Does restless legs syndrome impact cognitive function via sleep quality in adults with Parkinson’s disease?

Abstract

Purpose:

Restless legs syndrome (RLS) is a sleep disorder that results in sleep dysfunction. Sleep disruption can have profound negative consequences in adults with Parkinson’s disease (PD), potentially including cognitive dysfunction. This study examined the relationships among RLS, cognition, and sleep quality in persons with PD.

Materials and Methods:

Participants (N=79) with idiopathic PD completed six questionnaires evaluating RLS, sleep quality, daytime sleepiness, global cognitive function, sleep apnea risk, and depression. Participants were further examined for body composition (BMI) and motor symptom severity (MDS-UPDRS Part III).

Results:

Persons with RLS (n = 25) had significantly worse cognitive function (p = 0.035, d = − 0.56) and sleep quality (p < 0.0001, d= −1.19), and more daytime sleepiness (p = 0.009, d = 0.67) than those without RLS (n = 54). Cognitive function was not significantly correlated with sleep quality (r_s = 0.113) or daytime sleepiness (r_s = −0.001). The association between RLS and cognition was not attenuated by controlling for sleep quality or daytime sleepiness.

Conclusions:

This study is unique as it is the first to consider the possibility that RLS in PD may be associated with cognitive deficits through a pathway involving sleep quality. Persons with RLS and PD have greater deficits in both sleep quality and cognitive function than individuals without RLS; however, cognitive dysfunction among those with PD and RLS in this sample is not accounted for by sleep quality.

1. Introduction

Parkinson’s disease (PD) is a progressive, neurodegenerative movement disorder that results from the loss of dopamine-producing cells in the substantia nigra pars compacta (SNc). This disease is associated with the presence of α-synuclein-containing Lewy bodies in the SNc [1] and has a prevalence of between 100 and 300 per 100,000 persons in North America [2]. The hallmark features of PD include movement dysfunction (e.g., bradykinesia, rigidity, tremor, postural instability), as well as non-motor symptoms including restless leg syndrome (RLS), poor sleep quality, and cognitive impairment [3].

RLS is characterized by the uncontrollable urge to move the extremities, particularly the legs, and is a common and burdensome sleep-related movement disorder among persons with PD [4]. For example, the prevalence of RLS affects as many as 27% of persons with PD [5]. RLS has a range of consequences (e.g., insomnia, anxiety, depression, decreased quality of life) with one of the most notable being disruption of night-time sleep patterns. Persons with both PD and RLS report worse sleep quality [6, 7], greater sleep disturbances [8–12], and more excessive daytime sleepiness [11, 12] when compared with persons who have PD without RLS.

Disruption of sleep is common among persons with PD and negatively affects quality of life [4]. One recent study indicated that 77.1% of persons with PD reported poor sleep quality, with 32.3% reporting excessive daytime sleepiness. These persons further have significantly decreased sleep efficiency and prolonged sleep latency compared with healthy controls [13]. Such impairments in sleep have negative consequences, including functional disability, compromised quality of life, and cognitive impairment [14].

There is increasing focus on the prevalence and burden of cognitive impairment in persons with PD. Approximately 27% of persons with PD without dementia demonstrate mild cognitive impairment [15], and this increases in the later stages of PD, with an estimated 80% of persons with PD developing dementia over the course of the disease [3]. The influences of cognitive deficits in PD are multifactorial, with one mechanism including striatal dopaminergic deficits as the underlying neurochemical impairment [16]. Persons with PD and RLS demonstrate greater levels of cognitive decline than counterparts without RLS [11, 17]. One proposed mechanism for this is that the sleep disruptions associated with RLS may negatively influence cognitive function [18].

The current study explored the possibility that persons with PD who have RLS experience more sleep dysfunction and cognitive impairment, and that the symptoms of RLS may be indirectly linked with cognitive deficit through a pathway involving sleep. To that end, we examined the associations among the presence of RLS, sleep quality, and cognition in persons with PD. We hypothesized that (a) PD participants with RLS would have worse sleep quality, greater daytime sleepiness, and more cognitive dysfunction, and (b) cognitive dysfunction in persons with PD and RLS could be partially explained by reduced sleep quality and/or greater daytime sleepiness [19]. The current study expands on the work previously reported in a conference abstract [20].

