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)

The clinical characteristics of psychiatric side effects of bromocriptine in patients with Parkinson's disease were studied in 12 cases. The clinical picture was characterized by hallucinations and delirium. Daily doses of bromocriptine (more than 30 mg daily), not duration of the disease or pretreatment with levodopa or previous psychiatric diseases, appeared to be the most important causal factor.
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PMID:[Neuropsychic side effects of bromocriptine in Parkinson's disease]. 367 65

Falling occurs more often in patients with Parkinson's disease when there is inadequate--not excessive--effect of the antiparkinsonian agent. Thus, falling may be evidence of a need for increased dosage. Of PD patients participating in a study, 60% reported experiencing hallucinations, confusion, vivid dreams, or nightmares. Confusion (34%) was the most commonly reported mental complaint; 27% reported vivid dreams; 26%, hallucinations; and 20%, nightmares.
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PMID:Avoiding mental changes and falls in older Parkinson's patients. 373 9

Thirty-five patients with early mild Parkinson's disease were treated from the outset with small doses of L-dopa (mean dose, 396 to 454 mg daily) and a peripheral decarboxylase inhibitor, for a mean of 6 years. Overall mortality ratio was 1.2:1, worse for women than for men. After 6 years of treatment, only one-third of patients were better, and drug-related complications were common (peak-dose dyskinesias in 54% of patients, off-period dystonia 20%, wearing-off effects 52%, on-off oscillations 6%, visual hallucinations and toxic confusional states 17%). We found no evidence that long-term results were markedly improved with low-dose regimens.
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PMID:Low-dose L-dopa therapy in Parkinson's disease: a 6-year follow-up study. 376 73

Long-term management of patients with Parkinson's disease includes close monitoring and frequent dose adjustment. In a small selected group of patients, complete withdrawal of L-dopa (drug holiday) and slow reintroduction of lower doses of this drug assured continued benefit for six to 24 months. We studied 45 drug holidays in 45 patients with idiopathic Parkinson's disease. Average preholiday L-dopa dose was 2,970 mg/d; at 24 months, it was 263 mg/d. The drug holiday resulted in reduced adverse drug effects (dyskinesias, "on-off" phenomenon, hallucinations, and confusion), and improved functional ratings at one, six, 12, and 24 months after the drug holiday.
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PMID:Parkinson's disease: follow-up after "drug holiday". 379 59

One hundred and eighty-one patients with treated Parkinson's disease completed a self-administered questionnaire on symptoms, and their responses were compared with those of 263 control subjects randomly selected from a general practice population. Nine symptoms were reported by the patients with more than a fivefold excess when compared with the controls. These included jerking of the limbs, shaking of the hands, excessive salivation, poor mental concentration, grimacing, being frozen or rooted to the spot, and hallucinations. Compared with the general control population, the patients did not have an excess of stomach or limb pain, indigestion, headache, or any decrease of interest in sex. This observational survey, unlike a randomised controlled trial, could not ensure that the different treatment groups were comparable in important respects. However, certain associations were apparent; for example, patients receiving both a decarboxylase inhibitor and levodopa tended to report fewer attacks of being frozen to the spot, fewer problems with salivation, and a reduced frequency of defaecation. Patients receiving anticholinergic drugs reported an excess of dry mouth, faintness, and dyskinesia, and fewer hot flushes.
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PMID:The symptoms of patients treated for Parkinson's disease. 400 65

The authors studied 20 patients with Parkinson's disease and prominent hallucinations related to dopaminergic or anticholinergic therapy. The character of the hallucinations appeared distinct from the classic description of either acute anticholinergic or acute aminergic hallucinatory states. Manipulation of either kind of drug could precipitate or relieve hallucinations in a given patient, which suggests that the dopaminergic/cholinergic systems are reciprocally active in the pathophysiology of long-term drug-induced hallucinatory states in this population.
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PMID:Pharmacology of hallucinations induced by long-term drug therapy. 680 3

Pathological and biochemical evidence reviewed favours the hypothesis that the dementia seen in Parkinson's disease, particularly after long-term levodopa therapy, is akin to Alzheimer's disease. We postulate, in late Parkinson's disease, the development of a relative cholinergic deficiency due to the accelerated process of aging and the presence of neurofibrillary tangles (with choline acetyl transferase deficiency.) This process would be enhanced by the imbalance in favour of dopaminergic predominance caused by chronic levodopa therapy, and would partially explain the increase in dementia. As a test of this hypothesis we have given 10 levodopa-treated parkinsonian patients with dementia, a regimen of lecithin (average 20 gms/day). A clear improvement in Kohs block design test of constructive ability was noted with a decrease in the toxic symptoms of confusion, hallucinations and nightmares. In another study lecithin produced a decrease in levodopa-induced abnormal movements, but at the expense of motor performance. These preliminary investigations indicate that the progressive dementia of Parkinson's disease may not be irreversible.
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PMID:Lecithin in Parkinson's disease. 700 Sep 78

