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)

Twenty-five percent of 80 consecutive patients who met research criteria for persistent tardive dyskinesia (TD) were found to have an energy peak in the parkinsonian tremor band (3-6 Hz) of the frequency spectrum of their machine-measured resting hand movements in addition to the abnormalities consistent with TD (increased energy in the 0.5-3 Hz frequency spectrum). Twelve of these patients were studied again in double-blind fashion 2 hours after receiving a placebo and again 2 hours after a single 4 mg dose of trihexyphenidyl hydrochloride (HCl). Compared with the placebo condition, the trihexyphenidyl HCl markedly diminished the measured energy in the 4 Hz band and had no effect or slightly decreased the energy at all other points on the frequency spectrum. Simultaneous Abnormal Involuntary Movement Scale ratings revealed no change in the dyskinetic movements between the conditions; there was a significant subjective improvement reported by the patients following the trihexyphenidyl HCl administration. These observations indicate that electromechanical devices identify a subpopulation of TD patients who may acutely benefit from anticholinergic treatment.
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PMID:Effects of anticholinergic agents on patients with tardive dyskinesia and concomitant drug-induced parkinsonism. 257 92

Initially, the reality of the existence of tardive dyskinesia raised some controversy, but rapidly this syndrome was recognized as a complication arising from usually long-term administration of neuroleptics. These extrapyramidal abnormal movements represent an important problem due to their prevalence, their potential irreversibility, their complex and still disputed physiopathologic mechanism, the absence of specific and generally effective treatment, and more recently the medico-legal problems entailed. At first, it was believed that these dyskinetic movements, of various intensity, were localized only at the oro-facial area (face, tongue, maxillary), or consisted of limited or generalized choreo-athetosic movements, or were a mixture of both types of movements. However, digestive and respiratory tardive dyskinesia also occur. Tardive dyskinesia can develop insidiously during neuroleptic treatment, or appear when this medication is decreased or ceased. It can coexist with parkinsonian signs. Age (over 50) and gender (female) appear to be risk factors. Other types of tardive syndromes associated with neuroleptic administration have been reported, such as tardive akathisia, tardive dystonia and a tardive Tourette-like syndrome. Involuntary movements resembling tardive dyskinesia can be observed in elderly individuals who never received neuroleptic medication. With respect to the rabbit syndrome, a rapid tremor of the perioral area, with a rhythmicity similar to the parkinsonian tremor, it is clearly different from tardive dyskinesia. It is essential to detect as precociously as possible tardive dyskinesia. The diagnosis is sometimes difficult and even if the clinical features seem pathognomonic of tardive dyskinesia, it is nevertheless important to establish a differential diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical aspects of tardive dyskinesias induced by neuroleptics]. 290 48

Patients with proprioceptive loss due to a neuropathy affecting large myelinated sensory nerve fibres were studied to determine the role of somaesthetic sensory inputs in enhanced physiological tremor. Involuntary movements in patients and controls attempting to hold the outstretched arm immobile were recorded during prolonged arm extension. Fatigue led to increased movements in both controls and patients but only the controls developed a rhythmic tremor. These data indicate that enhanced physiological tremor is dependent on somaesthetic afferent input.
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PMID:Absence of enhanced physiological tremor in patients without muscle or cutaneous afferents. 403 8

Bromocriptine (Parlodel) was given for 2 years to 17 parkinsonian patients showing inadequate response to treatment over a mean of 7 years with levodopa combined with a decarboxylase inhibitor. 11 of the patients had developed dyskinesia and 13 the on-off phenomenon during levodopa therapy. When the dose of bromocriptine reached 30 mg daily, after 4 weeks' treatment, a highly significant improvement (p less than 0.001) was observed in the following six variables: bradykinesia, rigidity, tremor, feeding, dressing and speech. These improvements have now been maintained for 2 years. The on-off phenomenon disappeared in 9 out of 13 patients. Side effects were mild and transient. Involuntary movements existing prior to bromocriptine administration were improved by reducing the dose of levodopa. The mean daily dose--after progressive and individual adjustment--was 46 mg bromocriptine combined with 435 mg levodopa plus decarboxylase inhibitor.
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PMID:Bromocriptine combined with levodopa in Parkinson's disease. 711 8

An examination was developed for patients with PD. The four major signs--rigidity, tremor, bradykinesia, and gait disorder--were assessed through a series of specific maneuvers. Each sign was allocated a number of points reflecting its relative value. The scores for each of the major signs were added to yield a total score. There was a correlation between total score and stage of PD. Involuntary movements, functional disability, and dementia were assessed separately. The examination could be performed rapidly without special equipment and was particularly useful in evaluating patients exhibiting the "on-off" effect.
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PMID:Evaluation of Parkinson's disease. 739 19