2. Materials and Methods

2.1. Participants

Participants were recruited from the population of patients followed in the Movement Disorders Clinic at the University of Alabama at Birmingham. Participants were invited for participation in the study if they had a diagnosis of idiopathic PD based on the UK PD Society Brain Bank criteria, and age 40 or older. Participants were excluded if they have been previously diagnosed with narcolepsy, or had symptoms or health conditions that would prevent them from being able to complete questionnaires. The study was approved by the University’s Institutional Review Board and all participants agreed to participation through written, informed consent.

2.2. Procedure

Participants were contacted by a Movement Disorders physician by telephone 1–14 days prior to their scheduled clinic visit and were screened for inclusion and exclusion criteria. Subjects meeting criteria were given a minimum of 24 hours to discuss participation with their family and physician and decide whether or not to participate in the study. Those who chose to participate in the study reported to the Movement Disorders Clinic for their normally scheduled visit and completed written, informed consent as well as consent to review their medical records. Participants then completed six questionnaires that evaluated for sleep disorders, memory disorders, and depression. Participants also underwent a physical examination for measures of body composition and disease severity.

2.3. Assessments

The International Restless Legs Syndrome Study Group Rating Scale (IRLS) was used to screen for the presence of RLS as well as provide a descriptive measure of symptom severity [21]. The IRLS is a 10-item questionnaire with items rated on a 4-point scale of 0 (None) to 4 (Very Severe), with participants instructed to report their symptoms over the preceding 7-day period. The IRLS has a maximum score of 40, with higher scores indicating more severe symptoms. Participants were characterized as ‘RLS+’ (score > 0) or ‘No RLS’ (score = 0). The IRLS scale is the most common instrument for quantifying RLS severity among the PD population and has demonstrated reasonable evidence for validity and reliability in the general population with RLS [22, 23].

Additional measures included assessments of motor symptoms, sleep quality, excessive daytime sleepiness, global cognitive function, risk of obstructive sleep apnea, depression, and body composition. PD motor symptom severity was assessed with the Movement Disorders Society-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS), part III (motor examination), which consists of 18-items, rated on a scale of 0 through 4, where 0 = normal, 1 = slight, 2 = mild, 3 = moderate, and 4 = severe, with higher scores indicating more severe motor symptoms [24]. The MDS-UPDRS has demonstrated acceptable reliability and validity in persons with PD [24, 25].

Sleep quality was evaluated with the Parkinson’s Disease Sleep Scale (PDSS), a validated, visual analogue, 15-item scale which assesses symptoms of sleep disturbances over the preceding 7-day period [26]. PDSS was designed to evaluate sleep complaints specific to PD by addressing overall sleep quality, sleep onset and maintenance, nighttime restlessness, nocturnal psychosis, nocturia, nocturnal motor symptoms (i.e., limb movements), sleep fulfillment, and daytime sleepiness [26]. The maximum score is 150, with scores of less than 100 indicating poor sleep quality.

Excessive daytime sleepiness was evaluated with the Epworth Sleepiness Scale (ESS) [27], in which participants rate the likelihood of falling asleep in 8 different situations. The maximum score is 24, with higher scores representing more daytime sleepiness, and scores greater than 10 indicating excessive daytime sleepiness.

Global cognitive function was evaluated with the Montreal Cognitive Assessment (MoCA), which has high sensitivity and specificity for identifying mild cognitive impairment [28] and is accurate in detecting cognitive impairment in PD [29]. The MoCA is a brief 30-point questionnaire that assesses: (1) short term memory; (2) visuospatial memory; (3) executive function; (4) attention, concentration, and working memory; (5) language skills; and (6) orientation to time and place. Scores of 25 or below indicate cognitive impairment [30].

Obstructive sleep apnea (OSA) is commonly associated with symptoms of RLS [31] and is frequently encountered in the PD population [32]. The risk of OSA was assessed using the Berlin Questionnaire [33], which consists of 12-items from three main categories (snoring and cessation of breathing, symptoms of excessive daytime sleepiness, and BMI and hypertension). Overall scores of two or more positive responses indicate an elevated risk of OSA and scores of less than two indicate low risk of OSA.

Depression was evaluated with the Hamilton Depression Scale (HAMD-17) [34]. This scale contains 21 items, however, scoring is based on the first 17 questions in which eight items are scored on a 5-point scale ranging from 0 (not present) to 4 (severe), and nine items are scored from 0–2. The sum of scores is used to determine the level of depression and is validated as a diagnostic and screening tool for depression in PD, with a positive screen for depression in PD if the score is greater than or equal to 11 [34]. The Levodopa Equivalent Dose (LED) was calculated as previously described [35]. Participants also underwent a physical examination that included weight and height to calculate body mass index (BMI).

