Cervicogenic Headache

Questions and Answers

Question: In your view, if what appears to be a classical right C2,3 cervicogenic headache and it responds to a Triptan, is the diagnosis CxHA or migraine?

Answer: My understanding of CxHA is where (secondary to) a disorder in the upper cervical spine is misinterpreted as residing in the trigeminal field and head pain results; but to recognise and accept that noxious C1-3 afferents can sensitise the trigemino cervical nucleus (TCN) in primary headache is another concept again…

Taxonomists of classification systems differentiate between symptomatic and etiologic approaches to medical classification.1 Clinical or symptomatic classification systems are based on presentation of symptoms and in the case of pneumonia for example, would include the clinical features of chills, a productive cough, fever, and absence of breath sounds. An etiological classification is based on underlying pathology and in the case of pneumonia, differentiates between viral, pneumococcal and chlamydial pneumonias. Currently, the International Headache Society provides a clinical or symptomatic classification for primary headaches and an etiological classification system for secondary headaches.2

Migraine with aura is a diagnosis based on arbitrarily established2 (un-validated),3,4 symptomatic features. Diagnosing primary headache appears to be irrelevant; it is based on presenting features, not on etiology, and therefore is of little value to clinicians.

The TCN is at the heart of migraine pathophysiology.5 There is widespread agreement that the underlying disorder in migraine (at least, if not other primary headache presentations) is a sensitised TCN,6 and triptans abort headache by De-sensitising the TCN7,8 (without determining the reason for sensitisation) and a potential source of TCN sensitisation is noxious C1-3 afferents;9-14 it’s not about a diagnosis. The focus, for optimal management of the headache and migraine therefore, is the identification of the source of sensitisation.

What would I call the situation described above? If one prescribes to the notion that relief from a triptan confirms migraine, then it is ‘migraine’, but I am thinking ‘etiologically’, so, provided my examination has led to reproduction and resolution of typical head pain as the examination technique is sustained,13 (which I believe is the most powerful clinical pheomonenon confirming cervical relevancy), and I cringe, because I disdain labels – to use a term used decades ago ‘cervicogenic migraine’ – which probably best answers your question. Ultimately though, I won’t rely on a presentation of CxHA or otherwise, and a ‘diagnosis’ in primary headache is meaningless.

This is an example of the mockery of a classification system based on symptomatic presentation which has potentially arrested advancing our understanding of headache.4

Question: If a medical hypersensitivity exists in the neurovascular system in the brain of a five year old child and they have a right sided classic migraine with associated symptoms and behaviour, would you still assess their neck?

Answer: Firstly, I am not aware of how a ‘medical hypersensitivity exists in the neurovascular system’ is determined/ confirmed – how do we know? Secondly, I am assuming ‘classic migraine’ indicates the presence of an aura (M+A); therefore the ‘diagnosis’ is no doubt.

As mentioned above, the underlying disorder in M+A and M-A is a sensitised TCN.

I will examine the neck in any headache/migraine form. If my examination has led to reproduction and resolution of typical head pain as the examination technique is sustained,13 my clinical experience and research suggest that cervical afferents are relevant and I will treat. However, if there is reproduction without subsequent resolution, then other (non cervicogenic) reasons for sensitisation need to be considered.

and

Question: Lastly what percentage of clients with no neck pain and no headache do you produce HA like area of pain on end range palpation ?

Answer: I only treat headache/migraine and over 80% of clients, irrespective of the diagnosis, have associated cervical symptoms. I am not sure what you mean… someone who experiences headache and presents interictally i.e. in a headache free state? If so, reproduction (and resolution) of typical head pain occurs in 80-90%. It’s difficult to estimate the percentage of the 20% who do not have associated cervical symptoms.

If you mean someone who doesn’t experience headache, I have no idea as I don’t treat anything but headache/migraine or other symptoms potentially emanating for the upper cervical spine i.e. symptoms of TCN/brainstem sensitization.

References:

  1. Robins EG, S.B. . Establishment of diagnostic validiity in psychiatric illness: application to skizophrenia. In: Robbins LN BJ, eds, ed. The Validity of Psychiatric Diagnosis. . New York:: Raven Press;; 1989::1-7.
  2. Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition. Cephalalgia. Jan 2018;38(1):1-211.
  3. Shevel E SD. The international headache society classification of migraine headache-A call for substantiating data. Journal of Biomedical Science and Engineering. 2014;7(3):112-114.
  4. Spierings EL. Migraine, big and small. Headache. Oct 2001;41(9):918-922.
  5. Akerman S, Holland PR, Goadsby PJ. Diencephalic and brainstem mechanisms in migraine. Nat Rev Neurosci. Sep 20 2011;12(10):570-584.
  6. Goadsby PJ, Holland PR, Martins-Oliveira M, Hoffmann J, Schankin C, Akerman S. Pathophysiology of Migraine: A Disorder of Sensory Processing. Physiological reviews. Apr 2017;97(2):553-622.
  7. Hoskin KL, Bulmer DC, Goadsby PJ. Fos expression in the trigeminocervical complex of the cat after stimulation of the superior sagittal sinus is reduced by L-NAME. Neurosci Lett. May 14 1999;266(3):173-176.
  8. Hoskin KL, Kaube H, Goadsby PJ. Sumatriptan can inhibit trigeminal afferents by an exclusively neural mechanism. Brain. Oct 1996;119 ( Pt 5):1419-1428.
  9. Bartsch T, Goadsby PJ. Stimulation of the greater occipital nerve induces increased central excitability of dural afferent input. Brain. Jul 2002;125(Pt 7):1496-1509.
  10. Goadsby PJ, Knight YE, Hoskin KL. Stimulation of the greater occipital nerve increases metabolic activity in the trigeminal nucleus caudalis and cervical dorsal horn of the cat. Pain. Oct 1997;73(1):23-28.
  11. Piovesan EJ, Kowacs PA, Tatsui CE, Lange MC, Ribas LC, Werneck LC. Referred pain after painful stimulation of the greater occipital nerve in humans: evidence of convergence of cervical afferences on trigeminal nuclei. Cephalalgia. Mar 2001;21(2):107-109.
  12. Busch V, Jakob W, Juergens T, Schulte-Mattler W, Kaube H, May A. Functional connectivity between trigeminal and occipital nerves revealed by occipital nerve blockade and nociceptive blink reflexes. Cephalalgia. Jan 2006;26(1):50-55.
  13. Watson DH, Drummond PD. Cervical referral of head pain in migraineurs: effects on the nociceptive blink reflex. Headache. Jun 2014;54(6):1035-1045.
  14. Piovesan EJ, Kowacs PA, Oshinsky ML. Convergence of cervical and trigeminal sensory afferents. Curr Pain Headache Rep. Oct 2003;7(5):377-383.

Until next time

If you are new to Watson Headache®, welcome to the Watson Headache® Approach, an evidence-informed practice when considering the role of the neck in Cervicogenic and Primary Headache.

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