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 effects of the NMDA antagonist dextromethorphan (DM) on levodopa-associated dyskinesias and motor fluctuations were studied in patients with advanced Parkinson's disease. During initial open-label dose escalation, 6 of 18 patients reported a beneficial effect at their individually determined optimal DM dose (range, 60-120 mg/day). The 12 remaining patients either experienced reversible side effects, particularly mild drowsiness, or decreased levodopa efficacy, and were therefore excluded from the study. The six responders entered the double-blind, placebo-controlled, crossover study with two 2-week arms separated by 1 week wash-out. On the last day of each arm, motor ratings were performed every 20 minutes for 8 consecutive hours. In addition, motor complications and Activities of Daily Living (ADL) were assessed using the Unified Parkinson's Disease Rating Scale (UPDRS) and patient diaries. With DM, dyskinesias improved by 25% according to physician's ratings and by 40% according to UPDRS interviews, without compromising the anti-Parkinson effect of levodopa. Motor fluctuations and ADL scores also improved significantly. Although the narrow therapeutic index of DM limits its clinical usefulness, these findings support the view that drugs acting to inhibit glutamatergic transmission at the NMDA receptor can ameliorate levodopa-associated motor complications.
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PMID:A trial of dextromethorphan in parkinsonian patients with motor response complications. 961 30

Ropinirole is a novel, nonergoline, selective D2-type dopamine agonist developed to treat Parkinson's disease. Safety data from therapeutic studies involving 1364 patients receiving ropinirole are reported (mean daily dose 8.7 mg, early therapy; 8.2 mg adjunct therapy). In early therapy, the emergent adverse experiences more common with the ropinirole group compared with placebo were nausea, somnolence, leg edema, abdominal pain, vomiting, dyspepsia, and hallucinations. In adjunct therapy, they were dyskinesia, nausea, hallucinations, and confusion. Most adverse experiences were mild and associated with a similar withdrawal rate compared with the placebo group. Except for hallucinations, the incidence of emergent adverse experiences decreased with time, despite increasing doses. Long-term adverse experiences particularly associated with ergoline-type dopamine agonists have so far not been observed with ropinirole. Only 1.2% of patients receiving ropinirole developed dyskinesia compared with 11.2% receiving L-dopa in early therapy over a mean period of 17 months. There were no clinically significant changes in cardiovascular parameters or laboratory data. The incidence of adverse experiences in the bromocriptine group was low, possibly because of a slow titration scheme and low average dose. Overall, the safety profile of ropinirole appears similar to that of other dopamine agonists. Clinical studies are continuing to assess the long-term safety and efficacy of ropinirole.
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PMID:The safety of ropinirole, a selective nonergoline dopamine agonist, in patients with Parkinson's disease. 961 8

The surnames that honor the title of this work belong to individuals fascinated by the function of sleep and its integration in neurological illness. Sleep is a function of the brain exhibiting changes with age that are predictable. There are two major manifestations of sleep alteration: somnolence and insomnia. A rich variety of sleep alterations is associated with numerous neurological disorders. Some occur acutely like in stroke whereas others appear gradually like those associated with Parkinson's disease and the dementias. The pathology of sleep is a new area of involvement in the scope of practice of the neurologist. In the future the sleep specialist will also intervene in the prevention of mental fatigue and traffic accidents and in the promotion of sleep hygiene in primary medicine.
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PMID:[Neurosomnology: in the cutting-edge of neurology]. 981 Jul 96

We report sinus bradycardia induced by talipexole hydrochloride in a 65-year-old man with Parkinson disease. Approximately four hours after he had taken 0.8 mg of talipexole hydrochloride, he acutely developed sleepiness, delusion, akinesia, and faintness associated with hypotension and sinus bradycardia. Another similar episode occurred when he had taken talipexole hydrochloride 1.2 mg/day in combination with a daily dose of 200 mg of levodopa and 20 mg of carbidopa. These symptoms persisted for 12 hours and diminished gradually without any specific treatments. Talipexole hydrochloride, a stimulator of both the D2 and alpha 2 receptors probably induced bradycardia and hypotension in the present case.
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PMID:[Sinus bradycardia induced by talipexole hydrochloride in a patient with Parkinson disease]. 991 27

