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)

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

Modification of cocaine's stimulant and local anesthetic behavioral effects as a function of chronic treatment was evaluated in seven female cats. Video tape of behavior pre- and post-cocaine (iv) on days 1, 4, 7, 10, and 13 in seven cats, and in addition, on days 21, 28, and 35 for s subset of four cats, was rated for several scales of the Behavioral Rating Inventory for Drug-Generated Effects (BRIDGE), developed to quantify stimulant-induced behaviors. Preseizure events were measured using scales for Tremor Intensity and Preseizure-Seizure Intensity (PSI), developed to quantify local anesthetic-induced behaviors. Behaviors associated with cocaine's local anesthetic effects, i.e., Tremor Intensity and PSI levels, showed tolerance over the treatment period, while behaviors associated with cocaine's psychomotor stimulant effects, i.e., the BRIDGE measures, showed augmentation, or reverse tolerance. These data are discussed in terms of catecholamine supersensitivity, kindling mechanisms, and stimulant models of psychosis.
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PMID:Behavioral analysis of chronic cocaine intoxication in the cat. 66 28

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

The correcting action of tropatepine hydrochloride upon the extrapyramidal effects induced by neuroleptics has been studied in 32 acute psychotic states. A satisfying result has been obtained with daily doses of 10 to 20 mg in 30 cases (excellent results: 20, good results: 10 patients). The action upon dyskinetic crises is particularly good and quickly obtained, avoiding a recourse to an i.m. corrector in 7 cases out of 8. The akineto-hypertonic syndrome has been efficiently corrected in 18 cases out of 23. The hyperkinetic manifestations (akathisia, tasikinesia) reacted favourably in 8 cases out of 11, dysarthria in 7 cases out of 11. The lessening of tremor was less satisfying (8 cases out of 15); same thing for the dryness of the mouth (7 cases out of 16) and disorder of visual accomodation (6 cases out of 12). The clinical tolerance was excellent. With the used doses, we found neither inconvenient atropinic effect, nor disorder of the vigilance, nor pharmacodependence. The one daily administration of a 10 mg tablet turned out to be sufficient in 19 cases. This possibility of only one administration a day appeared to us as a great advantage.
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PMID:[Clinical study of a new agent correcting the syndrome of neuroleptic impregnation in acute psychotic states]. 109 47

In 38 patients with Parkinson's syndrome Madopar preparation was used (L-dopa with peripheral decarboxylase inhibitor) in 33 cases as the main drug and in 5 cases as an addition to L-dopa. In the group of 33 patients 39 could complete the treatment, one patient died suddenly, three had the treatment withdrawn in view of side effects. The effectiveness of Madopar was assessed by means of five-rate scoring systems NUDS and ART. Clinical improvement was found in 22 cases (about 67%). The improvement included mainly bradykinesia and rigidity, while tremor was only slightly improved. Side effects developed in about 40% of patients and were slight and transient (apart from 3 cases). The main contraindications seem to be psychotic disturbances. In the group of 5 cases treated with Madopar as an additional drug in low doses improved the result of long-term treatment with L-dopa.
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PMID:[Treatment of parkinsonism with L-dopa and peripheral decarboxylase inhibitor]. 116 36

Drug-induced parkinsonism is usually reversible, except in a small percentage of elderly patients. We describe two relatively young patients, who developed drug-induced parkinsonism during chronic treatment with neuroleptics for a psychotic disorder. Parkinsonism persisted, and markedly and progressively deteriorated after discontinuation of neuroleptic drugs. One patient had tremor as the most prominent sign and the other had mainly an akinetic-rigid syndrome. Neither had ever developed tardive dyskinesia. Both responded to levodopa therapy. Persistent drug-induced parkinsonism in our, and other reported on, elderly patients may be due to unmasking of preexisting subclinical idiopathic Parkinson's disease by neuroleptics. Theoretically, these drugs may precipitate degeneration of vulnerable, nigrostriatal neurons by generating cytotoxic free radicals or by attrition, due to accelerated neuronal firing rates.
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PMID:Persistent and progressive parkinsonism after discontinuation of chronic neuroleptic therapy: an additional tardive syndrome? 167 33

The introduction of levodopa in the treatment of Parkinson's disease had modified both the prognosis and the current concepts of the disease, Although levodopa remains the most potent drug for the treatment of Parkinson's disease, its long-term use is associated with fluctuations in motor performance, abnormal movements and psychotic hallucinations. These late side-effects remain difficult to treat and thus raise questions as to the benefits and risks of first-time treatment with levodopa. Levodopa mainly alleviates akinesia and rigidity and to a lesser extent, tremor. Levodopa increases life expectancy. This paper reviews some recent developments in the pharmacology of Parkinson's disease. Recent findings indicate that not only central dopamine but also several other central neurotransmitter and receptor changes are involved in the pathophysiology of Parkinson's disease. New data on autonomic dysfunction in Parkinson's disease are presented. New methods of investigation (clinical rating scales, pharmacological tests, imaging techniques, etc.) are reviewed. Finally, future strategies, e.g. the development of potent new symptomatic drugs (selective D2 and D1 agonists, new formulations of apomorphine, COMT inhibitors, new routes of administration, etc.) and etiopathogenic agents (antioxidative and anti-free radical drugs, etc.) are discussed.
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PMID:Recent advances in the clinical pharmacology of Parkinson's disease. 168 24

