ARTHRITIS & RHEUMATOLOGY

Vol. 66, No. 5, May 2014, pp 13881394

DOI 10.1002/art.38329
2014, American College of Rheumatology
Poor Sleep Quality Is Strongly Associated With
Subsequent Pain Intensity in Patients With
Acute Low Back Pain
Saad M. Alsaadi,
1
James H. McAuley,
2
Julia M. Hush,
3
Serigne Lo,
4
Chung-Wei Christine Lin,
4
Christopher M. Williams,
4
and Christopher G. Maher
4
Objective. Recent research suggests that sleep
quality and pain intensity are intimately linked. Al-
though sleep problems are common in patients with low
back pain, the effect of sleep quality on the levels of pain
intensity is currently unknown. The aim of this study
was to investigate the effect of sleep quality on subse-
quent pain intensity in patients with recent-onset low
back pain.
Methods. Data on 1,246 patients with acute low
back pain were included in the analysis. Sleep quality
was assessed using the sleep quality item of the Pitts-
burgh Sleep Quality Index, scored on a 03-point scale,
where 0 very good sleep quality and 3 very bad
sleep quality. Pain intensity was assessed on a numer-
ical rating scale (range 010). A generalized estimating
equation (GEE) analysis modeled with an exchangeable
correlation structure was used to examine the relation-
ship between sleep quality and pain intensity. The
model further controlled for symptoms of depression
and prognostic factors for low back pain.
Results. The GEE analysis demonstrated a large
effect of poor sleep on subsequent pain intensity, such
that for every 1-point decrease in sleep quality (based
on a 03-point scale), pain intensity (based on a 010-
point scale) increased by 2.08 points (95% confidence
interval 1.992.16). This effect was independent of
depression and common prognostic factors for low back
pain.
Conclusion. Sleep quality is strongly related to
subsequent pain intensity in patients with acute low
back pain. Future research is needed to determine
whether targeting sleep improvement contributes to
pain reduction.
Low back pain is a major global health problem
(1). Despite the expenditure of billions of dollars and the
publication of thousands of research articles, low back
pain is the leading cause of disability worldwide, and
management is only moderately effective (2,3). Epide-
miologic studies have shown that a large proportion of
patients with low back pain also present with comorbidi-
ties such as depression and anxiety, which along with
other psychological factors can exacerbate the condition
and complicate management (4,5). Interventions based
on these findings have led to moderate reductions in
pain and disability (6,7). Antidepressant drugs (e.g.,
heterocyclics and tricyclics) have been shown to signifi-
cantly reduce pain and improve disability in patients
with chronic low back pain, relative to placebo (8,9).
Such medications are thought to increase the number of
neurotransmitters released at the spinal cord level and
reduce the patients fear of movement related to low
back pain (10). Recently, sleep problems have also been
identified as common in patients with low back pain;
5060% of patients with either acute or chronic low back
pain report problems with their sleep (1113). Despite
The study reported herein used data from a consecutive
subset of participants from the PACE study, an investigator-initiated
study funded by the National Health and Medical Research Council,
Australia, with supplementary industry funding. The current study
did not receive any funding. Dr. Maher is recipient of an Australian
Research Council Fellowship.
1
Saad M. Alsaadi, PhD: King Fahd University Hospital and
the University of Dammam, Khobar, Saudi Arabia;
2
James H.
McAuley, PhD: Neuroscience Research Australia and University of
New South Wales, Sydney, New South Wales, Australia;
3
Julia M.
Hush, PhD: Macquarie University, Sydney, New South Wales, Austra-
lia;
4
Serigne Lo, PhD, Chung-Wei Christine Lin, PhD, Christopher M.
Williams, PhD, Christopher G. Maher, PhD: The George Institute for
Global Health and University of Sydney, Sydney, New South Wales,
Australia.
Address correspondence to Saad Alsaadi, PhD, Department
of Physical Therapy, King Fahd University Hospital, University of
Dammam, PO Box 40035, Khobar 31952, Saudi Arabia. E-mail:
alsaadis@gmail.com.
Submitted for publication February 5, 2013; accepted in
revised form December 17, 2013.
