Chronic Headache and Potentially Modifiable Risk Factors: Screening and Behavioral Management of Sleep Disorders

Authors


  • Conflict of Interest: None

Jeanetta C. Rains, Center for Sleep Evaluation, Elliot Hospital, One Elliot Way, Manchester, NH 03103-3599, USA.

Abstract

Sleep-related variables have been identified among risk factors for frequent and severe headache conditions. It has been postulated that migraine, chronic daily headache, and perhaps other forms of chronic headache are progressive disorders. Thus, sleep and other modifiable risk factors may be clinical targets for prevention of headache progression or chronification. The present paper is part of the special series of papers entitled “Chronification of Headache” describing the empirical evidence, future research directions, proposed mechanisms, and risk factors implicated in headache chronification as well as several papers addressing individual risk factors (ie, sleep disorders, medication overuse, psychiatric disorders, stress, obesity). Understanding the link between risk factors and headache may yield novel preventative and therapeutic approaches in the management of headache. The present paper in the special series reviews epidemiological research as a means of quantifying the relationship between chronic headache and sleep disorders (sleep-disordered breathing, insomnia, circadian rhythm disorders, parasomnias) discusses screening for early detection and treatment of more severe and prevalent sleep disorders, and discusses fundamental sleep regulation strategies aimed at headache prevention for at-risk individuals.

Abbreviations:
DSM-IV

Diagnostic and Statistical Manual of Mental Disorders, 4th Ed.

ICSD

International Classification of Sleep Disorders

OR

odds ratio

UARS

upper airway resistance syndrome

INTRODUCTION

Lipton and Pan1 recently postulated that migraine might be conceptualized as a chronic progressive disorder. The progression or chronification of headache from episodic to “chronic daily headache” is a well-described clinical phenomenon.2 Potential mechanisms for headache chronification3 and needed research4 are described elsewhere. Sleep abnormalities were identified among risk factors associated with chronic headache,5 along with medication overuse,6 stress,7 psychiatric disorders,8 and obesity.9 The present paper describes sleep disorders associated with chronic headache in epidemiological research (that may potentially be relevant to chronification), clinical implications, and sleep regulation strategies aimed at risk factor reduction.

SLEEP “RISK FACTORS” FOR CHRONIC HEADACHE

Representative epidemiological studies are presented below as a means of quantifying and conveying risk, while a more complete review of the epidemiological and clinical literature concerning sleep-related headache is available elsewhere.10 This literature, especially epidemiological studies, tends to lack diagnostic precision in the classification of headache with many studies characterizing headache by patterns of frequency or proximity to sleep (ie, chronic daily, “awakening” or morning headache) rather than specific International Classification of Headache Disorders or International Classification of Headache Disorders-Edition II diagnoses. Headache has been most extensively examined in relation to sleep-disordered breathing, but other sleep disorders have also been addressed.

Snoring, Habitual Snoring, and Obstructive Sleep Apnea.— Epidemiological studies generally find that headache occurs more commonly among snorers than nonsnorers among adults as well as children, although degree of risk varies with headache and snoring definitions and other research methods.10 For example, a Swedish cross-sectional study (324 diagnosed obstructive apneics compared with random sample of the general population classified as snorers [n = 448] and nonsnorers [n = 583]) found that heavy snorers were more likely than nonsnorers in the population to have “headache at least once a week” vs “morning headache” in men (odds ratio [OR] = 2.2 [1.4-3.2] vs OR=7.9 [3.5-18.0], respectively) and women (OR = 2.7 [1.6-4.4] vs OR = 5.8 [3.0-11.0]), and such headache was similar to that observed in a comparable sample of confirmed sleep apneics of men (OR = 2.2 [1.4-3.3] vs OR = 8.6 [3.8-20]) and women (OR = 3.0 [1.3-6.8] vs OR = 3.7 [1.3-11]).11 A similar study of 3323 Danish men only observed headache more common among snorers than nonsnorers (OR = 1.5 [1.3-1.8]) after adjusting for age, body mass index (BMI), alcohol, and tobacco.12

In a case–control study in the United States, Scher et al13 compared the prevalence of habitual snoring in a group of 206 chronic daily headache sufferers with a group of 507 episodic headache sufferers. Habitual (daily) snoring was more common among chronic daily than among episodic headache sufferers (OR = 2.02 [1.2-3.3; P < .005]) and increased after adjusting for traditional risk factors for obstructive sleep apnea (ie, age, gender, BMI, alcohol intake, hypertension) (OR = 2.86 [1.7-5.0; P < .005]). The relationship was not accounted for by other factors such as caffeine consumption and depression. Likewise, considering the study sample authors reported “in addition to and independent of snoring, patients were more likely than control subjects to report sleep problems, being tired, and sleeping for short or long periods of time” although these sleep variables were not elaborated (p. 490).

