Open access peer-reviewed chapter
Abstract
Headache is one of the most common and bothersome problems in neurology practice. The frequency of headache has been substantially increased over the last 30 years due to changes in lifestyle. Controlling the trigger factors and lifestyle changes (e.g. regular sleep, meal time, exercise, etc.) are the first step management strategies in headaches. Sleep and headache have bidirectional effects on each other. While diminished and poor quality of sleep can be a trigger factor for headache (e.g. migraine and tension-type headache (TTH)), some types of headache like hypnic headache and cluster-type headache mainly occur during sleep. Patients with headache may have poor sleep quality, reduced total sleep time, more awakenings, and alterations in architecture of sleep recorded by polysomnography. Progression to chronic forms of headache may also be associated with the duration and quality of sleep. Even though pathophysiology of headache and sleep disorders shares the same brain structures and pathways, sleep disturbances are commonly underestimated and underdiagnosed in headache patients. Clinicians should consider and behold the treatment of accompanying sleep complaints for an effective management of headache.
Keywords
- primary headache
- sleep
- polysomnography
1. Introduction
Headache disordes lead to significant disability worldwide, impairing quality of life, damaging productivity, and substantial burdens of financial cost on both the individual and societies. For this reason, these disorders effectuate a major public health problem in all countries and world regions. In Global Burden Disease (GBD) study 2019, headache disorders have been estimated to account for 46.6 million years lived with disability [YLDs] globally, which has been 5.4% of all YLDs, with 88.2% of them attributed to migraine [1]. The frequency of headache has been substantially increased over the last 30 years due to changes in lifestyle. Controlling the trigger factors and lifestyle changes (e.g. regular sleep, meal time, exercise, etc.) are the first step management strategies in headaches [2]
Sleep disorders and headache have bidirectional effects on each other [3, 4]. The nature of this relationship and whether sleep disturbance or headache has more impact on one another is still poorly understood [5, 6, 7]. Headache may be intrinsically related to sleep such as hypnic headache or cluster headache (CH) [8, 9]. Poor quality, and excessive or diminished sleep can be a trigger factor for headache (e.g. migraine and tension-type headache (TTH)), or contrary sleep may have a a relieving effect on a migraine attack [10, 11].
Headache chronicity might be also associated with the duration and quality of sleep [12]. The severity of a sleep disorder may be in an adverse correlation with the intension of the pain [3]. Patients with headache may have poor sleep quality, reduced total sleep time, more awakenings, and alterations in architecture of sleep recorded by polysomnography (PSG) [13]. Prevalance of chronic headache was found to be higher in patients who underwent polysomnographic investigation due to sleep problems [14].
In this section, we aim to discuss the effects and relation of sleep and primary headaches on one another.
2. Common pathophysiology between headache and sleep disorders
Sleep is a recurrent, reversible, periodic, and cyclic active and physiological process that is essential for life [15]. Sleep has essential roles for health such as regulating immune system, releasing hormones (e.g. growth hormone), neurodevelopment, mental health, memory, etc. [16]. Several factors effect the total duration of sleep, time to fall asleep, time to wake-up, and total duration of wakefullness. Sleep and wake cycle is regulated by circadian and homeostatic rhythms. Light is a main factor for circadian rhythmicity, in addition to, time for meals, work or school schedules, social activites, or internal biological clock designate sleep and wake durations [17].
Sleep is composed of four to six recurrent sleep periods each lasting to 80–110 minutes [16]. These periods are constituted of two main sleep stages as rapid eye movement (REM) and non-rapid eye movement (NonREM). NonREM sleep is divided into three stages such as N1, N2, and N3 (slow-wave sleep) [18]. During the early hours of night, NonREM stages dominate the sleep while REM stage dominates the later part of the sleep [16].
Even though pathophysiology of headache and sleep disorders shares the same brain structures and pathways, sleep disturbances are commonly underestimated and underdiagnosed in headache patients [19].
Thalamus is one of the main centers for regulation of sleep and also pain by receiving ascending nociceptive stimulus from trigeminocervical system. Dysregulation in thalamocortical circuits may be predisposing to sleep and headache disorders [20, 21]. Sleep deprivation may induce hyperexcitability and may alter regulation of cortical circuits [22]. During the shift from wakefullnes to sleep, there is an increment in response to tactile, auditory, and propriseptive stimulus. Disturbed sleep seems to escalate pain by decreasing the activity of descending inhibitory pain control system leading to diminish pain treshold [23, 24].