Tremors in association with thalamic haemorrhage have been infrequently reported, and delayed rubral tremor as a complication of such an event is quite rare. We describe a patient with a combined resting-postural-kinetic tremor due a thalamic haemorrhage. Magnetic resonance imaging showed evidence of a subthalamic involvement but failed to reveal any mesencephalic lesion. Five years after the original stroke there was rapid and almost complete suppression of her abnormal movements, probably related to an ischaemic capsular lesion. Involuntary movements, which resemble rubral tremor, can be due to lesions upstream of the rubral and nigral outflow system.
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PMID:"Rubral" tremor after thalamic haemorrhage. 813 18

Involuntary movements caused by disorders in the central nervous system are peculiar, purposeless movements whose characteristics have been elaborately described in the literature of clinical neurology, although their neural mechanism has not yet been fully clarified. As involuntary movement is the result of abnormal contraction of the skeletal muscles, simultaneous recording from many muscles or muscle groups with different functions furnishes information on characteristic patterns of involuntary movements based on physiological features and provides us with a tool for differential diagnosis and for evaluation of the degree of disorder. For these purposes concurrent examination of muscle tone and of voluntary contraction is desirable. In this article, quantitation of movement and strength by EMG recorded with surface electrodes, characteristic patterns of EMG in various involuntary movements including tremor, chorea, ballism and dystonia were described.
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PMID:[EMG for study of involuntary movements]. 827 64

506 patients with schizophrenia, diagnosed according to Diagnostic and Statistical Manual of Mental Disorders (DSM-III) criteria, were included in a long term treatment programme with remoxipride, a selective dopamine (D2)-receptor antagonist. This overview includes pooled data from all patients who have been treated long term with remoxipride in clinical trials, focusing on patients treated for more than 6 months (n = 283). Remoxipride was administered in daily doses of 75 to 600mg. The assessment tools were Brief Psychiatric Rating Scale (BPRS), Clinical Global Impression (CGI), Simpson and Angus scale, Abnormal Involuntary Movements Scale (AIMS) for abnormal involuntary movements, adverse events/symptoms using a 26-item checklist, clinical chemistry, and haematology and cardiovascular investigations. The majority of patients had a long duration of illness (median 11 years). 67% of patients (340/506) withdrew from treatment before 12 months and 44% (223/506) stopped treatment before 6 months. The median BPRS total score decreased during the first 3 months from 23 to 12, and this level of improvement was maintained throughout the 12-month period. Treatment-emergent adverse events reported by more than 5% of the patients were insomnia, tiredness, drowsiness and tremor in the group treated for 6 to 12 months. No symptoms, including checklist extrapyramidal symptoms (EPS), were reported by more than 5% of patients treated for 12 months. Low frequencies of EPS according to the Simpson and Angus scale were seen in patients treated for more than 6 months (n = 147). A small but statistically significant reduction of the mean total AIMS score from baseline to last rating was observed. There were infrequent changes in heart rate, resting diastolic blood pressure and electrocardiogram (ECG). Clinical chemistry and haematology data showed no evidence of clinically significant changes over time during the 12 months of treatment. Among 506 patients, 7 suicides and 7 suicide attempts occurred during the study period. Other serious adverse events were abnormal liver function test (2 cases), gastrointestinal, urinary retention, status epilepticus (psychotic polydipsia), granulocytopenia (1 each) and myocardial infarction (5 cases). Remoxipride is of potential value as a drug which is both effective and well tolerated in the long term management of patients with schizophrenia.
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PMID:Tolerability of remoxipride in the long term treatment of schizophrenia. An overview. 832 49

Three siblings of a consanguineous parents with involuntary movements are reported. The mother had only a very slight neck tremor, without any other neurological abnormality, and the father had died. The 38-year-old son (Case 1) complained of involuntary movements at the age of 6. His involuntary movements were observed in the tongue, perioral region and upper and lower extremities: jerky movements with dystonic features. The 46-year-old elder brother (Case 2) experienced involuntary movements at the age of 18. Involuntary movements were observed in the upper extremities; he also had torticollis and tremulous movements in the neck, and jerky movements in the perioral region. They showed gait disturbance and dysarthria. The 35-year-old sister (Case 3) also experienced involuntary movements. When she was writing, her involuntary movements were obvious: dystonia and myoclonic jerks. Tremor in the neck was also seen. Their intelligence was below average. We concluded that this family had hereditary torsion dystonia, with myoclonus, and low intelligence. This condition may be associated with an autosomal recessive gene.
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PMID:Hereditary non-progressive torsion dystonia with intellectual disturbance. 858 May 54

Involuntary movements are an infrequent complication of treatment with phenytoin and include tremor, asterixis, myoclonus, parkinsonism, and dyskinesias. The mechanism by which phenytoin exerts its actions is unclear. Phenytoin has been observed to exert variable effects on dopamine metabolites and also may induce changes in serotonergic activity. In this report, we discuss the available experimental evidence concerning the possible mechanisms of involuntary movements induced by phenytoin. We describe a case of postural myoclonus during treatment with phenytoin.
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PMID:Postural myoclonus induced by phenytoin. 893 94


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