1388
the high prevalence of sleep disturbance in the popula-
tion of patients with low back pain, research has been
limited.
Sleep is essential, and its disturbance can lead to
serious consequences (14). With regard to pain, recent
evidence suggests that sleep can modulate the intensity
of pain (15). Experimental studies in healthy volunteers
(without pain) have demonstrated that induced sleep
deprivation, via either a reduction in sleep duration or
disruption of sleep architecture, leads to the develop-
ment of musculoskeletal pain and increased pain sensi-
tivity to noxious stimuli (1618). Clinical studies in
patients with cancer (19) and patients with rheumatoid
arthritis (20) have shown a significant correlation be-
tween pain intensity and reported sleep quality. In
addition, longitudinal studies have identified a bidirec-
tional relationship between sleep and pain, such that a
night of poor sleep quality was followed by a day with
more severe pain, which consequently worsened sleep
quality during the subsequent night (21,22).
Sleep recovery after a period of induced sleep
deprivation in healthy volunteers has also been shown to
produce an analgesic effect similar to that induced by
nonsteroidal antiinflammatory drugs (23). Furthermore,
improved sleep quality in patients with painful condi-
tions, such as osteoarthritis (24) and chronic musculo-
skeletal pain (25), is significantly associated with reduc-
tions in pain intensity. Finally, previous research also
indicates a strong association between sleep disturbance
and the development of musculoskeletal pain. A Finnish
study demonstrated that sleep disturbance is a strong
predictor of the development of low back pain among
adolescents (26). Likewise, a recent study showed that
women ages 45 years who reported sleep problems are
5 times more likely to develop fibromyalgia compared
with those who do not report sleep problems (27). Taken
together, these findings imply that disturbed sleep has an
important influence on pain and may hinder treatment
effectiveness.
Studies investigating the impact of sleep distur-
bance on the intensity of low back pain have shown a
significant association between the quality of sleep and
pain intensity, fatigue, subsequent-day function, and
psychological distress (28). It has also been reported that
persons with low back pain who have sleep problems
and more severe pain (11) are at higher risk of being
hospitalized for care of low back pain than those with
good sleep quality (29). These findings suggest that poor
sleep quality may be associated with exacerbations of
low back pain; however, to date, no direct association
has been measured over the course of low back pain.
Both pain intensity and sleep quality fluctuate
over time (30,31). As a consequence, identifying the
effect of sleep quality on pain intensity in the population
of patients with low back pain is severely hampered by
the paucity of longitudinal data. Currently, it remains
uncertain whether levels of pain intensity are dependent
on sleep quality at different time points throughout the
course of low back pain. Accordingly, the present study
aimed to determine whether poor sleep quality is asso-
ciated with subsequent increases in pain intensity in
patients assessed during an episode of acute low back
pain.
PATIENTS AND METHODS
Study design overview. This study used data from a
consecutive subset of participants in the PACE study, a
randomized double-dummy, placebo-controlled trial evaluat-
ing paracetamol (acetaminophen) for the treatment of acute
low back pain. The PACE study methods have been published
elsewhere (32). Briefly, the PACE study aimed to enroll 1,650
individuals seeking care for acute low back pain. All partici-
pants received guideline-recommended advice and were ran-
domized to receive study medication containing either active
paracetamol or placebo. Participants were asked to take the
study medication until recovery from back pain or for a
maximum of 4 weeks after randomization. Followup lasted for
12 weeks. Ethics approval for the PACE study was obtained
from the University of Sydney Human Research Ethics Com-
mittee.
Participants. We used data on all participants in the
PACE study who had completed the 12-week followup period
prior to the date of this analysis (October 12, 2012). Because
the PACE study had not been completed at this time, partic-
ipants from all treatment groups were used, and investigators
remained blinded to group assignment. The inclusion criteria
were as follows: primary symptom of pain in the area between
the twelfth rib and the buttock crease, with or without leg pain,
for 6 weeks; experiencing a new episode of low back pain,
preceded by a period of at least 1 month without low back pain,
and moderate intensity of pain as measured by an adapta-
tion of item 7 of the Short Form 36 (33), where the original
phrasing of the item how much bodily pain . . . was changed
to how much back pain . . . to reflect the study interest in
back pain. The exclusion criteria were as follows: low back pain
caused by serious spinal pathology (e.g., metastatic, infective,
or inflammatory spinal disease, cauda equina syndrome, spinal
fracture); receiving recommended doses of analgesics (based
on Australian guidelines for dosing of pain medicine) (34);
spinal surgery within the preceding 6 months; serious comor-
bidities preventing treatment with paracetamol (e.g., renal or
liver failure); currently receiving psychotropic medication for a
mental health condition that remained uncontrolled; or preg-
nant or intending to become pregnant during the study period.