Hypothalamus, containing suprachiasmatic nuclei (SCN) being the main brain structure to maintain sleep-wake cycle, seems to be responsible for the prodromal symptoms of migraine like mood, appetite or sleep changes, fatigue, or yawning [25, 26]. Accompanying autonomic symptoms like nausea, lacrimation, and rinorrhea suspect the role of hypothalamus also during a migraine attack [27].
A reduction in arousal index in REM sleep stage and a reduction in cyclic alternating pattern (CAP) in NonREM sleep stages of migraneous patients may show a dysfunction in the connection of brainstem and hypothalamus both of which are important in the pathophysiology of sleep disorders and migraine [28, 29].
In cluster headache [CH], hypothalamus has a crucial role both in autonomic sypmtoms and periodicity of the headache. During attacks, ipsilateral to the autonomic features hyperactivation in hypothalamus was shown by a positron emission tomography (PET) study [30]. In another study, volume of anterior hypothalamus was found to be increased suggesting a structured alteration in SCN [31].
Neuropeptides orexin A and B that are important for the maintenance of wakefullness are synthesized mainly in lateral and posterior hypothalamus. Orexinergic receptors are located in prefrontal cortex, thalamus, and subcortical areas and also take role in pain modulation, thermoregulation, and autonomic functions except maintaining wakefullness and wake-sleep rhytmicity [25]. Sarchielli et al have found lower levels of orexin in patients with episodic migraine and higher levels in patients with chronic migraine and medication overuse headache suggesting a dysfunction of orexin and a response of hypothalamus to headache [32]. There is an orexin deficiency in narcolepsy, and high prevalance of migraine in patients with narcolepsy may indicate a dysfunction of orexin in migraine pathophysiology as well [33, 34].
Melatonin also called as sleep hormone is synthesized in epiphysis (pineal gland), and the secretion is regulated by suprachiasmatic nuclei. Thus, having a role in circadian rhythm, melatonin also has an analgesic effect via anti-inflammation, inhibition of dopamine release, and GABAergic and antiglutamatergic effects [35]. Melatonin therapy seemed to be affective in headache treatment even with or without an accompanying sleep-wake disorder [36].
Locus cereleus (LC), periaquaductal gray matter (PAG), and dorsal raphe nucleus (DPN) are important brain structures for both headache and pain [34]. Ventrolateral part of PAG that is activated by lateral orexinergic neurons of hypothalamus is a section of REM off area, and it is active during wakefullness while silent at REM sleep stage [37]. LC takes role in stabilizing the switches from sleep to wake, and DPN mainly takes role in switches from NonREM to REM sleep [38, 39]. The decrease in cyclic alternating pattern in REM sleep of migraineous patients is suspected to be a dysfunction of serotonergic system [40]. Dopaminergic dysfunction is associated with prodromal symptoms of migraine, e.g. yawning and mood changes and also with enhanced risk of restless legs syndrome (RLS). The prodromal symptoms being more in patients with RLS may indicate the role of affected dopaminergic system in both of the diseases [41].
Another suspected mechanism is the role of glymphatic system which is a clearing system of interstitial waste products from central nervous system [42]. In an experimental model, it has been shown that glymphatic system was temporarily disturbed during cortical spreading depression and improved 30 minutes later, indicating the role of glymphatic system in migraine pathophysiology [43]. As during sleep glymphatic system is active, the ameliorating effect of sleep on migraine attacks may be explained by the glymphatic system [4].
3. Sleep disorders and headache
During the evaluation of sleep macrostructure by polysomnography, sleep latency, REM sleep latency, percentages of every sleep stages, total sleep time, and sleep efficiency are mainly analyzed. Polysomnography is a diagnostic test for the detection of both the existence and the type of the sleep disorder. Channels of electroencephalography, electrooculography, and electromyography are used to evaluate all of the sleep stages and wakefullnes. Thermistor, nasal canule, and sensors located on thorax and abdomen belts are used to detect the existence and type of abnormal sleep-related breathing disorders. At the same time, electromyographic channels are used to observe sleep-related movement disorders [44].
The time that the first sleep stage epoch seen is called as sleep latency (minute), and the time that first REM sleep stage seen is named as REM latency (minute) [45]. Sleep effciency (%) is the ratio of total sleep time (TST) to total recording time during polysomnography all night [46]. Microstructure of sleep is evaluated by the detection of arousals and the analysis of cyclic alternating pattern [CAP]. Either macrostructure or microstructure of sleep can be effected by primary headaches, and changes can be observed by polysomnography [47].
