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Recent advances in understanding migraine mechanisms, molecules and therapeutics.
Trends Mol Med 2007; 13(1):39-44TM

Abstract

Migraine is a complex, disabling disorder of the brain that manifests itself as attacks of often severe, throbbing head pain with sensory sensitivity to light, sound and head movement. There is a clear familial tendency to migraine, which has been well defined in a rare autosomal dominant form of familial hemiplegic migraine (FHM). FHM mutations so far identified include those in CACNA1A (P/Q voltage-gated Ca(2+) channel), ATP1A2 (N(+)-K(+)-ATPase) and SCN1A (Na(+) channel) genes. Physiological studies in humans and studies of the experimental correlate--cortical spreading depression (CSD)--provide understanding of aura, and have explored in recent years the effect of migraine preventives in CSD. Therapeutic developments in migraine have come by targeting the trigeminovascular system, with the most-recent being the proof-of-principle study of calcitonin gene-related peptide (CGRP) receptor antagonists in acute migraine. To understand the basic pathophysiology of migraine, brain imaging studies have firmly established reproducible changes in the brainstem in regions that include areas that are involved in sensory modulation. These data lead to the view that migraine is a form of sensory dysmodulatio--a system failure of normal sensory processing.

Authors+Show Affiliations

Institute of Neurology, The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK. peterg@ion.ucl.ac.uk

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

17141570

Citation

Goadsby, Peter J.. "Recent Advances in Understanding Migraine Mechanisms, Molecules and Therapeutics." Trends in Molecular Medicine, vol. 13, no. 1, 2007, pp. 39-44.
Goadsby PJ. Recent advances in understanding migraine mechanisms, molecules and therapeutics. Trends Mol Med. 2007;13(1):39-44.
Goadsby, P. J. (2007). Recent advances in understanding migraine mechanisms, molecules and therapeutics. Trends in Molecular Medicine, 13(1), pp. 39-44.
Goadsby PJ. Recent Advances in Understanding Migraine Mechanisms, Molecules and Therapeutics. Trends Mol Med. 2007;13(1):39-44. PubMed PMID: 17141570.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Recent advances in understanding migraine mechanisms, molecules and therapeutics. A1 - Goadsby,Peter J, Y1 - 2006/12/01/ PY - 2006/05/03/received PY - 2006/10/25/revised PY - 2006/11/20/accepted PY - 2006/12/5/pubmed PY - 2007/3/10/medline PY - 2006/12/5/entrez SP - 39 EP - 44 JF - Trends in molecular medicine JO - Trends Mol Med VL - 13 IS - 1 N2 - Migraine is a complex, disabling disorder of the brain that manifests itself as attacks of often severe, throbbing head pain with sensory sensitivity to light, sound and head movement. There is a clear familial tendency to migraine, which has been well defined in a rare autosomal dominant form of familial hemiplegic migraine (FHM). FHM mutations so far identified include those in CACNA1A (P/Q voltage-gated Ca(2+) channel), ATP1A2 (N(+)-K(+)-ATPase) and SCN1A (Na(+) channel) genes. Physiological studies in humans and studies of the experimental correlate--cortical spreading depression (CSD)--provide understanding of aura, and have explored in recent years the effect of migraine preventives in CSD. Therapeutic developments in migraine have come by targeting the trigeminovascular system, with the most-recent being the proof-of-principle study of calcitonin gene-related peptide (CGRP) receptor antagonists in acute migraine. To understand the basic pathophysiology of migraine, brain imaging studies have firmly established reproducible changes in the brainstem in regions that include areas that are involved in sensory modulation. These data lead to the view that migraine is a form of sensory dysmodulatio--a system failure of normal sensory processing. SN - 1471-4914 UR - https://www.unboundmedicine.com/medline/citation/17141570/Recent_advances_in_understanding_migraine_mechanisms_molecules_and_therapeutics_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1471-4914(06)00262-0 DB - PRIME DP - Unbound Medicine ER -