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 evaluated the risk factors for nursing home placement of patients with Parkinson's disease (PD) by matching 11 PD patients permanently admitted to nursing homes with two control PD patients remaining at home. Risk factors assessed were motor severity, presence of hallucinations/delusions, and presence of memory of problems. The only statistically significant risk factor was the presence of hallucinations/delusions. Motor severity and the presence of memory problems did not have an impact on nursing home placement. There was no risk factor synergy for hallucinations, motor disability, and mental impairment. Since all patients in this series who entered nursing homes remained there permanently, these data suggest that vigorous efforts to control hallucinations may be warranted to prevent nursing home placement.
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PMID:Risk factors for nursing home placement in advanced Parkinson's disease. 823 34

Prior studies of sleep in Parkinson's disease (PD) have been compromised by inadequate comparison groups, mixed medication regimens, and absence of quantitative data collection. This is the first study to compare polysomnographic sleep measures in PD patients on only dopaminergic medications with and without hallucinations. We performed two consecutive nights of polysomnography in 10 nondepressed, nondemented PD patients, 5 with and 5 without hallucinations. All patients were being treated with carbidopa/levodopa and a dopaminergic agonist only. Hallucinators and nonhallucinators were group-matched for age, PD duration, severity, and medication doses. Both groups had abnormal sleep records. In particular, there was a reduction in K-complexes and spindle formation, and the frequent occurrence of motor activation during rapid eye movement (REM) sleep consistent with REM behavior disorder. The hallucinator group had a significantly lower sleep efficiency (0.25 in hallucinators vs 0.61 in nonhallucinators, p = 0.006), a reduced total REM sleep time (mean total REM sleep time, 3 minutes in hallucinators vs 50 in nonhallucinators; p = 0.005), and a reduced REM percentage (mean, 5% in hallucinators vs 20% in nonhallucinators; p = 0.011). This study demonstrates that advanced PD patients treated with dopaminergic agents have abnormal sleep patterns and that those with dopaminergic-induced hallucinations have significantly greater REM aberrations than nonhallucinating PD patients.
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PMID:Polysomnographic sleep measures in Parkinson's disease patients with treatment-induced hallucinations. 823 65

The efficacy of PRD was evaluated in 21 patients with Parkinson's disease who presented motor fluctuations or a bad quality "on" time despite treatment with L-dopa or dopaminergic agonists. Eighteen of the 21 patients completed three months of treatment and only 14 (66.6%) were able to complete 12 months. The four patients who stopped treatment in this period did so because of subjective complaints despite obtaining good clinical response to PRD. Only three patients suspended the dietetic regime during first month of treatment. The 14 who completed the year of treatment showed a decrease in the "off" time (4.10 to 1.65: p < 0.01) and an improvement in motor response (14.89 to 10.39; p < 0.05) during the follow up period. Improvement appeared at the end of the second week of initiation of treatment. The diet was well tolerated with scarce complications, with only one patient presenting visual hallucinations. Other secondary effects were mild and did not require discontinuation of the diet. We conclude that proteic redistribution diet improves the "on" time in patients with Parkinson disease receiving L-dopa and delays the possibility of increasing the doses of L-dopa. The dietetic regimens with proteic redistribution seems a simple, useful and cheap approach without morbidity for the patients with Parkinson's disease showing a poor response or oscillation to L-dopa treatment.
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PMID:[Efficacy of the proteic redistribution diet (PRD) in the antiparkinsonian effect of L-dopa]. 824 Aug 36

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

1. This article reviews the prevalence, diagnosis, pathophysiology and management of psychosis in Parkinson's disease. 2. Psychosis in Parkinson's disease has been associated with all antiparkinsonian medications. The most common symptoms are vivid disturbing dreams, visual hallucinations and paranoid delusions. 3. The emergence of psychosis reduces the patient's functional capacity and increases caregiver burden. It also poses a therapeutic dilemma because effective treatment of psychotic symptoms may result in worsening of motor symptoms and vice versa. 4. Increased physician awareness is essential for proper diagnosis and management. Withdrawal of anticholinergic medications and amantadine followed by levodopa dose adjustment is effective in many patients. 5. Atypical neuroleptics, in low doses, may be successful when other measures have failed. However, these agents are not approved for treating Parkinsonian psychosis and must be considered as investigational therapies.
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PMID:Psychosis in Parkinson's disease: diagnosis and treatment. 853 22

