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)

Many of the manifestations of hyperthyroidism are secondary to increased adrenergic activity. In recent years the beta adrenergic blocking drugs, as represented by d,1-propranolol, have become the agents of choice for ameliorating the adrenergic signs and symptoms of hyperthyroidism. Propranolol improves the tachycardia, tremor, restlessness, anxiety, and myopathy.
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PMID:The heart and hyperthyroidism. Use of beta-adrenergic blocking drugs. 24 93

In recent years there are a considerable increase in alcohol consumption in Taiwan, which may have been accompanied by increased incidence of alcohol-related physical disease. This study was designed for an understanding of neurological problems in chronic alcoholic patients. One hundred and five cases of chronic alcoholics with neurological problems were collected. All had taken more than 100 g alcohol daily for more than 8 years. They were all males, with a mean age of 47.0 +/- 1.3 years, mean daily alcohol consumption of 185.1 +/- 9.0 g (mean +/- S.E.). These chronic alcoholic patients showed various neurological problems. Patients showing typical clinical features of alcoholic neurological disease are now rather rare. Most of the patients had manifestations of more than one problems: polyneuropathy (74.3%), alcoholic tremor (37.1%), hallucinosis (30.5%), myopathy (26.7%), head injury (24.8%), withdrawal seizures (18.1%), Wernicke encephalopathy (15.2%), paranoia (13.3%), and stroke (15.2%). Furthermore, we divided all the patients into 5 categories, they were: encephalopathy, 59 cases (56.2%); stroke, 16 cases (15.2%); cerebellar degeneration, 12 cases (11.4%); neuropathy, 78 case (74.3%); and myopathy, 28 cases (16.7%). The daily alcohol consumption and duration of daily drinking were different significantly (p less than 0.05) among five different syndrome categories.
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PMID:Neurological problems in chronic alcoholics. 165 33

The authors report a seven-month-old boy with severe hypotonia, poor spontaneous movements, breathing difficulties and recurrent respiratory infections, dysmorphisms and a peculiar movement disorder: minipolymyoclonus (MPM), previously reported only in spinal muscular atrophies. MPM is characterized by nonrhythmic myoclonic jerks associated with a rhythmic tremor of the extended fingers polygraphically detected. A muscle biopsy showed pathological changes typical of congenital nemaline myopathy (CNM). The relationship between MPM and CNM may be explained on the presumptive basis of the "neurogenic" nature of this congenital myopathy or by the non-specificity of this clinical sign.
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PMID:Minipolymyoclonus in congenital nemaline myopathy: a nonspecific clinical marker of neurogenic dysfunction. 178 61

The maximum number of different motor unit action potentials (MUAPs), their firing rates, and total MUAP spikes/second recorded by monopolar needle electrode were determined for the biceps brachii muscle during 45-degree elbow flexion. There were 4.2 +/- 1.6 different MUAPs exceeding 100 microV. Mean firing rate was 10.0 +/- 1.7 Hz, and total MUAP spikes/second were 40.3 +/- 18. Recordings from 16 patients with neurogenic atrophy (NA) and just detectable weakness revealed corresponding values of 3.1 +/- 1.7 different MUAPs, a mean rate of 10.2 +/- 1.5 Hz and 30.6 +/- 19 total MUAP spikes/second, not different from normal. In these patients, increased force of muscle contraction was required to activate high threshold motor units firing at high rates. In each of 4 patients just able to hold the arm against gravity, 1 or 2 "overdriven" motor units firing at a mean rate greater than 20 Hz were recorded. In 8 patients with myopathy and just detectable weakness, greater than 100 total MUAP spikes/second were recorded. Antigravity posture as a reference level of innervation has the advantage that motor unit firing rate is set about that of physiologic tremor (10-13 Hz). Its application was helpful in quantifying recruitment.
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PMID:Antigravity posture for analysis of motor unit recruitment: the "45 degree test". 235 48

One hundred two patients with recurrent, drug-refractory tachyarrhythmias were treated with amiodarone for nine +/- eight months (mean +/- SD) (range, one to 50 months). Forty-five patients exhibited some form of neurotoxic reaction that was severe enough in nine patients to require discontinuation of treatment or reduction in dosage of the drug. The most frequent neurotoxic findings were tremor (44 patients), peripheral neuropathy (ten patients), and ataxia (seven patients). Five patients developed unusual neurotoxic manifestations: brainstem dysfunction characterized by downbeat nystagmus, hemisensory loss and ataxia, severe dyskinesia, jaw tremor, and proximal myopathy. Neurophysiologic studies revealed varying degrees of predominantly demyelinating peripheral neuropathy. Neurotoxic symptoms improved after discontinuing treatment or decreasing the dosage of the drug. Age of the patient and total cumulative dose did not seem to be risk factors for development of neurotoxicity. These neurotoxic findings suggest that amiodarone-induced neurotoxic reactions are not only confined to the peripheral nervous system, but also that parts of the central nervous system (eg, basal ganglia, brain stem, or their connections) may also be involved.
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PMID:Unusual neurotoxicity associated with amiodarone therapy. 303 78

