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)

One of the major difficulties in the treatment of Parkinson's disease with L-Dopa alone or associated with a decarboxylase inhibitor lies in the frequent occurrence of involuntary movements. In some cases these movements can be prevented (eliminated) by increasing the plasma DCI concentration or by associating 3-oxy-methyl-dopa. In resistant cases the authors have conducted a trial with EP 19-088, which belongs to a new class of tricyclic derivatives of indenopyridine. The trial population comprised 42 patients. In 12 of these there was complete cessation of symptoms. In 9 patients a marked improvement was noted, while in 10 others the improvement was slight but definite. The treatment was discontinued in 2 cases due to episodes of increased confusion. In the other 9 patients the experimental treatment had no effect. No side effects were observed in 24 of the 42 patients tested. In addition to symptoms such as nausea or transient heartburn, the remaining patients reported either a slight worsening of their parkinsonian symptoms or an increase in diurnal fatigability.
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PMID:[Abnormal movements induced by L-dopa. New therapeutic possibilities]. 112 79

Irregularities in motor response after continuing levodopa therapy of Parkinson disease (the "on-off effect") were assessed with the addition of L-alpha-methyldopa hydrazine (carbidopa) in a double-blind study. Thirteen of 20 patients improved while receiving carbidopa and levodopa while only four of 17 patients improved while receiving placebo and levodopa. Twenty-three of 37 patients improved in a subsequent non-blind trial of carbidopa plus levodopa. Improvement was not dependent on an increase in dose or frequency of levodopa administration. Adverse effects included dyskinesia, imbalance, and confusion; nausea was eliminated. On patient died of glomerulonephritis that predated the drug trial, but worsened progressively during and after it. Carbidopa's suppression of the "on-off effect" suggests that extracerbral factors may be important in this phenomenon.
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PMID:Treatment of "on-off effect" with a dopa decarboxylase inhibitor. 115 14

Apomorphine, a dopamine-agonist was applied as s. c. infusions to 7 patients with idiopathic Parkinson's disease. The indications were longlasting akinetic episodes (4 patients) and therapeutically resistant invalidating motoric fluctuations ("on-off") as well as hyperkinesia (3 patients) on anti-Parkinson medication. The effect of apomorphine as an anti-Parkinson therapeutic was verified using clinical scales and a portable activity-monitoring device. The s. c. infusion therapy (20-90 mg/die, or 0.025-0.01 mg/kg/die respectively) was effective in the akinetic patients interrupting akinesia and the inability to swallow. An improvement was also registered in patients with "on-off" and hyperkinesia using longlasting subcutaneous apomorphine infusions. The therapy was continued over a longer period of time with 2 patients as outpatients. The side-effects were nausea and local subcutaneous indurations at sites of infusions.
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PMID:[Subcutaneous apomorphine infusion in the treatment of Parkinson disease]. 141 Sep 78

Deprenyl is a synthetic, selective inhibitor of the monoamine oxidase-B enzyme system. The mechanism of its beneficial effect in early and advanced Parkinson's disease is not settled. Increased striatal dopamine accumulation, sensitization of surviving dopamine neurons with increased dopamine production and reduced nigro-striatal toxicity may all contribute. The standard daily dose of deprenyl is 10 mg. Selectivity may be lost at higher doses. Deprenyl is especially indicated in untreated patients, improving up to 50 percent of patients with mild motor fluctuations. Major symptomatic benefit also occurs in occasional levodopa treated patients. Adverse effects are common, however. Increase dyskinesias, confusion and hallucinations, nausea and postural hypotension may necessitate drug withdrawal or the use of low dose regimens. Caution should be exercised with older patients, those with ulcer disease, which may be worsened by deprenyl, and individuals with active ischemic heart disease where the safety of this drug is not yet clear.
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PMID:Deprenyl in Parkinson's disease: mechanisms, neuroprotective effect, indications and adverse effects. 157 60

The cause of the degeneration of dopamine-containing cells in the zona compacta of the substantia nigra in Parkinson's disease remains unknown. The ability of the selective nigral toxin 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) (via its metabolite MPP+) to destroy nigral dopamine cells selectively by inhibiting complex I of the mitochondrial energy chain may provide a clue. Indeed, recent studies of post-mortem brain tissue have suggested the presence of an on-going toxic process in the substantia nigra in Parkinson's disease leading to excess lipid peroxidation. This appears also to involve a disruption of mitochondrial function since mitochondrial superoxide dismutase activity is increased and there is impairment of complex I. These changes may in turn relate to a selective increase in the total iron content of substantia nigra coupled to a generalised decrease in brain ferritin content. Piribedil is used in the symptomatic treatment of Parkinson's disease and is particularly effective against tremor. Piribedil (and its metabolites) acts as a dopamine D-2 receptor agonist. However, in our studies in contrast to other dopamine agonists, in vivo piribedil interacts with dopamine receptors in the substantia nigra and nucleus accumbens but not those in the striatum. In patients with Parkinson's disease the beneficial effects of piribedil may be limited by nausea and drowsiness. Indeed, in MPTP-treated primates piribedil reverses motor deficits but marked side-effects occur. However, pre-treatment with the peripheral dopamine receptor antagonist domperidone prevents the unwanted effects and piribedil produces a profound and longer-lasting reversal of all components of the motor syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parkinson's disease: pathological mechanisms and actions of piribedil. 163 7