Assessments. A baseline questionnaire was completed
during a telephone interview, to measure demographic char-
acteristics, pain intensity, global impression of recovery, dis-
ability, sleep quality, and symptoms of depression. All partic-
SLEEP QUALITY AND PAIN INTENSITY 1389
ipants were asked to record subsequent weekly outcome data,
including pain intensity, global impression of recovery, disabil-
ity, and sleep quality, in their outcome assessment booklet.
Participants could then elect to provide researchers with data
over the telephone or via an online database. The mode of data
reporting (by telephone or online) could vary for a participant
between data collection time points.
Sleep assessment. Sleep quality was assessed using the
sleep quality item (item 6) of the Pittsburgh Sleep Quality
Index (PSQI) (35). The item was modified to evaluate sleep
quality over the past 7 days instead of the past 4 weeks. Each
participant was asked to rate his/her sleep quality based on the
following question: During the past week, how would you rate
your sleep quality overall? The response categories were as
follows: 0 very good, 1 fairly good, 2 fairly bad, and 3
very bad.
Pain assessment. Participants were asked to rate aver-
age pain over the last 24 hours on a 010-point numerical
rating scale (NRS), where 0 no pain and 10 worst possible
pain. The NRS is widely used to measure pain and has been
shown to be valid and reliable (36).
Low back pain prognostic factors. The following prog-
nostic factors were collected at baseline and included in the
multivariate analysis, because they have been suggested to
impact the prognosis for low back pain (37): age, sex, duration
of current episode (number of days from the onset of pain to
the time of assessment), number of previous episodes, physical
disability related to low back pain, feelings of depression,
risk of pain persistence, paid compensation, leg pain, paid
employment, and number of days of limited activities of daily
living. Physical disability was assessed using the Roland
Morris Disability Questionnaire, which is scored from 0 (no
disability) to 24 (high disability) (38). Depression was assessed
through the participants response to the question How much
have you been bothered by feeling depressed in the past 7
days? on a 010-point scale, where 0 not at all and 10
extremely. The risk of pain persistence was assessed by the
participants view of the probability of having persistence of
current pain, based on the question How large is the risk that
your current pain may become persistent? on a 010-point
scale, where 0 no risk and 10 very large risk.
Statistical analysis. Statistical analyses were per-
formed using SPSS version 19. Continuous variables are
expressed as the mean SD, and categorical variables are
expressed as frequencies and percentages.
The relationship between pain intensity and sleep
quality was evaluated using repeated measurements of pain
intensity and sleep quality over 12 weeks. Generalized estimat-
ing equation (GEE) models (39) with an exchangeable corre-
lation structure and robust standard errors were used to
account for any correlation among the observations in a single
subject. GEE models extend generalized linear models by
allowing repeated measures. Both variables (pain intensity and
sleep quality) are considered to be continuous. GEE regres-
sion models with Gaussian distribution were used, because the
outcome (pain intensity) was assumed to be continuous. All
analyses were conducted at the level of each individual mea-
surement (i.e., baseline and 4 followup time points). In a
bivariate analysis, the models were adjusted for symptoms of
depression at baseline, and a multivariate analysis was adjusted
for intensity of pain at baseline and the previously mentioned
baseline prognostic factors. All P values were calculated with
the 2-tailed Wald test, and the nominal alpha value was set to
5%.
