Annals of Movement Disorders

: 2018  |  Volume : 1  |  Issue : 1  |  Page : 8--19

Sleep disturbances in patients with Parkinson’s disease: It’s time to wake up!

Abhishek Lenka1, Priyantha Herath2, Shivam O Mittal3, Pramod K Pal4,  
1 Department of Neurology, MedStar Georgetown University Hospital, Washington, DC, USA
2 Department of Neurology, Kansas University Medical Center, Kansas City, Kansas, USA
3 Department of Neurology, Vikram Hospital, Bangalore, India
4 Department of Neurology, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India

Correspondence Address:
Dr. Pramod K Pal
Department of Neurology, National Institute of Mental Health & Neurosciences (NIMHANS), Hosur Road, Bengaluru 560029, Karnataka


Patients with Parkinson’s disease (PD) develop a range of non-motor symptoms (NMS). Sleep disturbance is one of the common NMS of PD and the onset of sleep disorders often precede the onset of motor symptoms of PD. Motor symptoms of PD often receive the main clinical focus and the sleep disturbances often go unnoticed in clinical practice. Given that the prevalence of PD is higher in the elderly population, primary care physicians, geriatricians, and gerontologists are usually the first point of contact for a majority of patients with PD. Because of this, it is important that they have a clear understanding about the diagnosis and management of the sleep disturbances in PD. This review provides an overview of the full spectrum of sleep disturbances in PD that includes insomnia, excessive daytime sleepiness, rapid eye movement sleep behavior disorder, restless leg syndrome, periodic limb movements, and obstructive sleep apnea. Although these sleep disorders may be primarily associated with PD, it is crucial to delineate the other treatable causes of sleep disturbances such as side effects of medications and physical symptoms not related to PD. This review highlights the major sleep disorders observed in patients with PD and succinctly discusses their management aspects. In addition, we have briefly described the effect of deep brain stimulation on the natural course of several sleep disorders in PD in this article.

How to cite this article:
Lenka A, Herath P, Mittal SO, Pal PK. Sleep disturbances in patients with Parkinson’s disease: It’s time to wake up!.Ann Mov Disord 2018;1:8-19

How to cite this URL:
Lenka A, Herath P, Mittal SO, Pal PK. Sleep disturbances in patients with Parkinson’s disease: It’s time to wake up!. Ann Mov Disord [serial online] 2018 [cited 2023 Mar 28 ];1:8-19
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Parkinson’s disease (PD) is characterized by a set of core motor symptoms that includes rigidity, bradykinesia, tremor, and postural instability.[1] In addition, often undetected and untreated, a repertoire of non-motor symptoms (NMS) often complicates the clinical course of PD.[2] These NMS that affect all the physiological domains in patients with PD are often associated with greater disability than the motor symptoms as the disease progresses.[3]

Our current understanding of the pathology of PD is that there is a loss of dopaminergic neurons in the substantia nigra (SN) and a concurrent accumulation of Lewy bodies (LB).[4] These are the pathological hallmarks of PD. Onset of many of the NMS may precede the onset of motor symptoms. The caudo-cranial progression of the LB pathology (LBP) that first affects the dorsal motor nucleus of vagus (Braak staging system) and subsequently involves several brain stem nuclei (raphe nucleus, locus coeruleus, and pedunculopontine nucleus), SN, and neocortex, partially explains the observation of earlier occurrence of certain NMS than the motor symptoms in PD[5] [Figure 1].{Figure 1}

Sleep is a basic and indispensable physiological requirement for the humans. Majority of the patients with PD complain of sleep disturbances and the burden caused directly and indirectly by these symptoms is massive.[6] The sleep symptom repertoire that has been documented in PD is extensive and it includes insomnia of several types including difficulty in falling asleep (sleep-onset insomnia) or staying asleep (sleep maintenance insomnia), excessive daytime sleepiness (EDS), rapid eye movement sleep behavior disorder (RBD), restless legs syndrome (RLS), and periodic limb movement in sleep (PLMS), as well as PLM of wakefulness.[7],[8] Sleep disorders, such as RBD, have been reported to have strong association with other debilitating NMS such as psychosis, cognitive impairment, and impulse-control disorders.[9],[10] These sleep disorders are associated not only with substantial worsening of the quality of life of patients with PD but also with higher caregiver distress.[11] Furthermore, comorbid sleep disorders are reported to predict higher NMS burden in PD,[12] warranting prompt identification and adequate management of sleep disorders associated with PD.

