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Sleep dysfunction and its management in Parkinson's disease.

ABSTRACT: OPINION STATEMENT:Sleep disorders are among the most common non-motor symptoms in Parkinson's Disease (PD). In some cases, symptoms can precede a diagnosis of PD by many years, but otherwise they are commonly encountered during the clinical care of patients. Unfortunately, sleep problems are under-recognized and subsequently inadequately addressed. In our experience, when properly addressed, physicians and patients are quickly aware of the often-debilitating nature of sleep dysfunction. This does not mean that solutions are easily attainable. Sleep in PD is held in a delicate balance, influenced by the disease process, medications, co-morbid symptoms, and a variety of other factors. For this reason, management of sleep in PD often requires an inter-disciplinary approach. Physicians should have an intimate knowledge of the many sleep problems apparent in PD, as well as appreciate the challenge presented by diverse therapeutic options that can both ameliorate and aggravate symptoms.

SUBMITTER: Kutscher SJ

PROVIDER: S-EPMC4143423 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature

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Sleep dysfunction and its management in Parkinson's disease.

Kutscher Scott J SJ Farshidpanah Siavash S Claassen Daniel O DO

Current treatment options in neurology 20140801 8

<h4>Opinion statement</h4>Sleep disorders are among the most common non-motor symptoms in Parkinson's Disease (PD). In some cases, symptoms can precede a diagnosis of PD by many years, but otherwise they are commonly encountered during the clinical care of patients. Unfortunately, sleep problems are under-recognized and subsequently inadequately addressed. In our experience, when properly addressed, physicians and patients are quickly aware of the often-debilitating nature of sleep dysfunction. ...[more]

PMID: 24930678

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Project description:Purpose: Parkinson's disease (PD) patients frequently present with sleep disorders. This study was designed to assess the impact of nonmotor symptoms (NMSs) on sleep quality in early-stage PD patients with and without cognitive dysfunction. Materials and Methods: A sample of 389 early-stage PD patients (modified Hoehn and Yahr score ≤ 2.5, duration ≤ 5 years) was recruited for the present study. The Non-Motor Symptoms Questionnaire (NMS-Quest) was used to screen for global NMSs. Depressive symptoms were assessed using the Hamilton Rating Scale for Depression (HAMD). PD motor symptoms were measured with the Unified PD Rating Scale (UPDRS), part III. The Montreal Cognitive Assessment (MoCA) was used to evaluate global cognitive status, and the PD Sleep Scale (PDSS) was used to quantify sleep quality. Polysomnography (PSG) was used for objective assessment of sleep. Results: In our sample, approximately one-quarter of the PD patients suffered from sleep disturbances (23.7%). Our results also confirmed the high prevalence of cognitive dysfunction in patients with PD (39.8%). In patients with cognitive dysfunction, higher percentage of sleep disorders (34.8 vs. 16.2%, P < 0.01) was observed. They also with lower PDSS score, sleep efficiency (SE) and longer sleep lantency (SL) and wake after sleep onset (WASO) (All P < 0.05). In total, the patients who suffered from NMSs, such as depressive symptoms, anxiety symptoms, urinary tract symptoms and hallucinations/delusions, had poorer sleep quality. Better cognition may predict better sleep quality. In patients with cognitive dysfunction, the NMS-Hallucinations/delusions score was the most important risk factor for sleep disorders. In patients without cognitive dysfunction, NMSs such as anxiety and cognition and medication were related to sleep disorder. Conclusions: NMSs in early-stage PD are highly associated with and are determinants of subjective sleep quality. Future studies should focus on elucidating the pathophysiology of these symptoms.

Project description:PD is a complex, multifactorial neurodegenerative disease, which occurs sporadically in aged population, with some genetically linked cases. Patients develop a very obvious locomotor phenotype, with symptoms such as bradykinesia, resting tremor, muscular rigidity, and postural instability. At the cellular level, PD pathology is characterized by the presence of intracytoplasmic neurotoxic aggregates of misfolded proteins and dysfunctional organelles, resulting from failure in mechanisms of proteostasis. Nonmotor symptoms, such as constipation and olfactory deficits, are also very common in PD. They include alteration in the circadian clock, and defects in the sleep-wake cycle, which is controlled by the clock. These non-motor symptoms precede the onset of the motor symptoms by many years, offering a window of therapeutic intervention that could delay-or even prevent-the progression of the disease. The mechanistic link between aberrant circadian rhythms and neurodegeneration in PD is not fully understood, although proposed underlying mechanisms include alterations in protein homeostasis (proteostasis), which can impact protein levels of core components of the clock. Loss of proteostasis depends on the progressive pathological decline in the proteolytic activity of two major degradative systems, the ubiquitin-proteasome and the lysosome-autophagy systems, which is exacerbated in age-dependent neurodegenerative conditions like PD. Accordingly, it is known that promoting proteasome or autophagy activity increases lifespan, and rescues the pathological phenotype of animal models of neurodegeneration, presumably by enhancing the degradation of misfolded proteins and dysfunctional organelles, which are known to accumulate in these models, and to induce intracellular damage. We can enhance proteostasis by pharmacologically inhibiting or down-regulating Usp14, a proteasome-associated deubiquitinating enzyme (DUB). In a previous work, we showed that inhibition of Usp14 enhances the activity of the ubiquitin-proteasome system (UPS), autophagy and mitophagy, and abolishes motor symptoms of two well-established fly models of PD that accumulate dysfunctional mitochondria. In this work we extended the evidence on the protective effect of Usp14 down-regulation, and investigated the beneficial effect of down-regulating Usp14 in a Pink1 Drosophila model of PD that develop circadian and sleep dysfunction. We show that down-regulation of Usp14 ameliorates sleep disturbances and circadian defects that are associated to Pink1 KO flies.

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Sleep dysfunction and its management in Parkinson's disease.

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Sleep dysfunction and its management in Parkinson's disease.

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