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Neurobiology and sleep disorders in cluster headache.

Barloese MC - J Headache Pain (2015)

Bottom Line: Supported by endocrinological and radiological findings as well as the chronobiological features, predominant theories revolve around central pathology of the hypothalamus.The findings include: A distinct circannual connection between cluster occurrence and the amount of daylight, substantially poorer sleep quality in patients compared to controls which was present not only inside the clusters but also outside, affected REM-sleep in patients without a particular temporal connection to nocturnal attacks, equal prevalence of sleep apnea in both patient and control groups, reduced levels of hypocretin-1 in the cerebrospinal fluid of patients and finally a blunted response to the change from supine to tilted position in the head-up tilt table test indicating a weakened sympathoexcitatory or stronger parasympathetic drive.Future endeavors should focus on pathological changes which persist in the attack-free periods but also heed the possibility of long-lived, cluster-induced pathology.

View Article: PubMed Central - PubMed

Affiliation: Danish Headache Center, Glostrup Hospital, Nordre Ringvej 57, Glostrup, DK-2600, Denmark, mads@barloese.net.

ABSTRACT
Cluster headache is characterized by unilateral attacks of severe pain accompanied by cranial autonomic features. Apart from these there are also sleep-related complaints and strong chronobiological features. The interaction between sleep and headache is complex at any level and evidence suggests that it may be of critical importance in our understanding of primary headache disorders. In cluster headache several interactions between sleep and the severe pain attacks have already been proposed. Supported by endocrinological and radiological findings as well as the chronobiological features, predominant theories revolve around central pathology of the hypothalamus. We aimed to investigate the clinical presentation of chronobiological features, the presence of concurrent sleep disorders and the relationship with particular sleep phases or phenomena, the possible role of hypocretin as well as the possible involvement of cardiac autonomic control. We conducted a questionnaire survey on 275 cluster headache patients and 145 controls as well an in-patient sleep study including 40 CH-patients and 25 healthy controls. The findings include: A distinct circannual connection between cluster occurrence and the amount of daylight, substantially poorer sleep quality in patients compared to controls which was present not only inside the clusters but also outside, affected REM-sleep in patients without a particular temporal connection to nocturnal attacks, equal prevalence of sleep apnea in both patient and control groups, reduced levels of hypocretin-1 in the cerebrospinal fluid of patients and finally a blunted response to the change from supine to tilted position in the head-up tilt table test indicating a weakened sympathoexcitatory or stronger parasympathetic drive. Overall, these findings support a theory of involvement of dysregulation in hypothalamic and brainstem nuclei in cluster headache pathology. Further, it is made plausible that the headache attacks are but one aspect of a more complex syndrome of central dysregulation manifesting as sleep-related complaints, sub-clinical autonomic dysregulation and of course the severe attacks of unilateral headache. Future endeavors should focus on pathological changes which persist in the attack-free periods but also heed the possibility of long-lived, cluster-induced pathology.

No MeSH data available.


Related in: MedlinePlus

Hypnograms from night 1 (top) and 2 (bottom) from a patient suffering nine spontaneous CH attacks (arrows) during recordings. As is seen, the attacks occur in stages W, REM, N2 and N3 at remarkably regular intervals. With permission from Barloese et al. 2014 (Wiley) [51]
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Fig3: Hypnograms from night 1 (top) and 2 (bottom) from a patient suffering nine spontaneous CH attacks (arrows) during recordings. As is seen, the attacks occur in stages W, REM, N2 and N3 at remarkably regular intervals. With permission from Barloese et al. 2014 (Wiley) [51]

Mentions: In one patient a striking rhythmicity of nocturnal attacks was noticed (Fig. 3). This patient suffered a total of nine attacks during the two nights of recording. There was no relation with any particular sleep stage, rather the attacks occurred roughly every 90 min. During night 1, at 02.00, the patient wakes up but without an attack.Fig. 3


Neurobiology and sleep disorders in cluster headache.

