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)

The effect of ipratropium (Atrovent) 0.125 mg x 4 daily was compared to terbutalin (Bricanyl) 5 mg x 4 daily, given to 19 patients with chronic obstructive airways disease (15 with chronic bronchitis, 10 bronchial asthma, 7 pulmonary emphysema) as inhalation therapy with Monaghan IPPB-M 515, during 2 treatment periods of 3 days. The investigation was carried out as a controlled, double-blind, cross-over comparison. The effect of treatment was evaluated by measurement of PEFR, symptom scores, including the side-effects and the use of rimiterol MDI for the treatment of acute attacks. The PEFR values were all higher than the initial values (P less than 0.001) during the period of treatment (08.00-20,30 hrs). The highest values were recorded at 16.30 hrs, these were PEFR + 31.7% for the Atrovent period and PEFR + 28.0% for the Bricanyl period. No statistically significant difference was observed in the PEFR, symptom scores, side-effects and the use of rimiterol during the Atrovent and Bricanyl treatment periods. The authors suggest that Atrovent is a wellsuited alternative bronchodilatator, particularly for patients with tremor, muscle cramp, and "inner restlessness" following treatment with a beta 2-stimulator.
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PMID:A comparative study of the bronchodilatating effects of ipratropium and terbutalin inhaled with Monaghan IPPB-M 515 by 19 patients with chronic obstructive airways disease. 15 95

The clinical, electrophysiological and muscle biopsy findings of 7 cases with a peculiar form of X-linked hereditary degenerative motor neuron disease are presented. It is suggested that the disease might be a separate clinical entity with the following characteristics: (1) sex-linked recessive inheritance, (2) unusual but not invariable late onset, (3) slow progression, (4) facial-bulbar and proximal spinal muscle involvement, (5) consistent fasciculations, sometimes massive and more pronounced about the lips, chin and tongue, (6) fine tremor of the hands, (7) muscle cramps usually preceding the other symptoms, and (8) gynaecomastia as a frequent but not a constant feature.
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PMID:X-linked spinal and bulbar muscular atrophy of late onset. A separate type of motor neuron disease? 111 17

A 64-year-old man was admitted to our department because of muscle cramp, atrophy and weakness of the limbs together with difficulty in walking, which had gradually progressed from age 60. About 1 year prior to admission, he had noticed hand tremor and gynecomastia. On admission, neurological examination revealed diffuse muscle atrophy and weakness of the extremities, which were more obvious on the right side with preponderance in the right leg. Bilateral postural hand tremor was also more prominent on the right hand. Fasciculations were observed both in the extremities and tongue. The remaining cranial nerves and cerebellar functions were intact. Sensation was normal except for slightly decreased vibratory sense in the distal part of the legs. Deep tendon reflexes including jaw jerk were increased with the exception of hyporeflexia of the right leg. Babinski sign was negative bilaterally. Blood examination disclosed slight elevation of CK and fasting glucose level of 110 mg/dl. Glucose tolerance test showed a diabetic pattern. CSF examination showed total protein of 74 mg/dl and IgG of 12 mg/dl. On a series of endocrinological studies, there was no significant elevation of androgen and estrogen both in serum and urine except for slight elevation of serum E1 level. Serum LH and FSH, however, were markedly high, which responded far beyond the normal range following to 0.1 mg injection of LH-RH. These results suggested that gynecomastia might be caused by dysfunction of the hypothalamus-hypophysis system. Brain CT and spine MRI showed no abnormality. Muscle biopsy obtained from the right quadriceps femoris revealed neurogenic abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case presenting manifestations of bulbospinal muscular atrophy with senile onset, rapid progression and marked asymmetry]. 275 68

A 32 year old male is described with an onset of upper limb postural tremor in adolescence followed by muscle cramps. Progressive proximal amyotrophy and weakness in the limbs developed late in the third decade. Examination disclosed, in addition, bilateral facial weakness and mild dysarthria. Enzyme studies revealed hexosaminidase A and B deficiency, indicating a diagnosis of Sandhoff disease. Intra-axonal membranocytoplasmic bodies were present in a rectal biopsy. The presentation, which resembled that of X-linked bulbospinal neuronopathy, widens the clinical spectrum for disorders related to G(M2) gangliosidosis.
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PMID:Sandhoff disease mimicking adult-onset bulbospinal neuronopathy. 279 83

