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

The ABO blood-group distributions of 1460 patients who had died from a stroke were compared with those of a control group of 20 705 controls selected at random from the healthy population at risk (i.e., over thirty-five years of age and matched for age and sex ratio). The cause of death was certified as cerebral thrombosis in 329 cases and as cerebral haemorrhage in 482 cases, these diagnoses being established in neurological hospitals; the remaining 649 cases had an unspecified type of stroke, the diagnosis being made by general practitioners. In the group with unspecified type of stroke the blood-group distribution was practically the same as the distribution in the controls. In the thrombosis cases there was an excess of blood-groups A and AB and a deficiency of O and B; in cerebral haemorrhage this situation was reversed. However, these were only trends; the differences were not significant at the 5% level. A statistically significant difference did emerge when the A+AB excess in thrombosis was contrasted with the O+B excess in haemorrhage, suggesting that this difference might be accounted for the major A subgroup (A1) and, consequently, A1B.
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PMID:Cerebral thrombosis, cerebral haemorrhage, and ABO blood-groups. 5 89

One adolescent and two young adults had ulcerative colitis and cerebral thrombosis. All survived with neurologic deficit. These patients had no other predisposing factor for cerebrovascular disease. Systemic arterial and venous thromboembolic complications occur often in ulcerative colitis, but stroke is uncommon. Abnormalities in the early stages of clotting may be responsible, and the risk of thromboembolic phenomena in young patients seems to increase with exacerbations of this form of chronic inflammatory bowel disease, and possibly with regional enteritis as well.
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PMID:Strokes and ulcerative colitis. 56 88

In 100 consecutive patients with acute cerebrovascular accident, due to cerebral thrombosis in 72, cerebral hemorrhage in 12, embolus in 6, and subarachnoid hemorrhage in 10, there were 90 who had electrocardiographic abnormalities during the first three days after admission, compared to 50% in a control group. The patients with cerebrovascular accident had a 7- to 10-fold higher incidence of ST segment depression, prolonged Q-Tc interval and atrial fibrillation, and a 2- to 4-fold higher incidence of T wave inversion, conduction defects, premature ventricular beats and left ventricular hypetrophy. Patients who died had a 2-, 3- and 5-fold higher incidence of electrocardiographic evidence of recent myocardial infarction, atrial fibrillation and conduction defects than those who survived, but these changes occurred in only 5, 21 and 14% of all patients, and other electrocardiographic changes could not be correlated with mortality. During the first three days after admission 29 patients had elevation of serum enzymes which may be derived from cardiac muscle, particularly CPK, which was increased 6-fold, compared to 2-fold increases in HBDH, GOT, and LDH. Only 5 of these patients had electrocardiographic evidence of recent myocardial infarction. Patients with elevated serum CPK had a 2-fold higher incidence of ST segment depression, T wave inversion, conduction defects and atrial fibrillation than those with normal CPK, and a mortality of 66%, compared to 30%. Of 41 patients who died, 49% had elevated serum CPK, compared to 15% of 59 patients who survived. These differences were significant (P less than 0.01). Serum CPK was more frequently helpful than the electrocardiogram in evaluating the extent of cardiac damage and in predicting mortality. Patients with acute cerebrovascular accident should have repeated evaluation of serum CPK and the ECG, and be monitored for arrhythmias.
Stroke
PMID:Electrocardiographic changes and myocardial damage in patients with acute cerebrovascular accidents. 89 40

Platelet aggregability was measured using the screen filtration pressure (SFP) method in 50 elderly healthy people, 93 persons with essential hypertension, 166 patients with cerebral thrombosis at the recovery stage (more than two months after onset), and 74 patients with cerebral hemorrhage at the recovery stage. SFP by 3 muM ADP in the healthy persons, the hypertensive patients, and the patients in the recovery stages of hemorrhage and thrombosis were 148.7 +/- 53.5, 176.2 +/- 74.4, 189.8 +/- 58.3 and 206.3 +/- 58.9 mm Hg, respectively. The differences of the SFP between the Healthy and each of the diseased groups were statistically significant (P less than 0.01 to 0.05). Meanwhile, SFP of nine patients with cerebral thrombosis and 18 patients with hemorrhage was measured during their time course of disease from the onset to 180 days. SFP in the acute stage of thrombosis showed an increase and a gradual decrease during the time course, while SFP in the acute stage of hemorrhage showed the opposite -a decrease and a gradual increase. A statistically significant difference was observed between both groups within 30 days from onset (P less than 0.001). Screen filtration pressure in the acute stage of hemorrhage showed 95.2 +/- 17.7 mm Hg in nine survival cases and 194.0 +/- 96.2 mm Hg in nine deaths with ten days from the onset. The difference was statistically significant (P less than 0.001). Such results suggest a role of platelets in cerebral thrombosis and hemorrhage and a usefulness in differential diagnosis of both diseases.
Stroke
PMID:Platelet aggregability measured by screen filtration pressure method in cerebrovascular diseases. 96 Jan 62

