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

1. A review of the immediate and long-term results of prophylactic carotid endarterectomy for asymptomatic lesions of 78 carotid arteries in 72 patients between 1961 and 1976 is presented. 2. The inhospital operative mortality was zero. Two patients experienced postoperative transient neurologic deficit with complete recovery (2.6 per cent). There were no postoperative strokes. 3. Late follow-up data demonstrated that in only one patient did a stroke subsequently develop appropriate to the operative side, and it occurred 4 years after operation. Life table analysis for neurologic events carried out for up to 15 years indicated a 96 per cent stroke-free status of the surviving patients. 4. A 42 month survival rate of 83 per cent in patients treated by prophylactic carotid endarterectomy represented a statistically significant improvement over the 67 per cent survival of a comparable group of patients reported on in the literature. 5. Prophylactic carotid endarterectomy in the experience of vascular surgeons who can offer a low operative morbidity and mortality appears to be reasonable therapy in preventing stroke and prolonging survival until a randomized controlled study comparing surgery with the natural history of untreated patients shows evidence to the contrary.
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PMID:Asymptomatic carotid stenosis. Immediate and long-term results after prophylactic endarterectomy. 46 20

The effects of hemorrhagic shock on left ventricular dimensions and volume were studied in 15 splenectomized dogs. A 42 +/- 1% decrease in total blood volume caused arterial blood pressure to fall 60% (from 120 +/- 5 to 48 +/- 3 mmHg); the first derivative of left ventricular pressure at a developed pressure of 40 mmHg fell 54% (from 1,930 +/- 94 to 905 +/- 93 mmHg/s, P < 0.05). Cardiac output fell 76% due to a 73% decrease in stroke volume; heart rate was unchanged at the end of hemorrhage but increased 50% during 3 h of sustained shock (from 110 +/- 6 to 166 +/- 8 beats/min, P < 0.05). During hemorrhage the septal-lateral and the anterior-posterior end-diastolic dimensions fell to a greater extent (7.8 mm, -21% and 7.0 mm, -18%, respectively) than the apex-base dimension (2.3 mm, -3.3%, P < 0.05). As a result of these dimensional changes, left ventricular end-diastolic volume fell 39% (from 48 +/- 2 to 28 +/- 1 cm3, P < 0.01). End-systolic dimensions fell in the same proportion during hemorrhage, resulting in a 30% decrease in end-systolic volume (from 30 +/- 2 to 21 +/- 1 cm3, P < 0.05). After 120 min of sustained shock, all end-diastolic dimensions remained unchanged, but end-systolic dimensions and volume increased significantly from values measured at end hemorrhage (P < 0.05), causing ejection fraction and stroke volume to fall to a greater extent. This study confirms a pronounced reduction in the minor axes of the left ventricle during hemorrhagic shock with subsequent reduction in ventricular function.
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PMID:Left ventricular dimensions during hemorrhagic shock measured by biplane cinefluorography. 144 7

A 42-year-old woman suffered two focal right hemisphere strokes, sequentially damaging different components of a proposed cerebral network for the spatial distribution of attention. Her first stroke was centered in the right frontal lobe and resulted in left hemi-spatial neglect but only for tasks that emphasize exploratory-motor components of directed attention. A second stroke occurred 20 days later in the parietal lobe and led to the emergence of perceptual-sensory aspects of neglect. This case strongly supports the existence of a distributed anatomic-functional network subserving directed attention.
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PMID:Dissociated neglect behavior following sequential strokes in the right hemisphere. 237 43

A 42-year-old man presented with right temporal headache, dysarthria, and dysphagia. On examination, he had a right hypoglossal nerve palsy. The diagnosis of right internal carotid artery dissection was suggested by magnetic resonance imaging and confirmed by carotid angiography. A dynamic computed tomogram demonstrated enlargement of the carotid artery. In carotid dissection, the hypoglossal nerve may be compromised by local factors as it passes close to the carotid artery in the neck.
Stroke 1988 Sep
PMID:Spontaneous internal carotid artery dissection presenting as hypoglossal nerve palsy. 304 72

A 42-year-old man with diabetes mellitus and probably acromegaly had a pituitary apoplexy with left-sided oculomotor palsy. There was an immediate fall in blood glucose concentration. Pituitary insufficiency promptly developed. Blood glucose levels remained normal for the next two years. During the first year after the pituitary apoplexy, severe proliferative retinopathy developed in the left eye, which became almost blind. Only mild retinopathy was present on the right side. Plasma concentrations of growth hormone remained low after the apoplexy, and the acromegalic features subsided. The explanation of these findings may be that the proliferative retinal angiopathy was caused by compression of the cavernous sinus at the time of the apoplexy. This would lead to impaired venous drainage, thus resembling occlusion of the central retinal vein, which may cause retinopathy similar to that seen in diabetes mellitus.
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PMID:Pituitary apoplexy, the Houssay phenomenon, and accelerated proliferative retinopathy. 403 88

A 42-year-old woman developed headache and epistaxis followed by fever, stiff neck, and loss of vision of the right eye. The diagnosis of simple epistaxis was changed to mucormycosis, then to bacterial meningitis and then to sphenoid sinusitis, before the correct diagnosis of pituitary apoplexy was established by CT scan. Epistaxis is yet another confusing symptom of pituitary apoplexy.
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PMID:Pituitary apoplexy presenting with epistaxis. 623 14

