Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The entity of generalized livedo racemose and cerebrovascular bleeding disorders was introduced in 1965 by I. B. Sneddon describing 5 cases. it is not clear what role oral contraceptives and smoking play in the etiology of this syndrome. The case of a 44-year old multipara is described who had taken pills up to 1980 and smoked 5-10 cigarettes a day. In 1980 just before age 35 she suffered an apoplectic insult with hemisyndrome on the left side that she recovered from. An acute hypoglossal, and trigeminal paresis appeared on the left side. Computer tomogram showed a hypodense field in the area of both hemispheres of the brain. An audible mesosystolic click led to the diagnosis of suspecting cerebral embolism with mitral valve prolapse. Therapy was started with thrombocyte aggregation inhibitors. Although the prolapse could not be showed by echocardiography, the frontal mitral valve was slightly thickened. Another hospitalization in 1985 owing to a recurring attack of vertigo revealed higher blood pressure. She received betablocker treatment. In 1987 sudden weakness in the left arm and speech disorders ensued, and skin color alterations were manifest characteristic of generalized racemose livedo. Skin necrosis appeared on both toes. Sneddon syndrome was diagnosed, and full anticoagulation therapy was started with cumarin. The sensomotoric and speech symptoms receded only slightly. In 1988 a light cerebral insult occurred with the deterioration of the speech disorder. Laboratory finding showed immunoglobulin G (IgG) anticardiolipin antibodies (ACA) with 255 U/ml (normal range 0-10 U/ml), and normal IgM anticardiolipin antibodies with 8 U.ml (range of 0-10 U.ml). ACA has been detected in patients with lupus erythematosus and racemose livedo indicating the possible association of Sneddon syndrome with systemic lupus erythematosus.
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PMID:[Sneddon syndrome]. 187 23

Aneurysm of the extracranial internal carotid artery is a rarely observed condition. Intra-aneurysmatic thrombosis, cerebral embolism with possible neurological consequences, and rupture are the most common complications. Operations were performed on 20 patients for aneurysm of the internal carotid artery. The cases included 14 "genuine" arteriosclerotic aneurysms and seven "false" aneurysms in the wake of shell splinter injuries, tonsillectomy, thrombo-arteriectomy, and blunt traumata. Pulsating tumour was the most important clinical symptom in all aneurysm cases. Arterial continuity was restored by resection of aneurysm in all cases. Sixteen patients were dehospitalised without any complaint. Two patients with preoperative cerebral infarction were left with residual paresis. One patient died of pulmonary embolism, and one patient operated on for rupture died in shock.
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PMID:[Aneurysm of the extracranial internal carotid artery]. 354 7

Large subcortical infarctions may be due to cerebral embolism and cause cortical signs more frequently than small subcortical infarctions, which usually result from small-vessel disease and are not associated with cortical findings. We evaluated 51 consecutive patients with a subcortical infarct on CT that was 1.5 cm or larger for a potential carotid or cardiac source of embolism and determined how frequently aphasia, hemineglect, or gaze paresis occurred. A carotid or cardiac embolic source was identified in 63% of the total population with a carotid source occurring in 23% and a cardiac source occurring in 49%. More than one-half of the patients with hypertension or diabetes mellitus had an embolic source, whereas all patients without these risk factors had a possible carotid or cardiac source of embolism. Aphasia or hemineglect occurred in 39% of patients and gaze paresis occurred in 41%. Large subcortical strokes frequently result in a different clinical syndrome and from a different mechanism than small subcortical strokes.
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PMID:Stroke mechanisms and clinical presentation in large subcortical infarctions. 940 42

We report a 96-year-old Japanese man who developed a sudden onset of left hemiplegia and coma. He was found to have diabetes mellitus, hypertension, and atrial fibrillation since 1996 with occasional episodes of congestive heart failure. He was otherwise apparently well until July 5 of 1997 when he developed a sudden onset of unresponsiveness and convulsion involving his right hand and was admitted to our hospital. On admission, his BP was 210/120 mmHg, heart rate 76/min and irregular, BT 36.5 degrees C, and Cheyne-Stokes respiration. General medical examination was otherwise unremarkable. Neurologic examination revealed semicoma, conjugated deviation to the right, loss of oculocephalic response, left facial paresis of central type, flaccid left hemiplegia, and bilateral Babinski sign. Pertinent laboratory findings are as follows: BUN 47 mg/dl, creatinine 1.46 mg/dl, GPT 69 IU/l, LDH 1,142 IU/l, and CK 385 IU/l. A chest x-ray film revealed cardiac enlargement and EKG showed left ventricular hypertrophy and atrial fibrillation. Cranial CT scan revealed low density areas involving the right anterior cerebral and the right posterior cerebral artery territories. He was treated with an intravenous osmotic agent and short course of intramuscular steroid. He remained unconscious despite these treatment and developed sudden cardiopulmonary arrest three weeks after the admission. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had suffered from cerebral embolism of cardiac origin. The cause of the death was ascribed to acute subendocardial myocardial infarction. Most of the participants agreed with this conclusion. Postmortem examination revealed an old subendocardial myocardial infarction involving the posterior septal region and posterolateral wall of the left ventricle. Neuropathologic examination revealed hemorrhagic infarctions involving the territories of the right anterior cerebral, right middle cerebral, right posterior cerebral, and left anterior cerebral arteries. The left A1 portion of the anterior cerebral artery was hypoplastic, and the left pericallosal artery appeared to have been receiving blood supply from the right anterior cerebral artery through the anterior communicating artery. The large arteries in the base showed marked arteriosclerosis; particularly, the initial portion of the right posterior artery showed near complete arteriosclerotic occlusions. These characteristic arterial changes appeared to be the reason why this patient suffered from an extensive infarction from what appeared to have been a single episode of cerebral embolism probably initially involving the right internal carotid artery.
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PMID:[A 96-year-old man with consciousness disturbance, convulsion, and left hemiplegia of acute onset]. 1006 67

