Sleep and Headache

Chapter 63 Sleep and headache

TERESA PAIVA* Institute of Molecular Medicine, Medical Faculty of Lisbon, Lisbon, Portugal

INTRODUCTION functional links between sleep and headache, addres- sing the physiological, anatomic, chronobiological, Headache and sleep disturbances are commonly and genetic aspects as well as neurotransmitters and reported problems in neurological practice and both neuromodulators. have important individual and socioeconomic impacts. Their mutual relationships have been known for many years, but the full understanding of the underlying CLINICAL ASPECTS OF SLEEP^ mechanisms involved is still unclear. Basically, it is HEADACHE RELATIONS known that a headache may cause a sleep disturbance, Sleep and headache prevalence a sleep disturbance may be the cause of a headache, and both sleep and headache may be the consequence Headache patients more often report daytime symp- of another underlying condition (Paiva et al., 1995). toms (fatigue, tiredness, or sleepiness) and sleep pro- From clinical practice data it is clear that such a rela- blems (insomnia) (Paiva et al., 1995; Jennum and tion is complex, because a headache can be the result Jensen, 2002). In a specialized headache clinic, 17% of both too much and too little sleep, and can be both of the patients had awakening or nocturnal headache, cured by sleep and induced by it. This complexity must and 53% of them (9% of the total headache population) be considered in any scientific and clinical approach in had a sleep disorder (Paiva et al., 1997). order to achieve a deeper and clearer insight. A recent population study showed that poor sleep The recent publication of revised versions of the and anxiety have an important impact on the lives of International Classification of Headache Disorders headache sufferers. Those with moderate sleep pro- (ICHD-II) (Olesen, 2005) and International Classifica- blems had experienced significantly more headaches tion of Sleep Disorders (ICSD-2) (American Academy in the previous 3 months than controls (percentage of Sleep Medicine, 2005) implies an updated review occurrence 76% versus 24%; odds ratio 4.8), and the with some new concepts. In the ICHD-II, some sleep picture was still more impressive for severe sleep pro- entities are individualized, namely headache related to blems (percentage 87% versus 13% respectively; odds sleep apnea and hypnic headache, whereas in the ratio 13.0) (Boardman et al., 2005). ICSD-2 sleep-related headaches are referred to other The prevalence of chronic morning headache classifications in Appendix A. (CMH) is 7.6%, as determined in a European study The first section of this chapter describes clinical including a total of 1890 subjects from the UK, aspects of sleep–headache relations: sleep and head- Germany, Italy, Portugal, and Spain. CMH is more ache prevalence; clinical evaluation (parameters used common in females and in subjects between 45 and to characterize the mutual influences); sleep distur- 64 years of age. The most significant associated fac- bances coursing with headaches; headaches coursing tors are anxiety, depressive disorders, insomnia, dys- with sleep disturbances; sleep disturbances and head- somnia, and circadian rhythm disorder (Ohayon, ache as comorbid symptoms; and when to suspect a 2004). The picture is similar in young subjects: in the sleep disturbance in the evolution of a chronic head- USA, a national survey including 6072 adolescents ache, and vice versa. The second section deals with showed a clear relation between insomnia and headache

*Correspondence to: Teresa Paiva, M.D., Ph.D., Centro do Sono, CENC, Rua Conde das Antas, 5, 1700 Lisboa, Portugal. Tel: 351213715450, Fax: 351213715459, E-mail: [email protected] 1074 T. PAIVA in less than 10% (Rhee, 2000). A Hong Kong cross- severity, triggers, associated and premonitory symp- sectional questionnaire survey of 3355 secondary toms, relieving and aggravating factors, and family school students (response rate 98%), attempting to history of headache. investigate common illnesses, found a similar preva- Several other clinical parameters must also be con- lence for headache and insomnia: headache/dizziness sidered in order to evaluate sleep–headache relations: (23.6%) and chronic anxiety/insomnia (20.1%) (Lau (1) sleep as a trigger for headaches; (2) headaches et al., 2000). related to the duration of sleep or changes in the sleep schedule; (3) sleep stage-related headaches; (4) associa- Clinical evaluation tion with a specific sleep pattern; (5) sleep as a headache reliever; (6) headaches and dreams; and (7) Headache evaluation should include at least a brief headaches affecting sleep. A summary is shown in sleep history (Rains and Poceta, 2005), and this should Table 63.1. also be applied to sleep patients who also need a headache evaluation. As well as conventional questions, the SLEEP-TRIGGERED HEADACHES sleep history should specifically address symptoms of sleep onset (sleep latency, limb discomfort or restless- Headaches are classified as sleep related when 75% ness, anxiety); nocturnal symptoms (snoring, nocturia, of the episodes occur during sleep or upon awaken- dreaming, abnormal behaviors), morning symptoms ing. Several of the currently known headache entities (dry mouth, headache, body pain, fatigue), and diurnal sometimes fulfil these requirements: migraine, cluster symptoms (sleepiness, performance difficulties, headache (CH), chronic paroxysmal hemicrania (CPH), fatigue, depression, pain). Headache history should hypnic headache, exploding head syndrome, and noc- consider type, location, frequency, time of occurrence, turnal hypertension headache.

