Introduction

Sleep disturbance has been consistently linked to psychopathology [1, 2]. Despite this robust relationship, sleep disturbance has largely been considered an epiphenomenon of psychopathology and has thus remained understudied. However, given the cascade of downstream effects of sleep loss and overlap between neurobiological systems related to sleep and psychopathology, sleep disturbance has recently been proposed as a mechanistic transdiagnostic factor [3]. That is, sleep disturbance may contribute to the development of various forms of psychopathology through its negative impact on functioning across multiple systems.

Though extant research examining sleep and psychopathology has largely focused on depression and postraumatic stress disorder (PTSD), sleep disturbance has received recent attention within the context of obsessive-compulsive disorder (OCD). Indeed, a recent meta-analysis revealed alterations in multiple sleep parameters among those with OCD compared to controls, even when excluding those with comorbid depression [4]. Further, multiple sleep parameters are associated with OCD symptom severity, including slow-wave sleep percentage [5], rapid eye movement (REM) density [5, 6], and total number of subjective sleep problems [7]. Finally, sleep disturbance may interfere with the treatment of OCD. Preliminary evidence in pediatric OCD samples suggests that baseline sleep disturbance predicts worse treatment outcome, and those who do not respond to cognitive behavior therapy (CBT) are more likely to report residual sleep disturbance than responders [8].

Taken together, these findings highlight the role of sleep disturbance in OCD. Given increasing interest in this relationship in recent years, as well as the relatively small body of extant research, integration of the most up to date findings on sleep disturbance and OCD is necessary to identify the most fruitful areas for future research. As such, the purpose of the present review is to synthesize findings related to sleep disturbance and OCD over the past year. Conclusions and future directions for the role of sleep disturbance in OCD will be discussed, including ways in which sleep disturbance might be incorporated into existing models of OCD.

Recent Findings on Sleep and OCD

Recent research continues to link sleep disturbance to OCD, and this relationship is evident across a range of indices, including group differences, relation to symptom severity, and treatment outcome. In the only recent study of sleep in an OCD sample, those with OCD exhibited subjective and objective sleep disturbance compared to controls [9•]. For example, the OCD group reported increased global sleep disturbance, with evidence for specific disturbance in sleep quality, sleep onset latency (SOL), sleep efficiency, and daytime impairment [9•]. Evidence for subjective sleep disturbance in the OCD group was consistent with actigraphy assessment of sleep, which indicated decreased total sleep time (TST) and sleep efficiency and increased SOL compared to controls, with medium effect sizes [9•]. The concordance between subjective and objective sleep deficits suggests that the sleep disturbance reported by those with OCD represent genuine deficits in sleep rather than an overestimation of ancillary symptoms. Interestingly, this study found divergent results for TST, such that those with OCD reported comparable TST to controls, but objectively exhibited decreased TST. One interpretation of these findings is that individuals with OCD may experience restless sleep that accelerometers interpret as increased wakefulness. Such restlessness may then contribute to the interpretation of the sleep as poor quality.

Recent findings have also linked sleep disturbance to OCD symptoms in multiple nonclinical samples. In a sample of unselected college students, subjective sleep disturbance was associated with OCD symptoms [10]. A similar relationship was found in a nationally representative sample, even when controlling for depression [11]. This study also found that those who reported sleep disturbance reported increased OCD symptoms compared to those without sleep disturbance [11]. These findings highlight the relationship between sleep disturbance severity and OCD symptom severity. In contrast, one recent study found no relationship between subjective TST and OCD symptoms in an unselected sample [12]. This finding is consistent with Donse et al. [9•] and provides additional evidence that perceived sleep duration may not be a sensitive indicator of sleep disturbance in OCD.

While recent studies largely link sleep disturbance severity to OCD symptom severity, such cross-sectional approaches offer limited ability to examine temporality. That is, it is unclear from these findings whether sleep disturbance contributes to OCD symptoms or vice versa. However, one recent study utilizing a longitudinal design found that sleep disturbance predicted obsessions over 6 months [13•], suggesting that sleep disturbance may precede OCD symptoms. This finding is consistent with previous research indicating that insomnia predicts the development of anxiety disorders in children [14] and adults [15], but contradicts a recent study which found a unidirectional relationship between insomnia symptoms and OC symptoms in adolescents over 6 months [16]. Thus, the temporal link between sleep and OCD symptoms remains unclear, though extant findings may suggest a bidirectional relationship where sleep disturbance exacerbates OCD symptoms and vice versa.

Despite the consistent link between sleep disturbance and OCD, few studies have examined mechanisms that may account for this relationship. However, one recent study found that the relationship between sleep disturbance and obsessions over 6 months was mediated by focusing attentional control [13•], suggesting that the negative effects of sleep disturbance on cognitive function contribute to increased obsessions. This finding provides preliminary evidence for a potential mechanism that may link sleep disturbance and OCD; however, given the relative dearth of mechanistic studies in this field, considerable additional research is necessary to replicate this finding and identify other candidate mechanisms. Similarly, few studies have examined the downstream effects of this relationship on other processes. However, one recent study found that sleep disturbance moderated the effect of OCD symptoms on inhibitory control [12], such that those with high OCD symptoms and decreased TST exhibited increased commission errors on a Go/NoGo task. Importantly, findings from this study revealed no main effect of OCD symptoms on inhibitory control, suggesting the importance of considering sleep disturbance when examining the relationship between OCD and higher-order cognitive function. However, both of these studies are limited by reliance on unselected samples. Future research in this area will benefit from the utilization of OCD populations.

