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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an effort to call attention to a lesion which is possibly provoked by ingestion of oral contraceptives, this case report of a 23-year-old woman, who had been taking Minovlar for 3 years admitted to the hospital after sudden onset of complete right-sided hemiplegia and total motor aphasia is presented. There was no clinical evidence of deep vein thrombosis or other cerebral, coronary, or other arterial occlusions due to embolism on admission. 1 week later, bilateral leg venography showed a normal left leg but the right leg showed nonfilling of the deep veins of the calf. In the process of a right-heart catherization, an atrial communication was crossed which proved to be a patent foramen ovale by pulmonary artery pressures and dilution indicator curves. Hence, a clinical diagnosis of paradoxical embolism was made on the grounds of combined evidence of deep vein thrombosis, electrocardiogram changes of acute cor pulmonale, which were entirely different from those known to accompany primary cerebrosvascular lesions, and catheter studies typical of embolism rather than thrombosis. This case prompted the authors to call for prospective studies to reveal paradoxical embolism in oral contraceptive users, rather than venous thrombosis.
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PMID:Paradoxical embolism associated with oral contraceptives: an underdiagnosed lesion? 48 90

In fifteen patients with a cerebro-vascular accident resulting in an acute hemiplegia there was a subsequent rise in the platelet count and plasma fibrinogen level. There were no significant alterations in platelet adhesiveness, plasminogen activator, plasminogen, FR-antigen and haematocrit. Patients diagnosed as developing deep venous thrombosis with the 125I-fibrinogen technique had a significantly lower platelet adhesiveness and plasminogen level than those who were not.
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PMID:Platelet adhesiveness and fibrinolysis after recent cerebro-vascular accidents and their relationship with subsequent deep venous thrombosis of the legs. 103 1

Venous thrombo-embolism is a common complication in patients with acute ischaemic stroke. Without prophylaxis, deep vein thrombosis occurs in 60-75% of patients with dense hemiplegia, usually in the paralyzed limb, and 1-2% suffer fatal pulmonary embolism. Orgaran (Org 10172, low-molecular-weight heparinoid) has been evaluated for the prevention of deep vein thrombosis in patients with acute ischaemic stroke in two studies. In a double-blind study, 75 patients were randomized to receive Orgaran (50 patients) in a loading dose of 1,000 anti-Xa units intravenously followed by 750 anti-Xa units subcutaneously 12-hourly or placebo (25 patients). Deep vein thrombosis occurred in 2 of 50 (4%) in the Orgaran group and 7 of 25 (28%) in the placebo group (p = 0.005). The corresponding rates for proximal deep vein thrombosis were 0 and 16%, respectively (p = 0.01). There was one major haemorrhage in the treated group and one minor haemorrhage in the placebo group. In the second study, the safety and efficacy of Orgaran was compared with unfractionated heparin in the prevention of deep vein thrombosis in a double-blind randomized trial. Eighty-seven patients with marked lower limb paralysis secondary to stroke were randomized to receive Orgaran (45 patients) in a dose of 750 anti-factor Xa units subcutaneously 12-hourly or unfractionated heparin (42 patients) in a dose of 5,000 units subcutaneously 12-hourly. Venous thrombosis occurred in 4 of 45 (8.9%) of the Orgaran group and 13 of 42 (31%) in the unfractionated heparin group (2p = 0.014). The corresponding rates for proximal vein thrombosis were 4.4 and 11.9%, respectively (2p = 0.255).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Orgaran in the prevention of deep vein thrombosis in stroke patients. 137 69

The authors report 21 cases of heparin-induced thrombocytopenia with ischemic vascular complications. The clinical presentations were peripheral arterial ischemia (16 cases), hemiplegia (1 case) and deep vein thrombosis (4 cases). The vascular surgeon confronted by these complications in an emergency situation should recognise the difficulties of clinical diagnosis (atypical forms) and biological investigations (problems of tests of platelet aggregation). Arterial occlusions are usually accessible to disobliteration with a Fogarty catheter without peroperative heparinisation. Delayed diagnosis explains the seriousness of these complications; in our series of 21 patients, there were 2 deaths, 1 paraplegia, 4 amputations due to arterial problems, 4 severe post-deep vein thrombosis conditions, two of which followed trans-metatarsal amputation. The diagnosis of heparin-induced thrombocytopenia implies immediate withdrawal of heparin therapy. A relay with a low molecular weight heparin is not without risk and should only be undertaken after a negative platelet aggregation test (with the low molecular weight heparin). These tests are rarely practicable in emergency situations and a relay using oral anti-vitamin K antagonists with a rapid onset of action is probably the safest option.
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PMID:[Ischemic vascular complications following thrombopenia induced by heparin. Diagnostic and therapeutic problems]. 212 62

143 patients with acute onset of hemiplegia transferred to our unit for rehabilitation were analysed retrospectively for the development of deep vein thrombosis or pulmonary emboli. 26% of the patients had suffered thromboembolic events, in more than half of the cases within the initial four weeks after hospital admission. Hemiplegia seems to be the main risk factor for thromboembolic complications, whereas age and sex had no further impact on the rate of occurrence in our series. Nor did we find a correlation between the extent of the paresis in the involved lower extremity or the degree of restriction of mobility and the incidence of thromboembolic disease. Because of the high frequency of thromboembolic complications in our patients we recommended prophylactic treatment with low dose heparin given subcutaneously, followed by oral anticoagulant therapy with vitamin K antagonists, provided there are no contraindications.
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PMID:[Thromboembolism complications following acute hemiplegias]. 342 73

