Boris Dubrovsky

Introduction Exploring the relationship between OSA and pain, some studies showed hyperalgesia, and others, hypoalgesia. It was proposed that apnea-related sleep fragmentation causes hyperalgesia, and hypoxemia, hypoalgesia. However, SpO2 nadir had opposite relationships with pain measures in different studies. A 2018 review of over 1000 studies reported lack of consistent relationship between OSA and pain variables. Further, OSA was shown to relate to depressed mood, which may alter pain perception. Presently, retrospective reports of pain are analyzed as a function of polysomnographic and self-report sleep variables and depressive symptomatology in patients evaluated for OSA. Methods A total of 1,166 patients (923 women, 1136 minorities, 18-97 y.o., age M=53.1±15.2, BMI M=34.4±8.7) undergoing an overnight PSG filled out the Center for Epidemiologic Studies Depression Scale-Revised (CESDR), ISI, PSQI, ESS, and Chronic Pain Grade Scale yielding pain intensity (PI) and functional effect (FE) scores. PI and FE were separately regressed onto age, sex and BMI, followed by PSG and self-report variables meeting p<0.1 criterion. AHI and SpO2nadir were forced into the models. Results Mean AHI=29.6±34.7, range 0-167/hr, 72.3% had AHI≥5. Higher PI related to higher AHI (p=0.005, R2<1%), lower total arousal index (TAI, p=0.006, R2<1%), higher total sleep time (TST, p=0.003, R2<1%), higher PSQI (p<0.001, R2=5%), and higher CESD (p=0.001, R2<1%), without interactions with sex. Higher FE related to higher AHI (p=0.004, R2<1%), lower TAI (p<0.001, R2=1%), higher PSQI (p<0.001, R2=3%, and higher CESD (p<0.001, R2=2%). Sex had a significant interaction only with AHI (p=0.032); the FE-AHI relationship was significant in women (p=0.012), but not in men. Conclusion On retrospective reports of pain in this large sample, higher AHI related to greater pain intensity in both sexes and to greater functional effect in women only. Unexpectedly, higher pain measures were also related to lower TAI and higher TST. Higher depressive symptomatology and subjective sleep disturbance on PSQI were related to greater pain intensity and its functional effect. Only a small portion of the variance in pain measures was accounted for by PSG and self-report variables. Support none

Introduction OSA was found to alter pain experience, presumably due to apnea-related hypoxia and sleep disturbance. However, types of pain measures, demographic and subjective variables, such as mood, may influence pain experience in OSA. Presently, retrospective pain reports of patients referred for OSA evaluation were analyzed as a function of PSG measures, demographic variables, and self-reported mood and insomnia symptoms. Methods On the evening of a diagnostic in-lab PSG, patients reported pain intensity in the preceding 6 months (PI, rage 0-10, Chronic Pain Grade Scale), symptoms of depression (Center for Epidemiologic Studies Depression Scale-Revised, CESDR) and insomnia (Insomnia Severity Index, ISI). PI was regressed on age, sex, BMI, total sleep time (TST), sleep stage percentages, sleep efficiency, WASO, awakenings, respiratory arousal index, AHI, SpO2% nadir, time below SpO2 90%, desaturation index, CESDR and ISI using a stepwise entry. Results A total of 1293 patients w...

Patients with temporomandibular disorder (TMD) report poor sleep quality on the Pittsburgh Sleep Quality Index (PSQI). However, polysomnographic (PSG) studies show meagre evidence of sleep disturbance on standard physiological measures. The present aim was to analyse self-reported sleep quality in TMD as a function of myofascial pain, PSG parameters and depressive symptomatology. PSQI scores from 124 women with myofascial TMD and 46 matched controls were hierarchically regressed onto TMD presence, ratings of pain intensity and pain-related disability, in-laboratory PSG variables and depressive symptoms (Symptoms Checklist-90). Relative to controls, TMD cases had higher PSQI scores, representing poorer subjective sleep and more depressive symptoms (both P < 0·001). Higher PSQI scores were strongly predicted by more depressive symptoms (P < 0·001, R2 = 26%). Of 19 PSG variables, two had modest contributions to higher PSQI scores: longer rapid eye movement latency in TMD cases (P = 0·01, R2 = 3%) and more awakenings in all participants (P = 0·03, R2 = 2%). After accounting for these factors, TMD presence and pain ratings were not significantly related to PSQI scores. These results show that reported poor sleep quality in TMD is better explained by depressive symptoms than by PSG-assessed sleep disturbances or myofascial pain. As TMD cases lacked typical PSG features of clinical depression, the results suggest a negative cognitive bias in TMD and caution against interpreting self-report sleep measures as accurate indicators of PSG sleep disturbance. Future investigations should take account of depressive symptomatology when interpreting reports of poor sleep.