RESULTS
Data on 1,246 individuals with acute low back
pain were included in the analysis. The demographic and
clinical characteristics of the participants are presented
in Table 1. The mean SD age of the participants was
44.2 15.7 years, and 46% were female. The mean
SD pain intensity score at baseline was 6.3 1.9 on a
010-point NRS, and the mean SD duration of low
back pain was 9.8 9.8 days. Only 252 (20%) of the
participants reported pain radiating to the leg. The
mean SD score for physical disability, as assessed by
the 24-item RolandMorris Disability Questionnaire,
was 13.0 5.4, indicating moderate levels of disability.
The mean SD score for depression was 3.1 2.9 and
that for anxiety associated with the risk of pain persis-
tence was 4.5 2.8, as measured on a 010-mm scale,
indicating low levels of depression and anxiety. During
their first visit, 766 patients (62%) reported that their
pain was either unchanged or worse compared with the
level at the onset of pain. At baseline, 633 participants
(51%) reported that their sleep quality was either very
bad or fairly bad. Both sleep quality and pain intensity
improved over the 12-week followup period, and 118
Table 1. Baseline demographic and clinical characteristics of the
study participants
Age, mean SD years 44.2 15.7
Duration of current symptoms, mean SD days 9.8 9.8
Pain rating, mean SD (010 scale) 6.3 1.9
No. of previous episodes, mean SD 6.7 14.0
Days of reduced activity, mean SD 3.3 5.3
Depression rating, mean SD (010 scale)* 3.1 2.9
Risk of pain persistence rating, mean SD
(010 scale)
4.5 2.8
Physical disability rating, mean SD (024 scale) 13.0 5.4
Female sex, no. (%) 567 (46)
Leg pain, no. (%) 252 (20)
Receiving compensation, no. (%) 80 (6)
Paid employment, no. (%) 925 (74)
Global perceived effect, no. (%)
Unchanged 375 (30)
Better 476 (38)
Worse 391 (32)
Sleep quality rating, no. (%) (03 scale)
Very bad 135 (11)
Fairly bad 498 (40)
Fairly good 506 (41)
Very good 104 (8)
* Feelings of depression during the past 7 days.
Assessed using the RolandMorris Disability Questionnaire.
Assessed using the Pittsburgh Sleep Quality Index.
1390 ALSAADI ET AL
subjects (10%) reported that their sleep quality was
either very bad or fairly bad at week 12 (mean SD
pain intensity score 1.3 2.2). Figures 1 and 2, respec-
tively, show ratings for sleep quality and pain intensity
over time.
The percentage of missing data for each time
point (baseline and 4 followup time points) for both
sleep quality and pain intensity was very low (i.e., never
9%). We expected to include 6,230 assessment occa-
sions in the GEE analysis (i.e., 1,246 participants as-
sessed at 5 time points). Due to missing data, 5,831
assessments (93.6%) were included in the final analyses.
Full details about the number and ratio of missing data
for each variable included in the analysis are available
from the corresponding author.
The results of the GEE analysis, as shown in
Table 2, demonstrated evidence of an association be-
tween sleep quality and subsequent pain intensity (P
0.001). These findings can be interpreted that for every
1-point decrease in sleep quality (based on a 03-point
scale), pain intensity (based on a 010-point NRS)
increased by 2.08 points (95% CI 1.992.16). The asso-
ciation between sleep quality and subsequent pain in-
tensity was independent of baseline symptoms of depres-
sion ( 2.05 [95% CI 1.962.14]). The strength of the
association between sleep quality and subsequent pain
also remained after adjusting for important low back
pain prognostic factors (age, sex, duration of current
episode, number of previous episodes, physical disabil-
ity, symptoms of depression, risk of persistence of pain,
paid compensation, leg pain, paid employment, and days
of limited activities of daily living) ( 2.00 [95% CI
1.902.09]).
The interpretation of the analysis is that, on
average, a patient with a sleep quality score of 0 (very
good) on a 03-point scale would be expected to have a
pain intensity score of 1.08 on a 110-point NRS (the
intercept), a patient with a sleep quality score of 1 (fairly
good) would have a pain intensity score of 3.16, a sleep
Figure 1. Prevalence of poor sleep quality from baseline to week 12.
Figure 2. Mean pain intensity from baseline to week 12.
