RESTLESS LEGS SYNDROME

Polysomnography Findings in Patients with Restless Legs Syndrome and in

Healthy Controls: A Comparative Observational Study
Magdolna Hornyak, MD; Bernd Feige, PhD; Ulrich Voderholzer, MD; Alexandra Philipsen, MD; Dieter Riemann, PhD

Center for Sleep Research and Sleep Medicine, Department of Psychiatry and Psychotherapy, University Medical Center, Freiburg, Germany
Study objectives: Sleep disturbances and their sequelae are the most to the one-epoch criterion), shorter total sleep time, lower sleep efficiency,
common complaints of patients with restless legs syndrome (RLS). We higher arousal index, higher number of stage shifts, and longer REM sleep
compared polysomnography (PSG) findings in a large cohort of patients latency. During the sleep period time, percentage of wake and sleep stage
with idiopathic RLS and of healthy subjects. 1 were increased, and sleep stage 2 and REM sleep were decreased in
Design: Comparative observational study. RLS patients. The PLMS indices and the sleep fragmentation index were

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Setting: University hospital sleep laboratory. markedly increased in the RLS group.
Patients: Age- and sex-matched patients with idiopathic but untreated Conclusions: We present the largest polysomnography study to date
RLS versus healthy controls. that compares patients with idiopathic RLS with age- and sex-matched
Interventions: N/A healthy subjects. The findings demonstrate markedly fragmented sleep
Results: Each group consisted of 29 females and 16 males. RLS subjects with deterioration of both NREM and REM sleep in RLS patients.
and controls were 47.4 ± 10.9 and 47.3 ± 10.5 years old, respectively. Keywords: Polysomnography, restless legs syndrome, sleep fragmenta-
RLS severity was 24.0 ± 6.2 points on the IRLS scale, indicating moder- tion index, healthy controls, comparative study
ately severe RLS symptoms. We found strong multivariate group effects Citation: Hornyak M; Feige B; Voderholzer U et al. Polysomnography
on PSG parameters (Wilks’ lambda, P <0.001): RLS patients exhibited findings in patients with restless legs syndrome and in healthy controls: a
prolonged sleep onset latencies (according to the 10-min criterion but not comparative observational study. SLEEP 2007;30(7):861-865.

cohort of RLS patients and healthy subjects. The only comparable

INTRODUCTION PSG study examined 12 patients and 12 matched controls and
reported NREM sleep abnormalities, with increased sleep stage
RESTLESS LEGS SYNDROME (RLS) DESCRIBES A COM- 1 and awakenings during sleep and decreased sleep efficiency in
S: 9.5 in

B: 12 in
T: 11 in

MON SENSORIMOTOR DISORDER WHICH IN MOST CAS- RLS;9 the spectral analysis of sleep EEGs did not find differences
ES TAKES A CHRONIC COURSE. THE DIAGNOSIS OF RLS in the sleep EEG spectra.10
relies on the patient’s history.1 Due to the nocturnal occurrence We compared the PSG findings from patients with idiopathic
of symptoms, patients with moderate or severe RLS usually suf- RLS with those of age- and sex-matched controls in order to de-
fer from sleep disruption. In patients seeking medical help, sleep termine characteristic differences between them and to uncover
disturbances and their consequences are the primary morbidity of any macroarchitectural pattern in RLS. We hypothesized that RLS
the disorder and have a negative impact on quality of life.1,2 patients would exhibit lower sleep efficiency, longer sleep onset
While RLS severity is usually evaluated with questionnaires latency, and more fragmented sleep than controls. For assess-
like the International RLS Study Group Rating Scale (IRLS),3 ment of sleep fragmentation, we applied the sleep fragmentation
polysomnography (PSG) recordings may support diagnosis.4 Pe- index (SFI).11,12 The SFI was introduced as an estimate of sleep
riodic leg movements (PLM),5,6 sleep efficiency, and sleep onset disruption in patients with sleep disordered breathing.11 The main
latency are the most frequently used assessment parameters for advantage of the SFI is that it can be determined without hav-
determining symptom severity and treatment efficacy.7 In a typical ing to score arousals. The assessment of arousals is considered
RLS patient, one expects to find an increase of PLM during sleep to be the “gold standard” in detecting sleep fragmentation, but
(PLMS), increased sleep onset latency, increased wake periods af- arousal scoring is time consuming and requires trained observers.
ter sleep onset, increased sleep stage shifts, as well as an increase The SFI has shown a good correlation with the arousal index and
of sleep stage 1 and a decrease in slow wave sleep.8 Although indices of sleep discontinuity and high inter-night reliability in
alterations of sleep are a common finding, no study has yet been previous studies.11,12
published that compares polysomnographic parameters in a larger
METHODS

