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The most widely accepted theory of pathogenesis of cluster headaches is hypothalamic activation with secondary activation of the trigeminal-autonomic reflex. Compared with the general population, the risk of cluster headache for first-degree relatives is increased by 14- to 39-fold, and for second-degree relatives by 2- to 8-fold (http://www.uptodate.com/contents/cluster-headache-epidemiology-clinical-features-and-diagnosis?source=search_result&search=cluster+headache&selectedTitle=1~57). Clinical features include attacks of severe orbital, supraorbital, or temporal pain, accompanied by autonomic phenomena and/or restlessness or agitation (patients will move around the room and won’t be able to sit still). Autonomic symptoms include ptosis, miosis, lacrimation, conjunctival injection, rhinorrhea, and nasal congestion, which only occur during the pain attack and are ipsilateral to the pain. Attacks are abrupt in onset and may occur as often as eight times a day and are generally short lived, from 45 minutes to 2 hours. These “clusters” occur over days to weeks. Cluster headaches are strictly unilateral, and the symptoms remain on the same side of the head during a single cluster attack. In some cases the symptoms can switch to the other side during a different cluster attack. In contrast to migraines, in which the patients are still, patients with cluster headaches are restless and prefer to pace around or sit and rock back and forth. There is also circadian rhythmicity of the cluster attacks. The episodic form, which is most common, is characterized by periods of attacks and remissions. The chronic form lacks remissions and is diagnosed after a year without remission, or if remission has lasted less than 1