Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

134 cases of dyskinesia caused by various CNS diseases were treated with a new type of DA blocker L-Stepholidine (1-SPD). Good response was obtained in 72% (29/40) of L-dopa induced abnormal involuntary movements in Parkinson disease, 79% (34/43) of Tourette syndrome, and 65% (15/23) of tardive dyskinesia through a short-term follow-up. No serious side effects were found within the therapeutic dosage of 50-225mg/day The results showed that L-SPD is a new type of anti-dyskinesia agent deserving further pharmacological investigation.
 ...
PMID:[Clinical study on the treatment of dyskinesia by L-stepholidine]. 270 Jun 94

Abnormal involuntary movements complicate the management of a majority of patients with advanced Parkinson's disease. The ability of levodopa to induce dyskinesias and alleviate parkinsonism has generally been considered a continuous dose-dependent pharmacological spectrum. In this study, the acute dose-response profile of intravenously administered levodopa for both inducing dyskinesia and alleviating parkinsonism, and its duration of action on these motor manifestations were evaluated in 52 parkinsonian patients. The minimum dose of levodopa required to produce mild dyskinetic movements was significantly lower in patients with fluctuations in motor response compared with those who had a stable response to standard oral therapy; the minimum dose for antiparkinsonian benefit, however, failed to show significant differences. The rate of disappearance of dyskinetic movements was faster than the rate of reappearance of parkinsonian signs following withdrawal of a steady-state infusion of levodopa. The dissociation of the pharmacodynamic profile of the two major motor effects of levodopa suggests their mediation through two different central pharmacological mechanisms, perhaps involving the two classes of dopamine receptors or other transmitter systems, and could have important implications for the design of future antiparkinsonian agents.
 ...
PMID:Pathogenesis of dyskinesias in Parkinson's disease. 277 96

The densities of D1- and D2-type dopamine receptors were measured with [3H]SCH23390 and [3H]spiperone, in the caudate nucleus and putamen of a large series of patients with Parkinson's disease or progressive supranuclear palsy, in relation to markers of dopaminergic and cholinergic innervation of the striatum ([3H]dihydrotetrabenazine binding and choline acetyltransferase activity). Correlations were sought between these parameters and clinical characteristics of the patients (abnormal involuntary movements, dementia, confusional syndrome or treatment). In Parkinson's disease, the densities of both types of receptors were unchanged, whereas in PSP, the density of D2, but not D1-type dopamine receptors, was decreased in the caudate nucleus and the putamen. No correlations between the biochemical and clinical data were found.
 ...
PMID:D1 and D2-type dopamine receptors in patients with Parkinson's disease and progressive supranuclear palsy. 297 99

Among the various deficiencies in neurotransmitters and neuropeptides in the brains of patients with Parkinson's disease, the loss of dopamine (DA) is implicated in a major way in the occurrence of L-dopa-induced abnormal involuntary movements (AIMs). Whatever the clinical pattern, they are triggered by drugs which stimulate DA transmission and can be modified by DA agonists and antagonists. They occur when DOPA plasma concentrations, and thus central DA receptor stimulation, reach a critical level. They are observed in patients with severely damaged central DA neurons, but involvement of other neurotransmitter-containing cells cannot be excluded. L-Dopa-induced AIMs have clinical and somatotopic characteristics, which vary from patient to patient. One might speculate that variable damage to DA neurons, associated or not with other neurotransmitter-containing cells in the affected brain structures, causes these differences in AIM patterns. By analogy with behavioral experiments in animals, the hypersensitivity of DA receptors observed in the basal ganglia of parkinsonian patients post mortem might reasonably be considered to mediate L-dopa-induced AIMs. However, the role of various subtypes of DA receptors or of changes in DA metabolism in the cell bodies and dendrites (substantia nigra) or nerve terminals (striatolimbic areas) must also be considered. In brief, the features, topography, and timing of L-dopa-induced AIMs are dependent upon alterations of the functional expression of striatal DA output, which is not yet well understood.
 ...
PMID:Pathophysiology of L-dopa-induced abnormal involuntary movements. 298 4

