Insomnia is a common complaint, and like most headaches, it is more frequent in women. Different recent studies highlighted the strict relation between headache and insomnia. In a study of 50 insomniacs, 24 subjects (48 %) also complained of headache, mostly migraine without aura (37.5 %) or episodic tension-type headache (50 %) [3], but only 10 % had headache upon awakening.

A national survey in the United States recruited 5484 adults; it showed a significant association between frequent and severe headache, including migraine with and without aura, and insomnia, without differences between specific headache subtypes. Adults with headache were more likely than those without headache to report at least one of four insomnia symptoms: difficulty initiating sleep, maintaining sleep, waking up early, and daytime fatigue. Subjects with headache were more than twice as likely to report three or more of these symptoms than those without headache (1.83 % vs. 0.60 %; OR 2.5; CI 2.0–3.1) [88].

A Chinese study showed that the prevalence of DSM-IV insomnia was higher in women with headache than in those without headache (19.9 % vs. 5.3 %; p < 0.01). After adjusting for age and menopausal status, women with migraine, tension-type headache, and unspecified headache were significantly more likely than women without headache to report insomnia symptoms of difficulty in initiating and maintaining sleep and waking up early. Women with insomnia had a 4.0-fold increased risk of having headache at least once per week: in particular, a 3.2-fold increased risk of migraine, a 2.3-fold increased risk of tension-type headache, and a 2.2-fold increased risk of headache in general [152].

A population study in Norway showed that subjects with insomnia were significantly more likely, compared to those without insomnia, to suffer from headache in general (17.6 % vs. 11.8 %; OR 1.68; CI 1.58–1.79, p < 0.001) and migraine (16.8 % vs. 13.3 %; OR 1.41; CI 1.29–1.55, p < 0.001) [73].

A follow-up of the same study reported that, after adjusting for age, gender, and sleep medication, insomnia among headache-free subjects at baseline was associated with a significantly increased risk of headache 11 years later (p < 0.001). There was also a significant association between insomnia at baseline and headache frequency at follow-up, specifically for migraine (p = 0.02) and tension-type headache (p < 0.001) [104].

It is evident that headache and migraine are associated with insomnia, while only severe insomnia is associated with headache or migraine. In addition, it was found that insomnia is a risk factor for headache or migraine onset and for increased headache frequency, specifically for tension headache and migraine.

As insomnia appears to be a risk factor for headache or migraine onset, insomnia patients should probably be routinely evaluated for headache, and, on the other hand, tension headache and migraine patients should probably be routinely treated for insomnia, if present, as part of their overall management [142].

There is evidence that sleep-disordered breathing is associated with headaches. Self-reported snoring has been associated with morning and daytime headache [27, 103, 132, 144], and habitual snoring was more frequent in patients with chronic daily headaches (24 %) vs. controls (14 %) [131].

The prevalence of headache in a population of patients with OSAS has been evaluated by different authors [4, 13, 61, 63, 75, 103, 119, 131, 144] and ranged from 32.9 to 58.5 %. However, when evaluating in a headache clinic, the prevalence of OSAS was not different from that in the general population [77].

Guilleminault et al. [65] reported a 36 % incidence of morning headaches in 50 patients with sleep apnea. Dexter [37] reported 11 patients with chronic recurring headaches with a history suggestive of sleep apnea that was confirmed polysomnographically: ten of these patients had sleep apnea and one had mixed sleep apnea. Mathew et al. [97] also reported headache in patients with sleep apnea: 3 out of 18 patients with chronic headaches and 1 out of 4 patients with cluster headache had sleep apnea. Kudrow et al. [86] found a 60 % prevalence of sleep apnea among ten patients with cluster headaches: four of these patients had central apneas and two obstructive apneas.

The clinical presentation is a morning tension-type headache, mainly frontal, frontotemporal, or temporal (38.9 %) in location, tightening or pressing (78.9 %), and mild to moderate (84.2 %) [3]. Chronic headache was seven times more common among subjects with OSAS than in the general population, and treatment of sleep apnea (nCPAP) leads to headache improvement [47].

