A systematic review of sleep disturbance in anxiety and

Prévia do material em texto

Accepted Manuscript
Title: A systematic review of sleep disturbance in anxiety and
related disorders
Author: Rebecca C. Cox Bunmi O. Olatunji
PII: S0887-6185(15)30038-4
DOI: http://dx.doi.org/doi:10.1016/j.janxdis.2015.12.001
Reference: ANXDIS 1789
To appear in: Journal of Anxiety Disorders
Received date: 21-8-2015
Revised date: 20-11-2015
Accepted date: 1-12-2015
Please cite this article as: Cox, Rebecca C., & Olatunji, Bunmi O., A systematic review
of sleep disturbance in anxiety and related disorders.Journal of Anxiety Disorders
http://dx.doi.org/10.1016/j.janxdis.2015.12.001
This is a PDF file of an unedited manuscript that has been accepted for publication.
As a service to our customers we are providing this early version of the manuscript.
The manuscript will undergo copyediting, typesetting, and review of the resulting proof
before it is published in its final form. Please note that during the production process
errors may be discovered which could affect the content, and all legal disclaimers that
apply to the journal pertain.
http://dx.doi.org/doi:10.1016/j.janxdis.2015.12.001
http://dx.doi.org/10.1016/j.janxdis.2015.12.001
Sleep In Anxiety and Related Disorders 1 
 
A Systematic Review of Sleep Disturbance in Anxiety and Related 
Disorders 
 
Running Head: SLEEP IN ANXIETY AND RELATED DISORDERS 
 
Rebecca C. Cox, Bunmi O. Olatunji 
 
Vanderbilt University 
 
Author Note. Correspondence concerning this article should be addressed to Bunmi O. Olatunji, 
Department of Psychology, Vanderbilt University, 301 Wilson Hall, 111 21st Avenue South, Nashville, 
TN 37240, email: olubunmi.o.olatunji@vanderbilt.edu 
 
mailto:olubunmi.o.olatunji@vanderbilt.edu
Sleep In Anxiety and Related Disorders 2 
 
Highlights 
 Sleep disturbance is present in the majority of anxiety and related disorders 
 Sleep disturbance often exacerbates symptom severity 
 Role of sleep disturbance often depends on objective vs subjective assessment 
 Sleep disturbance may contribute to anxiety and related disorders 
 Understanding comorbid sleep and anxiety may have treatment implications 
 
Abstract 
Recent research suggests that sleep disturbance may be a transdiagnostic process, and there is increasing 
interest in examining how sleep disturbance may contribute to anxiety and related disorders. The current 
review summarizes and synthesizes the extant research assessing sleep in anxiety and related disorders. 
The findings suggest that sleep disturbance exacerbates symptom severity in the majority of anxiety and 
related disorders. However, the nature of sleep disturbance often varies as a function of objective versus 
subjective assessment. Although sleep disturbance is a correlate of most anxiety and related disorders, a 
causal role for sleep disturbance is less clear. A model of potential mechanisms by which sleep 
disturbance may confer risk for the development of anxiety and related disorders is discussed. Future 
research integrating findings from basic sleep research with current knowledge of anxiety and related 
disorders may facilitate the development of novel treatments for comorbid sleep disturbance and clinical 
anxiety. 
 
Keywords: Sleep; Anxiety Disorder; Subjective; Objective 
 
Sleep In Anxiety and Related Disorders 3 
 
A Systematic Review of Sleep Disturbance in the Anxiety and Related Disorders 
Sleep is a vital process linked to neural restoration and physiological maintenance across multiple 
systems (Siegel, 2005; Xie et al., 2013). For example, healthy sleep is linked to clearance of metabolic 
waste from the brain (Xie et al., 2013) and enhancement of cognitive function, including the consolidation 
of memory (Diekelmann, 2014; Inostroza & Born, 2013). Conversely, sleep loss is linked to a diverse 
range of adverse effects, including deficits in cognitive function (Goel, Rao, Durmer, & Dinges, 2009; 
Harrison & Horne, 2000) and dysregulation of circadian processes, such as cortisol secretion (Omisade, 
Buxton, & Rusak, 2010; Spiegel, Leproult, & van Cauter, 1999). Further, poor sleep is implicated in 
impaired emotional function (Goldstein & Walker, 2014; Zohar, Tzichinsky, Epstein, & Lavie, 2005), 
including deficits in emotion regulatory abilities (Baum et al., 2014; Mauss, Troy, & LeBourgeois, 2013). 
Likewise, sleep disturbance is highly prevalent in psychopathology, and sleep impairments are found in 
almost every major psychiatric disorder (Benca, Obermeyer, Thisted, & Gillin, 1992). While the majority 
of extant research has focused on impaired sleep in affective disorders (Armitage, 2007; Benca et al., 
1992; Krystal, Thakur, & Roth, 2008), a small body of developing research is addressing the role of sleep 
disturbance in the anxiety and related disorders. 
The present paper aims to review the existing literature on sleep disturbance in the anxiety and 
related disorders, including generalized anxiety disorder (GAD), obsessive-compulsive disorder (OCD), 
panic disorder (PD), phobias, posttraumatic stress disorder (PTSD), and social anxiety disorder (SAD). 
For the purposes of this review, the term “sleep disturbances” will be used to refer to self-reported poor 
sleep quality, clinical insomnia, and/or alterations or deficits in sleep parameters compared to a control 
group. Reviewed studies include those utilizing single sample and controlled comparison methods, as 
well as studies employing subjective and objective measurement of sleep. Additionally, the review 
includes studies of both adult and child samples. This paper will begin with a brief overview of 
definitions regarding the physiology and measurement of sleep, followed by a review of sleep disturbance 
in anxiety and related disorders. The literature review will be followed by a comparison of subjective 
versus objective differences in sleep disturbances, as these methods yield discrepant results in some cases 
and are both critical for the assessment of sleep (Buysse, Ancoli-Israel, Edinger, Lichstein, & Morin, 
2006). Additionally, potential mechanisms by which sleep disturbance may confer risk for the 
development of anxiety and related disorders will be proposed. Finally, treatment implications and future 
directions for the study of sleep disturbance in the anxiety and related disorders will be discussed. 
 
 
 
 
Sleep In Anxiety and Related Disorders 4 
 
1. Sleep Measurement: Terminology and Methods 
 The assessment of sleep can be grouped into two broad categories: objective sleep assessment and 
subjective sleep assessment. While objective assessment offers an unbiased measure of sleep parameters 
and increased precision, subjective measures are also critical for the assessment of sleep disturbance, as 
subjective sleep complaints are linked to dsyregulated emotional processes (Takano, Iijima, & Tanno, 
2012) and are necessary for diagnosing insomnia (Buysse, 2008). 
There have been significant advancements in sleep methodology in recent decades, including 
advances in sleep-related technology and recommendations for standard assessment of sleep and insomnia 
(see Buysse et al., 2006 for a review). The most commonly measured sleep parameters assessed with both 
subjective and objective methods include the following (see Table 1): total sleep time (TST), or amount 
of spent asleep during the night; sleep onset latency (SOL), or the amount of time it takes to fall asleep; 
sleep efficiency (SE), or the percentage of time asleep while in bed; and wake after sleep onset (WASO), 
or the amount of time awake during the night after initiating sleep. Polysomnography, an objective sleep 
methodology, provides data on these indices and also provides information on progression through stages 
of sleep, or sleep architecture (Bastien, 2011). Sleep architecture can be divided into Non-Rapid Eye 
Movement (NREM) sleep and Rapid Eye Movement (REM) sleep. Within NREM sleep, there are 3 
stages ofsleep with increasing delta wave frequency and decreasing alpha wave frequency (Iber, Ancoli-
Israel, Chesson, & Quan, 2007). However, as previous sleep scoring methods included 4 stages of sleep, 
the present paper will include results dividing Stage 3 into Stages 3 and 4 sleep, which were also 
considered slow-wave sleep (SWS). NREM stages and SWS are typically assessed as percentage of time 
spent in each stage during the night. REM sleep is characterized by a mixture of theta and beta waves, 
rapid eye movements, and muscle atonia (Iber et al., 2007). Common REM sleep parameters include 
REM onset latency, or the amount of time before the first REM period, REM percentage, or time spent in 
REM sleep during the night, and REM density, or the frequency of rapid eye movements. 
 
1.1 Objective Sleep Measurement 
 Polysomnography (PSG). PSG is the most comprehensive objective measure of sleep and 
provides data on multiple indices that are used to delineate sleep parameters, including four 
electroencephalogram recordings (EEG) to assess electrical brain activity, vertical and horizontal 
electrooculogram recordings (EOG) to assess eye movements, and electromyogram recordings (EMG) to 
assess muscle tone (Bastien, 2011). PSG is considered the gold-standard method for sleep measurement 
and is the only method that allows for assessment of sleep stages (Bastien, 2011). However, PSG is 
limited by its relative expense, burden to the participant (Miller, Kyle, Melehan, & Bartlett, 2015; Ancoli-
Israel et al., 2003), and lack of ecological validity (Buysse et al., 2006). 
Sleep In Anxiety and Related Disorders 5 
 
 Actigraphy. Actigraphy measures movement using accelerometers typically worn on the wrist 
(Ancoli-Israel et al., 2003). Actigraph data can be scored by hand or by algorithms that differentiate sleep 
from wake (Buysse et al., 2006). Studies indicate that actigraphy correlates highly with PSG (Cellini, 
Buman, McDevitt, Ricker, & Mednick, 2013; Kushida et al., 2001). Further, actigraphy has the advantage 
of allowing for data collection across multiple days in the participants’ natural sleeping environment, is 
relatively inexpensive, and is less invasive than PSG (Ancoli-Israel et al., 2003; Buysse et al., 2006). 
However, actigraph recordings are less reliable at detecting wakefulness compared to PSG (Paquet, 
Kawinska, & Carrier, 2007) and should be used in conjunction with a sleep diary in order to differentiate 
sleep from other times of stillness, such as when watching TV or reading (Buysse et al., 2006). 
 
