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)

We treated 17 patients with Parkinson's disease (PD) complicated by psychosis with the atypical antipsychotic drug, clozapine, for 6 to 24 months (mean, 15 months) in a prospective, open-label trial. At 3-month intervals we evaluated patients, using a simplified brief Psychiatric Rating Scale (PRS), the motor examination portion of the Unified Parkinson's Disease Rating Scale, and the Mini-Mental State Examination (MMSE). Mean PRS score was significantly improved when compared with baseline over 1 year (p < 0.01) and nonsignificantly improved for the second year. We maintained the levodopa dose at levels that were 17 to 68% higher than baseline, and the mean motor examination score improved by 11 to 22% in the first 15 months. Clozapine dosage utilized in the trial ranged from 6.25 mg every other day to 150 mg/d. Adverse effects, including sedation and confusion, were common. These results demonstrate that clozapine therapy can be effective in treating psychosis in PD patients over 1 to 2 years. The decline in efficacy in the second year was most likely related to an increase in daily levodopa dose, progression of dementia (illustrated by a decline in MMSE score), and an inability of PD patients to tolerate higher doses of clozapine.
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PMID:Clozapine: a 2-year open trial in Parkinson's disease patients with psychosis. 814 29

Clinical diagnoses of Parkinson's disease (PD) is highly inaccurate. Olivopontocerebellar atrophy (OPCA) is a major source of diagnostic confusion. We have studied the clinical characteristics of 50 patients with PD, 24 patients with OPCA judged by the presence of selective atrophy of the cerebellum and brainstem (diagnosed by CT brain scan) and 30 normal controls of similar age. The typical triad of PD, tremor, rigidity and akinesia, did not distinguish among patients from either group. The presence of severe postural imbalance and reflex myoclonus (in OPCA but not in PD) were the 2 most highly discriminative clinical features.
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PMID:[Olivopontocerebellar atrophy and Parkinson's disease: diagnostic problems]. 816 68

There is now considerable evidence to support a defect of the mitochondrial respiratory chain, and complex I in particular, in Parkinson's Disease (PD). However, the site specificity of the defect within the chain, its anatomical selectivity within the brain, and its presence in other tissues still remain controversial. Much of the present confusion surrounding the mitochondrial defect can be dispelled by careful analysis of the available data. The molecular basis of the deficiency and its relevance to the pathogenesis of PD remain unknown. Nevertheless, the complex I deficiency in PD provides a direct biochemical link between the idiopathic disease and the MPTP toxin model. The relationship between the mitochondrial defect and other abnormalities within the PD substantia nigra suggests that a self amplifying cycle of events might be precipitated either by a genetic or environmentally induced abnormality of mitochondrial function or free radical metabolism. Alternatively, a biochemical event separate from these might precipitate a cascade which terminates in complex I dysfunction and free radical formation. An understanding of the molecular basis of the complex I defect in PD and its relationship to other biochemical changes will provide important insight into the potential chain of events that lead to dopaminergic cell death in PD.
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PMID:Evidence for mitochondrial dysfunction in Parkinson's disease--a critical appraisal. 819 73

All medications currently used to treat Parkinson's disease carry some risk of causing confusion, hallucinations, or disruption of such higher-order mental operations as problem-solving and learning. Although the elderly demented patient is at greatest risk, such complications have also been noted during treatment of younger patients. Treatment with anticholinergics may lead to a confusional state and decreased memory function in some patients, especially the elderly and those with preexisting dementia. Monoamine oxidase inhibition is considered quite benign when used alone, but may potentiate certain side effects when used in combination with other compounds. Ergot alkaloid medication, which is usually combined with levodopa, often induces severe psychiatric complications. Typical findings with levodopa treatment indicate little or no positive impact on cognition, apart from nonspecific arousal and alleviation of concomitant depressive affect. Guidelines for the management of neuropsychological and psychiatric side effects are suggested.
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PMID:Neuropsychological and psychiatric side effects in the treatment of Parkinson's disease. 826 12

The prevalence of Parkinson's disease rises with age. The clinical features can be the typical ones or those associated with the "late-onset" type, with more gait and balance problems and a mild progressive dementia. Other disorders, such as stroke and essential tremor, may be mistaken for Parkinson's disease, or multiple conditions may be present which modify the response to treatment. The treatment of choice is a low dose of one of the L-dopa-decarboxylase inhibitor drugs. Other agents have a high incidence of side effects, particularly confusion, which also occurs with L-dopa in higher doses.
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PMID:Parkinson's disease. 841 92

The issue of whether there is a relationship between essential tremor (ET) and Parkinson's disease (PD) is controversial partly due to the confusion regarding the accurate diagnosis of these conditions. The presence of postural tremor, which often occurs in PD, by itself is insufficient for the diagnosis of ET. Most epidemiological studies have shown that there is no association between these two conditions. Some studies, but not others have found a higher prevalence of tremor in family members of PD patients. Clinical, positron emission tomography scan, and neuropathological data have failed to show any relationship between these two conditions. It is concluded that there is no relationship between ET and PD and that when these two conditions are seen in the same patient, this represents a chance occurrence of two common diseases.
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PMID:Is there a relationship between Parkinson's disease and essential tremor? 842 55