Several reports showed that migraine attacks in sleep apnea patients occur usually during nighttime or early morning [4, 13, 65]. Subjects with obstructive sleep apnea and other sleep disorders evaluated in a sleep laboratory had a higher headache frequency, mostly morning headaches, compared with healthy subjects [61].

In a population-based cohort study, the authors evaluated the effects of sleep-related breathing disorders (SBDs) on migraine development in patients aged 20 years or more and diagnosed with SBD. The cumulative incidence of migraine was significantly higher in the SBD cohort than in the control cohort. The risk of developing migraine was higher in men than in women with SBD; moreover, the incidence of migraine was higher in patients aged 20–44 years and 45–64 years. The findings indicated increased risk of developing migraine in adults, but not elderly, with SBD [66].

Jensen et al. [77] assessed the frequency of OSA in a population of headache patients. Seventy-five of 903 headache patients reported heavy snoring and episodes of interrupted nocturnal breathing (8 %). Among 43 patients examined with polysomnography (PSG), 14 (1.5 % of the total study population) had an apnea/hypopnea index (AHI) of 5/h or higher. Eleven of the patients reported morning headache. They concluded that OSA’s prevalence is not higher than what is reported for the general population but that chronic daily headache appeared to be more frequent in patients with OSA. Idiman et al. [69] did not find a statistically significant relationship between headache and AHI or minimal oxygen saturation. Kallweit et al. [78] reported that 11 (10.3 %, 8 % male) of 107 consecutive patients with OSA fulfilled diagnostic criteria for migraine (migraine with aura [MA] in four, migraine without aura [MO] in six, and CM in one). They did not find significant differences between patients with or without migraine. After 1 year, however, continuous positive airway pressure (CPAP) treatment was effective for sleep apnea, sleep quality, and migraine. Kristiansen et al. [85] concluded that migraine and OSA are unrelated in the general population. They investigated the relationship between migraine and OSA in a random age- and gender-stratified sample of 40,000 persons aged 20–80 years. Three hundred and seventy-six subjects with high risk and 157 with low risk of sleep apnea aged 30–65 years were identified based on screening questionnaires. They underwent clinical evaluation, a structured headache interview, and PSG. No relationship was found between MO or MA and OSA. This was true for moderate and severe OSA. Greenough et al. [63] found no relationship between the duration of nocturnal hypoxemia and headache complaints in patients with OSA.

Few data are available on the relationship between sleep apnea and migraine in children. Guilleminault et al. first reported that 18 of 50 OSA patients suffered from frontal or diffuse morning headache; afterward, several other reports supported this important relationship [65, 110].

A varied range of symptoms and signs are associated with OSAS in the pediatric population. In children and adolescents with OSAS, the most common clinical manifestation reported is snoring but also obesity, excessive daytime sleepiness, heavy habitual snoring, and neuropsychological disturbances [103]. Morning headaches and poor appetite may also present in OSAS, particularly in school-aged children, and it is one of the Diagnostic Criteria of Pediatric Obstructive Sleep Apnea by the American Academy of Sleep Medicine which may be due to carbon dioxide retention, sleep fragmentation, or gastroesophageal reflux [71].

A polysomnographic study in children with headaches indicated that sleep-disordered breathing was more frequent among children with migraine (56.6 %) and nonspecific headache (54 %) vs. chronic migraine (27 %) [44].

In synthesis, the prevalence of headaches is higher in OSA patients. The data concerning the higher prevalence of OSAS in migraine patients are controversial and point to an inexistent impact upon prevalence.

The association between headache and OSAS is probably based on a combination of factors: hypercarbia, hypoxemia, altered cerebral blood flow, increased intracranial pressure, alterations in sympathetic nerve activity and increases in blood pressure secondary to multiple arousals, and brainstem dysfunction. However, it has been hypothesized that migraine attacks could be secondary to sleep disruption rather than to sleep apnea by itself [142].