1.2 Subjective Sleep Measurement 
 Sleep Diary. A sleep diary is a form of experience sampling that captures the subjective 
perception of the previous nights sleep across an extended period of time, typically one week (Carney et 
al., 2012). Sleep diaries typically include self-reported TST, SOL, sleep efficiency, time in bed, WASO, 
and a rating of perceived sleep quality (Buysse et al., 2006), and sleep diaries are considered the gold-
standard for subjective sleep assessment (Carney et al., 2012). Relative to PSG, sleep diaries are more 
ecologically valid and are able to capture sleep data over a longer period of time; however, sleep diaries 
are limited by the inability to verify whether data were actually collected at the indicated times (though 
this problem can be addressed by using electronic sleep diaries) and rely on the participants ability to 
accurately estimate their own sleep (Buysse et al., 2006). 
 Questionnaires. Sleep questionnaires assess global subjective sleep quality and disturbances over 
a specified period of time (Buysse et al., 2006). The two most common sleep questionnaires and those 
recommended for use (Buysse et al., 2006) are the Pittsburgh Sleep Quality Index (PSQI; Buysse, 
Reynolds, Monk, Berman, & Kupfer, 1989) and the Insomnia Severity Index (ISI; Bastien, Vallieres, & 
Morin, 2001). The PSQI is a 19-item self-report measure of broad sleep disturbances over the past month 
and yields 7 component scores (subjective sleep quality, sleep latency, sleep duration, habitual sleep 
efficiency, sleep disturbances, and daytime dysfunction), which are added to create a total score. Scores 
range from 0-21, and a score of 5 or higher indicates poor sleep (Buysse et al., 1989). The ISI is a 7-item 
self-report measure of the perceived severity of insomnia over the past two weeks. Scores range from 0-
28, and a score of 15 or higher indicates clinical insomnia. The ISI also specifies ranges for subthreshold 
insomnia, moderate insomnia, and severe insomnia and can be used to screen for insomnia and as a 
treatment outcome measure (Bastien et al., 2001). 
 Other subjective sleep assessments. Some studies, including studies reviewed here, have 
assessed subjective sleep disturbances by creating composite scores of sleep-related items from other 
Sleep In Anxiety and Related Disorders 6 
 
standardized measures (see Alfano, Ginsburg, & Kingery, 2007 for an example). While these methods 
likely provide useful information about sleep disturbances, the use of standardized questionnaires is 
recommended for maximum reliability and comparability across studies (Buysse et al., 2006). 
 
2. Sleep Disturbance and Anxiety and Related Disorders 
 Sleep disturbance is commonly observed in individuals with anxiety and related disorders 
(Babson & Feldner, 2010; Ramsawh, Stein, Belik, Jacobi, & Sareen, 2009; Roth et al., 2006; Soehner & 
Harvey, 2012), and this link is found in both adults and children (Johnson, Roth, & Breslau, 2006; 
Alfano, Beidel, Turner, & Lewin, 2006; Forbes et al., 2008). Further, sleep problems are included in the 
symptom criteria for posttraumatic stress disorder (PTSD) and generalized anxiety disorder (GAD) 
(American Psychiatric Association, 2013), and recent research suggests that sleep disturbance may predict 
the development of an anxiety disorder (Batterham, Glozier, & Christensen, 2012; Neckelman, Mykletun, 
& Dahl, 2007). In order to better understand the role of sleep disturbance in anxiety and related disorders, 
it is necessary to delineate how sleep may be impaired in each disorder. The following sections critically 
examine the extant literature assessing objective and subjective sleep disturbances in GAD, OCD, PD, 
phobias, PTSD, and SAD. 
 
2.1 Selection of Studies 
 A literature search was conducted using PsycINFO and PubMed utilizing the following search 
terms: sleep and generalized anxiety disorder; sleep and GAD; sleep and obsessive compulsive disorder; 
sleep and OCD; sleep and panic disorder; sleep and phobia; sleep and posttraumatic stress disorder; sleep 
and PTSD; sleep and social anxiety disorder; sleep and SAD; sleep and social phobia. Abstracts from 
these searches were reviewed to identify relevant articles, and a total of 117 articles were included for 
review. Only empirical articles that assessed sleep in one of the specified disorders were included. 
 
3. Generalized Anxiety Disorder 
Objective Sleep. Although a relatively limited body of work has compared the objectively 
measured sleep of individuals with GAD to healthy controls, the existing literature indicates differences 
between these groups on multiple sleep parameters. Compared to healthy controls, those with GAD 
exhibit decreased TST (Arriaga & Paiva, 1991; Papadimitriou, Kerkhofs, Kempanaers, & Mendlewicz, 
1988a) and increased Stage 2% (Arriaga & Paiva, 1991) and time (Papadimitriou, Kerkhofs, Kempanaers, 
& Mendlewicz, 1988a), and evidence of increased SOL is found in both children (Alfano, Reynolds, 
Scott, Dahl, & Mellman, 2013) and adults (Papadimitriou et al., 1988a). Further, one study found 
evidence for increased WASO and decreased Stage 4% in adults with GAD (Arriaga & Paiva, 1991). In 
Sleep In Anxiety and Related Disorders 7 
 
contrast, evidence of diminished sleep efficiency in those with GAD is mixed. While most studieshave 
found no differences in sleep efficiency between those with GAD and healthy controls (Alfano et al., 
2013; Lund et al., 1991; Papadimitriou et al., 1988a), one study indicates decreased sleep efficiency in 
adults with GAD (Arriaga & Paiva, 1991), and one study actually found higher sleep efficiency in GAD 
children compared to healthy controls (Patriquin et al., 2014). 
Similarly, evidence for alterations in REM sleep parameters in GAD is inconclusive. Only one 
study has found evidence for increased REM latency in adults with GAD (Lund, Bech, Eplov, Jennum, & 
Wildschiodtz, 1991). Interestingly, children with GAD evidence decreased REM latency (Alfano et al., 
2013) and fewer REM periods (Patriquin, Mellman, Glaze, & Alfano, 2014). These seemingly discrepant 
findings may be a reflection of the development of sleep regulatory processes, as healthy sleep in 
childhood and adolescence is characterized by increased SWS and REM (Kopasz et al., 2010). As healthy 
adolescents exhibit decreases in SWS and REM sleep during development (Colrain & Baker, 2011), these 
findings of decreased REM latency and REM periods may reflect pathological abnormalities in time spent 
in SWS and REM sleep in children with GAD. Finally, in contrast to the studies reviewed in this section, 
one study comparing children with GAD to healthy controls found no evidence for objective differences 
on any sleep parameters (Alfano, Patriquin, & de los Reyes, 2015). 
 Differences in sleep parameters also distinguish individuals with GAD from those with MDD. 
Consistent differences are observed in REM parameters between GAD and MDD, with considerable 
evidence for increased REM latency in those with GAD (Lund et al., 1991; Papadimitriou et al., 1988a; 
Papadimitriou, Linkowski, Kerkhofs, Kempenaers, & Mendlewicz, 1988b; Reynolds, Shaw, Newton, 
Coble, & Kupfer, 1983; Reynolds et al., 1984). Further, reduced REM percentage, time (Reynolds et al., 
1983; Reynolds et al., 1984), and density (Reynolds et al., 1983; Reynolds et al., 1984) are also found in 
GAD compared to MDD. In addition to differences in REM parameters, those with GAD exhibit 
increased Stage 2 percentage (Reynolds et al., 1983; Reynolds et al., 1984), but fewer nocturnal 
awakenings (Papadimitriou et al., 1988b). Further, in one study comparing individuals with GAD to those 
with insomnia, only increased REM density among those with GAD distinguished the two groups 
(Reynolds et al., 1984), which suggests that the sleep of individuals with GAD is similar to those with 
insomnia. 
Subjective Sleep. As with the work on objective sleep in GAD, several studies have assessed the 
subjective perception of sleep in GAD. Compared to healthy controls, adults with GAD consistently 
report worse subjective sleep (Brenes et al., 2009; Tempesta et al., 2013; Wetherell, Le Roux, & Gatz, 
2003). Similarly, those with GAD are more likely to have a sleep disorder than healthy controls (Berger et 
al., 2009). Further, children with primary GAD also report more subjective sleep complaints compared to 
healthy controls (Alfano et al., 2015). There is also evidence of subjective sleep impairment in primary 
Sleep In Anxiety and Related Disorders 8 
 
GAD compared to other anxiety disorders. For example, among children with an anxiety disorder, sleep 
complaints are most common in primary GAD (Alfano et al., 2006; Alfano et al., 2007), and a higher 
percentage of children with GAD report sleep problems compared to children with SAD or OCD (Alfano, 
Pina, Zerr, & Villalta, 2010). However, one study found no difference in the number of sleep problems 
reported by anxiety-disordered children with and without GAD, although the results indicated that 90% of 
the anxiety-disordered sample reported at least one sleep problem (Chase & Pincus, 2011). In community 
samples of adults, those with GAD have higher odds of sleep disturbance (Marcks, Weisberg, Edelen, & 
Keller, 2010; Roth et al., 2006), and one study found that this relationship was significant after 
controlling for comorbid MDD (Ramsawh et al., 2009). Further, subjective sleep disturbance is linked to 
the development of GAD over time in both adults (Batterham, Glozier, & Christensen, 2012) and children 
(Shanahan, Copeland, Angold, Bondy, & Costello, 2014; Steinsbekk & Wichstrom, 2015), which 
suggests that subjective sleep impairment may contribute to the etiology of GAD. 
 