Lewy bodies (LBs) are intracytoplasmic neuronal inclusions sometimes found in the brain stem, diencephalon, basal ganglia, and cerebral cortex. Cases designated as diffuse Lewy body disease (DLBD) demonstrate widespread cortical and subcortical Lewy body formation. The fact that DLBD is possibly the second most common cause of dementia after Alzheimer's disease is not generally recognized. We hope to emphasize the importance of this common neurodegenerative disorder by reviewing the literature and our own experience with DLBD. The English-language literature dealing with the clinical and pathological features of DLBD was reviewed. Pathological material from the Canadian Brain Tissue Bank, Toronto, Ontario, was reviewed over a 2-year period from 1991 through 1993. Prominent LB pathology may occur in isolation or mixed with pathological changes seen in Alzheimer's disease. Lewy body diseases include Parkinson's disease that presents with a classic movement disorder and sometimes dementia, and DLBD where LBs occur in a widespread distribution in the cortex in addition to the usual subcortical sites. Diffuse LB disease usually presents with a neurobehavioral syndrome that may include hallucinations, delusions, and psychosis; all patients eventually become demented. A day-to-day fluctuating mental state may be an important distinguishing clinical feature. Parkinsonism may follow the psychiatric disturbance although occasionally it is a presenting feature. Serious life- threatening side effects may occur with the use of standard neuroleptics. The variable clinical features and additional presence of Alzheimer-type pathological changes in many cases of DLBD has led to a confusing and inconsistent classification of LB disease and, together with little awareness of its existence, its misdiagnosis. Although DLBD may be the second most common cause of dementia, the terminology and classification of LB disorders and their relationship to Alzheimer's disease remain sources of intense debate. Further research is needed to resolve these issues and to provide insight into the pathogenesis of LB formation and accompanying neuronal degeneration.
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PMID:Lewy body disease and dementia. A review. 860 54

Remoxipride is a novel substituted benzamide that more effectively blocks mesolimbic than striatal D2 dopamine receptors. We used remoxipride in the management of nine patients with Parkinson's disease (PD) who were experiencing visual hallucinations due to dopaminergic therapy. Remoxipride was begun in a dose of 25 mg three times daily and gradually increased to 75-225 mg/d (mean 161 mg). The psychiatric status improved in eight patients. Little or no change in the severity of parkinsonism was noted in five, a mild increase in two, and a moderate increase in two. Because one patient with moderately severe levodopa-induced dyskinesias experienced a reduction in the abnormal movements without a substantial increase in parkinsonism, we began a trial of remoxipride for disabling peak-dose dyskinesias. The trial was abandoned after every one of the first four patients entered experienced an immediate, severe, and prolonged increase in off periods with single 10- to 25-mg doses. This striking differential response to an atypical neuroleptic with weak striatal D2 antagonist properties indicates that different states of postsynaptic dopamine receptor sensitivity or synaptic dopamine levels may be associated with various disease- and treatment-related problems found in late-stage PD.
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PMID:Remoxipride in Parkinson's disease: differential response in patients with dyskinesias fluctuations versus psychosis. 866 33

A long-term follow-up evaluation on the clinical usefulness of selegiline hydrochloride (selegiline) was performed in 13 patients with Parkinson's disease. All patients, except one case, subjected to the study were symptomatically improved by combination therapy of selegiline with L-DOPA in the preceding short-term evaluation. One patient continued the therapy after an evaluation of no symptomatic improvement in the short-term study, because this patient strongly requested continuation of medication, expecting to stop the progression of the disease. The average daily dose of selegiline at the last evaluation was 7.0 +/- 2.8 mg. The average daily dose of L-DOPA at each evaluation point in the patients who continued the therapy for 12 months remained low compared to that prior to the therapy (before: 450 +/- 138 mg, at the 12th month: 383 +/- 98 mg). In the analysis of individual parkinsonian symptoms, the improvement in the mean score for most of the symptoms, especially the wearing-off phenomenon and frozen gait, persisted for the entire period of study. Global improvement rates (moderately improved) at the 6th and 12th month, and the last evaluation were 60.0%, 50.0% and 50.0%, respectively. Among 10 patients, therapy was discontinued only in one case due to hallucination. Although the global improvement rate declined in the course of the therapy, selegiline seems to be useful for improving L-DOPA responsive symptoms in long-term therapy for Parkinson's disease.
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PMID:[A long-term clinical effect of selegiline hydrochloride on Parkinson's disease]. 867 6

