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Biomedical subjects

Y Saku

Publications and source records attributed to Y Saku.

17 recordsLinked to original sources
PubMed1996

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↗
PubMed1996

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↗
PubMed1996

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↗
PubMed1994

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↗
PubMed1994

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↗
PubMed1994

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↗
PubMed1992

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↗
PubMed1991

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↗
PubMed1990

Hemorrhagic infarct induced by arterial hypertension in cat brain following middle cerebral artery occlusion.

The purpose of this experiment was to determine whether an acute rise in brain perfusion pressure causes hemorrhagic transformation of an infarct without a reopening of the occluded artery. We raised the blood pressure of 22 cats by aortic obstruction 5-24 hours after transorbital middle cerebral artery clipping; hemorrhagic infarcts were induced in 11. Mean arterial blood pressure increased by 57.2 +/- 16.9 mm Hg (mean +/- SD) in the 11 cats with hemorrhagic infarcts and by 40.4 +/- 16.9 mm Hg in the 11 remaining cats with pale brain infarcts (p less than 0.05). Induction of hypertension increased regional cerebral blood flow in the ischemic cortical gray matter more in three cats with hemorrhagic infarcts than in seven with pale infarcts. Our results demonstrate that hemorrhagic transformation of an infarct can be induced by a rapid increase in perfusion pressure to brain tissue already exposed to focal ischemia. We also suggest that the restoration of blood flow through leptomeningeal collaterals plays an important role in the pathogenesis of hemorrhagic infarction in cases without reopening of occluded arteries.

Animals↗
PubMed1990

[A case of left internal capsular infarction with auditory hallucination and peculiar amnesia and dysgraphia].

A 46-year-old businessman suddenly became to behave curiously on the morning, September 1, 1988. He forgot how to go through an automatic ticket gate, which he used every day. In his company, he also forgot how to open the cash box, and he wrote a meaningless report for his business. From the night on that day, he had experienced auditory hallucination in which whispering words of some criticism to his performance for a few days. On the next day, he was admitted to a psychiatric hospital because he was suggested to have schizophrenia. By day 6 after the onset, his curious symptoms completely disappeared. However, slight verbal memory disturbance and cognitive dysfunction still remained. Because the brain CT on day 6 showed a small localized subcortical infarction in the left hemisphere he was transferred to our clinic on day 20 to elucidate the relation between the abnormal behavior and the infarction. His blood pressure was 116/64 mmHg and pulse was regular 63/min. He was clear and did not have any neurological deficit. He kept his episodic memory regarding the events at the onset and could almost recall them precisely. Results of standard blood tests, electrocardiogram, ultrasound cardiogram, electroencephalogram as well as cerebral angiography were normal. Computed tomography and magnetic resonance imaging showed an infarcted lesion in the genu of the left caudate nucleus, adjacent to the anterior part of the thalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Agraphia↗
PubMed1989

Hemorrhagic infarct of the brain without a reopening of the occluded arteries in cardioembolic stroke.

We examined the brains of 14 patients (four men and 10 women, mean age 68.9 years) who died from brain herniation after cardioembolic stroke with persistent occlusion of the internal carotid-middle cerebral arterial axis. Our examination showed hemorrhagic infarct in seven patients and pale infarct in the other seven, contradicting the commonly proposed pathophysiologic mechanism for the development of hemorrhagic infarct that the opening of previously occluded vessels makes an infarct hemorrhagic. Analysis of blood pressure after stroke revealed one or more surges of arterial hypertension or rapid rise of blood pressure in patients with hemorrhagic infarct without a reopening of the occluded artery. Such arterial hypertension was not always present in patients with pale infarct. Hemorrhage into an infarct with persisting occlusion of the proximal artery is assumed to occur when the involved blood vessels are exposed to the force of arterial blood pressure from the leptomeningeal collaterals. This occurs when arterial blood pressure rises after stroke in the presence of efficient leptomeningeal collaterals and before occlusion of these collaterals by a swollen cerebral hemisphere containing a large infarct.

Adult↗
PubMed1989

[Disturbances of fluid and electrolyte balance in patients with acute stroke].

Serum sodium and potassium concentrations were measured in 196 patients with acute cerebral infarction and 56 with cerebral hemorrhage. All patients were admitted within 7 days of onset and the data within 2 weeks of admission were recorded. The incidences of hypernatremia (serum Na greater than or equal to 149 mEq/l), hyponatremia (less than or equal to 134 mEq/l), hyperkalemia (serum K greater than or equal to 4.8 mEq/l) and hypokalemia (less than or equal to 3.2 mEq/l) were higher in patients with hemorrhage (18, 7, 13 and 14%, respectively) than infarction (4.5, 4.5, 11 and 6%, respectively). The incidences of hypernatremia and hyponatremia in infarction were higher in those who had cortical lesions than in those who had lesions in the basal ganglia or infratentorium. In cerebral hemorrhage, the incidence of hypernatremia was the highest in those with brain stem lesion. Hypernatremia was found in 27% of large sized hematoma, being significantly higher than that of those with medium (16%) or small (1%) hematoma. A similar tendency was also observed in hyponatremia and hyperkalemia. In elderly patients, electrolyte disturbances were more common than in young or middle-aged patients. Renal insufficiency and diabetes mellitus were frequent complications in stroke patients with hypernatremia (42 and 32%, respectively), of which 57% died within one month of admission.

Acute Disease↗