Among children, Isik et al14 reported on 2756 children randomly selected from school districts in Istanbul. Complete data from 2228 children aged 8.4 ± 1.4 years included 74 with migraine and 626 other nonmigraine headaches. Snoring (parent-rated child's snoring as often or always) and daytime sleepiness in children were associated with migraine (OR = 1.97 [1.22-3.16; P < .005] and OR = 2.17 [1.28-3.65; P < .004]) and other nonmigraine headaches (OR = 1.39 [1.14-1.68; P < .01] and OR = 1.78 [1.41-2.25; P < .001]). Snoring, sleepiness, and parasomnias (below) were more frequent among children with migraine than among nonmigraine headache and no headache groups. In a Chinese community survey of sleep disorders among 3047 children aged 6 to 12 years, habitual (6-7 days/week) snoring was associated with morning headache (adjusted OR = 1.53 [1.05-2.21; P < .05]).15

Insomnia.— Insomnia has been associated with chronic headache and may be a negative prognostic indicator at least for tension-type headache. In a United Kingdom cross-sectional study, Boardman et al16 identified a relationship between headache severity and sleep (ie, trouble falling asleep, wake up several times, trouble staying asleep, or waking after usual amount of sleep feeling tired or worn out); among 2662 respondents, headache frequency was associated with slight (age/gender adjusted OR = 2.4 [1.7-3.2]), moderate (OR = 3.6 [2.6-5.0]), and severe (OR = 7.5 [4.2-13.4]) sleep complaints. Authors identified “likely migraine” but did not describe migraine separate from other headaches. Likewise, Ohayon17 reported a European study using 18,980 telephone interviews associated “chronic morning headache” with insomnia (OR = 2.14 [1.79-2.57]) using strict Diagnostic and Statistical Manual of Mental Disorders, 4th Ed. (DSM-IV) and International Classification of Sleep Disorders (ICSD) criteria for insomnia.

In a large cross-sectional epidemiological study conducted in 1989 and using a random sample of 1000 Copenhagen residents18 found “sleep problems” were more common among tension-type than migraine headache sufferers and the general population and waking nonrefreshed more common among male and female migraineurs and female tension headache than the population. In 2001, a follow-up survey of the cohort from 198919 found sleep problems were associated with a poorer outcome for tension-type headache (defined as at least 180 headache days/year at follow-up due to increased frequency from episodic to chronic or unremitting) with sleep complaints (OR = 2.7 [1.1-6.3]) but not migraine. Negative prognostic indicators for tension-type headache included fewer hours sleep (OR = 1.4 [1.1-2.0]), waking nonrefreshed (OR = 2.0 [1.1-3.7]), and fatigue (OR = 2.5 [1.3-4.6]).20

Circadian Rhythm Disorders.— Although circadian rhythms have been closely linked to migraine, cluster and hypnic headache in clinical studies, circadian rhythm disorders were addressed in only one epidemiological study. In the European study by Ohayon17 described above, “chronic morning headache” was associated with circadian rhythm disorder using strict DSM-IV and ICSD diagnostic criteria (OR = 1.97 [1.31-2.94; P < .001]), and the relationship strengthened when the data were reanalyzed in a model that only used information obtained from individuals with “daily” morning headache (OR = 2.61).

Parasomnias.— Parasomnias have seldom been addressed, but 2 epidemiological studies were available indicating that a number of parasomnias are related to headache in children and adults. Concerning adults, the Ohayon17 study (described above in relation to insomnia and circadian rhythm disorders) also associated chronic morning headache with nightmares ≥ 1 per week (OR = 1.76 [1.30-2.39; P < .001]) and dyssomnias not otherwise specified (OR = 2.30 [1.94-2.72; P < .001]). Concerning children, the Isik et al14 study (described above in relation to snoring) also observed significant ORs in migraine and nonmigraine headache for nightmares (OR = 7.11 [4.07-12.41; P < .001] and OR = 1.93 [1.55-2.41; P < .001] respectively), sleep bruxism (OR = 2.80 [1.70-4.61; P < .001] and OR = 1.78 [1.43-2.22; P < .001]), sleepwalking (OR = 2.77 [1.20-6.39; P < .02] and OR = 1.28 [0.80-2.06; P < .05]), sleep vocalizations (OR = 3.58 [2.17-5.88; P < .001] and OR = 1.87 [1.53-2.29; P < .001]), and bedtime struggles (OR = 3.19 [1.81-5.61; P < .001] and OR = 1.94 [1.59-2.37; P < .001]).

