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)

N-carbamoyl-2-(2,6-dichlorophenyl) acetamidine hydrochloride (LON 954) causes a reproducible rest tremor in mice, of rapid onset and short duration with no associated rigidity or akinesia and in the absence of any marked changes in body temperature or accompanying peripheral parasympathomimetic effects. This tremor can be antagonised by the dopamine receptor agonists L-Dopa, bromocriptine, nomifensine and piribedil, as well as by anticholinergic anti-Parkinson drugs having an inhibitory effect on dopamine uptake such as benapryzine and benztropine. In contrast, benzhexol, orphenadrine and amantadine had no effect. LON 954 appears to be more specific than oxotremorine for the detection of drugs having therapeutic potential in the treatment of Parkinson's disease, particularly those exerting their effect through dopaminergic systems. An antagonist (BS 100-141), which is a structural isomer of LON 954, is also described.
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PMID:The production of an alternative laboratory model of the Parkinson syndrome using a new benzylimidoylurea derivative LON 954. 40

Since there is degeneration of substantia nigra concomitant with that of locus coeruleus (LC) in patients with Parkinson's disease, the study was performed to determine the role of central norepinephrine (NE) on harmaline induced tremor. The duration of harmaline (10 mg/kg IP) induced tremor was significantly reduced by intraventricular administration of L-thero-3,4-dihydroxyphenylserine (200 micrograms/rat) and 1-NE (50 micrograms/rat) was increased NE levels in the cerebral cortex, striatum, diencephalon, cerebellum and brain stem. Electrical stimulation of bilateral LC suppressed harmaline-induced 10-12/sec EMG activities in the neck muscle. Bilateral LC lesion upon electrocoagulation and 6-hydroxydopamine treatment resulted in a significant prolongation of the duration of harmaline induced tremor, reducing NE levels in the brain. These data suggest that central NE originating in the LC neurons has an inhibitory effect on the development of the tremor induced by harmaline.
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PMID:Significance of central noradrenergic system on harmaline induced tremor. 45 Sep 52

This paper reports and illustrates in figurine style results obtained by electrical stimulation of the cortex in 20 patients and by recording of cortical evoked potentials (EPs) in 13 of these patients, whose surgery required wide exposure of the Rolandic or paracentral regions of the cortex. This study is unique in that cutaneous receptive fields related to specific cortical sites were defined by mechanical stimulation, as is done in animals, in contrast to electrical stimulation of peripheral nerves at fixed sites, as in scalp EP recordings. Observations were made on pre- and postcentral gyri, on the second somatic sensory-motor area, on the supplementary motor area, and on the supplementary sensory area. In two patients with phantom limb pain, the pain was elicited in one on stimulation of the postcentral arm area, and in the other on stimulation of the supplementary sensory leg area. Surgical removal of these areas had the immediate effect of abolishing the phantoms and the pain. Long-term follow-up review was not possible. In one patient with severe Parkinson's disease, stimulating currents subthreshold for the elicitation of movement resulted in disappearance of tremor and rigidity for short periods after stimulation of the precentral gyrus. The possible patterns of organization of the human pre- and postcentral areas are considered and compared with those of the chimpanzee and other primates. In patients in whom data from pre- and postcentral gyri were adequate, it appeared that the precentral face-arm boundary is situated 1 to 2 cm higher than the corresponding postcentral boundary.
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PMID:Localization in somatic sensory and motor areas of human cerebral cortex as determined by direct recording of evoked potentials and electrical stimulation. 47 34

Bromocriptine was administered to 66 patients with advanced Parkinson disease (PD) and increasing disability despite optimal treatment with levodopa/carbidopa (Sinemet). Forty-five patients tolerated at least 25 mg per day of bromocriptine (the "adequately treated" group) in addition to Sinemet and had significantly decreased rigidity, tremor, bradykinesia, gait disturbance, and total score, but increased involuntary movements. Twenty-five of these 45 patients improved by at least one stage. Among the 45 patients, 27 had "on-off" effects, and in 19 the "on-off" effects decreased on bromocriptine. The mean dose of bromocriptine in adequately treated patients las 47 mg, permitting a 10 percent reduction in the dose of levodopa. Twelve adequately treated patients received bromocriptine for at least 1 year, and 8 continued for longer than this. Bromocriptine was discontinued in 29 of 66 patients because of adverse effects, including mental changes (14 patients) and involuntary movements (9 patients). All adverse effects were reversible. Despite adverse effects, expense, and scarcity, bromocriptine, when added to levodopa, is useful in patients with advanced disease who no longer respond satisfactorily to levodopa, and for whom no other treatment is available.
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PMID:Bromocriptine in Parkinson disease: further studies. 57 81

Patients with Parkinson's disease performed several different stereotyped elbow flexion tasks, and the electromyographic (EMG) patterns from biceps and triceps were compared with previously established normal standards. The EMG pattern during a smooth flexion task was almost always abnormal and was characterized by alternating activity in biceps and triceps. The EMG patterns during a fast flexion task were also usually abnormal although they were always composed of bursts of EMG activity of normal duration appearing alternately in the agonist and antagonist muscles. These bursts, associated with movements of the limb, have a superficially similar appearance to the EMG bursts seen with tremor-at-rest, but certain physiological differences are demonstrated. This study demonstrates that both slow (ramp) and fast (ballistic) movements are clearly abnormal in these patients with disease of the basal ganglia. In a task designed to investigate antagonist inhibition before agonist activity, a majority of the patients performed normally. This suggests that, contrary to previous claims, slowness of movement (akinesia/bradykinesia) is not due either to failure to relax or to rigidity of antagonist muscle.
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PMID:Analysis of stereotyped voluntary movements at the elbow in patients with Parkinson's disease. 59 80

