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)

This review considers the evidence for possible involvement of central nervous system pacemaker neurons in several clinical disorders of movement. Two basic types of tremor are discussed from this point of view, i.e., 4--7/sec parkinsonian tremor, of possible thalamocortical origin, and 7--11/sec essential tremor of possible olivo-cerebellar origin. The importance of motor programs and abnormalities in their utilization are considered with reference to the loss of motor function in parkinsonism (? loss of motor programs), and the inappropriate release of such programs as a possible basis for the involuntary movements seen in other movement disorders, such as chorea, athetosis, dystonia, and hemiballismus. The possible role of pacemaker neurons controlling such programs is considered. Finally, the subject of locomotion and the pacemaker model of the spinal locomotor pattern generator for stepping are considered in relation to clinical disorders of gait. While critical evidence is lacking for pacemaker inovlvement in any of these disorders, their possible role is emphasized.
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PMID:Possible involvement of central pacemakers in clinical disorders of movement. 35 Jun 32

An historical review is presented of the evolution of the clinical apomorphine treatment. Some of the results from the last 10 years of psychopharmacological research have led us to the hypothesis that there exists a close relationship between abstinence and craving symptoms in drug and alcohol addicts, and that anxiety, depression, and tremor symptoms in Parkinsonism (and dementia senilis), are due to disturbances of the same, mainly dopaminergic, pathways in the CNS. In such cases, by means of effective preparations for oral use, we have utilized the synergistic effect of small amounts of apomorphine, L-dopa, and decarboxylase inhibitor with considerable therapeutic effect.
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PMID:Apomorphine revived: fortified, prolonged, and improved therapeutical effect. 35 69

Fifty chronic schizophrenics were randomly assigned to a 16-week treatment either with fluspirilene or with fluphenazine decanoate. The aim of the study was to compare the antipsychotic action and the side effects of the two neuroleptics. Fluphenazine decanoate caused more side effects and the difference between the two groups was statistically significant in the items tremor, severe extrapyramidal effects and parkinsonism. More patients in the fluspirilene group (nine patients) compared with only three in the fluphenazine decanoate group remained free of side effects during the whole trial. Judged from the BPRS fluspirilene proved an equally potent neuroleptic with fluphenazine decanoate although statistically significant improvement has been obtained in more items of the scale in the fluspirilene group. The improvement in the NOSIE-30 was much more clear in the fluspirilene group. Although Clinical Global Impressions of the investigators and the nursing personnel favored fluspirilene, the differences between the two groups were not statistically significant.
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PMID:Double-blind therapeutic evaluation of fluspirilene compared with fluphenazine decanoate in chronic schizophrenics. 35 31

A clinical evaluation was carried out in 20 elderly patients with parkinsonism to assess the effectiveness and acceptability of treatment with a combination preparation of levodopa and benserazide over a period of 9 months. Mean daily maintenance dosage was 612.5 mg levodopa and 140 mg benserazide. The effects of treatment on clinical features and activities of daily living were monitored at monthly intervals. Significant improvement occurred in the first month and optimal improvement was usually reached by the end of 3-months' treatment. Akinesia and rigidity were abolished or improved in the majority of patients but the effect on tremor was less satisfactory. The preparation was well tolerated and side-effects were not troublesome.
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PMID:Levodopa/benserazide ('Madopar') combination therapy in elderly patients with parkinsonism. 37 53

Results of electrostimulation and destruction of the median centre of the thalamus in 15 patients with parkinsonism and in 7 patients with uncontrollable pain are presented. Reactions of activation and inhibition in the psychoemotional, somatic and vegetosensory spheres in response to the stimulation are described. Data on bioelectrical activity changes in the cortex of the large hemispheres are presented. Special studies of the effect of the median centre destruction on the muscular tone and tremor were carried out. In the akinetic forms of parkinsonism the effect of reactivation after the median centre destruction was found to be of little clinical importance.
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PMID:[Effects of electric stimulation and destruction of the centrum medianum of the optic thalamus in patients with akinetic forms of parkinsonism]. 38 71

In a study of 16 psychotic patients with neuroleptic-induced tardive dyskinesia and 16 patients with Parkinson's disease and L-Dopa-induced hyperkinesia it was found that (1) tardive dyskinesia, compared to L-Dopa hyperkinesia, was localized almost exclusively to the oral region (P mean value of 0.01), whereas theL-Dopa hyperkinesia was more pronounced in the neck (P mean value of 0.05) and the extremities (P mean value of 0.05); (2) L-Dopa hyperkinesia showed an increasing tendency to oral preponderance with age, irrespective of the severity ofParkinsonism and extra-oral hyperkinesia, while tardive dyskinesia only itensified with age, without any change in distribution; and (3) extra-oral L-Dopa hyperkinesia was related to the localization and severity of pretreatment Parkinsonism, and more to bradykinesia than to rigidity and tremor. It is concluded that the irreversible neurotoxic effect of neuroleptic drugs may be associated with age-related changes in the oral somatotopic region of the basal ganglia (to be given consideration in any future search for the pathogenetic process underlying irreversible tardive dyskinesia), and that the pathophysiology of involuntary hyperkinesia in neuroleptic-treated psychiatric patients and in L-Dopatreated parkinson patients may consist of a primary dopamine deficiency (pharmacological or structural), and a secondary relative hyperactivity in the dopaminergic system ("dopaminergic hypersensitivity") possibly corresponding to hypoactivity in the cholinergic system.
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PMID:Relationship between tardive dyskinesia, L-Dopa-induced hyperkinesia and parkinsonism. 40 41