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, dosage and administration, and formulary considerations of ropinirole are reviewed. Ropinirole is a nonergoline dopamine agonist that binds to dopamine D2-receptors; the drug is indicated for use in the symptomatic treatment of early and late Parkinson's disease (PD). Ropinirole is rapidly absorbed after oral administration and undergoes extensive hepatic metabolism to active metabolites. The elimination half-life averages about six hours. Ropinirole has a low potential to interact with other drugs likely to be administered to PD patients. In patients with early PD, initial monotherapy with ropinirole was more effective than placebo or bromocriptine in the absence of selegiline and was as effective as bromocriptine in the presence of selegiline. Ropinirole was as effective as levodopa in patients with earlier stages of PD. In one subset of patients with advanced PD not adequately controlled by levodopa, adjunctive ropinirole was more effective than placebo and bromocriptine. Ropinirole was more effective than bromocriptine in patients previously given high-dose levodopa and was as effective in patients previously given low-dose levodopa or adjunctive dopamine agonist therapy. The most frequent adverse effects are nausea, somnolence, and dizziness; the dosage should be increased gradually to minimize adverse effects. Ropinirole is less expensive than bromocriptine and pergolide and similar in cost to pramipexole. Ropinirole appears to be a useful addition to existing therapeutic approaches to PD and is approved for both early and later stages of the disease.
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PMID:Ropinirole: a dopamine agonist for the treatment of Parkinson's disease. 1003 May 5

Twenty-one patients with Parkinson's disease and psychosis were included in an open-label 8-week trial of olanzapine. Eight subjects had dementia. Six subjects (29%) discontinued treatment prematurely because of drowsiness. Delusions and hallucinations improved significantly, and 80% were rated as much or very much improved. There was no worsening of parkinsonism or cognition.
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PMID:Olanzapine for psychosis in patients with Parkinson's disease with and without dementia. 1044 17

The objective of this study was to investigate the frequency of excessive daytime sleepiness (EDS) and the beneficial effect of sleep on motor performance in an unselected community-based sample of patients with Parkinson's disease (PD). Furthermore, we wanted to identify possible risk factors to these phenomena. Detailed information on somnolence and sleep during daytime, as well as sleep benefit (SB) on awakening, was collected through a questionnaire among 245 patients with PD. Daytime somnolence was graded in groups of no somnolence, mild daytime sleepiness, and EDS. In addition, the occurrence of somnolence in the patients with PD was compared with the occurrence among control groups of patients with diabetes mellitus and of healthy elderly subjects. The correlations between EDS and SB and various motor- and non-motor symptoms of PD were evaluated. Among the patients with PD, 15.5% experienced EDS, significantly more than in the patients with diabetes mellitus (4%) and the healthy control subjects (1%). The frequency of mild daytime sleepiness was similar (10%) in patients with PD and control subjects. The patients with EDS had significantly higher staging of PD, were more disabled, and showed a higher frequency of cognitive decline compared with the patients without somnolence. They also had been using levodopa for a longer time and had more hallucinations. The occurrence of nocturnal sleeping problems and the use of sleeping pills was similar in the two groups, as was the mean age at examination, duration of PD, and presence of fluctuations and dyskinesias. SB was found in 42.2% of the patients with PD. These patients had been using levodopa for significantly longer and had significantly more fluctuations and dyskinesias compared with the patients without SB. Our results suggest that mild daytime sleepiness may be a result of normal aging, whereas more severe EDS can be explained by the neuropathologic changes of PD. The data from this community-based study confirms the previously reported high frequencies of SB.
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PMID:Excessive daytime sleepiness and sleep benefit in Parkinson's disease: a community-based study. 1058 65

