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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nimodipine is a calcium antagonist which improves learning and memory in brain-lesioned or aged animals (LeVere & Sandin, 1989; Schuurman & Traber, 1989). It also accelerates the recovery of experimentally damaged sciatic nerves (van der Zee et al., 1987) and reduces age-associated gait abnormalities in aging rats (Schuurman et al., 1987). Selective action on cerebral vessels has also been proven. Vasoconstriction was prevented or reduced with nimodipine under experimental conditions (Toward, 1981) and cerebral blood flow could be increased (Kazda et al., 1982). The drug has been tested in subarachnoid hemorrhage, stroke, severe head injury, cerebral resuscitation after cardiac arrest, impaired brain function in old age, and dementia. Methodological aspects of clinical studies with this agent are examined in this paper.
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PMID:Global rating, symptoms, behavior, and cognitive performance as indicators of efficacy in clinical studies with nimodipine in elderly patients with cognitive impairment syndromes. 150 90

Risk factors for intracerebral hemorrhage (ICH) and cerebral infarction (CI), were studied by a prospective study of 7,390 men and women aged 40-69 without a history of stroke living in three rural populations in Japan. Baseline examinations were done for populations in Akita-Ikawa and Akita-Ishizawa in 1975-1979, and for Ibaraki-Kyowa in 1981-1987, and followed until 1989 for Akita-Ikawa and Ibaraki-Kyowa and 1987 Akita-Ishizawa. There were 246 stroke cases diagnosed by clinical criteria during the follow-up period in which 74 percent (n = 181) had data from computed tomography (CT) performed within three weeks of the onset. According to these CT-findings, 181 stroke were classified as 48 with ICH, 50 with CI in penetrating artery regions (penetrating artery infarction), 33 with CI in cortical artery regions (cortical artery infarction), and 31 with subarachnoid hemorrhage while there were 19 with stroke without any evident CT abnormality. Cortical artery infarction was further classified as embolic type (n = 17) and thrombotic type (n = 9) according to clinical findings of the onset and presence of possible embolic sources such as atrial fibrillation, congenital heart disease, myocardial infarction and heart valve diseases. Using a nested case-control design, risk variables at baseline examination were compared between 131 stroke cases, 48 ICH and 83 CI, with 655 controls matched for sex, age (+/- 3), and the follow-up year. Univariate analysis showed that high blood pressure was associated with all types of stroke. From conditional logistic regression analysis significant risk variables were found to be high blood pressure for ICH and penetrating artery infarction, while atrial fibrillation and ST-T abnormality in electrocardiogram (ECG) were risk variables for cortical artery infarction. Associations with hypertensive or arteriosclerotic changes in ocular fundus were stronger for penetrating artery infarction than ICH and cortical artery infarction. ST-T abnormality in ECG was associated with embolic type cortical artery infarction and high blood pressure was associated with the thrombotic type, although the number of cases were small. Compared to controls, cortical artery infarction showed a higher mean value of serum total cholesterol for thrombotic type cortical infarction, and lower mean values for embolic type and ICH, but none of them reached statistical significance. The present study also suggests that duration of hypertension varied with type of stroke. ICH may develop due to acute effects of hypertension, while penetrating artery infarction and cortical artery infarction develop by chronic effects of hypertension.
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PMID:[A nested case-control study of risk factors for intracerebral hemorrhage and cerebral infarction classified by computed tomographic findings]. 150 35

Nimodipine is a dihydropyridine calcium antagonist which dilates cerebral blood vessels and increases cerebral blood flow in animals and humans. Preliminary findings reveal its potential benefit for the treatment of a wide range of cerebrovascular disorders, particularly for prophylaxis and treatment of delayed ischaemic neurological deficits resulting from cerebral vasospasm in patients with subarachnoid haemorrhage. Studies involving patients aged up to 79 years have confirmed these preliminary findings by showing that nimodipine reduces the incidence of severe ischaemic deficit after subarachnoid haemorrhage. Initial results from studies of patients with acute ischaemic stroke indicate that nimodipine, started within 72 hours of onset, improved recovery, particularly in patients over 65 years. However, other investigators have found no marked difference in 6-month mortality or morbidity rates of stroke patients aged up to 97 years. Findings from other studies suggest that nimodipine may improve symptoms of cognitive dysfunction in elderly patients. Nimodipine is well tolerated by both younger and older patients. The most frequently reported adverse event has been hypotension. Thus, nimodipine therapy offers important benefits as part of the approach to management of patients with subarachnoid haemorrhage and has potential in other cerebral disorders, including stroke and impaired cognitive function, although confirmation of initial results in patients with cerebral impairment are required.
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PMID:Nimodipine. A review of its pharmacological properties, and therapeutic efficacy in cerebral disorders. 150 42