Barloese MC - J Headache Pain (2015)

Hypnograms from night 1 (top) and 2 (bottom) from a patient suffering nine spontaneous CH attacks (arrows) during recordings. As is seen, the attacks occur in stages W, REM, N2 and N3 at remarkably regular intervals. With permission from Barloese et al. 2014 (Wiley) [51]
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4542772&req=5

Fig3: Hypnograms from night 1 (top) and 2 (bottom) from a patient suffering nine spontaneous CH attacks (arrows) during recordings. As is seen, the attacks occur in stages W, REM, N2 and N3 at remarkably regular intervals. With permission from Barloese et al. 2014 (Wiley) [51]
Mentions: In one patient a striking rhythmicity of nocturnal attacks was noticed (Fig. 3). This patient suffered a total of nine attacks during the two nights of recording. There was no relation with any particular sleep stage, rather the attacks occurred roughly every 90 min. During night 1, at 02.00, the patient wakes up but without an attack.Fig. 3

Bottom Line: Supported by endocrinological and radiological findings as well as the chronobiological features, predominant theories revolve around central pathology of the hypothalamus.The findings include: A distinct circannual connection between cluster occurrence and the amount of daylight, substantially poorer sleep quality in patients compared to controls which was present not only inside the clusters but also outside, affected REM-sleep in patients without a particular temporal connection to nocturnal attacks, equal prevalence of sleep apnea in both patient and control groups, reduced levels of hypocretin-1 in the cerebrospinal fluid of patients and finally a blunted response to the change from supine to tilted position in the head-up tilt table test indicating a weakened sympathoexcitatory or stronger parasympathetic drive.Future endeavors should focus on pathological changes which persist in the attack-free periods but also heed the possibility of long-lived, cluster-induced pathology.

View Article: PubMed Central - PubMed

Affiliation: Danish Headache Center, Glostrup Hospital, Nordre Ringvej 57, Glostrup, DK-2600, Denmark, mads@barloese.net.

ABSTRACT
Cluster headache is characterized by unilateral attacks of severe pain accompanied by cranial autonomic features. Apart from these there are also sleep-related complaints and strong chronobiological features. The interaction between sleep and headache is complex at any level and evidence suggests that it may be of critical importance in our understanding of primary headache disorders. In cluster headache several interactions between sleep and the severe pain attacks have already been proposed. Supported by endocrinological and radiological findings as well as the chronobiological features, predominant theories revolve around central pathology of the hypothalamus. We aimed to investigate the clinical presentation of chronobiological features, the presence of concurrent sleep disorders and the relationship with particular sleep phases or phenomena, the possible role of hypocretin as well as the possible involvement of cardiac autonomic control. We conducted a questionnaire survey on 275 cluster headache patients and 145 controls as well an in-patient sleep study including 40 CH-patients and 25 healthy controls. The findings include: A distinct circannual connection between cluster occurrence and the amount of daylight, substantially poorer sleep quality in patients compared to controls which was present not only inside the clusters but also outside, affected REM-sleep in patients without a particular temporal connection to nocturnal attacks, equal prevalence of sleep apnea in both patient and control groups, reduced levels of hypocretin-1 in the cerebrospinal fluid of patients and finally a blunted response to the change from supine to tilted position in the head-up tilt table test indicating a weakened sympathoexcitatory or stronger parasympathetic drive. Overall, these findings support a theory of involvement of dysregulation in hypothalamic and brainstem nuclei in cluster headache pathology. Further, it is made plausible that the headache attacks are but one aspect of a more complex syndrome of central dysregulation manifesting as sleep-related complaints, sub-clinical autonomic dysregulation and of course the severe attacks of unilateral headache. Future endeavors should focus on pathological changes which persist in the attack-free periods but also heed the possibility of long-lived, cluster-induced pathology.

No MeSH data available.


Related in: MedlinePlus