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)

We have examined bromocriptine, levodopa and trihexyphenydil ins ingle-blind design in 16 chronic productive schizophrenics having the same degree of tardive dyskinesias. Treatment time for each patient was 60 days: Bromocriptine was given in mean daily doses of 32 mg, levodopa 3,2 g and trihexyphenydil 27 mg. Bromocriptine and trihexyphenydil allowed the continued use of neuroleptics, without necessitating an increase in dosage. On the other hand, with levodopa 25% of the patients deteriorated, and this could not be prevented by increasing the dose of neuroleptics. Bromocriptine and trihexyphenydil permitted treatment of tardive dyskinesias, whereby bromocriptione was clinically (and statistically) superior to trihexyphenydil. Trihexyphenydil had only a slight effect on tremor, whilst treatment with levodopa was ineffective.
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PMID:[Dopamine-receptor stimulators and neuroleptic-induced dyskinesia (author's transl)]. 3 97

Bromocriptine and lergotrile were administered to 81 patients with Parkinson disease (PD) and increasing disability despite optimal treatment with levodopa (secondary levodopa failures). Sixty-six patients were treated with bromocriptine and 53 patients were treated with lergotrile. Both groups had significantly decreased rigidity, tremor, bradykinesia and gait disturbance upon addition of bromocriptine or lergotrile to levodopa. Twenty-five patients improved at least one-stage on bromocriptine, and 21 improved at least one-stage on lergotrile. The mean dose of bromocriptine was 47 mg, and the mean dose of lergotrile was 49 mg, permitting a 10% reduction in levodopa. Bromocriptine was discontinued in 29 of 66 patients because of adverse effects, including mental changes (14 patients) and involuntary movements (9 patients). Lergotrile was discontinued in 33 of 53 patients because of adverse effects including hepatotoxicity (11 patients) and mental changes (12 patients). The results of treatment with bromocriptine or lergotrile were comparable, with patients either responding or not. Bromocriptine will shortly be available for use in PD. Lergotrile, because of the hepatotoxicity, will not.
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PMID:Treatment of Parkinson's disease with dopamine agonists: a review. 3 52

Bromocriptine, a dopamine receptor agonist, was administered to 20 patients with idiopathic parkinsonism taking levodopa (L-dopa) or "Sinemet" (levodopa combined with carbidopa in a 10/1 ratio) at optimum doses. In a double-blind randomised cross-over study lasting 6 months, the addition of bromocriptine (mean daily dose 79 mg) led to a significant (P less than 0.01) 74% reduction in the dose of sinemet and levodopa. "Total disability score" showed a significant (P less than 0.01) improvement at both low and high doses of bromocriptine. Tremor improved 50% (P less than 0.01), with significant improvements in gait, posture, writing, balance, rigidity, finger dexterity, and drooling. Adverse reactions were similar to those observed with sinemet and levodopa. Although both the cause and the cure of idiopathic parkinsonism remain elusive, bromocriptine appears to represent a therapeutic advance.
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PMID:Bromocriptine and levodopa (with or without carbidopa) in parkinsonism. 5 50

Nine patients suffering from Parkinson's disease and 2 cases of Parkinsonian syndrome were treated with bromocriptine, for 41 to 117 days, with a daily dose of 20 to 40 mg. The results were very good in 4 cases, satisfactory in 6 and nil in one case. Improvement concerned akinesias, rigidity and tremor, and was more marked in patients with more advanced signs. In 2 patients, amantadine was stopped. The dose of L-dopa was decreased by 2/3 without any change in clinical condition and L-dopa could be withdrawn in 5 cases out of 8. Bromocriptine appears to be an interesting development in the treatment of Parkinson's disease.
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PMID:[Treatment of parkinsonian syndromes by bromocriptin]. 31 21

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

A double-blind crossover study was performed in 12 patients with idiopathic parkinsonism to compare their response to bromocriptine with their response to previous optimal drug treatment, including levodopa. There was a 26 percent overall improvement with bromocriptine; rigidity, tremor, and facial expression showed the greatest response. Seven of eight patients who were taking levodopa at the beginning of the study was taken off the drug completely. Adverse reactions were transient and dose-dependent. Bromocriptine promises to be an effective new therapeutic agent in the treatment of idiopathic parkinsonism.
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PMID:Studies with bromocriptine. Part 2. Double-blind comparison with levodopa in idiopathic parkinsonism. 77 55

