Liesl N Close1, Sajedeh Eftekhari2, Minyan Wang3, Andrew C Charles2, Andrew F Russo4,5,6. 1. 1 Department of Neurosurgery, University of Iowa, Iowa City, IA, USA. 2. 2 UCLA Goldberg Migraine Program, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA. 3. 3 Centre for Neuroscience, Department of Biological Sciences, Xi'an Jiaotong-Liverpool University (XJTLU), SIP, Suzhou, China. 4. 4 Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, USA. 5. 5 Department of Neurology, University of Iowa, Iowa City, IA, USA. 6. 6 Veterans Affairs Medical Center, Iowa City, IA, USA.
Abstract
PREMISE: Migraine is a complex neurologic disorder that leads to significant disability, yet remains poorly understood. PROBLEM: One potential triggering mechanism in migraine with aura is cortical spreading depression, which can activate the trigeminal nociceptive system both peripherally and centrally in animal models. A primary neuropeptide of the trigeminal system is calcitonin gene-related peptide, which is a potent vasodilatory peptide and is currently a major therapeutic target for migraine treatment. Despite the importance of both cortical spreading depression and calcitonin gene-related peptide in migraine, the relationship between these two players has been relatively unexplored. However, recent data suggest several potential vascular and neural connections between calcitonin gene-related peptide and cortical spreading depression. CONCLUSION: This review will outline calcitonin gene-related peptide-cortical spreading depression connections and propose a model in which cortical spreading depression and calcitonin gene-related peptide act at the intersection of the vasculature and cortical neurons, and thus contribute to migraine pathophysiology.
PREMISE: Migraine is a complex neurologic disorder that leads to significant disability, yet remains poorly understood. PROBLEM: One potential triggering mechanism in migraine with aura is cortical spreading depression, which can activate the trigeminal nociceptive system both peripherally and centrally in animal models. A primary neuropeptide of the trigeminal system is calcitonin gene-related peptide, which is a potent vasodilatory peptide and is currently a major therapeutic target for migraine treatment. Despite the importance of both cortical spreading depression and calcitonin gene-related peptide in migraine, the relationship between these two players has been relatively unexplored. However, recent data suggest several potential vascular and neural connections between calcitonin gene-related peptide and cortical spreading depression. CONCLUSION: This review will outline calcitonin gene-related peptide-cortical spreading depression connections and propose a model in which cortical spreading depression and calcitonin gene-related peptide act at the intersection of the vasculature and cortical neurons, and thus contribute to migraine pathophysiology.
Authors: Anthony J Strong; Martin Fabricius; Martyn G Boutelle; Stuart J Hibbins; Sarah E Hopwood; Robina Jones; Mark C Parkin; Martin Lauritzen Journal: Stroke Date: 2002-12 Impact factor: 7.914
Authors: N Hadjikhani; M Sanchez Del Rio; O Wu; D Schwartz; D Bakker; B Fischl; K K Kwong; F M Cutrer; B R Rosen; R B Tootell; A G Sorensen; M A Moskowitz Journal: Proc Natl Acad Sci U S A Date: 2001-04-03 Impact factor: 11.205