A Micro-Longitudinal Study of Naps, Sleep Disturbance, and Headache Severity in Women with Chronic Migraine.

OBJECTIVE: To examine the relationship between headaches, naps, and nocturnal sleep in women with chronic migraine (CM) using micro-longitudinal data from diaries and actigraphy. METHODS: 20 women with CM and 20 age and sex-matched healthy controls (HC) completed self-report questionnaires, electronic diaries, and wrist actigraphy over a 4-week period. Between-group comparisons were conducted with naps (frequency and duration) as the primary variable of interest. Within-group analyses were conducted on the CM group using hierarchical linear mixed models to examine the temporal relationships between headache severity, sleep behaviors, and sleep parameters. The primary variables of interest were naps (number and duration) and nocturnal sleep efficiency (diary and actigraphy). RESULTS: The CM group reported significantly more days with naps (25.85%) compared to the HC group (9.03%) during the study period (p = .0025). Within-group analyses in CM revealed that greater headache severity was associated with longer nap duration (p = .0037) and longer nap duration was associated with lower sleep efficiency measured using diaries (p = .0014) and actigraphy (p < .0001). CONCLUSIONS: Napping is more frequent in CM than HC and nap duration in CM is associated with headache severity and nocturnal sleep disturbance. These findings provide initial support for the hypothesis that daytime napping is a behavioral coping strategy used in CM that could contribute to insomnia.

Sleep Disorders Among People With Migraine: Results From the Chronic Migraine Epidemiology and Outcomes (CaMEO) Study.

OBJECTIVES: We examined the cross-sectional association of sleep apnea and indices of sleep quality with both episodic migraine (EM) and chronic migraine (CM). BACKGROUND: Sleep apnea and abnormal patterns of sleep, such as insomnia, were associated with migraine onset, severity, and progression in previous research. METHODS: The Chronic Migraine Epidemiology & Outcomes Study, a longitudinal study, used a series of web-based surveys to assess migraine symptoms, burden, and patterns of health care utilization. Quota sampling was used from September 2012 to November 2013 to generate a representative sample of the US population. Persons who screened positive for sleep apnea on the Berlin Questionnaire are said to be at "high risk" for sleep apnea. Respondents indicated if they believed that they had sleep apnea, if a physician had diagnosed it, and if and how they were treated. Other aspects of sleep quality were assessed using the Medical Outcomes Study (MOS) Sleep Measures. RESULTS: Of 12,810 eligible respondents with migraine and data on sleep, 11,699 with EM (91.3%) and 1111 with CM (8.7%) provided valid data for this analyses. According to the Berlin Questionnaire, 4739/12,810 (37.0%) were at "high risk" for sleep apnea, particularly persons with CM vs EM (575/1111 [51.8%] vs 4164/11,699 [35.6%]), men vs women (1431/3220 [44.4%] vs 3308/9590 [34.5%]), people with higher body mass index, and older people (all P < .001). Among respondents to the MOS Sleep Measures, persons with CM were more likely to report poor sleep quality than those with EM, including sleep disturbance (mean [SD] values: 53.2 [26.9] vs 37.9 [24.3]), snoring (38.0 [33.9] vs 31.0 [32.1]), shortness of breath (34.9 [29.8] vs 15.3 [20.6]), somnolence (44.1 [23.4] vs 32.2 [21.2]), and less likely to report sleep adequacy (34.0 [24.2] vs 39.2 [22.1]). CONCLUSIONS: Compared with respondents with EM, a larger proportion of those with CM were at "high risk" for sleep apnea and reported poor sleep quality. This reflects an association between CM vs EM and sleep apnea and poor sleep quality; the potential relationships are discussed.

Sleep and Migraine: Assessment and Treatment of Comorbid Sleep Disorders.