A case of cerebral venous thrombosis with familial antithrombin III (AT III) deficiency was reported and we discussed the anticoagulant therapy of cerebral venous thrombosis from the viewpoint of AT III. The patient, a 17-year-old boy, was admitted to our clinic with severe bifrontal headache, generalized convulsions and progressive disturbance of consciousness. He developed deep vein thrombosis in his right leg and pulmonary emboli two years earlier when he was placed on heparin and so forth, followed by warfarin sodium. Warfarin was terminated 9 months prior to his recent illness. On neurological examination on admission, he was semicomatous with blurred disc margins, roving eye movements with right abducens nerve palsy, nuchal stiffness and right flaccid hemiplegia. Left carotid angiogram and CT scan revealed extensive superior sagittal sinus thrombosis, complicated with hemorrhagic infarcts in bilateral frontal lobes. When examined for coagulation studies, the patient and his father had decrease in AT III activity and antigen levels. He was treated successfully with antiedematous agents and anticonvulsants during acute phase of illness. He was thereafter placed on warfarin 5-6 mg/day with no further clinical thromboembolic event for 2 years 9 months. There was no neurological abnormality when he was last examined, although he was treated with valproic acid 1,200 mg/day and phenytoin 250 mg/day to control occasional adversive seizures. A coagulation study following infusion of 5,000 units of AT III was carried out. Warfarin was discontinued the day before the study. 0.64 U/kg of AT III administration resulted in a 1% increase in AT III level after the infusion. The biological half life of AT III was 14.4 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral venous thrombosis with familial antithrombin III deficiency]. 404 Dec 90

In 35 Chinese patients suffering from strokes resulting in hemiparesis or hemiplegia, deep venous thrombosis, as detected with 125I-fibrinogen scan, occurred in the paralysed leg in five and in the normal leg in one. The total incidence of 17% was lower than that reported in the West. No clinical evidence of pulmonary embolism was seen. This report represents an objective confirmation of the low incidence of venous thrombosis in the Chinese.
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PMID:Deep venous thrombosis after strokes in Chinese. 693 63

We report a case of pulmonary embolism complicated by paradoxical cerebral embolism in a patient with atrial septal aneurysm and patent foramen ovale. The patient was a 65-year-old obese woman, admitted because of sudden development of right-sided hemiplegia and dysarthria. In the few days before hospitalization she noted painful edema of the right leg and suffered from increasing dyspnea. Echo-Doppler examination of the venous bed confirmed the clinical suspicion of deep vein thrombosis. A pulmonary scan showed multiple perfusion defects in both lungs. On cerebral computerized tomography there were two non-haemorrhagic infarct zones. Contrast transesophageal echocardiography revealed a type II atrial septal aneurysm with right-to-left shunting through a patent foramen ovale. The patient was treated by warfarin, followed by implantation of a caval filter, with a good outcome. Paradoxical embolism may be more common than currently thought. In cases of pulmonary embolism, a careful check for clinical symptoms indicative of a possible paradoxical embolism should be performed and, consequently, a search for possible atrial septal aneurysm or patent foramen ovale.
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PMID:[Paradoxical embolism in a patient with aneurysm of the interatrial septum]. 792 85

Hereditary protein S deficiency (HSPD) is a predisposing factor to recurrent venous thrombosis but is not currently associated with stroke. We report two cases of HSPD revealed by stroke in young adults. The first one was a 36-year-old patient whith a pure motor hemiplegia, who gradually recovered without sequelae. Total and free protein S was decreased (55 and 10%). One of his brothers died from pulmonary embolism at 20 years and a sister had low protein S level without clinical signs. The second case was a 26-year-old patient who had a right hemiplegia with aphasia due to an infarction in middle cerebral artery area. He partially recovered, but the course of the illness was complicated by deep venous thrombosis of the lower limbs and pulmonary embolism. Total and free serum protein S level was severely decreased (25 and 0%). The patient's mother and one of his sisters also had low protein S but never had clinical complications. In both case, dupplex scanning, transcranial doppler, echocardiography, serum antithrombin III and protein C were normal. Cigarette smoking was the only risk factor for arterial disease. These two cases suggest that HSPD must be investigated in young patients with stroke, even in cases of lacunar stroke.
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PMID:[Cerebrovascular complications and hereditary protein S deficiency: 2 cases]. 876 59

In medical patients there are numerous and variable risk factors for deep vein thrombosis. Placebo-controlled clinical trials are rare. The efficacy of standard heparin or low molecular weight heparin for the prevention of deep vein thrombosis is clearly demonstrated for patients with recent myocardial infarction, ischaemic stroke with hemiplegia or severe pulmonary sepsis with lung failure. Pharmacological prophylaxis is probably also efficient in patients with a severe acute disease and a certain history of deep vein thrombosis. For all other medical and especially for bedridden elderly patients, use of low molecular weight heparin might decrease the incidence of deep vein thrombosis but might not modify the overall mortality. In these situations, placebo-controlled clinical trials are needed for best evaluation of the benefit-risk ratio.
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PMID:[Synthesis: certainties/uncertainties in the prevention of venous thrombosis in medical patients]. 1007 Feb 35


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