These findings revealed a strong relationship between migraine and sleep-disordered breathing, while chronic migraine was associated with more disrupted sleep and tension-type headache with bruxism. It is hypothesized that sleep-disordered breathing may predispose patients to sleep fragmentation, which in turn may exacerbate or aggravate preexisting signs of migraine, because sleep deprivation is known to trigger or worsen migraine attacks [40].

Restless legs syndrome (RLS) is commonly represented by an urge to move the legs, accompanied by unpleasant leg sensations, occurring at night, worsened by rest, and improved by movements [155].

There is evidence that restless legs syndrome (RLS) is another condition frequently reported by migraine patients [21]. RLS prevalence in migraine ranged from 8.7 to 39.0 % with no apparent differences based on gender and aura status, while migraine prevalence in RLS ranged from 15.1 to 62.6 % [54].

The first study suggesting an association between RLS and migraine in the pediatric population was conducted by Seidel et al. [134] and assessed the frequency of RLS in children and adolescents with migraine compared to headache-free controls. The authors included two control groups. The first group was recruited from an outpatient clinic of pediatrics and adolescent medicine (group 1). These children and adolescents were exclusively screened at follow-up after recovery from a minor illness and did not suffer from a significant medical, neurological, or psychiatric condition at the time they were included in this study. The second control group was recruited from primary school (group 2); the aim of the study and the objects of the questionnaires were explained to the children and teachers.

In 111 consecutive patients with a sole diagnosis of migraine with or without aura and 73 headache-free controls, the frequency of RLS in migraine patients was significantly higher (22 % vs. 5 % [p < 0.001] group 1 and 8 % [p < 0.001] group 2 [134]).

A common pathophysiological origin for migraine and RLS has been proposed [21], and a link involving a disturbance of iron metabolism has been considered. A recent study investigated daytime dysfunction in children with RLS and the effects of treatment primarily with iron supplements on RLS symptoms and daytime dysfunction in 25 children with RLS showing that after treatment, participants’ daytime function had improved to levels similar to those of controls. Sixteen out of 23 cases were successfully treated primarily with iron supplement [57].

A link between RLS and a dysfunction within the dopaminergic system has also been suggested [21, 54, 155]. It is supported by the rapid improvement of RLS symptoms after treatment with dopaminergic agents. Dopamine is also involved in migraine pathophysiology. Dopaminergic symptoms (DPS) like yawning, irritability, and mood changes as well as nausea and vomiting occurring both during the premonitory and headache phases are present in 47.6 % migraine patients with RLS vs.13.1 % of those without RLS (p < 0.001). A further support to a “dopaminergic link” between migraine and RLS is the observation that antiemetics with antidopaminergic properties are effective in aborting migraine attacks [21].

The prevalence of both RLS and periodic limb movements in sleep (PLMS) increases with age. Complaints of morning or daytime headaches are three to five times more frequent in patients with RLS [145]. Fifty patients with severe headaches who qualified for the treatment with dopamine receptor-blocking agents had a prevalence of RLS of 34 %; this group had a higher risk of developing akathisia as a treatment side effect.

A recent study [146] investigated the prevalence, severity, and correlation between sleep quality and RLS in a large population of migraine patients and non-migraine controls as poor sleep presumably triggers migraine attacks. Restless legs syndrome prevalence in migraine was higher than in controls (16.9 % vs. 8.7 %; multivariable-adjusted odds ratio 1.83; 95 % confidence interval 1.18–2.86; p = 0.008) and more severe (adjusted severity score 14.5 ± 0.5 vs. 12.0 ± 1.1; p = 0.036). Moreover, poorer sleep quality was independently associated with RLS occurrence and RLS severity in migraine patients.

