DSM-5 insomnia disorder in pregnancy: associations with depression, suicidal ideation, and cognitive and somatic arousal, and identifying clinical cutoffs for detection.

Study Objectives: The study had three primary goals. First, we estimated survey-assessed DSM-5 insomnia disorder rates in pregnancy, and described associated sociodemographics, and sleep-wake and mental health symptoms. Second, we derived cutoffs for detecting DSM-5 insomnia disorder using common self-report measures of sleep symptoms. Third, we identified clinically relevant cut-points on measures of nocturnal cognitive and somatic arousal. Methods: Ninety-nine women (85.9% in the 2nd trimester) completed online surveys including DSM-5 insomnia disorder criteria, the Insomnia Severity Index (ISI), Pittsburgh Sleep Quality Index (PSQI), Presleep Arousal Scale's Cognitive (PSASC) and Somatic (PSASS) factors, and Edinburgh Postnatal Depression Scale. Results: DSM-5 insomnia disorder rate was 19.2%. Insomnia was associated with depression, suicidality, nocturnal cognitive and somatic arousal, and daytime sleepiness. An ISI scoring method that aligns with DSM-5 criteria yielded excellent metrics for detecting insomnia disorder and good sleep. Regarding quantitative cutoffs, ISI ≥ 10 and ISI ≥ 11 (but not ISI ≥ 15) were supported for detecting DSM-5 insomnia, whereas ISI ≤ 7 and ISI ≤ 9 performed well for detecting good sleep. PSQI cutoff of 5 was supported for detecting insomnia and good sleep. The optimal cutoff for nocturnal cognitive arousal was PSASC ≥ 18, whereas the optimal cutoff for somatic arousal was PSASS ≥ 13. Conclusions: Insomnia disorder affects a large segment of pregnant women. Empirically derived cutoffs for insomnia, good sleep, cognitive arousal, and somatic arousal may inform case identification and future perinatal sleep research methodology.

Hyperarousal and sleep reactivity in insomnia: current insights.

Hyperarousal is a key component in all modern etiological models of insomnia disorder. Overall patterns in the literature suggest that over-active neurobiological and psychological systems contribute to difficulty sleeping. Even so, mixed results regarding the specific mechanisms linking hyperarousal to sleep disturbance limit current etiological conceptualizations. Similar basal arousal profiles between individuals with high vs low risk for insomnia in the absence of stress exposure suggest that dysregulated stress "response" rather than general hyperarousal may be a more pertinent marker of risk. In this report, we discuss evidence for hyperarousal in insomnia and explore the role of sleep reactivity. A trait characteristic, sleep reactivity is the degree to which stress disrupts sleep, manifesting as difficulty falling and staying asleep. Premorbid sleep reactivity has been shown to identify individuals at risk for future insomnia disorder, such as highly reactive sleepers (whose sleep systems are sensitive to stress) who are at elevated disease risk. Research points to genetics, family history of insomnia, gender, and environmental stress as factors that influence sleep reactivity. Importantly, stress-related cognitive-emotional reactivity (e.g., rumination, worry) may exploit the vulnerability of a highly reactive sleep system. We propose that sleep reactivity and cognitive-emotional reactivity may share a bidirectional relationship, conferring an insalubrious environment for sleep in response to stress. Future research on sleep reactivity is needed to identify its neurobiology, characterize its relationship with cognitive-emotional reactivity, and explore the potential clinical utility of sleep reactivity in treatment planning.