Affective Consequences of Sleep Deprivation

Surprisingly little is known about the effects of sleep deprivation on affective processes. Although clinical evidence and introspection suggest that emotional function is sensitive to sleep loss, there are only three published studies that have experimentally manipulated both stress and emotion in a single experiment, the earliest of which was published in 2007. This dissertation presents findings from three studies that were designed to improve our understanding of the influence of sleep loss on affective functioning in healthy adults. Study 1 (Sleep and Mood) measured the effects of sleep loss on affect in the absence of specific probes. Three facets of mood (Fatigue, Vigor and Confusion) were found to be sensitive to sleep restriction, increasing in a dose-response manner with extended wakefulness and covarying with a well validated behavioral assay of alertness (the PVT reaction time task). Three other facets of mood (Depression, Anxiety, and Anger) were not sensitive to sleep restriction and did not covary with objective alertness. Study 2 (Sleep and Emotion) found that sleep deprivation decreased facial expressiveness in response to positive and negative emotion probes. There was also a trend toward decreased intensity of positive and negative subjective emotional reactions for sleep deprived subjects as well. Study 3 (Sleep and Stress) found that sleep deprived subjects reported a more negative subjective response than control subjects to a mild stressor, but not to a more intense stressor. When taken together, these studies offer a more nuanced account of the relationship between sleep deprivation and affective functioning. This dissertation ends with a discussion of the implications of these findings for both healthy and clinical populations and proposes future direction for research on sleep and emotion

Sleep quality and neural circuit function supporting emotion regulation.

UNLABELLED: BACKGROUND: Recent laboratory studies employing an extended sleep deprivation model have mapped sleep-related changes in behavior onto functional alterations in specific brain regions supporting emotion, suggesting possible biological mechanisms for an association between sleep difficulties and deficits in emotion regulation. However, it is not yet known if similar behavioral and neural changes are associated with the more modest variability in sleep observed in daily life. METHODS: We examined relationships between sleep and neural circuitry of emotion using the Pittsburgh Sleep Quality Index and fMRI data from a widely used emotion regulation task focusing on cognitive reappraisal of negative emotional stimuli in an unselected sample of 97 adult volunteers (48 women; mean age 42.78±7.37 years, range 30-54 years old). RESULTS: Emotion regulation was associated with greater activation in clusters located in the dorsomedial prefrontal cortex (dmPFC), left dorsolateral prefrontal cortex (dlPFC), and inferior parietal cortex. Only one subscale from the Pittsburgh Sleep Quality Index, use of sleep medications, was related to BOLD responses in the dmPFC and dlPFC during cognitive reappraisal. Use of sleep medications predicted lesser BOLD responses during reappraisal, but other aspects of sleep, including sleep duration and subjective sleep quality, were not related to neural activation in this paradigm. CONCLUSIONS: The relatively modest variability in sleep that is common in the general community is unlikely to cause significant disruption in neural circuits supporting reactivity or regulation by cognitive reappraisal of negative emotion. Use of sleep medication however, may influence emotion regulation circuitry, but additional studies are necessary to determine if such use plays a causal role in altering emotional responses

Determining Effective Methadone Doses for Individual Opioid-Dependent Patients

BACKGROUND: Randomized clinical trials of methadone maintenance have found that on average high daily doses are more effective for reducing heroin use, and clinical practice guidelines recommend 60 mg/d as a minimum dosage. Nevertheless, many clinicians report that some patients can be stably maintained on lower methadone dosages to optimal effect, and clinic dosing practices vary substantially. Studies of individual responses to methadone treatment may be more easily translated into clinical practice. METHODS AND FINDINGS: A volunteer sample of 222 opioid-dependent US veterans initiating methadone treatment was prospectively observed over the year after treatment entry. In the 168 who achieved at least 1 mo of heroin abstinence, methadone dosages on which patients maintained heroin-free urine samples ranged from 1.5 mg to 191.2 mg (median = 69 mg). Among patients who achieved heroin abstinence, higher methadone dosages were predicted by having a diagnosis of posttraumatic stress disorder or depression, having a greater number of previous opioid detoxifications, living in a region with lower average heroin purity, attending a clinic where counselors discourage dosage reductions, and staying in treatment longer. These factors predicted 42% of the variance in dosage associated with heroin abstinence. CONCLUSIONS: Effective and ineffective methadone dosages overlap substantially. Dosing guidelines should focus more heavily on appropriate processes of dosage determination rather than solely specifying recommended dosages. To optimize therapy, methadone dosages must be titrated until heroin abstinence is achieved

Optimizing the Pharmacologic Treatment of Insomnia Current Status and Future Horizons

A number of medications are available for treating patients with insomnia. These medications include agents approved as insomnia therapies by the U.S. Food and Drug Administration (FDA), agents approved by the FDA for another condition that are used "off-label" to treat insomnia, and agents available "over-the-counter" that are taken by individuals with insomnia. These agents differ in their properties, their safety and efficacy when used for different insomnia patient subtypes, and the available data on their efficacy and safety in these subtypes. As a result, optimizing the medication treatment of insomnia for a given patient requires that the clinician select an agent for use which has characteristics that make it most likely to effectively and safely address the type of sleep difficulty experienced by that individual. This article is intended to assist clinicians and researchers in carrying out this optimization. It begins by reviewing the basic characteristics of the medications used to treat insomnia. This is followed by a review of the fundamental ways that individuals with insomnia may differ and affect the choice of medication therapy. This review includes discussions that illustrate how to best choose a medication based on the characteristics of the available medications, the key differences among insomnia patients, and the available research literature. Lastly, we discuss future directions for the optimizing pharmacologic management of insomnia. It is hoped that the treatment tailoring methods discussed herein serve as a means of improving the clinical management of insomnia and, thus, improve the lives of the many patients who suffer from this common and impairing condition

