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)

Sleep disorders are common in patients with Parkinson's disease (PD), and preliminary work has suggested viable treatment options for many of these disorders. For rapid eye movement sleep behavior disorder, melatonin and clonazepam are most commonly used, while rivastigmine might be a useful option in patients whose behaviors are refractory to the former. Optimal treatments for insomnia in PD have yet to be determined, but preliminary evidence suggests that cognitive-behavioral therapy, light therapy, eszopiclone, donepezil, and melatonin might be beneficial. Use of the wake-promoting agent modafinil results in significant improvement in subjective measures of excessive daytime sleepiness, but not of fatigue. Optimal treatment of restless legs syndrome and obstructive sleep apnea in PD are not yet established, although a trial of continuous positive airway pressure for sleep apnea was recently completed in PD patients. In those patients with early morning motor dysfunction and disrupted sleep, the rotigotine patch provides significant benefit.
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PMID:Treatment of the sleep disorders associated with Parkinson's disease. 2427 58

Sleep quality and architecture as well as sleep's homeostatic and circadian controls change with healthy aging. Changes include reductions in slow-wave sleep's (SWS) percent and spectral power in the sleep electroencephalogram (EEG), number and amplitude of sleep spindles, rapid eye movement (REM) density and the amplitude of circadian rhythms, as well as a phase advance (moved earlier in time) of the brain's circadian clock. With mild cognitive impairment (MCI) there are further reductions of sleep quality, SWS, spindles, and percent REM, all of which further diminish, along with a profound disruption of circadian rhythmicity, with the conversion to Alzheimer's disease (AD). Sleep disorders may represent risk factors for dementias (e.g., REM Behavior Disorder presages Parkinson's disease) and sleep disorders are themselves extremely prevalent in neurodegenerative diseases. Working memory , formation of new episodic memories, and processing speed all decline with healthy aging whereas semantic, recognition, and emotional declarative memory are spared. In MCI, episodic and working memory further decline along with declines in semantic memory. In young adults, sleep-dependent memory consolidation (SDC) is widely observed for both declarative and procedural memory tasks. However, with healthy aging, although SDC for declarative memory is preserved, certain procedural tasks, such as motor-sequence learning, do not show SDC. In younger adults, fragmentation of sleep can reduce SDC, and a normative increase in sleep fragmentation may account for reduced SDC with healthy aging. Whereas sleep disorders such as insomnia, obstructive sleep apnea, and narcolepsy can impair SDC in the absence of neurodegenerative changes, the incidence of sleep disorders increases both with normal aging and, further, with neurodegenerative disease. Specific features of sleep architecture, such as sleep spindles and SWS are strongly linked to SDC. Diminution of these features with healthy aging and their further decline with MCI may account for concomitant declines in SDC. Notably these same sleep features further markedly decline, in concert with declining cognitive function, with the progression to AD. Therefore, progressive changes in sleep quality, architecture, and neural regulation may constitute a contributing factor to cognitive decline that is seen both with healthy aging and, to a much greater extent, with neurodegenerative disease.
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PMID:Sleep-dependent memory consolidation in healthy aging and mild cognitive impairment. 2465 8

Some sleep disorders and sleep problems are reported as risk of dementia. It is reported that 50-80% of idiopathic REM sleep behavior had a later conversion to a synucleinopathy, thus this parasomnia is regarded as early marker of Parkinson disease, dementia with Lewy bodies and multiple system atrophy. Obstructive sleep apnea syndrome causes reversible decline of cognitive functions in children and adults, and it increases the risk of dementia and mild cognitive impairment in elderly women. A decrease of amplitude of circadian activity rhythm and habitual long sleep duration (> or = 9 hours) are reported to increase the risk of dementia in elderly people. Some reports indicate that hypnotic use may be a risk factor of dementia. However, it is not cleared whether insomnia itself related with dementia or not, since no study evaluated the risk of insomnia without hypnotic treatment.
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PMID:[Sleep disorders]. 2479 8

Sleep disorders could be associated with neurodegenerative diseases. This study aimed to determine the risk of Parkinson's disease in patients with obstructive sleep apnea. The incident cases of newly diagnosed obstructive sleep apnea were identified between 2000 and 2009 from the medical claims database of National Health Institute of Taiwan. The risk of Parkinson's disease onset at least 1 year after the diagnosis of obstructive sleep apnea was measured during and up to 11 years of period, compared to that of age- and gender-matched controls estimated in the same period. A total of 5864 patients with newly diagnosed obstructive sleep apnea and 23,269 subjects without obstructive sleep apnea were identified for data analysis. The study reported that the incidence of Parkinson's disease in the obstructive sleep apnea cohort was approximately two times higher than that in the control cohort (2.57 versus 1.32 per 1000 person-years), with an adjusted hazard ratio of 1.84. Furthermore, the risk of Parkinson's disease was particularly greater for the obstructive sleep apnea with insomnia subgroup (adjusted hazard ratio = 1.97, 95% confidence interval = 1.44-2.69) than for the control cohort. The sex-age-specific analysis further discovered that the most elevated risk of Parkinson's disease onset was noted in female obstructive sleep apnea patients aged 50-69 years (adjusted hazard ratio = 2.82). This population-based study indicated that patients with obstructive sleep apnea, especially those who suffered from insomnia, are at an increased risk of Parkinson's disease onset.
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PMID:Obstructive sleep apnea and risk of Parkinson's disease: a population-based cohort study. 2581 19

