Is migraine a neuropathic pain syndrome?

Abstract

The understanding of migraine pathophysiology has evolved from the belief that migraine is a vascular disorder, to evidence that better defines migraine as a neurogenic disorder associated with secondary changes in brain perfusion. There is evidence to suggest that the early phase of migraine pain results from neurogenic inflammation affecting cranial blood vessels and dura. Allodynia, hyperalgesia, and expansion of nociceptive fields occur during most well-established migraine attacks. These clinical features of migraine are evocative of those traditionally associated with neuropathic pain. A hypothesis that defines migraine pain as a unique neuropathic pain disorder can imply the potential for neural plasticity and may provide insight into the mechanisms that underlie the transformation of episodic to chronic forms of migraine. The neuropathic pain model of migraine pathophysiology not only paves the way for mechanism-based treatment strategies that can improve the acute and preventive management of migraine attacks, but also opens the door for the discovery of novel therapeutic targets. It also lends momentum to an understanding of clinically intriguing topics such as opiate-induced hyperalgesia and medication-overuse headache (rebound headache), opioid resistance in the treatment of chronic headache, and disease modification in defending against the potential for migraine transformation.

Genetics of migraine in the age of genome-wide association studies

“…TRPM8 is investigated as a target in animal models of neuropathic pain [65]. Since migraine and neuropathic pain share some characteristics [66], a role for TRPM8 in migraine as well as a link between both pain syndromes is plausible.…”

Von Frey's hairs – a review of their technology and use – a novel automated von Frey device for improved testing for hyperalgesia

“…Some features of migraine suggest that there are short-or longterm changes (Liu-Chen et al, 1983) which involve neuropathic processes (Biondi, 2006;Dodick and Silberstein, 2006). Migraine pain itself may be a consequence of centrally generated alterations in neurotransmission, in which innocuous sensory traffic becomes amplified and is perceived as noxious (Lambert, 2007;Yarnitsky et al, 2003).…”

Genetics of Migraine - Is There any Progress?

“…This gene encodes cold-and menthol-activated ion channels and participates in the generation of cold-induced pain [110]. Studying the role of TRPM8 in animal models with neuropathic pain also confirms the functional association with migraine [111]. LRP1 expresses in the brain tissues and in many other tissues [31], modulates synaptic transmission and interacts with the NMDA glutamatergic receptors.…”