In this review, we focus on the mechanism of sleep disturbance in PD, characteristics of common sleep disorders observed in patients with PD, their effect on disease course and quality of life, and approaches to their optimal management.

 Physiology of Normal Sleep

On the basis of polysomnographic features, normal human sleep is categorized into two stages that have distinct physiological and neurochemical signatures. First is the non-rapid eye movement (NREM) sleep, which is predominantly present in the first half of sleep and comprises approximately 65% of the total sleep time. It is further divided into three stages, that is, stage-N1, stage-N2, and stage-N3. The other one is the REM sleep, which is often termed as stage-R.[13] It is now presumed that NREM sleep is crucial for the maintenance of the synaptic plasticity and restorative functions at cellular, molecular, and network levels. The REM sleep is characterized by low amplitude, mixed frequency electroencephalograph waves similar to that of stage-N1. Biological roles of REM sleep are not clear; however, burgeoning evidence indicates the possible role of REM sleep in consolidation of memory and in processing of emotional information.[14]

The neurochemistry of the sleep–wake cycle involves complex interactions of several neurotransmitters (NTs), released from various loci in the brain. For example, hypocretin (orexin), a neuropeptide, secreted from the posterior and lateral hypothalamus, is essential in promoting wakefulness.[15] There is also evidence that NTs such as histamine, serotonin, norepinephrine, and dopamine promote wakefulness,[16] whereas acetylcholine (Ach) has an important dual role in regulating wakefulness as well as REM sleep. With these, the state of wakefulness is regulated through a coordinated expression of multiple NTs dependent on several external and internal stimuli. Combinations of these NTs appear to be active under specific circumstances. For example, dopamine promotes wakefulness when an individual is motivated and physically activated, whereas norepinephrine is important for arousal in response to novel or important stimuli. [Figure 2] summarizes the role of the NTs that regulate sleep–wake cycle in humans.{Figure 2}

It is important to be aware of the role of the aforementioned NTs in the regulation of sleep–wake cycle as these NTs are often implicated in several other NMS of PD. Functional derangements in these NTs perhaps result in higher NMS burden in Patients of PD with sleep disturbances.[12]

 Pathophysiology of Sleep Disturbances in PD

The pathophysiology of sleep disorders in PD remains largely elusive. It is now known that certain sleep disorders may precede the onset of motor symptoms of PD by several years. This observation correlates well with the predicted caudo-rostral spread of LBP. As reticular-activating system and majority of the NTs, which maintain the sleep–wake cycle are located within the brain stem, alpha-synuclein deposition in the form of LB in brain stem structures (Braak stage-II) might be the preliminary neuropathologic disturbance that explains the onset of certain sleep disorders such as insomnia and RBD earlier than the motor symptoms. Here, the LBP likely involves the local dopaminergic neurons in the ventral tegmental area and the hypothalamus. Given the importance of dopamine as a modulator of wakefulness, the resultant local brain stem hypodopaminergic state in PD may partially explain the various early- and late-onset parasomnias and other sleep disturbances in patients with PD.

Although some of the sleep disorders such as RBD and RLS are intrinsic to the pathology of PD, most of the sleep disorders occur possibly secondary to the motor and psychiatric symptoms of PD. For example, patients with severe nocturnal akinesia would have difficulty in maintaining the sleep and would present with multiple nocturnal awakenings. Similarly, patients of PD with depression and anxiety would present with more frequent sleep disturbances compared to those without any psychiatric symptoms.