2.4. Statistical Analysis

The data were analyzed using the SPSS Statistics program, Version 24 (IBM Corporation, Armonk, NY) and analyses were interpreted with an a priori p-value of 0.05. Descriptive statistics for demographic and clinical characteristics are expressed as mean and standard deviation and range for scaled variables or as frequency (n) and percentage of participants (%) for categorical variables. We conducted independent samples t-tests and Chi-Square analyses to determine differences between RLS+ and No-RLS groups followed by Spearman rho rank-order correlations (r_s) among RLS groups, sleep, clinical characteristics of PD and cognition. Spearman correlation coefficients of 0.2, 0.5, and 0.8 were interpreted as weak, moderate, and strong, respectively [36]. Linear regression analyses were performed, with cognition (MoCA score) as the dependent variable and presence of RLS (Step 1) and presence of RLS plus each sleep parameter (i.e., PDSS, ESS, and OSA) (Step 2) as predictor variables. Of note, only variables that demonstrated significant associations in the Spearman rho rank-order correlation analysis with both cognition and RLS were included in Step 2.

3. Results

3.1. Sample Characteristics

The demographic and clinical characteristics of the sample (N = 79) are presented in Table 1. As expected based on PD characteristics, the sample included more men than women. Participants had a broad range of motor symptom severity and PD duration. Among the 31.5% of participants who reported symptoms of RLS, symptom severity was moderate, with a mean IRLS score of 16.7 ± 6.1 (range 6–32). The sample demonstrated a range of severity of non-motor symptoms, including cognitive dysfunction (MoCA), sleep quality (PDSS), daytime sleepiness (ESS), and depression (HAMD-17). Approximately 35% of the participants screened as having high risk of OSA.

Table 1:

Demographic and clinical characteristics of participants (N=79) with Parkinson’s disease.

	Descriptive Statistic
Age (years)	66 ± 9
Sex (n (%))	51 M (65), 28 F (35)
BMI (kg/m2)	27.1 ± 4.6
PD Duration (years)	10 ± 6
Range (years)	1–30
LED (mg)	863.5 ± 522.7
MDS-UPDRS Part III	33.0 ± 13.6
Range	11–68
IRLS
Total Sample	5.0 ± 8.2
RLS +	16.7 ± 6.1
RLS (n (%))
No RLS (0)	54 (68)
Mild (1–10)	4 (5)
Moderate (11–20)	16(20)
Severe (21–30)	4 (5)
Very Severe (31–40)	1 (1)
PDSS	103.5 ± 25.4
Range	43–150
ESS	9.2 ± 5.6
Range	0–21
MoCA	24.1 ± 4.2
Range	11–30
OSA (n (%))
High Risk (Score ≥ 2)	28 (35)
Low Risk (Score < 2)	51 (65)
HAMD-17	6.7 ± 5.4
Range	0–21

Data are presented in mean ± standard deviation unless otherwise specified. M male; F female; BMI Body Mass Index; PD Parkinson’s disease; LED Levodopa Equivalent Dose; MDS-UPDRS Movement Disorders Society-Unified Parkinson’s Disease Rating Scale; IRLS International Restless Legs Syndrome Study Group Scale; RLS Restless Legs Syndrome; PDSS Parkinson’s Disease Sleep Scale; ESS Epworth Sleepiness Scale; MoCA Montreal Cognitive Assessment; OSA Obstructive Sleep Apnea; HAMD-17 Hamilton Depression Scale

3.2. Restless Legs Syndrome in Parkinson’s disease

Demographic and clinical characteristics of PD participants with and without RLS are provided in Table 2. The RLS+ group had significantly greater cognitive dysfunction (MoCA; p = 0.035), worse sleep quality (PDSS; p < 0.0001), more daytime sleepiness (ESS; p = 0.009), and a greater risk of OSA (p = 0.036) compared to those without RLS. Moreover, PD participants with RLS reported scores consistent with poor sleep quality and excessive daytime sleepiness, based on cut scores of less than 100 and greater than 10, respectively. RLS had a moderate-sized effect on MoCA (d = −0.56) and ESS (d = 0.67), and a strong effect on PDSS (d= −1.19). There were no significant differences between participants with and without RLS in terms of age, sex, body composition, PD disease duration, medication dose, motor symptom severity, or depression.

