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)

Parkinson's disease (PD) is associated with sleep disorders which are attributed mainly to dopamine deficiency, nocturnal akinesia, drug therapy, and cofactors such as age and depression. These disturbances affect the macro- and microstructure of both REM and non-REM sleep and motor, respiratory, and autonomic functions. Excessive daytime sleepiness and the interactions between sleep and daytime motor performance in PD are not yet completely understood. Correct diagnosis and treatment of sleep disorders is essential due to the risk of harm to the patient and others and due to their effect on quality of life for all concerned. As sleep disorders in PD are extremely common (about 70%) and may have severe consequences, a systematic sleep history and specific therapy should be considered integral to treatment in every PD patient.
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PMID:[Pathophysiology, clinical aspects and therapy of sleep disorders in Parkinson disease]. 1143

Somatic and psychiatric illnesses are commonly associated. Cardiovascular disorders, Parkinson's disease and stroke are especially often associated with depression as also anxiety and sleep disturbances. Psychophytopharmaceuticals, which are usually well tolerated, are highly suitable for this purpose. To treat mild to moderate episodes of depression, extracts of St. John's Wort are employed, but recently reported interactions with coumarin, theophylline and also estrogen preparations, need to be considered. Unspecific anxiety states can be treated with extracts of kava. At present, no herbal preparation can be recommended for the treatment of sleep disorders, as no unequivocal proof of efficacy in patients with such problems has yet been established.
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PMID:[Psychiatric comorbidity in somatic disorders. Psychophytopharmaceuticals are worth a try]. 1143 62

Patients with Parkinson's disease can experience a number of sleep disorders, including insomnia, parasomnias and daytime somnolence [specifically, excessive daytime sleepiness (EDS) and sleep attacks]. Insomnia is a frequent and important complaint of patients with the disease. Both the pathology of Parkinson's disease and dopaminergic drugs may contribute to the much higher than expected frequency of sleep fragmentation and disrupted sleep among these patients. In addition, coexisting depression seems to be a major and frequent risk factor for insomnia in Parkinson's disease. After recognising a sleep problem, the first step in management is to examine and diagnose the type of insomnia and possible medical or psychological factors that may disturb nocturnal sleep. The next step is to give the patient appropriate advice on sleep hygiene. Increasing the dosage of dopaminergic drug treatment will often increase sleep disruption and should be avoided unless the patient's sleep is primarily disturbed by the motor manifestations of parkinsonism during the night. Depression should be looked for and if appropriate be treated in any patients with insomnia. If it becomes necessary to treat the patient with an hypnosedative agent, it is important to use a drug with a short half-life and that manifests as few adverse effects as possible the next morning. Up-to-date guidelines for the use of hypnosedatives should be followed. Patients with Parkinson's disease experience a wide range of parasomnias. The majority of behaviours may be related to rapid eye movement (REM) sleep behaviour disorder (RBD) or to a spectrum of symptoms ranging from vivid dreaming to psychosis. RBD is effectively treated with clonazepam. In addition, the atypical antipsychotics have given physicians new and better treatment options for psychotic symptoms in individuals with Parkinson's disease. EDS is common in Parkinson's disease, while sleep attacks seem to be rare manifestations of the disease or its treatment. Significant EDS is found in 15% of patients with Parkinson's disease compared with in 1% of healthy elderly people. Sleep attacks are observed in patients treated with all dopaminergic medications but have recently been brought to prominence because of their association with the newer dopamine agonists ropinirole and pramipexole. Patients with Parkinson's disease should be informed about the possibility of developing sleep problems during the day when prescribed new drugs. Appropriate actions with regard to driving must be taken if significant and persistent daytime somnolence or sleep attacks appear.
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PMID:Sleep disorders in patients with Parkinson's disease: epidemiology and management. 1146 32