3.1 Summary Analysis of Sleep Disturbance in GAD 
 Taken together, these findings indicate the presence of sleep disturbance in GAD across objective 
and subjective sleep measures (see Tables 2a and 3a, respectively, for summaries of these studies). 
Objective studies of sleep in those with GAD have found evidence for decreased TST, increased SOL, 
and variations in NREM sleep architecture compared to healthy controls. In contrast, the evidence for 
differences in sleep efficiency and REM parameters among those with GAD compared to healthy controls 
is mixed. However, REM parameters seem to distinguish those with GAD from those with MDD. Studies 
assessing subjective sleep have also found consistent sleep disturbance in GAD compared to healthy 
controls, as well as evidence for increased sleep problems in GAD compared to other anxiety disorders. 
Additionally, subjective sleep disturbance predicts the development of GAD. Future research assessing 
objective sleep disturbance as a contributing factor in GAD would compliment this finding. Despite the 
evidence for both objective and subjective sleep impairment in GAD, limited research has assessed both 
of these parameters together (Alfano et al., 2015). Future research would benefit from utilizing both 
subjective and objective sleep assessment in order to more fully understand how these factors may 
contribute to GAD. Further, although sleep disturbance is included in the symptom criteria for GAD 
(APA, 2013), a relatively small body of research has examined objective sleep disturbance in this 
population, and there is a notable lack of recent research in adults. Finally, although sleep disturbance is 
implicated in GAD, the question of why sleep impairment is present in GAD remains unanswered. 
Additional research is necessary to identify mechanisms that may link GAD and sleep disturbance. 
 
 
Sleep In Anxiety and Related Disorders 9 
 
4. Obsessive-Compulsive Disorder 
 Objective Sleep. The available research suggests that individuals with OCD also exhibit 
alterations in objective sleep parameters. For example, compared to healthy controls, those with OCD 
exhibit significantly reduced TST, an effect found in both adults (Insel et al., 1982; Voderholzer et al., 
2007) and children (Alfano & Kim, 2011; Rapoport et al., 1981). Similarly, individuals with OCD also 
exhibit increased WASO compared to healthy controls (Alfano & Kim, 2011; Hohagen et al., 1994; Insel 
et al., 1982; Voderholzer et al., 2007). Further, reduced sleep efficiency is found in both adults (Hohagen 
et al., 1994; Voderholzer et al., 2007) and children (Rapoport et al., 1981) with OCD. In contrast, one 
study found no evidence for objective differences in sleep variables between adults with and without 
OCD, but did find trends in negative correlations between TST and sleep efficiency and OC symptoms 
(Robinson, Walsleben, Pollack, & Lerner, 1998). 
 A small number of studies have also found differences in the sleep architecture of NREM sleep in 
individuals with OCD. Compared to healthy controls, adults with OCD exhibit increased Stage 1 
percentage and time (Insel et al., 1982) and decreased Stage 4% (Insel et al., 1982) and time (Insel et al., 
1982; Kluge, Schussler, Dresler, Yassouridis, & Steiger, 2007). Further, Insel et al., (1982) found 
evidence of a trend toward a negative correlation between Stage 4 sleep and obsessions. In contrast, one 
study of NREM architecture in children with OCD found decreased Stage 2% and timeand increased 
Stage 4% (Rapoport et al., 1981). However, some studies have found no evidence of NREM sleep 
architecture differences between individuals with OCD and healthy controls (Robinson et al., 1998; 
Voderholzer et al., 2007). 
 There is also evidence for altered REM parameters in individuals with OCD, though the findings 
are mixed. One study found that children with OCD exhibit decreased REM time and latency (Rapoport 
et al., 1981). Similarly, there is also evidence that adults with OCD exhibit decreased REM latency (Insel 
et al., 1982) and higher REM density in the first REM period (Voderholzer et al., 2007). In contrast, other 
studies have found no differences between individuals with OCD and healthy controls on any REM 
parameters (Hohagen et al., 1994; Kluge et al., 2007; Robinson et al., 1998). However, three studies 
found evidence of a link between REM parameters and OC symptoms, including a positive correlation 
between REM density and OC symptoms (Insel et al., 1982; Voderholzer et al., 2007) and increased 
severity of OC symptoms in individuals with OCD with sleep-onset REM periods (Kluge et al., 2007). 
 Finally, few studies have compared the objective sleep of individuals with OCD to that of 
individuals with MDD. One study found increased Stage 1% and time and increased Stage 3% and time 
in those with OCD compared to those with MDD (Insel et al., 1982). However, another study comparing 
these two groups found no differences on any objective sleep parameters (Armitage et al., 1994). 
Sleep In Anxiety and Related Disorders 10 
 
Additional research is necessary to determine whether differences in objective sleep distinguish OCD and 
MDD. 
Subjective Sleep. In contrast to the previous research on objective sleep in OCD, less attention 
has been given to the assessment of subjective sleep in this population. Only one study to date has 
compared the subjective sleep of adults with OCD to healthy controls, and no differences were found 
(Bobdey, Fineberg, Gale, Patel, & Davis, 2002). This study also found that individuals with depression 
and those with comorbid OCD and depression reported comparable sleep that was significantly worse 
than those with OCD without comorbid depression and healthy controls. However, it is worth noting that 
the OCD only group still exceeded the PSQI cutoff for poor sleep, which suggests sleep disturbance in 
this group. Further, the healthy control group also met criteria for poor sleep, which may have masked 
group differences. Similarly, one study utilizing a community sample of adults found an increased 
likelihood of sleep disturbance in those with OCD; however, this association was no longer significant 
after controlling for comorbid mood and substance use disorders (Ramsawh et al., 2009). 
Studies assessing subjective sleep disturbance in children with OCD are also inconclusive. In one 
study comparing children with OCD to healthy controls, both groups of children reported similar sleep 
quality (Alfano & Kim, 2011). However, the number of self-reported sleep problems in children with 
OCD is positively correlated with OC symptom severity (Storch et al., 2008). Further, subjective sleep 
disturbance may play a role in the treatment of OCD in children. Specifically, children who report sleep 
disturbance prior to OCD treatment have worse treatment outcome compared to those without pre-
treatment sleep disturbance, and children who do not respond to CBT are more likely to report a persistent 
sleep problem than children who do respond to CBT (Ivarsson & Skarphedinsson, in press). 
A small, but developing body of literature suggests that adults with OCD report delayed phase 
shifting (Bobdey et al., 2002) and have an increased incidence of comorbid Delayed Sleep Phase Disorder 
(DPSD; Mukhopadhyay et al., 2008; Turner et al., 2007). These findings point to a potential circadian 
rhythm disturbance in OCD (see Nota, Sharkey, & Coles, 2015 for a review). 
 
4.1 Summary Analysis of Sleep Disturbance in OCD 
 Extant research on sleep in OCD has yielded mixed results (see Tables 2b and 3b for summaries 
of these studies). First, previous research has consistently found evidence for decreased TST and 
increased WASO in adults and children with OCD. In conjunction with the finding that reduced TST is 
associated with increased OC symptom severity, these results indicate that short sleep duration may be 
particularly important to the presentation of OCD. In contrast, the evidence for altered REM and NREM 
architecture in OCD is less clear. While multiple studies have found evidence for various differences in 
these parameters, the results are not consistent across studies. Further, limited research has compared 
Sleep In Anxiety and Related Disorders 11 
 
subjective sleep in OCD to that of healthy controls, and the present findings indicate no differences; 
however, subjective sleep disturbance is associated with OCD symptom severity and treatment outcome. 
The null findings on subjective sleep in OCD may be driven in part by the small number of studies 
utilizing subjective sleep assessment. More research is necessary to assess for the presence of subjective 
sleep disturbance in OCD. Further, recent studies have found links between OCD and delayed sleep 
phase, which suggests the presence of circadian rhythm disruption in OCD. Additional research is 
necessary to replicate these findings, particularly in child samples. As with the previous research on 
objective sleep in GAD, the objective findings in OCD are limited by a relative lack of recent research, 
and only one study to date has employed actigraphy in the assessment of sleep in OCD (Alfano & Kim, 
2011). Future research utilizing a multi-method approach that employs both objective and subjective 
assessment is necessary to more fully understand the role of sleep in OCD. 
 