Bromocriptine in high doses (up to 100 mg per day) was administered to 14 patients with advanced Parkinson's disease whose disorder was progressing despite optimum treatment with levodopa combined with a peripheral dopa decarboxylase inhibitor (carbidopa). In 10, bromocriptine (mean dose, 57 mg) induced a statistically significant (P less than 0.01) improvement in rigidity, tremor, bradykinesia, gait disturbance and total score. In seven patients levodopa with carbidopa was completely replaced by bromocriptine (mean dose, 70 mg), with improvement in four. Adverse effects were similar to those observed with levodopa and carbidopa, except that in individual patients abnormal involuntary movements and diurnal oscillations in performance (on-off effect) were decreased whereas orthostatic hypotension and mental changes were increased. Bromocriptine appears to be a major new agent in Parkinson's disease that is especially promising in patients no longer responding to levodopa.
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PMID:Treatment of parkinson's disease with bromocriptine. 98 85

The interim results obtained up to the end of the 3rd year of the multicenter nationwide cooperative study on the long-term effects of bromocriptine in parkinsonian patients are reported. Bromocriptine monotherapy could be continued in approximately 33% of the patients at the mean maintenance dose of 11.4 mg/day. The combined use of bromocriptine (11.1 mg/day) in parkinsonian patients already treated with levodopa had a favorable influence on the long-term side effects of levodopa such as the on-off phenomenon and dyskinesia. The beneficial effects of bromocriptine, levodopa and an early combination on parkinsonian symptoms such as rigidity and tremor remained at the end of the 3rd year. However, the effects of each mode of therapy on another parkinsonian symptom, akinesia, ceased by the end of the 3rd year.
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PMID:Third interim report of the nationwide collaborative study on the long-term effects of bromocriptine in the treatment of parkinsonian patients. 217 38

Sebum secretion was measured on the forehead of 47 patients with Parkinson's disease before and after treatment with anticholinergic (biperiden), levodopa + AAID and bromocriptine, by the osmic acid technique. Another 100 patients under biperiden, levodopa + AAID or association of both, for at least one year, were also evaluated. The male parkinsonian "de novo" patients have shown greater sebum secretion than female patients. It was also concluded that biperiden failed to reduce sebum secretion rate. On the other hand, it was found that L-dopa + AAID reduces the sebum secretion (CL = casual level and SER = sebum excretion rate) on both male and female patients. Bromocriptine (10mg/day) was the second dopaminergic therapy employed in the present work. Similarly to L-dopa, this dopaminergic agonist was able to significantly reduce sebum secretion (both CL and SER) of male patients. There was a positive and significant correlation for the 50-59 years old male patients "de novo" between CL and tremor, hypokinesia, gait and posture or functional incapacity, before treatment. After a period of treatment correlation was no more found. In relation to parkinsonians under chronic treatment was found a positive and significant correlation between sebum secretion and hypokinesia. The level of sebum secretion on parkinsonian "de novo" patients before treatment was equal to parkinsonian patients under chronic treatment regardless the treatment, except for greater than or equal to 60 years old parkinsonians who have shown CL and SER higher than "de novo" parkinsonian patients with the same age but without treatment. The treatment with L-dopa + AAID significantly decreased both CL and SER of "de novo" parkinsonian patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[L-dopa, biperiden and sebum excretion in Parkinson disease]. 276 50

The etiology, pathophysiology, diagnosis and clinical presentation, and clinical management of Parkinson's disease are reviewed. The cause of Parkinson's disease, a progressive, degenerative neurologic motor disorder, is unknown. Both endogenous and environmental factors appear to play a role. The clinical features of parkinsonism result from a depletion in dopaminergic transmission in the corpus striatum; the dopamine deficiency is caused by a loss of melanin-containing nerve cells within the substantia nigra and locus ceruleus. In the remaining neurons, hyalin-like masses called Lewy bodies increase in number, but the importance of this is unclear. The diagnosis of Parkinson's disease is based on the clinical presentation of the patient, which initially includes sensory complaints of aching pains, paresthesias, numbness, and coldness. As the disease progresses, the four classic symptoms become prominent: tremor, rigidity, bradykinesia, and postural difficulties. Drug therapy is the cornerstone of clinical management of Parkinson's disease, but no treatment has been found that will retard or reverse the disease. Therapy is usually initiated with anticholinergic agents such as biperiden hydrochloride or trihexyphenidyl hydrochloride with or without amantadine. The mainstay of therapy is levodopa, which is used in combination with dopa decarboxylase inhibitors to decrease the peripheral conversion of levodopa to dopamine. Bromocriptine is a dopamine agonist useful in treating Parkinson's disease. Therapy, which must continue for life, eventually becomes less effective or completely ineffective in all patients. Drug therapy has improved greatly the functional ability of patients with Parkinson's disease, but new agents that can extend the length of effective treatment or reverse the disease are needed.
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PMID:Current concepts in clinical therapeutics: Parkinson's disease. 353 Jun 16


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