Twenty-six patients affected by Parkinson's disease were treated with a 2-Br-alpha-ergocriptine (CB 154): 14 cases were given CB 154 alone, and 12 were given CB 154 along with L-dopa plus benserazide (Madopar). Both CB 154 and combined therapy (CB 154+Madopar) induced a significant improvement in total disability score, tremor, rigidity, akinesia, self-sufficiency, and some motor performance tests (dynamic tests). No significant difference was found between results obtained with CB 154 therapy and with Madopar treatment, while the improvement induced by combined therapy (CB 154+Madopar) was significantly higher than that obtained by Madopar alone. The averse reactions caused by CB 154 alone or associated with Madopar are similar to those observed during other dopaminergic treatment. CB 154 alone or combined with Madopar appears to be a useful advance in the management of Parkinson's disease.
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PMID:Bromocriptine alone or associated with L-dopa plus benserazide in Parkinson's disease. 59 82

Before and during a standardized course of trifluoperazine therapy, 18 schizophrenic patients underwent repeated examinations for extrapyramidal motor signs, clinical psychopathology, and urinary excretion of free and conjugated forms of dopamine and its metabolites. Patients excreting more free dopamine and metabolites, or showing less complete conjugation, before drug treatment, were much less likely than others to develop parkinsonian akinesia and rigidity during drug treatment. Neither catatonic rigidity nor akinesia before treatment was predictive of a parkinsonian response to trifluoperazine, but pretreatment tremor may have been. The severity of schizophrenic psychopathology was unrelated to dopamine excretion. This study of schizophrenic patients, and our previous research in Parkinson's disease, suggest that urinary dopamine excretion may reflect dopaminergic function of the extrapyramidal motor system in both conditions.
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PMID:Dopamine excretion and vulnerability to drug-induced Parkinsonism. Schizophrenic patients. 61 44

Acturial methods are used to study the correlation between the initial condition and early therapeutic results, and the present condition of 164 parkinsonian patients treated with L. dopa for 4 to 8 years. There is an ineluctable deterioration in motility. There is a lower risk in patients who are autonomous and only slightly akinetic at the beginning of treatment. Intellectual deterioration is seen in some patients only. The risk factors are: males, the clinical forms of Parkinson's disease in which tremor is not predominant, onset of the disease before 60 years of age, and depression and transitory psychotic disorders during the first year of treatment. This deterioration appears 3 to 5 years after starting dopatherapy, which could be the cause. Life expectancy is still reduced by the disease at the present time. It is longer in patients in whom the disease started with isolated tremors, absence of Babinski's sign, and no loss of autonomy, and those in whom a good initial therapeutic result was obtained.
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PMID:[Long-term prognostic factors in Parkinson's disease (author's transl)]. 72 3

Coretal -- an agent blocking the beta-adrenergic receptors -- was given to 12 patients with Parkinson's syndrome with evident tremor and to 4 patients with benign essential tremor. In the group of Parkinson's syndrome the effectiveness of this treatment was evaluated by the blind method. The whole period of observation was 6 weeks, during 3 weeks the patients received Coretal 60-120 mg daily, during the next 3 weeks they were given placebo. The intensity of tremor was assessed by means of a scoring system. Improvement was achieved in 7 patients with Parkinson's syndrome and in 3 out of 4 cases of idiopathic tremor. Complete disappearance of tremor was never observed. Transient side effects were observed in 2 causes. The authors think that Coretal may be used with good result in treatment of parkinsonian tremor and benign essential tremor.
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PMID:[Effect of Coretal Polfa (Oxprenolol) on parkinsonian tremor and benign essential tremor]. 76 93

Twenty patients with paralysis agitans took part in a double-blind, cross-over investigation of CB 154 (2-bromo-alpha-ergocryptine) and Madopar (L-Dopa + benserazid (a peripheral decarboxylase inhibitor), dose ratio 4:1). Each treatment phase lasted for 8 weeks. Modapar was found to be significantly superior to CB 154 in the treatment of the Parkinson state as a whole (Webster total score) and the individual symptoms of hypokinesia, rigidity and tremor. Compared with pretreatment score, CB 154 had a weak, but significant effect on tremor, but not on the Webster total score, hypokinesia and rigidity. The effect of CB 154, however, varied: four patients preferred CB 154 to Madopar on account of its satisfactory therapeutic effect and fewer side-effects ("on-off" phenomena, hyperkinesia, psychiatric complications); other patients showed neither therapeutic effect nor side-effects of CB 154, which in some cases may be related to too low a dose-level of CB 154 (median 30 mg daily, range 20-60 mg). In the four cases first mentioned which showed a good effect of CB 154, the ratio between the dose of CB 154 and the dose of L-Dopa (in Madopar) was 3.5-10 mg/100 mg, i.e. in certain cases it must be assumed that the maximum dose of CB 154 lies around 120 mg daily.
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PMID:Effect of CB 154 (2-bromo-alpha-ergocryptine) on paralysis agitans compared with Madopar in a double-blind, cross-over trial. 77 80


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