The relationship of sleep and migraine is unequivocal and familiarity with the nature and magnitude of these associations may inform clinical practice. Recent prospective, longitudinal, and time-series analysis has begun to unravel the magnitude and temporal patterns of sleep and migraine. Prospective evidence has shown that sleep variables can trigger acute migraine, precede and predict new onset headache by several years, and indeed, sleep disturbance and snoring are risk factors for chronification. The presence of a sleep disorder is associated with more frequent and severe migraine and portends a poorer headache prognosis. Interestingly, the disorders linked to migraine are quite varied, including insomnia, snoring and obstructive sleep apnea, restless legs, circadian rhythm disorders, narcolepsy, and others. Insomnia is by far the most common sleep disorder in headache patients. In fact, the majority of patients with chronic migraine presenting for treatment have insomnia. Despite a rapidly expanding literature, very few controlled treatment studies have been published to guide clinical practice. This paper focuses on clinical assessment and treatment of sleep disorders. An algorithm is presented for sleep disorders management in the migraine patient, which highlights major sleep disorders and psychiatric comorbidity. Diagnostic procedures are recommended that are conducive to clinical practice. Suggested tools include the sleep history, screening mnemonics, prediction equation, and sleep diary. New developments in treatment have produced abbreviated and cost-effective therapies for insomnia and obstructive sleep apnea that may reach a larger population. Revisions in the diagnostic manuals for sleep and headache disorders enhance recognition of sleep-related headache. Recommendations include behavioral sleep regulation, shown in recent controlled trials to decrease migraine frequency, management for sleep apnea headache, cognitive behavioral therapy (CBT) for insomnia abbreviated for the physician practice setting, sleep-related headache trigger, and others. There is no empirical evidence that sleep evaluation should delay or supersede usual headache care. Rather, sleep management is complimentary to standard headache practice.

Cognitive-Behavioral Therapy for Insomnia to Reduce Chronic Migraine: A Sequential Bayesian Analysis.

BACKGROUND: Insomnia is frequently comorbid with chronic migraine, and small trials suggest that cognitive-behavioral treatment of insomnia (CBTi) may reduce migraine frequency. This study endeavored to provide a quantitative synthesis of existing CBTi trials for adults with chronic migraine using Bayesian statistical methods, given their utility in combining prior knowledge with sequentially gathered data. METHODS: Completer analyses of 2 randomized trials comparing CBTi to a sham control intervention (Calhoun and Ford, 2007; Smitherman et al, 2016) were used to quantify the effects of a brief course of treatment on headache frequency. Change in headache frequency from baseline to the primary endpoint (6-8 weeks posttreatment) was regressed on group status using a Gaussian linear model with each study specified in the order of completion. To estimate the combined effect, posterior distributions from the Calhoun and Ford study were used as informative priors for conditioning on the Smitherman et al data. RESULTS: In a combined analysis of these prior studies, monthly headache frequency of the treatment group decreased by 6.2 days (95%CrI: -9.7 to -2.7) more than the control group, supporting an interpretation that there is a 97.5% chance that the treatment intervention is at least 2.7 days better than the control intervention. The analysis supports the hypothesis that at least for those who complete treatment, there is high probability that individuals who receive CBTi experience greater headache reduction than those who receive a control intervention equated for therapist time and out-of-session skills practice. CONCLUSION: Cognitive-behavioral interventions for comorbid insomnia hold promise for reducing headache frequency among those with chronic migraine. These findings add to a small but growing body of literature that migraineurs with comorbid conditions often respond well to behavioral interventions, and that targeting comorbidities may improve migraine itself.

Can Circadian Dysregulation Exacerbate Migraines?

OBJECTIVE: This observational pilot study examined objective circadian phase and sleep timing in chronic migraine (CM) and healthy controls (HC) and the impact of circadian factors on migraine frequency and severity. BACKGROUND: Sleep disturbance has been identified as a risk factor in the development and maintenance of CM but the biological mechanisms linking sleep and migraine remain largely theoretical. METHODS: Twenty women with CM and 20 age-matched HC completed a protocol that included a 7 day sleep assessment at home using wrist actigraphy followed by a circadian phase assessment using salivary melatonin. We compared CM vs HC on sleep parameters and circadian factors. Subsequently, we examined associations between dim-light melatonin onset (DLMO), the midpoint of the sleep episode, and the phase angle (time from DLMO to sleep midpoint) with the number of migraine days per month and the migraine disability assessment scale (MIDAS). RESULTS: CM and HC did not differ on measures of sleep or circadian phase. Within the CM group, more frequent migraine days per month was significantly correlated with DLMO (r = .49, P = .039) and later sleep episode (r = .47, P = .037). In addition, a greater phase angle (ie, circadian misalignment) was significantly correlated with more severe migraine-related disability (r = .48, P = .042). These relationships remained significant after adjusting for total sleep time. CONCLUSIONS: This pilot study revealed that circadian misalignment and delayed sleep timing are associated with higher migraine frequency and severity, which was not better accounted for by the amount of sleep. These findings support the plausibility and need for further investigation of a circadian pathway in the development and maintenance of chronic headaches. Specifically, circadian misalignment and delayed sleep timing could serve as an exacerbating factor in chronic migraines when combined with biological predispositions or environmental factors.

Randomized Controlled Pilot Trial of Behavioral Insomnia Treatment for Chronic Migraine With Comorbid Insomnia.

