Page 132 - The clinical aspects and management of chronic migraine Judith Anne Pijpers
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Chapter 7
chronic migraine.6 This conclusion is based on comorbidity and sick-leaf related data, and disability, headache impact or phenotypic characteristics such as allodynia or photo- and phonophobia are not taken into account. Nonetheless, a similar disability of both groups appears reasonable. Figure 3 in chapter 4 shows the reversion of chronic migraine to episodic migraine upon treatment and highlights the potential overlap between the different subgroups.
Hence, for future revision of the ICHD criteria, I propose a discernment between chronic migraine with and without medication use. Furthermore, criteria for chronic migraine should be based on number of migraine days, without taking any non-migraine headache days into account.
Pathophysiology
Migraine headache is caused by activation of the trigeminal system, either by cortical events or central generators, causing intracranial hypersensitivity and thereby experience of headache.8–12 As described more elaborate in the introduction of this thesis, migraine chronification can be considered as a state of increasing susceptibility for migraine attacks.11 This increased susceptibility is assumed to be the consequence of both enhanced pain facilitation of the ascending pain pathway, known as central sensitisation,10,13,14 and lack of pain inhibition by alterations in the descending pain modulating pathways.15,16
New insights on central sensitization
This thesis touches on these assumed mechanisms in migraine chronification by studying cutaneous allodynia, a clinical marker of central sensitisation. Sensitisation of second order neurons in the brainstem (trigeminal nucleus caudalis) results into referred hypersensitivity of the skin (cutaneous allodynia) of the ipsilateral cephalic region. Sensitisation of third order neurons in the thalamus causes extracephalic allodynia (see Introduction, Figure 1 and 2). Chapter 6 stresses the importance of central sensitization in migraine chronification and reversibility as the absence of cutaneous allodynia is a predictor of good response to acute withdrawal. Moreover, this predictive value of cutaneous allodynia was more pronounced when subdivided based on spatial distribution: no allodynia versus cephalic allodynia (second order sensitization) versus extracephalic allodynia (third order sensitization), suggesting that in



























































































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