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 have carried out a case-control survey of the prevalence of restless legs syndrome (RLS) in 118 Parkinson's disease out-patients with different stage of disease severity by using the International restless legs syndrome Study Group clinical criteria. This study failed to demonstrate a significantly augmented prevalence of either primary and secondary restless legs syndrome pooled together or primary restless legs syndrome alone among Parkinson's disease patients as compared to age and gender matched controls. The results of our survey do not confirm a significant co-morbid occurrence of the two disorders. However, an unavoidable limitation of this and all previous studies is that most of the patients examined were already treated with dopaminomimetic drugs, which could have abolished a mild unrecognized RLS anteceding the diagnosis of Parkinson's disease or possibly masked the subsequent emergence of the sensory-motor disorder following the onset of Parkinson's disease.
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PMID:Absence of co-morbidity of Parkinson disease and restless legs syndrome: a case-control study in patients attending a movement disorders clinic. 1927 34

A middle-aged architect, suffering from familial, idiopathic, levodopa-responsive restless legs syndrome (RLS) progressively abused levodopa for 10 years, to the point of taking 20 tablets/day (4000 mg/day) for 6 months. Such abuse (possibly linked to the rewarding effect of dopamine) has been recently monitored in the context of Parkinson's disease (PD) (the "dopamine dysregulation syndrome"). Physicians who now routinely treat RLS patients with dopaminergic agents should be aware of this abuse potential. This case also constitutes an experimental model. As levodopa abuse has only been described in patients with PD, it was suspected to be promoted by central dopamine depletion (with consequent sensitization of dopamine receptors). This idea should be revised because functional imaging showed that this RLS patient had no dopamine depletion. Later, he had no impulse disorders (no gambling, hypersexuality, excessive shopping), which occur with dopamine agonists, suggesting that levodopa abuse and impulse disorders can result through different mechanisms.
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PMID:Dopamine dysregulation syndrome in a patient with restless legs syndrome. 1941 Jan 83

Restless legs syndrome (RLS) is characterized by paraesthesias-dysesthesias and motor restlessness worsening at rest-in the evening, with at least temporary relief by activity. Its etiology is unknown, though it could be secondary to various conditions. It is well known, however, that dopamine plays a crucial role in the pathophysiology of RLS, as dopaminergic agonists achieve marked improvement. Pramipexole is a nonergoline compound with selectivity for D3 dopamine receptors. This drug is very effective in the treatment of idiopathic and secondary RLS and in treatment-resistant patients, as shown by double-blind, placebo-controlled studies in adults. In children, studies are much more limited, and RLS is often misdiagnosed as "growing pain" or attention deficit hyperactivity disorder. Pramipexole has been successful in open studies, eliminating clinical symptoms. This medication has the advantage of being free of the frequently encountered problems seen with ergot derivatives. The side-effects are limited, particularly at the dosages usually prescribed for RLS treatment: They are much lower than in Parkinson's disease, and inappropriate sleepiness and sleep attacks, particularly while driving, or compulsive behavior have not been seen. Compared with the adverse reactions of levodopa, including tolerance, rebound, and augmentation phenomena in RLS, which led to usage of dopamine agonists as first line of treatment for RLS, pramipexole has had one of the best profiles. Augmentation can still be noted with the drug, but after longer usage time compared with many other dopamine agonists. Although excessive daytime sleepiness has been noted, sleep attacks have not been encountered in RLS patients treated with pramipexole.
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PMID:Pramipexole: new use for an old drug - the potential use of pramipexole in the treatment of restless legs syndrome. 1941 89

Rotigotine (Neupro((R))) is a new non-ergolinic dopamine agonist transdermal patch that can be applied once daily. To date, it is approved for the treatment of early Parkinson's disease as monotherapy and has been shown to be effective in the treatment of advanced-stage Parkinson's disease and restless legs syndrome in several clinical trials. This review gives an overview of physical, chemical, and pharmaceutical characteristics, pharmacokinetics, biotransformation and elimination, drug interactions, and adverse events of rotigotine. Further, the rationale for the treatment of Parkinson's disease and restless legs syndrome with rotigotine is discussed.
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PMID:Rotigotine transdermal system: a short review. 1941 91

