Project description:ObjectiveThere is an unexplained association between disturbed sleep and migraine. In this blinded crossover study, we investigate if experimental sleep restriction has a different effect on pain thresholds and suprathreshold pain in interictal migraineurs and controls.MethodsForearm heat pain thresholds and tolerance thresholds, and trapezius pressure pain thresholds and suprathreshold pain were measured in 39 interictal migraineurs and 31 healthy controls after two consecutive nights of partial sleep restriction and after habitual sleep.ResultsThe effect of sleep restriction was not significantly different between interictal migraineurs and controls in the primary analyses. Pressure pain thresholds tended to be lower (i.e., increased pain sensitivity) after sleep restriction in interictal migraineurs compared to controls with a 48-hour preictal-interictal cut-off (p = 0.061). We found decreased pain thresholds after sleep restriction in two of seven migraine subgroup comparisons: heat pain thresholds decreased in migraineurs with lower pain intensity during attacks (p = 0.005) and pressure pain thresholds decreased in migraineurs with higher severity of photophobia during attacks (p = 0.031). Heat pain thresholds tended to decrease after sleep restriction in sleep-related migraine (p = 0.060). Sleep restriction did not affect suprathreshold pain measurements in either group.ConclusionThis study could not provide strong evidence for an increased effect of sleep restriction on pain sensitivity in migraineurs compared to healthy controls. There might be a slightly increased effect of sleep restriction in migraineurs, detectable using large samples or more pronounced in certain migraine subgroups.
Project description:BackgroundPatients with migraine are vulnerable to insufficient sleep, but the impact of sleep restriction is largely unknown. In addition, the importance of sleep may be different in patients with migraine who mostly have attack onsets during sleep, so called sleep-related migraine, compared to patients with non-sleep-related migraine. In this study we investigate the effect of sleep restriction on endogenous pain modulation in patients with migraine and healthy controls. We also compared the effect of sleep restriction in sleep-related and in non-sleep-related migraine.MethodsMeasurements were conducted in 39 patients with migraine between attacks and 31 controls, once after habitual sleep and once after two consecutive nights of partial sleep restriction. There were 29 and 10 patients with non-sleep-related and sleep-related migraine respectively. Test stimulus was 2-min tonic noxious heat to the left volar forearm. Temporal summation was calculated as the regression coefficient for rated pain in the late part of this 2-min stimulation. Conditioning stimulus was right hand-immersion in 7 °C water. Conditioned pain modulation was defined as the difference in rated pain with and without the conditioning stimulus and was calculated for temporal summation and mean rated pain for the test stimulus. The effect of sleep restriction on temporal summation and conditioned pain modulation was compared in migraine subjects and controls using two-level models with recordings nested in subjects.ResultsConditioned pain modulation for temporal summation of heat pain tended to be reduced after sleep restriction in patients with migraine compared to controls (p = 0.060) and, in an exploratory analysis, was reduced more after sleep restriction in sleep-related than in non-sleep-related migraine (p = 0.017). No other differences between groups after sleep restriction were found for temporal summation or conditioned pain modulation.ConclusionPatients with migraine may have a subtly altered endogenous pain modulation system. Sleep restriction may have an increased pronociceptive effect on this system, suggesting a mechanism for vulnerability to insufficient sleep in migraine. This effect seems to be larger in sleep-related migraine than in non-sleep-related migraine.
Project description:IntroductionObservational studies suggested that diabetes mellitus [type 1 diabetes mellitus (T1DM), type 2 diabetes mellitus (T2DM)], multiple sclerosis (MS), and migraine are associated with Alzheimer's disease (AD). However, the causal link has not been fully elucidated. Thus, we aim to assess the causal link between T1DM, T2DM, MS, and migraine with the risk of AD using a two-sample Mendelian randomization (MR) study.MethodsGenetic instruments were identified for AD, T1DM, T2DM, MS, and migraine respectively from genome-wide association study. MR analysis was conducted mainly using the inverse-variance weighted (IVW) method.ResultsThe result of IVW method demonstrated that T2DM is causally associated with risk of AD (OR: 1.237, 95% CI: 1.099-1.391, P: 0.0003). According to the IVW method, there is no causal association between TIDM, MS, migraine, and the risk of AD (all p value > 0.05). Here we show, there is a causal link between T2DM and the risk of AD.ConclusionThese findings highlight the significance of active monitoring and prevention of AD in T2DM patients. Further studies are required to actively search for the risk factors of T2DM combined with AD, explore the markers that can predict T2DM combined with AD, and intervene and treat early.