Strokes occurred in 17 of 310 children with homozygous sickle cell disease who were followed from birth, representing an incidence of 7.8% by the age of 14 years. Two children had subarachnoid hemorrhage, one having resolution of symptoms after aneurysm surgery and another dying of a presumed second hemorrhage 14 days later. The remaining 15 strokes were presumed to be cerebral infarction, although autopsy, angiographic, or computed tomographic evidence was available in only 8 children. There were 6 deaths, 2 in the acute event and 4 after recurrence, which occurred in 6 (46%) of 13 patients who survived the initial episode. There were 10 recurrent episodes at a median interval of 9 months after the initial event. Steady-state hematologic data revealed significantly higher leukocyte counts than in control subjects without strokes at age 1 year and in the last study preceding the stroke. The initial stroke coincided with an acutely lowered hemoglobin value in 5 patients (3 aplastic crises, 1 acute splenic sequestration, 1 probable pulmonary sequestration) and with painful crises in another 7 patients. We conclude that a high leukocyte count and an acute decrease of hemoglobin are risk factors for stroke in patients with homozygous sickle cell disease.
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PMID:Stroke in a cohort of patients with homozygous sickle cell disease. 153 80

Measures to prevent ischemic stroke after aneurysmal subarachnoid hemorrhage include management of fluids to avoid dehydration, use of calcium entry blocking drugs, and when necessary, therapy with drug-induced hypertension and hypervolemic hemodilution. Promising treatments that may also prove to be effective include 21-aminosteroids, intrathecal thrombolytic therapy, and transluminal angioplasty.
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PMID:Prevention of brain ischemia after aneurysmal subarachnoid hemorrhage. 155 6

Regular red blood cell transfusions reduce the rate of recurrent cerebral infarction in sickle cell disease but lead to accumulation of excessive iron. We studied the effect on the prevention of recurrent stroke and the volume of blood transfused of a modified transfusion program in which the pretransfusion percentage of hemoglobin S (HbS) was maintained at 50%, rather than the conventional 30%. Fifteen patients with sickle cell disease and cerebral infarction who had been free of recurrent stroke for at least 4 years during which the pretransfusion HbS was maintained below 30% were assigned to a transfusion program in which the HbS was allowed to increase to 50%. Transfusion regimens included simple transfusion and manual and automated partial exchange transfusion. The duration of follow-up was 14 to 130 months with a median duration of 84 months. None of the 15 patients had a recurrent cerebral infarction during 1,023 patient-months in which the target pretransfusion HbS was 50%. Analysis of this finding, using a binomial distribution, indicates that there is less than a 5% chance that the risk per patient of recurrent stroke in the first year of the modified transfusion program is greater than 18%. One 23-year-old patient had a fatal intraventricular hemorrhage when the HbS was 30% and a 21-year-old patient had a fatal subarachnoid hemorrhage in the 40th week of pregnancy when the HbS was 29%. Blood requirements with simple transfusions decreased by 17% to 48% (mean 31%) when the target pretransfusion HbS level was increased from 30% to 50% (P less than .001). Manual or automated partial exchange transfusions and a target HbS level of 50% in eight patients reduced blood requirements by 33% to 99% (mean 67%) in comparison with simple transfusion and a target HbS level of 30% (P less than .001). This study offers evidence that a target pretransfusion HbS level of 50% affords a continuing high rate of protection against recurrent cerebral infarction in sickle cell disease after 4 years of a conventional transfusion program. Increasing the target HbS level from 30% to 50% provides a major reduction in blood requirements and lowers the rate of iron accumulation.
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PMID:A modified transfusion program for prevention of stroke in sickle cell disease. 155 63

