Treatment needs associated with pain in substance use disorder patients: implications for concurrent treatment.

Although pain problems are prevalent in substance use disorder (SUD) patients, the special treatment needs of SUD patients with pain have not been investigated. This study examines the problems and behaviors associated with reported pain among veterans treated at eight opioid substitution treatment clinics. Patients reporting pain had more severe medical and psychiatric problems and greater health care utilization. Pain was associated with an increased propensity for misuse of substances with analgesic effects, suggesting that ongoing pain contributes to an altered and more severe pattern of drug-seeking behavior. Patients without pain rarely abused sedatives or opioid medication, indicating that misuse of these substances is unique to co-morbid pain and SUD patients. Patients reporting pain did not differ from patients without pain in use of heroin, alcohol, cocaine or in injection practices, demonstrating that they are truly SUD patients in need of SUD treatment. Pain complicates the treatment of SUD and should be addressed as an important co-morbidity during treatment.

Sleep quality and neural circuit function supporting emotion regulation.

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.

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 = 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.