We report a right-handed 78-year-old man with early onset parkinsonism. The patient had an onset of micrographia at 23 years of the age in 1939. Seven years later he started to drag his right foot, and at 38 years of age, he walked with small steps with festination. Tremor was also present in his right hand. His daily life was independent as a otorhinolaryngologist. He visited our clinic on March 24, 1977 when he was mentally sound and showed mild parkinsonism consisting of masked face, stooped posture, small step gait, bradykinesia, and right side dominant rigidity and tremor. He showed good response to trihexyphenidyl and amantadine HCl. Two month later, he developed dyskinesia and some worsening of parkinsonism, and was admitted to our hospital for the first time. He was treated with 400 to 600 mg/day of levodopa/ carbidopa. He showed marked improvement, however, dyskinesia remained in his mouth. He was doing well until 77 years of age (June of 1993) when he developed hallucination and motor fluctuations. He was admitted again to our hospital on June 22, 1993. On admission, he was alert and appeared mentally sound. However, Hasegawa dementia scale was 18/30. Upward gaze was slightly restricted (3/5). Voice was somewhat small but no masking was noted. His posture was stooped and the gait was of small step. Dyskinesia was noted during walk. No rigidity nor tremor was noted. Deep tendon reflexes were lost but no sensory loss or motor weakness was noted. Routine laboratory studies were unremarkable. A cranial CT scan revealed only mild to moderate cortical atrophy. Motor and sensory conduction velocities were within normal limits, however, motor action potentials could not be obtained with stimulation to the right common peroneal nerve. He was treated with 600 mg/day of levodopa with carbidopa, 100 mg of amantadine HCl, 300 mg of Dops, and 25 mg of tiapride. He continued to show motor fluctuations, and was discharged on July 23, 1993. Since then his motor functions had become progressively worse with frequent falls, but he was still able to walk without support. On October 3 of 1994, he went to bed as usual. On the next morning, he was found dead in his bed at 9: 30. The patient was discussed in neurological CPC, and the chief discussant arrived at the conclusion that the patient had young-onset Parkinson's disease with Lewy bodies in the substantia nigra. Opinions were divided between Parkinson's disease and Lewy body negative young onset parkinsonism. Postmortem examination revealed obstruction of the trachea by aspirated foods, and the cause of death appeared to have been suffocation by the foods. Macroscopically, the external appearance of the brain was unremarkable except for slight frontal atrophy. The substantia nigra showed depigmentation in the lateral part, but the pigmentation of the medial part was well preserved. Upon histologic examination, the number of pigmented neurons in the dorsomedial part was well preserved. In the lateral part, pigmented neurons were well preserved in the dorsal area, however, in the ventral area, only non-pigmented neurons were seen; they appeared to be neurons in the pars reticulata. No gliosis was seen in any of the nigral areas. No Lewy bodies were seen in the remaining neurons. So-called immature neurons with rounded shape without neuromelanin could not be detected. The locus coeruleus neurons were well preserved. The putamen and the other basal ganglia structures were also intact. Slight myelin pallor was noted in the subcortical white matter, however, otherwise cerebral cortices were normal. The histology of this patient is unique in that only the ventrolateral part of the substantia nigra showed abnormal finding consisting of lack of pigmented neurons without gliosis. It is not clear whether the nigral change represents degeneration or a congenital "hypoplasia'. To our knowledge, such a unique pathology of the substantia nigra has not been reported in the literature. Our patient ma
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PMID:[A 78-year-old man with young onset parkinsonism and sudden death]. 867 9

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


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