 Specific Sleep Disturbances in PD


Insomnia is a common disturbance of sleep in patients with PD. It has three forms: (i) sleep-onset insomnia (difficulty in falling asleep), (ii) sleep maintenance insomnia (difficulty in staying asleep), and (iii) early morning awakenings. It is the most commonly observed sleep disorder in PD.[17] Sleep maintenance insomnia has been reported as the most common form of insomnia in PD as majority of the patients attribute insomnia to the physical discomfort they get during the sleep.[18],[19] In a study by Gjerstad et al.,[20] difficulty in turning on the bed and frequent nocturnal awakenings were the two most commonly associated symptoms in patients of PD with insomnia. Other medical conditions may contribute to this. In addition, the presence of other NMS such as nocturia, depression, and anxiety, and the anticipation of wearing off can also disrupt the sleep. Antiparkinsonian medications can also result in sleep disruption in some patients. It has been reported that dopaminergic agents at low dosage promote sleep, whereas they cause significant sleep disruption at higher doses.[21] The dose-dependent effect of levodopa and dopamine receptor agonists on the quality of sleep is possibly secondary to their differential action on D1, D2, and D3 receptors in the brain.[22] Contribution of medications such as antihypertensives (atenolol, propranolol, and clonidine), bronchodilators, hormones (thyroxine and estrogen), caffeine, and nicotine to insomnia must always be considered.

Approach to insomnia in PD

PD may not be the only source of insomnia. Other common comorbidities should be sought. The treatment for insomnia should be individualized because of its multifactorial origin in patients with PD. However, the first step towards management of insomnia in PD is to optimally control the motor symptoms as they are the major source of physical discomfort during sleep. For this, adequate titration of the antiparkinsonian medications is essential. Although no consensus regarding the dosage and distribution of antiparkinsonian medications in patients with insomnia is observed, maintaining dopamine receptor agonists at a low dose in the evenings is useful as is the judicious use of slow-release preparations. Proper sleep hygiene, relaxation techniques, and cognitive behavior therapy should be used before starting pharmacological therapy for insomnia. As neuropsychiatric symptoms are common in PD, treatment of the underlying depression and anxiety remains an essential step. The options for medical management of insomnia have been expanding. Newer hypnotics such as zopiclone and eszopiclone have almost replaced the benzodiazepines for the management of insomnia. Eszopiclone provides significant improvement in the quality of sleep, especially for sleep maintenance in patients of PD with insomnia.[23] Doxepin has also yielded encouraging results in patients of PD with insomnia.[24] Patients not getting good results with the newer hypnotics and doxepin could still benefit from melatonin.[25]

Excessive daytime sleepiness

EDS can be severely debilitating in patients with PD. A multifactorial etiology, including the severity of motor symptoms, disrupted nocturnal sleep, and adverse effects of antiparkinsonian medications, especially the dopamine receptor agonists are contributory.[26] A study based on a cohort from the Parkinson progression marker initiative revealed no significant difference in the prevalence of EDS in de novo untreated patients with PD and controls.[26] However, as the prevalence of EDS in PD ranges from 20% to 60%[27] and the prevalence progresses with advancing disease,[28] it appears that the duration of the disease and the effect of antiparkinsonian medications possibly play an important role in the natural course of EDS. Several risk factors for EDS in PD have been identified and these include the male sex, use of DA, insomnia, disability, cognitive impairment, and depression.[28],[29] Use of dopamine receptor agonists has been reported to have association with sleep attacks in patients with PD. In a comprehensive review on sleep attacks in PD, Homann[30] reported that up to 30% of the patients who take dopamine receptor agonists develop sleep attacks. Later, Yeung and Cavanna,[31] in a meta-analysis, reported the presence of sleep attack in 13% of patients taking dopamine receptor agonists. Importantly, PD patients with EDS have higher severity of depression and autonomic dysfunction[26] and increased frequency of falls[32] compared to those without EDS; thus, necessitating prompt management of this debilitating sleep disorder.