Table 2. Effect of poor sleep quality on subsequent pain ratings,
using a GEE model with an exchangeable correlation*
Model 1 Model 2 Model 3
Intercept
coefficient 1.08 0.90 0.54
95% CI 0.971.19 0.771.02 0.041.03
P 0.001 0.001 0.001
Sleep quality
coefficient 2.08 2.05 2.00
95% CI 1.992.16 1.962.14 1.902.09
P 0.001 0.001 0.001
* GEE generalized estimating equation; 95% CI 95% confidence
interval.
Dependent variable pain; independent variable sleep.
Dependent variable pain; independent variables sleep and symptoms
of depression at baseline.
Dependent variable pain; independent variables sleep, baseline pain,
disability, female sex, presence of leg pain, presence of compensation,
paid employment, age, duration of current symptoms, number of
previous episodes, number of days of reduced activity, and risk of
persistence of pain.
SLEEP QUALITY AND PAIN INTENSITY 1391
quality score of 2 (fairly bad) would be associated with a
pain intensity score of 5.24, and a patient with a sleep
quality score of 3 (very bad) would be expected to have
a pain intensity score of 7.32.
DISCUSSION
In this study, we investigated the association
between sleep quality and subsequent pain intensity in
patients with acute low back pain. The results showed a
strong relationship between the quality of a patients
sleep and subsequent pain intensity that remained of
the same magnitude even after controlling for symptoms
of depression and important prognostic factors. The
effect of poor sleep was large: for every 1-point decrease
in sleep quality, pain intensity increased by 2 points.
This study demonstrates that sleep quality has a
profound impact on the experience of pain intensity.
Our data show that the difference in pain intensity
among individuals with a favorable sleep quality score
(0 on a 03-point scale) and those with a very bad sleep
quality score (3 on a 03-point scale) was 6 points on
a 010-point NRS. This clearly indicates that untreated
sleep problems in individuals with low back pain are
likely to hinder pain management. The literature sug-
gests that untreated sleep problems in patients with
painful conditions can lead to a vicious circle of pain and
poor-quality sleep, which adversely affects an individu-
als quality of life, including social integration, physical
activity, and emotional well-being (40). In fact, previous
studies investigating sleep quality in patients with
chronic low back pain have shown sleep quality to be
associated with psychological distress and physical dis-
ability (41,42). Therefore, it seems prudent that clini-
cians should consider performing a sleep assessment
early in the management of low back pain.
Most contemporary treatments of low back pain
have disappointingly small treatment effects, and a focus
of research in this field is the identification of more
effective treatments. Against this background, the re-
sults of this study are quite significant. The difference in
pain intensity following a fairly good nights sleep com-
pared with a very poor nights sleep is 4 points on a
010-point NRS. This effect is at least double the size
of the effect that is expected for the majority of low back
pain treatments, such as spinal manipulative therapy or
exercise therapy (43). There is evidence that sleep
improvement plays a role in pain reduction of a magni-
tude similar to that of most common analgesic drugs
(23). Clinically, good-quality sleep has been reported to
contribute to the resolution of painful conditions (44).
Furthermore, treatment targeting sleep improvement in
various pain conditions contributed significantly to the
pain reduction. For example, cognitive behavioral ther-
apy targeting insomnia in patients with chronic muscu-
loskeletal pain and arthritic pain has been shown to
significantly reduce pain intensity (45). Although the
effect size was reported to be small to medium, it
persisted for 1 year posttreatment (24). Considering the
findings of the current study, future research in patients
with low back pain should evaluate whether targeting
sleep improvement can contribute to a reduction in pain
intensity.
The current study has several limitations that
must be considered when interpreting the findings. First,
the trial had not been completed at the time of this
analysis, which makes it impossible to determine the
potential effect of active treatment (paracetamol) on the
study results. However, because our analyses are within-
subject, we believe that any effects are likely to be small.