L-Dopa is still the most effective drug for the treatment of Parkinson's Disease, but after 5 years or more of therapy fluctuations in motor performance and abnormal involuntary movements commonly appear. Continuous intravenous infusions of L-Dopa abolish or strikingly reduce such fluctuations. Unfortunately, this is not suitable for daily treatment because of the low solubility of L-Dopa. Lisuride is a potent dopamine agonist and is very soluble in water. In this study the clinical effects of L-Dopa and lisuride continuous intravenous infusions were compared in a group of 20 fluctuating parkinsonian patients. L-Dopa controlled fluctuations in almost all the subjects, whereas only seven patients were continuously mobile while taking lisuride. Another seven patients showed a fluctuating response and the remaining six did not satisfactorily respond to lisuride. Dyskinesias were present in all patients during "on" phases, with both levodopa and lisuride treatment.
 ...
PMID:Comparison between L-dopa and lisuride intravenous infusions: a clinical study. 321 Nov 76

Lisuride at a mean daily dose of 3.2 mg was given to 15 untreated idiopathic Parkinson's disease patients. There were 10 dropouts, due mainly to inefficacy in the first months of therapy. The parkinsonian pattern in the patients who remained in the study for the full 4 years showed distinct improvement, which was maintained for less than 2 years. The patients did not develop "on-off" phenomena or abnormal involuntary movements during follow-up.
 ...
PMID:Lisuride in de novo parkinsonian patients: a four-year follow-up. 329 46

23 parkinsonian patients, 11 men and 12 women with an average age of 62 +/- 10 years, were recruited for an open substitution study of standard Madopar by Madopar HBS (hydrodynamically balanced system). All patients were presenting fluctuations in efficacy associated or not with abnormal involuntary movements. The patients in this study had been suffering from Parkinson's disease for 16 +/- 6 years and were severely disabled (Hoehn and Yahr grade III-V). The substitution was carried out dose for dose from one day to another. During the first month the dosage titration was aimed at finding the optimal therapeutic effect. After 120 days 13 patients were continuing the treatment while 10 had stopped it because of lack of therapeutic advantage. After 120 days, as compared to the initial state, end-of-dose fluctuations improved by 47%, the parkinsonian symptomatology by 54% and the abnormal involuntary movements improved by 33%. The daily dose of Levodopa had to be increased from 580 +/- 230 to 710 +/- 240 mg. The results obtained were excellent in 5 cases, good in 6 and moderate in 2 cases.
 ...
PMID:Clinical trial of Madopar HBS in parkinsonian patients with fluctuating drug response after long-term levodopa therapy. 332 35

Lisuride at a mean daily dose of 3 mg was given to 48 patients with idiopathic Parkinson's disease. Twenty received lisuride alone (Group A) and 36 received lisuride + L-Dopa + peripheral decarboxylase inhibitors (Group B). Dropouts were due primarily to lack of efficacy in Group A patients and to mental side effects in Group B patients. The patients who remained in the study for the full 4 years showed distinct improvement, which was maintained. Group A patients did not have the on-off phenomenon or abnormal involuntary movements.
 ...
PMID:Lisuride in Parkinson's disease. 4-year follow-up. 340 56

We studied the possible deleterious effect of levodopa therapy on 185 patients with Parkinson's disease and concluded that the time when levodopa is introduced, the daily dose, and the duration of treatment do not aggravate Parkinson's disease. We also studied 72 parkinsonian patients with levodopa-induced abnormal involuntary movements to see whether early initiation of levodopa therapy affected the time of onset of abnormal involuntary movements. The results suggested that it did not, and that levodopa was started early in these patients because of the severity of their motor disability.
 ...
PMID:Does levodopa aggravate Parkinson's disease? 341 89

Mean-age of onset of Parkinson's disease is 56 years. The older the patient is the more rapid is on average the progression of disability. In the early phase the motor symptoms respond well to therapy. Later, variations of response to therapy and side-effects of therapy occur (wearing-off, end-of-dose akinesia, end-of-dose dystonia, dopaminergic abnormal involuntary movements, pharmacogenic psychoses etc.). Due to the modern pharmacologic treatment of Parkinson's disease with dopaminergic substances disabling stages of the disease occur mean 3 to 5 years later than before levodopa-substitution was initiated. The incidence of depression, distinct cognitive deficits (impairment of memory, visuospatial deficits) and dementia increases in the course of the disease. The tremulous form of Parkinson's disease generally leads to less motor impairment than the rigid-akinetic form. Parkinson's disease of early onset (onset before the age of 40), may be regarded as a subtype of Parkinson's disease. Benign and malignant types of Parkinson's disease may be distinguished, as well as overlaps with multisystem atrophies.
 ...
PMID:Nosography of Parkinson's disease. 346 66


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>