The aim of this study was to determine the frequency and predictors of correctly initiated continuous positive airway pressure (CPAP) settings on the initial night of hospitalization in patients with known obstructive sleep apnea-hypopnea syndrome (OSAHS). Hospital records of all patients who underwent an outpatient therapeutic polysomnogram (PSG) at our institution between January 2005 and December 2010 were retrospectively reviewed. Data collected included initial CPAP settings on hospital admission, latency to hospitalization (from sleep study), hospital length of stay, demographic variables, and PSG variables. One hundred seventy subjects were included in the analysis: 51 % were male, average age (±SD) was 55.3 ± 13.7 years, and body mass index was 43.7 ± 10.4 kg/m(2). OSAHS was generally severe (apnea-hypopnea index (AHI) 52.8 ± 37.3 event/h). Mean CPAP setting during in-laboratory titration was 11.1 ± 3.1 cm H2O and during the first night of hospitalization was 9.5 ± 2.8 cm H2O (p < 0.0001). Of 170 subjects, only 71 (42 %) received the correct laboratory-derived CPAP setting on the first night of hospitalization. In a multivariable logistic regression analysis, higher body mass index (BMI), lower CPAP level determined during PSG, and shorter latency (months) between PSG and hospitalization were associated with receiving the correct CPAP setting during the first night of hospitalization: Each 1 kg/m(2) increase in BMI was associated with a 7 % increase odds of receiving the correct CPAP setting during the first night of hospitalization (OR 1.07, 95 % CI 1.02-1.12), while each 1 cm H2O increase in CPAP during PSG and each 1 month longer latency between PSG and hospitalization was associated with a 15 and 7 %, respectively, decrease in the odds of receiving the correct CPAP setting during the first night of hospitalization (CPAP OR 0.85, 95 % CI 0.74-0.97 and latency OR 0.93, 95 % CI 0.90-0.97). There was no in-hospital mortality, and correct CPAP settings did not affect hospital length of stay. Among patients admitted to the hospital, a correct, laboratory-derived CPAP setting is infrequently prescribed during the first night of hospitalization. Predictors for correctly ordering CPAP include latency from the time of in-laboratory CPAP titration, BMI, and laboratory-derived CPAP level.

To determine whether total sleep time (TST) and specific sleep stage duration are associated with bodily pain perception and whether sex, age, or subjective sleepiness modifies this relationship. Data from adults ages 39-90 y (n = 5,199) who took part in the Sleep Heart Health Study Exam 1 were analyzed. TST, rapid eye movement (REM) sleep time, and slow wave sleep (SWS) time were measured by unattended, in-home nocturnal polysomnography. Bodily pain perception was measured via the Short Form-36 questionnaire bodily pain component. We used logistic regression to examine associations between total and individual sleep stage durations and bodily pain perception controlling for age, sex, race, body mass index, apnea-hypopnea index, antidepressant use, and important cardiovascular conditions (smoking [pack-years], history of diabetes, and history of percutaneous coronary intervention and/or coronary artery bypass graft). In the fully adjusted model, REM sleep time and SWS time were not ...

Sleep bruxism (SB), primarily involving rhythmic grinding of the teeth during sleep, has been advanced as a causal or maintenance factor for a variety of oro-facial problems, including temporomandibular disorders (TMD). As laboratory polysomnographic (PSG) assessment is extremely expensive and time-consuming, most research testing this belief has relied on patient self-report of SB. The current case-control study examined the accuracy of those self-reports relative to laboratory-based PSG assessment of SB in a large sample of women suffering from chronic myofascial TMD (n = 124) and a demographically matched control group without TMD (n = 46). A clinical research coordinator administered a structured questionnaire to assess self-reported SB. Participants then spent two consecutive nights in a sleep laboratory. Audiovisual and electromyographic data from the second night were scored to assess whether participants met criteria for the presence of 2 or more (2+) rhythmic masticatory mu...