Sleep disorders are classified as sleep-related breathing disorders, insomnia, hypersomnia, circadian sleep-wake disorders, parasomnia, sleep-related movement disorders, and other sleep diseases [18]. Polysomnography (PSG), multiple sleep latency test (MSLT), wakefullness maintenance test (WMT), and actigraphy are the main diagnostic tests for sleep disorders. Sleep-related breathing disorders, parasomnias, sleep-related movement disorders, and some types of insomnia can be diagnosed by polysomnography. Actigraphy is a diagnostic test that detects limb movements by using a device worn either on ankle or wrist or both. Whether the patient is awake or asleep can be detected due to the limb movements, but neither sleep stages nor breathing disorders can be evaluated [48]. Actigraphy helps the detection of circadian sleep-wake disorders and insomnia, while MSLT and WMT are used for the diagnosis of hypersomnias [49].
We will discuss the effects of sleep disorders on primary headaches separately as follows:
3.1 Insomnia
Though the high incidence of comorbidity, insomnia is underestimated in patients with headache [19]. Insomnia is identified as difficulty to fall asleep, maintain sleep, or wake up earlier than planned, though all conditions, circumtances, and possibilities are sufficient to sleep [18]. Insomnia may be in relation with several painful symptoms like headache, especially with chronic forms rather than episodic [50, 51]. In patients with the diagnosis of fibromyalgia, insomnia related to pain was thought to be a result of increases in amount of arousals during sleep [52]. During night sleep, frequently seen awakenings may lead to a missing of pain inhibiton and patients may have decreased pain tresholds [24].
Insomnia is the most frequent disorder associated with chronic headache [53]. Nearly 50% of migraneurs may have insomnia symptoms, and insomnia is 1.8 times more in patients with tension-type headache (TTH) [54, 55]. Also, insomnia is a risk factor for the high rate of attacks and chronification for both migraine and TTH [56, 57].
Cognitive behavioral therapy widely used in the treatment of insomnia also decreases the frequency of accompanying headache [58].
3.2 Obstructive sleep apnea
Apnea-hypopnea index (AHI) is calculated by the detection of apneas (cessation of sleep for at least 10 seconds) and hypopneas (shallowing of breath for at least 10 seconds) by polysomnography. Obstructive sleep apnea syndrome (OSAS) is diagnosed when AHI is bigger than 5. AHI in the range of 5–15 is called mild, >15–30 as moderate, and >30 as severe OSAS. Obstructive sleep apnea headache is a secondary type of headache which is characterized by a headache attack that lasts upto 4 hours after awakening [18]. Morning headache is related to nocturnal hypoxemia (oxygen saturation ≤90 %) [59] and/or hypercapnia (PaCO2 > 45 mmHg) [60] due to recurrent apneas and/or hypopneas [61]. It has a good response to treatment and decreases or totally diminishes after an effective treatment of OSAS [5, 61, 62].
There may be a comorbidity with migraine, tension-type headache (TTH), cluster and hypnic headache, and OSAS [4, 63, 64]. Snoring which may be a component of sleep apnea is found to be more frequent in chronic types of headache than episodic forms [65]. Treatment of OSAS has favorable effects on the accompanying primary headache [66].
3.3 Parasomnia
Parasomnias are divided into two according to sleep stages as REM parasomnias and NonREM parasomnias. Somnambulism (sleepwalking), sleep terror, sleep-related eating disorders, and confusional arousal are NonREM parasomnias. Nightmare, recurrent isolated sleep paralysis, and REM sleep behavior disorder (RBD) are among REM parasomnias [18].
NonREM parasomnias are common in childhood and adolescent periods and mainly disappear in adulthood. Migraine with aura is more common than migraine without aura in sleepwalking patients [67]. The percentage of a history of sleepwalking in parents of the children with migraine is higher than the other types of headache [68]. As there is a circadian periodicity in NonREM parasomnias, serotonergic and orexinergic systems that have roles in migraine attacks were suspected to be responsible for the underlying comorbidity [69].
The frequency of nightmare, a REM parasomnia, is increased in migraneurs with an increase in awakenings during REM sleep [4, 70]. REM sleep behavior disease was also found to be in association with migraine headache and in relation with disability due to headache [71].
