Specific hypothalamic activation during a spontaneous cluster headache attack

Cluster headache, the most severe pain condition among the primary headache syndromes, is characterized by unilateral excruciating head pain and autonomic dysfunction.1 Functional neuroimaging has recently improved the pathophysiologic understanding of the different primary headache syndromes. Thereby, brainstem activation was found in migraine,2,3⇓ and hypothalamic overactivity was observed in nitrate-induced cluster headache4 and in short-lasting, unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT).5 Results of voxel-based morphometry support the role of the posterior hypothalamus in the pathogenesis of cluster headache because an increased gray matter density has been shown in this structure.6 However, the cluster headache attacks investigated so far were triggered with nitroglycerin (NTG). Although clinical and experimental data show NTG-provoked and spontaneous cluster attacks to be comparable and NTG does not alter regional cerebral blood flow (rCBF) significantly,4 the vasoactive properties of nitrates have to be considered, and data from spontaneous cluster attacks are desirable to confirm the mentioned results. We present a case of a spontaneous cluster attack during an ongoing H215O-PET study. A man (aged 30 years, right-handed, no medication) with a 2-year history of chronic cluster headache …