Sleep Deprivation and Stressors: Evidence for Elevated Negative Affect in Response to Mild Stressors When Sleep Deprived

Stress often co-occurs with inadequate sleep duration, and both are believed to impact mood and emotion. It is not yet known whether inadequate sleep simply increases the intensity of subsequent stress responses or interacts with stressors in more complicated ways. To address this issue, we investigated the effects of one night of total sleep deprivation on subjective stress and mood in response to low-stress and high-stress cognitive testing conditions in healthy adult volunteers in two separate experiments (total N ϭ 53). Sleep was manipulated in a controlled, laboratory setting and stressor intensity was manipulated by changing difficulty of cognitive tasks, time pressure, and feedback about performance. Sleep-deprived participants reported greater subjective stress, anxiety, and anger than rested controls following exposure to the low-stressor condition, but not in response to the high-stressor condition, which elevated negative mood and stress about equally for both sleep conditions. These results suggest that sleep deprivation lowers the psychological threshold for the perception of stress from cognitive demands but does not selectively increase the magnitude of negative affect in response to high-stress performance demands

Dynamic Resting-State Functional Connectivity in Major Depression

Major depressive disorder (MDD) is characterized by abnormal resting-state functional connectivity (RSFC), especially in medial prefrontal cortical (MPFC) regions of the default network. However, prior research in MDD has not examined dynamic changes in functional connectivity as networks form, interact, and dissolve over time. We compared unmedicated individuals with MDD (n=100) to control participants (n=109) on dynamic RSFC (operationalized as SD in RSFC over a series of sliding windows) of an MPFC seed region during a resting-state functional magnetic resonance imaging scan. Among participants with MDD, we also investigated the relationship between symptom severity and RSFC. Secondary analyses probed the association between dynamic RSFC and rumination. Results showed that individuals with MDD were characterized by decreased dynamic (less variable) RSFC between MPFC and regions of parahippocampal gyrus within the default network, a pattern related to sustained positive connectivity between these regions across sliding windows. In contrast, the MDD group exhibited increased dynamic (more variable) RSFC between MPFC and regions of insula, and higher severity of depression was related to increased dynamic RSFC between MPFC and dorsolateral prefrontal cortex. These patterns of highly variable RSFC were related to greater frequency of strong positive and negative correlations in activity across sliding windows. Secondary analyses indicated that increased dynamic RSFC between MPFC and insula was related to higher levels of recent rumination. These findings provide initial evidence that depression, and ruminative thinking in depression, are related to abnormal patterns of fluctuating communication among brain systems involved in regulating attention and self-referential thinking

The sleep-deprived human brain

How does a lack of sleep affect our brains? In contrast to the benefits of sleep, frameworks exploring the impact of sleep loss are relatively lacking. Importantly, the effects of sleep deprivation (SD) do not simply reflect the absence of sleep and the benefits attributed to it; rather, they reflect the consequences of several additional factors, including extended wakefulness. With a focus on neuroimaging studies, we review the consequences of SD on attention and working memory, positive and negative emotion, and hippocampal learning. We explore how this evidence informs our mechanistic understanding of the known changes in cognition and emotion associated with SD, and the insights it provides regarding clinical conditions associated with sleep disruption

The role of sleep in emotional processing

Abstract In this chapter, we have reviewed an extensive literature supporting the 4 critical role of sleep for several aspects of emotional processing and regulation. In the first part, we discussed the main behavioral and psychophysiological studies that examined how sleep influences the processes of encoding and consolidation of emotional memory. In addition, we examined how sleep modulates emotion regulation, emotional reactivity, and empathy. Further, we discussed the implication of sleep in fear conditioning memory, threat generalization, and extinction memory. In the second part, we discussed evidence specifically suggesting the implication of REM sleep in the consolidation of emotional memory and in the modulation of emotional reactivity. In particular, we will focus on the specific physiological REM features that contributed to suggest its critical involvement in emotional processing. In the third part, we overviewed the functional neuroimaging studies on the brain mechanisms that underlie the relations between sleep and emotions. Finally, we focused on the most important psychiatric disorders that express abnormalities of sleep and emotional alterations, briefly reviewing our knowledge about the relationships between sleep disturbances and mood in major depression, anxiety disorders, and post-traumatic stress disorder. We showed that sleep helps in the formation of emotional memories at every stage of this process. On the contrary, sleep loss induces deficit in encoding of emotional information, leading to a disruptive interference with emotional memory consolidation. The reviewed literatures clearly suggest that sleep loss significantly influences emotional reactivity. Whether sleep acts to protect, potentiate, or de-potentiate emotional reactivity is, however, still debatable. Future studies will have to elucidate, at the behavioral level, the specific direction of the sleep-dependent emotional modulation. Sleep seems to be crucial also for our ability to correctly process emotional information that allows us to understand the others’ feelings and to be empathic with them, as well as for our ability to encode and consolidate fear conditioning and extinction learning. As far as the role of REM sleep is concerned, it seems to be crucial for the consolidation of emotional memory, while its specific contribution on next-day emotional reactivity is less clear. In fact, REM sleep could act to potentiate or, conversely, de-potentiate the emotional charge associated to a memory along with its consolidation. This topic could be also relevant for its implications in clinical settings. Indeed, further explaining how sleep influences the next-day emotional brain functioning will be crucial to open a new perspective for the understanding and treatment of affective or anxiety disturbances in patients with disturbed sleep