Is There An Imposter In Migraine?

The Accompanying Neck Pain

The findings and subsequent assumption from a recent observational Italian study,¹ ‘When cervical pain is actually migraine: An observational study in 207 patients.’, challenge basic neuro/anatomical/physiological principles.

This survey sought to assign a headache diagnosis to a cohort of 132 participants who had self-diagnosed their headache as being of cervical in origin. The main factors influencing participants’ self-diagnoses were the presence of pain in the back of the head/ neck and/ or that episodes started with pain in these regions.

After applying the IHCD-IIIβ criteria² the authors’ concluded that 91% of participants suffered from migraine or probable migraine, and that there had been ‘a false neuroanatomical attribution of cause and symptoms’ (by the participants), creating ‘strong and diffuse beliefs that go against science.’

What science?

I am not rejecting the extremely valuable medical research that has been done recently; we know that the trigeminocervical nucleus (TCN) is sensitised, but the science surrounding the reason for sensitisation is incomplete. To ignore elementary neuro anatomy, i.e., the C1-3 afferents influence the TCN significantly, an equal (to trigeminal afferents) player in the ‘migraine’ game, is pseudo or ‘assumed’ science. Genuine scientific research excludes no possibilities in its search for understanding and progress.

Currently, despite decades of vast financial resources and brilliant minds, the reason for the underlying disorder in migraine – a sensitised brainstem – remains elusive. Whilst recognising that occipital/ sub occipital symptoms, because of the bi directional nature of the TCN, may be referred from a disorder in the trigeminal field,^3-6 to assume that C1-3 afferents are irrelevant is incomprehensible.

The former perspective is perpetuated by the erroneous conclusion that because migraine associated neck pain responds to triptan therapy, the neck pain is not cervical in origin.⁷ Triptan therapy alleviates symptoms by de sensitising the TCN and confirms that migraine pain and neck pain share an underlying pathophysiology – a sensitised TCN. This is all it does; it does not enlighten as to the source of sensitisation. Cervical afferent sensitisation of the TCN remains a possibility.

Over the past 25 years, many of my patients have described ‘migraine in their neck’ (i.e. no head pain), because it responded to ‘triptans’; appropriate cervical treatment resolved their symptoms.

This is not about cervicogenic headache i.e. a cervical disorder misinterpreted as residing in the trigeminal field; it is about the potential sensitising influence of noxious cervical afferents on the TCN – two different concepts. The absence of macroscopic lesions does not rule out nociceptive relevance.^8-11

A substantial body of evidence^12-21 from animal models has demonstrated the development of mechanical spinal hyperexcitability, plasticity of dorsal horn neuronal activity and pain from controlled, non injurious (sub clinical trauma?) loading of zygapophyseal joint capsules. Moreover there is significant research^22-28 involving deep cervical paraspinal musculature, which provides additional support for cervical afferent sensitisation of the TCN.

I presume (for it is not clear from the publication) the basis of the authors’ statement that there was no discernible ‘… evidence of causative conditions of the cervical spine.’ was based on the absence of pathology on radiological imaging. If this was the case, enough said.

The title of the publication could easily have been:

‘When migraine is actually cervical in origin: An observational study in 207 patients.’ … were it not for a blinkered conclusion… and the public continue to be fed by pseudoscience.

We owe it to our patients to prove otherwise!

Here’s to changing a generation of assumptions…

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References:

1. Viana M, Sances G, Terrazzino S, Sprenger T, Nappi G, Tassorelli C. When cervical pain is actually migraine: An observational study in 207 patients. Cephalalgia. Dec 07 2016.
2. The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia. Jul 2013;33(9):629-808.
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22. Makowska A, Panfil C, Ellrich J. Long-term potentiation of orofacial sensorimotor processing by noxious input from the semispinal neck muscle in mice. Cephalalgia. Feb 2005;25(2):109-116.
23. Makowska A, Panfil C, Ellrich J. ATP induces sustained facilitation of craniofacial nociception through P2X receptors on neck muscle nociceptors in mice. Cephalalgia. Jun 2006;26(6):697-706.
24. Hu JW, Yu XM, Vernon H, Sessle BJ. Excitatory effects on neck and jaw muscle activity of inflammatory irritant applied to cervical paraspinal tissues. Pain. Nov 1993;55(2):243-250.
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