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

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

This review evaluates the long-term results of Levodopa therapy in Parkinson's disease upon quality of life, prolongation of survival and excess mortality. It also focuses on recent and new therapeutic approaches: Levodopa in combindation with a Dopa-decarboxylase inhibitor or MAO-B inhibitor, dopamine agonists and an active tripeptide: L-prolyl-L-leucylglycine amide (MIF-I). It ends by looking at new avenues of etiological research in Parkinson's disease which may indicate specific accelerated ageing of catecholaminergic (pigmented) neuronal systems.
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PMID:Progress in understanding and treating Parkinson's disease. 77 22

Seventeen patients with either Parkinson's disease or post-encephalitic parkinsonism were treated with Piribedil, an apomorphine-like drug, in single blind conditions for a period ranging from five weeks to twenty-four months. The analysis of the results shows that Piribedil modifies the extrapiramidal symptomatology being specially effective against the tremor either when used alone or in association with L-Dopa. The side effects noticed during treatment with Piribedil are similar to those of Apomorphine, and are dose-dependent.
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PMID:[Piribedil in the treatment of Parkinson disease (author's transl)]. 77 98

Twenty-one patients suffering from Parkinson disease were treated with L-Dopa together with an extra-cerebral dopa-decarboxylase inhibitor (Ro4-4602) and with triesyphenidyl. Seven assessments of the patient's clinical condition were carried out over a period of two years with a number of neurological and psychometric tests. At the beginning of the second year of treatment, the signs and symptoms of Parkinson disease began to worsen with an increased disability. In the present paper two possibilities are discussed, namely whether the deterioration was the consequence of L-Dopa administration or whether this was simply the outcome of inadequacy of drug treatment during a period of natural worsening of the disease.
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PMID:[Outcome of Parkinsonism after two years of levodopa plus R04-4602 (author's transl)]. 78 78

In Parkinson's disease there is a derangement of the metabolism of at least 3 major brain monoamines, namely, dopamine (DA), norepinephrine (NE) and serotonin (5-HT). Of these alterations the severe deficiency of DA in the striatum is most characteristic, being (a) found in Parkinsonian syndromes of any etiology and (b) significantly correlated with the degree of cell loss in the substantia nigra, and the severity of the main symptoms. On the basis of neurochemical-clinical correlations Parkinson's disease may be subdivided into (a) an asymptomatic stage during which the striatal DA deficiency may reach a marked degree but can be compensated by the remaining DA neurons, and (b) the stage of decompensation (i.e. clinically manifest disease) which ensues when the depetion of striatal DA reaches 70% or more. L-Dopa's main feature as a specific antiparkinson drug may be seen in its potential to revert the decompensated stage of the disease to the stage of functional compensation. This is in many cases possible because (a) the DA turnover in the remaining DA neurons is increased, providing for a high rate of formation (from L-dopa) and release of DA; (b) the "denervated" striatal receptors are supersensitive to DA; and (c) the newly-formed DA can be expected to reach a wide area of the striatum due to the high degree of divergence of the dopaminergic innervation. Compared with the striatal DA deficiency, the degree of NE and 5-HT decrease in the Parkinsonian brain is moderate. The decrease in NE may be due to the (moderate) cell loss in the locus coeruleus; at present no morphological basis for the lowering of brain 5-HT is known. The functional significance of the changes in brain NE may be an aggravation of akinesia. The decrease in brain 5-HT may be related to aspects of Parkinson's disease in turn related to affective behavior and mood.
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PMID:Brain monoamines and parkinsonism. 78 96

The authors describe the results of biochemical analysis carried out on 28 patients with Parkinson's disease who had been treated by L-dopa. Twenty of them showed either no abnormal movements at all or very few, eight others had considerable dyskinesia. Biochemical analysis of the urinary degradation products of L-Dopa revealed the existence of a swing in the degradation of dopamine towards 4-O-methylate derivatives in dyskinetic patients (significant difference at .01). The results confirm those obtained in their initial analysis carried out in 1973. The authors express the view that abnormal movements while under L-Dopa treatment are dependent on two factors: one, the hypersensitivity of dopaminergic reception, the other, the greater or lesser preponderance of the COMT isozyme giving rise to 4-O-methylates;
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PMID:[Abnormal movements of patients with Parkinsonism treated with L-dopa and anomalies of dopamine metabolism]. 84 19