We describe multiple sleep latency test (MSLT) results in 27 adult patients with idiopathic Parkinson's disease (PD). Pathological sleepiness (i.e. mean sleep latency </=5 min) was common (40 of 134 nap opportunities), and sleep-onset REM periods were also observed (13 of 134 nap opportunities). These findings bore little relationship to disease specific variables (e.g. level of disability, medication use), or sleep architecture measures (e.g. total sleep time, sleep stage percentage's). Our findings speak against a simple association of excessive sleepiness and the quality and quantity of prior night's sleep, but rather, argue for primary impairments of waking arousal and REM-sleep expression in a sizeable subpopulation of PD patients.
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PMID:FAST TRACK: daytime sleepiness in Parkinson's disease. 1073 91

Hallucinations, mainly of a visual nature, are considered to affect about one-quarter of patients with Parkinson's disease. They are commonly viewed as a side-effect of antiparkinsonian treatment, but other factors may be involved. The aim of this study was to determine the phenomenology, prevalence and risk factors of hallucinations in Parkinson's disease. Two-hundred and sixteen consecutive patients fulfilling clinical criteria for Parkinson's disease were studied. Demographic and clinical variables were recorded, including motor and cognitive status, depressive symptoms and sleep-wake disturbances. Patients with and without hallucinations were compared using non-parametric tests, and logistic regression was applied to significant data. Hallucinations had been present during the previous 3 months in 39.8% of the patients, and fell into three categories: minor forms, consisting of a sensation of a presence (person), a sideways passage (commonly of an animal) or illusions were present in 25.5% of the patients (an isolated occurrence in 14.3%), formed visual hallucinations were present in 22.2% (isolated in 9.3%) and auditory hallucinations were present in 9.7% (isolated in 2.3%). Patients with minor hallucinations had a higher depression score than non-hallucinators but did not differ in other respects. Logistic regression analysis identified three factors independently predictive of formed visual hallucinations: severe cognitive disorders, daytime somnolence and a long duration of Parkinson's disease. These findings indicate that, when minor hallucinations are included, the total prevalence is much higher than previously reported. A simple side-effect of dopaminergic treatment is not sufficient to explain the occurrence of all visual hallucinations. The main risk factor in treated patients is cognitive impairment, although sleep-wake cycle disturbances, and possibly other factors related to the duration of the disease, act as cofactors.
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PMID:Hallucinations in Parkinson's disease: prevalence, phenomenology and risk factors. 1073 5

A review of stereotactic medial pallidotomy of the 1950s in five neurosurgical centers is presented. The surgical technique varied from one center to the other. The results of surgery, however, seemed to be quite equal, being positive in 70-90% of the patients. The surgical mortality ranged from 0 to 13%. Behavioral complications were adequately analyzed and reported from one center only and published by three independent neurologists. The side effects included drowsiness (12%), confusion (13.6%), mental deterioration (5%), memory deficit (13.6%), and dysphasia (7.5-24%, the rate depending on the concomitant brain atrophy). Among permanent side effects, 5% of the patients presented with a mild postoperative mental deterioration, whereas 13.6% had a severe memory deficit. In the four other centers, the results and side effects were analyzed only by the surgeons and were more biased. A comparison of the results and complications between Leksell's early medial pallidotomy of 1951-1957 and recent medial pallidotomies of the 1990s from two centers showed that 40 years ago Leksell had at least as good results as, and less serious complications than, two representative neurosurgeons of today. Even when positive clinical results of GPi pallidotomy have recently been reported from several centers, the patients seem to have improved relatively little, the dyskinesias excepted, and the rate of side effects has been quite high. The author is afraid that medial pallidotomy will soon be abandoned as a method of choice in the surgical treatment of Parkinson's disease, as in fact happened 40 years ago. One should look for better surgical alternatives and targets outside of the medial pallidum.
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PMID:Behavioral complications of early pallidotomy. 1075 82


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