SIGNIFICANCE OF SNORING

In epidemiological research, snoring is the cardinal symptom and a marker for obstructive sleep apnea (high sensitivity/low specificity). The designation “habitual” snoring, typically defined as either “daily” or “6 to 7 days/week,” increases specificity while maintaining a high degree of sensitivity. Snoring frequency positively correlates with polysomnographic indices of respiratory disturbance and daytime sequela (hypersomnolence).21 Despite increasing specificity, habitual snoring as a primary exposure variable probably still represents a range of conditions along the spectrum of sleep-disordered breathing (Table 1), including obstructive sleep apnea and upper airway resistance syndrome (UARS).

Table 1.—. Spectrum of Obstructive Sleep-Disordered Breathing
  • Sleep-disordered breathing (abnormalities of the respiratory pattern or quality of ventilation during sleep) may be secondary to varying levels of airway obstruction represented in this Table, dysregulation of respiratory control (eg, central sleep apnea, Cheyne-Stokes respiration), or both (eg, mixed and complex sleep apnea).

• Quiet Breathing
 Absence of snoring or breathing-related sleep disturbance
• Primary Snoring (Intermittent to Persistent)
Snoring without apnea or hypopnea or oxygen desaturation; intermittent snoring usually presents without significant daytime sequela while varying degrees of sleep disturbance may occur with persistent snoring
• Upper Airway Resistance Syndrome
 Snoring with arousals from sleep, but without apnea, hypopnea or oxygen desaturation (symptomatic with sleep complaint, daytime sleepiness, risk for hypertension, etc.)
• Obstructive Sleep Apnea/Hypopnea Syndrome (Mild to Severe)
 Snoring, repeated complete collapse (apnea) or partial collapse (hypopnea) of the pharyngeal airway during sleep, oxygen desaturation, resuscitative arousals from sleep

The prevailing viewpoint is that UARS represents an intermediate condition along the spectrum of sleep-disordered breathing. Pharyngeal properties in patients with UARS are intermediate between those with obstructive sleep apnea and normal controls.22 UARS may be identified in nonapneic snorers presenting with a variety of somatic complaints. On polysomnography, UARS is characterized by sustained or repeated airflow limitations (in the absence of obstructive apnea/hypopnea) correlating with arousals that fragment sleep, yielding daytime fatigue or sleepiness and increased risk for hypertension.23 The syndrome was initially described in 199124 and is readily identified through polysomnography using esophageal or intranasal pressure monitoring. UARS is associated with significant abnormalities in the macrostructure25 and microstructure of sleep,26 and correlates with measures of daytime sleepiness and fatigue.27

Unfortunately, UARS is not easily distinguished from other forms of snoring by research methods in epidemiological studies and is believed to account for some health risks previously assigned to simple snoring. Likewise, UARS is a fairly recently recognized phenomenon and represents a potential confound in earlier polysomnographic research on sleep-related headache, none of which employed the sensitive polysomnographic measures currently recommended to detect UARS.28 Likewise, epidemiological research described in this paper linking habitual snoring to headache in the absence of prototypical risk factors for obstructive sleep apnea (eg, age, male gender, obesity, hypertension) does not rule out the possibility of UARS contributing to chronic headache.

CLINICAL IMPLICATIONS

Headache patients may benefit from early identification and treatment of at least the most severe (sleep-disordered breathing) and prevalent (insomnia) sleep disorders. Screening questionnaires and algorithms are reviewed elsewhere.10 The mnemonic REST is a useful prompt for four key questions to screen for the presence of a sleep disorder: the Restorative nature of the patient's sleep, Excessive daytime sleepiness, tiredness or fatigue, the presence of habitual Snoring, and whether the Total sleep time is sufficient. A significant proportion of sleep apnea-related headaches will improve or resolve with treatment of apnea29–31 and preliminary evidence suggests transformed migraine may improve with behavioral insomnia treatment.32 Likewise, basic sleep regulation and measures to avoid development of a sleep disorder may be considered as preventative measures to reduce risk for chronic headache.