Results og an open, controlled three-month clinical trial of therapeutical efficacy of a combination of a low doses of levodopa/carbidopa and bromocriptine in 20 de novo patients with Parkinson's disease (PD) are presented. All patients received the same daily doses of levodopa/carbidopa (250 mg), while daily dosage of bromocriptine was gradually increased from 1.25 mg to 30 mg. Owing to development of adverse effects 3 patients dropped out of the study, while in 70% of the patients who completed the protocol improvement of motor functioning exceeded 50%. Those with bradykinesia and rigidity responded most favorably. For all our patients the mean daily dose of bromocriptine was 26.25 mg. The most common adverse effects of the therapy were orthostatic hypotension (7 pts) and nausea (5 pts). The results of the study coincide with the hypothesis that comparative administration of low doses of bromocriptine and levodopa is the best approach to treatment of early phases of PD.
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PMID:[Comparison of administration of low doses of bromocriptine and levodopa in the early treatment of Parkinson disease]. 164 93

The effects of naloxone on side effects provoked by apomorphine (APO) administration in patients with parkinsonian syndrome have been studied. The group under study included eight patients with Parkinson's disease and four with parkinsonism who received 100 micrograms/kg s.c. APO acutely to test dopaminergic responsiveness. All patients were treated with 20 mg domperidone tablets t.i.d. and then for 2 consecutive days (in double blind fashion) were given a 2-hour i.v. saline infusion alone or with naloxone (8 mg) starting 30 min before APO administration. In both groups, naloxone delayed the appearance of sleepiness, and reduced the intensity of yawning, sleepiness, nausea, and vomiting as compared with saline. These findings indicate a potential usefulness of naloxone and other opioid antagonists in preventing acute APO side effects.
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PMID:Naloxone partly counteracts apomorphine side effects. 174 54

We have investigated the prevalence of gastrointestinal (GI) symptoms in 98 individuals with Parkinson's disease (PD) and in a control group of 50. Seventy-nine of those with PD were being treated with dopaminergic medications and 19 were untreated. Those symptoms occurring more frequently in PD patients than in controls included abnormal salivation, dysphagia, nausea, constipation, and defecatory dysfunction. Except for defecatory dysfunction, symptoms did not correlate with treatment but instead correlated with disease severity. This suggests that the GI symptoms of PD reflect direct involvement in the GI tract by the primary disease process.
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PMID:Gastrointestinal symptoms in Parkinson's disease. 205 6

The Home Visiting Exercise Project assessed the impact (benefit) of a weekly home exercise regimen for ambulatory patients with Parkinson's disease (PD). The exercises were taught by senior nursing students. In a case control study with 29 patients, half were assigned to a home-supervised exercise regimen and the other half were assigned a home visit without an exercise regimen. The hypothesis was that PD patients who received a weekly home nursing student-supervised exercise regimen would experience better mobility, feeding and self-care as compared to patients who received a weekly home visit from a nursing student without exercises. Patients who participated in the exercise regimen showed significant improvement in recent memory, diminution of nausea, improved sucking ability, and less urinary retention and incontinence. This research was supported by a grant from the National Parkinson's Foundation, Miami, Florida.
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PMID:The benefit of a home exercise regimen for ambulatory Parkinson's disease patients. 252 59

(+)-4-propyl-9-hydroxynaphthoxazine (PHNO) is a novel selective D2 agonist. The efficacy and safety of PHNO was studied in 10 Parkinsonian patients (Hoehn and Yahr Stage II or III) who continued to receive levodopa/carbidopa. At the lowest dose administered (0.25 mg tid), nine of the 10 patients improved with respect to rigidity, bradykinesia and tremor. At this dose there was one dropout because of severe orthostasis. Although there was a trend towards improvement in motor scores with the higher doses (0.5-1.0 mg tid), this was not statistically significant. At higher doses there were a total of four dropouts because of adverse effects such as nausea, vomiting and orthostatic hypotension. It appears that PHNO may prove to be efficacious in the treatment of Parkinson's disease.
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PMID:The efficacy of (+)-4-propyl-9-hydroxynaphthoxazine as adjunctive therapy in Parkinson's disease. 274 65


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