BACKGROUND: Migraine frequently co-occurs with and is triggered by sleep disturbance, particularly insomnia, and the large majority of patients with chronic migraine (CM) have comorbid insomnia. Limited evidence suggests that behavioral regulation of sleep may reduce migraine frequency, but studies to date have not assessed the viability of stimulus control and sleep restriction interventions or included objective measurement of sleep parameters. The aim of this study, thus, was to pilot-test the efficacy of a brief behavioral insomnia intervention for adults with CM and comorbid insomnia; headache diaries and actigraphy were included to assess outcomes throughout the trial. METHODS: This randomized parallel-arm pilot trial recruited adults with both CM and comorbid insomnia. Participants were randomly assigned to three 30-minute biweekly sessions of cognitive-behavioral therapy for insomnia (CBTi) or control treatment. Participants were blinded to treatment and control conditions to control for outcome expectations. Each treatment condition involved training in and daily practice in 5 instructions/skills. The CBTi group learned and practiced skills pertaining to stimulus control and sleep restriction. The control intervention was the same as used by Calhoun and Ford (2007) and involved training in and daily practice of skills pertaining to keeping a consistent food/liquid intake, range of motion exercises, and acupressure. Participants provided outcome data via daily headache diaries, actigraphy, and self-report measures. The primary outcome was reduction in headache frequency at 2 weeks post-treatment and 6-week follow-up; secondary outcomes included other headache parameters, objective actigraphic and subjective changes in sleep, and treatment effect sizes and perceived credibility. Generalized estimating equations with a binomial logit link and inverse probability weights were used to assess the primary outcome among the intent-to-treat sample, and repeated measures generalized linear models were used to assess changes in secondary outcomes after controlling for baseline values. RESULTS: The intent-to-treat analyses included 31 adults (M age = 30.8 [12.9] years; 90.3% female; 80.6% white) with CM and comorbid insomnia. Both interventions yielded reductions in headache frequency at post-treatment (26.9% reduction for CBTi vs. 36.2% for control) and follow-up (48.9% for CBTi vs. 25.0% for control). At follow-up the odds of experiencing headache were 60% lower for CBTi than for control treatment, indicative of a large effect size that did not reach statistical significance after Bonferroni correction for assessing two primary endpoints (odds ratio: 0.40; 95% CI: 0.17, 0.91; P = .028). CBTi produced significantly larger increases than control treatment in total sleep time and sleep efficiency as quantified by actigraphy, as well as in self-reported insomnia severity. Adherence was high and treatments were perceived as credible without differences between groups, but the control group experienced a higher rate of dropouts. No adverse events were reported. CONCLUSIONS: Behavioral treatment of comorbid insomnia in individuals with CM produced large reductions in headache frequency, though some improvement in headache occurred with a behavioral intervention not focused on modifying sleep. Among the CBTi group only, both headache frequency and sleep parameters continued to improve after treatment, suggesting the presence of enduring effects over time. Directly treating insomnia using components of stimulus control and sleep restriction holds promise for reducing comorbid migraine. Development of and comparison to a truly inert pseudotherapy control presents unique challenges that future studies should address.

Well-Established and Empirically Supported Behavioral Treatments for Migraine.

This paper provides an overview of the well-established and empirically supported behavioral interventions for the treatment of migraine. The considerable evidence base addressing behavioral interventions amassed since 1969 has conclusively established the efficacy of therapies featuring combinations of relaxation, biofeedback, and stress management training, and demonstrated they are capable of yielding benefits on par with pharmacological therapies for migraine. Behavioral interventions also are well suited for delivery across a variety of different contexts (e.g., group vs. individual, standard clinic vs. limited therapist contact, face-to-face vs. technology-assisted). Despite the amply established efficacy and effectiveness of these self-management interventions for the treatment of migraine, the availability and implementation of these approaches remain limited for many headache sufferers. We anticipate the technological advances in delivery platforms will provide better access to behavioral self-management strategies for migraine.

Tension-type headache and sleep.

This review describes empirical evidence for a bidirectional relationship between tension-type headache (TTH) and sleep. In its most severe form, chronic TTH (CTTH) affects 2-3 % of the population and can be very disabling. Sleep dysregulation triggers episodic TTH, and sleep disorders may complicate and exacerbate headache. The majority of CTTH sufferers also have insomnia, and longitudinal data suggest that insomnia is a risk factor for new-onset TTH. Similarly, observational studies suggest that sleep disturbance is a risk factor for new-onset TTH and for progression from episodic to chronic TTH (i.e., headache "chronification"). CTTH is the most common headache secondary to sleep apnea and other sleep-related breathing disorders. Psychiatric disorders are comorbid with both TTH and insomnia and may further complicate diagnosis and treatment. Developments in diagnostic classification of sleep-related headache are presented.