The aim of our study was to assess the prevalence of the specific disorders of the circadian rhythm of cortisol and melatonin in the patients with sleep disorders. The group of our patients consisted of 93 persons (25 men, 68 women), from 4-72 years (mean age 38.3 years) with a sleep disorders. These patients were studied on Department of Neurology of 1st Medical Faculty of Charles University in Prague during years 1997-1999. Patients were divided by the clinical diagnosis into many subgroups: idiopathic hypersomnia (IH) 24 patients and other hypersomnias 8, narcolepsy 22, degenerative disorders 9, delay sleep phase syndrome (DSPS) 7, periodic leg movements syndrome (PLMS) 6, insomnia 7 and Parkinson's disease 10 patients. Twelve salivary samples were taken from each patient during a period of 24 hours in order to investigate the circadian secretion pattern of melatonin and cortisol. Salivary melatonin and cortisol levels were estimated by radioimmunoassay in the Department of Physiology of the Academy of Science, Czech Republic. Significant differences were found between our patients and the control group in idiopathic hypersomnia--acrophase of melatonin was delayed and secretion was prolonged. Patients suffered from narcolepsy often displayed multiple peak of melatonin secretion. The peak of the melatonin concentration occurred later in DSPS (non significantly). Low level of melatonin and prolonged signal of melatonin was in Parkinson's disease patients.
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PMID:[Sleep disorders and the 24-hour profile of melatonin and cortisol]. 1170 73

Non-motor symptoms may considerably reduce parkinsonian quality of life, particularly in advanced stages of the disease. Autonomic features, such as seborrhoea, hyperhidrosis, orthostatic hypotension, excessive salivation, bladder dysfunction and GI disturbances, and neuropsychiatric symptoms, such as depression, sleep disorders, psychosis and dementia, appear in the course of Parkinson's disease. Pharmacotherapy of these non-motor symptoms complicates long-term antiparkinsonian combination drug therapy due to possible drug interactions, side effects and changes in metabolism. Moreover, antiparkinsonian compounds themselves contribute to the onset of these non-motor symptoms to a considerable extent. This complicates differentiation between the disease process itself and drug-related effects, thus influencing therapeutic options, which are often limited because of comorbidity and polypharmacy. Therefore, standardised recommendations are questionable, since drug tolerability and response differ between patients. Nevertheless, this review tries to provide a survey of possible therapeutic options for the treatment of the symptoms of Parkinson's disease other the dopamine-sensitive motor features.
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PMID:Drug treatment of non-motor symptoms in Parkinson's disease. 1193 40

During the past 10 years, there has been an increasing interest in the study of rapid-eye-movement (REM) sleep in neurodegenerative diseases and more particulary in Parkinson's disease (PD). This interest is justified by the strong association observed between these diseases and REM sleep behavior disorder (RBD). In the first section of this paper, a critical review of the literature on the presence of REM sleep disorders in PD is presented. Studies that show an association between PD and RBD are reviewed. Studies that report the presence of other REM sleep disorders in PD (short latency, abnormal length and/or proportion of REM sleep, increasing occurrence of hallucinations) are then discussed. Limitations of the criteria proposed by Rechtschaffen et Kales (1968) for the quantification of REM sleep are also presented. Some authors believe that dopaminergic (DA) agents used in the treatment of PD (levodopa, bromocriptine, pergolide, pramipexole and selegiline) could be a responsable factor for the occurence of REM sleep disorders observed in this disease. The literature concerning the impact of these DA agents on human REM sleep is therefore critically reviewed. It is concluded that DA agents cannot explain on their own the presence of REM sleep disorders in PD. Other causes, among which the disturbance of some neurochemical systems linked to the neuropathological process of the disease, must be considered in order to explain these REM sleep disorders. In the second section of this paper, we present the different pathophysiological hypotheses proposed to explain REM sleep disorders in PD, such as a dysfunction of the cholinergic, noradrenergic, serotonergic, dopaminergic or GABAergic neurons. Emphasis is placed on the role of cholinergic neurons of the pedunculopontine and laterodorsal tegmental nuclei, structures shown to be particularly impaired in PD. Neurophysiological, neuroanatomical and neuropharmacological studies demonstrate that these neurons are strongly implicated in the different REM sleep parameters (muscular atonia, electroencephalographic desynchronisation, ponto-geniculo-occipital spikes). Finally, future research directions are proposed.
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PMID:[Rapid-eye-movement sleep disorders in Parkinson's disease]. 1196 70

