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

Stroke is increasingly becoming a major cause of death and morbidity in African population among most of which the frequencies of hypertension are considerable, although hard data based on community surveys are lacking and most of the information available is from hospital data. The epidemiology of stroke in the Africans is reviewed. The frequencies in hospital populations varied from 0.9% to 4.0% and stroke accounted for 0.5% to 45% of neurological admissions. There is male predominance in published series. The main risk factors are hypertension, diabetes mellitus and homozygous sickle cell disease (in children only). Ischaemic stroke is by far the commonest clinical type encountered. These conclusions are further supported by experience at Ibadan, of over 1100 Africans seen over 18 years reported briefly in this communication. The results of the first community study over a 2-year period on the incidence of stroke in an African Urban (Ibadan) Community are presented. The study was carried out as part of a multinational multicentric study initiated and sponsored by the World Health Organization. The male to female ratio was five to two. Incidence rates reached peaks in the eighth decade in males and in seventh decade in females and were higher in males in all age groups, and the rates are comparable with those recorded in European populations, except in those under the age of 40 in Ibadan, in which age-specific incidence rates are considerably lower than in European and Japanese populations. Hypertension, diabetes mellitus constituted the main risk factors. Mortality and recurrence rates are described and are similar to experience in the Caucasians. Hypertension in the Nigerians predispose to a high frequency of cerebrovascular disease other than through mainly cerebral atherosclerosis. With increasing longevity of Nigerians and other Africans, the mortality and morbidity caused by cerebrovascular disease would probably become of enormous dimensions and adequate control of high blood pressure on a community basis may be the only way of preventing this: this would be desirable as myocardial infarction in contradistinction to hypertensive heart disease is an uncommon complication of high blood pressure in the Africans and prevention of hypertensive heart disease as shown by experience elsewhere can be achieved by control of high blood pressure, which does not seem to prevent ischaemic myocardial disease.
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PMID:Stroke in the Africans. 41 66

In vivo circulating platelet aggregates (CPA) were evaluated in 18 patients aged 6 to 17 years with sickle cell disease and in 11 age and sex matched normal subjects. Twelve patients with sickle cell disease were in steady state and 6 had vaso-occlusive crises. CPA in patients in steady state were similar to those in normal subjects (mean 6 +/- 1% compared to 5 +/- 2%, respectively), whereas patients with vaso-occlusive crisis in acute state had significantly higher CPA (mean 39 +/- 8%) than patients in steady state or normal control individuals (both p less than 0.001). CPA decreased in patients with vaso-occlusive crisis (mean 11 +/- 4%) on the tenth day, in association with clinical improvement. This study suggests that in vivo platelet aggregate formation activity, although normal in sickle cell disease patients in steady state, is significantly increased in patients with vaso-occlusive crises.
Stroke
PMID:Circulating platelet aggregates in sickle cell disease patients with and without vaso-occlusion. 50 86

An opportunity to study cerebrovascular changes in sickle cell anemia (SCA) presented itself when a black child with this disorder died of bihemispheric strokes. Angiography demonstrated severe occlusive vascular disease involving primarily the circle of Willis and major bifurcations of both internal carotid arteries. Collateral circulation to the distal branches of the internal carotid arteries occurred through transdural anastomoses from the external carotid system and via the leptomeningeal route. Perfusion of the basal ganglia was accomplished by vessels arising from the proximal internal carotid arteries. These changes resembled those of Moyamoya disease. Autopsy showed old and recent cerebral infarcts. Two vascular processes were responsible for the arterial occlusions: (1) exuberant intimal hyperplasia, and (2) old and recent thrombi with partial recanalization. The former has been described only once before in SCA. Small vessels in the basal ganglia were exceptionally numerous and dilated. We conclude that intimal hyperplasia within large cerebral arteries may be responsible for infarction and small vessel prliferation in basal ganglia in patients with SCA.
Stroke
PMID:Cerebrovascular disease in sickle cell anemia: a clinical, pathological and radiological correlation. 62 45

The echocardiographic measurements of cardiac chamber dimension, ejection phase indices of left ventricular function and the systolic time intervals of 23 adult patients with sickle cell anemia were compared to those of normal control subjects. Patients with sickle cell anemia had a significantly greater mean left ventricular systolic dimension index, left ventricular diastolic dimension index, left ventricular mass, stroke volume index, interventricular septal width, aortic root index and left atrial index. No significant differences were noted between the mean velocity of circumferential fiber shortening, ejection fraction or systolic time intervals. The anemic population was divided into two groups; one consisting of patients less than 30 years old and the other of patients over 30 years old. There was no significant differences between the ventricular dimensions, velocity of circumferential fiber shortening, ejection fraction and systolic time intervals of the two groups. These data indicate that the chronic volume overload of sickle cell anemia is well tolerated without development of left ventricular dysfunction.
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PMID:Evaluation of left ventricular function in patients with sickle cell anemia. 93 58

