Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0233565 (bradykinesia)
 2,352 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 In the group of 33 patients 39 could complete the treatment, one patient died suddenly, three had the treatment withdrawn in view of side effects.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

In an open pilot study, 10 patients with Parkinson's disease and nocturnal and/or early-morning disabilities were given Madopar HBS (hydrodynamically balanced system; mean dose 250 mg) shortly before retiring in addition to their usual daytime antiparkinsonian treatment. Eight patients derived worthwhile improvement; the most gratifying responses were seen in the relief of nocturnal bradykinesia, rigidity and tremor. Early-morning symptoms were also improved in 3 out of 5 patients, possibly as a secondary response to an improved nights sleep. Cramps, early-morning dystonia and pain, however, responded poorly. Overall results are sufficiently encouraging to warrant further controlled studies with Madopar HBS in what has been a relatively neglected area of distress for many patients with Parkinson's disease.
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PMID:A sustained-release formulation of L-dopa (Madopar HBS) in the treatment of nocturnal and early-morning disabilities in Parkinson's disease. 342 6

Intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in four cats produced akinesia, bradykinesia, crouched posture, feeding difficulty, and so on, lasting for two weeks. Madopar therapy ameliorated these motor impairments. Reduction of the concentration of dopamine and its metabolites was determined in the substantia nigra and putamen by high performance liquid chromatography (HPLC). Depletion of noradrenaline, serotonin and their metabolites was also seen. Loss of nerve cells and proliferation of glial cells in the substantia nigra were observed under the light microscope. The results indicate that MPTP-induced Parkinsonism in the cat provides an animal model that can be used for basic and therapeutic research on Parkinson's disease.
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PMID:Parkinsonism induced with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in cats: behavioral, biochemical and pathological studies. 803 69

Ten free monoamines and their metabolites in plasma and cerebrospinal fluid (CSF) were simultaneous measured in 6 levodopa-untreated (LU), 18 levodopa-treated (LT) and 37 levodopa-withdrawn (LW) Chinese patients with Parkinson's disease (PD) and 26 controls. We found that the levels of these substances in LW patients were not significantly different from those in LU patients. In LU- and LW-PD patients, CSF epinephrine (EPI) was higher (P < 0.05) than that of the controls. 3-methoxy-DOPA (3-OMDOPA) might not inhibit the accumulation of 3,4-dihydroxyphenylalanine (DOPA) and dopamine metabolites in CSF. Levodopa treatment might change the dopaminergic and serotoninergic neuronal systems, but not the noradrenergic or adrenergic neuronal systems, in CNS of PD patients. Benserazide (a peripheral decarboxylase inhibitor) in Madopar might decrease the levels of serotonin (5-HT) and norepinephrine (NE), but not those of DOPA and homovanillic acid (HVA), in plasma. HVA, NE and EPI in plasma were not good indices for those in CSF. Otherwise, our results were consistent with some other studies by showing a significantly lower level (P < 0.01) of HVA in CSF of LU- and LW-PD patients than that of the controls, while no difference for NE, 3-methoxy-4-hydroxyphenylglycol (MHPG), 5-hydroxyindole acetic acid (5-HIAA) or 3-OMDOPA was noted. The severity of clinical disability was related to the deficiency of CSF HVA and DOPAC in LU- and LW-PD patients; however, there was no relationship between clinical symptoms of tremor, rigidity-bradykinesia, autonomic dysfunction, dementia, depression or levodopa-induced dyskinesia and CSF monoamines or their metabolites.
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PMID:Monoamines and their metabolites in plasma and lumbar cerebrospinal fluid of Chinese patients with Parkinson's disease. 833 58