Controversial reports of sudden onset 'sleep attacks' resulting in road traffic accidents have recently been reported in patients with Parkinson's disease (PD) taking the non-ergot dopamine D(2 )/D(3) receptor agonists pramipexole and ropinirole. These reports have generated considerable debate as the concept of 'sleep attacks' is disputed amongst sleep specialists and most believe that isolated 'sleep attacks' not preceded by warning on the background of chronic sleepiness or 'unintended sleepiness' do not exist. A series of case reports suggested that this phenomenon may not be exclusive to the non-ergot dopamine agonists such as pramipexole or ropinirole and indeed may occur with most dopaminergic agents. Recent evidence suggest that a 'sleepiness' or 'hypoactivity' reaction to dopaminergic therapy may be related to underlying dopamine deficiency of PD rather than a drug effect. In this report we provide the evidence for the phenomenon being a class effect attributable to all dopamine agonists currently employed in the management of PD. Controversy surrounding excessive daytime sleepiness (EDS) in PD and the use of the Epworth Sleepiness Scale (ESS) in relation to PD is also discussed. In spite of variable reports, EDS is recognised to be common in PD and is likely to be related to both the disease process and drug therapy. Studies using multiple sleep latency tests have also reported differing results in PD although a recent study indicated that a subset of 'sleepy' patients with PD may experience pathological somnolence with resultant detrimental consequence on daytime and cognitive functions. We recommend that the issue of 'sleepiness' or 'sleep attacks' in PD should be routinely checked in all patients with PD and indirectly assessed by using either the ESS or the recently introduced Parkinson's Disease Sleep Scale. Those with reported 'sleep attacks' or 'unintended sleep episodes' and excessive daytime sleepiness while taking dopamine agonists or dopaminergic agents such as levodopa should have a review of their medication, should not be driving a car on their own and some may merit formal sleep architecture studies. The latter may identify sleep disorders such as secondary narcolepsy which may benefit from the use of a wakefulness promoting agent.
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PMID:'Sleep attacks' or 'unintended sleep episodes' occur with dopamine agonists: is this a class effect? 1209 5

Sleep problems are an under-emphasised cause of disability in Parkinson's disease (PD) and may be seen independently of PD, associated with primary PD pathology, or as a result of antiparkinsonian medications. Common sleep disorders include excessive daytime sleepiness, rapid eye movement (REM) sleep behaviour disorder, night-time wakefulness and restless legs syndrome. A number of strategies may be used to improve sleep cycle disturbances, and often these interventions do not require pharmacological manipulation. Restoring traditional mealtimes and scheduling activities during predicted periods of sleepiness may help alleviate daytime somnolence; the use of controlled-release levodopa preparations or administration of a catechol-O-methyl transferase (COMT) inhibitor with levodopa at bedtime may reduce periods of night-time wakefulness. Administration of clonazepam at bedtime may assist with REM sleep behaviour disorder but, because this agent can result in daytime somnolence, experimentation with dosage times is recommended. Sleep attacks are described as a sudden, unavoidable transition from wakefulness to sleep and, although rare, have been described with pramipexole, ropinirole and other dopamine agonists. Although the condition has yet to be recognised by the International Association of Sleep Disorders, patients with PD who report rapid sleep onset should be evaluated for the possibility of sleep attacks. If sleep attacks are suspected, it is reasonable to strongly caution patients regarding potentially risk-associated activities such as driving, and to consider careful withdrawal of dopaminergic therapy.
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PMID:Sleep disorders in Parkinson's disease: epidemiology and management. 1239 50