Clinical and neuropathologic data in 45 patients with Parkinson's disease (PD) were compared. Twenty-seven patients suffered from marked akinesia and rigidity (AR-type) and 18 patients from predominant resting tremor (T-type). Dementia, depression, and psychosis occurred in 26, 18, and 18 patients, respectively. Neuronal counts were performed in defined areas of the medial and lateral substantia nigra (SNM, SNL), locus ceruleus (LC), and dorsal raphe nucleus (DRN). The AR-type (compared with the T-type) showed higher neuronal loss of LC, SNL, SNM, and more severe gliosis, extraneuronal melanin deposits, and neuroaxonal dystrophy in substantia nigra. Demented PD patients showed more intense cortical Alzheimer lesions and higher neuronal depletion in the SNM, whereas PD subjects with moderate or marked dementia differed from mildly or not demented ones only in the higher degree of cortical Alzheimer lesions. More severe neuronal cell loss of DRN was observed in PD patients with depression. Occurrence of psychosis was not associated with any pathologic feature. Our findings indicate that some major clinical features of PD are related to distinct neuropathologic lesions.
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PMID:The neuropathologic basis of different clinical subgroups of Parkinson's disease. 174 81

Trimipramine and clozapine show some similarities in their receptor binding profiles. Since both have the same affinity for the D2 receptor and since the affinity for this receptor correlates closely with the antipsychotic potency of a drug, an antipsychotic efficacy of trimipramine in acute schizophrenia could be expected. Therefore 28 schizophrenic patients in an acute phase were treated with trimipramine up to 400 mg/d in an open clinical trial. For the whole group of patients the BPRS total score changed from 58 +/- 5 before treatment to 46 +/- 18 at the last rating (p less than 0.05). According to our clinical judgement the patients were divided into three subgroups. Thirteen patients showed a good remission under trimipramine so that they could be discharged on a trimipramine maintenance treatment. They improved on the BPRS from 58 +/- 6 before treatment to 32 +/- 8 at endpoint. Six patients deteriorated during the first week of treatment and had to be withdrawn from the study. Nine patients showed insufficient improvement or became worse after an initial improvement. The observed side-effects (dry mouth, sedation, sweating, increased appetite, constipation, tremor, vertigo) are well known under trimipramine and were therefore expected. Beyond these, one patient developed a cardiac insufficiency. No clinical relevant extrapyramidal side-effects occurred. Since the improvement of florid psychotic symptoms seems to be markedly higher under trimipramine than the one reported under placebo, our results indicate that trimipramine may have an antipsychotic potency.
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PMID:Trimipramine--an atypical neuroleptic? 180 21

A total of 240 patients of Parkinson's disease (PD) were studied (125 male, 115 female). The age of onset was 60.0 +/- 9.9 years(Y) (mean +/- S.D.) (range 30-87). A 0-4 rating score was applied on each of 6 major symptoms: i.e. tremor, rigidity, bradykinesia, gait, activities of daily living and fluctuation with maximum score of 24. According to the Hoehn and Yahr's stages, there were 44 cases in stage I, 141 in stage II, 31 in stage III, 19 in stage IV and 5 in stage V. Fluctuation in symptoms occurred in 42.9%, dyskinesia in 7.1%, psychosis in 9.6%, depression in 4.6%, and dementia in 2.9%. The mean duration of PD was 4.9 +/- 4.5 Y with 40% 5 years or longer. Significantly longer duration of PD was seen in the patients suffering from fluctuation (6.7 +/- 4.7 Y), dyskinesia (10.7 +/- 6.7 Y) and psychosis (9.4 +/- 6.5 Y). The mean duration of L-dopa treatment was 4.1 +/- 3.4 Y. The patients showing fluctuation (6.2 +/- 4.0 Y) or dyskinesia (7.6 +/- 4.7 Y) had significantly longer duration of L-dopa treatment. The mean daily dose of L-dopa was 370 +/- 203 mg. The patients with fluctuation (430 +/- 187 mg) or dyskinesia (545 +/- 265 mg) received significantly higher dose of L-dopa. Dementia tended to occur in the patients having later age of onset of PD (71.2 +/- 11.2 Y). The symptom score was significantly worse in those with fluctuation, dyskinesia, psychosis and dementia. It was well correlated with the Hoehn and Yahr's staging system.
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PMID:Abbreviated rating score for Parkinson's disease. 184 38


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