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)

In 13 elderly patients, 12 of whom had Parkinson's disease, visual hallucinations and delirium developed as a side effect of amantadine hydrochloride (Symmetrel) therapy. The symptoms promptly disappearred when amantadine was discontinued. Thereafter, each parkinsonian patient was treated satisfactorily with levo-dopa. Treatment with a combination of amantadine and an anticholinergic agent increases the likelihood of delirium because of the hazard of retention of urine. Although amantadine is effective in the treatment of Parkinson's disease in the elderly, the incidence of delirium as a complication seems higher in this age group.
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PMID:Visual hallucinations and delirium during treatment with amantadine (Symmetrel). 12 40

Twenty-two patients entered a double-blind trial to test the efficacy of bromocriptine therapy in patients with Parkinson's disease who were already stabilized on conventional L-Dopa therapy. Of these, three patients who were receiving placebo withdrew when no improvement occurred and control became complicated. Another four patients taking active drug withdrew because of side effects, but only in one case was the symptom (nausea and vomiting) thought to be a true effect of the drug. Of the 15 patients who completed the trial, nine were taking active drug and six took placebo. Although more than half the patients in each group were subjectively improved, measurement scales of functional disability and physical examination revealed no significant change in either group. Side effects encountered included nausea, dyskinesia, and hallucinations. It was concluded that bromocriptine does not offer any additional benefit to patients with Parkinson's disease who are stabilized on L-Dopa therapy, but may have a place in those patients who encounter side effects due to fluctuations in serum and tissue levels of L-Dopa.
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PMID:A double-blind trial of bromocriptine in Parkinson's disease. 37 May 27

22 patients entered a double-blind trial to test the efficacy of bromocriptine therapy in patients with Parkinson's disease already established on conventional levodopa therapy. 3 patients on placebo withdrew when no improvement occurred and control became complicated. 4 patients on active drug withdrew because of various symptoms, but in only 1 case were these (nausea and vomiting) thought to be a real drug effect. Of the 15 patients who completed the trial, 9 were on active drug and 6 were on placebo. Although more than half the patients in each group were subjectively improved, measurement scales of functional disability and physical examination revealed no significant change in either group. Side effects encountered included nausea, dyskinesiae and hallucinations. It is concluded that bromocriptine does not offer any additional benefit in most patients with Parkinson's disease who are well stabilised on levodopa therapy, but may have a place in those patients who encounter side effects due to fluctuations in serum and tissue levels of levodopa.
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PMID:An evaluation of bromocriptine in the treatment of Parkinson's disease. 38 7

Lergotrile mesylate, a direct-acting dopamine agonist, was administered for up to 10 months to 25 patients with Parkinson disease. Of six patients not receiving levodopa concurrently, five showed definite improvement in parkinsonian signs and symptoms. These results are the first clear indication that lergotrile is efficacious, independently of any interaction with levodopa, in the treatment of Parkinson disease. The drug was also effective in relieving some complications of long-term levodopa therapy. Lergotrile was more effective in alleviating on-off problems than in reversing loss of levodopa efficacy. Side effects of lergotrile included exacerbation of hallucinations, dyskinesias, hypotension, and alterations in liver function tests.
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PMID:Lergotrile in the treatment of parkinsonism. 56 68

Of 88 patients with idiopathic Parkinson's disease, without prior psychotic symptoms, and without significant dementia, nearly half had experienced vivid dreams, hallucinations, illusions, and nonconfusional as well as confusional psychoses as side effects of chronic levodopa therapy within the previous year of treatment. It was found that 61.3% of all hallucinations were associated with preexistent or concurrent vivid dream phenomena, that all psychotic states were associated with preexistent or concurrent vivid dreams and/or hallucinations, and that nonconfusional psychotic states tended to become confusional. These findings raise the possibility that chronic levodopa therapy may result in dopaminergic kindling and support the hypothesis that chronic dopaminergic agonism may, via such a kindling mechanism, play a role in the development of some types of psychoses.
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PMID:Levodopa-induced psychosis: a kindling phenomenon. 65 76

