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 ability of the selective GABA-receptor agonist, progabide, to suppress abnormal involuntary movements was evaluated in a preliminary open pilot study. 17 patients, 10 males and 7 females, aged 10-78 years, with hyperkinetic movement disorders were included in the study. Daily doses of progabide ranged from 900 to 3600 mg (median 2400 mg) corresponding to 14-45 mg/kg (median 45 mg/kg), while the duration of treatment varied from 2 to 52 weeks. Improvement, with a reduction of involuntary movements exceeding 25%, occurred in two of four patients with Gilles de la Tourette's syndrome, and in two of three patients with postanoxic intention myoclonus, while no consistent beneficial effects were registered in ten patients with Huntington's chorea, postanoxic choreoathetosis, torsion dystonia, tardive dyskinesia, action tremor, essential myoclonus, or oro-branchio-respiratory myoclonus.
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PMID:Progabide in the treatment of hyperkinetic extrapyramidal movement disorders. 386 33

Research in Parkinson's disease has given little attention to the reliability of subjective-qualitative assessment, or to the empirical aggregation of physical signs to supraordinate indexes of motor disturbance. We illustrate methods for examining observer reliability and discuss the importance of reliability to the interpretation of results. Observers rated patients (n = 70) for physical signs (selected Columbia Scale scores), disability stages, and abnormal involuntary movements. Observer agreement was achieved for Columbia scores and disability stages (range of Spearman rho = 0.67-0.95), but not for dyskinesias or dystonic postures. A factor analysis of Columbia scores revealed two indexes of motor disturbance: motor deficiency and tremor.
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PMID:Qualitative assessment of Parkinson's disease: study of reliability and data reduction with an abbreviated Columbia Scale. 397 53

The effects of the 8-alpha-amino-ergoline CU 32-085 on central dopamine neuronal systems was investigated. Two h after administration of CU 32-085 a slight increase of dopamine levels was observed in the nucleus caudatus-putamen. Radioligand binding studies in vitro have shown that CU 32-085 has a low affinity for striatal dopamine receptors labeled by [3H]n-propylapomorphine or [3H]spiroperidol. However, CU 32-085 effectively displaces in vivo [3H]n-propylapomorphine and [3H]spiroperidol from their respective binding sites in the mouse striatum. Functional studies have shown that CU 32-085 elicits contralateral rotation in rats with unilateral 6-OH-dopamine induced lesions of the meso-striatal dopamine neurons, and ipsilateral rotation in rats with unilateral intrastriatal ibotenic acid lesions. CU 32-085 relieves tremor in monkeys with ventromedial tegmental lesions and produces only slight abnormal involuntary movements. The biochemical and functional studies suggest that CU 32-085 and/or its metabolite exerts central dopamine agonist activity in vivo. Studies in monkeys with ventromedial tegmental lesions suggest that CU 32-085 might be an effective antiparkinsonian agent which produces less dyskinesias than the other tested dopamine agonists.
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PMID:Central dopamine agonist activity on the 8-alpha-amino-ergoline CU 32-085. 398 30

Arteriovenous malformations have only rarely been implicated as a cause of basal ganglia dysfunction. In four instances where such a lesion was uncovered, abnormal involuntary movements were present. In two, tremor involving the contralateral limbs occurred, while in others the head and neck were involved in dystonic movements and posture. The clinical and angiographic characteristics of these four patients have been assessed and are presented in detail in this report. The possible mechanism by which arteriovenous malformations may disturb the internal circuitry of the basal ganglia and induce symptoms are discussed.
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PMID:Extrapyramidal dysfunction with cerebral arteriovenous malformations. 482 31

The antiparkinsonian activity of several dopamine agonists was investigated in an animal model and clinically in parkinsonian patients. The semisynthetic ergoline, pergolide, the partial ergoline, LY 141865 and the 8-alpha-aminoergoline, CU 32-085 were found to be effective antitremor agents in monkeys with ventromedial tegmental lesions. The administration of pergolide or LY 141865 results in a relief of tremor with a concomitant occurrence of severe abnormal involuntary movements, while the administration of CU 32-085 results in a relief of tremor with the occurrence of only minor abnormal involuntary movements. Clinical studies have revealed that pergolide is an effective drug in patients with advanced Parkinson's disease, and it reduces the "on-off" phenomena. The possible regulation of dopamine neurotransmission by the norepinephrine neuronal systems was reviewed. Preliminary data suggest that clonidine may interact with presynaptic dopamine receptors.
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PMID:Therapeutic potentials of centrally acting dopamine and alpha 2-adrenoreceptor agonists. 613 44