3.4 Sleep-related movement disorders
Restless legs syndrome (RLS) is the most common disorder in this group. It is an upleasant sensation that develops when patient lies to sleep or during inactivity or even resting and makes patients to be in need of moving the legs. The symptoms are mainly seen after evening, but in time they may also develop earlier in a day during resting. Sleep-related periodic limb movements also accompany in a majority of these patients [18]. Prevalance of migraine is high in RLS patients with a high frequency of headache attacks and more disability [72, 73]. Migraine prevalance in RLS is more than RLS in migraine [74].
Also there is an increased association with TTH and RLS [73, 75]. Dopaminergic dysfunction and iron metabolism are claimed for the common pathophysiology of migraine and RLS, while in TTH dopaminergic dysregulation is suspected to connect depression with RLS [76, 77].
Bruxism can occur both in sleep and wakefullness. Sleep bruxism is characterized by recurrent tightening or clenching of teeth with an increased jaw muscle activity during night [78]. Headache comorbidity was found to be higher in adults than children [79]. Bruxism is found to be mainly associated with chronic migraine; nevertheless, the combination of bruxism with temporomandibular dysfunction is associated with both episodic and chronic migraine as well as TTH [53].
3.5 Hypersomnia
In this group, narcolepsy with cataplexia (type 1), narcolepsy without cataplexia (type 2), idiopathic hypersomnia, and recurrent hypersomnia have the main complaint of sleepiness during day [18]. As the disrupted orexinergic system is the main pathology in narcolepsy, migraine is claimed to be in association [80], but the results are conflicting. In a study, no association was found between narcolepsy and migraine, while the others found an increase of migraine attacks in narcoleptic patients and have suspected migraine as an independent risk factor [10, 33, 80].
4. Effects of headache on sleep
4.1 Migraine
Migraine is one of the most disabling primary headache with a pulsating quality and moderate to severe intensity, mainly located unilaterally and lasting for 4 to 72 hours. It may be aggrevated with physical activity and nausea and/or phonophobia, and photophobia may accompany [81]. Migraneurs have higher scores of Pittsburg Sleep Quality Index (PSQI) showing a poor sleep quality [13]. Frequency of attacks were found to be related with decrease in sleep quality, and prevalance of poor sleeper is high in migraine [70]. Poor sleep quality may be in association with chronic migraine, and patients with chronic migraine may have more sleep disorders comparing episodic migraine [8, 54]. Bertisch et al have investigated sleep efficiency of patients with episodic migraine with actigraphy. They have found a relation with poor sleep efficiency characterized by fragmentations during sleep and a migraine attack on the following day. No temporal association was found between poor sleep quality and shorter duration of sleep. They have concluded that fregmantations rather than duration of sleep have a role in inducing frequent attacks in episodic migraine [82]. On the other hand, some studies have not found an association between headache and fregmantations in sleep during night [25, 83].
Obesity is a common risk for both migraine and OSAS, and migraineous patients may be sensitive to hypoxemia which is also associated with OSAS headache [4]. Comorbidity of OSAS increases the frequency of migraine attacks, and chronicity of migraine can be due to sleep apnea [65]. Morning headache attacks in migraineurs can be associated with sleep apne or snoring [84].
The polysomnographic features of migraneurs may show alterations compared to nonheadache population. Sleep latency is found to be normal or longer, and the percentage of NonREM1 sleep is slightly higher, while NonREM3 sleep stage is decreased interictally [40, 84]. The latency of rapid eye movement (REM) sleep may be longer. The total amount of REM sleep may decrease, and sleep efficiency may also be low [13, 84]. In the microstructure of sleep in migraneous patients, rate of CAP and amount of CAP cycles and arousal index in REM and NonREM sleep stages may be low [28, 40], or arousals may be frequent especially in patients with aura [38]. Pediatric patients with chronic migraine or migraine attacks with severe intensity may have short duration of sleep with an increased sleep latency as well as decreased percentages of NonREM 3 and REM sleep stages [84].
Migraneous patients have more complaints of insomnia [85], and the rate increases with the comorbidity of psychiatric diseases such as anxiey disorder and/or depression [86]. Sleep may be fragmentated cause of headache. The patients may also complain of symptoms of insomnia previous night before a morning headache attack with a decrease in the amount of NonREM3 sleep stage [83].
Treatment of associated sleep disorder has beneficial effects on migraine therapy. It has been shown that if the sleep disorder is treated, accompanying migraine may turn from chronic form to episodic one (Case 1) [9, 13, 87].