Table 63.1

Clinical evaluation of sleep and headaches

Sleep history Sleep onset (sleep latency, limb restlessness, anxiety) Nocturnal symptoms (snoring, nicturia, dreaming, abnormal behaviors) Morning symptoms (dry mouth, headache, body pain, fatigue) Diurnal symptoms (sleepiness, performance difficulties, fatigue, depression, pain) Headache Type and location Frequency Time of occurrence (time of the day, relation to sleep and to awakening) Severity Associated and premonitory symptoms Triggers Relieving and aggravating factors Familiar cases Sleep–headache interactions Sleep as a trigger for headaches Migraine, CH, CPH, hypnic headache, exploding head syndrome Headaches related to the duration of sleep Migraine: excess, lack, scheduling of sleep or changes in sleep schedule Tension headache: lack of sleep Sleep phase-related headaches Most headaches occur in REM and NREM sleep, with higher probability for REM Exploding head syndrome and turtle headache in sleep–wake transitions Association with a specific sleep pattern Migraine: signs of lower cortical activation Tension headache: decreased sleep efficiency Sleep as a headache reliever Migraine Headaches and dreams Dreams culminating in a migraine Greater anger and apprehension Headaches affecting sleep CH, CPH, and hypnic headache may induce insomnia and awakenings

CH, cluster headache; CPH, chronic paroxysmal hemicrania; NREM, nonrapid eye movement; REM, rapid eye movement. SLEEP AND HEADACHE 1075 SLEEP DURATION AND SLEEP SCHEDULE main trigger for CH attacks (Kudrow et al., 1984; Kudrow, 1994; Nobre et al., 2003). CPH has been con- Normal subjects, when sleep deprived, may experience sidered a REM-locked headache (Kayed et al., 1973), a dull or pressing bilateral headache in the forehead but polysomnographic studies have shown that the (Blau, 1990). Migraine attacks can be precipitated by trigger is not the sleep state but a sustained increase excessive sleep or lack of sleep (Sahota and Dexter, in blood pressure (Concili et al., 1994). 1990). A recent population study evaluating the preva- Hypnic headache occurrence across the night may lence of migraine and tension headache in Japan, by vary, but for the majority of patients (60% of 71 cases) means of structured questionnaires in adult residents the pain started 3 hours after falling asleep (Evers and of Daisen (n ¼ 5758; 4795 responders, 83.3% response Goadsby, 2003). A few patients have been recorded by rate) showed that “lack of sleep” triggered 51.6% of polysomnography during attacks; some had REM- cases of migraine with aura, 44.1% of migraine without related and others NREM-related headaches (Arjona aura, 32.0% of episodic tension headache, and 36.6% et al., 2000; Evers and Goadsby, 2003). In nocturnal of chronic tension headache; the “excess sleep” trigger headache hypertension syndrome, pain can appear in was significantly less common, being 3.3%, 8.9%, the morning hours. In exploding headache syndrome, 5.6%, and 1.4% respectively (Takeshima et al., 2004). attacks occur during the transition from wakefulness Migraineurs sleeping for fewer than 6 hours had to sleep, and in the turtle syndrome pain appears after more severe headaches and more sleep-related head- morning awakening when the patient pulls the sheet aches (Kelman and Rains, 2005). Lack of sleep is also over their head (Evers and Goadsby, 2003). a cause for tension headaches (Drake et al., 1990).

