Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is sometimes very difficult to diagnose dissecting aortic aneurysms (DAA), particularly in its early stage, due to manifold signs and symptoms. The purpose of this study is to clarify the reasons for such erroneous diagnoses. A total of 41 patients with DAA were referred to our hospitals for further examination and/or surgery from April 1986 to August 1989. In 18 of these patients, the diagnostic possibility of an underlying DAA was overlooked by the referring physicians. Among these 18 patients, 2 were mistakenly diagnosed as uncomplicated myocardial infarction (MI), one as pneumonia, 2 as cerebral infarction, 6 as acute abdominal disease, one as cholelithiasis, 5 as thrombosis of the lower extremities, and one as malignant metastasis to the pericardium. The following is the detail: In 2 cases thought to be uncomplicated MI, an expanding dissecting ascending aorta had crushed the lumen of the left coronary artery, causing MI, in turn, wasting clinical treatment and consuming precious time. In one case, enlargement of the descending aorta on the chest radiography was overlooked and the patient's symptoms were mistakenly attributed to pneumonia. In 2 cases in which symptoms of cerebral ischemia were thought to be attributed to cerebral thrombosis, the real cause turned out to be occlusion of the brachiocephalic artery following aortic dissection. Among 6 cases which were initially considered to have only acute abdominal disease, 3 presented with symptoms and signs of ileus, and their exploratory laparotomies yielded no positive findings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The pitfalls in the clinical diagnosis of dissecting aortic aneurysm]. 133 5

A 61-year-old man developed progressive weakness, numbness, and exercise-induced vascular symptoms in the left hand. There was left thenar wasting. The presence of a supraclavicular bruit and vascular studies indicated left subclavian artery stenosis, but electrophysiological studies demonstrated no evidence for brachial plexopathy. Subsequent neuroimaging studies revealed multifocal right cerebral infarction. Focal atrophy and weakness from a cerebral lesion can simulate a branchial plexus lesion.
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PMID:Pseudoneurogenic thoracic outlet syndrome. 793 37

Hyponatremia is a common feature after subarachnoid hemorrhage. Hyponatremia is complex in its origin because different neuroendocrine disturbances are involved: elements of inappropriate secretion of ADH, cerebral salt wasting, and blunted response of the reninangiotensin-aldosterone system may occur simultaneously. Hyponatremia is accompanied by hypovolemia which implies a major risk for vasospasm and cerebral infarction. Hyponatremia itself might cause cerebral edema and intracranial hypertension. Fluid restriction is therefore contraindicated in hyponatremia following subarachnoid hemorrhage because of the negative impact on intravascular volume. On the contrary, replacement of both volume and sodium should be vigorously accomplished.
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PMID:[Hyponatremia in patients with subarachnoid hemorrhage]. 977 67

Peters made the original description of the cerebral salt wasting syndrome (CSWS) in 1950 in three patients with hyponatremia that he assumed to be secondary to natriuresis of cerebral mechanism. Few years later, Schwartz describe the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in two patients with bronchial carcinoma, with characteristics similar to CSWS. Wijdicks gave clinical entity to CSWS when referring that it is the prevalent cause of hyponatremia in patients with subarachnoid hemorrhage, and stressed the risk of secondary cerebral infarction if restrictive plans of water and salt were used as a consequence of a miss diagnosis. However, CSWS has been recently questioned because of its atypical characteristics, not shared by other saline wasting syndromes. The volume status of patients with hyponatremia and natriuresis determines whether the cause of this disorder is SIADH or CSWS. Nevertheless the evidence are contradictory, the vasopressin level can be recognized only in relation to the tonicity of body fluids, and the natriuresis is a common final pathway for both syndromes. In this literature review, some issues of CSWS that are associated or opposed with SIADH and other saline wasting syndrome are discussed. We conclude that the reports that sustain CSWS are insufficient in their methodology and interpretation of the results. The absence of strict metabolic studies has been negatively replaced by the original information casually quoted, and the strength of tradition. Thereafter, the paradigm generates unfounded ethical dilemmas which render difficult any further investigations with appropriate controls.
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PMID:[Cerebral salt wasting. Half a century of a largely undefined syndrome]. 1180 34

A 50-year-old woman presented with drowsiness, severe dysarthria, left facial palsy, and left hemiparesis. Diffusion-weighted MRI showed cerebral infarction in the left pontine tegmentum and right cerebellum and angiography revealed basilar artery occlusion. Altered consciousness and hemiparesis fully resolved following successful recananlisation of the basilar artery by emergent intra-arterial thrombolysis. However, about 8 months later, obvious wasting of the left temporal and buccal area without sensory signs was detected. Electrophysiological evaluation revealed a chronic denervation process in the left masseter and temporalis muscles. We suggest that a small infarction in the trigeminal nucleus of the pontine tegmentum can cause an isolated trigeminal motor neuropathy with masticatory muscle atrophy.
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PMID:Pure motor trigeminal neuropathy in a woman with tegmental pontine infarction. 2383 66