Disclosure Statement
Patients and healthy controls
This was not an industry supported study. The authors have reported no
financial conflicts of interest. Only data from subjects with simultaneous PSG and PLM re-
cordings on 2 consecutive nights were analyzed. Forty-five of the
Submitted for publication May, 2006 100 consecutive idiopathic RLS patients investigated between
Accepted for publication March, 2007 1999 and 2005 (64 females, 36 males, mean age 55.3 ± 12.4 yrs)
Address correspondence to: Asso. Prof. Dr. Magdolna Hornyak, Department were pair-matched to healthy controls derived from our labora-
of Psychiatry and Psychotherapy, University Medical Center, Hauptstrasse 5, tory database, using a computer program. The selected subgroup
D-79104 Freiburg, Germany; Tel: ++49-761-270-6501; Fax: ++49-761-270- was younger on average (see below) because of the lack of older
6619; E-mail: magdolna.hornyak@uniklinik-freiburg.de healthy controls, while the sex distribution did not differ from the
SLEEP, Vol. 30, No. 7, 2007 861 PSG in RLS and Healthy Controls—Hornyak et al
original population of 100 patients (chi-square test, P = 0.956). ochs); REM density defined as (number of eye movements dur-
Each patient and healthy subject underwent a semi-structured ing REM/number of REM epochs) x 10; number of stage shifts
interview to ascertain history of sleep disturbance, physical and (number of stage shifts during SPT); and number of wake periods
psychiatric examination, laboratory examination, electrocardiog- (number of wake periods during SPT). The following PLMS indi-
raphy (ECG), electroencephalography (EEG), and polysomnog- ces were calculated: 1) the PLMS index (number of all PLMS per
raphy (PSG). hour of TST) and 2) the PLMS-arousal index (PLMS associated
with arousals per hour of TST). As PLMS data was only available
RLS Patients in the first night for all controls, only PLMS data from the first
night of PSG recording are presented. The sleep fragmentation in-
RLS was diagnosed according to the criteria of the Internation- dex (SFI) was determined as previously described11 (total number
al Restless Legs Syndrome Study Group.1 All patients suffered of awakenings and shifts to stage 1 sleep divided by the TST) but
from idiopathic RLS and were unmedicated for at least 2 weeks modified to include any sleep stage shift and the total number of
prior to PSG. Exclusion of secondary RLS was based on labora- awakenings divided by TST in hours.12
tory analysis (blood cell count, serum ferritin, serum creatinine),