We report of 51-year-old man with early onset parkinsonism. The patient was well until 38 years of age, when he noted a difficulty in the use of his right leg; this difficulty improved after he received a medicine from his physician. He did not take medicine regularly, and he noted difficulty in standing up from a chair and in rolling over at age 40. Tremor was not a feature, but he noted slowness in his movements at age 42; at age 49, he noted diurnal fluctuation in his symptoms and at times he experienced hallucination. He was admitted to our hospital in September of 1992 for the first time when he was 50-year-old. At that time, neurologic examination revealed an alert and somewhat bradyphrenic man; Hasegawa dementia rating scale was 20/30. Cranial nerves were intact except for masked face and small voice. He showed stooped posture and small step gait cogwheel rigidity was noted in the four limbs more on the left; tremor was absent. Deep reflexes were within normal range and the sensation was intact. As he showed diurnal fluctuation in his symptoms, his medication was switched to levodopa 3,000 mg/day without a peripheral decarboxylase inhibitor. He was discharged for out patient follow up. But he did not take drugs regularly, and his neurologic condition deteriorated; he was admitted to another hospital. Neurologic examination at that time was essentially similar to that of his first admission to our hospital, except that he showed more severe rigidity and akinesia; again tremor was not detected. His cranial CT scan showed a mild ventricular dilatation without cortical or brain stem atrophy. During his hospital stay, he developed episodes of oculogyric crisis during peak dose of levodopa, and orthostatic hypotension. He developed pneumonia and expired on October 28, 1993. He was discussed in a neurological CPC, and the chief discussion arrived at the conclusion that the patient had early onset Parkinson's disease of Lewy body type. As differential diagnoses, early onset parkinsonism without Lewy body, pure form of diffuse Lewy body disease, pallidoluysian atrophy, and other conditions were considered; however, all of those possibilities were excluded. Early onset parkinsonism without Lewy body would have much earlier onset than this patient, and diffuse Lewy body disease would show more profound dementia 13 years after the onset. Pallidoluysian atrophy would be complicated with some dystonic features. Post-mortem examination showed marked discoloration and degeneration of the substantia nigra. The degeneration was most prominent in the ventrolateral tier of the substantia nigra.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 51-year-old man with early onset parkinsonism]. 760 92

Psychosis, linked to chronic levodopa and other antiparkinsonian drug treatments, is a common and incapacitating complication of advanced Parkinson's disease (PD). The psychosis may be due, in part, to overstimulation of central serotonergic (5-HT) receptors. We treated 16 PD patients who had psychosis of 6 to 60 months' duration with the 5-HT3 receptor antagonist ondansetron (12 to 24 mg daily) in an open-label, short-term (4 to 8 weeks) trial. There was marked to moderate improvement (p < 0.01) in measures of visual hallucinations, paranoid delusions, confusion, and the associated global functional impairment in all but one of the patients, and there was moderate improvement in the Brief Psychiatric Rating Scale and the Nurse's Observation Scale for Inpatient Evaluation; the Mini-Mental State Examination scores remained unaltered. Ondansetron did not cause any worsening in basic PD symptoms or levodopa efficacy and was well tolerated with no major side effects. Our study suggests that pharmacologic blockade of central 5-HT receptors may become a strategy to attenuate PD psychosis without inducing motor deterioration or suppression of antiparkinsonian action of levodopa, and it lends support to the hypothesis that serotonergic mechanisms are pathogenetically important in the emergence of psychosis in PD.
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PMID:Psychosis in advanced Parkinson's disease: treatment with ondansetron, a 5-HT3 receptor antagonist. 896 Jul 64

We performed fetal nigral transplantations in 4 Parkinson's disease (PD) patients. Solid grafts were bilaterally implanted into the postcommissural putamen using 3 to 4 donors per side aged 6 1/2 to 9 weeks postconception. Transplant deposits were separated by no more than 5 mm in three dimensions. Cyclosporine was employed for a total of 6 months. Patients were evaluated at baseline and at 1, 3, and 6 months postoperatively. Striatal 18-fluorodopa uptake was assessed by positron emission tomography at baseline and at 6 months postoperatively. The procedure was well tolerated in all patients. One patient had a clinically asymptomatic superficial cortical hemorrhage along the needle tract and a second had transient postoperative confusion and hallucinations. All patients experienced clinically meaningful benefit. Significant improvement (p < 0.05) was detected in total UPDRS score during the "off" state, Schwab-England disability score during the "off" state, percent "off" time, and percent "on" time with dyskinesia. Increased striatal fluorodopa uptake was observed bilaterally in each patient, with mean increases of 53% on the right (p = 0.01) and 33% on the left (p = 0.08). Our study demonstrated clear and consistent improvement in clinical features and striatal fluorodopa uptake following fetal tissue transplantation in patients with advanced PD whose condition was not improved preoperatively by drug manipulation. These preliminary results are encouraging and support further studies to evaluate grafting strategies as a therapy for PD.
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PMID:Bilateral fetal nigral transplantation into the postcommissural putamen in Parkinson's disease. 766 23


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