5. Panic Disorder 
Objective Sleep. Individuals with PD consistently exhibit objective sleep disturbance across 
multiple parameters1. Compared to healthy controls, those with PD exhibit increased SOL (Lauer, Krieg, 
Garcia-Borreguero, Ozdaglar, & Holsboer, 1992; Lydiard et al., 1989; Mellman & Uhde, 1989), 
decreased sleep efficiency (Lauer et al., 1992; Lydiard et al., 1989; Mellman & Uhde, 1989; Sloan et al., 
1999), and decreased TST (Mellman & Uhde, 1989; Stein, Enns, & Kryger, 1993). Though less robust, 
some findings also indicate increased Stage 1% (Ferini-Strambi et al., 1996), decreased Stage 2 time 
(Lydiard et al. 1989), increased Stage 2% (Stein et al., 1993), and decreased Stage 3% (Stein et al., 1993) 
and Stage 4% (Sloan et al., 1999; Stein et al., 1993) in those with PD compared to healthy controls. 
Alterations in REM parameters are also found in PD, though the evidence is relatively limited. Some 
studies indicate decreased REM latency (Lauer et al., 1992; Uhde et al., 1984), decreased number of REM 
periods (Mellman & Uhde, 1989), and decreased REM density (Uhde et al., 1984). In contrast to these 
findings, other studies found no differences in the objective sleep of those with PD compared to healthy 
controls (Aikins & Craske, 2008; Dube et al., 1986; Todder & Baune, 2010). 
Subjective Sleep. Although a smaller body of work has assessed subjective sleep in those with 
PD, extant research indicates subjective sleep impairment in this population. Compared to healthy 
controls, individuals with PD report increased sleep disturbance (Hoge et al., 2011; Overbeek, van Diest, 
Schruers, Kruizinga, & Griez, 2005; Todder & Baune, 2010). Further, in a study comparing individuals 
with PD with and without depression and nocturnal panic, significantly more participants in each of the 
four groups reported sleep problems than not (Singareddy, 2009), which indicates the presence of sleep 
 
1 Although nocturnal panic attacks often characterize PD (Craskeet al., 2002), a discussion of nocturnal 
panic attacks is not within the scope of this review. 
Sleep In Anxiety and Related Disorders 12 
 
impairment across multiple subtypes of PD. Further, self-reported sleep disturbance is associated with PD 
in community samples (Ramsawh et al., 2009; Roth et al., 2006) and veterans (Swinkels et al., 2013) and 
predicts the development of PD at a 4-year follow-up in a community sample (Batterham et al., 2012). 
There is also evidence that treatment of PD does not successfully treat comorbid insomnia (Cervena, 
Matousek, Prasko, Brunovsky, & Paskova, 2005), which suggests that sleep disturbance may not merely 
be a secondary symptom of anxiety. Although limited research has attempted to delineate how sleep 
disturbance may contribute to specific dimensions of PD, one study found that increased anxiety 
sensitivity, or fear of sensations related to anxiety due to the perception that these sensations are harmful 
(Olatunji & Wolitzy-Taylor, 2009), was associated with increased SOL among those with PD (Hoge et 
al., 2011). Difficulty initiating sleep may increase anxiety sensitivity by bringing attention to seemingly 
uncontrollable pathological sleep processes in the absence of distractors (i.e., in a dark bedroom), and this 
increase in anxiety sensitivity may then contribute to PD. Alternatively, the increased attendance to 
internal sensations characteristic of anxiety sensitivity may disturb sleep initiation. Additional research is 
needed to clarify this finding and identify other processes that may link sleep disturbance and PD. 
 
5.1 Summary Analysis of Sleep Disturbance in PD 
 Overall, these findings indicate the presence of sleep disturbance in panic disorder (see Tables 2c 
and 3c for summaries of these studies). Specifically, those with PD report increased subjective sleep 
disturbance, and objective studies indicate decreased sleep efficiency and TST and increased SOL, which 
may be due in part to increased anxiety sensitivity. In contrast to the findings on SOL, TST, and sleep 
efficiency, the evidence for alterations in other objective sleep parameters is less consistent. As in GAD 
and OCD, extant research assessing objective sleep in PD is limited by a relative lack of recent work, as 
well as research utilizing actigraphy. Further, few studies of sleep in PD have attempted to move beyond 
characterization to examine why sleep disturbance is implicated in PD. While one study points to a role of 
anxiety sensitivity, future research is necessary to delineate specific mechanisms that may explain the 
relationship between sleep and PD. This question may have important implications for the treatment of 
PD, as the utilization of treatments targeting anxiety sensitivity (Smits, Berry, Tart, & Powers, 2008) may 
improve sleep in those with PD. Likewise, identifying other processes that link sleep and PD may also 
highlight new treatment options for individuals with PD. 
 
6. Phobias 
No study to date has compared the sleep of individuals with a phobia to that of healthy controls. 
In one study comparing objective sleep in depressed individuals with and without a comorbid phobia, no 
differences were found (Clark, Gillin, & Golshan, 1995). However, two studies assessing subjective sleep 
Sleep In Anxiety and Related Disorders 13 
 
disturbance in community samples of adults indicate increased likelihood of sleep disturbance in 
individuals with phobias (Ramsawh et al., 2009; Roth et al., 2006). While little is known about sleep in 
phobias, recent research indicates that sleep may enhance the efficacy of spider phobia treatment. 
Specifically, those who had a night of sleep between exposure therapy sessions exhibited lower heart rate 
and skin conductance response (SCR) to a novel spider, while those who remained awake between two 
same-day sessions exhibited increased SCR to a novel spider (Pace-Schott, Verga, Bennett, & Spencer, 
2012). Further, phobic individuals who slept for 90 minutes following exposure therapy reported 
decreased fear and catastrophic spider-related cognitions in a spider approach task one week later 
compared to those who remained awake following exposure therapy, and both of these changes were 
associated with higher Stage 2% (Kleim et al., 2014). Additionally, Kleim et al. (2014) found that the 
sample of spider phobic individuals exceeded the cut-off for poor sleep quality on the PSQI. Although 
more research is necessary to characterize sleep in those with phobias, these findings offer preliminary 
evidence for sleep disturbance in phobias and suggest that healthy sleep may be important for the 
consolidation of information learned in exposure therapy (see Tables 2d and 3d for summaries of these 
studies). Future research is necessary to assess whether these findings generalize to the treatment of other 
anxiety disorders. 
 
7. Posttraumatic Stress Disorder 
Objective Sleep. Relative to other anxiety-related disorders, PTSD has the largest body of sleep 
research. The most consistent objective finding among those with PTSD is decreased sleep efficiency 
compared to healthy controls (Calhoun et al., 2007; Germain & Nielsen, 2003; Glaubman, Mikulincer, 
Porat, Wasserman, & Birger, 1990; Habukawa, Uchimura, Maeda, Kotorii, & Maeda, 2007; Lipinska, 
Timol, Kaminer, & Thomas, 2014; Mellman, Kumar, Klulick-Bell, Kumar, & Nolan, 19952; Mikulincer, 
Glaubman, Wasserman, Porat, Birger, 1989; Straus, Drummond, Nappi, Jenkins, & Norman, 20153; 
Ulmer, Calhoun, Edinger, Wagner, & Beckham, 2009). Further, compared to healthy controls, those with 
PTSD exhibit decreased TST (Germain, Hall, Shear, Nofzinger, & Buysse, 20064; Straus et al., 2015) and 
increased SOL (Calhoun et al., 2007, Germain et al., 2006; Ulmer et al., 2009; van Liempt et al., 2013). 
Similarly, individuals with PTSD exhibit increased problems with sleep maintenance compared to healthy 
controls, including increased number of awakenings (Germain & Nielsen, 2003; Glaubman et al., 1990; 
Lipinska et al., 2014; Mikulincer et al., 1989; van Liempt, Vermetten, Lentjes, Arends, & Westenberg, 
 
2 Healthy control group were non-combat exposed veterans 
3 PTSD sample was seeking treatment for PTSD-related sleep problems 
4 Germain et al., 2006 reported effect sizes only due to small sample size 
Sleep In Anxiety and Related Disorders 14 
 
20115), increased WASO (Germain & Nielsen, 2003; Glaubman et al., 1990; Ulmer et al., 2009), and 
increased sleep fragmentation (Calhoun et al., 2007; Ulmer et al., 2009). Interestingly, although those 
with PTSD exhibit consistent problems with sleep maintenance, some studies have found higher 
awakening thresholds in those with PTSD compared to healthy controls (Dagan, Lavie, & Bleich, 1991) 
and veterans without PTSD (Lavie, Katz, Pillar, & Zinger, 1998). These findings may indicate that 
individuals with PTSD develop higher awakening thresholds as a compensatory mechanism in response 
to difficulties with sleep maintenance. Future research is necessary to clarify these findings. 
Individuals with PTSD also exhibit differences in sleep architecture compared to healthy controls, 
including increased Stage 2% (Glaubman et al., 1990) and decreased SWS% (Fuller, Waters, & Scott, 
1994; Glaubman et al., 1990; Habukawa et al., 2007; Mikulincer et al., 1989). Further, some studies 
indicate that individuals with PTSD exhibit alterations in REM parameters compared to healthy controls, 
including increased REM latency (Glaubman et al., 1990; Mikulincer et al., 1989), increased REM 
density (Mellman et al., 1995; Ross et al., 19996), decreased REM% (Lipinska et al., 2014; Mikulincer et 
al., 1989), and decreased REM duration (Mellman, Bustamante, Fins, Pigeon, & Nolan, 2002). In 
contrast, one study found evidence for increased REM% in those with PTSD compared to healthy 
controls (Rosset al., 1999). Although the majority of extant research indicates objectively impaired sleep 
in those with PTSD compared to healthy controls, some studies found no differences between these 
groups (Hurwitz, Mahowald, Kuskowski, & Engdahl, 19987; Mellman, Kobayashi, Lavela, Wilson, & 
Brown, 2014), and one study found increased TST in those with PTSD 12 months following a trauma 
(Klein, Koren, Arnon, & Lavie, 2003). 
 In contrast to the relatively consistent evidence of objective sleep disturbance among those with 
PTSD compared to healthy controls, the findings of studies comparing trauma-exposed individuals with 
and without PTSD are mixed. While some studies have found evidence for various differences between 
these groups, including decreased sleep efficiency (Lipinska et al., 2014), increased SOL (van Liempt et 
al., 2013), increased WASO (Lipinska et al., 2014; van Liempt et al., 2011; van Liempt et al., 2013), and 
increased REM density (Ross et al., 1994), a considerable number of studies have found no evidence for 
any objective sleep differences between trauma-exposed individuals with and without PTSD (Cohen et 
al., 2013; Cowdin, Kobayashi, & Mellman, 2014; Dagan, Zinger, & Lavie, 1997; Klein, Koren, Arnon, & 
Lavie, 2002; Kobayashi, Lavela, & Mellman, 2014; Lavie et al., 1998; Mellman, Knorr, Pigeon, Leiter, & 
Akay, 2004; Mellman et al., 2014). Further, some studies have yielded contradictory results. For example, 
while some studies found evidence for increased REM% in those with PTSD compared to trauma-
 