Beta 2 agonists are best administered by inhalation since this route provides maximum therapeutic effect with minimum side effects. Plasma levels are lower and muscle cramps, tachycardia and tremor less common. Inhalation may be carried out by use pressurised inhalers (with various modification if necessary), by a Rotahaler with Salbutamol powder, and by nebulisers. All have their uses. Apart from their immediate bronchodilator effect, it is customary to give Beta 2-agonists routinely before inhalation beclomethasone, and there is evidence that regular use of Beta 1-agonists has a useful suppressive effect. In severe chronic asthma high doses may be indicated and be effective where conventional doses have failed. The introduction of reliable sustained-release preparation of theophylline and its derivatives together with plasma assays theophylline levels has enabled therapy to be optimal and side effects to be lessened. The therapeutic range is a plasma concentration of 10-20 mg/l. There are large individual variations in hepatic clearance of theophylline, which may also be influenced by age, liver disease, drugs and viral infections. Theophyllines are less effective as bronchodilators than Beta 2-agonists but in chronic severe asthma have a place for their additive effect. They are used most frequently to suppress nocturnal asthma and early morning wheezing.
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PMID:Bronchodilators: beta 2 agonists versus theophylline. 289 40

Three patients from two families had an unusual phenotypical variant of late-onset hexosaminidase-A deficiency. The clinical picture was dominated by spinal motor neuron involvement mimicking juvenile-onset spinal muscular atrophy. Atypical features included prominent muscle cramps, postural and action tremor, recurrent psychosis, incoordination, corticospinal and corticobulbar involvement, and dysarthria. The presence of these atypical features in patients whose lower motor neuron involvement would otherwise be consistent with juvenile-onset spinal muscular atrophy should raise the suspicion of the presence of hexosaminidase-A deficiency and GM2 gangliosidosis that can be proved by appropriate enzyme assays.
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PMID:Hexosaminidase-A deficiency presenting as atypical juvenile-onset spinal muscular atrophy. 293 15

In an open pilot study, 10 patients with Parkinson's disease and nocturnal and/or early-morning disabilities were given Madopar HBS (hydrodynamically balanced system; mean dose 250 mg) shortly before retiring in addition to their usual daytime antiparkinsonian treatment. Eight patients derived worthwhile improvement; the most gratifying responses were seen in the relief of nocturnal bradykinesia, rigidity and tremor. Early-morning symptoms were also improved in 3 out of 5 patients, possibly as a secondary response to an improved nights sleep. Cramps, early-morning dystonia and pain, however, responded poorly. Overall results are sufficiently encouraging to warrant further controlled studies with Madopar HBS in what has been a relatively neglected area of distress for many patients with Parkinson's disease.
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PMID:A sustained-release formulation of L-dopa (Madopar HBS) in the treatment of nocturnal and early-morning disabilities in Parkinson's disease. 342 6

We treated 105 patients with advanced breast cancer, using the progestational agent medroxyprogesterone acetate (MPA), 200 mg orally tds in a non-randomised trial. In general they were a poor risk population, since 78 had received prior endocrine therapy (21 more than one type) and 58 prior chemotherapy. Treatment was well tolerated. Side effects included weight gain, muscle cramps, fine tremor and fluid retention, but these were usually mild, resolved if the dose of drug was reduced, and only one patient stopped treatment because of toxicity. Seventeen patients died within six weeks of starting MPA, and disease progression occurred in a further 58. Nine have had stable disease for periods ranging from two to 11 months, and there were 21 who showed disease regression. Response to treatment continues in 13 of these patients, and at the time of writing the median duration of response is 10 months. Response rates were similar in pre- and post-menopausal patients. The dose of MPA was double to 400 mg tds in 16 patients whose disease had progressed on 200 mg tds, but no additional responses were seen in this group. Seven out of 24 (29%) patients who had not received prior endocrine therapy responded to high dose oral MPA, a response rate similar to that seen following other hormonal manipulations, but because the drug also has activity against hormone-resistant tumours and is well tolerated, it should have role in the treatment of advanced breast cancer.
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PMID:Advanced breast cancer: response to high dose oral medroxyprogesterone acetate. 623 89

Among patients with renal failure, there have been impressive modifications of both the duration and quality of life as a result of dialysis, renal transplantation, and improved medical management. However, patients who have renal failure continue to manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. Even after the institution of otherwise adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous system dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. The central nervous system disorders of both untreated renal failure and that persisting despite dialysis are referred to as uremic encephalopathy. The dialytic treatment of end stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system: Dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. This disease also appears to be a complication of the therapy for renal failure.
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PMID:Pathogenesis of dialysis encephalopathy. 636 3

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
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PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30


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