Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042571 (vertigo)
 7,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reported a case of opsoclonus-myoclonus syndrome. A 63-year-old man was admitted to Kenwakai Hospital with rapidly progressing symptoms, including lumbago, whole body pain, vertigo, nausea, and anorexia. He became bed-ridden because of severe vertigo and truncal ataxia. Five days after admission, he developed opsoclonus followed by myoclonus and mild disturbance of consciousness, but he showed no appendicular ataxia or pyramidal tract sign. He was treated with prednisolone, 40 mg/day, which was effective for disturbance of consciousness, but opsoclonus and myoclonus persisted. He died of liver dysfunction and ventricular fibrillation 3 weeks after onset. Blood examination revealed high LDH (1,106 IU/l), Al-P, and gamma-GTP titers. Tumor markers were normal except for increase NSE activity (129 ng/ml). The cerebrospinal fluid showed normal cell count, 63.9 mg/dl of protein, 7.3 mg/dl of IgG, and normal glucose. A cranial CT scan showed an old lacune only. Chest rentgenogram and CT scan revealed mediastinal and hilar lymph node enlargement. An abdominal CT scan showed multiple low density masses in the liver. Small cell lung cancer associated with opsoclonus-myoclonus syndrome was suspected. Western blot analysis revealed that his serum reacted with protein in the cerebellum, cerebrum, and dorsal root ganglion with a molecular weight of 77 kDa. This is the first time such an antibody was ever been detected in patients with opsoclonus-myoclonus syndrome. The molecular weights of the antigens previously found by the serum of patients with this syndrome, were 55 kDa and 80 kDa in patients with breast cancer, and 210 kDa in patients with neuroblastoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of opsoclonus-myoclonus syndrome associated with anti-central nervous system antibody]. 782 Sep 64

We present the case of a 72-year-old woman referred for dyspnea and vertigo when admitted to the hospital with a diagnosis of aortic stenosis. She had hypertension with previous deep venous thrombosis with no known hypercoagulable diathesis. She underwent aortic valve replacement with a Carpentier-Magna bioprosthesis without intraoperative complications; selective cardioplegia before aortic wall suture confirmed that coronary ostia were free. After extracorporeal circulation weaning, an episode of ventricular fibrillation occurred; sinus rhythm was restored using 20 J shock. Considering new episodes of ventricular fibrillation, the increasing number of polymorph ectopic ventricular systoles and the worsening of patient condition despite the use of high doses of inotropes, an intra-aortic balloon pump 1: 1 was inserted via the right femoral artery. Echocardiography (ECG) did not show alteration of the bioprosthesis in the presence of severe left ventricular impairment (ejection fraction <30%) with ipokinesia of the anterior-lateral wall and moderate-severe mitral regurgitation. Considering the rapid decline of the patient's condition despite the use of high doses of inotropes and an intra-aortic balloon pump, the aortic wall was reopened to control bioprosthesis. The intraoperative finding was unexpected; a thrombus of length 3-4 cm was found, attached to the prosthetic annulus and protruding into the left main trunk. The thrombus was immediately sucked up to avoid coronary embolization and, after that, the prosthesis was replaced with a Mitroflow 19 (Sorin Group Inc, Mitroflow Division, Vancouver, Canada) bioprosthesis. Probably, an association between factors could induce thrombosis-like aortic sinuses: annulus dimensions, endothelium damage caused during decalcification, tears in the bioprosthetic sewing ring, unknown coagulation diathesis and the structure of the Carpentier-Magna support may have induced this very unusual complication. However, we do not have enough information to establish with certainty the causes of this complication, but discussion of this topic may be useful.
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PMID:Acute bioprosthetic thrombosis immediately after aortic valve replacement. 1919 76

Gitelman's syndrome, or congenital hypokalemic hypomagnesemic hypocalciuria with metabolic alkalosis, is widely described as a benign or milder variant of Bartter's syndrome and most commonly presents with transient periods of weakness and fatigue, presyncope, vertigo, ataxia, and blurred vision, though aborted sudden cardiac death has also been rarely reported. Despite this there are limited data in the literature regarding the formal cardiac evaluation of patients with Gitelman's syndrome. We present the case of a gentleman with Gitelman's syndrome who initially presented to his primary physician with symptoms suggestive of an upper respiratory tract infection and subsequently survived a ventricular fibrillation (VF) cardiac arrest in the community. We review the literature regarding possible life-threatening cardiac complications in these patients.
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PMID:An unusual presentation of primary renal hypokalemia-hypomagnesemia (Gitelman's syndrome). 2037 Apr 62

A 55-year-old man underwent surgical replacement of a mitral valve 10 years earlier. In a retrospective evaluation of a chest radiograph, the diaphragm was intact at the time of initial surgery. He was then admitted to our emergency room with a complaint of vertigo. During evaluation, he developed decreased consciousness. Ventricular fibrillation was diagnosed, and external massage and full cardiopulmonary resuscitation were performed. After 20 minutes, his sinus rhythm returned and hemodynamic status stabilized with inotropic drugs. Transthoracic echocardiography showed normal valvular function and no evidence of left cardiac malfunction or clot. Electrocardiography showed ST elevation in inferior leads, and levels of cardiac enzymes were elevated. Angiography showed an embolic lesion in the mid right coronary artery that was treated with percutaneous coronary intervention (PCI) and insertion of a stent. After 24 hours, the patient was extubated in good condition, but had mild dyspnea that progressed to CO2 narcosis and subsequent reintubation. Post-extubation chest radiography showed herniation of abdominal organs into the right hemithorax. The diaphragmatic defect was closed with a polytetrafluoroethylene patch by a thoracic surgeon, and the postoperative course was uncomplicated.
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PMID:Diaphragmatic Rupture and Hernia after Cardiopulmonary Resuscitation. 2930 83