Excerpt
The frequency of head pain episodes is one of the most relevant aspects that influence the impact of headache disorder on the quality of life. It may be modified by many endogenous and exogenous factors, including a series of co-pathologies and multiple lifestyle aspects, especially sleep and related disorders; among which, obstructive sleep apnea syndrome (OSAS) seems particularly able to influence or to induce headache. OSAS is one of the most common disorders of breathing during sleep, characterized by recurrent apneas and hypopneas and snoring, which is able to modify a preexisting primary headache but also to induce a specific secondary headache, labeled as OSAS headache, in subjects who were free from any kind of headache before OSAS’ onset. Notwithstanding the existence of specific diagnostic criteria, the presence of headache in a patient with OSAS is often directly considered a secondary headache caused by OSAS, even if clinical characteristics of headache do not fit the criteria. Moreover, the history of headache is an element that, nowadays, is not enough taken in account when it comes to international diagnostic criteria. Consequently, it seems to be relevant to individuate elements that may help to distinguish between OSAS headache and a preexisting headache modified by OSAS and, in parallel, to determine, in general population, the proportion of these two conditions. In order to find out elements that may help in this difficult challenge, we designed a study to investigate, in general population, the following features: onset latency and fragmentation of sleep, snoring, headache presence, and characteristics. We also aimed to evaluate the reciprocal relationship between sleep behavior/disorders and headache characteristics in terms of type, frequency, intensity, and clinical symptoms; at last, we purpose to assess, among OSAS patients with recurrent headache, whether OSAS treatment may have effects on headache, independently by its primitive or secondary nature. Clinical data were collected using a telematic ad hoc questionnaire in Google Form format, distributed to population through social media territorial groups. Questions were focused on these three items: sleep behavior, such as latency, fragmentation, and snoring; presence of OSAS and its treatments; and headache and its features in terms of side and kind of pain, modification with physical activity, association with nausea, vomit, photophobia, phonophobia, osmophobia, allodynia, tearing, and rhinorrhea. All of these questions were intended to distinguish between different kinds of headache, according to the ICHD-III criteria. For statistical analysis,
T test was applied to compare mean values in different groups, whereas a chi square test was used to compare the distribution of a variable in different groups. We received 3112 (408 from males, 2697 from females, and 7 not declared) responses to our questionnaire: 1817 had recurrent headache with migraine characteristics, 889 a non-migraine headache, and 406 were free from recurrent headache. A prolonged sleep onset latency was more frequent among migraineurs (695 out of 1817; 38.2%) with respect to non-migraine headache sufferers (279 out of 889; 31.4%) and to headache-free subjects (102 out of 406; 25.1%),
p < 0.0001 at chi square test. Allodynic migraineurs showed a longer sleep onset latency with respect to non-allodynic ones (278 out of 695 vs 368 out of 1119,
p = 0,002). Sleep resulted more frequently fragmented in headache patients with respect to non-headache subjects (1539/2706 vs 180/406,
p < 0.001), especially among migraineurs with respect to non-migraine headache sufferers (1105 out of 1817 vs 434 out of 889,
p < 0.001), and in particular if allodynic (440 out of 646 vs 663 vs 1168,
p < 0.001). A codified diagnosis of OSAS was more frequent among non-headache subjects with respect to headache sufferers (31/2701 vs 14/404,
p < 0.001 at chi square test); OSAS was reported less frequently in migraine (19 out of 1814, 1%) with respect to subjects without migraine (26 out of 1291; 2.0%;
p = 0.02) and also with respect to non-headache ones (14 out of 404; 3.4%),
p < 0.001. Limited to the headache group, OSAS was slightly less frequent in migraineurs (1%) with respect to non-migraine headache (1.35%), but without a significant difference. Among headache sufferers, OSAS was more frequent in subjects complaining of sided “tearing” and “red eye” during headache attacks, resembling trigeminal-autonomic cephalalgias, than the remaining individuals with headache (respectively 21 out of 926 vs 14 out of 1775;
p = 0.001). Also headache at the awakening, which should evoke OSAS headache, was found more frequently among patients with clinical features of migraine instead of OSAS headache. As previously described in outpatients [
1], also in general population, sleep in migraineurs seems to be more fragmented and sleep onset latency longer. Migraine, especially if chronic and allodynic, is the headache in which these evidences are more relevant: headache may disrupt sleep and a poor sleep is able to worsen headache. Headaches that may be diagnosed as secondary to OSAS according to the ICHD-III criteria seem to be infrequent in OSAS patients without a preexisting history of primary recurrent headache. In other words, a transformation of a preexisting headache seems to be more frequent than a new secondary headache, and, commonly, this preexisting headache was of migraine type. In the presence of OSAS, the frequency of migraine attacks increases but the average intensity of pain and associated symptoms may be unchanged or reduced. In chronic migraine, many headache attacks are of non-migraine type: OSAS can increase the amount of headache days in a migraineur, adding non-migraine headache episodes. By another point of view, migraine associated with sleep fragmentation may counteract OSAS effects by inducing a more rapid awake during apneas that consequently shorten the apnea duration and deepness. Migraine and allodynia may be consequently considered protective, as an alarm system activated when a metabolically dangerous situation is present. Migraine is associated with energy metabolic impairment of the brain [
2]: an increment of energy demand may induce metabolic preconditions for the onset of the migraine attack, but also a reduction of energy production, as in oxygen low availability, may bring to the same situation. The defect of oxidative energy metabolism in migraine is known and generalized but it remains unclear if the mitochondrial deficit in migraine is primary or secondary [
2]: for sure, a chronic reduction of oxygen levels provoked by apneas may be one of the factors that favors such energetic impairment. …
