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)

A double-blind, placebo-controlled, crossover study with long-term follow-up of amantadien i- Parkinson's disease was performed on 26 patients. Other antiparkinsonian medications were discontinued in all but three patients. Amantadine resulted in a statistically significant 12 percent overall improvement over placebo. Twenty of 26 patients, without breaking the code, selected amantadine for long-term usage. Ten patients continued treatment for 10 to 12 months, and an overall statistically significant improvement was noted at 2 weeks and at 1, 2, 3, and 10 to 12 months. Improvements in tremor and rigidity remained relatively constant, while there was some apparent loss of efficacy in timed tests and quality of timed tests. Amantadine appears effective in the long-term treatment of some patients with Parkinson's disease.
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PMID:Amantadine in Parkinson's disease. A double-blind, placebo-controlled, crossover study with long-term follow-up. 80 67

The author treated 83 patients with parkinsonism by analouges of amantadin--the Soviet preparation midantan and Swiss preparation simmetril. Twenty patients received only Amantadin and 63 Amantadin in combination with other antiparkinsonic drugs. Optimal doses of other antiparkinsonic drugs were determined prior to amantadin treatment. The preparation exerted a higher influence on such symptoms of parkinsonism as akinesis and rigidity and less on tremor. In 1/3 of the cases a positive effect of the treatment was temporary and disappeared altogether after 2--4 weeks despite the continuation of therapy. The preparation was well tolerated. Side effects observed in 32 of the 83 patients were usually expressed very midly and disappeared without special treatment. The author compares such preparations al 1-Dopa and Amantadin (Midantan).
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PMID:[The effectiveness of amantadine (midantan) in the treatment of the parkinsonian syndrome]. 94 14

Treatment of Parkinson's disease (PD) can be divided into two categories: symptomatic therapy (restoring dopamine levels toward normal and reversing functional disability) and preventive therapy (interfering with the pathophysiologic mechanism of PD to prevent or decrease the rate of progression of the disease). Regarding symptomatic treatment, although anticholinergic preparations generally are considered effective for the symptoms of tremor and rigidity without altering bradykinesia, their effectiveness is limited and adverse reactions are common; their role should be restricted to use as adjuvants to levodopa therapy. Amantadine has been shown to be as effective as anticholinergics, but it lacks long-term efficacy. Dopamine agonists--bromocriptine, pergolide mesylate and lisuride in Europe--are not as effective as levodopa and therefore rarely are used as initial therapy; their proposed role, too, is as adjuvants to levodopa therapy. Levodopa is the most effective drug presently available for the treatment of PD; its introduction is accompanied by rapid and dramatic reduction of symptoms and signs. Initial adverse reactions are not usually a major problem; and although there is speculation that initiation of therapy should be delayed because of possible long-term complications, clinically distinguishing these from problems related to disease progression itself is difficult. The possibility that nigral cell death is mediated by oxidative mechanisms provides the basis for considering antioxidant therapy as protective treatment; selegiline, an antioxidant, has been found to delay the need for symptomatic therapy. It is suggested that initial treatment of Parkinson's disease begin with both preventive therapy with selegiline and symptomatic treatment with the sustained-release preparation of levodopa, which may be associated with fewer long-term complications.
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PMID:Initiating treatment of Parkinson's disease. 134 9

Amantadine is one of the most commonly used drugs for the control of tremor in Parkinson's disease. Additionally, it has an antiviral action in the prevention of type A influenza. It has been previously reported that amantadine is nearly completely eliminated in the urine. No metabolites have been detected. Surprisingly, in a case of amantadine overdose, several metabolites could be identified by gas chromatography/mas spectrometry. This finding prompted us to re-investigate the metabolism of amantadine under a therapeutic dosing regimen. The bulk of the dose was eliminated unchanged. However, eight metabolites could be identified. Besides N-acetylation which is the major metabolic pathway, several rather unusual metabolic pathways were observed: N-methylation, formation of Schiff bases and N-formiates. No metabolites with a hydroxylated adamantane ring system could be detected.
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PMID:A revision of the metabolic disposition of amantadine. 293 78

