Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between 1984 and 1989, orthotopic cardiac transplantations were done in 90 patients from 10 to 65 years of age for end-stage, refractory congestive cardiomyopathy. Two patients had had ischemic strokes 5 months and 18 years, respectively, before transplantation. Six patients (7%) suffered acute neurologic events perioperatively. Three patients suffered cerebral infarctions. In 1 case this occurred 10 days before transplantation--probably as a result of systemic hypoperfusion--with the placement of ventricular assist devices. Two others suffered infarctions 5 and 21 days, respectively, after transplantation, each of probable embolic origin. Two patients had an acute intracerebral hemorrhage 21 and 36 days, respectively, after transplantation; both were located within the basal ganglia and subcortical regions. Both patients had moderate to severe hypertension, and in 1, renal failure and a coagulopathy developed before hemorrhage. Tremor, seizures, and an altered level of consciousness developed in 1 patient as an apparent toxic reaction to cyclosporine treatment. Only 1 patient died as a result of the neurologic complication--of an acute intracerebral hemorrhage. Three patients recovered fully, 2 partially. Only the case of drug toxicity could be directly attributed to the transplantation procedure itself. We conclude that the risk of an acute neurologic insult with orthotopic cardiac transplantation is low but may result from drug toxicity, cerebral ischemia, or hemorrhagic mechanisms.
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PMID:Neurologic complications of cardiac transplantation. 221 70

The pharmacologic treatment of dilated cardiomyopathy encompasses measures such as temporary administration of amino acids and calories for those who may be undernourished and avoidance of drugs such as alcohol, nicotine, amphetamines and high doses of tricyclic antidepressants. Anticoagulants should be used in patients with persistent failure or marked dilatation of the cardiac chambers since about 20% suffer from major embolic complications. In patients with ventricular tachycardia, R-on-T, or multifocal ventricular ectopic beats, class I antiarrhythmic drugs, or if unsuccessful, amiodarone should be administered since the risk of sudden death is substantial. In addition to digitalis and diuretics, the use of vasodilators is generally accepted to be of clinical value for reduction of symptoms in heart failure. Reports concerned with long-term clinical and hemodynamic effects with drugs such as prazosin, captopril and the combination of hydralazine and isosorbide dinitrate are conflicting and, so far, there is no evidence that any vasodilator prolongs survival. The beta-agonists, such as prenalterol, are limited in their usefulness by tachycardia induction, a tendency to provoke serious arrhythmias, tremor and anxiety as well as hemodynamic tolerance development. While the noncatecholamine inotropics such as milrinone may provide symptomatic relief in severe congestive heart failure, they also increase heart rate, induce ventricular arrhythmias and are associated with high one-year mortality rates. The beneficial effect of long-term beta-blockade, which we first reported in 1975 to include a decrease in functional class, increase in exercise tolerance, improvement in physical findings, increase in ejection fraction and enhanced survival, has been met with scepticism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacologic treatment of dilated cardiomyopathy with special reference to the role of beta-blockers. 286 98

Wilson's disease is a multisystem disorder. Heart involvement in Wilson's disease, however, has rarely been recognized. A prospective study was undertaken of 53 consecutive patients (28 men and 25 women, mean age of 21.4 years) with Wilson's disease. Electrocardiographic abnormalities occurred in 18 of 53 patients (34 percent), including left ventricular hypertrophy, biventricular hypertrophy, early repolarization, ST depression and T inversion, premature atrial or ventricular contractions, atrial fibrillation, sino-atrial block, Mobitz type 1 atrioventricular block, and tremor artifact. In contrast, 26 medical students and 14 carriers of Wilson's disease as control subjects (mean age of 22.6 years) all showed normal ECG. Eight out of 43 patients (19 percent) demonstrated asymptomatic orthostatic hypotension. An abnormal response to the Valsalva maneuver occurred in six of 18 patients (33 percent). There were two cardiac deaths; one died of repeated ventricular fibrillation (the copper content in the myocardium was 2.28 micrograms/g, and in the bundle of His 1.21 micrograms/g wet weight in the autopsy specimen); and the other, of dilated cardiomyopathy. It is concluded that four modes of cardiac manifestations in Wilson's disease include arrhythmias, cardiomyopathy, cardiac death, and autonomic dysfunction. Such possible cardiac involvement should be added to the clinical picture of Wilson's disease involving the hepatic and central nervous system.
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PMID:Cardiac Wilson's disease. 382 52