Five patients developed neurological symptoms during treatment with amiodarone for intervals ranging between five and 40 months. In each case the daily maintenance dose did not exceed 600 mg. The neurological manifestations included gait ataxia, tremor, polyneuropathy, and myopathy. In all five patients, the neurological symptoms were severe and disabling. In one patient with a myopathy, there was no improvement after amiodarone was withdrawn. The neurological side effects of amiodarone may be disabling and are not always reversible with drug withdrawal. Neurological complications may arise during treatment with usual maintenance doses.
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PMID:Disabling neurological complications of amiodarone. 386 21

There is an increasing use and variety of beta-adrenoceptor blocking agents (beta-blockers) available for the treatment of hyperthyroidism. Recent comparative studies suggest that atenolol (200mg daily), metoprolol (200mg daily); acebutolol (400mg daily), oxprenolol ( 160mg daily), nadolol ( 80mg daily) and timolol (20mg daily) produce a beneficial clinical response equal to that seen with propranolol ( 160mg daily). Most beta-blockers reduce resting heart rate by approximately 25 to 30 beats/min, although a lesser reduction is seen with those possessing intrinsic sympathomimetic activity such as oxprenolol and pindolol. While earlier studies employing large doses of intravenous propranolol concluded that beta-blockade reduced myocardial contractility, more recent non-invasive studies suggest that the predominant cardiac effect is on heart rate. In patients with cardiac failure, beta-blockers may, however, produce a profound fall in cardiac output. Nevertheless, in combination with digoxin they may be useful in controlling the atrial fibrillation of thyrocardiac disease. beta-Blockers improve nervousness and tremor (although to a lesser extent with cardioselective agents) and severe myopathy, and they also reduce the frequency of paralysis in patients with thyrotoxic periodic paralysis. There is often subjective improvement in sweating but usually no major effect on eye signs. Recent studies show a 10% reduction in oxygen consumption/basal metabolic rate with long term oral use of selective or nonselective beta-blockers. In addition, many agents (propranolol, metoprolol, nadolol and sotalol but not acebutolol, atenolol or oxprenolol) reduce circulating tri-iodothyronine (T3) concentration by between 10 and 40%, although the clinical significance of this effect (if any) is not established. beta-Blockers may also have endocrinological effects on gastrin, cyclic AMP, catecholamines and other hormone levels. Given in adequate dosage, propranolol has been shown to control thyrotoxic hypercalcaemia. Minor side effects (nausea, headaches, tiredness, etc.) are quite common but overall beta-blockers are well tolerated by the thyrotoxic patient. The major use of these drugs is in symptomatic control while awaiting definitive diagnosis or treatment. As an adjunct to antithyroid drugs or radioactive iodine, beta-blockers will produce a satisfactory clinical response in the weeks to months before these forms of therapy produce a euthyroid state. beta-Blockers are more convenient than antithyroid drugs in the control of patients receiving therapeutic radioiodine, in that continuous therapy and assessment of biochemical response is possible.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of beta-adrenoceptor blocking drugs in hyperthyroidism. 614 1

A 51 years old patient underwent 3 urological operations within a short space of time. The anaesthetic procedures (NLA and spinal anaesthesia) caused a rise of temperature, hyperventilation and tremor, suggesting a malignant hyperthermia. The patient refused a muscle bioptical investigation. Biopsies were performed in the patient's children. In the daughter, some "whorled fibres" and single fibre necrosis, interpreted as signs of myopathy, were detected. The clinical syndrome of the father and the histological results of the daughter point out to the possibility that in this family a predisposition to malignant hyperthermia is present.
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PMID:["Malignant hyperthermia" following NLA and spinal anaesthesia (author's transl)]. 710 33

Inherited neurological diseases in animals are of interest to a wide range of scientific disciplines, particularly because such animals may be suited as genetic animal models for respective human disorders. Because the pig has a number of anatomic and physiologic features similar to those of human beings, this species is becoming increasingly popular in biomedical research. The usefulness of pigs as genetic models of neurological diseases is illustrated by the porcine model of malignant hyperthermia (MH), i.e., a frequently fatal myopathic disease in both pigs and humans. In the present study, we describe a new hereditary movement disorder in Pietrain pigs, which may represent a useful genetic animal model of high-frequency tremor. Because the disorder was first detected in the offspring of a boar named "Campus," we use the term "Campus syndrome" in this respect. Segregation analysis of breeding studies indicates that the syndrome is inherited as a monogenic dominant trait. DNA-based testing of the mutation involved in MH myopathy showed that expression of the Campus syndrome in pigs is not dependent on homozygosity for the MH mutation. In affected pigs, the Campus syndrome develops at an average age of 27 days. The syndrome is characterized by muscular weakness and a very intense tremor of the legs when standing and walking but not when at rest in a lying position. The intensity of tremor and muscular weakness progressively increases with age, resulting in pronounced postural instability. Despite these neurological abnormalities, body weight gain in affected pigs does not differ from that in unaffected siblings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The "campus syndrome" in pigs: neurological, neurophysiological, and neuropharmacological characterization of a new genetic animal model of high-frequency tremor. 755 40

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


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