The relative efficacy of trihexiphenidyl hydrochloride, amantadine hydrochloride, and low-dose carbidopa-levodopa in reducing parkinsonian tremor was investigated using objective techniques. Trihexiphenidyl and carbidopa-levodopa decreased tremor by greater than 50%. Some patients responded to one drug but not to the other. Amantadine decreased tremor less than 25%. Monotherapy with trihexiphenidyl or carbidopa-levodopa should be the initial treatment for the tremor of Parkinson's disease.
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PMID:Pharmacologic treatment of parkinsonian tremor. 394 48

Fourteen slightly disabled patients with Parkinsonism were treated separately with benzhexol, amantadine, and levodopa. Benzhexol and amantadine both gave a 15% reduction in functional disability and levodopa a 36% reduction. Benzhexol lessened the rigidity and improved the flexion of posture of Parkinson's disease, but had little or no effect on akinesia and tremor. Amantadine and levodopa caused improvement in all these symptoms. The combination of benzhexol and amantadine was as effective after four weeks of treatment as levodopa was after six months.
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PMID:Comparative trial of benzhexol, amantadine, and levodopa in the treatment of Parkinson's disease. 483 13

Chronic valproate therapy induces symptomatic tremor in about 10% of patients. We studied the effects of propranolol, amantadine, diphenhydramine, benztropine, and cyproheptadine on these tremors in 19 patients by using serial accelerometric recordings. Propranolol was clearly the most therapeutic. Amantadine was moderately effective, but cyproheptadine, diphenhydramine, and benztropine gave little or no relief.
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PMID:Treatment of valproate tremors. 641 57

The effects of anticholinergic and dopaminergic drugs used for Parkinson's disease were studied on the tremor induced by physostigmine (0.3-3.0 mg/kg) in rats. For the measurement of tremor a new electronic device was employed. Atropine (0.3-1.2 mg/kg) and biperiden (0.01-1.0 mg/kg) reduced the physostigmine-induced tremor in a dose-related manner and could abolish it. Biperiden was less potent than atropine. Methylatropine in a dose of 1.2 mg/kg slightly inhibited the tremor. Amantadine (0.3-3.0 mg/kg) reduced the tremor but only to a certain degree. Bromocriptine (0.1-10.0 mg/kg) reduced it in a manner that was not dose-related. Pimozide potentiated the tremor in the dose of 0.2 mg/kg but not in larger doses. At the onset of the tremor, a small decrease in rectal temperature occurred. The hypothermia lasted significantly longer than the tremor. Neither the anticholinergic nor the dopaminergic anti-Parkinson drugs altered the hypothermic effect of physostigmine. The results show that those anti-Parkinson drugs, which act by increasing the dopaminergic activity can counteract the tremor induced by physostigmine. However, these drugs are clearly less active than th anticholinergic anti-Parkinson drugs.
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PMID:Drugs for Parkinson's disease reduce tremor induced by physostigmine. 662 15

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

The initial treatment of Parkinson's disease should be addressed to improve symptoms, slow down the progression of the illness and avoid long and short term complications. Drugs currently available for symptomatic treatment are levodopa, dopaminergic agonists, anticholinergics and amantadine. Levodopa is still the goldstandard. Both the standard preparations of carbidopa/levodopa or benserazide/levodopa and the slow release preparations are suitable for initial treatment. However, when to start levodopa remains controversial. Dopaminergic agonists are useful symptomatic drugs. They can be used in monotherapy, but usually require the addition of levodopa to obtain a satisfactory long term therapeutic response. Used as adjuvant treatment to levodopa, they help lowering the dosage of levodopa. Anticholinergic drugs effectively improve symptoms such as tremor and rigidity but their use is limited by their side effects, particularly in older people. Amantadine may be a useful drug for initial treatment of Parkinson's disease when symptoms are not severe. Symptomatic treatment should be considered individually in each patient. If there is only slight disability, treatment may be started with amantadine alone or with a dopaminergic agonist. If there is greater disability, levodopa or the simultaneous use of levodopa and a dopaminergic agonist should be considered. Anticholinergic drugs should be reserved for young patients with tremor as the main symptom. The newer dopamine agonists and inhibitors of catachol-o-methyltransferase (COMT) are coming therapeutic options. Selegiline, a MAOB inhibitor with a possible neuroprotective effect, should also be considered as initial option for Parkinson's disease.
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PMID:[Initial treatment of Parkinson's disease]. 928 Jun 84


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