Electromyographic (EMG) activity of abnormal involuntary movements and their modifications after Piribedil, a dopaminergic agonist, were analysed in patients presenting with tremor or tardive dyskinesia induced by treatment with neuroleptics. Quantitative analysis of EMG bursts and of their phase relationships with bursts of antagonist muscles revealed differences between tremor and tardive dyskinesia; three separate EMG types of the latter were found. In tremor, EMG activity was coordinated between agonists and antagonists. Length and frequency of bursts are characteristic. In tardive dyskinesia, phase histograms of antagonist muscle bursts showed an absence of reciprocal organisation of EMG activity. This activity was made up of either rhythmical bursts (type I and II according to the frequency) or irregular discharges (type III). Piribedil decreased tremor but facilitated EMG activity in tardive dyskinesia. These results give an objective measurement or classification of tremor and tardive dyskinesia induced by neuroleptics.
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PMID:EMG patterns in abnormal involuntary movements induced by neuroleptics. 614 81

We present a 77-year-old woman with myoclonus and epilepsy. She was well until 35 years of age, when she noted an onset of trembling of the legs upon standing. Her symptom slowly progressed, and she felt a difficulty in standing when she was 39-year-old. She had a major motor seizure without an apparent focal onset when she was 46-year-old. She also developed tremor in her hands, and she felt difficulty in holding a glass filled with water. She was admitted to our service for the first time in 1965 when she was 51-year-old. She showed wide-based ataxic gait with truncal titubation. In finger to nose test, myoclonic jerks were induced in the upper extremities. Otherwise neurological examination was unremarkable. She was treated with primidone and phenobarbital, and was discharged for out patient follow up. Her symptoms slowly progressed, and gait and station became more difficult. Mentally she was sound. Three months prior to the present admission, she developed more difficulty in gait, and decrease in food intake. On the 14th of September in 1991, she was seen by a local physician who found an abnormal shadow in her chest X-ray, and she was admitted to our service for further work-up on September 18, 1991. On admission, the patient was a chronically ill and emaciated woman. Her blood pressure was 140/84 mmHg, heart rate 115/minutes and regular, and the body temperature 36.9 degrees C. The palpebral conjunctivae were anemic. No cervical adenopathy was noted. The lung fields were clear, and no heart murmur was audible. The abdomen was soft, and no organomegaly was present. On neurologic examination, she looked somnolent with disorientation to time and place. Her memory was poor, and she could not do well serial 7s. The disc was flat and the ocular movements appeared intact. Other cranial nerves were also unremarkable. She showed diffuse muscle wasting. She was unable to stand or walk. Maintaining the sitting position was also difficult. She was able to raise her arms, but almost unable to move her lower extremities. The precise muscle testing was impossible. No abnormal involuntary movement was seen. Finger to nose test could not be performed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 77-year-old woman with myoclonus and epilepsy]. 812 9

We studied 1086 AIDS patients in the last six years. Of these 389 (35.82%) had neurological manifestation and 7 (1.8%) male patients had abnormal involuntary movements (parkinsonism in 3, hemichorea-hemiballism in 2, spinal myoclonus in 1 and rubral tremor in another). All patients were men, 5 white and 2 black. Four were homosexual, 2 drug-users and 1 bisexual. The mean age was 33.14 years. The time between AIDS diagnosis and the onset of movement disorders was 23.8 months in 5 patients and in 2 it was the first symptom. The parkinsonian patients did not show any opportunistic infection in connection with the neurological symptoms but in the remaining four cases this relationship was suggested. The data showed that not only the opportunistic infection but also the AIDS virus may play an important role on the development of involuntary movements.
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PMID:Involuntary movements and AIDS: report of seven cases and review of the literature. 814 50

Dyskinesia, here, is considered to be synonymous with abnormal involuntary movement (AIM). AIMs are recognized in various infections of the central nervous system, of which Creutzfeldt-Jakob disease (CJD) and subacute sclerosing panencephalitis (SSPE) are thought to be the most important. The two show myoclonus and other similar features in common except age of onset. The myoclonus is classified under the non-stimulus-sensitive and periodic one characterized by a long duration and a relationship to periodic synchronous discharge (PSD) in EEG. The rhythm is, however, somewhat different and quicker in CJD (0.5-2 Hz) than in SSPE (0.05-0.2 Hz). In the acquired immunodeficiency syndrome (AIDS), AIMs, including tremor, myoclonus and some others are also noted.
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PMID:[Dyskinesias in infections of the central nervous system]. 827 70

A variety of inheritable metabolic disorders produce movement disorders. A lists of conditions associated with tremor, athetosis, chorea, dystonia and myoclonus are presented as a guide for the differential diagnosis of such abnormal involuntary movements. The list includes aminoacidopathies, lipidoses, mucopolysaccharidoses, mucolipidoses, organic acidemias, mitochondrial cytopathies and disorders of carbohydrate, purine, and metal metabolism. Clinical, pathological and biochemical features of movement disorders of three typical examples, Wilson's disease, Lesch-Nyhan syndrome and glutaric acidemia type 1, are described.
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PMID:[Movement disorders in miscellaneous disorders--inherited metabolic diseases]. 827 72


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