In recent years, several studies have been devoted primarily to investigating the relationship between migraine and sleep disorders, suggesting a significant correlation between these two conditions.6
This was also confirmed in this study by the higher prevalence, according to parents’ reports, of sleep disorder symptoms (SDSC TOT, P
< 0.001) in the MoA group than in the control group.
Uncertain and not yet clarified mechanisms seem to be the biological basis for this association, although many studies tend to support a sort of cause–effect and/or, alternatively, a common pathogenesis39
as a putative effect of an alteration in the control of the core of the serotoninergic median raphe, which is important in circadian rhythm regulation and in genesis migraine.6
Herein, our findings regarding the higher prevalence of disorders in initiating and maintaining sleep (P
< 0.001) and disorders of arousal (P
< 0.001) corroborate the results of a recent polysomnographic study that suggested the presence of a peculiar macrostructural alteration in sleep organization in children with migraine, such as increased sleep latency, decreased total sleep time, and nocturnal awakenings rate, as well as the presence of respiratory disorders.6
On the other hand, our results may confirm the role of MoA in disorders of initiating and maintaining sleep and in excessive daytime sleepiness, as suggested in a previous study.5
These findings may suggest a putative role in the negative influences on academic performance, mood regulation, and behavior in the developmental age.40
For this reason, we have focused on MoA and not on other types of headaches because there are few specific studies about the relationship between MoA and sleep disturbances.
In 2010, Ødegård et al reported that subjects with chronic headache were 17 times more likely to have severe sleep disturbances, and the association was stronger for chronic migraine than for chronic tension type headache,41
pinpointing the impact of migraine pathology on body homeostasis.42
Migraine is a common condition in the developmental age with a prevalence between 3% and 10.6%21
in school-age children, and EDS can be considered to be a frequent and disabling symptom, ranging from 10% to 20% in the general population and greater in the youth and old age groups.44
Alternatively, EDS is a symptom with specific underlying pathogenic mechanisms, and it could be generally caused by many disturbances, including obesity and/or metabolic syndrome,5
mood disorders, sleep related breathing dis-orders,47
and poor sleep efficiency. In this light, our results about the higher prevalence of sleep disorders in children with migraine can be interpreted as such disorders being a potential trigger of EDS in these subjects. Conversely, somnolence may be considered as part of the different phases of migraine attacks, even if there have been few studies on this.48
With regard to the presence of EDS subjectively perceived in the daily life activities of migraine patients, compared to previous studies that found a higher percentage of EDS in an adult population of migraineurs,48
our MoA children experienced EDS more frequently than healthy controls.
On the other hand, several brain structures and neuro-transmitter systems involved in sleep regulation may be involved in the genesis of primary headaches like migraine, such as monoamine, acetylcholine, GABAergic structures, the orexin–hypocretin system, prostaglandins (viz PGD2), cytokines (IL1), and adenosine,51
but an alternative theory is the other way around, postulating that poor sleep can alter pain processing and therefore could alter the pain threshold.51
Conversely another interesting finding of the present study is the discrepancy between the questionnaire results (filled out by parents) and the PDSS about the presence of daytime somnolence. This may be explained by the fact that migraineurs tend to perceive subjectively a high grade of tendency for sleep not explained by other medical conditions. We can then hypothesize that this report can be interpreted as a sort of disequilibrium in excitatory and inhibitory neurotransmissions in children affected by migraine.