A 55-year-old man with a mild fever and sweating developed severe headache for the days before admission. Cerebral computed tomography and selected cerebral angiography on the day of admission revealed subarachnoid hemorrhage due to rupture of an aneurysm of a distal branch of the left middle cerebral artery. Detection of vegetation on the aortic valve by two dimensional echocardiography confirmed the diagnosis of infective endocarditis with a ruptured mycotic cerebral aneurysm. Because of rapid growth of the vegetation on the aortic valve and progression of heart failure despite antibiotic therapy, emergency cardiac surgery was performed. To prevent re-rupture of the aneurysm, the aortic valve was replaced with a bioprosthetic valve, and no anticoagulant was administered postoperatively. Repeated cerebral angiography revealed that the aneurysm was becoming progressively smaller during the next 9 months. No cerebrovascular accident occurred postoperatively. We believe that it is safe to treat a ruptured mycotic cerebral aneurysm without involvement of a hematoma mass in the brain conservatively, and that use of a bioprosthetic valve, if valve replacement is mandatory, and avoidance of anticoagulant therapy during the postoperative period are advisable in the treatment of a patient with infective endocarditis and a ruptured cerebral mycotic aneurysm.
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PMID:[Valve replacement in a patient with infective endocarditis and ruptured mycotic cerebral aneurysm]. 156 43

Neurogenic mechanisms are important in the maintenance of most forms of hypertension, yet the brain is highly vulnerable to the deleterious effects of elevated blood pressure. Hypertensive encephalopathy results from a sudden, sustained rise in blood pressure sufficient to exceed the upper limit of cerebral blood flow autoregulation. The cerebral circulation adapts to chronic less severe hypertension but at the expense of changes that predispose to stroke due to arterial occlusion or rupture. Stroke is a generic term for a clinical syndrome that includes focal infarction or hemorrhage in the brain, or subarachnoid hemorrhage. Atherothromboembolism and thrombotic occlusion of lipohyalinotic small-diameter end arteries are the principal causes of cerebral infarction. Microaneurysm rupture is the usual cause of hypertension-associated intracerebral hemorrhage. Rupture of aneurysms on the circle of Willis is the most common cause of nontraumatic subarachnoid hemorrhage. Stroke is a major cause of morbidity and mortality, particularly among persons aged 65 years or older. Treatment of diastolic hypertension reduces the incidence of stroke by about 40%. Treatment of isolated systolic hypertension in persons aged 60 years and older reduces the incidence of stroke by more than one third. Blood pressure management in the setting of acute stroke and the role of antihypertensive therapy in the prevention of multi-infarct dementia require further study.
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PMID:Hypertension and the brain. The National High Blood Pressure Education Program. 158 Jul 19

We studied 925 consecutive patients hospitalised with acute stroke to determine how stroke type, age, gender and risk factors influence acute, in-hospital outcome. Stroke types included carotid territory cortical or large subcortical infarction (52%), vertebrobasilar infarction (12%), lacunar infarction (11%), intracerebral haemorrhage (16%), and subarachnoid haemorrhage (9%). Mean age (mean +/- 1 SD) was 66 +/- 15 years, but patients with cerebral infarction were older than those with cerebral haemorrhage. The prevalence of hypertension, diabetes mellitus and cardiac disease increased with age across all stroke types, while the prevalence of smoking decreased with age. Mortality was 19% overall, but varied significantly between stroke types, highest in intracerebral haemorrhage (34%), and lowest in lacunar infarction (1%). Age had a marked adverse effect on mortality, independent of stroke type, the probability of death increasing by 3 +/- 0.5% per year from 20-92 years, whereas gender had no effect. Cardiac disease and diabetes were independent adverse prognostic factors (Odds Ratios 1.6 and 1.5 respectively). Cerebral haemorrhage, age, cardiac disease and diabetes all independently worsen acute stroke outcome.
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PMID:Acute stroke outcome: effects of stroke type and risk factors. 158 Aug 59

A retrospective follow-up of 200 consecutive stroke patients [ischemic brain infarction (IBI) 157, intracerebral hemorrhage (ICH) 20, subarachnoid hemorrhage (SAH) 23] who were in need of ambulatory rehabilitation was conducted for a mean period of 40 months after stroke. Epilepsy developed in 33 (17%) patients. The occurrence of epilepsy was 14% in IBI, 15% in ICH, and 35% in SAH. Significantly more patients developed epilepsy in the SAH group than in the IBI group (8 of 23 vs. 22 of 157, p less than 0.05). Of the 33 patients, 15% had their first seizures within the first 2 weeks after stroke, and 55% developed epilepsy in 6 months. Forty-eight percent of the patients had generalized seizures. Antiepileptic drug (AED) treatment was started in 28 of 33 patients, of whom 17 still had seizures during follow-up. Epilepsy was an important consequence of stroke among patients who needed rehabilitation, especially in SAH patients. In most, this was due to arterial spasm leading to IBI.
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PMID:Epilepsy after stroke. 159 26


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