Restless legs syndrome (RLS) is a common movement disorder wherein sensory motor symptoms are observed in the limbs mainly during sleep and quiet wakefulness. The diagnostic criteria for RLS were established in 1995 by the International RLS Study Group (IRLSSG) and revised in 2003. The prevalence of RLS in Europe and North America was reported to be between 5% and 12%. On the other hand, the prevalence of RLS in Asia was lesser than that in Europe and North America: it was estimated to be less than 4%. This difference might be associated with vacial, cultural, and language differences. Genetic factors are known to contribute to the etiology of RLS in up to two-thirds of these patients. Furthermore, RLS might complicate an already existing medical condition. The development of secondary RLS is associated with renal failure, iron deficiency, frequent blood donation, Parkinson disease, neuropathy, as well as pregnancy. Generally, these medical condition are more frequently complicated in patient with RLS than in healthy controls. However, there is no conclusive evidence to prove an association between these medical conditions and RLS. Genetic contribution, environmental factors and other covariates such as gender, age, iron deficiency, as well as medical conditions play an important role in the development of RLS. In conclusion, epidemiological evidence suggests that both the primary and secondary forms of RLS are common neurological disorders. Future epidemiological studies are required to determine the potential risk factors contributing to the development of this disorder.
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PMID:[Prevalence of restless legs syndrome]. 1951 11

Restless legs syndrome (RLS) is a sensorimotor disorder, characterized by an irresistible urge to move the legs and usually accompanied or caused by uncomfortable and unpleasant sensations. It begins or worsens during periods of rest or inactivity, is partially or totally relieved by movement and is exacerbated or occurs mainly in the evening or night. People suffering from RLS are estimated to represent 2-3% of the general Japanese population, which is relatively lower than the estimated prevalence in western countries. Supportive diagnostic critevia include family history, the presence of periodic-leg movements (PLM) when awake or asleep, and a positive response to dopaminergic treatment. RLS phenotypes include an early onset form that is usually idiopathic with frequent familial history and a late onset form that is usually secondary to other somatic conditions that are causative factors in RLS occurrence. In all patients presenting with complaints of insomnia or discomfort in the lower limbs, diagnosis of RLS should be considered. RLS should be differentiated from akathisia, which is an urge to move the whole body in the absence of uncomfortable sensations. Polysomnographic studies and the suggested immobilization test (SIT) can detect PLM in patients that are asleep or awake. RLS may cause severe sleep disturbances, poor quality of life, depressive and anxious symptoms, and may be a risk factor for cardiovascular disease. Secondary RLS may occur due to iron deficiency, end-stage renal disease, pregnancy, peripheral neuropathy and drug use including antipsychotics and antidepressants. Small fiber neuropathy can trigger RLS or mimic its symptoms. RLS is associated with many neurological disorders, including Parkinson disease and multiple system atrophy; althoughit does not predispose to these diseases. A symptom rating scale for RLS authorized by the International RLS Study Group (IRLS) would facilitate accurate diagnosis of this condition.
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PMID:[Diagnosis and symptom rating scale of restless legs syndrome]. 1951 13

(1) Pathological gambling and increased sexual activity can occur in patients taking dopaminergic drugs. Detailed case reports and small case series mention serious familial and social consequences. The frequency is poorly documented; (2) Most affected patients are being treated for Parkinson's disease, but cases have been reported among patients prescribed a dopamine agonist for restless legs syndrome or pituitary adenoma; (3) Patients treated with this type of drug, and their relatives, should be informed of these risks so that they can watch for changes in behaviour. If such disorders occur, it may be necessary to reduce the dose or to withdraw the drug or replace it with another medication.
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PMID:Dopamine agonist: pathological gambling and hypersexuality. 1953 37