Excessive daytime sleepiness (EDS) can cause negative behavioral, physiologic, and cognitive effects, which limit patients' function and quality of life. Clinicians can screen for EDS using patient-report scales like the Epworth Sleepiness Scale or objective tests, such as the Multiple Sleep Latency Test. EDS and fatigue are common symptoms in many sleep disorders (eg, narcolepsy, obstructive sleep apnea), medical and neurologic conditions (eg, Parkinson's disease), and psychiatric disorders (eg, depression, substance abuse). Recognizing and managing comorbid conditions along with EDS can improve patients' quality of life.
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PMID:Effects of excessive daytime sleepiness and fatigue on overall health and cognitive function. 2645 83

Psychiatric, neurologic, and medical conditions frequently coexist with sleep disorders and contribute to poor treatment outcomes when unrecognized and untreated. For patients who present with excessive daytime sleepiness (EDS) or fatigue, clinicians should screen for sleep disorders (eg, obstructive sleep apnea, narcolepsy), medical and neurologic conditions (eg, cancer, Parkinson's disease), and psychiatric disorders (eg, depression, substance abuse) to determine if they are the cause or a contributing factor to sleep symptoms. Once recognized, comorbid conditions may be targeted along with EDS or fatigue using behavioral and pharmacologic treatment strategies.
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PMID:The effect of comorbid psychiatric and medical illnesses on sleep disorder treatment. 2645 84

Sleep disturbance is a common nonmotor phenomenon in Parkinson's disease (PD) affecting patient's quality of life. In this study, we examined the association between clinical characteristics with sleep disorders and sleep architecture patterns in a PD cohort. Patients underwent a standardized polysomnography study (PSG) in their "on medication" state. We observed that male gender and disease duration were independently associated with obstructive sleep apnea (OSA). Only lower levodopa equivalent dose (LED) was associated with periodic limb movement disorders (PLMD). REM sleep behavior disorder (RBD) was more common among older patients, with higher MDS-UPDRS III scores, and LED. None of the investigated variables were associated with the awakenings/arousals (A/A). Sleep efficiency was predicted by amantadine usage and age, while sleep stage 1 was predicted by dopamine agonists and Hoehn & Yahr severity. The use of MAO-B inhibitors and MDS-UPDRS part III were predictors of sleep stages 2 and 3. Age was the only predictor of REM sleep stage and gender for total sleep time. We conclude that sleep disorders and architecture are poorly predictable by clinical PD characteristics and other disease related factors must also be contributing to these sleep disturbances.
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PMID:A Polysomnographic Study of Parkinson's Disease Sleep Architecture. 2650 12

Parkinson's disease (PD) is a relentlessly progressive neurodegenerative disorder associated with hallmark motor and nonmotor symptoms (NMS) such as sleep disturbances and cognitive dysfunction. While dopaminergic treatments have improved the motor aspects of PD, progression remains inevitable. Research has recently increasingly focused on strategies to modify disease progression and on nonmotor manifestations of PD, given their impact on patients' quality of life. Obstructive sleep apnea (OSA) is a treatable sleep disorder, common in the general population, associated with excessive daytime sleepiness and neurocognitive deficits. Neuroimaging has demonstrated structural and functional changes in OSA patients; in animal models, OSA causes brain inflammation and oxidative injury, including in key areas involved in PD pathophysiology such as locus coeruleus. The prevalence of OSA in PD has been variable in studies to date, and potential consequences and interrelationship between the two disorders have not been well studied. There is however emerging evidence that OSA is associated with increased NMS in PD, particularly cognitive dysfunction. This review focuses on the possible interrelationship between OSA and PD. Mechanisms promoting OSA in PD will be reviewed, as well as mechanisms whereby OSA can affect the neurodegenerative process in PD.
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PMID:The Interaction between Obstructive Sleep Apnea and Parkinson's Disease: Possible Mechanisms and Implications for Cognitive Function. 2650 97

Excessive daytime sleepiness (EDS) is a common and bothersome phenomenon. It can be associated with insufficient sleep syndrome, narcolepsy, idiopathic hypersomnia, obstructive sleep apnea, shift work disorder, Kleine-Levin syndrome, or Parkinson's disease. Once the underlying cause of the excessive sleepiness is determined, clinicians must select the most appropriate behavioral and pharmacologic interventions to reduce daytime sleepiness, alleviate other symptoms, improve functioning, and ensure the safety of patients and those around them. Patient history, adverse effects, and efficacy in specific conditions should be considered in pharmacologic treatment options for patients with EDS.
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PMID:Recommended treatment strategies for patients with excessive daytime sleepiness. 2652 60

Purpose. Obstructive sleep apnea (OSA) is frequent in Parkinson's disease (PD) and may contribute to nonmotor symptoms. Polysomnography (PSG) is the gold standard for OSA diagnosis. Unattended portable monitoring (PM) may improve access to diagnosis but has not been studied in PD. We assessed feasibility and diagnostic accuracy in PD. Methods. Selected PD patients without known OSA underwent home PM and laboratory PSG. The quality of PM signals (n = 28) was compared with matched controls. PM accuracy was calculated compared with PSG for standard apnea hypopnea index (AHI) thresholds. Results. Technical failure rate was 27.0% and airflow signal quality was lower than in controls. Sensitivity of PM was 84.0%, 36.4%, and 50.0% for AHI cut-offs of 5/h, 15/h, and 30/h, respectively, using the same cut-offs on PM. Specificity was 66.7%, 83.3%, and 100%, respectively. PM underestimated the AHI with a mean bias of 12.4/h. Discrepancy between PM and PSG was greater in those with more motor dysfunction. Conclusion. PM was adequate to "rule in" moderate or severe OSA in PD patients, but the failure rate was relatively high and signal quality poorer than in controls. PM overall underestimated the severity of OSA in PD patients, especially those with greater motor dysfunction.
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PMID:Diagnosis of Obstructive Sleep Apnea in Parkinson's Disease Patients: Is Unattended Portable Monitoring a Suitable Tool? 2655 May 19


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