It has been suggested that the therapeutic response to levodopa in patients with Parkinson's disease may be related to changes in plasma growth hormone concentration. In order to examine this problem, we have determined plasma DOPA and growth hormone levels after a standard oral levodopa load in 32 patients with Parkinson's disease. Levodopa caused an increase in plasma growth hormone concentration in 30 subjects. The magnitude and timing of this growth hormone response was not related to the clinical response, the presence or absence of response swings, or the occurrence of dyskinesias. The growth hormone response to levodopa is normal in patients with Parkinson's disease and not altered by long-term levodopa treatment.
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PMID:Plasma DOPA levels and growth hormone response to levodopa in parkinsomism. 86 80

We have studied the urinary excretion of 1,4-methylhistamine (1,4-MeHm), 5-hydroxyindole-3-acetic acid (5-HIAA) and homovanillic acid (HVA) in patients with Parkinson's disease, choreiform movements and essential tremor. The effect of amantadine on urinary excretion has been measured in each group of patients as well as the effect of levodopa in patients with Parkinson's disease. In patients with Parkinson's disease, excretion of 1,4-MeHm and HVA was significantly lower than in controls. Patients with choreiform movements had a reduced excretion of HVA but trends toward low levels of 1,4-MeHm and, in patients with Huntington's chorea, elevated excretion of 5-HIAA, were not significant. In patients with essential tremor, urinary excretion of the amine metabolities studied did nof differ significantly from controls. Administration of amantadine to patients with Parkinson's disease was not followed by increased excretion of monoamine metabolites except in those patients who were already receiving anticholinergic drugs. This increase is not significant and there was no effect in other groups of patients. These findings lend no support to the view that amantadine has a general amine-releasing action although there is limited evidence for such an effect in Parkinson's disease. In addition to the expected increase in HVA excretion, administration of levodopa to Parkinsonian patients was followed by significantly reduced excretion of 1,4-MeHm and 5-HIAA. However, if amantadine and levodopa were given together, excretion of 5-HIAA was still reduced, but that of 1,4-MeHm was normal. Levodopa may thus modify the turnover of histamine, which appears to be reduced in Parkinson's disease, and this effect may be modified by amantadine.
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PMID:Urinary monoamine metabolite excretion in disorders of movement. Effects of amantadine and levodopa. 87 21

It is widely known that administration of L-Dopa benefits patients with Parkinson's syndrome and combination of this drug with decarboxilase does it to a greater extent. In the present study 20 patients with Parkinson's syndrome received MK 486, a combination of L-Dopa and Carbidopa 10:1 (250 mg of the fomer and 25 mg of the latter). The aim of this study was to evaluate therapeutic activity of this drug combination. It was found that MK 486 is effective for controlling clinical manifestation in Parkinson's syndrome. Although side effects were seen frequently, they diminished or disappeared after time of drug administration.
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PMID:[Treatment of Parkinson's syndrome with a combination of levodopa and carbidopa]. 90 17

In a group of patients suffering from Parkinson's disease, beside neurogenic bladder dysfunction, we have also found dysfunction affecting the external sphincter musculature. Treatment with L-Dopa probably improves the urethral symptoms by providing a relaxing effect on the urethral closure pressur together with better coordination of the pelvic floor and external sphincter Mechanism during micturition. The effect was parallel to the improvement in Parkinsonion symptoms. Experimental studies demonstrate the ability of L-Dopa to reduce urethral closure pressure and this effect was related to a central effect on the skeletal musculature.
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PMID:Parkinsonism and neurogenic bladder. Experimental and clinical observations. 103 92


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