5 Healthy control group included non-combat exposed veterans and civilians 
6 Healthy control sample included two veterans 
7 Healthy control sample were non-combat exposed veterans 
Sleep In Anxiety and Related Disorders 15 
 
exposed controls (Engdahl, Eberly, Hurwitz, Mahowald, & Blake, 2000; Ross et al., 1994; Woodward, 
Murburg, & Bliwise, 20008), one study found decreased REM% in PTSD compared to trauma-exposed 
controls (Lipinska et al., 2014). Similarly, while one study comparing those with PTSD to trauma-
exposed controls found increased REM period duration in those with PTSD (Ross et al., 1994), another 
study found evidence for decreased REM period duration (Mellman, Pigeon, Nowell, & Nolan, 2007). It 
is worth noting that the studies yielding contradictory results used samples with distinct sources of trauma 
exposure. Likewise, several studies that found no differences between those with PTSD and trauma-
exposed controls utilized samples including multiple forms of trauma exposure. It may be the case that 
objective sleep disturbances vary as a function of trauma type, which may mask differences in sleep 
disturbance between those with PTSD and trauma-exposed individuals without PTSD. Future research 
comparing the objective sleep of diverse trauma subtypes may elucidate unique patterns of sleep 
disturbance. 
Subjective Sleep. Studies assessing subjective sleep have found consistent subjective sleep 
impairment in individuals with PTSD. Compared to healthy controls, individuals with PTSD consistently 
report increased sleep disturbance (Calhoun et al., 2007; Germain et al., 2006; Glaubman et al., 1999; 
Klein et al., 2003; Straus et al., 2015; van Liempt et al., 2013; Woodward et al., 2009; van Heughten-van 
der Kloet, Huntjens, Giesbrecht, & Merckelbach, 2014), including increased SOL, decreased sleep 
efficiency (Calhoun et al., 2007; Straus et al., 2015), decreased TST (Calhoun et al., 2007; Hurwitz et al., 
1998; Straus et al., 2015), lower sleep quality (Calhoun et al., 2007), and increased WASO (Straus et al., 
2015; van Liempt et al., 2013). In contrast, one study found no evidence of subjective sleep disturbance in 
those with PTSD compared to healthy controls (Lipinska et al., 2014). 
Similar evidence of subjective sleep disturbance in PTSD has emerged from studies comparing 
veterans with PTSD to veterans without PTSD (Cohen et al., 2013; Engdahl et al., 2000; Lewis, Creamer, 
& Failla, 2009; Pietrzak, Morgan, & Southwick, 2010; Talbot, Neylan, Metzler, & Cohen, 2014), 
including decreased sleep quality, increased SOL, decreased daytime functioning (Lewis et al., 2009; 
Pietrzak et al., 2010), and decreased TST (Lewis et al., 2009) in veterans with PTSD Similarly, although 
one study found no differences between trauma exposed individuals with and without PTSD (Klein et al., 
2002), the majority of research indicates that individuals with PTSD report more subjective sleep 
impairment compared to trauma-exposed controls (Babson, Badour, Feldner, & Bunaciu, 2012; Giosan et 
al., 2015; Klein et al., 2003; Mellman et al., 2007; Meyerhoff, Mon, Metzler, & Neylan, 2014; van 
Liempt et al, 2013), including increased SOL and WASO (van Liempt et al., 2013). Further, in studies of 
community samples of adults, PTSD is associated with an increased likelihood of experiencing sleep 
disturbance (Marcks et al., 2010; Roth et al., 2006). 
 
8 Control group including 10 veterans with trauma exposure and 4 without trauma exposure 
Sleep In Anxiety and Related Disorders 16 
 
 Studies assessing the role of sleep disturbance in PTSD indicate that subjective sleep impairment 
may exacerbate the disorder. For example, several studies found that increased sleep disturbance was 
associated with increased PTSD symptom severity in those with PTSD (Belleville, Guay, & Marchand, 
2009; Casement, Harrington, Miller, & Resick, 2012; Fairholme et al., 2013; Germain, Buysse, Shear, 
Fayyad, & Austin, 2004), veterans (Lang, Veazey-Morris, & Andrasik, 2014; Pietrzak et al., 2010; 
Plumb, Peachey, & Zelman, 2013), and trauma-exposed individuals (Giosan et al., 2015; Krakow et al., 
2001; Krakow et al., 2004; Kuroda, Wada, Takeuchi, & Harada, 2013). 
Further, pre-trauma sleep disturbance may contribute to the development of PTSD. In veterans, 
pre-deployment sleep problems are linked to an increased likelihood of developing PTSD post-
deployment (Gehrman et al., 2013) and predict PTSD at two years post-deployment (Koffel, Polusny, 
Arbisi, & Erbes, 2013). Similarly, in trauma-exposed individuals, subjective sleep disturbance at time one 
predicts PTSD symptom severity at follow-up (Brown, Mellman, Alfano, & Weems, 2011; Garthus-
Niegel, Ayers, von Soest, Torgersen, & Eberhard-Gran, 2015; Gerhart, Hall, Russ, Canetti, & Hobfoll, 
2014). Interestingly, one study of automobile accident survivors found that those with and without PTSD 
at a 12-month follow up reported comparable sleep disturbance one week following the accident, but only 
those who would go on to develop PTSD reported continued sleep disturbance in the months following 
the accident (Klein et al., 2003). This finding suggests that persistent sleep impairment following trauma 
may contribute to the development of PTSD. 
Sleep disturbance has also been implicated as a mediator of the association between various 
psychological processes and PTSD symptoms. For example, in veterans, self-reported sleep disturbances 
mediate the relationship between rumination and PTSD symptoms (Borders, Rothman, & McAndrew, 
2015) and combat stressors and PTSD symptoms (Picchioni et al., 2010). These findings suggest that 
sleep disturbance may amplify the effects of factors that increase the likelihood of developing PTSD and 
suggest that targeting sleep disturbance following a stressor may be a effective intervention strategy. 
Finally, sleep disturbance is linked to PTSD treatment. Sleep disturbances often persist following 
treatment for PTSD (Belleville, Guay, & Marchand, 2011; Zayfert & DeViva, 2004), and residual sleep 
problems are linked to increased severity of post-treatment PTSD symptoms (Belleville et al., 2011) and 
decreased likelihood of remission (Marcks et al., 2010). 
 
7.1 Summary Analysis of Sleep Disturbance in PTSDThe respective literatures on objective and subjective sleep have established the presence of sleep 
disturbance in PTSD (see Tables 2e and 3e, respectively, for summaries of these studies). Studies 
assessing objective sleep indicate particular disturbances in sleep efficiency and sleep maintenance among 
those with PTSD, as well as shorter TST and increased SOL. Further, several studies indicate various 
Sleep In Anxiety and Related Disorders 17 
 
alterations in REM parameters among those with PTSD compared to healthy controls. While a relatively 
small number of studies have yielded null findings, the majority of extant research comparing those with 
PTSD to healthy controls indicates objective sleep disturbance across multiple sleep parameters. 
In contrast, the findings from studies comparing individuals with PTSD to trauma-exposed 
controls are mixed and preclude any conclusion on the role of sleep disturbance in trauma exposure 
broadly. However, as noted, these discrepant findings may be a function of studies utilizing samples with 
diverse trauma exposure, which may have differential effects on sleep. Given that individuals with PTSD 
report more sleep disturbance than their trauma-exposed counterparts, specific differences in objective 
sleep parameters may be masked by these mixed samples and efforts to compare studies utilizing samples 
with distinct forms of trauma exposure. These inconclusive results indicate a need for additional research 
comparing objective sleep between trauma-exposed individuals with and without PTSD that have been 
exposed to the same type of trauma, as well as studies that group samples by trauma type. 
Studies assessing subjective sleep have found robust evidence for subjective sleep disturbances in 
PTSD. Further, subjective sleep impairment is linked to PTSD symptom severity, and baseline sleep 
problems may contribute to the development of PTSD following a trauma. Further, residual sleep 
disturbances following PTSD treatment are linked to diminished treatment efficacy. Taken together, these 
findings indicate that subjective sleep disturbances play a critical role in the development, maintenance, 
and treatment of PTSD and indicate a particular need to address sleep problems in the treatment of PTSD. 
Further, these results suggest that healthy sleep may function as a protective factor against developing 
PTSD following trauma. Additional research is necessary to examine how healthy sleep may be utilized 
as a preventative measure against PTSD. 
Interestingly, while the majority of research comparing the sleep of those with PTSD to trauma-
exposed controls has found inconclusive evidence for objective differences, studies assessing subjective 
sleep indicate that individuals with PTSD report more sleep impairment than their trauma-exposed 
counterparts. In addition to the proposed function of mixed trauma samples, this discrepancy may also 
indicate an important role of sleep quality appraisal in PTSD. For example, it may be the case that 
individuals who perceive their sleep as more disturbed may be more likely to develop PTSD compared to 
trauma-exposed individuals who do not perceive a disturbance in sleep. Similar to the findings linking 
anxiety sensitivity and SOL in PD, increased attendance to perceived pathological processes may increase 
anxiety symptoms and contribute to PTSD. Future research is necessary to better understand the role of 
perceived sleep disturbance in PTSD. 
Finally, while some authors have suggested that individuals with PTSD may subjectively 
overestimate sleep disturbance, the results of studies utilizing both objective and subjective sleep 
assessments have found evidence for both objective and subjective sleep disturbance in those with PTSD 
Sleep In Anxiety and Related Disorders 18 
 
compared to healthy controls, which offers objective support for the subjective sleep complaints indicated 
by those with PTSD. It is worth noting that some studies suggesting a lack of objective sleep disturbance 
in PTSD utilized veterans without PTSD as the control group, which may mask the differences in 
objective sleep indicated by studies comparing those with PTSD to healthy controls. Additional research 
is necessary to further examine differences between objective and subjective sleep in those with PTSD, 
trauma-exposed controls, and healthy controls. 
 