The clinical signs of thyroid disease in older people may differ considerably from those in younger patients. The symptoms are often incorrectly interpreted and attributed to old age. The age is also important to the kind of therapy. The normal clinical hyperthyroidism-indices are not relevant in the diagnosis of hyperthyroidism in older patients. Organic symptoms predominate in old age (loss of weight, muscular asthenia, tremor, cardiac arrhythmia, stenocardia, congestive cardiomyopathy). Most of the time they are wrongly interpreted as additional symptoms of old age. Probably it is not the age that causes the difficulties in hyperthyroidism-diagnostics in old age, but the atypical symptoms of solitary or multilocular adenomas, which increase with advancing age. A special symptom of hyperthyroidism in old age, often misinterpreted, is "apathetic" hyperthyroidism. Radioiodotherapy is indicated in older patients with hyperthyroidism.
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PMID:[Thyroid diseases in old age. Clinical aspects and therapy. Part 1: Hyperthyroidism]. 727 38

The results of laboratory investigations in concerning 15 patients suspected of mitochondrial disease (MD) are presented. Our purpose is to provide an outline of the investigative modalities that support the clinical suspicion and have been found to be useful in the diagnosis. Five clinical groups were studied including 5 exercise intolerances (2 with inflammatory myopathy), 3 with myopathies (1 with dilated cardiomyopathy), 2 with progressive external oftalmoplegia (1 associated with cerebellar ataxia+epilepsy+hypertrophic cardiomyopathy+pes cavus), 4 with encephalopathies (3 with myoclonic encephalopathies with ataxia and dementia and 1 with epilepsy and tremor), and 1 with metabolic acidosis and cardiomyopathy. We used the following categories of investigative procedures: clinical phenotype analysis including pedigree study, neurophysiological tests, bicycle ergometric evaluation, neuroimaging, microscopic study of skeletal muscle biopsy, post-mortem examination, biochemical assays and molecular genetic studies. EMG showed myopathic changes in 5 cases, features of neuropathy in 2, mixed myopathic and neuropathic pattern in 1 and nonspecific changes in 3. EMG was normal in 3 patients. The most common skeletal muscle abnormalities were variation in fiber size (60%), lipid inclusions (33.3%), oxidative subsarcolemmal aggregates (26.7%) and ragged-red fibers (26.7%). Electron microscopy revealed mitochondrial abnormalities in 8 out of 14 patients' muscle biopsies, and in myocardiac and hepatic tissues of another. Site of biochemical defect was located in 12 patients. Complex I defect in 6, complexes I+IV deficiencies in 3, complex II defect in 1, complex IV deficiency in 1, complexes II+IV deficiencies in 1, and complex III defect in 1. In 2 patients the biochemical defect was not located. Mitochondrial DNA alterations were not found in 7 investigated patients. The clinical spectrum of MD has become increasingly wider. After the clinica suspicion, the diagnosis depends up on the appropriate use of skeletal muscle biopsy, biochemical investigations and molecular genetic techniques. Conventional EMG and automatic measurement of the electromyogram are particularly helpful in confirming the clinical suspicion in patients with predominantly central nervous system disease or in cases in which clinical signs are few.
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PMID:[Clinical and investigative approaches in mitochondrial diseases. A review of 15 cases]. 780 49

An apparently new cardioskeletal myopathy is reported in three unrelated families. Five infants were affected by rapidly progressive generalized muscle weakness, with onset shortly after birth, and dilated cardiomyopathy. All had generalized tremor (clonus) starting in the first week of life. The disease was lethal in all cases between 4 and 6 months. Muscle biopsy, performed in four of the five patients, showed a light microscopic pattern of small type I and normal-sized type II fibres. By electron microscopy small fibres were affected by myofibrillar disruption and swelling of organelles. Findings in blood and urine suggested a disturbance in energy metabolism but an extensive search for respiratory chain disorders and disorders of mitochondrial fatty acid oxidation in frozen muscle and cultured fibroblasts was negative. The findings support a new progressive autosomal recessive infantile cardioskeletal myopathy in which type I muscle fibres are preferentially affected.
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PMID:Infantile fibre type disproportion, myofibrillar lysis and cardiomyopathy: a disorder in three unrelated Dutch families. 967 82