Sleep-related headaches.

Irrespective of diagnosis, chronic daily, morning, or "awakening" headache patterns are soft signs of a sleep disorder. Sleep apnea headache may emerge de novo or may present as an exacerbation of cluster, migraine, tension-type, or other headache. Insomnia is the most prevalent sleep disorder in chronic migraine and tension-type headache, and increases risk for depression and anxiety. Sleep disturbance (e.g., sleep loss, oversleeping, schedule shift) is an acute headache trigger for migraine and tension-type headache. Snoring and sleep disturbance are independent risk factors for progression from episodic to chronic headache.

Stress and sleep duration predict headache severity in chronic headache sufferers.

The objective of this study was to evaluate the time-series relationships between stress, sleep duration, and headache pain among patients with chronic headaches. Sleep and stress have long been recognized as potential triggers of episodic headache (<15 headache days/month), though prospective evidence is inconsistent and absent in patients diagnosed with chronic headaches (≥15 days/month). We reanalyzed data from a 28-day observational study of chronic migraine (n=33) and chronic tension-type headache (n=22) sufferers. Patients completed the Daily Stress Inventory and recorded headache and sleep variables using a daily sleep/headache diary. Stress ratings, duration of previous nights' sleep, and headache severity were modeled using a series of linear mixed models with random effects to account for individual differences in observed associations. Models were displayed using contour plots. Two consecutive days of either high stress or low sleep were strongly predictive of headache, whereas 2 days of low stress or adequate sleep were protective. When patterns of stress or sleep were divergent across days, headache risk was increased only when the earlier day was characterized by high stress or poor sleep. As predicted, headache activity in the combined model was highest when high stress and low sleep occurred concurrently during the prior 2 days, denoting an additive effect. Future research is needed to expand on current findings among chronic headache patients and to develop individualized models that account for multiple simultaneous influences of headache trigger factors.

Direct costs of preventive headache treatments: comparison of behavioral and pharmacologic approaches.

OBJECTIVES: This study provides preliminary data and a framework to facilitate cost comparisons for pharmacologic vs behavioral approaches to headache prophylactic treatment. BACKGROUND: There are few empirical demonstrations of cumulative costs for pharmacologic and behavioral headache treatments, and there are no direct comparisons of short- and long-range (5-year) costs for pharmacologic vs behavioral headache treatments. METHODS: Two separate pilot surveys were distributed to a convenience sample of behavioral specialists and physicians identified from the membership of the American Headache Society. Costs of prototypical regimens for preventive pharmacologic treatment (PPT), clinic-based behavioral treatment (CBBT), minimal contact behavioral treatment (MCBT), and group behavioral treatment were assessed. Each survey addressed total cost accumulated during treatment (ie, intake, professional fees) excluding costs of acute medications. The total costs of preventive headache therapy by type of treatment were then evaluated and compared over time. RESULTS: During the initial months of treatment, PPT with inexpensive mediations (<0.75 $/day) represents the least costly regimen and is comparable to MCBT in expense until 6 months. After 6 months, PPT is expected to become more costly, particularly when medication cost exceeds 0.75$ a day. When using an expensive medication (>3 $/day), preventive drug treatment becomes more expensive than CBBT after the first year. Long-term, and within year 1, MCBT was found to be the least costly approach to migraine prevention. CONCLUSIONS: Through year 1 of treatment, inexpensive prophylactic medications (such as generically available beta-blocker or tricyclic antidepressant medications) and behavioral interventions utilizing limited delivery formats (MCBT) are the least costly of the empirically validated interventions. This analysis suggests that, relative to pharmacologic options, limited format behavioral interventions are cost-competitive in the early phases of treatment and become more cost-efficient as the years of treatment accrue.

Processes of change in acceptance and commitment therapy and cognitive therapy for depression: a mediation reanalysis of Zettle and Rains.

Several articles have recently questioned the distinction between acceptance and commitment therapy (ACT) and traditional cognitive therapy (CT). This study presents a reanalysis of data from Zettle and Rains that compared 12 weeks of group CT with group ACT. For theoretical reasons, Zettle and Rains also included a modified form of CT that did not include distancing, and no intent-to-treat analysis was included. Particularly because that unusual third condition did somewhat better than the full CT package, it contaminated the direct comparison of ACT and CT, which has of late become theoretically interesting. In the present study, data from participants in the ACT and CT conditions were reanalyzed. ACT was shown to produce greater reductions in levels of self-reported depression using an intent-to-treat analysis. Posttreatment levels of cognitive defusion mediated this effect at follow-up. The occurrence of depressogenic thoughts and level of dysfunctional attitudes did not function as mediators. This study adds additional evidence that ACT works through distinct and theoretically specified processes that are not the same as CT.