Project description:Cognitive decline is a major concern in patients with migraine. Depression, anxiety, and/or poor sleep quality are well-known comorbidities of migraine, but available evidence on the subjective cognitive decline (SCD) is limited. This study aimed to investigate the presence and frequency of SCD and its relationship with anxiety, depression and sleep quality in patients with migraine.We enrolled patients with migraine who scored within the normal range of the Korean-Mini Mental State Examination and the Korean-Montreal Cognitive Assessment. Using the Subjective Cognitive Decline Questionnaire (SCD-Q), participants with ≥7 were assigned to the SCD group. The Headache Impact Test-6, Generalized Anxiety Disorder-7, Patient Health Questionnaire-9, and Pittsburgh Sleep Quality Index were used and analyzed between the two groups.A total of 188 patients with migraine, aged 38.1 ± 9.9 years, were enrolled. The mean SCD-Q score was 6.5 ± 5.5, and 44.7% of participants were identified as SCD. Migraineurs with SCD reported higher headache pain intensity and headache impact, as well as greater prevalence of anxiety, depression, reduced quality of sleep, and shorter sleep duration during weekdays compared to migraineurs without SCD. There were no significant differences in terms of age, sex, migraine type (chronic/episodic), medication, or sleep duration during weekends between the two groups. Upon multivariate logistic analysis adjusted for age, sex, headache characteristics, and psychological variables, depression was associated with increased risk of SCD (Odds ratio 1.31, 95% confidence interval 1.16-1.49) and sleep duration during weekdays was associated with decreased risk of SCD (Odds ratio 0.66, 95% confidence interval 0.44-0.97).A non-negligible number of patients with migraine complained of SCD. Depression and short sleep duration during weekdays were related to SCD among adult migraineurs.
Project description:IntroductionVeterans with chronic pain frequently report comorbid disruptions in sleep and psychological dysfunction. The purpose of this study was to investigate whether psychological function variables mediate the sleep-pain relationship. Knowledge regarding such contributing factors can inform the development and optimization of treatments for sleep disturbances and pain.Materials and methodsIn an IRB-approved, registered clinical trial, we collected objective sleep data from U.S. military Veterans with chronic pain (N = 184, ages 23-81) using wrist actigraphy for 7 days and self-reported survey data assessing sleep quality, pain intensity, and psychological function (depression, anxiety, post-traumatic stress disorder, and pain catastrophizing). We investigated the associations between objectively measured and self-reported sleep quality and self-reported pain intensity. In addition, using parallel mediation analyses, we examined whether psychological function variables mediated these associations.ResultsActigraphy showed suboptimal sleep duration (less than 7 hours) and sleep fragmentation for most participants. Self-reported poor sleep quality and pain intensity were significantly correlated. Pain catastrophizing was found to mediate the association between self-reported sleep quality and pain intensity.ConclusionsSleep disturbances in this sample of Veterans with chronic pain included insufficient sleep, fragmented sleep, and perceived poor sleep quality. Analyses suggest that poor perceived sleep quality and pain intensity are mediated via pain catastrophizing. The finding highlights the potential importance of pain catastrophizing in Veterans with chronic pain. Future longitudinal research is needed to determine the extent to which treatments that reduce pain catastrophizing might also improve both sleep and pain outcomes.
Project description:BackgroundThere is a bidirectional link between sleep and migraine, however causality is difficult to determine. This study aimed to investigate this relationship using data collected from a smartphone application.MethodsSelf-reported data from 11,166 global users (aged 18-81 years, mean: 41.21, standard deviation: 11.49) were collected from the Migraine Buddy application (Healint Pte. Ltd.). Measures included: start and end times of sleep and migraine attacks, and pain intensity. Bayesian regression models were used to predict occurrence of a migraine attack the next day based on users' deviations from average sleep, number of sleep interruptions, and hours slept the night before in those reporting ≥ 8 and < 25 migraine attacks on average per month. Conversely, we modelled whether attack occurrence and pain intensity predicted hours slept that night.ResultsThere were 724 users (129 males, 412 females, 183 unknown, mean age = 41.88 years, SD = 11.63), with a mean monthly attack frequency of 9.94. More sleep interruptions (95% Highest Density Interval (95%HDI [0.11 - 0.21]) and deviation from a user's mean sleep (95%HDI [0.04 - 0.08]) were significant predictors of a next day attack. Total hours slept was not a significant predictor (95%HDI [-0.04 - 0.04]). Pain intensity, but not attack occurrence was a positive predictor of hours slept.ConclusionsSleep fragmentation and deviation from typical sleep are the main drivers of the relationship between sleep and migraine. Having a migraine attack does not predict sleep duration, yet the pain associated with it does. This study highlights sleep as crucial in migraine management.
Project description:Chronic pain is a common and disabling condition in adolescents. Disturbed sleep is associated with many detrimental effects in adolescents with acute and chronic pain. While sleep and pain are known to share a reciprocal relationship, the sleep-pain relationship in adolescence warrants further contextualization within normally occurring maturation of several biopsychological processes. Since sleep and pain disorders begin to emerge in early adolescence and are often comorbid, there is a need for a comprehensive picture of their interrelation especially related to temporal relationships and mechanistic drivers. While existing reviews provide a solid foundation for the interaction between disturbed sleep and pain in youth, we will extend this review by highlighting current methodological challenges for both sleep and pain assessments, exploring the recent evidence for directionality in the sleep-pain relationship, reviewing potential mechanisms and factors underlying the relationship, and providing direction for future investigations. We will also highlight the potential role of digital technologies in advancing the understanding of the sleep and pain relationship. Ultimately, we anticipate this information will facilitate further research and inform the management of pain and poor sleep, which will ultimately improve the quality of life in adolescents and reduce the risk of pain persisting into adulthood.