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and assessment of patient history and physical examination. One Scales
patient without REM sleep during the first night (having slept for
only 84 min of the 8-hour bedtime period) and the matching con- RLS severity was assessed with the International RLS Severity
trol were excluded from the statistical analysis. Score (IRLS), a validated questionnaire developed by the Interna-
tional RLS Study Group.3
Healthy Subjects
Statistics
Healthy subjects were recruited through relatives and friends of
the clinic staff over a period of 12 years by word of mouth. None Sleep variables were statistically analyzed using repeated
had a history of sleep or psychiatric disorders, substance abuse, or measures MANOVA (SPSS 9.0 GLM, SPSS Inc, Chicago, IL)
intake of hypnotics or other substances known to influence sleep with the factor GROUP. MANOVAs were employed to avoid
(e.g., antihistamines). Exclusion of any relevant medical condi- alpha error inflation. Correspondingly, the univariate ANCOVA
tion potentially influencing sleep was based on a semi-structured F is considered only when the corresponding multivariate test
interview to ascertain history of sleep disturbance, physical and was significant, and single factors or covariates were considered
psychiatric examination, serum biochemistry, and polysomnog- only when the corresponding univariate ANCOVA F was sig-
raphy. nificant. As an additional exploratory analysis, nonparametric
Spearman rank order correlations were performed. The level of
Polysomnographic and PLM recordings significance (two-tailed if not indicated otherwise) was set at P
≤0.05. For descriptive purposes, mean ± standard deviation was
Polysomnographic assessments included EEG (C3-A2, C4- calculated.
A1), EOG, submental EMG, ECG, and superficial EMG of both
anterior tibial muscles. Oronasal air flow, thoracic and abdominal RESULTS
breathing efforts, and transcutaneous oximetry were monitored in
all patients, usually in the first night. Patients with clinically rel- Patients
evant sleep disordered breathing (apnea-hypopnea index >10 per
hour) were excluded. PSG recordings were performed for an 8-h For each group, 45 patients and healthy controls were matched
bedtime period, usually from 23:00 (“lights out”) to 07:00 (“lights for age and sex. Patients and controls were 47.4 ± 10.9 years old
on”); an adjustment of ± 30 min was allowed. Sleep recordings and 47.3 ± 10.5 years old, respectively. Each group consisted of
were visually analyzed according to Rechtschaffen and Kales by 29 females and 16 males. Females were aged 45.6 ± 11.3 years
experienced raters.13 Arousals were scored as described by the (range: 19–68 years) in the RLS group and 45.5 ± 11.0 years
American Sleep Disorders Association.14 PLMS were scored ac- (range: 19–69 years) in the control group. Males were 50.6 ± 9.6
cording to standard criteria.15 years old (range: 31–66 years) in the RLS group and 50.7 ± 8.7
PSG parameters were calculated as follows: sleep onset latency years old (range: 32–63 years) in the control group. RLS sever-
(time from “lights out” until the first epoch of any sleep stage ity as assessed with the IRLS scale was 24.0 ± 6.2 points, thus
excluding sleep stage 1); sleep onset latency-10 (“10-minute cri- indicating moderately severe symptoms. The apnea index of both
terion,” latency to persistent sleep) defined as time from “lights groups was the same (0.5 ± 0.8/h in the RLS and 0.3 ± 0.5/h in the
out” until any sleep stage, excluding sleep stage 1, lasting at least control group, P = 0.092), while the apnea-hypopnea index was
10 min; sleep period time (SPT) defined as the time between sleep 1.0/h of sleep higher in RLS patients (1.8 ± 2.1 in the RLS and 0.8
onset (according to the one-epoch criterion) and last sleep epoch ± 1.7 in the control group, P = 0.017).
of the recording (not regarding sleep stage 1); total sleep time
(TST) defined as time spent in any sleep stage during SPT; sleep Polysomnography parameters
efficiency (SE) defined as percentage of TST during time in bed;
arousal index (number of arousals per hour of TST); REM sleep Group Effects
latency (time from sleep onset until the first epoch of REM sleep);
REM sleep latency-3 (“3-minute criterion”) defined as time from Data for sleep variables and statistical results are presented in
sleep onset until the first REM sleep lasting at least 3 min (6 ep- Table 1. We found strong overall group effects (P <0.001): RLS
SLEEP, Vol. 30, No. 7, 2007 862 PSG in RLS and Healthy Controls—Hornyak et al
 Table 1—Polysomnography Parameters in RLS Patients and the Healthy Control Group. SPT: Sleep Period Time.

Adaptation night Baseline night Group Night Night*Group

Controls RLS Controls RLS P P P
Multivariate test (Wilks’ lambda) <0.001 <0.001 0.058
Sleep onset latency (min) 24.3 ± 23.3 26.2 ± 24.3 17.1 ± 12.2 19.9± 24.5 0.536 0.013 0.859
Sleep onset latency-10 (min) 34.2 ± 32.8 56.2 ± 41.3 25.4 ± 17.8 41.6 ± 44.6 0.004 0.005 0.469
REM sleep latency (min) 100.7 ± 61.9 123.1 ± 73.0 70.0 ± 30.3 92.4 ± 76.3 0.044 <0.001 0.998
REM sleep latency-3 (min) 117.7 ± 65.7 142.2 ± 86.5 84.2 ± 32.7 97.6 ± 80.4 0.135 <0.001 0.461
Sleep period time (min) 454.2 ± 38.8 447.0 ± 29.7 462.8 ± 30.1 454.9 ± 26.6 0.186 0.023 0.932
Total sleep time (min) 403.5 ± 51.2 345.2 ± 80.2 425.4 ± 34.3 383.9 ± 67.0 <0.001 <0.001 0.172
Sleep efficiency (%) 82.5 ± 10.8 72.4 ± 16.5 87.6 ± 7.6 80.0 ± 13.9 <0.001 <0.001 0.305
Arousal index (/h) 13.9 ± 9.1 25.9 ± 13.0 12.4 ± 7.2 23.4 ± 12.6 <0.001 0.007 0.497
Number of stage shifts 144.2 ± 40.8 168.0 ± 44.9 145.8 ± 44.6 168.3 ± 47.9 0.007 0.826 0.882