Treatment with dopamine receptor agonists has been associated with impulse control disorders and pathological gambling (PG) secondary to medication in previously unaffected patients with Parkinson's disease or restless legs syndrome (RLS). In a within-subjects design, we investigated the underlying neurobiology in RLS patients using functional magnetic resonance imaging. We scanned 12 female RLS patients without a history of PG. All patients were scanned twice: once whilst taking their regular medication with low dose dopamine receptor agonists and once after a washout phase interval. They performed an established gambling game task involving expectation and receipt or omission of monetary rewards at different levels of probabilities. Upon expectation of rewards, reliable ventral striatal activation was detected only when patients were on, but not when patients were off medication. Upon receipt or omission of rewards, the observed ventral striatal signal under medication differed markedly from its predicted pattern which by contrast was apparent when patients were off medication. Orbitofrontal activation was not affected by medication. Chronic dopamine receptor agonist medication changed the neural signalling of reward expectation predisposing the dopaminergic reward system to mediate an increased appetitive drive. Even without manifest PG, chronic medication with dopamine receptor agonists led to markedly changed neural processing of negative consequences probably mediating dysfunctional learning of contingencies. Intact orbitofrontal functioning, potentially moderating impulse control, may explain why none of the patients actually developed PG. Our results support the notion of a general medication effect in patients under dopamine receptor agonists in terms of a sensitization towards impulse control disorders.
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PMID:At-risk for pathological gambling: imaging neural reward processing under chronic dopamine agonists. 1956

The dopamine agonist rotigotine was developed for the treatment of Parkinson's disease and restless legs syndrome. Disposition, metabolism, elimination, and absolute bioavailability of rotigotine were determined in six healthy male subjects by using two different forms of administration in a randomized sequence with a crossover design. Treatment A (continuous infusion) consisted of a single radiolabeled 12-h intravenous infusion of 1.2 mg of rotigotine (0.6 mg of [(14)C] and 0.6 mg of unlabeled rotigotine, 3.7 MBq) solution. Treatment B (transdermal application) consisted of a single 10-cm(2) patch containing 4.5 mg of unlabeled rotigotine with a patch-on period of 24 h. During the 12 h-infusion, total radioactivity concentration rapidly increased within 2 h; there was a slight additional increase toward the end of infusion. Plasma concentrations of total radioactivity declined by 75% within 12 h after completion of infusion. More than 94% of the radioactivity was excreted 216 h after the start of infusion, 71% by the kidneys and 23% by feces. Renal elimination of the parent compound was <1%. Systemically absorbed rotigotine was rapidly metabolized. The major rotigotine biotransformation pathway was conjugation of the parent compound, mainly by sulfation; a second pathway was the formation of phase 1 metabolites (N-desalkylation) with subsequent conjugation. Plasma concentration-time profiles of unchanged rotigotine during and after infusion and during and after patch administration were comparable. Absolute bioavailability of transdermally applied rotigotine was 37%.
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PMID:Absorption, disposition, metabolic fate, and elimination of the dopamine agonist rotigotine in man: administration by intravenous infusion or transdermal delivery. 1960 95

Parkin gene mutations cause a juvenile parkinsonism. Patients with these mutations may commonly exhibit REM sleep behaviour disorders, but other sleep problems (insomnia, sleepiness, restless legs syndrome) have not been studied. The aim of this study was to evaluate the sleep-wake phenotype in patients with two parkin mutations, compared with patients with idiopathic Parkinson's disease (iPD). Sleep interview and overnight video-polysomnography, followed by multiple sleep latency tests, were assessed in 11 consecutive patients with two parkin mutations (aged 35-60 years, from seven families) and 11 sex-matched patients with iPD (aged 51-65 years). Sleep complaints in the parkin group included insomnia (73% patients versus 45% in the iPD group), restless legs syndrome (45%, versus none in the iPD group, P = 0.04), and daytime sleepiness (45%, versus 54% in the iPD group). Of the parkin patients, 45% had REM sleep without atonia, but only 9% had a definite REM sleep behavior disorder. All sleep measures were similar in the parkin and iPD groups. Two parkin siblings had a central hypersomnia, characterized by mean daytime sleep latencies of 3 min, no sleep onset REM periods, and normal nighttime sleep. Although the patients with two parkin mutations were young, their sleep phenotype paralleled the clinical and polygraphic sleep recording abnormalities reported in iPD, except that restless legs syndrome was more prevalent and secondary narcolepsy was absent.
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PMID:Restless legs syndrome, rapid eye movement sleep behavior disorder, and hypersomnia in patients with two parkin mutations. 1967 85


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