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)

269 patients suffering from progredient, chronic either primary or secundary cerebral diseases (Parkinson's disease, cerebral vascular diseases, cerebral atrophic dystrophy, Huntington's chorea, muliple sclerosis have been studied in the last two years. 44 of these patients developed pharmaco-toxic psychoses during drug treatment (low and medium dosis). The psycho-pathological rating resulted in an acute organic brain syndrome with predominance of confusion, sometimes progressing to delirium. EEG was changed during the psychotic stage. These changes cannot be decided from organic psychoses, which are not related to drugs. Patients with Parkinson's disease showed a relatively high incidence to psychoses during drug treatment (51.47%). In patients without Parkinson's disease, but on treatment with antidepressants, neuroleptics, diuretics and digitalis, pharmacotoxic psychoses only could be observed in 4.4% of the patients. However, the same group of patients showed an acute organic brain syndrome in 12.43%, when not on treatment. Combined treatment with L-DOPA plus peripherally acting decarboxylase inhibitors resulted in a high incidence to psychoses in idiopathic Parkinsonism but the same dosis produced this side effect only in a few patients with cerebral atrophic dystrophy. The ratio was 5:1 between the former group and the later one. That means, that L-DOPA is a much more psychotoxic substance in Parkinsonism when compared to other cerebral diseases. These pharmacotoxic psychoses could be correlated with the progredience of the disease. These pharmacotoxic psychoses are not only dependent from age and duration of treatment. Evidence exist, that there might be a correlation between the incidence for pharmacotoxic psychoses and the lack of surviving dopaminergic neurons in the nigro-striatal areas. Treatment with very low doses of neuroleptics suppresses pharmacotoxic psychoses but allow a further anti-Parkinson therapy which is of vital necessity.
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PMID:[Acute pharmacotoxic psychoses in patients with chronic cerebral disorders]. 3 35

Mental symptoms increased in frequency among 100 patients with parkinsonism treated with levodopa. Dementia was found in about one-third of patients throughout the 6-year treatment period. Thirteen patients became demented during the study, and dementia worsened severely in seven others. Agitated confusion became increasingly frequent and was observed in 60 percent of patients taking levodopa for 6 years. Withdrawal from levodopa decreased agitation, but not dementia. Ten patients received L-tryptophan along with levodopa, but no change in mentation was observed. In view of previous studies of mentation in Parkinson's disease and reports of widespread neuronal changes in the brain of autopsied patients with parkinsonism, our results suggest that the high incidence of dementia in patients with Parkinson's disease who take levodopa reflects prolongation of the course of the illness rather than a direct effect of the medication.
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PMID:Mental symptoms in Parkinson's disease during chronic treatment with levodopa. 94 87

Piribedil, a dopamine agonist, was administered to 13 patients with long-standing Parkinson's disease whose major symptoms were not well controlled on levodopa, anticholinergics, alpha-methyldopa, amantadine, or a combination of these agents. Twelve of the 13 clearly benefited from the addition of Piribedil although side effects precluded long term use in two cases. Beneficial results were obtained by using a combination of Piribedil, levodopa, and anticholinergic drugs. Side effects (hallucinations, confusion, dyskinesias) were frequent, but were usually reversible by lowering the dosage of levodopa or the accompanying anticholinergic medication. The synergistic effect of Piribedil and other antiparkinsonian drugs emphasizes the need for careful titration of all available medications in difficult cases and demonstrates the usefulness of dopamine receptor stimulators when drugs acting presynaptically have failed.
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PMID:Piribedil: its synergistic effect in multidrug regimens for parkinsonism. 94 94

The effect of a new dopaminergic agonist, piribedil, was studied in 16 patients with Parkinson's disease and compared with placebo and L-DOPA. Piribedil appeared to have a moderate therapeutic effect that was significantly less than that of L-DOPA. Tremor appeared to be the main clinical feature to benefit. Nausea, vomiting, and somnolence were most frequent during the buildup of treatment and confusion and hallucinations during long-term treatment. Piribedil caused a significant decrease in probenecid-induced accumulation of HVA in the CSF, suggesting reduced turnover of endogenous dopamine in the brain. There was a significant relationship between dopamine receptor activation by piribedil and improvement of parkinsonian disability.
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PMID:Dopaminergic agonist effects on Parkinsonian clinical features and brain monamine metabolism. 109 75

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

Delirium is commonly defined as a transient organic brain syndrome characterized by concurrent disorders of attention, perception, thinking, memory, psychomotor behavior, and the sleep-wake cycle. One of the difficulties in studying delirium is that symptoms tend to fluctuate over the course of the day. Pre-existing organic brain disease appears to be a significant risk factor for the development of delirium, and numerous studies have shown a high rate of delirium in patients with cerebrovascular disease, Parkinson's disease, and Alzheimer's disease. The cognitive deficits associated with delirium have not been widely studied in a systematic, quantitative fashion. Following resolution of the frank delirium, documented cognitive deficits can be observed, and may persist in a diluted form for a period of months. Residual cognitive deficits may be due to a minimal and persistent confusion or to an underlying brain disorder.
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PMID:Cognitive deficits in delirium: assessment over time. 129 18

Memantine is a 1-amino-adamantane derivative which has been proposed to be useful in the treatment of Parkinson's disease. Its beneficial effect has been related to its novel properties as an NMDA receptor blocker which can neutralize the effect of glutamate at striatal and subthalamic levels. In the present study, conducted in an open-fashion, 14 parkinsonian patients with motor fluctuations taking L-dopa, were given a supplement of memantine 30 mg/day. After one month, 10 patients completed the treatment (4 discontinued it due to abdominal pain, psychomotor agitation, confusion and dizziness). In 5 patients, the main parkinsonian features improved significantly (1 point or more on the Webster scale). In 6 patients, "off" episodes improved (from daily mean of 273 minutes, to 172 minutes). In summary, memantine addition to parkinsonian features, could form a basis for novel therapeutic strategies directed to neutralize the effects of glutamate at striatal and subthalamic levels.
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PMID:Efficacy of memantine, an NMDA receptor antagonist, in the treatment of Parkinson's disease. 138 98

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

There are a number of ways in which drugs might increase the risk of an elderly person falling. The most important of these are sedation, impaired balance and reaction time, hypotension and drug-induced Parkinson's disease. Demonstrating the association between drugs and falls has been difficult because of certain methodological problems. However, there is now strong evidence that the use of psychotropic drugs, with the possible exception of short-acting benzodiazepines and hypnotics, is associated with a clinically important increase in the risk of falling. This increased risk is present after controlling for confounding factors such as confusion and depression. The evidence linking other drug groups to an increased risk of falls is conflicting. Decreasing the risk of drug-induced falls requires both careful individual adjustment of therapy and also a public health programme to ensure safe drug prescribing for older people.
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PMID:Drug treatment as a cause of falls in old age. A review of the offending agents. 179 21


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