The objective was to compare the prevalence and severity of fatigue in patients with Parkinson's disease (PD) with that in two control groups, one consisting of randomly chosen control subjects of the same age and sex distribution and the other consisting of patients with coxarthrosis waiting to receive total hip replacement. We also explored the possible correlation of demographic and clinical data to the presence and severity of fatigue. Sixty-six patients with PD, 131 randomly chosen controls and 79 patients with coxarthrosis, waiting to receive total hip replacement, were evaluated for fatigue. Patients and controls with a depressive mood disorder or cognitive impairment had been excluded from the study. Fatigue was measured by the Fatigue Severity Scale (FSS). For the patients with PD the mean total FSS score was 4.1, compared with 2.7 amongst the randomly chosen control group and 2.9 in the group consisting of patients with coxarthrosis. Fifty per cent of the patients with PD had a mean total FSS score of 4 or higher, compared with 25% in both of the two control groups. There was no correlation between pain, presence of self-reported nocturnal sleep disorders or duration of PD and fatigue. The patients with fatigue did have a more advanced disease, measured both by Unified Parkinson's Disease Rating Scale score and Hoehn and Yahr stage. Although the univariate analyses indicated that more severe parkinsonism was correlated to the symptom, the multivariate analysis showed that none of the studied variables were significant explanatory factors for fatigue. Fatigue is a common symptom in patients with PD without depression or dementia. The study indicates that fatigue is an independent symptom of the disease without relation to other motor or non-motor symptoms.
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PMID:Measuring fatigue in patients with Parkinson's disease - the Fatigue Severity Scale. 1245 74

The present article is meant to suggest an approach to the guidelines for the therapy of sleep disturbances in Parkinson's Disease (PD) patients.The factors affecting the quality of life in PD patients are depression, sleep disturbances and dependence. A large review of the literature on sleep disturbances in PD patients, provided the basis for the following classification of the sleep-arousal disturbances in PD patients. We suggest a model based on 3 steps in the treatment of sleep disturbances in PD patients. This model allowing the patient, the spouse or the caregiver a quiet sleep at night, may postpone the retirement and the institutionalization of the PD patient. I. Correct diagnosis of sleep disorders based on detailed anamnesis of the patient and of the spouse or of the caregiver. One week recording on a symptom diary (log) by the patient or the caregiver. Correct diagnosis of sleep disorders co morbidities. Selection of the most appropriate sleep test among: polysomnography (PSG), multiple sleep latency test (MSLT), multiple wake latency test (MWLT), Epworth Sleepiness Scale, actigraphy or video-PSG. II. The nonspecific therapeutic approach consists in: a) Checking the sleep effect on motor performance, is it beneficial, worse or neutral. b) Psycho-physical assistance. c) Dopaminergic adjustment is necessary owing to the progression of the nigrostriatal degeneration and the increased sensitivity of the terminals, which alter the normal modulator mechanisms of the motor centers in PD patients. Among the many neurotransmitters of the nigro-striatal pathway one can distinguish two with a major influence on REM and NonREM sleep. REM sleep corresponds to an increased cholinergic receptor activity and a decreased dopaminergic activity. This is the reason why REM sleep deprivation by suppressing cholinergic receptor activity ameliorates PD motor symptoms. L-Dopa and its agonists by suppressing cholinergic receptors suppress REM sleep. The permanent adjustment according to the progression of the degenerative process of the disease will diminishe aggravation. The following types of sleep-arousal disturbances have to be considered in PD patients: - Sleep Disturbances, Light Fragmented Sleep (LFS), Abnormal Motor Activity During Sleep (AMADS), REM Behavior Disorders (RBD), Sleep Related Breathing Disorders (SRBD), Sleep Related Hallucinations (SRH), Sleep Related Psychotic Behavior (SRPB). - Arousal Disturbances, Sleep Attacks (SA), Excessive Daytime Sleepiness (EDS), Each syndrome has to receive a score according to its severity. III. The specific therapy consists in: LFS: Benzodiazepines & Nondiazepines. AMADS: Clonazepam, Opioid, Apomorphine infusion; RBD: Clonazepam and dopaminergic agonists; SRBD: CPAP, UPPP, nasal interventions, losing weight; SRH: Clozapine, Risperidone; SRPD: Nortriptyline, Clozapine, Olanzepine; SA-adjustment; EDS-arousing drugs. Each therapeutic approach must be tailored to the individual PD patient.
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PMID:Sleep disturbances in Parkinsonism. 1258 74


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