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Number of awakenings 22.3 ± 11.3 30.8 ± 14.1 20.8 ± 16.2 26.8 ± 11.7 0.005 0.038 0.347
Sleep fragmentation index 25.3 ± 8.1 35.8 ± 11.1 23.8 ± 8.7 31.6 ± 11.0 <0.001 0.004 0.174
Wake (% of SPT) 11.1 ± 9.0 23.0 ± 16.1 7.9 ± 7.0 15.6 ± 13.8 <0.001 <0.001 0.069
Sleep stage 1 (% of SPT) 9.0 ± 5.5 11.6 ± 4.9 8.6 ± 5.1 9.8 ± 3.6 0.042 0.010 0.087
Sleep stage 2 (% of SPT) 56.1 ± 8.2 46.0 ± 10.8 56.2 ± 7.8 50.6 ± 10.8 <0.001 0.013 0.017
Slow wave sleep (% of SPT) 4.3 ± 5.6 4.2 ± 6.0 5.1 ± 6.8 4.9 ± 7.1 0.922 0.017 0.766
REM sleep (% of SPT) 19.1 ± 5.7 15.0 ± 6.1 21.7 ± 4.6 19.0 ± 6.0 0.001 <0.001 0.259
REM density (%) 22.8 ± 8.0 25.8 ± 10.7 24.2 ± 9.1 25.2 ± 8.5 0.248 0.628 0.210
PLMS index (/h) 0.6 ± 1.2 22.9 ± 31.8 - - <0.001 - -
PLMS-arousal index (/h) 0.1 ± 0.3 8.1 ± 12.1 - - <0.001 - -

patients exhibited longer sleep onset latencies (according to the (SFI) was significantly higher in the RLS group (Figure 1). The
10-min criterion but not to the one-epoch criterion), shorter total PLMS index and the PLMS-arousal index, assessed in the first
sleep times, lower sleep efficiencies, higher arousal indices, more night, were elevated in patients, as expected. As PLMS monitor-
stage shifts, and longer REM sleep latency (for the one-epoch cri- ing was not performed in every subject in the second night, an
terion). During sleep period time, percentage of wake, sleep stage analysis of the PLMS parameters has been done only for the first
1, sleep stage 2, and REM sleep were different in patients com- (adaptation) night.
pared with controls (see Table 1). The sleep fragmentation index

80
*** ***
Sleep Fragmentation Index

60

40

20

RLS Controls RLS Controls

Night 1 Night 2

Figure 1—Scatterplots of the sleep fragmentation indices of the first and second nights. Thick lines indicate means. ***: P < 0.001.

SLEEP, Vol. 30, No. 7, 2007 863 PSG in RLS and Healthy Controls—Hornyak et al
Night Effects tients.12 This study reported somewhat higher indices than in our
RLS group, possibly because of the study’s heterogenous patient
The multivariate repeated measures factor “NIGHT” was sig- population.12 In our study, the slightly elevated apnea-hypopnea
nificant for both groups. In the second night, patients and controls index in the RLS group (1.8 ± 2.1/h vs. 0.8 ± 1.7 /h) might have
showed decreased sleep onset latencies for both the one-epoch contributed to the difference in SFI. A substantial influence is un-
criterion and the 10-min criterion, increased total sleep time and likely as the apnea-hypopnea index was only minimal, (1/h high-
sleep period time, improved sleep efficiency, and decreased arous- er) and its magnitude was not comparable to the main correlate
al index. During sleep period time, fractions of waking and sleep of SFI, the arousal index. As shown in Figure 1, SFI values of the
stage 1 were significantly reduced, and REM sleep increased in RLS and the healthy group overlap to some extent. The overlap
night 2 compared with the first night recording. REM latency was might stem from the calculation method used. This method has
shorter in the second night in both groups. Sleep fragmentation, been validated12 and was developed to provide a measure of the
as assessed with the SFI, decreased on the second night compared fragmented sleep in sleep apnea syndrome, but it might not en-
with the adaptation night. tirely capture the fragmented sleep in RLS patients.
A difference in the patients’ preferred bedtimes and the bed-

