Previous evidence demonstrates that the incidence of chronic sleep disturbance is high in patients with temporomandibular joint disorder (TMD). However, there has been little examination of whether heightened daytime pain sensitivity in this population is associated with alter sleep architecture at night. We aimed to test the extent to which daytime pain sensitivity, measured using quantitative sensory testing (QST) is associated with objective markers of sleep physiology, including sleep architecture and power spectral density bands, in patients with TMD. Female participants (n=149) with insomnia and TMD were recruited as part of a randomized-controlled trial. Pre-randomization, we performed a quantitative sensory testing (QST) battery to measure General Pain Sensitivity, a Central Sensitization Index, and Masseter Pressure Pain Threshold, and performed polysomnography (PSG) that night to calculate sleep architecture parameters (N1%, N2%, SWS%, REM%) and derive relative power in the Delta (0.5-3.5 Hz), Theta (3.5-8.0 Hz), Alpha (8.0-15.0 Hz), and Beta (15-30.0 Hz) spectral bands during sleep. We fit linear regression models with sleep parameters as the outcome, and pain sensitivity as the predictor, controlling for age, depressive symptom severity, and race. Higher Central Sensitization (B = -2.863, P = <0.01) and General Pain Sensitivity Indices (B = -3.069, P = <0.01) were significantly associated with lower REM% both before after controlling for covariates, however masseter pressure pain threshold was not significantly associated with REM% (B = -0.0259, P = 0.0743). Pain sensitivity measures were not significantly associated with relative power in any of the spectral bands, or with any other sleep architectural stages. Heightened pain sensitivity, measured using QST is associated with objective features of sleep architecture in TMD patients, potentially due to heightened pain interfering with sleep. These findings may contribute to understanding of physiological mechanisms through which acute and chronic pain result in sleep disruption. Grant support from NIH Grant R01 DE019731. Previous evidence demonstrates that the incidence of chronic sleep disturbance is high in patients with temporomandibular joint disorder (TMD). However, there has been little examination of whether heightened daytime pain sensitivity in this population is associated with alter sleep architecture at night. We aimed to test the extent to which daytime pain sensitivity, measured using quantitative sensory testing (QST) is associated with objective markers of sleep physiology, including sleep architecture and power spectral density bands, in patients with TMD. Female participants (n=149) with insomnia and TMD were recruited as part of a randomized-controlled trial. Pre-randomization, we performed a quantitative sensory testing (QST) battery to measure General Pain Sensitivity, a Central Sensitization Index, and Masseter Pressure Pain Threshold, and performed polysomnography (PSG) that night to calculate sleep architecture parameters (N1%, N2%, SWS%, REM%) and derive relative power in the Delta (0.5-3.5 Hz), Theta (3.5-8.0 Hz), Alpha (8.0-15.0 Hz), and Beta (15-30.0 Hz) spectral bands during sleep. We fit linear regression models with sleep parameters as the outcome, and pain sensitivity as the predictor, controlling for age, depressive symptom severity, and race. Higher Central Sensitization (B = -2.863, P = <0.01) and General Pain Sensitivity Indices (B = -3.069, P = <0.01) were significantly associated with lower REM% both before after controlling for covariates, however masseter pressure pain threshold was not significantly associated with REM% (B = -0.0259, P = 0.0743). Pain sensitivity measures were not significantly associated with relative power in any of the spectral bands, or with any other sleep architectural stages. Heightened pain sensitivity, measured using QST is associated with objective features of sleep architecture in TMD patients, potentially due to heightened pain interfering with sleep. These findings may contribute to understanding of physiological mechanisms through which acute and chronic pain result in sleep disruption. Grant support from NIH Grant R01 DE019731.
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