Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

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

The therapeutic efficacy of Madopar HBS was investigated in 5 patients with advanced parkinsonism. They were under treatment with standard Madopar and suffered from marked fluctuations, mainly end-of-dose akinesia. All patients were abruptly switched from standard Madopar to the HBS formulation. For the first few days (up to 1 week) dosage and number of daily intakes of HBS were the same as those of the standard formulation. Under this treatment there was some deterioration of the clinical state. The dosage was then gradually increased, on average to about twice the daily amount. After 4 weeks therapy with Madopar HBS there was an improvement of akinesia and rigidity. End-of-dose akinesia was also improved, but all patients reported prolonged periods of early-morning akinesia; tremor remained unchanged. Hourly measurements of plasma levodopa and 3-O-methyldopa concentrations showed markedly increased values under Madopar HBS. The concentrations still were found to fluctuate in a similar extent as before and did not closely correlate with the actual stage of mobility. In contrast to the initial benefit, follow-up observation up to 40 weeks revealed a marked deterioration, either with permanent akinesia, or reappearance of fluctuations with a tendency from predictable to unpredictable forms.
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PMID:Preliminary experience with Madopar HBS: clinical observations and plasma levodopa concentrations. 332 40

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

Stereotaxic surgical operations on the basal cerebral ganglia are effective in the tremor and tremor-rigid forms of parkinsonism. Surgery is followed by an increased excretion of dopamine with a good clinical effect in most cases. Madopar (L-DOPA with an inhibitor DOPA-decarboxylase) is most effective in the akinetic and rigid-akinetic forms of the disease. Prolonged treatment with this drug leads to a sharp increase in DOPA and less significant in dopamine secretion. The effect of a single low dose of madopar on DOPA and dopamine excretion can be detected for six hours. When stereotaxic operation is indicated, the combined (surgery plus drug therapy) treatment of parkinsonism is most optimal. Following effective stereotaxic surgery, drug therapy should be continued with reduced dosage of the drugs.
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PMID:[Combined (surgical and drug) therapy of parkinsonism]. 638 98

The authors report the results of treatment of hereditary extrapyramidal diseases with new preparations acting upon neurotransmitter systems. Patients with torsion dystonia, Huntington's chorea, Parkinson's disease, hereditary tremor, myoclonic epilepsy were followed-up for several years.. The best results in akinetic-rigidity syndromes (Parkinson's disease, rigid froms of torsion dystonia, Hallevorden-Spatz disease) were obtained with L-DOPA (including Sinemet, Nacom, Madopar) and in many patients these preparations were given in combination with other drugs (cholinolytic agents, Midantan) which contributed to compensation of the disturbed equilibrium of neurotransmitter systems and reduction of side effects. For decreasing the side effects of L-DOPA (hyperkineses of dystonic type, chorea and myoclonia) preparations from the group of phenothiazine and diazepine were given. In many cases improvement was achieved by slover increase of L-DOPA doses. In the hyperkinetic syndromes (Huntington's chorea, idiopathic tremor, myoclonic epilepsy, hyperkinetic torsion dystonia) preparations of phenothiazine, butyrophenone and new drugs active on the GABAergic system (Baclophen, Lyoresal, Pantogam) and diazepine (Clonazepam) were used. The analysis of the results shows that disturbed equilibrium of central neurotransmitters plays and important role in the pathogenesis of hereditary extrapyramidal system diseases.
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PMID:[Pathogenetic treatment of various hereditary extrapyramidal disorders with new drugs]. 732 7

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