Sleep and headache.

OPINION STATEMENT: Headache has been linked to a wide range of sleep disorders that may impact headache management. There are no evidence-based guidelines, but the authors believe that literature supports the following clinical recommendations: 1. Diagnose headache according to standardized criteria. Specific diagnoses are associated with increased risk for specific sleep and psychiatric disorders. 2. Collect sleep history in relation to headache patterns. Screening questionnaires and prediction equations are cost-effective. 3. Rule out sleep apnea headache in patients with awakening headache or higher-risk headache diagnoses (cluster, hypnic, chronic migraine, and chronic tension-type headache); patients with signs and symptoms of obstructive sleep apnea warrant polysomnography and treatment according to sleep medicine practice guidelines. There is no evidence for suspending conventional headache treatment in suspected or confirmed cases of sleep apnea. Treatment of sleep apnea with CPAP may improve or resolve headache in a subset of patients. The impact on sleep apnea headache of other treatments for sleep apnea (eg, oral appliances, surgery, weight loss) is largely untested. At a minimum, sedative-hypnotic drugs should be avoided in suspected apneics until the sleep apnea is treated. 4. Among patients with migraine and tension-type headache, insomnia is the most common sleep complaint, reported by one half to two thirds of clinic patients. Patients who suffer from chronic migraine or tension-type headache may benefit from behavioral sleep modification. Pharmacologic treatment may be considered on a case-by-case basis, with hypnotics, anxiolytics, or sedating antidepressants used to manage insomnia, tailoring treatment to the symptom pattern. 5. Individuals with chronic headache are at increased risk for psychiatric disorders. Assessment for depression and anxiety may be warranted when either insomnia or hypersomnia is present. Psychiatric symptoms affect the choice of sedating versus alerting versus neutral pharmacologic agents for headache. 6. All headache patients, particularly those with episodic migraine and tension-type headaches, may benefit from inclusion of sleep variables in trigger management.

Psychiatric comorbidities and migraine chronification.

A growing body of literature has implicated comorbid psychopathology as a potential risk factor for the chronification of migraine. Of the psychiatric disorders, depressive and anxiety disorders have been most consistently associated with the chronification of migraine. A shared dysfunction of the serotonergic system, medication overuse, and psychological factors have been proposed to mediate this relationship, although the responsible mechanisms are still largely unclear. This article overviews literature on psychiatric comorbidities and migraine chronification, considers mechanisms underlying this relationship, and notes directions for future clinical and empirical work.

Optimizing circadian cycles and behavioral insomnia treatment in migraine.

Sleep regulation may play a key role in headache management for individuals with migraine. At least among individuals with a predisposition to headache, episodes may be provoked by sleep deprivation or excess, as well as by sleep disorders. Chronobiological patterns have been identified in some forms of headache, including migraine. Insomnia is the most common sleep disorder in headache clinic populations, observed in half to two thirds of migraineurs. Recent evidence suggests migraine may improve with regulation of sleep. Because sleep represents a potentially modifiable vulnerability to headache, practitioners may wish to consider strategies that restore sleep homeostasis. Behavioral strategies are effective for regulation of sleep and may be abbreviated for headache medical practice settings. This article discusses the nature and prevalence of sleep complaints in migraineurs, conceptualization, and behavioral management of insomnia in the headache practice setting.

Change mechanisms in EMG biofeedback training: cognitive changes underlying improvements in tension headache.

Forty-three college students suffering from recurrent tension headache were randomly assigned to 1 of 4 electromyographic (EMG) biofeedback training conditions. Although all subjects were led to believe they were learning to decrease frontal EMG activity, actual feedback was contingent on decreased EMG activity for half of the subjects and increased EMG activity for the other half. Within these 2 groups, subjects also viewed bogus video displays designed to convince them they were achieving large (high success) or small (moderate success) reductions in EMG activity. Regardless of actual changes in EMG activity, subjects receiving high-success feedback showed substantially greater improvement in headache activity (53%) than subjects receiving moderate success feedback (26%). Performance feedback was also related to changes in locus of control and self-efficacy. Changes in these 2 cognitive variables during biofeedback training were also correlated with reductions in headache activity following treatment, whereas changes in EMG activity exhibited during training were uncorrelated with outcome. These results suggest that the effectiveness of EMG biofeedback training with tension headache may be mediated by cognitive changes induced by performance feedback and not primarily by reductions in EMG activity.