Project description:BackgroundProbable migraine (PM) is a subtype of migraine that is prevalent in the general population. Previous studies have shown that poor sleep quality is common among migraineurs and is associated with an exacerbation of migraine symptoms. However, information on the prevalence and clinical implication of poor sleep quality among individuals with PM is scarce. Thus, the aim of this study was to assess the prevalence and clinical impact of poor sleep quality in individuals with PM in comparison with those with migraine.MethodsTwo-stage cluster random sampling was used to perform the survey for sleep and headache in Korean general population. Participants with Pittsburgh Sleep Quality Index > 5 were considered as having poor sleep quality.ResultsOf 2695 participants, 379 (14.1%) had PM and 715 (26.5%) had poor sleep quality. Prevalence of poor sleep quality was 35.4% in the PM group, which was lower than that in the migraine group (47.6%, p = 0.011), but higher than that in the non-headache group (21.4%, p < 0.001). The PM participants with poor sleep quality showed increased headache frequency (median [interquartile range]: 2.0 [0.3-4.0] vs. 1.0 [0.2-2.0]; p = 0.001) and headache intensity (visual analogue scale, 6.0 [4.0-7.0] vs. 5.0 [3.5-6.0]; p = 0.003) compared to PM participants who had no poor sleep quality.ConclusionsPoor sleep quality was prevalent among participants with PM. It was associated with an exacerbation of PM symptoms. Our findings suggest that proper evaluation and treatment for poor sleep quality are needed in the management of PM.
Project description:Background25-hydroxyvitamin D [25(OH)D] deficiency in patients with Obstructive Sleep Apnea (OSA) has long been noted, but identifying the exact causal relationship remains hard. Investigation of the causality between 25(OH)D deficiency and OSA would help facilitate disease prevention.MethodsWe conducted a two-sample bi-directional Mendelian randomization (MR) study. For forward analysis, 237 newly identified genetic variants are used as proxies for 25(OH)D to estimate the unconfounded effect on OSA among 16,761 OSA cases and 201,194 controls of European ancestry. Reverse analysis was performed to detect the causal impact of OSA on 25(OH)D levels. The inverse variance weighted (IVW) method was used as the primary analysis. Sensitivity analysis was performed to evaluate the robustness of our results. Multivariate MR analysis was conducted to evaluate the direct link between 25(OH)D and OSA after accounting for body mass index (BMI).ResultsIVW indicated that OSA causally associated with a lower level of 25(OH)D ((β = -0.03, 95% CI = -0.06 ~ -0.007, P = 0.01). No evidence of the causal link from 25(OH)D to OSA was detected (OR = 0.99, 95% CI = 0.88 ~ 1.12, P = 0.85). Sensitivity analysis suggested the MR estimates were not biased. Multivariate MR analysis indicated the effect of OSA on 25(OH)D vanished upon accounting for BMI (β = -0.011, 95% CI = -0.028 ~ 0.007, P = 0.23).ConclusionThis MR study provided evidence that OSA was causally associated with a lower level of 25(OH)D, which might be driven by BMI. Obesity management should be enhanced in patients with OSA to prevent 25(OH)D deficiency.
Project description:Objectives: Pain Pattern Classification (PPC) and Directional Preference (DP) have been shown to be predictive of health care outcomes and serve to guide orthopedic clinical decision making. We conducted a prospective, observational cohort study to verify the association between PPC, DP, and clinical outcomes. Methods: Clinical outcome measures including pain intensity and disability were completed at first examination and follow-up by 335 patients. A Pearson's chi-squared test was used to determine differences in prevalence rates for the categorical variables, and two-sample t-tests were used to determine differences in rates for the continuous variables. A Tukey's range test was used to determine differences in follow-up pain intensity and disability for neck pain dual-classification schemes. Results: The prevalence of DP was 82.4%. The prevalence of CEN, Non-CEN, and Non-Classifiable (NC) was 15.2%, 42.1%, and 25.1%, respectively. The prevalence of DP was lowest for patients with sub-acute symptoms and who were <45 years old. Patients classified as DP CEN had, on average 2.62 NDI units less than patients classified as Non-DP. Patients classified as DP CEN had, on average, 0.90 pain intensity units less than patients classified as Non-DP at follow-up. Patients who demonstrated DP CEN did not have clinically significant lower pain intensity or disability at follow-up than patients who demonstrated Non-DP. Discussion: The results of this investigation need to be interpreted with caution with respect to the study design and it's subsequent strengths and limitations. Level of Evidence: 1b.