EDS has become a prime topic of research in PD. Several neuroimaging studies have explored the neural correlates of EDS in PD and have reported widespread structural and functional brain abnormalities. A voxel-based morphometric study that explored the neural correlates of EDS in PD reported significant gray matter atrophy in frontal, temporal, occipital, and limbic cortex including the basal nucleus of Meynert.[33] In a study comparing the functional connectivity of drug-naive patients of PD with and without EDS, Wen et al.[34] observed alterations in the regional homogeneity in the left cerebellum, inferior frontal gyrus, and left paracentral lobule. More recently, Yousaf et al.[35] reported abnormal caudate [123I]FP-CIT uptake in patients of PD with EDS, suggesting the putative role of greater dopaminergic deficit in the pathogenesis of EDS.

Approach to EDS in PD

Identifying and managing comorbidities is the cornerstone of management of EDS in patients with PD. Emphasis must be given to underlying depression, fatigue, disruption in night sleep, and obstructive sleep apnea (OSA), which may result in EDS. Considering the strong association of EDS with the use of D2-receptor agonists, titration of D2-receptor agonists to the lowest possible dose or completely eliminating them in patients with EDS is a useful step in the management of EDS. Physicians must also be cognizant of potential overdose of hypnotic medications at night, which may result in EDS. Specific pharmacotherapy for EDS includes modafinil, caffeine, and atomoxetine; however, given that the data regarding their efficacy are conflicting,[36] their use should be tailored to individuals. In a recent study, Büchele et al.[37] provided class I evidence for the efficacy of sodium oxybate in treating EDS. However, larger longitudinal studies are warranted to validate this result.

 Rapid eye movement sleep behavior disorder in patients with PD

RBD is characterized by abnormal behaviors during REM sleep, especially dream enactments along with heightened muscle tone and/or phasic muscle twitching.[38],[39] In fact, the excessive muscle tone during REM sleep, often termed as REM sleep without atonia, is the central objective finding in RBD.[38] Bed partners of patients with RBD often report various vocalizations and abnormal movements (limb jerks, falling out of bed, and violent assaults), which are parts of dream enactment behaviors. Sometimes, violent limb movements could result in injury to the individual or to their sleep partner. The neuroanatomical substrates of RBD have been reported to be localized in some of the brain stem nuclei. Several animal studies in cats and rodents where the subcoeruleus nucleus and ventral medial medulla were damaged by different methods have consistently yielded enhanced electromyography activity during REM sleep associated with aberrant motor behaviors (e.g., prominent twitching and attack-like behaviors).[40] It is important to note that the onset of RBD may precede the onset of motor symptoms of several synucleinopathies such as PD, multiple system atrophy, dementia with Lewy bodies (DLB), and pure autonomic failure by several decades.[41],[42] This important epidemiological observation is consistent with the Braak’s hypothesis, which emphasizes the association of various NMS of PD with the progressive accumulation of LB in caudo-cranial manner.[5] Considering this, RBD is often regarded as the clinical biomarker of PD and has been a prime topic of research in recent times.

There is discordance in the reported prevalence of RBD in PD, mostly because of the difference in the diagnostic criteria used for the diagnosis of RBD. A recently published meta-analysis revealed that approximately half of the patients with PD have symptoms of RBD.[43] Presence of RBD not only increases the odds of future occurrence of PD but also is associated with a faster motor progression and a higher risk of cognitive dysfunction in patients with PD.[44],[45] A large study involving 475 patients with early PD reported greater somnolence, depression, and cognitive impairment in those with RBD compared to those without RBD,[46] suggesting poor functional outcome related to RBD. For these reasons, it is important to identify and manage this sleep disorder.

Approach to RBD in PD

In most cases, a thorough history from the bed partner clinches the diagnosis of RBD. The RBD screening questionnaire (RBDSQ) is a validated questionnaire that is useful in research settings.[47] A score of >6 is a strong evidence for the presence of RBD. Polysomnography is warranted for a confirmatory diagnosis of RBD, especially in patients with clinically probable RBD (score >6 on RBDSQ) as it may reveal other sleep disorders such as PLMS and OSA, which can co-occur along with RBD. An early diagnosis of RBD in PD is crucial not only for a treatment standpoint but also for recruitment in neuroprotective trials for PD and other synucleinopathies. RBD in some patients may occur secondary to the use of specific drugs that include selective serotonin reuptake inhibitors (SSRIs), serotonin and noradrenaline reuptake inhibitors (SNRIs), tricyclic antidepressants such as clomipramine, and beta-blockers such as bisoprolol.[39] Hence, the detailed history of the medication use should be carried out and the aforementioned medications should be discontinued.

