographic findings, it is suggested that the vasospasm associated with migraine played an important role in developing multiple brain hemorrhage in this patient.

Cerebral Amyloid Angiopathy↗

Circadian blood pressure in patients in a persistent vegetative state.

We examined circadian variations in blood pressure, pulse rate, and other physiological variables, including hormone levels, in 16 patients in a persistent vegetative state (mean age -/+ SE; 66.1 -+/ 3.9 yr). Cerebrovascular accident was responsible for brain damage in 12 (75%) of the 16 patients. Blood pressure was measured for 24 h with an ambulatory blood pressure monitoring device. We monitored the temperature of the urinary bladder and measured urinary excretion of epinephrine, norepinephrine, 17-hydroxycorticosteroids, water, and sodium. When data were analyzed by analysis of variance, significant circadian changes were observed in body temperature and urinary excretion of hormones and sodium, but not in blood pressure or pulse rate. Individual analysis of rhythmicity using the cosinor method detected small but significant circadian variations in blood pressure and pulse rate in five of six patients who showed a simple organized response to noxious external stimuli. The disappearance of variation in blood pressure in patients in a vegetative state appeared to be related, in part, to the lack of response to external stimuli. Our findings suggest that the circadian variation in blood pressure may largely depend on external environmental factors.

Adult↗

Serial changes in blood pressure and neurohormone levels after the onset of lacunar stroke.

To assess serial changes in blood pressure and its circadian variation following a lacunar stroke, the authors studied 7 patients who developed a single lacunar infarction in either the internal capsule or the corona radiata. Blood pressure and pulse rate were monitored noninvasively for twenty-four hours by an ambulatory blood pressure monitoring device in the acute, subacute, and chronic phases of the strokes. In the acute and chronic phases, the authors also measured urinary excretion of catecholamines every 6 hr, and serum cortisol concentration at 9:00, 17:00, and 21:00 hr. The patients were free from antihypertensive agents during the study. The twenty-four-hour averages of both systolic and diastolic blood pressure in the chronic phase were lower than those in the acute phase (P < 0.05). A nighttime fall in blood pressure was observed in the subacute and chronic phases (P < 0.05), but not in the acute phase. Urinary excretion of epinephrine at night in the acute phase was significantly higher than that in the chronic phase (P < 0.05). Serum levels of cortisol at 17:00 and 21:00 hr in the acute phase also exceeded those in the chronic phase (P < 0.05 and P < 0.01, respectively). The authors conclude that an increased secretion of epinephrine and cortisol might, at least in part, contribute to a high blood pressure and a lack of circadian variation in blood pressure in the acute phase of lacunar stroke.

Acute Disease↗

Medial medullary infarction: analyses of eleven patients.

Of 2,130 consecutive patients admitted to two hospitals with acute brain infarction, we examined 11 patients (0.52%) with medial medullary infarction. The infarcts documented by MRI were unilateral in 9 patients and bilateral in 2 patients, and located in the anteromedial arterial territory of the upper or middle part of the medulla. Atherosclerosis of the vertebral arteries was the predominant vascular pathology. The vertebral artery was occluded at its terminal portion in 7 patients. Nine patients had hypertension, and 8 of these had additional risk factors. Male gender (10 patients) and smoking habits (7 patients) were more prevalent compared with patients with pontine infarction. One patient had a medial medullary infarction attributed to dissection of the vertebral arteries following blunt head injury. Limb weakness was the major symptom in all patients, and gaze-evoked nystagmus was also frequent (6 patients). Tongue weakness ipsilateral to the infarct, the classic sign of medial medullary syndrome, was evident in only 3 patients. The outcome was usually excellent.

Adult↗

Pontine infarction extending to the basal surface.