An epidemiological study of cerebrovascular disease in Akabane and Asahi, Japan, was made. (These cities are located near Nagoy, Japan.) The study population included 4,737 men and women aged 40 to 79 at the time of entry into the study. There were 4,186 persons who were examined and, of these, 264 cases of cerebrovascular attacks were observed between 1964 and 1970. The incidence rate of stroke in those persons not responding to the survey was 15.9 times higher than in those persons examined according to person-year observation in Akabane. The risk factors for cerebral hemorrhage and thrombosis were evaluated by age-adjusted and sex-adjusted relative risks. The predisposing factors to cerebral hemorrhage appeared to be high blood pressure, high left R wave, ST depression, T abnormality, capillary fragility counts, previous medical history of stroke and albuminuria. For cerebral thrombosis, the predisposing factors appeared to be high blood pressure, ST depression and funduscopic sclerotic findings, and those factors assumed to be significant were glycosuria and smoking habits. Ocular funduscopic abnormality was the most prominent risk factor for cerebral thrombosis, while high blood pressure and ECG abnormalities were highly related to cerebral hemorrhage. It was suggested that those subjects with a relatively higher blood pressure may have a higher relative risk of cerebral hemorrhage than those with a lower (normal range) blood pressure. A previous or family history of stroke also appeared significantly related to cerebral hemorrhage.
Stroke
PMID:A prospective study of cerebrovascular disease in Japanese rural communities, Akabane and Asahi. Part 1: evaluation of risk factors in the occurrence of cerebral hemorrhage and thrombosis. 100 36

Antibodies directed against phospholipids are highly associated with episodes of venous and arterial thrombosis, which are often recurrent. There seems to be a skewed frequency of cerebral thrombosis when the arterial circulation is affected. Clinical clues that should lead to evaluation for aPL include stroke in a young adult, recurrent thrombosis or miscarriage, and thrombocytopenia. Associated laboratory abnormalities include a biologically false-positive test for syphilis, abnormal antinuclear antibody titers, and a high erythrocyte sedimentation rate. If the activated partial thromboplastin time is prolonged on routine screening and does not correct with mixing studies, a lupus anticoagulant should be suspected. However, more sensitive and specific tests are usually necessary to detect aPL. Many in vitro and more recently in vivo systems strongly suggest that aPL may be directly implicated in the pathogenesis of thrombosis. Optimal management of patients with aPL-associated thrombosis is unknown. The use of aggressive therapeutic management schemes with such agents as warfarin or corticosteroids is sometimes required.
Heart Dis Stroke
PMID:Antiphospholipid antibodies and ischemic stroke. 134 35

A 52-year-old Chinese female with recurrent cerebral thrombosis associated with hereditary protein S deficiency is described. The need to consider clotting disorders in young patients with no known risk factors for stroke is emphasized.
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PMID:Recurrent cerebral thrombosis associated with protein S deficiency in a Chinese female. 141 82

40 patients of stroke were studied. The results showed that in Cerebral hemorrhage the correlation between ascending Growth hormone (GH) of CSF and insulin of serum was negative, but the positive correlation between ascending GH (CSF) and hyperglycemia. In patients of cerebral thrombosis the results of values above were no correlation. The pathological significance in such cases was discussed.
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PMID:[Relationship among hyperglycemia growth hormone (CSF) and insulin in serum of cerebral hemorrhage]. 149 6

We examined the relationship between free protein S deficiency and cerebrovascular disease by reviewing the records of all patients with the diagnoses of cerebral thrombosis, cerebral embolism, and cerebral vascular occlusion who were referred for coagulation studies over a 12-month period. We assayed for free protein S antigen, protein C antigen, and antithrombin III and tested for lupus-like anticoagulant and anticardiolipin antibody. Twenty-two of 267 patients (8.2%) admitted with thrombotic strokes were referred for coagulation studies. Free protein S antigen was significantly lower in women than in men (62 +/- 25% versus 88 +/- 24%, p = 0.03; n = 11 in each group). Six women had free protein S antigen levels below the range recorded for a contemporary group of 24 age-matched normal women (17 to 59% versus 70 to 102%, p less than 0.001); four of these women had cerebral arterial thrombosis and two had venous dural sinus thrombosis. The six women were aged 29 to 55 at the time of their first strokes; two had family members with protein S deficiency, and one of these had died of a stroke at age 52. Other abnormalities in this population included a positive test for lupus-like anticoagulant or anticardiolipin in five patients, a modest decrease in protein S in two men, and one patient with an isolated deficiency of antithrombin III. We conclude that protein S deficiency may be an important risk factor for stroke in middle-aged women but this requires confirmation by prospective studies in unselected patients.
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PMID:Protein S deficiency in middle-aged women with stroke. 153 5

Polycythemia in CAPD patients has been rarely described. Over an eight year period, 4 out of 123 CAPD patients (3%) were identified as having Hct values exceeding 50% for 1 month or longer. All of the 4 patients were insulin dependent diabetics (4/47 diabetic patients, 8.5%). Charts were reviewed on 3 of these 4 patients. Polycythemia developed after a mean of 21 +/- 7 months on peritoneal dialysis. Prior to the development of polycythemia, ferritin levels were low and ferrous sulfate therapy was begun at a time the Hct values were 36 to 40%. Erythropoietin levels were obtained in 2 patients, and were 22 U/L (Hct 51%) and less than 5 U/L (Hct 55%). Renal ultrasound failed to show renal masses or cysts. One patient had a plasma volume of 2.1 L (normal 2.4-3.2 L); another patient was clinically volume depleted. Complications during the period of polycythemia included gangrenous feet requiring amputation in 2 patients, CVA in 2 patients, and splenic infarct in 1 patient. One patient died of cerebral thrombosis. We conclude that polycythemia is uncommon in CAPD patients and occurs most often in diabetic patients. Volume depletion and iron therapy may play a role in its etiology. In this high risk group of patients polycythemia may contribute to vascular complications and should be avoided.
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PMID:Polycythemia in diabetic patients on CAPD. 168 Apr 62


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