Pharmacological options for RBD in patients with PD are limited to clonazepam and melatonin.[48] Both these drugs reduce the frequency as well as the severity of RBD symptoms. Use of these two drugs should be tailored to clinical status of the patients. For example, clonazepam should be avoided in elderly patients with PD, especially those with severe gait disturbances, cognitive dysfunction, and OSA. In these patients, melatonin may be a good therapeutic alternative (gradually up to a maximum dose of 12mg per night).

 Restless legs syndrome

RLS, also known as Willis–Ekbom disease, is the most commonly observed movement disorder. It is a sensorimotor neurological disease with an estimated prevalence of 5%–12%.[49] Its clinical symptomatology includes urge to move the legs, which is usually accompanied by, or felt to be caused by, uncomfortable and unpleasant sensations in the legs. These symptoms usually occur during periods of rest or inactivity and tend to improve after moving the legs. RLS often has a diurnal pattern with worsening toward the evening.

Diagnosis is based on the history and can be validated by adhering to International RLS Study Group (IRLSSG) diagnostic criteria.[50] In some cases, patients may give a history of urge to move the legs but they may not fulfill the criteria for a diagnosis of RLS. The term “leg motor restlessness” has been used for such cases.[51] It is thought that the symptoms of RLS occur secondary to certain dopaminergic dysfunctions. Forty to sixty percent of patients report strong family history of RLS with an autosomal-dominant pattern of transmission.[52] Three loci in chromosomes 12q, 14q, and 9q indicate vulnerability to RLS.[53] These have been labeled RLS1, RLS2, and RLS3, respectively. However, specific causative mutations need further exploration.

RLS in the absence of any other pathology is termed as idiopathic RLS; secondary RLS occurs in PD, pregnancy, iron deficiency, renal failure, and peripheral neuropathy.[54] Estimation of the frequency of RLS in patients with PD has been conflicting. Although several studies have reported an increased prevalence of RLS in patients with PD,[55] other studies show a prevalence closer to that of the general population.[56] This discordance may be due to confounding effect of the dopaminergic agents that can mask the RLS symptoms resulting in false negative reporting. A study on drug-naive patients with PD reported significantly higher prevalence of RLS in patients with PD compared to healthy controls.[57] Moreover, patients of PD with RLS are more likely to have certain NMS such as impulse control disorder,[58] pain,[59] and constipation.[60] In addition, individuals with RLS have poor quality of life[61] and higher mortality rate[62] compared to those without RLS. Hence, it is important to diagnose and manage this sleep disorder in patients with PD early.

Approach to RLS in PD

Initial steps include identification of secondary causes of RLS including an evaluation for iron deficiency anemia, uremia because of renal insufficiency, peripheral neuropathy, myelopathy, and diabetes. The patients with low serum ferritin level (less than 50 μg/L) improve significantly with iron supplements. The dopaminergic medications such as pramipexole, ropinirole, rotigotine, and levodopa have been the mainstay of treatment for RLS. Equal efficacy of pramipexole and ropinirole is observed in reducing the RLS symptoms,[63] and transdermal rotigotine patch is also similarly effective.[64] However, there are several issues with the use of DA for the treatment of RLS, which include the side effects such as impulsive behavior disorders, pedal edema, and EDS; and most notably, the morning rebound phenomenon or augmentation with long-term therapy with dopaminergic medications.[65] Considering all these side effects, the joint task force of the IRLSSG, European RLS Study Group, and the RLS Foundation has recommended the use of α2δ ligands (gabapentin, pregabalin, and gabapentin enacarbil) as the first-line agents for the treatment of RLS.[66],[67] α2δ ligands are excellent therapeutic option, especially when pain is a prominent component of the RLS symptoms.[68] A study comparing the efficacy of pregabalin (300mg/day) versus pramipexole (either 0.25 or 0.5mg) in RLS revealed significant improvement in symptoms at 12 and 52 weeks of follow-up with significantly lower rates of augmentation.[69] Opiates and benzodiazepines can be useful but the adverse effect profiles make them less favorable. Although controversial, some patients with refractory RLS may benefit from intravenous ferric carboxymaltose. High-molecular-weight iron dextran should be avoided due to fear of severe anaphylaxis.[70]