Transient modification in sleep schedule (weekends, SLEEP PATTERN trips, etc.) by sleeping too little, too much, or by chang- ing routines can precipitate headaches (Spierings et al., A total of 164 children with migraine evaluated by 2001), particularly migraine (Olesen, 2005). A short nap questionnaire had longer sleep latency and poorer may also precipitate an attack (Blau, 1982). Further- sleep quality than 893 controls (Bruni et al., 1997). more, it is known that both migraine (Fox and Davies, In an actigraphic study in children with migraine, 1998) and cluster headache (Russel, 1981; Manzoni the only difference observed was decreased nocturnal et al., 1983) have a circadian distribution of the attacks motor activity on the day before the crisis (Bruni (Peres, 2005). et al., 2004). Adult migraineurs recorded in nonheadache periods SLEEP STAGE AND SLEEP-STATE LEVEL had normal sleep patterns and muscular (EMG) activity in spite of a clear increase in REM sleep duration The fact that headaches may be related to the sleep and latency (Drake et al., 1990). Adult migraineurs stage implies that they will occur during specific showed, the day before the crisis, a decreased number moments of the night. For instance, an event related of arousals, lower REM density and alpha power, sug- to slow-wave sleep will usually occur during the first gesting a decrease in cortical activation (Goder et al., 60 minutes of sleep; the first rapid eye movement 2001). In line with these findings, a decreased EEG (REM) period has a latency around 90 minutes; complexity was observed in the first two NREM cycles REM-related events tend to occur during the last hours in patients with spontaneous nocturnal attacks (Strenge of sleep; and those with no special sleep-stage relations et al., 2001). will have no specific temporal profile. Events related to Patients with tension-type headaches also have per- wake–sleep or sleep–wake transitions appear at sleep sistently poor sleep with reduced sleep efficiency and onset, upon morning awakening, or during awakening slow-wave sleep, as observed in a polysomnographic from sleep. study of 10 patients (Drake et al., 1990). It has been stated that certain headache entities occur in relation to specific sleep stages (Sahota and SLEEP-RELIEVED HEADACHES (SLEEP AS A HEADACHE Dexter, 1990), but the available data provide RELIEVER) conflicting results. Migraine occurrence after diurnal or nocturnal sleep seems to be related to excessive per- A migraine attack is often ended by a short nap or by centages of stages 3 and 4 nonrapid eye movement nocturnal sleep (Blau, 1982), particularly in children (NREM) sleep, but also to REM sleep (Dexter, 1979). (Barlow, 1994). In 1283 migraineurs, 85% chose to sleep CH is often triggered by REM sleep (Dexter and or rest because of headache and 75% were needed to do Riley, 1975; Kudrow et al., 1984) and by NREM sleep so in order to relieve the pain (Kelman and Rains, 2005). (Pfaffenrath et al., 1986). Some researchers have pro- This was also true for confusional migraine (Ehyai and posed hypoxia, and not the sleep stage per se, as the Fenichei, 1978; Parrino et al., 1986). 1076 T. PAIVA DREAMS AND HEADACHES According to the ICHD-II (Olesen, 2005), the headache in sleep apnea is classified in the group with There are possible relationships between unpleasant homeostasis disturbance (item 10.1.3). The diagnostic dreams and migraine. In a study of 37 patients, the criteria imply the existence of recurrent headaches, dream contents before a nocturnal migraine involved present upon awakening, with apnea confirmed by mostly anger, misfortune, apprehension, and aggres- polysomnography, and clinical improvement with sive interactions (Heather-Greener et al., 1996). In effective treatment of the apnea. Furthermore, at least some patients, dreams with terrifying content may one of the fulfilling criteria should be present: a fre- terminate in a migraine, but only on certain occasions quency greater than 15 days per month; pressing qual- (Levitan, 1984). ity without nausea; no photophobia or phonophobia; EFFECT OF HEADACHES ON SLEEP resolution within 30 minutes. To determine the prevalence of this association, two Insomnia and sleep disruption may occur in patients strategies have been used: evaluation of headache in a with CH and CPH due to fear of nocturnal attacks population of patients with OSAS, and evaluation of (Kayed et al., 1973; Kudrow et al., 1984; Paiva et al., OSAS in a headache population. In the past two dec- 1995). In chronic daily headaches, sleep disruption is ades, many authors have followed the first strategy considered to have a psychogenic origin because the (Boutros, 1989; Aldrich and Chauncey, 1990; Jennum pain starts after awakening (Sahota and Dexter, et al., 1994; Poceta and Dalessio, 1995; Ulfberg et al., 1990). Hypnic headaches also induce nocturnal awa- 1996; Greenough et al., 2002; Neau et al., 2002; Goder kenings (Raskin, 1988; Newman et al., 1990). et al., 2003; Sand et al., 2003; Idiman et al., 2004). Patients with OSAS often complain of headache, which Sleep disturbances associated is reduced with continuous positive airway pressure with headaches (CPAP) treatment (Wright and White, 2000). Headache INSOMNIA frequency in OSAS ranges from 32.9% to 58.5%; it is mainly a morning tension-type headache, mainly fron- Insomnia is defined as a repeated difficulty in sleep tal, frontotemporal, or temporal (38.9%) in location, initiation, duration, consolidation, or quality that tightening or pressing (78.9%), and mild to moderate occurs despite an adequate time and opportunity for (84.2%) (Alberti et al., 2005). However, when evaluat- sleep (American Academy of Sleep Medicine, 2005). ing in a headache clinic the prevalence of OSAS in The relation between insomnia and headache is proba- 903 patients was no different from that expected from bly very complex. Insomnia is a common complaint; data in the general population (Jensen et al., 2004). like most headaches, it is more frequent in women. OSAS severity and headache is another contradictory Headache and insomnia have a variety of causes and aspect: the relationship found in some studies (Alberti both can be defined as a “complaint” or as a “clinical et al., 2005) was not confirmed in others (Greenough entity”, inducing frequent equivocal estimates. et al., 2002; Neau et al., 2002). A significant association The problem of comorbidity arises from several between headache and depression in OSAS was found studies, in the sense that both may reflect another in a controlled study (Neau et al., 2002). clinical problem, such as depression. In a study of 50 Self-reported snoring has also been associated with insomniacs, 24 subjects (48%) also complained of head- morning and daytime headache, but the relation is con- ache, but only 10% had headache upon awakening. sidered weaker than with sleep apnea (Jennum et al., Most headaches that did not occur upon awakening 1994; Ulfberg et al., 1996; Neau et al., 2002). However, fulfilled the criteria of migraine without aura (37.5%) habitual snoring was more frequent in patients with or episodic tension-type headache (50%) (Alberti chronic daily headaches (24%) than in controls (14%) et al., 2005). (Scher et al., 2003). The relations between sleep apnea

