Sleep abnormalities are extremely common in anxiety disorders and may contribute to their development and persistence. Their shared pathophysiological mechanisms could thus serve as biomarkers or targets for novel therapeutics. Individuals with Primary Insomnia were age- and sex-matched to controls and to persons with Generalized Anxiety Disorder. All underwent fMRI resting-state scans at 3-T. In Primary Insomnia and controls, sleep was recorded for 2 weeks using diaries and actigraphy. All participants completed state-anxiety and neuroticism inventories. Whole-brain connectivity of 6 fear- and extinction-related seeds were compared between the 3 groups using ANOVA. The only significant between-group main effect was seen for connectivity between the left amygdala seed and a bilateral cluster in the rostral anterior cingulate cortex. The latter is believed to exert top-down control over amygdala activity and their interaction may thus constitute an emotion regulatory circuit. This connectivity was significantly greatest in controls while Primary Insomnia was intermediate between that of controls and Generalized Anxiety Disorder. Across Primary Insomnia and control subjects, mean connectivity decreased with poorer sleep. Across all 3 groups, connectivity decreased with greater neuroticism and pre-scan anxiety. Decreased top-down control of the amygdala may increase risk of developing an anxiety disorder with preexisting Primary Insomnia.

Study Objectives Formation and maintenance of fear-extinction memories are disrupted in post-traumatic stress disorder (PTSD) and anxiety disorders. Sleep contributes to emotional memory consolidation and emotion regulation. Insomnia disorder (ID) is characterized by persistent sleep disturbance as well as rapid eye movement (REM) sleep abnormalities and often precedes or develops in parallel with PTSD and anxiety disorders. Here, we explore the impact of chronic poor sleep and sleep immediately following fear conditioning and extinction learning on preservation of extinction memories. Methods Twenty-four ID age- and sex-matched to 24 healthy, good sleeper controls (GS) completed up to 2 weeks of habitual sleep monitoring with daily sleep–wake diaries and actigraphy, and then participated in a two-session fear conditioning, extinction learning and extinction recall procedure. Fear Conditioning and Extinction Learning occurred during session 1, followed by Extinction Recall approximately 24 hours later. Skin-conductance responses (SCR) and shock expectancies were recorded throughout all experimental phases to evaluate associative learning and memory. Overnight sleep between sessions 1 and 2 was recorded using ambulatory polysomnography. Results ID showed greater physiological reactivity during Fear Conditioning. REM sleep physiology was associated with poorer extinction memory in ID but better extinction memory in GS. Conclusion REM sleep physiology may differentially support emotional memory retention and expression in ID and GS. In the former, REM may enhance retention of fear memories, while in the later, REM may enhance the expression of extinction memories.

Empirical evidence demonstrates mental health disparities between sexual and gender minority individuals (SGM) compared with cisgender heterosexual individuals. SGM individuals report elevated rates of emotional distress, symptoms related to mood and anxiety disorders, self-harm, and suicidal ideation and behavior. Social support is inversely related to psychiatric symptoms, regardless of SGM status. The COVID-19 pandemic—with its associated limited social interactions—represents an unprecedented period of acute distress with potential reductions in accessibility of social support, which might be of particular concern for SGM individuals' mental well-being. In the present study, we explored the extent to which potential changes in mental health outcomes (depressive symptoms, worry, perceived stress, positive and negative affect) throughout the duration of the pandemic were related to differences in perceptions of social support and engagement in virtual social activity, as a function of SGM status. Utilizing a large sample of US adults (N = 1,014; 18% reported SGM status), we assessed psychiatric symptoms, perceptions of social isolation, and amount of time spent socializing virtually at 3 time windows during the pandemic (between March 21 and May 21). Although SGM individuals reported greater levels of depression compared with non-SGM individuals at all 3 time points, there was no interaction between time and SGM status. Across all participants, mental health outcomes improved across time. Perceived social isolation was associated with poorer mental health outcomes. Further, time spent engaging in virtual socialization was associated with reduced depression, but only for those in self-reported quarantine. We discuss these results in terms of the nature of our sample and its impact on the generalizability of these findings to other SGM samples as well as directions for future research aimed at understanding potential health disparities in the face of the COVID-19 pandemic.

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Sleep disturbances are common in post-traumatic stress disorder (PTSD), although which sleep microarchitectural characteristics reliably classify those with and without PTSD remains equivocal. Here, we investigated sleep microarchitectural differences (i.e., spectral power, spindle activity) in trauma-exposed individuals that met (n = 45) or did not meet (n = 52) criteria for PTSD and how these differences relate to post-traumatic and related psychopathological symptoms. Using ecologically-relevant home sleep polysomnography recordings, we show that individuals with PTSD exhibit decreased beta spectral power during NREM sleep and increased fast sleep spindle peak frequencies. Contrary to prior reports, spectral power in the beta frequency range (20.31–29.88 Hz) was associated with reduced PTSD symptoms, reduced depression, anxiety and stress and greater subjective ability to regulate emotions. Increased fast frequency spindle activity was not associated with individual differences in psychopathology. Our findings may suggest an adaptive role for beta power during sleep in individuals exposed to a trauma, potentially conferring resilience. Further, we add to a growing body of evidence that spindle activity may be an important biomarker for studying PTSD pathophysiology.