A 63 year-old woman who had had mitral valve commissurotomy 12 years earlier was seen because of rheumatic mitral stenosis and left brachial paresis due to cerebral embolism. On clinical evaluation, a diastolic rumble was heard over the mitral area, and the echocardiogram revealed a mass attached to the mitral subvalvular apparatus. The patient was operated on, and both the surgical and histologic findings depicted papillary fibroelastoma. This tumor may occur as an isolated lesion or be associated with mitral valve stenosis or other cardiac abnormalities, and it is an important source of emboli. Early echocardiographic diagnosis, followed by surgical excision, may avoid serious complications such as stroke, myocardial infarction, and sudden death.
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PMID:Papillary fibroelastoma of the mitral valve 12 years after mitral valve commissurotomy. 1054 80

Recently, patent foramen ovale(PFO) has been highlighted as an important risk factor of cerebral infarctions in young adults. We report a patient of multiple cerebral embolism associated with PFO and deep venous thrombosis caused by a uterine myoma. A 40-year-old woman suddenly suffered from right hemiparesis with motor aphasia. Brain angiography showed an occlusion of M2 portion of the left middle cerebral artery, but atherosclerotic changes were not seen. She developed left facial paresis 23 days later and admitted to our hospital. Brain MRI revealed multiple cerebral infarcts in the left insular cortex, the deep white matter of the right frontal lobe, and bilateral thalamus. Hypoxia with the perfusion defects of S1 and S2 sections of the right lung demonstrated by scintigraphy suggested pulmonary embolism. Transesophageal echocardiography showed a PFO with spontaneous left-to-right shunt and right-to-left shunt evoked by the Valsalva maneuver. Although venography could not detect thrombi, it revealed severe compression of the right external iliac vein by a uterine myoma. These findings suggested thrombi in the right external iliac vein were the embolic source when combined with elevated coagulation markers. An uterine myoma should be considered as an important risk factor for an embolic source in case of cerebral embolism with PFO.
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PMID:[Multiple cerebral embolism caused by a patent foramen ovale and a uterine myoma]. 1367 5

Veillonella species is a rare cause of endocarditis. We report a case of a 49-year-old man with Veillonella parvula prosthetic valve endocarditis who presented with acute cardiac failure due to valvular dehiscence. His clinical course was complicated by cortical blindness and limb paresis as a result of cerebral embolism. The endocarditis was successfully treated with urgent valve replacement surgery and a prolonged course of metronidazole.
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PMID:Prosthetic valve endocarditis caused by Veillonella parvula. 1560 47

Economy class stroke syndrome is a cardiovascular complication associated with long periods of travel, only a few cases have been reported after long drives, however. The patient, a 62-year-old professional driver, had driven a truck for 2 days with minimal rest. While driving, he noted left foot paresis and numbness, along with geographical disorientation. Magnetic resonance imaging of the brain revealed multiple cerebral embolisms in the bilateral cerebral hemisphere. The only complications representing a stroke risk in this patient were a patent foramen ovale and an anterior septal aneurysm, as detected by transesophageal echocardiography. The patient was diagnosed with paradoxical cerebral embolism following his long drive. This case report examines the paradoxical cerebral emboli documented in a patient following a long period of driving.
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PMID:Economy class stroke syndrome after a long drive. 2065 11

Paradoxical embolism is the passage of venous thrombi into the arterial circulation through a pulmonary or intracardiac shunt. We report the management of a 31-year-old patient who initially presented with chest pain and right brachiofacial paresis. A diagnosis of paradoxical cerebral embolism associated with a spontaneous venous thromboembolism and a patent foramen ovale was made. The patient benefited from thrombolytic therapy and lifelong anticoagulation with good recovery. This case showed that percutaneous closure of a patent foramen ovale needs to be discussed individually.
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PMID:Cerebral paradoxical embolism associated with patent foramen ovale and idiopathic venous thromboembolism in a 31-year-old patient. 3272 55