We present the results obtained using low doses of clozapine (mean dose 26.4 mg at bedtime) in the treatment of nocturnal akathisia in nine patients with Parkinson's disease for a mean period of 12.5 months. The results were excellent in all the patients. Furthermore, three patients experienced a remarkable improvement in rest tremor and in five patients the confusional state that accompanied the akathisia also disappeared. No serious side-effects were observed. We believe that clozapine is a very useful drug for the relief of nocturnal akathisia in parkinsonian subjects.
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PMID:Nocturnal akathisia in Parkinson's disease: treatment with clozapine. 847 84

A better understanding of the mechanisms underlying movement disorders, coupled with refinements in surgical technique, has led to a resurgence of interest in the surgical treatment of patients with tremor. We retrospectively analyzed the outcomes of 60 patients (62 patient sides) with medically intractable tremor who underwent stereotactic thalamotomy. Of these 60 patients, 42 had Parkinson's disease (of whom 2 patients underwent bilateral surgery for a total of 44 patient sides), 6 had essential tremor, 6 had cerebellar tremor, and 6 had post-traumatic tremor. The patients received follow-up for as long as 13 years (mean, 53.4 mo) after their operations. At the most recent follow-up visit, 86% of the patients with Parkinson's disease, 83% of the patients with essential tremor, 67% of the patients with cerebellar tremor, and 50% of the patients with post-traumatic tremor had cessation of or moderate-to-marked improvement in their contralateral tremor, with a concomitant improvement in function. The mean daily dose of levodopa for those patients preoperatively taking levodopa (n = 35) was reduced by approximately 156 mg at a mean of 53.4 months after thalamotomy. Immediate postoperative complications were common, occurring in 58% of patients. The most common complications were contralateral weakness (34%), dysarthria (29%), and confusion (23%). These complications generally resolved rapidly during the postoperative period.
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PMID:Outcome after stereotactic thalamotomy for parkinsonian, essential, and other types of tremor. 883 86

Adjunctive cabergoline or placebo, in doses up to 5 mg daily, were administered to Parkinson's disease patients with short-duration levodopa responses in a 6-month double-blind trial. The 13 patients randomized to cabergoline and completing the study had significantly improved Unified Parkinson's Disease Rating Scale (UPDRS) motor scores and timed hand-tapping test scores. Serial measurements on test days documented improved scores: (a) before the first levodopa (and cabergoline) dose of the day, (b) at the time of the peak levodopa effect, and (c) at the end of the levodopa response cycle, 5 h after test doses. Continued testing verified that these therapeutic responses were sustained for at least 48 h after the last cabergoline dose. Patients randomized to placebo failed to improve on any of these measures. In a subsequent open-label dose-escalation phase, further improvement was documented as the dosage was gradually raised to 10 mg daily. As in the double-blind phase, levodopa reduction allowed the improvement to occur in the absence of significantly increased dyskinesias. Other side effects were more substantial with higher doses, however, including two of 11 patients with hallucinations and confusion. In summary, adjunctive single-daily-dose cabergoline therapy resulted in long-lasting, dose-related improvement in parkinsonism not seen in patients receiving placebo.
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PMID:Adjunctive cabergoline therapy of Parkinson's disease: comparison with placebo and assessment of dose responses and duration of effect. 872 39

In the present study we compared the efficacy and safety of the new dopamine agonist cabergoline (CBG) with bromocriptine (BCR) in Parkinson's disease (PD). CBG has a very long half-life and can be administered as a single daily dose. Forty-four PD patients with uncontrolled motor fluctuations participated in the study. Patients were randomly and blindly assigned to equivalent doses of either CBG or BCR in addition to preexisting levodopa. Dosage was titrated to optimal, using up to 6 mg of CBG or 40 mg of BCR daily. CBG was given as a single morning dose whereas BCR was administered tid. Sixteen patients were followed for 1 year and 16 additional patients for 6 months. The mean follow-up duration was 9 +/- 5 months. The main effect of both drugs was observed on motor UPDRS scores, rigidity, bradykinesia items, and the percentage of awake hours spent during "on" and "off". In general, the effect of CBG was similar to that of BCR. The percentage of awake hours spent during "on" was higher with CBG as compared with BCR. Adverse events included dyskinesias, orthostatism, confusion, edema, and paresthesias in limbs. These effects were seen at similar frequencies with both drugs. The study shows that CBG given as a single morning dose is at least as efficacious as BCR given tid. CBG is a promising dopamine agonist for the treatment of motor fluctuations in PD.
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PMID:Double-blind comparison of cabergoline and bromocriptine in Parkinson's disease patients with motor fluctuations. 879 80


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