Table 2:

Clinical characteristics for samples of persons with and without restless legs syndrome and Parkinson’s disease (N = 79).

	RLS+ (n = 25)	No RLS (n = 54)	p-value	Cohen’s d
Age (years)	68 ± 9	65 ± 9	0.12	0.37
Sex (n (%))	18 M (72), 7 F (28)	33 M (61), 21 F (39)	0.34	--
BMI (kg/m2)	26.5 ± 4.5	27.4 ± 4.7	0.43	−0.19
PD Duration (years)	11 ± 6	9 ± 5	0.22	0.32
LED	949.4 ± 427.7	823.8 ± 560.5	0.23	0.24
MDS-UPDRS Part III	35.7 ± 13.2	31.8 ± 13.7	0.23	0.29
IRLS	16.7 ± 6.1	--	<0.0001	--
MoCA	22.5 ± 4.5	24.8 ± 3.9	0.035	−0.56
PDSS	85.4 ± 22.0	111.9 ± 22.5	<0.0001	−1.19
ESS	11.7 ± 5.5	8.1 ± 5.3	0.009	0.67
OSA (n (%))			0.036	--
High Risk (Score ≥ 2)	13 (52)	15(28)
Low Risk (Score < 2)	12 (48)	39 (72)
HAMD-17	8.1 ± 5.9	6.0 ± 5.1	0.14	0.39

Data are presented in mean ± standard deviation unless otherwise specified. RLS Restless Legs Syndrome; M male; F female; BMI Body Mass Index; PD Parkinson’s disease; LED Levodopa Equivalent Dose; MDS-UPDRS Movement Disorders Society-Unified Parkinson’s Disease Rating Scale; IRLS International Restless Legs Syndrome Study Group Scale; MoCA Montreal Cognitive Assessment; PDSS Parkinson’s Disease Sleep Scale; ESS Epworth Sleepiness Scale; OSA Obstructive Sleep Apnea; HAMD-17 Hamilton Depression Scale

3.3. Correlation Analysis

The correlations among RLS group, cognition, sleep, and possible confounding variables are presented in Table 3. Presence of RLS was significantly correlated with worse sleep quality as measured by PDSS (r_s = −0.501), more daytime sleepiness, as measured by ESS (r_s = 0.298), worse cognitive impairment, as measured by MoCA (r_s = −0.296), and higher risk for OSA, as measured by the Berlin Questionnaire (r_s = 0.236). However, there were no significant correlations between presence of RLS and PD motor symptom severity, depression, or dopaminergic medications (LED). Cognitive impairment was significantly correlated with PD motor severity (MDS-UPDRS III; r_s = −0.317), but not with sleep quality, daytime sleepiness, depression, dopaminergic medications, or OSA risk. Worse sleep quality, based on PDSS, was significantly correlated with more excessive daytime sleepiness (ESS; r_s = −0.330), more depression (HAMD-17; r_s = −0.549), higher LED (r_s = − 0.307), and higher risk of OSA (r_s = −0.426).

Table 3:

Summary of correlations among restless leg syndrome, cognition, sleep quality, disease severity, depression and medication in persons (N=79) with Parkinson’s disease.

	1	2	3	4	5	6	7	8
1. RLS	--
2. MoCA	−0.296**	--
3. PDSS	−0.501**	0.113	--
4. ESS	0.298**	−0.001	−0.330**	--
5. MDS –UPDRS III	0.140	−0.371**	−0.144	0.114	--
6. HAMD-17	0.196	0.062	−0.549**	0.144	0.248*	--
7. LED	0.157	0.008	−0.307**	0.187	0.081	0.078	--
8. OSA	0.236*	−0.029	−0.426**	0.228*	−0.057	0.409**	0.001	--

^*p < 0.05;

^**p < 0.01.

