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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 evidence12-21 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 research22-28 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…

____________________________________________________________________________

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.
  3. Goadsby PJ, Bartsch T. On the functional neuroanatomy of neck pain. Cephalalgia. Jul 2008;28 Suppl 1:1-7.
  4. Bartsch T, Goadsby PJ. The trigeminocervical complex and migraine: current concepts and synthesis. Curr Pain Headache Rep. Oct 2003;7(5):371-376.
  5. Bogduk N. Cervicogenic headache: anatomic basis and pathophysiologic mechanisms. Curr Pain Headache Rep. Aug 2001;5(4):382-386.
  6. Bartsch T. Migraine and the neck: new insights from basic data. Curr Pain Headache Rep. Jun 2005;9(3):191-196.
  7. Kaniecki RG. Migraine and tension-type headache: an assessment of challenges in diagnosis. Neurology. May 14 2002;58(9 Suppl 6):S15-20.
  8. Packard RC. Epidemiology and pathogenesis of posttraumatic headache. J Head Trauma Rehabil. Feb 1999;14(1):9-21.
  9. Packard RC. The relationship of neck injury and post-traumatic headache. Curr Pain Headache Rep. Aug 2002;6(4):301-307.
  10. Sterling M. Whiplash-associated disorder: musculoskeletal pain and related clinical findings. J Man Manip Ther. Nov 2011;19(4):194-200.
  11. Radanov BP, Di Stefano G, Augustiny KF. Symptomatic approach to posttraumatic headache and its possible implications for treatment. Eur Spine J. Oct 2001;10(5):403-407.
  12. Lee KE, Winkelstein BA. Joint distraction magnitude is associated with different behavioral outcomes and substance P levels for cervical facet joint loading in the rat. J Pain. Apr 2009;10(4):436-445.
  13. Lee KE, Thinnes JH, Gokhin DS, Winkelstein BA. A novel rodent neck pain model of facet-mediated behavioral hypersensitivity: implications for persistent pain and whiplash injury. J Neurosci Methods. Aug 30 2004;137(2):151-159.
  14. Quinn KP, Winkelstein BA. Cervical facet capsular ligament yield defines the threshold for injury and persistent joint-mediated neck pain. J Biomech. 2007;40(10):2299-2306.
  15. Lee KE, Davis MB, Winkelstein BA. Capsular ligament involvement in the development of mechanical hyperalgesia after facet joint loading: behavioral and inflammatory outcomes in a rodent model of pain. J Neurotrauma. Nov 2008;25(11):1383-1393.
  16. Winkelstein BA, Santos DG. An intact facet capsular ligament modulates behavioral sensitivity and spinal glial activation produced by cervical facet joint tension. Spine (Phila Pa 1976). Apr 15 2008;33(8):856-862.
  17. Dong L, Winkelstein BA. Simulated whiplash modulates expression of the glutamatergic system in the spinal cord suggesting spinal plasticity is associated with painful dynamic cervical facet loading. J Neurotrauma. Jan 2010;27(1):163-174.
  18. Quinn KP, Dong L, Golder FJ, Winkelstein BA. Neuronal hyperexcitability in the dorsal horn after painful facet joint injury. Pain. Nov 2010;151(2):414-421.
  19. Kras JV, Dong L, Winkelstein BA. The prostaglandin E2 receptor, EP2, is upregulated in the dorsal root ganglion after painful cervical facet joint injury in the rat. Spine (Phila Pa 1976). Feb 1 2013;38(3):217-222.
  20. Quinn KP, Bauman JA, Crosby ND, Winkelstein BA. Anomalous fiber realignment during tensile loading of the rat facet capsular ligament identifies mechanically induced damage and physiological dysfunction. J Biomech. Jul 20 2010;43(10):1870-1875.
  21. Kallakuri S, Singh A, Lu Y, Chen C, Patwardhan A, Cavanaugh JM. Tensile stretching of cervical facet joint capsule and related axonal changes. Eur Spine J. Apr 2008;17(4):556-563.
  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.
  25. Ellrich J, Makowska A. Nerve growth factor and ATP excite different neck muscle nociceptors in anaesthetized mice. Cephalalgia. Nov 2007;27(11):1226-1235.
  26. Reitz M, Makowska A, Ellrich J. Excitatory and inhibitory purinergic control of neck muscle nociception in anaesthetized mice. Cephalalgia. Jan 2009;29(1):58-67.
  27. Vernon H, Sun K, Zhang Y, Yu XM, Sessle BJ. Central sensitization induced in trigeminal and upper cervical dorsal horn neurons by noxious stimulation of deep cervical paraspinal tissues in rats with minimal surgical trauma. J Manipulative Physiol Ther. Sep 2009;32(7):506-514.
  28. Hu JW, Tatourian I, Vernon H. Opioid involvement in electromyographic (EMG) responses induced by injection of inflammatory irritant into deep neck tissues. Somatosensory & motor research. 1996;13(2):139-146.

 

Until next timedean-signatureDr Dean H Watson
PhD (APA Titled Musculoskeletal Physiotherapist);
MAppSc(Res); GradDipAdvManipTher(Hons); DipTechPhty
If you are new to Watson Headache®… Welcome.To learn more about how we can help you click on the link if:
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and access your complimentary resources.Posted in: Health Professionals, Researching HeadacheTagged: cervicogenic headache, migraine, neck pain, sensitisation, sensitised brainstemAuthor: Dr Dean Watson

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