Nine cases have been presented in detail to illustrate some of the varied causes of sudden neurological deficit in childhood: arteriovenous malformation, cryptic hamartoma, berry aneurysm, mycotic aneurysm, intraspinal arteriovenous malformation, brain tumor, migraine, arteritis, and multiple sclerosis. The Boston Children's Hospital experience with aneurysms and intracranial arteriovenous malformation has been summarized. It is noteworthy that a cutaneous hemangioma overlay one cranial and one intraspinal arteriovenous malformation. One small but deep cerebral arteriovenous malformation apparently destroyed itself after its second hemorrhage. Not only have multiple sclerosis and a brain tumor mimicked a vascular lesion, but a series of vascular accidents was misdiagnosed first as multiple sclerosis then as a thalamic tumor. The many possible causes of childhood strokes has been thoroughly cataloged in the Report of the Joint Committee for Stroke Facilities in 1973 (11). Children may be more susceptible to strokes because of congenital abnormalities such as congenital heart disease, hemophilia, and sickle cell anemia, or by diseases which more commonly occur in this age group, such as leukemia. The likelihood of brain abscess in cyanotic congenital heart disease is stressed. Arteriographic studies in our series have been safe; however, there have been reports of probable worsening of symptoms in children with multiple cerebral occlusive lesions in the presence of homocystinuria.
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PMID:Strokes in children. 98 45

Cerebral angiograms were performed in patients with sickle cell disease and symptoms of stroke to evaluate transfusion therapy for cerebrovascular accidents. Three patients who were transfused repeatedly for one year to maintain less than 30% hemoglobin S were compared to two patients who were not transfused. All patients had abnormal angiograms initially. After one year the angiographic abnormalities resolved in two and improved in one transfused child. The two children who were not transfused showed progressive vascular disease. For all arteriograms, the patients were prepared by transfusion with normal red cells and careful hydration.
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PMID:Transfusion therapy for cerebrovascular abnormalities in sickle cell disease. 124 48

Localized proton nuclear magnetic resonance spectroscopy (MRS), obtained with stimulated echo and spin echo sequences, MR imaging (MRI) and MR angiography (MRA) were used to study the brain in 13 children and adolescents with sickle cell disease. Regions of interest (ROI) studied by MRS included regions appearing normal on MRI as well as regions showing complications of sickle cell disease, including focal deep white matter areas of high signal intensity (deep white matter ischemia, DWMI) seen on long TR images, focal atrophic brain areas, and infarcts. The findings in these studies are summarized as follows: Normal-appearing regions on MRI have normal MRS. In ROI including small areas of DWMI, lactate elevation was not detected, but the levels of N-acetyl-aspartate (NAA) appeared slightly elevated. In areas of DWMI 1-2 cm in size, reduced blood flow could be seen on MRA and lactate elevation could be detected with MRS. When blood flow to a DWMI region was normal, NAA was reduced and there was little lactate elevation, as cell death had already occurred. ROI consisting of atrophic tissue had reduced NAA levels but total creatine levels were not changed. Sometimes lipids, presumably from broken cell membrane, could be detected. In regions of past massive stroke, all metabolites were absent except for small amounts of lactate or lipids.
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PMID:Investigation of stroke in sickle cell disease by 1H nuclear magnetic resonance spectroscopy. 128 41

In a five year retrospective study of 360 patients with homozygous (SS) sickle cell disease, eighteen (5%) were found to have neurological complications. Their ages ranged from 7 months to 21 years with a mean of 11.1 +/- 6 years. Of those with neurological complications, twelve (67%) of the patients had cerebrovascular accident, six (33.3%) convulsions, three visual disturbance; one sensorineural deafness, one cerebellar degeneration and the last one confusion and hallucinations. Four of the patients had multiple neurological complications. There was only one patient with recurrence of neurological complications. Two patients were hypertransfused and up to the end of the study period none of them had any recurrence. The pattern of neurological complications are similar to that observed in other studies. However, in this study, there were fewer recurrences of neurological complications.
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PMID:Neurological complications of sickle cell anaemia at KNH: a five year retrospective study. 129 28

Twenty-four patients presenting an acute stroke with watershed cerebral infarct on CT scan or MRI were included in this retrospective study. Age was 63 +/- 14 years (mean +/- SD), and sex ratio was 2 men for 1 woman. Main clinical features were: in anterior location, lower limb weakness and frontal syndrome with transcortical motor aphasia in left lesions or spatial dyscalculia in right ones; in posterior location, brachiofacial weakness with constant quadranopsia and hypoesthesia, and Gerstmann syndrome in left lesion. There was no distinctive feature for subcortical and multiple infarcts. In bilateral infarcts, there were one pseudobulbar syndrome, and 2 pseudo brainstem syndromes with neuropsychological signs. Aetiologies were severe carotid artery disease in 14 cases, severe cardiopathy in 6, isolated cerebral angiitis in 1, essential thrombocythemia in 1, protein C deficiency with sickle cell disease in 1, and cholesterol emboli in 1 anatomical case. CBF performed in carotid artery occlusions or tight stenoses showed evidence of haemodynamic changes. Microembolic process can be proposed in the case with cholesterol emboli. Preventive treatment is discussed.
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PMID:Watershed cerebral infarcts: retrospective study of 24 cases. 135

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


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