SLEEP APNEA AND SNORING and headache are more pronounced in the elderly (Barthlen, 2002). There is controversy concerning the Obstructive sleep apnea syndrome (OSAS) is charac- underlying mechanisms. Headache has been attributed terized by repetitive episodes of total or partial cessa- to intracranial pressure variations, lower oxygen tion of breathing (American Academy of Sleep saturations, and hypercapnia during apnea (Jennum Medicine, 2005). Patients snore and are often obese and Borgesen, 1989; Doyle and Tami, 1991; Alberti with a large neck and/or craniofacial abnormalities et al., 2005). However, none of these features was (micrognathia and retrognathia, and bird-like face); detected in other controlled studies (Neau et al., 2002). they also have excessive daytime sleepiness, nocturia, In intracranial disorders associated with sleep apnea, dry mouth upon waking, or hypertension. some studies have measured intracranial pressure (ICP). SLEEP AND HEADACHE 1077 Most of them found increased B waves of ICP, mostly legs syndrome, and manifest as repetitive and stereo- during REM sleep, and in some studies headaches typed movements that occur during sleep (American remitted with CPAP treatment (Hanigan and Zallek, Academy of Sleep Medicine, 2005). 2004). Obstructive sleep apnea was considered to be The prevalence of both RLS and PLMS increases the cause of increasing headaches in two shunted with age. Complaints of morning or daytime headaches patients with low-pressure ventriculoperitoneal shunts. are three to five times more frequent in patients with Neurophysiological evaluation in these patients during RLS (Ulfberg et al., 2001). Fifty patients with severe REM sleep showed multiple Lundberg A waves in ICP headaches who qualified for treatment with dopamine in association with obstructive sleep apneas; in one receptor blocking agents had a prevalence of RLS of patient, headaches during nocturnal awakenings were 34%; this group had a higher risk of developing associated with a sudden increase in ICP (Hanigan and akathisia as a treatment side-effect (Young et al., Zallek, 2004). 2003). In children, PLMS and RLS show a significant association with morning headaches (Chervin and NARCOLEPSY Hedger, 2001). Nobre et al. (2003) found no significant increase in Narcolepsy is characterized by irresistible daytime the prevalence of PLMS in patients with CH. There is sleepiness, cataplexy, hypnagogic hallucinations, and a case report of excessive PLMS in a patient with hyp- sleep paralysis (American Academy of Sleep Medicine, nic headaches (Kocasoy Orhan et al., 2004). 2005). The association between narcolepsy and migraine (Dahmen et al., 1999) is controversial. In a OTHER SLEEP DISORDERS population of 100 narcoleptics, Dahmen et al. (2003) found a migraine prevalence of 44% in women and Hypersomnia and nocturnal bruxism are associated 28.3% in men. The German Migraine and Headache with increased occurrence of a tension-like headache. Society Study Group (2003), however, had different In bruxism, this may eventually be related to sleep results: in an evaluation of 96 narcoleptics, a similar fragmentation and increased muscular activity during prevalence of migraine was observed in patients sleep. Sleep disorders associated with headache are (21.9%) and controls (19.8%). summarized in Table 63.2.

RESTLESS LEGS SYNDROMES AND PERIODIC LIMB Headaches associated with sleep MOVEMENTS IN SLEEP disturbances

Restless legs syndrome (RLS) is characterized by a Headache disorders related to sleep complaints are pri- strong and nearly irresistible urge to move the legs. mary headaches such as migraine, tension-type head- The sensations are worse at rest and more frequent ache, cluster headache, and hypnic headache. Other in the evening and during the night; they are relieved rare entities, not included in the ICHD-II (Olesen, by moving or walking (American Academy of Sleep 2005), may occur exclusively in relation to sleep: Medicine, 2005). Periodic limb movements in sleep exploding head syndrome and the turtle headache (PLMS) may or may not be associated with restless (Evers and Goadsby, 2003)(Table 63.3).

Table 63.2

Sleep disturbances that may be present with headaches

Sleep disturbance Headache Headache type Comorbidity

Insomnia 48% (Alberti et al, 2005) Daytime headache, morning headache, Depression migraine, tension-type headache OSAS Sleep apnea headache (32–58.5%) Morning headache Depression(?) (American Academy of Sleep Medicine, 2005) Narcolepsy Migraine(??) Restless legs, PLMS ? Morning headache, daytime headache

OSAS, obstructive sleep apnea syndrome; PLMS, periodic limb movements in sleep. 1078 T. PAIVA Table 63.3

Headaches relations with sleep and sleep disturbances

Headache Sleep disturbance Trigger Reliever Sleep stage Circadian influences

Migraine Insomnia Yes, often Yes, often REM/NREM Yes Tension headache Insomnia Sometimes Variable No No CH OSAS, PLMS Yes No REM/NREM Yes CPH ? Yes No REM Yes Hypnic headache Insomnia Yes No REM/NREM Yes Exploding head syndrome Insomnia Yes No Wake–sleep transition No

CH, cluster headache; CPH, chronic paroxysmal hemicrania; NREM, nonrapid eye movement; OSAS, obstructive sleep apnea syndrome; PLMS, periodic limb movements in sleep; REM, rapid eye movement.

