Contingency management (CM) is associated with decreases in off-target drug and alcohol use during primary target treatment. The primary hypothesis for this trial was that targeting alcohol use or tobacco smoking would yield increased abstinence in the opposite, nontargeted drug. We used a 2 [CM vs. noncontingent control (NC) for alcohol]×2 (CM vs. NC for smoking tobacco) factorial design, with alcohol intake (through urinary ethyl glucuronide) and tobacco smoking (through urinary cotinine) as the primary outcomes. Thirty-four heavy-drinking smokers were randomized into one of four groups, wherein they received CM, or equivalent NC reinforcement, for alcohol abstinence, smoking abstinence, both drugs, or neither drug. The CM for alcohol and tobacco group had only two participants and therefore was not included in analysis. Compared with the NC for alcohol and tobacco smoking group, both the CM for the tobacco smoking group [odds ratio (OR)=12.03; 95% confidence interval (CI): 1.50-96.31] and the CM for the alcohol group (OR=37.55; 95% CI: 4.86-290.17) submitted significantly more tobacco-abstinent urinalyses. Similarly, compared with the NC for the alcohol and tobacco group, both the CM for smoking (OR=2.57; 95% CI: 1.00-6.60) and the CM for alcohol groups (OR=3.96; 95% CI: 1.47-10.62) submitted significantly more alcohol-abstinent urinalyses. These data indicate cross-over effects of CM on indirect treatment targets. Although this is a pilot investigation, it could help to inform the design of novel treatments for alcohol and tobacco co-addiction.
Introduction The baseline non-REM sleep EEG of individuals with insomnia has been found to display increased spectral power at frequencies >14Hz, which may reflect hyperarousal. There is some evidence in this population of reduced slow wave activity after total sleep deprivation (TSD), potentially indicating altered sleep homeostasis. We investigated non-REM sleep EEG spectra at baseline and after TSD in individuals with sleep-onset insomnia. Methods 10 individuals with sleep-onset insomnia and 5 healthy controls (ages 22-40y, 11 females) completed a 5-day laboratory study with an adaptation night, baseline night, assignment to 38h TSD (n=5 insomnia, n=5 control) or equivalent non-TSD control (n=5 insomnia), and recovery night. Sleep periods were 10h (22:00-08:00) with digital polysomnography (250Hz; Nihon Kohden). Following artifact rejection, 5s subepochs of the non-REM (stages N2, N3) sleep EEG (C3-M2 derivation) in baseline and recovery nights were subjected to spectral analysis. Spectra (0.2Hz bins) were averaged over subepochs in 30s epochs. Repeated-measures ANOVA compared baseline spectra between insomnia and controls, and baseline-recovery difference spectra between TSD insomnia, non-TSD insomnia, and TSD controls. Results Average non-REM sleep amount was 5.9 at baseline, increasing by 1.1h after TSD, with no differences between groups (p≥0.20). At baseline, the insomnia group showed increased power in theta/alpha (~4–12Hz), reaching significance in the lower spindle range, compared to controls (p<0.05). As anticipated, no differences emerged between baseline and recovery nights in the non-TSD insomnia group. However, the TSD insomnia group showed increased delta (~1–3Hz) and theta/alpha (~6–10Hz) power (p<0.05) during recovery. Healthy controls showed expected power increases in delta and lower spindle range, and decreases in upper spindle range (~14–15Hz), after TSD (p<0.05). Conclusion Compared to healthy controls, individuals with sleep-onset insomnia showed increased non-REM sleep EEG power in the theta/alpha bands and low spindle frequency range, with further significant increases in theta/alpha in addition to delta power following TSD, despite small sample size. The increase in delta power following TSD was equivalent to that in healthy controls, suggesting no sleep homeostasis abnormality. Whether the elevated theta/alpha power may be related to hyperarousal is unclear. Support (if any) ONR grant N00014-13-C-0063
Introduction Opioids are a common pain treatment in the United States with approximately 143 million prescriptions dispensed in 2020. Long-term opioids for chronic pain increase risk of misuse and overdose. Opioids can also disrupt sleep and cause respiratory depression while poor sleep can exacerbate pain. In-lab polysomnography is the standard for diagnosing sleep disorders. However, polysomnography is less effective for observing patterns over multiple days and is not always representative of at-home sleep. This study investigates the feasibility of using a disposable home sleep test device with adults prescribed opioids for chronic pain and its ability to screen for sleep disorders and overnight oxygenation. Methods Participants were recruited from clinics and public advertisements. Key inclusion criteria were: ≥18 years of age, moderate daily level of pain (≥5 on the 0-10 Numeric Pain Scale [NPS]), prescribed opioids, and internet access. The NightOwl mini disposable home sleep test (Ectosence, Leuven, Belgium) was used to record total sleep time (TST), time in bed (TIB), sleep efficiency (SE), oxygen saturation (SaO2) and apnea-hypopnea index (AHI) for 5 consecutive nights. Results All enrolled participants (N=9) completed 5 days with no missing data. The sample was 66% female with an average age of 60±12 (Mean ± SD). Mean NPS scores indicated moderate pain intensity (6.3±1.9). Participants spent an average of 8.0±1.4h TIB and slept for 5.4+/-1.3h TST resulting in a SE of 68.5±17.9%. On average, AHI was 7.3±7.7 (mild range for sleep apnea). 56% of participants displayed a SaO2 nadir below 88%, the recommended threshold for supplemental oxygen. All individuals agreed that they were at least somewhat satisfied with the ease and amount of time participating in the study. All agreed or strongly agreed that they felt comfortable participating. Conclusion Participants used the disposable sleep test device at home with relative ease as indicted by complete data recording, values within expected norms, and satisfaction survey responses. The device could be an acceptable screening tool for sleep disorders and respiratory events that may otherwise go undetected in this population prescribed opioids and at risk for apnea and respiratory depression. Support (if any) NCATS/NIH # Ul1 TR002319 and The Rayce Rudeen Foundation
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