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Abstract

Cluster headache is a stereotyped primary pain syndrome that is probably the most severe cause of headache existing. It is characterized by strictly unilateral headache, predominantly nocturnal, lasting from 15 to 180 minutes, accompanied by at least one ipsilateral autonomic phenomena. Symptoms occur several times a day (clusters) having a rhythmic periodicity and a circadian behavior. Its incidence is 4-15 cases per 100000, the annual prevalence is 53 cases per 100000., and has a radius male: female 4-9:1. The most common age of onset is 27 to 31 years. There is a genetic predisposition for the disease with the existence of a frst line family member in 3,4-12% of affected patients. Pathophysilogically it involves changes in the trigémino-vascular system, the cavernous sinus, the ventral-posterior thalamus, frontal cortex, the cingulum, the Ínsula, basal ganglia, the inferior and posterior hypothalamic gray matter. Autonomic changes are due to parasympathetic activation by the facial nerve through the pterygopalatine ganglion and transitory defciency of the cervical sympathetic system. There is a modifcation in the levéis of gene-related peptide calcitonin, vasoactive intestinal peptide, L-arginine-nitric oxide, endothelin-1, testosterone, thyrotropin, cortisol, growth hormone, luteinizing hormone, prolactin and melatonin. The treatment is divided in: acute pharmacology including oxygen, the use of hyperbaric chamber, triptans, sumatriptan, zolmitriptan, ergotamine and ¡ntranasal lidocaine, transitional and chronic prophylactic containing steroids, ergotamine, verapamil, metisergide, lithium carbonate, valproic acid and melatonin, and invasive treatment consisting on blockade, surgery, among others. 

Key words: Cluster Headache. Autonomic Changes. Trigeminal Vascular System.