A 42-year-old man had ischemic infarction from an occlusion of the left posterior cerebral artery (PCA), but had no visual field defect by examination or Goldmann perimetry. Arteriograms showed distal filling of the occluded PCA, but no collateral blood flow from the carotid circulation, suggesting collateral flow from leptomeningeal anastomoses. Visual field sparing may occur in surgical occlusion of the PCA, but rarely occurs in stroke. An infarction from PCA occlusion is not excluded by complete visual field sparing, and studies looking for other causes of the neurologic deficit may not be necessary.
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PMID:Posterior cerebral artery occlusion without hemianopia. 673 7

The authors report the occurrence of vascular occlusion due to hyperhomocysteinemia without significant underlying atherosclerotic disease. This unique observation supports the potential of hyperhomocysteinemia to induce thrombosis and the independence of the thrombosis from hyperhomocysteinemia's associated atherosclerosis. The case demonstrates the clinical relevance of the effects of hyperhomocysteinemia on the coagulation cascade. A 42-year-old woman who lacked signs of classic homocystinuria developed disseminated thrombosis with a 24-hour urine homocysteine concentration of 384 mg, twelve times the upper limit of normal. Thrombosis was present in the aortic arch and its major branches and in the mesenteric arteries and veins. A fatal stroke resulted from the thrombosis. Autopsy revealed minimal atherosclerotic disease and no complicated plaques. This case demonstrates an expanded role of hyperhomocysteinemia in clinically significant vascular occlusion. Serum homocysteine concentration determination may be a factor in the evaluation of a hypercoagulable state. Hyperhomocysteinemia should be considered when evaluating arterial or venous thrombosis in a young person regardless of whether atherosclerosis or other signs of abnormal homocysteine metabolism are present.
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PMID:Homocysteine associated hypercoagulability and disseminated thrombosis--a case report. 975 29

A 42-year-old house wife presented with worsening headaches over 6 months in the absence of visual symptoms or symptoms suggestive of focal neurology. She was a life-long smoker. Systems review was unremarkable apart from secondary amenorrhoea and galactorrhoea of 6 months duration. Her serum prolactin was found to be 620 mU/l (60-400), FT4 12.6 nmol/l (9.8-23.1), TSH 1.38 mU/l (0.35-5.5), oestradiol < 73 pmol/l, LH and FSH of 4.4 and 12.6 mIU/l, respectively. She was on bromocriptine. A presumptive diagnosis of pneumonia, based on pyrexia and CXR findings, was made and she was started on IV antibiotics. Two days later she developed meningism and deterioration of conscious level. (Lumbar puncture results: no organisms, 312 neutrophils and 164 lymphocytes). CT scan revealed a 2.5-cm pituitary adenoma, with suprasellar extension. A repeat hormonal profile revealed FSH 1.4, LH < 0.3 mU/l, oestradiol < 73 pmol/l, prolactin 488 mU/l (60-400), and low random cortisol at 29 nmol/l. T1-weighted MRI revealed a large pituitary mass with evidence of haemorrhage. The patient subsequently underwent a transsphenoidal exploration with resection of the pituitary lesion. Whilst awaiting the histopathology results, CT of chest revealed a 1. 5-cm diameter rounded well defined density in the right lower lobe associated with hilar, pre- and right para-tracheal lymphadenopathy. The histopathology of the pituitary lesion, obtained piecemeal, revealed fragments of fibrous tissue infiltrated by sheets of acidophilic prolactin-positive cells, in keeping with a prolactinoma. In addition, other fragments with blood clot included highly atypical epithelial cells with mitotic figures. These were negative for prolactin but showed HMFG-and CEA-positivity, excluding them from a pituitary lineage. Transbronchial biopsy revealed moderately differentiated adenocarcinoma, with evidence of lymphatic spread. The overall conclusion was of bronchogenic adenocarcinoma, metastasizing to a prolactinoma and complicated by apoplexy.
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PMID:Pituitary apoplexy following metastasis of bronchogenic adenocarcinoma to a prolactinoma. 1046 19

A 42-year-old man and a 31-year-old man with congestive heart failure caused by the thyroid stimulating hormone(TSH) secreting pituitary adenoma were reported. Heart failure was improved after transsphenoidal resection of the pituitary adenoma in each patient. The syndrome of inappropriate secretion of TSH causes hyperthyroidism. Thyroid hormone acts directly on cardiac muscle to increase the stroke volume. Hyperthyroidism itself reduces the peripheral vascular resistance and an elevated basal metabolism which is the basic physiologic change in hyperthyroidism dilates small vessels and reduces vascular resistance. The reduced vascular resistance contributes to increase stroke volume. Thyroid hormone also acts directly on the cardiac pacemakers to be apt to cause tachycardiac atrial fibrillation. These mechanical changes in hyperthyroidism increase not only the cardiac output but also the venous return. The increased blood volume and the shortened ventricular filling time due to tachycardia result in congestive heart failure. TSH secreting pituitary adenoma is a rare tumor, however heart failure is common disease. TSH secreting pituitary adenoma should be taken into consideration in patients with heart failure. The presented cases were very enlightening to understand the relation between brain tumor and heart disease.
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PMID:[Congestive heart failure caused by the thyroid stimulating hormone(TSH) secreting pituitary adenoma: report of two cases]. 1157 21


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