MIGRAINE intensity (Hering-Hanit et al., 2000). Sleep problems evaluated by the Nottingham Health Profile provided Migraine with and without aura is characterized by one of the highest scores affecting negatively the quality paroxysmal episodes of pain, lasting from 4 to 72 of life of patients with migraine (Passchier et al., 1996). hours, associated with some of the following symp- Several authors have described a strong association toms: nausea, vomiting, photophobia, and phonopho- between somnambulism and migraine (Barabas et al., bia. When associated with aura, migraine is preceded 1983; Dexter, 1986; Giraud et al., 1986; Pradalier et al., by neurological symptoms, mostly visual, that subside 1987; Paiva et al., 1994). when the pain starts; for a detailed description, see

ICHD-II (Olesen, 2005). TENSION-TYPE HEADACHE Relations between migraine and sleep have been established in several studies, in both children (Bruni In tension-type headache the pain is usually bilateral, et al., 1997; Aaltonen et al., 2000; Miller et al., 2003; and is felt as pressure or tightening with a duration Bruni et al., 2004) and adults (Kelman and Rains ranging from 30 minutes to several days, fluctuating 2005). Patients with chronic migraine reported shorter in intensity but not associated with nausea and vomit- sleep duration than those with episodic migraine; they ing. Tension-type headache can be subdivided into epi- were also more likely to have trouble falling and stay- sodic (less than 15 days of headaches per month) and ing asleep, to have a headache triggered by sleep, and chronic (more than 15 days of headache per month) to choose sleep as a headache reliever (Kelman and types (see ICHD-II; Olesen, 2005). Here, too, sleep Rains, 2005). problems evaluated by the Nottingham Health Profile The most common migraine triggers are emotional provided one of the highest scores negatively affecting stress, hypoglycemia, lack or excess of sleep (weekend quality of life (Passchier et al., 1996). In 245 patients migraine), sensorial stimulation (loud noise, bright with chronic tension-type headache, sleep was impaired light, strong odor, heat, or cold), or physical stimula- in one-third for more than 10 days per month (Holroyd tion (physical exercise) (Rasmussen, 1993). Rest and et al., 2000). sleep usually bring pain relief (Blau, 1982). Sleep disturbances were confirmed by polysomno- Headaches and migraine with aura may be related graphic studies in 10 individuals with tension-type head- to extended sleep duration: subjects experienced headache and in 10 mixed (migraine plus tension) headache ache (but not migraine) with extended sleep night sufferers. Patients with tension headache had reduced (Moss et al., 1987). Changes in the quality of sleep may sleep duration and efficiency, frequent awakenings, arise up to 2 days before a migraine attack (Spierings increased nocturnal movements, and a marked reduc- et al., 2001). A circadian distribution of attacks has tion in slow-wave sleep. Those with mixed headaches been studied. In 3582 attacks in 1689 adult migraineurs, had reduced sleep and slow-wave sleep, increased awa- crisis occurred mainly in the early morning (Fox and kenings, and reduced REM sleep and REM latency Davies, 1998). (Drake et al., 1990). Overuse of medication may worsen the sleep pattern In order to identify possible physiological mechan- and the headache of migraineurs. Withdrawal of the isms, temporalis EMG activity was measured during misused medications can alleviate the associated sleep sleep and wake in patients with tension-type headache disturbance, and reduce headache frequency and and controls, but no significant differences were found SLEEP AND HEADACHE 1079 during sleep (Clark et al., 1997). Tension-type headache CH (Pfaffenrath et al., 1986). The circadian influence is often described in patients with insomnia, hyper- is presumed to be due to the fact that serum levels somnia, and circadian disturbances. of melatonin are low during clusters and melatonin is useful in CH treatment (Costa et al., 1998; Peres, 2005). CLUSTER HEADACHE