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Relationship of the Sleep Fragmentation Index, PLMS, and Arousal times in the sleep laboratory might have influenced the PSG pa-
Parameters rameters. RLS patients tend to go to bed later and to get up later
because they have the most restorative sleep period during the
In an additional exploratory analysis, we investigated the rela- early morning hours. But this explanation is unlikely because
tionship between the SFI, the PLMS indices, and the arousal in- most of our patients were employed and had to get up regularly
dex. The SFI correlated with the arousal index in both groups and in the early morning during the week. A possible limitation of the
in both nights (RLS group: 1st night: r = 0.562, P <0.001; 2nd night: results is the younger age of the analyzed population compared
r = 0.544, P <0.001; control group: 1st night: r = 0.646, P <0.001, with the original population of 100 patients. Also, the subgroups
2nd night: r = 0.611, P <0.001). There was a slight but significant of females tended to be younger. However, because of the rela-
correlation between the SFI and the PLMS-arousal index in the tively small number of the patients in the subgroups we did not
1st night in both groups (RLS: r = 0.307, P = 0.040; controls: r = perform an additional subgroup analysis.
0.296, P = 0.048). The apnea index (AI) and the apnea-hypopnea The alteration of REM sleep, with reduction of REM sleep
index (AHI) did not correlate with the SFI in the RLS (AI: r = duration and increase of REM sleep latency, is a novel finding.
-0.202, P = 0.184; AHI: r = -0.029, P = 0.851) or in the control It might have occurred as a consequence of sleep interruptions
group (AI: r = 0.170, P = 0.264; AHI: r = 0.273, P = 0.070). which were in turn due to the nocturnal occurrence of RLS symp-
toms. We cannot however exclude the possibility that in some
DISCUSSION patients, bedtimes in the sleep laboratory began earlier and that
REM phases subsequently occurred later. The REM sleep abnor-
In the present study, we compared the polysomnography data malities we described may also be related to the pathology of
of a large cohort of patients with idiopathic RLS with that of age- RLS. However, no data is available which would explain such a
and sex-matched healthy subjects. As hypothesized, RLS patients relationship.
showed numerous periods of waking, increased arousals, dimin- The consequences of chronic sleep loss have been investigated
ished sleep duration and sleep efficiency, and an elevated sleep intensively in recent years. Chronic sleep deprivation, as in un-
fragmentation index. In addition, we found evidence of REM sleep treated RLS, may lead to increased risk of insulin resistance and
disturbance, with increased REM sleep latency and decreased per- type 2 diabetes17 or to impairment of sleep-dependent memory
centage of REM sleep for both nights in the RLS group. consolidation.18 Prefrontal cognitive deficits similar to those re-
In a previous study, Saletu and coworkers 9 described simi- ported for loss of one night of sleep were shown recently in pa-
lar changes in NREM sleep in a group of 12 RLS patients and tients with RLS.19 Interestingly, modest reductions of sleep time
age- and sex-matched healthy subjects. In their study, the patients and specific loss of REM sleep in healthy subjects appear to be
showed increased REM sleep latency and decreased REM dura- related to hyperalgesia the following morning,20 an observation
tion, however, REM parameters were not significantly different which may be especially relevant in RLS patients in light of the
from those of healthy controls. This may be due to the small num- mechanical hyperalgesia described in this disorder.21
ber of subjects investigated. Interestingly, sleep onset latency and In summary, we present the first comparative analysis of poly-
sleep period time were comparable in RLS patients and healthy somnography parameters of RLS and age- and sex-matched
controls in both our study and in the aforementioned study.9 This healthy subjects in a larger cohort. Our findings show markedly
finding is surprising, as most patients complain about difficul- fragmented sleep with deterioration of both NREM and REM
ties in initiating sleep. The discrepancy might be explained by sleep in RLS. The long-term consequences of sleep loss in this
the clinical observation that RLS patients fall asleep rapidly but patient population should be investigated further.
cannot maintain sleep. This is supported by our finding that it is
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