Screening/Management of Sleep-Disordered Breathing.— Headache related to sleep-disordered breathing may present as tension-type, migraine, cluster, mostly morning, or other nonspecific headaches.33 Those with chronic or awakening headaches should be questioned about symptoms (eg, habitual snoring, witnessed apnea, hypersomnolence) and risk factors (eg, obesity, male gender, increasing age, craniofacial/oral/neuromuscular factors that diminish size or patency of the airway, chronic alcohol, sedatives, hypnotics, or muscle relaxants) for obstructive sleep apnea.34,35 Patients with UARS may present at any age, 1:1 male-to-female gender ratio, normal body habitus, and with a chief complaint of insomnia more often than hypersomnia.36 Suspected sleep-disordered breathing warrants referral for polysomnography to diagnose and calibrate treatment efforts to disease severity, symptoms, and comorbidities. Primary treatments for sleep apnea and UARS include weight loss, treatment of nasal allergies, positional treatment for supine-related apnea, upper airway surgery, oral appliances for mandibular advancement, and continuous positive airway pressure.37 Because of the potential for headache to improve, reevaluation of headache is advised 1 month following treatment of sleep-disordered breathing.

Screening/Management of Insomnia.— Insomnia is the most common sleep complaint in clinical headache populations, observed in half to two-thirds of clinical headache patients.10 Insomnia is usually diagnosed based on the history of recurrent difficulty with onset, maintenance, duration or quality of sleep despite an adequate opportunity to sleep. Insomnia results in daytime impairment, usually fatigue or sleepiness, or other somatic, cognitive or emotional complaints. Insomnia is most often diagnosed by clinical history and quantified by sleep diary or questionnaires,10 although empirically based quantitative diagnostic criteria have been proposed defining sleep onset latency or wake time after sleep onset >31 minutes, minimum frequency >3 nights/week, and duration of symptoms >6 months.38

A variety of behavioral and pharmacologic treatments for sleep regulation are compatible with headache care. Behavioral interventions for both headache and insomnia include daily self-monitoring, progressive relaxation training, behavior modification, and cognitive therapy.10 Individuals already receiving behavioral treatment for headache may be participating in some form of relaxation training or cognitive-behavioral therapy and sleep elements can be easily integrated to standard behavioral headache treatments. Behavioral and cognitive-behavioral interventions for insomnia are described in Table 2.

Table 2.—. Behavioral Treatment Strategies Suggested for Insomnia Based on Symptoms
Treatment [Rationale]IndicationInstructions
  • Restriction may initially create a modestly increased sleep loss or sleep deprivation and daytime sleepiness; though this deprivation heightens sleep drive to facilitate sleep at night, it may also result in daytime sleepiness. Patients should be warned about this, especially if often engaged in hazardous activities. Over successive weeks, the sleepiness will remit as time in bed is gradually increased and the individual's maximum efficient sleep time is achieved.

Relaxation training
[Skills to gain voluntary control over and reduce the state of hypervigilance that is incompatible w/sleep]
High physiologic, cognitive, or emotional arousalProgressive relaxation training to reduce physical tension (may be facilitated by EMG or other forms of biofeedback)
Autogenic training to establish calm mental state and deter intrusive and arousing thoughts
Stimulus control
[Based on operant conditioning principles and reinforces associations between the “state of sleepiness” and the sleep environment]
Difficulty falling asleep or staying sleep1. Go to bed only when sleepy.
2. If unable to fall asleep 10-20 minutes (without watching clock, 10-20 minutes is equal to repositioning twice to try to fall asleep), leave the bedroom. Return only when sleepy again.
3. Use the bed and bedroom for sleep only.
4. Set alarm and rise daily at a regular time – do not snooze.
5. Do not nap during the day.
Sleep restriction
[Maximizes homeostatic “sleep drive” by restricting time in bed to approximately the actual sleep time (based on sleep diary)]
Excessive time spent in bed not sleeping; frequent awakenings1. Use the sleep diary to determine: “time in bed” and “actual sleep time.”
2. Restrict “time in bed” to approximately the average number of hours of “actual sleep time” per night. (Prescribe specific bed/wake times)
3. As diary demonstrates actual sleep time is 85% of time in bed, increase by 15-30 minute increments.
4. Keep a fixed wake time, regardless of the actual sleep duration (short nights are expected and increase sleep drive on subsequent night).
5. If sleeping <85% time in bed for 10 days, restrict time in bed further by 15-30 minutes increments.
Cognitive therapy
[to identify, challenge, and replace irrational beliefs and fears about sleep and sleep loss which provoke anxiety and perpetuate insomnia]
Racing, obsessive thoughts at bedtime; unrealistic expectations; catastrophizing or ruminative worry about sleep1. Patients may be asked to self-monitor or solicit beliefs and fears about sleep (or questionnaire42).
2. Identify anxiety-provoking insomnia-perpetuating cognitions.
3. Cognitive techniques are taught to challenge dysfunctional beliefs and restructure rational statements that the patient will apply when the dysfunctional thought or emotional state occurs.
Sleep hygiene education
[Basic sleep-promoting behaviors and avoiding activities not conducive to sleep]
Any of the above or poor sleep habits1. Avoid daytime naps.
2. Eliminate stimulants (caffeine, nicotine, etc.).
3. Maintain a regular bed/wake schedule 7 days per week.
4. Dark, quiet, comfortable sleep environment.
5. Avoid alcohol.
6. Regular exercise (avoid exercising 5 hours before bed).
7. Use the bed only for sleep and sex (behaviors conducive to sleep).