CH is characterized by episodes of intense lateralized HYPNIC HEADACHE pain over and around the eye, lasting for 15–180 minutes, with a daily frequency of episodes ranging from First described by Raskin (1988), hypnic headache is 1 to 8, and accompanied by homolateral symptoms now included in the ICHD-II. Pain occurs exclusively (tearing, rhinorrhea, myosis, and ptosis) and agitation during sleep and induces awakening. One of the fol- or restlessness. The cluster of pain has a duration of lowing features must exist: more than 15 episodes per weeks or months, and repeats with long intervals of month, duration after awakening longer than 15 min- one or more years (see ICHD-II; Olesen, 2005). utes, and complaints beginning after 50 years of age; The clockwise onset of attacks suggests a circadian there are no associated autonomic symptoms and no influence. The temporal profiles of pain in CH have intracranial pathology (see ICHD-II; Olesen, 2005). been investigated. Of a total of 77 attacks in 22 patients, The pain is usually dull, moderate, and bilateral. In 75% began between 9 pm and 10 am, with two overnight the majority of reported cases, pain starts between peaks at 9–11 pm and 4–7 am (Russel, 1981). These data 120 to 180 minutes after sleep onset; pain may some- have been confirmed in other series (Manzoni et al., times worsen in the supine position, improving in the 1983). There was no difference in the severity of diurnal upright position (Evers and Goadsby, 2003). and nocturnal attacks (Russel, 1981). Headache attacks occur predominantly during noc- Patients with CH have a higher prevalence of sleep turnal sleep but may also occur during daytime naps. apnea (Kudrow et al., 1984; Chervin et al., 2000; Nath Some authors describe an association between head- and Chervin, 2000), which varies from 58.3% (Nobre ache episodes and slow-wave sleep (Arjona et al., et al., 2003) to 80.6% (Graff-Radford and Newman, 2000) or REM sleep, or with nocturnal desaturations 2004). They have an 8.4-fold increased risk of sleep (Dodick, 2000; Evers and Goadsby, 2003; Pinessi apnea compared with controls. This risk increases to et al., 2003); others found no special association with 24.38 if the body mass index is above 25 kg/m2 and any of these features (Manni et al., 2004). Sleep effi- the patient is male and aged 50 years or more (Nobre ciency is reduced due to pain-induced awakenings, et al., 2003). CPAP treatment of sleep apnea in patients but other sleep parameters are usually normal (Evers with CH reduces the severity (Nath and Chervin, 2000). and Goadsby, 2003). A circadian disturbance has been Sleep-disordered breathing probably does not cause described (Peres, 2005). Treatment includes lithium CH, but may worsen CH attacks. Transient situational and caffeine at bedtime (Olesen, 2005). insomnia has been described in association with CH, normalizing when the cluster period subsides (Sahota OTHER HEADACHE ENTITIES and Dexter, 1993). Nobre et al. (2003) found no significant increase in the prevalence of periodic limb move- There are some rare disorders not included in the ments, although the prevalence rate was relatively high: ICHD-II that are related exclusively to sleep. Explod- 37.5% in patients with CH and 28% in controls. ing head syndrome occurs mostly at sleep onset. It is According to Kudrow et al. (1984), patients with CH not a pain but an explosive noise in the head that have a higher prevalence of prior parasomnias, mostly prevents sleep onset; it also appears after the age of enuresis and sleepwalking, but also night terrors, tooth 50 years, and there is an occasional description of its grinding, and sleep talking. appearance in all sleep stages (Evers and Goadsby, Sleep studies have suggested that clusters may 2003). Turtle headache occurs in the morning after be provoked by the transition phase from REM the final awakening when the subject pulls the covers to NREM sleep and/or are related to hypoxemia over their head, retracting beneath the sheet (Evers (Kudrow et al., 1984; Chervin et al., 2000; Nobre and Goadsby, 2003). et al., 2003; Weintraub, 2003). However, associations with other sleep stages and states have been observed; Sleep disturbances and headache as only 20% were REM sleep related (Pfaffenrath et al., comorbid symptoms 1986). Headache attacks are related to REM sleep in episodic CH, although this relationship is unclear in Headaches and sleep disturbances may have a common chronic CH; most chronic CH evolves from episodic cause, either “intrinsic” or “extrinsic”. 1080 T. PAIVA affected dimension of poor sleep was sleep duration. HEADACHES AND SLEEP DISTURBANCES HAVE These patients also presented higher levels of psycholog- A COMMON “INTRINSIC” CAUSE ical distress (Vasquez-Delgado et al., 2004). Psychological and psychiatric disturbances (mostly Headache and sleep problems are often associated depression) are a frequent cause of both headache with other medical diseases. Patients with nocturnal and insomnia (Sahota and Dexter, 1990; Marazziti hypoxemia and hypercapnia, as in chronic obstructive et al., 1995; Paiva et al., 1995; Pine et al., 1996; Maizels lung disease (George, 2000) and neuromuscular disease and Burchette, 2004); this is true for migraine (Breslau (Barthlen, 1997), often complain of insomnia, daytime and Davis, 1993; Merinkangas and Angst, 1993; Swartz sleepiness, and headaches. et al., 2000) and for tension headache (Puca et al., 1999). Depression per se has a negative impact upon HEADACHE AND SLEEP DISTURBANCES HAVE sleep as it induces insomnia, reduction of slow-wave A COMMON “EXTRINSIC” CAUSE sleep, and, in some cases, REM sleep abnormalities. These situations may cause a vicious cycle, which is Snorers’ spouses or companions have a higher preva- difficult to handle clinically: depression induces head- lence of insomnia, morning headaches, daytime sleepi- ache and insomnia, which, when chronically main- ness, and fatigue (Ulfberg et al., 2000). Chronic tained, reinforce depressive symptoms maintaining substance abuse, particularly of ergot derivatives and/ the disturbed cycle. or analgesics, is a frequent cause of daily chronic head- In a recent publication from a headache clinic, 289 aches; these patients also have insomnia. In some patients were evaluated; psychiatric association showed patients, discontinuation of the abused substance was a clear influence in somatic