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Abstract
SUMMARY Our understanding of migraine pathophysiology is a work in progress, largely because of the absence of any identifiable cephalic pathology. There are currently two main theories on the genesis of migraine pain. One hypothesizes that the origin is in the periphery, requiring the activation of primary afferent nociceptive neurons that innervate cephalic tissue. The other theorizes that the origin of migraine pain is in the CNS, as a result of abnormal processing of sensory signals, rather than the activation of nociceptors. After briefly reviewing the clinical presentation and diagnosis of migraine, this article focuses on explaining the traditional and current theories of migraine pathogenesis.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.
Notes
Reproduced with permission from Citation[2] © John Wiley & Sons Ltd (2004).
Reproduced with permission from Citation[2] © John Wiley & Sons Ltd (2004).