4.2 Tension-type headache
Tension-type headache is the most common primary headache, mainly bilaterally with a pressing or tightening quality and a mild to moderate intensity. The duration may be 30 minutes to 7 days. Routine physical activity does not worsen the pain. Though photophobia or phonophobia may be present, nausea does not accompany [81]. Several sleep disturbances like hypersomnia, insomnia, or circadian sleep-wake disorders may accompany TTH [8, 88]. The decrease in sleep quantity is one of the most important triggers, and many of the patients with TTH report unsatisfied sleep [8].
CASE 1.
Chronic migraine.
Thirty years old male patient was a shift-worker in a factory. He was admitted to the headache outpatient clinic. Since childhood, he had a pulsatile and throbbing unilateral headache mainly on the right orbitotemporal side. Localization might change at different attacks. Pain duration wass 8 to 10 hours, and pain frequency has increased after he began to work as a shift-worker [>15 days/month]. Pain intensity was severe (with a visual analog score of 10). Phonophobia, photofobia, and nausea and sometimes vomiting accompanied the headache, and pain was elevating by climbing stairs or walking. There was no preceeding aura. Stress and inadequate sleep triggered the pain, while pain alleviated if the patient could sleep during the attack. His mother had a diagnosis of migraine without aura.
As he also complained of snoring without any witnessed apnea and paresthesia on his legs when he lied down for sleep which alleviates as he got up and walked around, he underwent a polysomnographic investigation at the sleep center of University of Health Sciences Erenkoy Mental Health and Neurological Diseases Training and Research Hospital.
On his polysomnographic investigation, we have detected slightly reduced sleep efficiency. NonREM1 percentage was high, while NonREM3 and REM sleep percentages were found to be low during all night. Arousal index in NonREM sleep stages and snoring index both in REM and nonREM sleep stages were increased. Apne-hypopnea index was 2.1 (not pointing out an obstructive sleep apnea syndrome).
Hypnogram of the patient that has been recorded by polysomnography. Gray horizantal lines show NonREM sleep stages ( N1, N2, and N3) and wakefullness [W], red lines show REM sleep stage [R], and green vertical lines show arousals.
Eppworth sleepiness scores and PSQ scores are higher in TTH patients indicating poor sleep quality and daytime sleepiness [83]. Decreased sleep quality is in relation with higher intension of headache attacks and can be a factor for the chronification of TTH [57, 89]. Patients with sleep disorders tend to have lower threshold of pain [83]. Accompanying depression may contribute to decrease the pain treshold [90].
On polysomnographic investigation, NonREM 1 [N1] latency was found to be decreased with an increase in NonREM 3 [N3] sleep, while the structure of REM (both the latency and total amount) was not effected. Decrease in total sleep time and poor sleep efficiency due to increased sleep fregmentation with arousals may also be observed [83].
Sleep-related movements and restless legs syndrome can also accompany TTH [8, 73]. Association with OSAS is not clear, but if OSAS is diagnosed, it must be treated properly [7, 9]. In children, a relation between TTH and bruxism was also found (Case 2) [84].
CASE 2.
Chronic tension-type headache.
Twenty-three years old female student was admitted to the headache outpatient clinic with a bilateral headache on frontal regions with a pressing quality since 3 years. Pain duration was 3 to 72 hours with a pain frequency more than 15 days in a month. She had no phonophobia or photophobia. Nausea might be present. Short duration of sleep and working with computer for long hours triggered the attacks. Pain intensity was moderate (with a visual analogue score of 6). As she complained of difficulty in maintaining sleep more than 3 times a week and daily sleepiness and snoring, she underwent a polysomnographic investigation at the sleep center of University of Health Sciences Erenkoy Mental Health and Neurological Diseases Training and Research Hospital
On her polysomnographic test, we have found elongation of sleep latency with a reduced sleep efficiency. NonREM1 and NonREM3 percentages are slightly increased. Frequent awakenings and short arousals are observed in the microstructure. Abnormal sleep-related breathing events were not detected.
Hypnogram of the patient that has been recorded by polysomnography. Gray horizantal lines show NonREM sleep stages (N1, N2, and N3) and wakefullness (W), red lines show REM sleep stage (R), and green vertical lines show arousals.
4.3 Cluster headache
Cluster headache is one of the trigeminal autonomic cephalalgias. Pain is mainly located at orbital/supraorbital/temporal regions unilaterally. The duration of severe pain is 15 to 180 minutes with accompanying autonomic symptoms (ICD). The relation with sleep and cluster headache [CH] has been shown in previous studies. CH is thought to be provoked during the switching of REM sleep to NonREM sleep. In episodic CH, attacks are mainly related to REM sleep, though this relaton is not clear in chronic form [8].