symptoms. The most com- sufficient to treat headaches and insomnia; in others, mon comorbid symptoms were fatigue (73% of cases), insomnia and headaches fluctuated independently insomnia (60%), and indigestion (55%); the association (Paiva et al., 1995). of these three symptoms was present in 33% of A large set of external causes, involving either med- all patients. This comorbidity was more evident in ications (antiepileptics, beta-blockers, and nitroglycer- those suffering from chronic migraine (Maizels and ine), toxic agents, or infectious organisms, may Burchette, 2004). Nocturnal seizures may induce noc- induce headache as well as sleep disturbances. How- turnal or morning headache in children and adults ever, in these situations both symptoms appear among (Kohrman and Carney, 2000). a broader spectrum of disturbance and, more likely, Another possible cause is fibromyalgia syndrome represent a nonspecific response of the central nervous (FMS) (Wolf et al., 1990). This is a common and long- system to external aggression. Benzodiazepine with- lasting condition with widespread musculoskeletal pain drawal syndrome includes insomnia, headache, irrita- and tender points at specific anatomical sites. Head- bility, anxiety, hand tremor, sweating, concentration aches (tension-type or migraine), insomnia, nonrestora- difficulties, nausea, weight loss, palpitations, and tive sleep, and restless legs are common (Jennum muscular pain (Potursson, 1994). Caffeine withdrawal et al., 1993; Clauw, 1995; Paiva et al., 1995). Patients also includes headaches, decreased wakefulness and motor have fatigue, orthostatic hypotension, tachycardia, activity, but has no evident effects on nocturnal sleep effort intolerance, cognitive psychological disturbances, (Hufer and Buttig, 1994). Caffeine withdrawal head- paresthesias, irritable bowel syndrome, and bladder dys- ache is, however, relatively rare: around 0.4% in epi- kinesia. Alpha–delta sleep is very common but not demiological studies (Sjaastad and Bakketeig, 2004). pathognomonic of FMS (Moldofsky et al., 1988; Branco Psychoactive substance use is also associated with et al., 1994); it is a specific sleep electroencephalo- headaches, sleep disorders, and psychiatric distur- graphic pattern. bances (Ardila and Bateman, 1995). Exposure to The association between headache and sleep distur- organic solvents may induce headache, sleepiness, bances is weaker in the chronic fatigue syndrome (Bell vertigo, concentration difficulties, and mood swings et al., 1994; Komaroff et al., 1996). It is characterized (Indulski et al., 1996). by chronic fatigue, impairment of cognitive functions, Infectious diseases, such as pertussis in adults, are poor sleep, headache, recurrent sore throat, muscle often associated with sleep disturbances (52%) and headaches, arthralgias, and postexertional malaise (Jennum aches (14%) (Postels-Multani et al., 1995). In infection et al., 1993). with human immunodeficiency virus, the 12 common In one study, 61 patients with myofascial pain also symptoms are fatigue, fever, imbalance, paresthesias, reported important sleep complaints, with an average memory loss, cough, nausea, diarrhea, sadness, skin Pittsburgh Sleep Quality Index (PSQI) score of problems, headache, and sleep disturbances (Whalen 11.1 4.5 (the PSQI cutoff point is 5). The most et al., 1994). SLEEP AND HEADACHE 1081 Posttraumatic stress following acts of violence Table 63.4 includes excitability, distrust, avoidance, concentration Morning headaches difficulties, fatigue, headaches, nightmares, and insomnia (De Mol, 1994). The main symptoms of acute Alerting Possible mountain sickness are headache, nausea, loss of appe- symptoms entity Polysomnography tite, fatigue, dizziness, and sleep disturbances. High- altitude headache (Silber et al., 2003) is considered in Snoring, sleepiness, OSAS Always required the ICHD-II – in item 10.1.1, which is headache with a obesity, large neck, homeostasis disturbance (Olesen, 2005). The influ- bird-like face, other ence of altitude upon sleep is also recognized: peri- typical symptoms of odic breathing, frequent awakenings, suffocation, apnea Nonrestorative sleep, PLMS Always required and lighter sleep stages and arousals on resolution more tired in the of apnea (Weil, 2005). Both headache and sleep dis- morning, jerks, RLS, turbance share the same treatment recommendations: unexplained progressive adjustment to altitude and acetazolamide. depression Mobile phone radiation is another possible extrinsic Urge to move legs at RLS Clinical evaluation cause of headache and sleep disturbance (Al-Khlaiwi sleep onset is sufficient; and Meo, 2004). PSG required to evaluate PLMS When to suspect a sleep disturbance in Persistent pain FMS PSG required the evolution of a chronic headache, and fatigue, eventually and vice versa nonrestorative sleep Inability to initiate and Insomnia Clinical evaluation Identification of sleep disorders in patients with chronic maintain sleep, is sufficient; headache is worthwhile as treatment of sleep disorders nonrestorative sleep PSG required in these patients may improve their headaches. to evaluate organic causes MORNING HEADACHES FMS, fibromyalgia syndrome; OSAS, obstructive sleep apnea Morning and nocturnal headache may be a warning syndrome; PGS, polysomnography; PLMS, periodic limb move- symptom of a sleep disturbance. In headache clinics, ments in sleep; RLS, restless legs syndrome. 