Second, sleep was subjectively assessed using a single
item, the sleep quality item of the PSQI. Thus, it is
unknown which aspects of disturbed sleep (e.g., sleep
duration, latency, or fragmentation) contributed to the
intensity of low back pain. In addition, retrospective
evaluation of an individuals quality of sleep for the past
several days has the potential for recall bias that results
from memory distortion (46). Given the order in which
pain and sleep quality were assessed, it is possible that
more intense pain inflated the patients recall or percep-
tion of sleep quality by focusing on the poor nights of
sleep and therefore to underestimate sleep quality over
a 7-day period. It is therefore important for future
research to evaluate the daily association between sleep
disturbance and low back pain, using both subjective
(e.g., sleep diary) and objective (e.g., actigraph) assess-
ments of sleep.
Finally, sleep quality is a general construct that is
difficult to define and complex to measure. A patients
report of poor sleep quality can be related to factors
such as disturbance of sleep parameters (e.g., difficulty
falling asleep), psychological distress, tiredness on wak-
ing, or impaired daytime functioning (47). In addition,
polysomnographic investigation of patients with pain has
shown that pain can disturb a patients sleep architecture
(i.e., sleep cycle), which can also be responsible for not
feeling refreshed upon waking, leading to the reporting
of poor sleep quality (48). Further research is required
to determine the factors that are responsible for the
reporting of poor sleep quality by patients with low back
pain, so that management of sleep disturbance in these
patients can be optimized.
1392 ALSAADI ET AL
In summary, this study demonstrates a large
effect of poor sleep quality on subsequent pain intensity
in patients with acute low back pain. The magnitude of
this effect was considerably larger than that of most
contemporary treatments for low back pain. The results
suggest that research into the role of interventions
designed to improve sleep quality in patients with low
back pain are warranted.
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Errata
DOI 10.1002/art.38669
In the article by Duval et al in the October 2009 issue of Arthritis & Rheumatism(pages 30383048), the primer
sequences for the aggrecan gene, listed in the Chromatin Immunoprecipitation (ChIP) Assay section of
Materials and Methods, were shown incorrectly. The sequences actually used in the study (taken from the
human sequence of the promoter of AGC1 gene [accession no. AF031586] and corresponding to nucleotides
6082 [forward] and 220240 [reverse]) were as follows: forward 5-AATTTGAAGACCCAGAGACTCGC,
reverse 5-GCTACTGTCGGCCACGATTT.
DOI 10.1002/art.38673
In the article by Park et al in the December 2013 issue of Arthritis & Rheumatism (pages 31413152), the grant
number of one of the Korea Healthcare Technology R&D Project grants was shown incorrectly. The
statement in the footnotes on the first page of the article should have read, Supported by the Ministry of
Health, Welfare, and Family Affairs (Korea Healthcare Technology R&D Project grants A084026 and
A110274).
DOI 10.1002/art.38653
In the article by Kuller et al in the March 2014 issue of Arthritis & Rheumatology (pages 497507), there were
several typographical errors in Table 4, column 5 (age-adjusted death rates per 1,000 person-years in the
group of anti-CCPnegative patients with DMARD use at baseline). The corrected values for age-adjusted
death rates (with 95% confidence intervals in parentheses) are as follows: general health excellent/very good
10.2 (3.233.6), general health good 16.7 (9.232.6), general health fair/poor 29.8 (14.262.8); no diabetes
16.8 (10.427.4), diabetes 27.5 (8.692.0); no CHD at baseline 16.7 (10.327.3), CHD at baseline 26.1
(10.271.6); physical function score on the SF-36 85 17.9 (11.229.3), physical function score on the SF-36
85 13.5 (3.656.6); waist circumference 88 cm 15.5 (8.030.3), waist circumference 88 cm 19.8
(11.137.7); total METs per week 2.5 20.0 (10.936.6), total METs per week 2.518.24 16.9 (9.032.1), total
METs per week 18.25 18.2 (6.750.6); no hypertension 18.2 (10.332.5), hypertension 17.5 (8.836.4).
Additionally, there were some typographical errors in Table 4, column 4 (weighted total in the group of
anti-CCPnegative patients with DMARD use at baseline). The corrected values are as follows: general health
excellent/very good 64, general health good 125, general health fair/poor 55. Finally, there was a
typographical error in Table 1, column 3: the correct 95% confidence interval for the age-adjusted death rate
in the group of anti-CCPpositive patients with no diabetes was 14.022.7.
We regret the errors.
1394 ALSAADI ET AL