Abstract
Cluster headache (CH) can be viewed as a periodic disturbance of bodily adaptive responses to internal or external environmental changes. In the pathophysiology of this disorder many factors must be considered such as autonomic reactivity, neuroendocrine integrative mechanisms, nociceptive sensory function, lifestyle, and personality characteristics [16]. A dyschronic hypothesis for CH has been proposed on the basis of the cyclical course of cluster periods and attacks and of the prophylactic effect exerted by some drugs (lithium) and procedures (sleep deprivation) known to affect biorhythms [11,12,13]. This hypothesis implies a certain vulnerability of CNS oscillators with a time-structure alteration of the neurotransmitters and neurohormones involved in adaptive responses; headache occurs when the delicately balanced systems of these subjects are forced by cyclic stimuli to shift or to cope with rapidly changing activity requirements.
This work was partly supported by CNR: Sottogruppo SP8 “Controllo del dolore” (Grant no. 8202253).
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Nappi, G. et al. (1985). Lack of β-Endorphin and β-Lipotropin Circadian Rhythmicity in Episodic Cluster Headache: A Model for Chronopathology. In: Pfaffenrath, V., Lundberg, PO., Sjaastad, O. (eds) Updating in Headache. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-88581-5_43
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