12–41.7% of patients with severe morning and nocturnal headaches had sleep apnea (Neau et al., 2002) and 53% had headaches associated with a sleep disorder In summary, morning headaches raise a high suspi- (Paiva et al., 1997). The subgroup of patients with sleep cion of OSAS, PLMS, RLS, FMS, and other sleep dis- disorders had a high prevalence of daytime sleepiness, orders. The specific signs and diagnostic procedures to nocturnal sleep disturbance, suffocation, sleepwalking, be used are summarized in Table 63.4. sleep paralysis, and work-related problems due to sleepiness (in 80% of cases), a predominance of men, HEADACHES WITH A HIGHER RISK OF SLEEP and several patients had a late-onset or late-worsening DISTURBANCE headache (Paiva et al., 1995, 1997). Of 432 subjects in a sleep laboratory, patients with Patients with cluster headache have a higher prevalence obstructive sleep apnea and other sleep disorders had of sleep apnea; the risk increases in patients aged over a higher headache frequency, mostly morning head- 40 years who have a body mass index above 25 kg/m2 aches, compared with healthy subjects (Goder et al., (Nobre et al., 2003). Migraine has a clear relationship 2003). Occurrence of headaches was associated with with sleep and sleep disturbances, mainly insomnia. a decrease in total sleep time, sleep efficiency, and In sleep-related headaches (CPH and hypnic headache), amount of REM sleep, and an increase in wake time a brief sleep questionnaire is also mandatory. during the preceding night. In the remaining headache entities, sleep disturbances Morning headaches are more frequent in RLS and should be evaluated because poor sleep worsens the PLMS (Ulfberg et al., 2001). In a polysomnographic course of headache. Furthermore, over-the-counter sleep study of headache sufferers with morning head- medications, often not mentioned by patients, should be aches, FMS was suspected whenever the alpha–delta known, as habituation is likely to develop and some may sleep pattern was found by polysomnography (Paiva aggravate sleep apnea. Increasing headaches in shunted et al., 1995). patients with low-pressure ventriculoperitoneal shunts 1082 T. PAIVA should raise the suspicion of obstructive sleep apnea (i.e., delta sleep or slow-wave sleep) affects the restor- (Hanigan and Zallek, 2004). ative function of sleep with tiredness, lack of concentration, and performance difficulties the following RISK OF HEADACHES IN SLEEP DISTURBANCES morning, whereas increased amounts of these stages are associated with abnormal arousal functions seen In OSAS, RLS, PLMS, circadian sleep disorders, sleep- in some of the parasomnias, such as sleep terrors and walking, and bruxism, an inquiry about headaches is somnambulism. Signs of cortical depression in the mandatory. This is still controversial in narcolepsy nights preceding a migraine attack (Goder et al., and other parasomnias. In addition, headaches should 2003; Strenge et al., 2001; Bruni et al., 2004) may be be investigated in all situations associated with a sleep premonitory manifestations of cortical spreading restriction. depression observed during an attack, and offer a pos- FUNCTIONAL LINKS BETWEEN sible explanation for the influence of sleep. HEADACHES AND SLEEP Abnormalities in REM sleep occur mainly in depression and narcolepsy, with decreased REM sleep Sleep is a recurrent phenomenon during which a com- latency and abnormal distribution of REM sleep across plex set of functions occur that promote tissue repair the night. REM sleep is reduced in situations causing (Adam and Oswald, 1983), for example thermoregula- fragmented sleep, such as sleep apnea and periodic limb tion (Parmeggiani, 1987), immune function (Moldofsky movements. Unpleasant REM sleep-related dreams may et al., 1986; Dinges et al., 1995), regulation of norad- be associated with migraine headaches (Heather-Greener renergic sensitivity (Siegel and Rogawski, 1988), and et al., 1996). maintenance of memory (Davis, 1985; Maquet, 1995). Sleep and pain regulation share common anatomical However, many sleep functions are either incompletely pathways within the central nervous system (Jensen, understood or are still unknown. 2001; Jones, 2005; Mason, 2005), namely in what con- Sleep researchers usually focus on the brain/body cerns the hypothalamus, the brainstem regions, and restorative effects of sleep. These effects are achieved cortical modulators. Appropriate knowledge of these by a sophisticated organization of nocturnal sleep, anatomicofunctional links that influence sleep and which implies a recurrent alternation of two basic sleep headache simultaneously is crucial. states intermixed with small amounts of the awake Several neuromodulators have been proposed in state. Awake is expressed in terms of transient awa- order to explain the association between sleep and head- kenings or brief arousals; the two basic sleep stages aches, especially involving the restorative function of are REM and NREM sleep. Minimal sleep distur- slow-wave sleep. Serotonin (5-hydroxytriptamine, 5HT) bances, as well as more severe disturbances, arise is implicated in the modulation of slow-wave sleep, whenever an imbalance of these states occurs. The and lesions of the raphe serotonin nuclei in animals basic effects of disturbed sleep, relevant to the produc- and humans induce insomnia. Furthermore, serotonin tion of headaches, can be summarized as follows. facilitates sleep onset, attenuating systems that normally Sleep deprivation induces sleepiness, fatigue and tired- activate cortical activation and arousal (Jones, 2005). ness, headaches, anxiety, lack of concentration, confu- Serotonin has opposite effects on migraine: 5HT-related sion, perception disturbances, learning deficits, growth compounds may induce migraine attacks, or prevent problems, and increased health risks and accidents them as prophylactic treatment or abort the acute epi- (Bonnet, 2005). sodes. These discrepancies may be explained by the Sleeplessness may present either as an initiation, interaction with multiple 5HT receptors, and may con- maintenance, or early morning insomnia or as sleep tribute to our understanding of the relationship between fragmentation, i.e., sleep is frequently interrupted by sleep and headaches (Hamel, 2000). short awakenings. Insomnia shares some of the fea- Adenosine, a central neuroprotector (Ribeiro et al., tures of sleep deprivation and is often associated with 2002), is another possible neuromodulator, as it is a fatigue and tiredness, headaches, lack of concentra- sleep-inducing factor that accumulates in the brain dur- tion, anxiety, and depression. For these reasons, in ing prolonged wakefulness, mainly in the extracellular patients with chronic headaches insomnia aggravates space of the basal forebrain. This increase reduces the and perpetuates the complaints. activity of wakefulness-promoting cell groups, mostly In normal subjects, sleep propensity increases in the basal forebrain cholinergic cells. Adenosine receptor course of wakefulness, and the longer the previous antagonists, such as caffeine and theophylline, induce wakefulness the longer and deeper is the following higher vigilance, promoting wakefulness (Porkka- sleep, namely delta activity of stages 3 and 4 (Borbe´ly Heiskanen, 1999). 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