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Neurobiology in primary headaches.
Brain Res Brain Res Rev. 2005 Jun; 48(3):438-56.BR

Abstract

Primary headaches such as migraine and cluster headache are neurovascular disorders. Migraine is a painful, incapacitating disease that affects a large portion of the adult population with a substantial economic burden on society. The disorder is characterised by recurrent unilateral headaches, usually accompanied by nausea, vomiting, photophobia and/or phonophobia. A number of hypothesis have emerged to explain the specific causes of migraine. Current theories suggest that the initiation of a migraine attack involves a primary central nervous system (CNS) event. It has been suggested that a mutation in a calcium gene channel renders the individual more sensitive to environmental factors, resulting in a wave of cortical spreading depression when the attack is initiated. Genetically, migraine is a complex familial disorder in which the severity and the susceptibility of individuals are most likely governed by several genes that vary between families. Genom wide scans have been performed in migraine with susceptibility regions on several chromosomes some are associated with altered calcium channel function. With positron emission tomography (PET), a migraine active region has been pointed out in the brainstem. In cluster headache, PET studies have implicated a specific active locus in the posterior hypothalamus. Both migraine and cluster headache involve activation of the trigeminovascular system. In support, there is a clear association between the head pain and the release of the neuropeptide calcitonin gene-related peptide (CGRP) from the trigeminovascular system. In cluster headache there is, in addition, release of the parasympathetic neuropeptide vasoactive intestinal peptide (VIP) that is coupled to facial vasomotor symptoms. Triptan administration, activating the 5-HT(1B/1D) receptors, causes the headache to subside and the levels of neuropeptides to normalise, in part through presynaptic inhibition of the cranial sensory nerves. These data suggest a central role for sensory and parasympathetic mechanisms in the pathophysiology of primary headaches. The positive clinical trial with a CGRP receptor antagonist offers a new promising way of treatment.

Authors+Show Affiliations

Department of Internal Medicine, University Hospital, S-221 85 Lund, Sweden. lars.edvinsson@med.lu.seNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

15914251

Citation

Edvinsson, Lars, and Rolf Uddman. "Neurobiology in Primary Headaches." Brain Research. Brain Research Reviews, vol. 48, no. 3, 2005, pp. 438-56.
Edvinsson L, Uddman R. Neurobiology in primary headaches. Brain Res Brain Res Rev. 2005;48(3):438-56.
Edvinsson, L., & Uddman, R. (2005). Neurobiology in primary headaches. Brain Research. Brain Research Reviews, 48(3), 438-56.
Edvinsson L, Uddman R. Neurobiology in Primary Headaches. Brain Res Brain Res Rev. 2005;48(3):438-56. PubMed PMID: 15914251.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neurobiology in primary headaches. AU - Edvinsson,Lars, AU - Uddman,Rolf, Y1 - 2004/11/18/ PY - 2004/02/13/received PY - 2004/08/17/revised PY - 2004/09/08/accepted PY - 2005/5/26/pubmed PY - 2005/7/27/medline PY - 2005/5/26/entrez SP - 438 EP - 56 JF - Brain research. Brain research reviews JO - Brain Res. Brain Res. Rev. VL - 48 IS - 3 N2 - Primary headaches such as migraine and cluster headache are neurovascular disorders. Migraine is a painful, incapacitating disease that affects a large portion of the adult population with a substantial economic burden on society. The disorder is characterised by recurrent unilateral headaches, usually accompanied by nausea, vomiting, photophobia and/or phonophobia. A number of hypothesis have emerged to explain the specific causes of migraine. Current theories suggest that the initiation of a migraine attack involves a primary central nervous system (CNS) event. It has been suggested that a mutation in a calcium gene channel renders the individual more sensitive to environmental factors, resulting in a wave of cortical spreading depression when the attack is initiated. Genetically, migraine is a complex familial disorder in which the severity and the susceptibility of individuals are most likely governed by several genes that vary between families. Genom wide scans have been performed in migraine with susceptibility regions on several chromosomes some are associated with altered calcium channel function. With positron emission tomography (PET), a migraine active region has been pointed out in the brainstem. In cluster headache, PET studies have implicated a specific active locus in the posterior hypothalamus. Both migraine and cluster headache involve activation of the trigeminovascular system. In support, there is a clear association between the head pain and the release of the neuropeptide calcitonin gene-related peptide (CGRP) from the trigeminovascular system. In cluster headache there is, in addition, release of the parasympathetic neuropeptide vasoactive intestinal peptide (VIP) that is coupled to facial vasomotor symptoms. Triptan administration, activating the 5-HT(1B/1D) receptors, causes the headache to subside and the levels of neuropeptides to normalise, in part through presynaptic inhibition of the cranial sensory nerves. These data suggest a central role for sensory and parasympathetic mechanisms in the pathophysiology of primary headaches. The positive clinical trial with a CGRP receptor antagonist offers a new promising way of treatment. UR - https://www.unboundmedicine.com/medline/citation/15914251/Neurobiology_in_primary_headaches_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0165-0173(04)00128-6 DB - PRIME DP - Unbound Medicine ER -