The hypotheses to explain the coexistence of RLS and migraine are based on a common genetic basis and brain structures involved (like the A11 dopaminergic nucleus of the dorsal posterior hypothalamus that lays a crucial role in RLS and trigeminovascular nociception). Furthermore, cerebral dopamine imbalance and altered iron metabolism were implicated; in fact, dopamine antagonists are effective in migraine attacks, and usually iron deficiency is associated with an increase in extracellular dopamine levels and in the changes in dopamine levels with circadian rhythm that could explain the appearance of RLS symptoms at night and the relationship with migraine because of a dopaminergic hyperfunction reached during the day after lower trough levels [96]. On the other hand, sleep deprivation or sleep instabilities caused by RLS could trigger migraine [54].

There are only two case reports on increased periodic limb movements in adult headache patients: the first was a patient with hypnic headache syndrome [84] and the second was the case of a man with episodic cluster headache who suffered from severe obstructive sleep apnea and periodic limb movements during sleep [112].

To our knowledge, only one study investigated the presence of periodic limb movements in children with migraine [49]. The questionnaire survey showed that migraine children had a higher frequency of difficulty in falling asleep, non-rapid eye movement sleep parasomnias, and sleep-related movement disorders compared with the control group. In the migraine children group, the individuals with PLM pathological index (PLMI ≥ 5) represent the 26.47 % of the sample and present higher frequency (p < 0.001), intensity (p < 0.001), duration (p = 0.006), and life impairment as scored in the PedMIDAS (p < 0.001) of headache and lower efficacy of prophylactic (p = 0.001) and acute (p = 0.006) pharmacological treatment than migraine children without PLM pathological index. These findings suggest that PLMS might influence the clinical presentation of migraine, increasing its severity, frequency, and all disabling aspects and also affecting treatment efficacy.

Narcolepsy is a rare neurological condition characterized by persistent, excessive daytime sleepiness, and generally it is underdiagnosed causing serious problems in patients.

Narcolepsy is considered as a comorbidity of migraine [150], but the association between narcolepsy and migraine is a matter of debate. The German Migraine and Headache Society Study Group [83] reported a similar prevalence of migraine in narcoleptics (21.9 %) and controls (19.8 %).

In this case control study of 96 narcoleptic patients, headache fulfilling the criteria for tension-type headache was significantly more often reported by narcolepsy patients than by the control group (60.3 % vs. 40.7 %) [83].

In another study, migraine prevalence had twofold to fourfold increase in the narcoleptic patients and amounted to 44.4 % in women and 28.3 % in men [34]. The onset of narcolepsy symptoms was 12.3 years before the onset of migraine symptoms. The increased prevalence of migraine was not due to pharmacological treatment for narcolepsy and did not depend on the severity of the narcolepsy symptoms [34].

No studies are available on the prevalence of migraine in children and adolescents with narcolepsy; headache has often been reported as a side effect of treatment in children with narcolepsy.

The relations between narcolepsy and migraine could be mediated by the orexinergic neurons of the posterior hypothalamus that are involved both in inhibition of analgesia and in narcolepsy. Dysfunctional hypothalamic activity might contribute to both altered REM function and altered pain processing via orexinergic neurons [91, 114].

Several studies also demonstrated a significant relationship between migraine and nocturnal enuresis. A study highlighted a strong correlation between the clinical history of nocturnal enuresis and the diagnosis of migraine, hypothesizing that nocturnal enuresis is a precursor of migraine and a migraine comorbid condition [92].

The presence of enuresis in migraine children has been previously incidentally reported in earlier studies [6, 55].

Patients with episodic migraine (EM) or chronic migraine (CM) had significantly more often a history of nocturnal enuresis vs. the control group (CG.12 %, EM.41 %, CM.49 %). A common pathophysiological substrate in the hypothalamus could explain this comorbidity through the inhibition of vasopressin secretion that leads to increased urinary frequency during the attack of migraine [111]. Recently, Carotenuto et al. [23] proposed that nocturnal enuresis and migraine could be linked to a dysfunction of the arousal system with primary nocturnal enuresis being considered as a migraine equivalent.