As aforementioned, in a subset of patients, augmentation of RLS symptoms may occur secondary to treatment with dopamine receptor agonists. Augmentation of RLS refers to the onset of symptoms earlier in the afternoon or evening, a quicker onset of symptoms following rest, an increased intensity of symptoms, and a spread of symptoms to different body parts.[71] It is not clear why only a subset of patients with RLS develops augmentation of symptoms but there appears to be a close relationship with the dose of dopamine receptor agonists and the occurrence of augmentation. In patients having significant discomfort, the dopaminergic drugs should be maintained at the lowest possible dose or the dose may be split or should be replaced by α2δ ligands. Lower serum ferritin levels in patients with augmentation compared to those without augmentation have been noted,[72] suggesting the need for reevaluation of iron levels in these patients.

Botulinum neurotoxin (BoNT) has been tried for the treatment of RLS and has yielded mixed results. Recently, Mittal et al.[73] in a large double-blinded placebo-controlled crossover study with BoNT-type A injections in leg muscles (100 units per leg) reported significant improvement in patients with severe RLS to mild/moderate RLS at 4 and 6 weeks following the BoNT injections compared to that in the placebo group. This needs to be further confirmed by larger multicenter studies. The possible pathophysiology is twofold: First, there is evidence of hyperexcitability of spinal motor neurons because of hyperexcitability of cortical–thalamic–cortical network. Injection of BoNT into the muscles causes relaxation of the muscle spindles and thus reduces the peripheral and central hyperexcitability. Second, BoNT helps in reducing neuropathic pain by inhibiting the release of other NTs such as glutamate, substance P, and calcitonin gene-related peptide from the peripheral terminals and spinal cord neurons, which probably help in reducing the sensory afferent signals in patients with RLS.[74]

 Periodic limb movement in sleep

PLMS is characterized by episodes of repetitive stereotypical movements of the lower extremities. It primarily involves rhythmic extension of the big toe and dorsiflexion of the ankle and occasional flexion of the knee and hip.[75] Although PLMS may occur independently in patients with PD, it frequently coexists with RLS. Studies have reported significant association of PLMS with PD and it is more common in patients with PD of higher duration and severity.[76] The neural basis of PLMS is not known, but reports of negative correlation between striatal tracer binding and PLM index during polysomnography in a [123I]β-CIT-based Single photon emission computed tomography study implicating the role of loss of dopaminergic neurons in the pathogenesis of PLMS are available.[77]

Approach to PLMS

No clear guidelines are available for the pharmacological management of PLMS in PD. DA resulted in significant reduction in PLM index compared to those who were drug naive.[78] Other medications such as clonazepam, melatonin, selegiline, and valproate have been reported to improve the subjective quality of sleep, yet their effect on PLM index is not significant.[79]

 Obstructive sleep apnea in patients with PD

OSA is a common finding in patients with PD. However, it is not clear whether OSA is more common in PD compared to the non-PD population. Increased[80] or decreased[81] prevalence of OSA in patients with PD has been reported. Conversely, a higher risk of development in PD in patients with OSA has emerged.[82],[83] Regardless, OSA should be promptly diagnosed and treated as it is associated with poor health–related quality of life in patients with PD and others.[84] Several studies have reported higher cognitive dysfunction in patients of PD with OSA compared to those without OSA.[85],[86]