Thirty-one patients with Parkinson's disease were treated with the ergot alkaloid bromocriptine, a drug which stimulates dopamine receptors. Bromocriptine had a slight therapeutic effect in patients on no other treatment and an additional effect in patients on levodopa. The mean optimum dosage of bromocriptine, established over a 12 week period, was 26 mg daily. In 20 patients bromocriptine was compared with placebo in a double-blind controlled trial. Active treatment caused a significant (P less than 0.02) reduction in total disability and akinesia scores. The least disabled patients showed the greatest response. Side-effects of bromocriptine--nausea, vomiting, hallucinations, and abnormal involuntary movements--were similar to nature to those of levodopa. In most normal subjects, bromocriptine causes an increase in plasma growth hormone concentration. This was determined in 20 patients with Parkinson's disease after 1-15 mg bromocriptine. Only a single patient showed an obvious increase up to 120 minutes after dosage. Bromocriptine was not effective treatment in two patients who had not previously responded to levodopa and replacement of this drug by bromocriptine in patients with end-of-dose akinesia after chronic levodopa treatment did not totally abolish response swings.
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PMID:Bromocriptine treatment in Parkinson's disease. 77 75

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

We report an autopsied case of Parkinson's disease manifesting Shy-Drager syndrome. At the age of 63 years, the patient noticed an onset of progressive orthostatic dizziness, which was followed by constipation, dysuria, and sexual impotence. When he was 66 years old, syncopal attack for a few minutes, tremor in the bilateral hands, and memory disturbance developed. On admission, his blood pressure was 142/72 mmHg in supine position, which fell to 58/42 mmHg on standing with appropriate increase of heart rate. Neurological examination revealed hallucination, memory disturbance, masked face, muscular rigidity, bradykinesia, mild postural tremor, and autonomic dysfunction including severe orthostatic hypotension, hypohydrosis, constipation, dysuria, and sexual impotence. Electroencephalogram showed diffuse slowing. Brain CT demonstrated absence of severe atrophy of the cerebellum, and brain stem. Pharmacological study revealed denervation hypersensitivity to the intravenously administrated noradrenaline. A diagnosis of Shy-Drager syndrome was made, and he was treated with anti parkinsonian drugs. However, no improvement was observed in his clinical symptoms. Seven months later, he died of pneumonia. Neuropathological examination revealed marked neuronal cell loss and gliosis in the substantia nigra and locus ceruleus. Lewy bodies were seen in those pigmented nuclei, dorsal vagal nucleus, hypothalamus and nucleus basalis of Meynert. No abnormality was found in the intermediolateral nucleus of the spinal cord. This is the first report on a Japanese patient who presented clinically Shy-Drager syndrome and pathologically typical Parkinson's disease. In this patient, from the pharmacological and pathological findings, sympathetic ganglia were supposed to be the responsible lesion for orthostatic hypotension.
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PMID:[An autopsied case of Parkinson's disease manifesting Shy-Drager syndrome]. 130 25

Lewy bodies are intraneuronal inclusions initially found in the pigmented brainstem nuclei of patients with Parkinson's disease. Their aspect varies according to their neuronal or cerebral situation. They have been a long time the hallmark of Parkinson's disease, but in recent years it has emerged that a small group of rare disorders or rare variants of common degenerative diseases are also sometimes associated with Lewy bodies in the nervous system. Pathological studies have also individualized a new disorder characterized by the presence of numerous Lewy bodies throughout the cerebral cortex and the brainstem: Lewy body disease. The clinical syndrome associates dementia, parkinsonian features, dysautonomia and motor neuron disease. The dementia is cortical in type and psychiatric symptoms such as agitation, hallucinations or delusions are frequent. The pathological features are nerve cell loss, diffuse Lewy bodies, and sometimes senile plaques. The origin of this disorder remains unclear, but it could be a primitive abnormality of neuronal cytoskeleton.
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PMID:[From Parkinson's disease to Lewy body disease]. 153 93


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