Sleep apnea either obstructive or central seem to be frequent in patients with CH. Accompaying sleep apnea may induce CH by leading to nocturnal hypoxemia [91], and effective treatment of sleep apnea either with CPAP or dental device can also be effective to diminish the severity of clusters [9, 64, 92].
Poor sleep quality and short duration of sleep may be seen in both episodic and chronic CH [93]. During the bouts of CH, patients may suffer from transient insomnia which usually resolves after the end of the bout and may recur at the next cluster period in episodic CH [91].
Among shift-workers, episodic cluster headache incidence was found to be higher. This suggested that disturbed sleep due to the work schedule could trigger cluster headache [93, 94]. As shift-working is suspected to induce the attacks, patients with CH can be advised to have a steady daily working plan [93].
During a cluster period, elongated REM latency and diminished total percentage of REM sleep can be detected by polysomnography. Sleep-wake cycle may also be disturbed during this period (Case 3) [28, 95].
CASE 3.
Cluster headache.
Fifty-two years old male patient was admitted to the headache outpatient clinic with a complaint of a severe headache on right orbitofrontal region for 3 years. Attacks mainly began at autumn and lasted for 3 to 4 weeks. Each attack has begun early in the morning and awakened him with a duration of 45 to 60 minutes. Pitosis, lacrimation, rinorrhea, and redness on the right eye convoyed the headache, which was very severe (with a visual analog score of 10). Pain was resistant to analgesics, and resting did not alleviate the headache. He did not have a history of any other diseases. Neurological examination and cranial magnetic resonance imaging were normal. He also complained of snoring and witnessed apnea.
His polysomnographic investigation recorded at the sleep center of University of Health Sciences Erenkoy Mental Health and Neurological Diseases Training and Research Hospital shows a slightly increased sleep latency. Awakenings are seen during all night, and sleep efficiency is slightly reduced. He had an attack at 05:00 AM that awakened him from sleep (shown by an arrow). Apne-hypopnea index is 6.2 (mild obstructive sleep apnea syndrome).
Hypnogram of the patient that has been recorded by polysomnography. Gray horizantal lines show NonREM sleep stages (N1, N2, and N3) and wakefullness (W), and red lines show REM sleep stage)
Abnormal sleep-related breathing events (obstructive apneas and hypopneas) are shown by green vertical lines
4.4 Hypnic headache
Hypnic headache is a rare headache disorder that mainly occurs during night sleep as well as at naps during the day [96]. Headache causes wakening and lasts for up to 4 hours without associating characteristic symptoms [81]. Attacks may occur in every stages of sleep [97, 98]. Just before and during the headache attack, elevation in arterial blood pressure has been detected in some patients. It has been hypothesized that these alterations could typify an association with sleep apnea [63]. Sleep apnea may be a trigger for the attack, and the treatment of OSAS also reduces the hypnic headaches [9, 98]. Attacks arising either from REM sleep or NonREM sleep can be documented using polysomnography (Case 4) [96].
CASE 4.
Hypnic headache.
Fifty-eight years old female patient was admitted to the headache outpatient clinic. She had a pressing headache on vertex which awakened her from sleep nearly every night. Attacks occured in the first half of the night with a duration of 60–120 minutes. Neither phonophobia/photofobia nor nausea/vomiting were present. Autonomic symptoms did not accompany. Pain intensity was mild (with a visual analog score of 6). She did not have any other types of headache. She also complained of snoring, and there was witnessed apnea detected by her husband. She had a history of hypertension which was under control with ramipril.
On her polysomnographic investigation recorded at the sleep center of University of Health Sciences Erenkoy Mental Health and Neurological Diseases Training and Research Hospital, we have found an elongated sleep latency and a reduced sleep efficiency. On the first half of sleep, she has awakened after first REM sleep stage (shown by an arrow on hypnogram) with a headache attack. Apnea-hypopnea index was 8.7 (mild obstructive sleep apnea syndrome). Snoring index both in REM and NonREM sleep stages were increased.
Hypnogram of the patient that has been recorded by polysomnography. Gray horizantal lines show NonREM sleep stages (N1, N2, and N3) and wakefullness (W), and red lines show REM sleep stage)
Abnormal sleep-related breathing events (obstructive apneas and hypopneas) are shown by green vertical lines.
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