RLS Restless Legs Syndrome; MoCA Montreal Cognitive Assessment; PDSS Parkinson’s Disease Sleep Scale; ESS Epworth Sleepiness Scale; MDS-UPDRS Movement Disorders Society-Unified Parkinson’s Disease Rating Scale; HAMD-17 Hamilton Depression Scale; LED Levodopa Equivalent Dose; OSA Obstructive Sleep Apnea

3.4. Linear Regression Analysis

The summary of linear regression analysis for independent predictors of cognitive impairment in persons with Parkinson’s disease (N = 79) is presented in Table 4. The presence of RLS was the only significant predictor of MoCA scores. We further ran linear regression analyses for determining the relationship among sleep quality, daytime sleepiness, and risk of OSA with the presence of RLS and MoCA scores. The summary of linear regression analysis for variables predicting cognitive impairment in this sample of PD patients (N = 79) is presented in Table 5. All three models demonstrate that the presence of RLS explained a significant amount of variance in MoCA in Step 1. The addition of sleep quality, daytime sleepiness, or risk of OSA in Step 2 did not attenuate the relationship between RLS group and MoCA from Step 1, based on the magnitude of the standardized beta-coefficient. This suggests that neither sleep quality, daytime sleepiness, nor the risk of OSA accounts for the association between RLS and cognitive function in persons with PD.

Table 4:

Summary of linear regression analysis for independent predictors of cognitive impairment in persons with Parkinson’s disease (N = 79).

Variable	B	SE B	β
RLS	2.401	1.189	0.266*
PDSS	0.009	0.024	0.054
ESS	0.046	0.094	0.060
OSA	0.645	1.118	0.073

Note: R² = .074.

^*p < .05 with two-tailed test.

Table 5:

Summary of linear regression analysis for variables predicting cognitive impairment in persons (N = 79) with Parkinson’s disease.

	Variable	B	SE B	β
Step 1	RLS	2.310	1.003	0.256*
Step 2	RLS	2.273	1.155	0.251
	PDSS	0.001	0.021	0.008
Note: R2 = .065 for Step 1; ΔR2 = .000 for Step 2. *p < .05 with two-tailed test.

	Variable	B	SE B	β
Step 1	RLS	2.310	1.003	0.256*
Step 2	RLS	2.498	1.064	0.276*
	ESS	0.050	0.091	0.065
Note: R2 = .065 for Step 1; ΔR2 = .004 for Step 2. *p < .05 with two-tailed test.

	Variable	B	SE B	β
Step 1	RLS	2.310	1.003	0.256*
Step 2	RLS	2.447	1.035	0.271*
	OSA	0.576	1.007	0.065
Note: R2 = .065 for Step 1; ΔR2 = .004 for Step 2. *p < .05 with two-tailed test.

We conducted an exploratory analysis of other predictors of cognitive impairment. This secondary analysis included MDS-UPDRS, Part III and demographic variables as potential predictors of MoCA, and only motor symptom severity was a significant predictor of global cognitive function (B = − 0.124, SE B = 0.036, β = −0.374). Additionally, we ran an analysis of the predictors of RLS and, notably, motor symptom severity did not predict presence of RLS (B = − 0.001, SE B = 0.004, β = −0.034).

4. Discussion

This study examined the relationships among the presence of RLS, cognitive impairment and sleep (i.e., sleep quality, daytime sleepiness, and risk of sleep apnea) in persons with PD. In this sample, individuals with PD and RLS demonstrated significantly greater cognitive dysfunction, more sleep disturbance, more daytime sleepiness, and higher risk for OSA than those without RLS, consistent with previous studies [6, 7, 11, 12, 37]. The presence of RLS was significantly correlated with sleep quality, daytime sleepiness, risk for OSA, and cognitive impairment. These results suggest that RLS negatively influences sleep and cognitive function in PD. Interestingly, the influence of RLS on cognition was not attenuated by controlling for sleep quality or OSA, suggesting that there are additional factors to consider in the relationship between RLS and cognitive function in persons with PD. Based on a secondary, linear regression analysis, motor symptom severity was the most robust predictor of cognitive impairment, but it was not considered as a factor accounting for the association between RLS and cognition because it did not differ between RLS groups or correlate with the presence of RLS.

The uncontrollable urge to move the extremities associated with RLS typically occurs in the evening, when the individual is at rest or near sleep onset and regularly leads to significant sleep disturbance, which can exacerbate the significantly decreased sleep efficiency and prolonged sleep latency experienced in PD [13]. Consequently, persons with both PD and RLS report worse sleep quality [6, 7], greater sleep disturbances [8–12], and more excessive daytime sleepiness [11, 12]. A recent study demonstrated a significant effect of sleep on global cognitive function in persons with PD [14]; however, our results indicate that sleep quality was not responsible for the influence of RLS on cognition. This leads us to believe that there are other links between RLS and cognitive dysfunction.