In a randomized controlled trial of behavioral sleep modification in the headache clinic, Calhoun et al32 randomized 43 women with transformed migraine to either a behavioral sleep treatment (eg, consistent sleep schedule, avoiding naps, eliminating alerting activities in the sleep environment) or sham control group (eg, consistent meals, acupressure as instructed, range of motion exercises) while both groups received usual medical care. The behavioral sleep intervention yielded a significant reduction in headache frequency and intensity relative to the control group in a sample of patients diagnosed with transformed migraine. Notably, the improvement in headache was proportionate to the number of sleep behaviors changed. Though preliminary, the study suggests that a relatively brief behavioral sleep intervention may favorably impact headache outcomes.

Sleep Risk Factor Reduction Strategies.— Though yet untested in headache sufferers, snoring interventions and sleep regulation strategies could be considered for headache sufferers aimed at prevention. The natural history of sleep-disordered breathing indicates a progression of snoring to obstructive sleep apnea.39 To quantify the risk of developing sleep apnea over time, the longitudinal cohort Cleveland Family Study34 identified a subgroup of 286 individuals without sleep apnea at baseline; the 5-year incidence of developing mild-to-moderate sleep apnea (defined as Apnea/Hypopnea Index ≥5/hour) was 16% and the incidence of developing moderate-to-severe sleep apnea (Apnea/Hypopnea Index ≥15/hour) was 7.5%. Untreated snoring may worsen over time, influenced by aging and weight gain.

Weight maintenance or loss as indicated is a recommendation in managing snoring. Weight loss is an effective treatment for snoring as well as obstructive sleep apnea – most significantly documented in cases of surgically induced weight loss.40 As indicated, other snoring treatments include dental appliances (eg, tongue-retaining, mandibular advancement), sleep positional training to avoid supine sleep, antihistamines and anti-inflammatory nasal sprays, nasal/palatal/intrapalatal surgical interventions, smoking cessation and avoiding regular use of muscle relaxants, alcohol, sedatives, and other substances that may suppress respiration.41

Basic sleep regulation for headache sufferers would encourage a lifestyle and habits that optimize the duration, quality, and regularity of sleep.10 The circadian rhythm is reinforced by maintaining a consistent sleep/wake schedule, avoiding significant schedule changes on weekends, avoiding shift work (eg, rotating, third shift) and phase appropriate light exposure (dark sleep environment/light day environment). Unless a bona fide short- or long-sleeper, the average individual is encouraged to sleep 7 to 8 hours per night consistent with the average homeostatic sleep need and avoiding daytime naps. Generally, individuals should avoid or minimize sleep altering substances such as caffeine, nicotine, and alcohol.

CONCLUSION

Population studies are generally consistent in several findings: the prevalence of sleep disorders is greater among individuals with headache than individuals without headache; sleep disorders are more prevalent among individuals with chronic headache than episodic headache; and there is evidence from one longitudinal study that sleep complaints may be a negative prognostic indicator at least for tension-type headache. The majority of studies have addressed sleep-disordered breathing, but a wide range of sleep disorders are implicated. This is generally consistent with clinical literature suggesting sleep disorders are prevalent among headache sufferers seeking treatment, especially insomnia.10 These various sleep disorders linked to headache are diverse in nature but common to all is the dysregulation of sleep processes impacting headache vulnerability or threshold, and possibly progression of the headache disorder over time.

There is clinical evidence in the case of obstructive sleep apnea and insomnia that treatment of the sleep disorder may improve headache. Therefore, it is recommended that screening and management for the more severe and prevalent sleep disorders be considered in headache practice. It is also proposed that basic sleep regulation strategies that manage snoring and optimize the duration, quality, and regularity of sleep be encouraged in headache sufferers. Longitudinal studies in the future would help determine if regulation of sleep can reduce the risk of headache progression.

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