(2-Hydroxyethyl) methyldiethylammonium iodide (diethylcholine; DEC) was tested against trihexyphenidyl for its ability to block tremors in two animal models of Parkinsonism tremors. Both DEC (75 mg/kg) and trihexyphenidyl (10 mg/kg) antagonized physostigmine tremors in mice. Both drugs also blocked tremors in rats which received intracaudate injections of carbachol. DEC was more efficacious than trihexyphenidyl in the rat model. No dose-related inhibition of tremors was seen for trihexyphenidyl (5--20 mg/kg) but inhibition by DEC was dose-related (25--50 mg/kg). The ED50 for tremor inhibition in the rat model by DEC was 33 mg/kg. DEC was also shown to cross the blood-brain barrier in mice. The probable mechanism of action of DEC is discussed.
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PMID:Effects of diethylcholine in two animal models of Parkinsonism tremors. 46 5

Studies on rats with unilateral nigral lesions suggest that a new ergoline, CF 25-397, is a dopaminergic agonist that might improve parkinsonism. CF 25-397 induces less stereotyped behavior than other dopaminergic agents in rats, and might therefore cause less dyskinesia than levodopa in man. We investigated the clinical actions of CF 25-397 in nine patients. During treatment, severe deterioration resulted in hypokinesia and rigidity; five patients showed marked dysphagia and dysphonia. There was statistically significant deterioration in four timed tests. Mild improvement, not statistically significant, was noted in tremor. These results indicate that clinical implication of the response to potential therapeutic agents in rodent models of parkinsonism must be interpreted with caution.
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PMID:Experiences with a new ergoline (CF 25-397) in parkinsonism. 56 12

The paper is concerned with a study of the effect of metamizil in 45 patients with different forms of vascular parkinsonism. It was established that metamizil exerts a positive effect on the development of neurological symptoms (rigidity, bradykinesia, tremor) in mild and moderately expressed degrees of lesions. In most of the cases the drugs appeared effective in doses of 0.001 g thrice daily, and in separate cases 0.001 g 6 times daily. In the majority of patients metazil was tolerated without significant side effects. In some patients the side effects (vertigo, dryness in the mouth) were slightly expressed. The effect of treatment was seen after 2 days up to 2 weeks and lasted during the whole course of treatment and sometimes after it. Metamizil possessing a moderate sedative action, as well as spasmolytical and hypotensive is indicated for patients with vascular parkinsonism.
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PMID:[Experience in treating vascular parkinsonism with metamysil]. 64 11

1. Tremor force was recorded during stationary isometric contractions of intrinsic hand muscles of normal subjects. Subjects maintained a steady force level between their thumb and forefinger for 30 s. The force level varied from weak (0.2 kg) to strong contractions (7 kg). These experimental conditions were the same as those in two preceding studies, where single motor-unit activity (14) and the correlation between the discharges of two simultaneously recorded motor units and physiological tremor (11) have been investigated. 2. Two alterations of the power spectra were observed at successively stronger contractions: increase of tremor amplitude and changes in the shape of the power spectrum. At all force levels, the power spectra of tremor force show the well-known decay of tremor amplitude from the lower to the higher frequencies with a local peak at 6--10 Hz. This peak does not show a significant change with respect to frequency when the force level is varied. It is shifted toward lower frequencies in a pathological condition (Parkinsonism) where the recruitment firing rates of the motor units are significantly lower than in the normal. 3. Higher frequencies (greater than 20 Hz) are barely present in the power spectrum during the very weak contractions. They become significant as the contractions become stronger. 4. The steep decay of the power spectrum toward higher frequencies has a similar slope (--43 dB/decade) as the reduction in amplitude of the unfused part of the muscle contractions with increasing stimulus rates (--38 dB/decade). The cutoff of the power spectrum above 25 Hz parallels the achievement of total fusion of muscle twitches above this rate. 5. The results are consistent with the hypothesis that the power spectrum over the range of 6--25 Hz is mainly caused by the unfused parts of the twitch contractions of motor units firing between recruitment (6--8/s) and total fusion of the twitches (25--30/s). The decline of the power spectrum toward higher frequencies can be explained by mechanical damping, which results from increasing fusion of the twitch contractions. The low-frequency part of the power spectrum is assumed to be the result of the slow force deviations produced by changes in the net output of the motoneuron pool. 6. These assumptions were supported by additional animal experiments where the number and rate of force-producing elements could be controlled. Bundles of ventral root filaments innervating cat soleus and gastrocnemius muscles were stimulated synchronously and asynchronously at a number of different rates. The force output of the strain gauge was recorded, filtered, and analyzed in the same way as the human force records. 7. Stimualtion of one nerve bundle at one fixed frequency led to a sharp peak in the power spectrum at that frequency plus peaks of decreasing height representing the harmonics of the stimulation frequency. The height of the peaks decreased at --37 dB/decade. 8...
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PMID:Neuronal mechanisms underlying physiological tremor. 66 Feb 26


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