LAUSR

Migraine and sleep complaints are common and have a bidirectional relationship [1]. Indeed, sleep disturbance— especially poor sleep quality—could precede a migraine attack. Thus, different sleep disorders have been identified as possible migraine triggers. Conversely, headache itself may cause sleep disturbances. Finally, sleep can play a therapeutic role considering that some headache attacks can be partially restored by sleep. The interaction between headache and sleep disorders is somewhat complex and remains ill-understood. Several efforts have been made to recognize possible morphological and pathophysiological mechanisms at the basis of this relationship. Several studies conducted in patients with migraine evaluated the prevalence and the role of different sleep disorders in this specific population [2], such as insomnia, obstructive sleep apnea (OSA), and restless legs syndrome (RLS). Insomnia is the most frequent sleep complaint in the general population. The majority of patients with migraine reports insomnia, including difficulty initiating sleep, staying asleep, poor sleep quality, and decrease of total sleep time associated with significant daytime symptoms. The insomnia prevalence is reported to be higher in patients with chronic migraine with respect to those affected by episodic migraine, suggesting that insomnia could play a role on frequency and clinical presentation of migraine [3]. On the contrary, recent studies showed that the headache status does not influence insomnia severity. The frequent links between insomnia and migraine have led to the notion that poor sleep quality could represent an intrinsic feature of this headache subtype. Indeed, polysomnographic studies demonstrated that patients with migraine display a decrease of sleep efficiency and of slow wave sleep. From a clinical point of view, insomnia is frequently under-recognized and untreated in migraineurs. Recent studies demonstrated the effectiveness of cognitive-behavioral therapy of insomnia (CBTi) on migraine. In particular, this psychological approach seems to be able to induce an increase of sleep efficiency as well as a reduction of migraine attacks. Another frequent sleep disorder in the general population is represented by OSA. Recent studies demonstrated that OSA has the same prevalence in migraineurs with respect to general population. However, patients with migraine should be screened for OSA when appropriate, considering that both migraine and sleep apnea represent a risk factor for future vascular events. Different evidence highlights a bidirectional link between migraine and RLS. In particular, many studies found an increased risk of RLS in patients with migraine. Moreover, migraine is associated with more severe symptoms of RLS. These findings are in accordance also with polysomnographic observation of lower sleep efficiency and fragmented sleep in both of the diseases. From a pathophysiologic point of view, the association among these disorders could be explained by the role of dopamine in both. Indeed, dopamine is implicated in the prodromal symptoms of migraine. Moreover, RLS is considered to be related to an impairment of the dopaminergic system of the A11 neurons descending from the hypothalamus to the spinal cord. Considering the pathogenic mechanisms at the basis of the bidirectional relationship between sleep and migraine, different hypotheses have been postulated taking into account recent findings on the role of different brain structures and molecules regulating sleep and pain. Serotonin (5-HT) plays different functions in diverse human systems such as sleep and pain but also mood, appetite, and sexual function. In particular, 5-HT stimulates wakefulness and suppresses REM sleep. Moreover, patients with migraine usually display a low interictal serotoninergic tone, * Paola Proserpio [email protected]