Sleep enhances motor sequence learning (MSL) in young adults by concatenating subsequences ("chunks") formed during skill acquisition. To examine whether this process is reduced in aging, we assessed performance changes on the MSL task following overnight sleep or daytime wake in healthy young and older adults. Young adult performance enhancement was correlated with nREM2 sleep, and facilitated by preferential improvement of slowest within-sequence transitions. This effect was markedly reduced in older adults, and accompanied by diminished sigma power density (12-15 Hz) during nREM2 sleep, suggesting that diminished chunk concatenation following sleep may underlie reduced consolidation of MSL in older adults.[Supplemental material is available for this article.]Optimal execution of motor skills relies on precise temporal sequencing of associated events. For young adults, sleep following learning, in the absence of further practice, enhances performance on motor sequence learning (MSL) tasks (Walker et al. 2002;Fischer et al. 2005;Nishida and Walker 2007;Doyon et al. 2009;Barakat et al. 2011;Wilson et al. 2012;Pace-Schott and Spencer 2013). This enhancement is significantly greater than that observed over an equivalent interval of wake, and is not merely a consequence of general increases in motor responding (Fischer et al. 2002;Spencer et al. 2006Spencer et al. , 2007.Recent work has suggested the importance of stage 2 nonrapid eye movement sleep (nREM2) for enhancing MSL (Walker et al. 2002;Nishida and Walker 2007;Peters et al. 2007;Tucker and Fishbein 2009). High frequency (12-15 Hz) thalamocortical oscillations, or sleep spindles, occurring during nREM2 have been implicated as a possible mechanism for sleep-related MSL improvements. These electrophysiological events induce longterm potentiation in the neocortex, a process crucial for memory consolidation (Sejnowskli and Destexhe 2000;Rosanova and Ulrich 2005;Fogel and Smith 2006;Nishida and Walker 2007;Bergmann et al. 2008;Tucker and Fishbein 2009; Foge et al. 2013).As motor sequence learning develops, distinct subsequences of movements are grouped together, a process termed "chunking" (Rosenbaum et al. 1983;Klapp 1995;Sakai et al. 2003). For instance, during the execution of a seven-item sequence (e.g., 2 -4-2-3 -4 -1 -3), items may be represented in memory as smaller subsequences, or "chunks" (e.g., 2 -4 -2, 3 -4, and 1 -3; Kennerley et al. 2004;). With each chunk representing a distinct memory unit, slowest transitions are expected "between" chunks, reflecting additional memory retrieval effort. Conversely, the fastest transitions indicate movements "within" chunks, or within a memory unit. Consequently, efficient learning of the MSL task relies on motor chunk concatenation, represented behaviorally as faster transitions between chunks (Verwey 2001;Wright et al. 2010). Kuriyama et al. (2004) demonstrated that this selective enhancement of the slowest transitions occurs maximally over sleep in young adults.Post-sleep enhancement of MSL is reduced in older a...

Across extinction learning, GS but not ID activated both fear and extinction-related networks. At extinction recall, ID engaged similar regions whereas GS no longer did so. Individuals with ID may show a delayed acquisition of fear extinction memories.

Exposure therapy for Social Anxiety Disorder (SAD) utilizes fear extinction, a memory process enhanced by sleep. We investigated whether naps following exposure sessions might improve symptoms and biomarkers in response to social stress in adults undergoing 5-week exposure-based group SAD therapy. Thirty-two participants aged 18-39 (18 females) with SAD were randomized. Before and after treatment, participants completed the Liebowitz Social Anxiety Scale (LSAS) and underwent a Trier Social Stress Test with psychophysiological monitoring (mpTSST) that included skin conductance (SCL), electromyographic (EMG) and electrocardiographic recording, and an auditory startle procedure while anticipating the social stressor. At sessions 3 and 4, exposure was followed by either a 120-min polysomnographically monitored sleep opportunity (Nap, N=17) or wakefulness (Wake, N=15). Primary hypotheses about SAD symptom change (LSAS) and EMG blink-startle response failed to differ with naps, despite significant symptom improvement (LSAS) with therapy. Some secondary biomarkers, however, provided preliminary support for enhanced extinction learning with naps, with trend-level Time (pre-, post-treatment) × Arm interactions and significant reduction from pre- to post treatment in the Nap arm alone for mpTSST SCL and salivary cortisol rise. Because of the small sample size and limited sleep duration, additional well-powered studies with more robust sleep interventions are indicated.