Finally, recent evidence suggests that sleep disturbance may play a role in OCD treatment. Indeed, one study examining the efficacy of repetitive transcranial magnetic stimulation (rTMS) found that treatment non-responders reported increased pre-treatment sleep disturbance compared to responders [9•], suggesting that sleep disturbance may interfere with treatment efficacy. Alternatively, elevated sleep disturbance may be a marker of more severe, treatment-refractory OCD. This interpretation is consistent with previous evidence that baseline sleep disturbance predicted diminished response to CBT for pediatric OCD [8]. However, in discriminant analyses, Donse et al. [9•] found that sleep disturbance could not predict responders vs non-responders, though circadian rhythm disturbances did. Given recent attention to the role of circadian rhythms in psychiatric disorders [17], including OCD [4], sleep disturbance in OCD may represent a biomarker of underlying circadian rhythm abnormality.

Conclusions and Future Directions

Consistent with extant research, findings from the past year link sleep disturbance to OCD. Those with OCD exhibit both subjective and objective sleep disturbance, indicating that sleep problems among those with OCD represent a true physiological deficit rather than a misperception. Further, subjective sleep disturbance is linked to OCD symptoms in multiple samples both cross-sectionally and prospectively, suggesting that sleep disturbance is not only concurrent with but also precedes OCD symptoms. Recent attention has also been given to the role of cognitive control within the context of sleep and OCD, with results highlighting decreased cognitive control as a candidate mechanism in this relationship. Finally, findings from the past year replicate previous research linking sleep disturbance to diminished treatment response. Taken together, the results from the past year continue to implicate sleep disturbance in OCD. Further, these findings provide additional specificity to this relationship by highlighting the divergence of subjective and objective TST, providing preliminary evidence for the role of cognitive function, and extending treatment outcome results beyond CBT to rTMS.

Given accumulating evidence for a role of sleep in OCD, an important next question is how to incorporate sleep into etiological conceptualizations of OCD? Current models of OCD posit a diathesis-stress model in which the interaction of genetic vulnerabilities and environmental stressors results in hyperactivity in cortico-striato-thalamo-cortical circuitry [18, 19]. That is, the combination of certain genes and environmental factors is thought to cause abnormal brain activity, which then manifests as the intrusive cognition and repetitive behavior characteristic of OCD. How then might sleep disturbance function in such a model? It may be that sleep disturbance is an environmental stressor that interacts with genetic vulnerabilities to influence symptom expression. Indeed, sleep disturbance has recently been proposed as a stressor that can contribute to allostatic overload, or the hypo/hyperactivity of systems that maintain physiological homeostasis [20].

This hypothesis is supported by considerable research delineating the negative consequences of sleep disturbance for whole system function, including processes linked to OCD. For example, sleep loss is associated with alterations in immune system function [21], including increased inflammatory cytokines [22]. Similarly, dysregulated immune function has been implicated in OCD and related disorders, most clearly in the case of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections [PANDAS; [23]]. Further, sleep loss results in blunted cortisol reactivity to an acute stressor [24], and decreased sleep and sleep variability are linked to alterations in the diurnal cortisol rhythm [25]. Dysregulated cortisol has likewise been implicated in OCD [26]. Thus, immune and cortisol responses are two candidate stress responses to sleep disturbance that may interact with genetic predispositions to confer vulnerability for OCD.

Sleep disturbance and OCD also share linkages to deficits in cognitive function. Sleep loss and disturbance results in diminished executive function [27], including deficits in inhibitory control [28] and working memory [29]. These deficits are further linked to altered activity in frontal and thalamic regions [29, 30]. Importantly, these regions are also implicated in the neurocircuitry of OCD [19], and considerable research has identified higher-order cognitive deficits in OCD, particularly regarding inhibitory control and working memory [18]. Taken together, these findings suggest that sleep disturbance impairs multiple processes necessary for adaptive function in a similar fashion to a major stressor. When experienced in an individual with a genetic predisposition, sleep disturbance may contribute to the development of OCD.

Further, recent attention has been given to the role of epigenetic factors in OCD; that is, environmental influences may modify the expression of certain genes, and these alterations may have downstream effects on neural activity that contributes to OCD [19]. Indeed, recent research has linked epigenetic processes to OCD [31, 32]. One possibility is that sleep disturbance functions as an epigenetic factor that alters the expression of genes related to OCD. Indeed, recent findings suggest that both acute sleep deprivation and insomnia symptoms are associated with epigenetic indicators [33, 34]. Though these findings are preliminary, they suggest that examining sleep disturbance as an epigenetic factor in OCD may be fruitful.

Future research would benefit from beginning to test specific mechanisms that may account for the relationship between sleep disturbance and OCD. Further, extant research in this area is limited by an overreliance on correlational and cross-sectional methods. Additional research utilizing experimental sleep restriction paradigms and longitudinal designs are necessary to move beyond associating sleep disturbance with OCD toward determining whether sleep disturbance causally contributes to OCD. Finally, future research on the role of sleep disturbance in treatment outcomes is necessary to clarify how sleep disturbance may contribute to treatment nonresponse. OCD is a highly heterogeneous disorder; thus, OCD characterized by sleep disturbance may represent a unique variant of OCD that is less responsive to current treatments. Further, future research is necessary to examine the role of sleep disturbance in OCD treatment outcome among adult samples. These gaps in the literature represent important areas for future research to further clarify the relationship between sleep disturbance and OCD.