8. Social Anxiety Disorder 
Objective Sleep. Only one study to date has objectively assessed the sleep of adults with SAD, 
and results revealed comparable sleep to that of healthy controls (Brown, Black, & Uhde, 1994). 
Likewise, the only study to date comparing objective sleep in adolescents with SAD to healthy controls 
also found no significant differences (Mesa, Beidel, & Bunnell, 2014). Additional research is necessary to 
replicate these findings in both children and adults. 
Subjective Sleep. There is also limited research assessing subjective sleep in SAD, and the 
available findings are mixed. While one study comparing the subjective sleep of those with SAD to 
healthy controls found worse subjective sleep in SAD (Stein, Kroft, & Walker, 1993), this finding is not 
consistent (Brown et al., 1994; Mesa et al., 2014). However, the presence of SAD is associated with an 
increased likelihood of sleep disturbance (Ramsawh et al., 2009; Roth et al., 2006), and individuals with 
SAD exceed PSQI criteria for being poor sleepers (Zalta et al., 2013). Further, self-reported sleep 
impairment is associated with symptoms of social anxiety in those with SAD (Raffray, Bond, & Pelissolo, 
2011) and healthy samples (Buckner, Bernert, Cromer, Joiner, & Schmidt, 2008; Cheng et al., 2015). 
Insomnia is also linked to the development of SAD in children, and children with insomnia at age 4 have 
an increased likelihood of developing SAD at age 6 (Steinsbekk & Wichstrom, 2015). Further, sleep 
disturbance may diminish the effects of CBT for those with SAD. Indeed, a recent study found that 
increased self-reported sleep disturbance at baseline predicted worse treatment outcome, while individuals 
who reported restful sleep following a treatment session exhibited decreased SAD symptoms at the 
subsequent session (Zalta et al., 2013). 
 
8.1 Summary Analysis of Sleep Disturbance in SAD 
 The limited extant research on sleep in SAD has yielded mixed results (see Tables 2f and 3f for 
summaries of these studies). While no evidence has been found for the presence of objective sleep 
disturbance in SAD, a small body of research indicates a link between subjective sleep problems and 
social anxiety symptoms. Despite this link, current understanding of the role of sleep in SAD is limited by 
a lack of studies comparing the sleep of those with SAD to healthy controls. Future research comparing 
Sleep In Anxiety and Related Disorders 19 
 
the objective and subjective sleep of individuals with SAD to that of healthy controls is necessary to 
characterize sleep in SAD. Further, although extant research points to a role of sleep disturbance in the 
development and treatment of SAD, more research is needed to replicate these findings. 
 
9. The Role of Comorbid MDD 
Given the high prevalence of sleep disturbance among those with MDD (Soehner, Kaplan, & 
Harvey, 2014) and the high rates of comorbidity between MDD and the anxiety-related disorders (Kessler 
et al., 2003), it is important to consider whether the evidence of sleep disturbance in the anxiety-related 
disorders may be due to comorbid MDD. The number of studies utilizing pure-disorder samples versus 
samples with comorbid MDD were equivalent for GAD, OCD, and PD, while more studies in the PTSD 
and SAD sections utilized samples with comorbid MDD. As stated in the phobia section, no study to date 
compared sleep in phobia-only individuals to that of healthy controls. However, it important to note that 
across all the anxiety-relateddisorders reviewed here, there were comparable numbers of positive and 
negative results between studies utilizing pure disorder samples and samples with comorbid MDD (see 
Tables 2 and 3 for the comorbid MDD status of each study). The roughly equivalent distribution of results 
between these samples suggests that the evidence for sleep disturbance in the anxiety-related disorders is 
not entirely due to comorbid MDD. 
 
10. A Critical Analysis of Sleep Disturbance in Anxiety and Related Disorders 
 The findings of the studies reviewed here indicate a strong role of sleep disturbance in anxiety 
and related disorders. Further, for the majority of these disorders, including GAD, PD, and PTSD, there is 
considerable evidence for both subjective and objective sleep disturbances compared to healthy controls, 
such as decreased TST and sleep efficiency and increased SOL and WASO. The congruence of the 
findings between objective and subjective measures suggests that the sleep disturbance reported by those 
with GAD, PD, and PTSD is not likely due to misperception or underestimation of sleep quality. 
In contrast, extant research has found evidence for objective, but not subjective sleep disturbance 
in those with OCD. It may be the case that those with OCD overestimate their sleep quality, while 
objective assessments indicate less healthy sleep than that of controls. Likewise, there is no evidence for 
objective sleep disturbance in phobias or SAD compared to healthy controls and limited evidence for 
subjective sleep disturbances. However, relatively few studies have examined sleep disturbance in SAD 
and phobias or subjective sleep disturbances in OCD. The current dearth of support for sleep disturbances 
in these groups may be a function of the relative lack of existing research. 
Although the articles reviewed here indicate subjective and objective sleep disturbance in GAD, 
PD, and PTSD and objective sleep disturbance in OCD, the evidence for alterations of REM parameters 
Sleep In Anxiety and Related Disorders 20 
 
in anxiety and related disorders is mixed. Studies assessing REM sleep parameters in those with PTSD, 
OCD, and PD have found inconsistent results, and although some studies indicate alterations in REM 
latency in GAD, this literature is limited. Similarly, there is inconsistent and limited evidence for 
variations in NREM sleep architecture parameters. It may be the case that those with anxiety and related 
disorders exhibit disturbances in sleep quality parameters, such as TST and SOL, while sleep architecture 
remains relatively normal. More research is necessary to determine whether those with anxiety and 
related disorders exhibit altered NREM and REM sleep architecture compared to healthy controls. 
 
10.1 Sleep Disturbance as a Cause or Consequence of Anxiety and Related Disorders 
 The results of the studies reviewed here establish the presence of sleep disturbance in the majority 
of the anxiety and related disorders. However, the question remains as to why sleep disturbance is present 
in these disorders. While sleep problems have typically been conceptualized as a symptom of anxiety and 
related disorders (Harvey, 2008; Spoormaker & Montgomery, 2008), recent research indicates that sleep 
disturbance may precede and predict the development of these disorders in some cases (Gregory et al., 
2005). Similarly, sleep disturbance has been implicated as a transdiagnostic factor due to the interplay 
between sleep and neurophysiological processes associated with emotional function (Harvey, Murray, 
Chandler, & Soehner, 2011). However, despite the robust link between sleep disturbance and anxiety and 
related disorders, as well as the proposal of sleep as a transdiagnostic process, potential mechanisms that 
may explain why sleep disturbance predicts the development of anxiety and related disorders are lacking. 
A large body of research has established that sleep loss results in impaired executive function 
(Harrison and Horne, 2000; Nilsson et al., 2005), including deficits in inhibition (Drummond, Paulus, & 
Tapert, 2006), attention (Drummond, Gillin, & Brown, 2001), and memory (Goel et al., 2009). Further, 
one night of sleep deprivation leads to increased amygdala response to a negative stimulus and decreased 
functional connectivity between the amygdala and the medial-prefrontal cortex (Yoo et al., 2008). It may 
be the case that the decreased activation of and functional connectivity within brain regions associated 
with executive function observed following sleep loss (Ma et al., 2015, Verweij et al., 2014) may 
contribute to a diminished ability to inhibit or regulate anxiety-related processes, such as maladaptive 
repetitive thought (i.e., worry, rumination, and obsessions) and attentional biases. Indeed, impaired 
executive function is linked to repetitive thought (Segerstrom, Roach, Evans, Schipper, & Darville, 2010) 
and attentional and inhibitory deficits are found in individuals with anxiety and related disorders 
characterized by repetitive thought, such as GAD (Olatunji, Ciesielski, Armstrong, Zhao, & Zald, 2011), 
PTSD (Aupperle, Melrose, Stein, & Paulus, 2012; Olatunji, Armstrong, McHugo, & Zald, 2013), and 
OCD (Snyder, Kaiser, Warren, & Heller, 2015). Moreover, a growing body of research has highlighted 
the importance of sleep in emotional learning and memory (Goldstein & Walker, 2014; Vanderkerckhove 
Sleep In Anxiety and Related Disorders 21 
 