Approach to OSA in PD

A detailed general medical and sleep history is important for establishing the diagnosis of OSA. History should be obtained from both the patient and his/her bed partner. Specific questions regarding snoring, choking, shortness of breath, and daytime sleepiness should be asked. In addition to the aforementioned classical symptoms of OSA, patients of PD with fragmented sleep and frequent nocturnal awakenings should be evaluated for OSA. In severe cases, OSA may mimic the symptoms of RBD. In fact, a higher risk of sleep disordered breathing is observed in patients of PD with RBD.[87] Hence, patients of PD with symptoms of RBD and/or OSA should undergo overnight polysomnography. Given that obesity is one of the biggest risk factors for the development of OSA, weight reduction is strongly advised in patients with OSA. In severe cases of OSA, continuous positive airway pressure (CPAP) remains the mainstay of therapy as it leads to significant improvement in sleep quality. Importantly, long-term treatment with CPAP was reported to improve the overall NMS burden, including cognition dysfunction and anxiety in patients with PD having OSA.[88] This necessitates the early diagnosis of OSA and its management with CPAP. Currently, no specific guidelines are available for the titration of dose of antiparkinsonian medications. Still, a beneficial effect of sustained-release combination of levodopa and carbidopa in patients of PD with OSA has been reported.[89] This is possibly because of the fact that levodopa might improve the patency of upper airways by improving the coordination among muscles in upper airways, pharynx, and larynx during sleep. Although the result of this study needs to be further evaluated, sustained release formulations of levodopa may become an attractive option for patients of PD with OSA who are not compliant to CPAP therapy.

[Table 1] summarizes the spectrum of sleep disturbances in PD and the common issues related to management of those disturbances.{Table 1}

 Impact of Deep Brain Stimulation on the Sleep Quality in PD

Deep brain stimulation (DBS) has revolutionized the management of motor symptoms of PD. In addition, a growing evidence is available to suggest that DBS also improves several NMS of PD, most notably, urinary dysfunction and sleep dysfunction. Several recently published studies have reported that DBS may result in subjective improvement in sleep quality in patients with PD.[90],[91] However, there is paucity of data on the effect of DBS on objective sleep quality of patients with PD and conflicting results have been reported. Although Amara et al.[92] and Dulski et al.[93] reported no significant improvement in polysomnographic parameters of patients with PD after subthalamic nucleus-DBS (STN-DBS), a recent study revealed improved sleep quality after STN-DBS.[94] At present, it is not clear how exactly the DBS of STN improve the sleep quality. Although the most plausible mechanism appears to be improved nocturnal motor symptoms, further studies are warranted to obtain better insights into the effect of DBS on microarchitecture of sleep–wake cycle in PD. A recent study speculated that as STN is in close proximity with few of the wake-promoting regions in the midbrain, modulation of the connections of STN with these structures after DBS could be indirectly associated with changes in the sleep architecture.[94]

Few interesting studies that have assessed the effect of DBS on RLS are available. Ondo[95] reported significant improvement of symptoms in two patients with medically refractory RLS after DBS of the globus pallidus interna (GPi). Further evidence on the efficacy of DBS in the treatment of RLS comes from a report published by Okun et al.[96] in which the authors described a patient with generalized dystonia whose RLS resolved after bilateral GPi DBS and recurred unilaterally after leads were removed from one side because of infections. A recently published study by Klepitskaya et al.[97] highlighted the effect of STN-DBS on RLS in patients with PD. In this study on 22 patients with PD and RLS, a significant long-term improvement (up to 2-years) in RLS symptoms was observed after STN-DBS, reinforcing the therapeutic role of DBS in patients with RLS.[97]

Overall, the effect of DBS on sleep quality in PD remains an attractive area of research and more studies are warranted to explore it.

[Table 2] summarizes important take-home messages and [Figure 3] shows the approach to the management of sleep disorders in PD.{Table 2}, {Figure 3}


Sleep disorders in PD are extremely common and they may be present as pre-motor symptoms. Their spectrum is large and varied. The exact neural correlates of PD sleep problems are not fully understood. Most of the sleep disturbances lead to poor quality of life in patients with PD, which can be improved by attentive management of these symptoms. Therefore, identification and management of sleep disturbances in PD is essential. In majority of the patients, multiple comorbidities may be the primary cause of sleep disturbances and these should also be carefully managed. Medications can be a major cause of sleep disturbance in PD. In some instances, polysomnography is warranted. Basic research and clinical studies are needed for better insights into the natural course and treatment options of sleep disorders in PD.

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