Although the mechanism underlying the association between RLS and cognitive dysfunction in PD is not known, one potential explanation of this relationship involves inflammation. Inflammation likely contributes to the pathogenesis of PD and PD patients have elevated levels of pro-inflammatory cytokines compared to controls [38]. Additionally, these cytokines correlate with and predict cognitive dysfunction in PD [39]. Inflammation is also a proposed mechanism underlying the pathophysiology of RLS [40]. Further research is needed to explore whether RLS and cognitive dysfunction in PD could be concurrent consequences of an enhanced inflammatory state (i.e., sickness behavior) or another underlying mechanism, such as dopaminergic dysfunction. In fact, the primary affected region in PD is the nigrostriatal dopaminergic system and RLS is also suggested to have an underlying dopaminergic pathophysiology [41]. Previous research suggests that dysfunction in dopaminergic modulation may also contribute to cognitive deficits in non-demented patients with PD [16, 42]. The resultant dopaminergic dysfunction associated with increased PD severity may also explain the concomitant increase in cognitive dysfunction; however, future research is necessary to examine the effect of dopaminergic dysfunction with regard to PD, RLS, and cognition.

Although not statistically significant, our sample with RLS trended toward higher doses of medication, longer PD duration, greater motor symptom severity, and more depression than those without RLS. These findings are consistent with an earlier study, which demonstrated that RLS was significantly associated with longer duration of PD symptoms, longer duration of disease modifying therapies, greater PD severity, and greater cognitive impairment in persons with PD [17]. Prior studies also demonstrate significantly more depression in persons with PD and RLS than without RLS [11, 12, 43, 44]. For example, one study reported that depressive symptoms in PD patients accounted for 21% of nighttime sleep problems, and were also associated with LED and disease severity [37]. Our results are consistent with the literature; however, we did not find statistically significant differences within our sample. This suggests that our sample size may have precluded significant findings and a larger sample is necessary to detect these differences. Nevertheless, this study is unique to the field, as it is the first to consider sleep as a variable that accounts for the relationship between RLS and cognition in PD.

There are some important limitations of this study that should be considered when interpreting our results. Our sample size was relatively small and we did not include a non-PD control group for comparative purposes. Unfortunately, Hoehn and Yahr scoring was not recorded in this study for an additional measure of disease severity. Additionally, the cross-sectional design of this study precludes any inferences regarding causality among RLS, sleep quality, and cognitive impairment. We relied primarily on scores from the IRLS questionnaire to determine RLS prevalence rather than a confirmed diagnosis from a physician. To that end, the questionnaire was designed to encompass the four essential criteria for diagnosing RLS [23]; therefore, a positive response to any these questions suggests a positive diagnosis. Additionally, the IRLS questionnaire is a commonly used measure of RLS in the PD population [22]; however, it may not distinguish from RLS mimics (i.e., akathisia, dystonia, and peripheral neuropathy) associated with PD and the psychometric properties of the IRLS have not yet been assessed for this group. Additionally, we did not have objective measures of sleep (polysomnography or multiple sleep latency test), but relied on patient report of sleep quality and daytime sleepiness; however PDSS and ESS are validated in PD and have been reliable measures of these symptoms [45, 46]. Additionally, the MoCA is a global cognitive scale used to detect mild cognitive impairment, which did not allow us to evaluate if RLS impacts specific domains of cognition in PD (i.e., attention); however, this measure provides a good starting point to design future studies to better address that question. Additional appropriate measures should be considered in future studies to assess cognitive function (i.e., learning and memory, attention, problem solving, and executive function) with respect to RLS and sleep in persons with PD.

In summary, we provide subjective data on the relationships among RLS, sleep, and cognitive dysfunction in persons with PD. Persons with RLS and PD demonstrate greater deficits in both sleep quality and cognitive function than individuals without RLS; however, the impairment in cognitive function among those with PD and RLS is not seemingly accounted for by impairment in sleep quality. Such results should be considered when assessing and treating persons with RLS and PD, as the treatment of RLS has the potential to improve clinical outcomes, such as sleep quality and daytime sleepiness that would impact one’s participation in daily activities. Future research should evaluate the direct and indirect relationship between RLS and specific domains of cognitive function that may be more influenced by sleep, as a single measure of global cognitive dysfunction may preclude inferences of the impact of RLS on different domains of cognitive function in persons with PD.