A May1, A Bahra, C Büchel, R S Frackowiak, P J Goadsby. 1. University Department of Clinical Neurology, Institute of Neurology, National Hospital for Neurology and Neurosurgery, London, UK.
Abstract
BACKGROUND: Cluster headache (CH), like migraine, is still regarded as a vascular headache although in both conditions a CNS cause has been suggested. OBJECTIVE: To examine neurovascular mechanisms in CH. METHODS: The authors used functional imaging with PET to investigate 18 CH patients (25 to 62 years old). Ten were in the active period (nine patients with induced attacks and one with spontaneous attack) and eight were out of their bout. In addition, the authors studied spontaneous CH and experimental pain in volunteers using MR angiography. RESULTS: When an acute CH attack was triggered with nitroglycerin (NTG), activation occurred in the ipsilateral posterior inferior hypothalamic gray, the contralateral ventroposterior thalamus, the anterior cingulate cortex, the ipsilateral basal ganglia, the right anterior frontal lobe, and both insulae. In patients out of the bout who experienced only a mild NTG headache, activation was seen bilaterally in the insulae and frontal cortices, the anterior cingulate cortex, the right thalamus, and the left basal ganglia, but not in the hypothalamic gray area. In addition, the authors found a significant activation (vasodilatation) in the region of the major basal arteries that was caused in part by NTG but was also observed in the spontaneous case and could be induced by capsaicin injection into the forehead. Therefore, the vasodilatation is likely to be mediated by neural mechanisms involved in the acute CH attacks that are present in every human being. CONCLUSIONS: Dilatation of cranial vessels is not specific to any particular headache syndrome but generic to cranial neurovascular activation, probably mediated by the trigeminoparasympathetic reflex. These data confirm that CH is a CNS disorder best considered as a form of neurovascular headache.
BACKGROUND:Cluster headache (CH), like migraine, is still regarded as a vascular headache although in both conditions a CNS cause has been suggested. OBJECTIVE: To examine neurovascular mechanisms in CH. METHODS: The authors used functional imaging with PET to investigate 18 CH patients (25 to 62 years old). Ten were in the active period (nine patients with induced attacks and one with spontaneous attack) and eight were out of their bout. In addition, the authors studied spontaneous CH and experimental pain in volunteers using MR angiography. RESULTS: When an acute CH attack was triggered with nitroglycerin (NTG), activation occurred in the ipsilateral posterior inferior hypothalamic gray, the contralateral ventroposterior thalamus, the anterior cingulate cortex, the ipsilateral basal ganglia, the right anterior frontal lobe, and both insulae. In patients out of the bout who experienced only a mild NTGheadache, activation was seen bilaterally in the insulae and frontal cortices, the anterior cingulate cortex, the right thalamus, and the left basal ganglia, but not in the hypothalamic gray area. In addition, the authors found a significant activation (vasodilatation) in the region of the major basal arteries that was caused in part by NTG but was also observed in the spontaneous case and could be induced by capsaicin injection into the forehead. Therefore, the vasodilatation is likely to be mediated by neural mechanisms involved in the acute CH attacks that are present in every human being. CONCLUSIONS: Dilatation of cranial vessels is not specific to any particular headache syndrome but generic to cranial neurovascular activation, probably mediated by the trigeminoparasympathetic reflex. These data confirm that CH is a CNS disorder best considered as a form of neurovascular headache.