& Cluydts, 2010), including enhanced fear conditioning (Menz et al., 2013) and fear extinction 
(Spoormaker et al., 2012) and consolidation of emotional memory (Nishida, Pearsall, Buckner, & Walker, 
2009; Payne et al., 2012). Taken together, these findings highlight the importance of sleep for cognitive 
function and suggest that impaired executive function may be one mechanism by which sleep disturbance 
contributes to the development of an anxiety-related disorder. That is, sleep loss may impair executive 
function, which may then diminish the ability to regulate or inhibit symptoms of anxiety. Consistent with 
this view, a recent study found that decreased executive function accounted for the relationship between 
sleep disturbance and maladaptive repetitive thought, including worry and rumination, even when general 
distress was included in the model (Cox & Olatunji, in press). This finding highlights impaired executive 
function as a potential mechanism that may further elucidate the pathway between sleep and anxiety. 
Dysregulated cortisol may be another mechanism that links sleep disturbance to anxiety and 
related disorders. Previous research has established the circadian rhythm of cortisol: a steep increase upon 
morning awakening (the cortisol awakening response or CAR) followed by a gradual decline across the 
day and a nadir during sleep (Omisade et al., 2010; Spiegel et al., 1999). In healthy individuals, cortisol 
levels increase in response to an acute stressor (Dickerson & Kemeny, 2004). However, poor sleep can 
alter these patterns, and decreased sleep quality and quantity are implicated in dysregulated diurnal 
cortisol, including a blunted CAR, elevated evening cortisol levels (Omisade et al., 2010), and blunted 
cortisol reactivity to stressors (Wright et al., 2007). Further, dysregulated diurnal cortisol is also 
associated with deficits in executive function (Stawski et al., 2007), and elevated cortisol is linked to 
impaired inhibition (Gomez et al., 2009) and memory (Buss, Wolf, Witt, & Hellhammer, 2004). Similar 
patterns of dysregulated cortisol are found in those with an anxiety-related disorder. For example, 
compared to healthy controls, individuals with GAD exhibit a blunted CAR (Hek et al., 2013) and higher 
total cortisol output (Mantella et al., 2008), and individuals with OCD exhibit elevated overnight cortisol 
secretion (Kluge et al., 2007) and blunted cortisol reactivity to stressors(Gustafsson, Gustafsson, 
Ivarsson, & Nelson, 2008). These findings suggest that sleep disturbance leads to dysregulated diurnal 
cortisol, which may result in elevated physiological arousal in the absence of an objective stressor 
(Abercrombie, Kalin, & Davidson, 2005), and deficits in cortisol reactivity to stressors, which may result 
in an inability to mount an adaptive response to stressful events (McEwen, 1998). Over time, the 
downstream effects of dysregulated cortisol due to sleep disturbance may contribute to the development 
of an anxiety-related disorder. 
Recent research suggests that chronic sleep disturbance may constitute a stressor that contributes 
to allostatic overload, or bodily wear and tear due to an imbalance of physiological processes in which 
pathophysiology can occur (McEwen, 2015). Dysregulated cortisol and impaired neurocognitive function 
are two known consequences of allostatic overload that can contribute to the development of 
Sleep In Anxiety and Related Disorders 22 
 
physiological and psychological disorders over repeated exposure to stress (McEwen, 2015). Considering 
the links between sleep disturbance, cortisol, executive function, and anxiety-related disorders, 
dysregulated cortisol and impaired executive function may be two neurophysiological mechanisms that 
may mediate the relationship between acute sleep disturbance and symptoms of anxiety (see Figure 1). 
Over time, chronic sleep disturbance may contribute to the development of an anxiety-related disorder 
through repeated disruption in these psychobiological processes, i.e., allostatic overload (see Figure 2). 
 
11. Conclusions: Treatment Implications and Future Directions 
 The extant literature on the role of sleep in anxiety and related disorders indicates objective and 
subjective sleep disturbance in GAD, PTSD, and PD, objective sleep disturbance in OCD, and a potential 
role of sleep disturbance in SAD and phobias. Additional research is necessary to more thoroughly test 
for the presence of sleep disturbance in SAD and phobias, as well as examine the role of subjective sleep 
disturbance in OCD. Further, future research utilizing both subjective and objective sleep measurements 
is necessary across the anxiety and related disorders, as extant research has primarily relied on single-
measure methodology. Such research will be critical for testing for discrepancies between the perception 
of sleep and objective sleep physiology, as well as identifying particular symptoms of sleep disturbance 
that may characterize specific anxiety processes and/or disorders. Additionally, researchers should utilize 
standardized self-report measures instead of relying on composite scores of various sleep-related items 
from depression or anxiety scales, as the use of standard methods will enhance internal validity and 
improve comparability across studies (Buysse et al., 2006). 
 Having established the presence of sleep disturbance in anxiety and related disorders, the next 
step for programmatic research is to delineate specific mechanisms that account for this relationship. 
Basic sleep research has defined multiple adverse effects of sleep loss, including impaired executive 
function and dysregulated cortisol secretion. It is critical that the study of sleep disturbance in the anxiety 
and related disorders begins to integrate findings from basic sleep research to test for specific mechanisms 
that may link sleep disturbance to the development of an anxiety-related disorder. Further, given the 
negative impact of anxiety on sleep quality (Harvey, 2002; Yeh, Wung, & Lin, 2015), future research 
should assess the role of sleep disturbance as a maintenance factor in anxiety and related disorders, as 
sleep disturbance due to anxiety processes may further exacerbate and sustain the adverse downstream 
effects of sleep loss and increase anxiety symptom severity. Indeed, research indicates that sleep 
disturbance is linked to increased symptom severity in PTSD (Belleville et al., 2009; Casement et al., 
2012; Fairholme et al., 2013; Germain et al., 2004) and OCD (Storch et al., 2000), which suggests that the 
negative effects of sleep loss may exacerbate symptoms of anxiety and related disorders. 
Sleep In Anxiety and Related Disorders 23 
 
Sleep disturbance may also diminish treatment efficacy, and recent research indicates that sleep 
disturbance is linked to worse treatment outcome in PTSD (Belleville et al., 2011; Zayfert & DeViva, 
2004, OCD (Ivarsson & Skarphedinsson, 2015), and SAD (Zalta et al., 2013). These findings suggest that 
addressing sleep problems in the treatment of anxiety and related disorders may enhance treatment 
efficacy. Research assessing the effects of cognitive behavioral therapy for insomnia (CBT-I) on 
comorbid anxiety indicates treating sleep disturbance has only a moderate effect on the reduction of 
anxiety (Belleville, Cousineau, Levrier, St-Pierre-Delorme, 2011). Additional research is necessary to 
examine how addressing sleep disturbance may enhance the efficacy of CBT for anxiety and related 
disorders. It may be the case that a stepwise treatment approach is more effective than a concurrent 
approach. That is, treating sleep disturbance prior to addressing the disorder may be more efficacious than 
attempting to treat these problems simultaneously. Similarly, given the accumulating evidence for an 
important role of sleep in emotional learning and memory (Goldstein & Walker, 2014), including 
enhanced therapeutic effects (Kleim et al., 2014; Pace-Schott et al., 2012), improving sleep health prior to 
treating an anxiety or related disorder and including an opportunity for sleep following intervention may 
bolster cognitive processes critical to the consolidation and maintenance of therapeutic benefits. Future 
research is necessary to examine how addressing sleep disturbance and utilizing healthy sleep may 
improve the treatment of anxiety and related disorders. 
 Extant research has established a role of sleep disturbance in the majority of anxiety and related 
disorders. Future research synthesizing these findings with basic research on the adverse effects of sleep 
loss is necessary to identify specific mechanisms that may link sleep disturbance to the development and 
maintenance of anxiety and related disorders. Examination of mechanisms, such as impaired executive 
function and dysregulated cortisol, by which sleep disturbance may increase the likelihood of developing 
an anxiety-related disorder will be critical in developing an integrated biopsychological model that may 
then inform efficacious treatment of anxiety and related disorders. 
 
Acknowledgment 
The authors would like to thank Eliza Kramer for her assistance with the preparation of this paper. 
 