BACKGROUND AND PURPOSE: Etiology and symptomatology in pontine infarction extending to the basal surface are supposed to be different from those in deep pontine infarction of the lacunar type. The aim of this study was to compare the infarct size and location, vascular lesions, risk factors, and neurological deficits in three different types of acute pontine infarction. METHODS: We studied isolated pontine infarction extending to the basal surface on brain imaging (group 1, n = 30), deep pontine infarction without extension to the basal surface (group 2, n = 23), and pontine infarction with simultaneous extrapontine infarct in the posterior circulatory system (group 3, n = 20). Clinical features, angiographic findings, and risk factors such as emboligenic heart disease, hypertension, and hypercholesterolemia were compared among the groups. RESULTS: The infarct area was 2.5 times greater in group 1 than in group 2. On angiogram, atherosclerotic stenosis of the basilar trunk was observed in 50% of the patients studied in group 1, in 0% in group 2, and in 78% in group 3. Emboligenic heart diseases were observed in 23%, 0%, and 30% in groups 1, 2, and 3, respectively. However, hypertension (60% to 65%), diabetes mellitus (35% to 45%), and hypercholesterolemia (13% to 17%) were equally distributed among the three groups. Classic lacunar syndromes were seen in 14 patients (47%) in group 1, in 20 patients (87%) in group 2, but in none of the patients in group 3. Patients belonging to group 1 showed a higher incidence of hemiparesis involving the face (37%), sensorimotor stroke (20%), and hemiparesis with confusion (17%) than those in group 2 (22%, 0%, and 4%, respectively) or in group 3 (0%, 5%, and 0%, respectively). CONCLUSIONS: Pontine infarction in group 1 may have several different causes, such as cardioembolism, artery-to-artery embolism, or atherosclerosis of the basilar artery affecting pontine branches. Severe neurological symptoms often result that differ from those seen in the deep pontine lacunar infarction in group 2.

Adult↗

Multiple brain infarction and hemorrhage by nonbacterial thrombotic endocarditis in occult lung cancer--a case report.

A fifty-four-year-old woman died from multiple brain infarction and hemorrhage in the bilateral cerebrum, cerebellum, and brainstem, with renal infarction. She developed hematuria and transient blindness sixteen days before admission. Low-grade fever, heart murmur, and aortic valve vegetation on ultrasonic cardiography suggested infectious endocarditis. Autopsy study revealed occult adenocarcinoma in the lung and nonbacterial thrombotic endocarditis, but infective endocarditis was not histologically confirmed. The patient was considered to be a rare case of nonbacterial thrombotic endocarditis who developed multiple small infarctions mainly in the brainstem and cerebellum. Nonbacterial thrombotic endocarditis seems to be still an important disease as the embolic source, even if cryptic, of systemic thromboembolism.

Adenocarcinoma↗

Purulent meningitis after endoscopic injection sclerotherapy for esophageal varices.

A 57-year-old man with liver cirrhosis developed alpha-hemolytic streptococcal meningitis following endoscopic injection sclerotherapy for esophageal varices. Central nervous system infection is uncommon as a complication of sclerotherapy, however, when such an infection does develop, it is usually intractable. We therefore emphasize the importance of immediate antibiotic therapy right after the onset of inflammatory symptoms in order to prevent the development of undesired infectious complications following sclerotherapy.

Ampicillin↗

Effects of angiotensin and atrial natriuretic peptide on the cerebral circulation.

The purpose of the present study was to determine effects of angiotensin (ANG) II on the cerebral circulation. We measured the pial artery pressure (PAP) and CBF in anesthetized rabbits. ANG II (5 micrograms/min) was infused into each carotid artery, and systemic arterial pressure was maintained constant. During infusion of ANG II, there was a significant increase in CBF and fall of PAP, with no change in the large artery resistance (LAR) and a significant decrease in the small vessel resistance (SVR). To investigate whether prostaglandin modulated the ANG II-induced increase in CBF, indomethacin was administered (10 mg/kg i.v.) in another group of animals. Indomethacin itself reduced PAP and increased LAR significantly without changing CBF or SVR. Indomethacin did not attenuate the effects of ANG II on the cerebral circulation. The CMRO2 was assessed during ANG II intracarotid infusion in another group of rabbits. CMRO2 did not change during infusion of ANG II. We also investigated effects of alpha-atrial natriuretic peptide (ANP) on the cerebral circulation. Infusion of ANP (1 microgram/min) decreased LAR by 28% (p less than 0.05) without altering SVR. Administration of ANG II after ANP tended to reduce LAR (p greater than 0.05), with a significant decrease in SVR. The results of the present study suggest that high doses of ANG II can produce cerebral vasodilatation, particularly of small vessels. Blood-borne ANP dilated the large arteries of the cerebral circulation selectively and neither interfered with nor reversed the ANG II-induced increase in CBF.

Angiotensin II↗

Acquired C1 inhibitor deficiency associated with systemic lupus erythematosus affecting the central nervous system.

A 22 year old woman with systemic lupus erythematosus affecting the central nervous system had acquired C1 inhibitor deficiency. She was admitted for treatment of psychotic behaviour, but showed no signs of angioedema. The serum complement profile of the patient showed normal C3 concentration and a depletion of C4, C2, C1 inhibitor, and C1q. Her parents had normal complement profiles. An extremely reduced C4 concentration may lead to involvement of the central nervous system in systemic lupus erythematosus.

Adult↗