Sleep In Anxiety and Related Disorders 24 
 
References 
*indicates reviewed article 
Abercrombie, H.C., Kalin, N.H., & Davidson, R.J. (2005). Acute cortisol elevations cause heightened 
arousal ratings of objectively nonarousing stimuli. Emotion, 5, 354-359. 
http://dx.doi.org/10.1037/1528-3542.5.3.354 
*Aikins, D.E. & Craske, M.G. (2008). Sleep-based heart period variability in panic disorder with and 
without nocturnal panic attacks. Journal of Anxiety Disorders, 22, 453-463. 
http://dx.doi.org/10.1016/j.janxdis.2007.03.010 
*Alfano, C.A., Beidel, D.C., Turner, S.M., & Lewin, D.S. (2006). Preliminary evidence for sleep 
complaints among children referred for anxiety. Sleep Medicine, 7, 467-473. 
http://dx.doi.org/10.1016/j.sleep.2006.05.002 
*Alfano, C.A., Ginsburg, G.S., & Kingery, J.N. (2007). Sleep-related problems among children and 
adolescents with anxiety disorders. Journal of the American Academy of Child and Adolescent 
Psychiatry, 46, 224-232. http://dx.doi.org/10.1097/01.chi.0000242233.06011.8e 
*Alfano, C.A., Pina, A.A., Zerr, A.A., & Villalta, I.K. (2010). Pre-sleep arousal and sleepproblems of 
anxiety-disordered youth. Child Psychiatry and Human Development, 41, 156-167. 
http://dx.doi.org/10.1007/s10578-009-0158-5 
*Alfano, C.A. & Kim, K.L. (2011). Objective sleep patterns and severity of symptoms in pediatric 
obsessive compulsive disorder: A pilot investigation. Journal of Anxiety Disorders, 25, 835-839. 
http://dx.doi.org/10.1016/j.janxdis.2011.04.004 
*Alfano, C.A., Reynolds, K., Scott, N., Dahl, R.E., & Mellman, T.A. (2013). Polysomnographic sleep 
patterns of non-depressed, non-medicated children with generalized anxiety disorder. Journal of 
Affective Disorders, 147, 379-384. http://dx.doi.org/10.1016/j.jad.2012.08.015 
*Alfano, C.A., Patriquin, M.A., & de los Reyes, A. (2015). Subjective-objective sleep comparisons and 
discrepancies among clinically-anxious and healthy children. Journal of Abnormal Child 
Psychology. http://dx.doi.org/10.1007/s10802-015-0018-7 
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). 
Washington, DC: Author. 
Ancoli-Israel, S., Cole R, Alessi C., Chambers, M., Moorcroft, W., & Pollak, C.P. (2003). The role of 
actigraphy in the study of sleep and circadian rhythms. SLEEP, 26, 342-92. 
*Armitage, R., Debus, J., Kiger, B., Trivedi, M., Cain, J., Roffwarg, H. P., and Rush, A. J. (1994). 
Polysomnogram in major depressive and obsessive-compulsive disorders: A preliminary study. 
Depression, 2, 297-302. http://dx.doi.org/10.1002/depr.3050020604 
http://dx.doi.org/10.1037/1528-3542.5.3.354
http://dx.doi.org/10.1002/depr.3050020604
Sleep In Anxiety and Related Disorders 25 
 
Armitage, R. (2007). Sleep and circadian rhythms in mood disorders. Acta Psychiatrica Scandinavica, 
115, 104-115. http://dx.doi.org/10.1111/j.1600-0447.2007.00968.x 
*Arriaga, F. & Paiva, T. (1991). Clinical and EEG sleep changes in primary dysthymia and generalized 
anxiety: A comparison with normal controls. Neuropsychobiology, 24, 109-114. 
Aupperle, R.L., Melrose, A.J., Stein, M.B., & Paulus, M.P. (2012). Executive function and PTSD: 
Disengaging from trauma. Neuropharmacology, 62, 686-694. 
http://dx.doi.org/10.1016/j.neuropharm.2011.02.008 
Babson, K.A. & Feldner, M.T. (2010). Temporal relations between sleep problems and both traumatic 
event exposure and PTSD: A critical review of the empirical literature. Journal of Anxiety 
Disorders, 24, 1-15. http://dx.doi.org/10.1016/j.janxdis.2009.08.002 
*Babson, K.A., Badour, C.L., Feldner, M.T., & Bunaciu, L. (2012). The relationship of sleep quality and 
PTSD to anxious reactivity from idiographic traumatic event script-driven imagery. Journal of 
Traumatic Stress, 25, 503-510. http://dx.doi.org/10.1002/jts.21739 
Bastien, C.H., Vallieres, A., & Morin, C.M. (2001). Validation of the Insomnia Severity Index as an 
outcome measure for insomnia research. Sleep Medicine, 2, 297-307. 
http://dx.doi.org/10.1016/s1389-9457(00)00065-4 
Bastien, C.H. (2011). Insomnia: Neurophysiological and neuropsychological 
approaches. Neuropsychology Review, 21, 22-40. http://dx.doi.org/10.1007/s11065-011-9160-3 
*Batterham, P.J., Glozier, N., & Christensen, H. (2012). Sleep disturbance, personality and the onset of 
depression and anxiety: Prospective cohort study. Australian and New Zealand Journal of 
Psychiatry, 46, 1089-1098. http://dx.doi.org/10.1177/0004867412457997 
Baum, K.T., Desai, A., Field, J., Miller, L.E., Rausch, J., & Beebe, D.W. (2014). Sleep restriction 
worsens mood and emotion regulation in adolescents. Journal of Child Psychology and 
Psychiatry, 55, 180-190. http://dx.doi.org/10.1111/jcpp.12125 
*Belleville, G., Guay, S., & Marchand, A. (2009). Impact of sleep disturbances on PTSD symptoms and 
perceived health. The Journal of Nervous and Mental Disease, 197, 126-132. 
http://dx.doi.org/10.1097/nmd.0b013e3181961d8e 
Belleville, G., Cousineau, H., Levrier, K., & St-Pierre-Delorme, M.E. (2011). Meta-analytic review of the 
impact of cognitive-behavior therapy for insomnia on concomitant anxiety. Clinical Psychology 
Review, 31, 638-652. http://dx.doi.org/10.1016/j.cpr.2011.02.004 
*Belleville, G., Guay, S., & Marchand, A. (2011). Persistence of sleep disturbances following cognitive-
behavior therapy for posttraumatic stress disorder. Journal of Psychosomatic Research, 70, 318-
327. http://dx.doi.org/10.1016/j.jpsychores.2010.09.022 
http://dx.doi.org/10.1016/j.janxdis.2009.08.002
Sleep In Anxiety and Related Disorders 26 
 
Benca, R.M., Obermeyer, W.H., Thisted, R.A., & Gillin, J.C. (1992). Sleep and psychiatric disorders: A 
meta-analysis. Archives of General Psychiatry, 49, 651-668. 
http://dx.doi.org/10.1001/archpsyc.1992.01820080059010 
*Berger, A., Dukes, E., Wittchen, H.U., Morlock, R., Edelsberg, J., & Oster, G. (2009). Patterns of 
healthcare utilization in patients with generalized anxiety disorder in general practice in 
Germany. European Journal of Psychiatry, 23, 90-100. http://dx.doi.org/10.4321/s0213-
61632009000200003 
*Bobdey, M., Fineberg, N., Gale, T.M., Patel, A., & Davis, H.A. (2002). Reported sleep patterns in 
obsessive compulsive disorder (OCD). International Journal of Psychiatry in Clinical Practice, 
6, 15-21. http://dx.doi.org/10.1080/136515002753489371 
*Borders, A., Rothman, D.J., & McAndrew, L.M. (2015). Sleep problems may mediate associations 
between rumination and PTSD and depressive symptoms among OIF/OEF veterans. 
Psychological Trauma: Theory, Research, Practice, and Policy, 7, 76-84. 
http://dx.doi.org/10.1037/a0036937 
*Brenes, G.A., Miller, M.E., Stanley, M.A., Williamson, J.D., Knudson, M., & McCall, W.V. (2009). 
Insomnia in older adults with generalized anxiety disorder. The American Journal of Geriatric 
Psychiatry, 17, 465-472. http://dx.doi.org/10.1097/jgp.0b013e3181987747 
*Brown, T.M., Black, B., & Uhde, T.W. (1994). The sleep architecture of social phobia. Biological 
Psychiatry, 35, 420-421. http://dx.doi.org/10.1016/0006-3223(94)90009-4 
*Brown, T.H., Mellman, T.A., Alfano, C.A., & Weems, C.F. (2011). Sleep fears, sleep disturbance, and 
PTSD symptoms in minority youth exposed to Hurricane Katrina. Journal of Traumatic Stress, 
24, 575-580. http://dx.doi.org/10.1002/jts.20680 
*Buckner, J.D., Bernert, R.A., Cromer, K.R., Joiner, T.E., & Schmidt, N.B. (2008). Social anxiety and 
insomnia: The mediating role of depressive symptoms. Depression and Anxiety, 25, 124-130. 
http://dx.doi.org/10.1002/da.20282 
Buss, C., Wolf, O.T., Witt, J., & Hellhammer, D.H. (2004). Autobiographic memory impairment 
following acute cortisol administration. Psychoneuroendocrinology, 29, 1093-1096. 
http://dx.doi.org/10.1016/j.psyneuen.2003.09.006 
Buysse, D.J., Reynolds, C.F., Monk, T.H., Berman, S.R., & Kupfer, D.J. (1989). The Pittsburgh Sleep 
Quality Index: A new instrument for psychiatric practice and research. Psychiatry Research, 28, 
193-213. http://dx.doi.org/10.1016/0165-1781(89)90047-4 
Buysse, D.J., Ancoli-Israel, S., Edinger, J.D., Lichstein, K.L., & Morin, C.M. (2006). Recommendations 
for a standard research assessment of insomnia. SLEEP, 29, 1155-1173. 
http://dx.doi.org/10.1080/136515002753489371
Sleep In Anxiety and Related Disorders 27 
 
Buysse, D.J. (2008). Chronic insomnia. American Journal of Psychiatry, 165, 678-686. 
http://dx.doi.org/10.1176/appi.ajp.2008.08010129 
*Calhoun, P.S., Wiley, M., Dennis, M.F., Means, M.K., Edinger, J.D., & Beckham, J.C. (2007). 
Objective evidence of sleep disturbance in women with posttraumatic stress disorder. Journal of 
Traumatic Stress, 20, 1009-1018. http://dx.doi.org/10.1002/jts.20255 
Carney, C.E., Buysse, D.J., Ancoli-Israel, S., Edinger, J.D., Krystal, A.D., Lichstein, K.L., & Morin, 
C.M. (2012). The Consensus Sleep Diary: Standardizing prospective sleep self-monitoring. 
SLEEP, 35, 287-302. 
*Casement, M.D., Harrington, K.M., Miller, M.W., & Resick, PA. (2012). Associations between 
Pittsburgh Sleep Quality Index factors and health outcomes in women with