Secondary Headache or another Primary Headache?

Cervicogenic Headache

Headache is classified as either Primary or Secondary Headache.1  Primary Headaches are those headache and migraine conditions with unknown pathophysiology. Secondary Headache comprises headache arising from a recognised and accepted cause, i.e. secondary to a known source. Cervicogenic Headache (CeH) is classified as a secondary headache i.e. headache secondary to a cervical lesion.1

Elementary neuro anatomy2-7 dictates, and substantial evidence7-11 demonstrates cervical afferents are not only a key player in head pain, but a potential source of the sensitisation of the trigemino cervical nucleus (TCN), the underlying disorder in migraine,7,12-14 if not, in other Primary Headache conditions.13-16

However, the existence of CeH is debated,17,18 (because) and currently there is no identifiable pathology i.e. there no validated lesions for CeH.17,18 Thus, CeH suffers the same fate as those of Primary Headache conditions, for whilst in theory, the pathophysiology of CeH is recognised, there are no bona fide, accepted lesions initiating the physiological process.

But… does there need to be evidence of a macroscopic lesion for noxious cervical afferents to be instrumental in not only CeH, but also as a sensitising source of the TCN in Primary Headache?

As in humans, histological studies of zygapophyseal joints in rats and goats have identified nociceptive nerve fibres in the joint’s capsular ligament.19-21 Mechanical hyperalgesia or allodynia represents enhanced nociceptive processing and as such is commonly used as an indicator of pain outcomes in animal studies.22,23

A substantial body of evidence from animal models has demonstrated the development of mechanical hyperalgesia (pain) from controlled, non injurious loading of the zygapophyseal joint capsule.22-33

These results imply that zygapophyseal joint19,34,35 mediated spinal hyperexcitability, plasticity of dorsal horn neuronal activity and pain,28,29,31 occur in response to abnormal alterations in fibre patterns of the capsule’s collagen matrix during loading occurring at or preceding capsular tolerance.36

Pathophysiological effects identified in mechanistic studies of the zygapophyseal joint in animal studies can be extrapolated to human pain processes.37-39 In particular, animal studies indicate that nociceptive afferent information from zygapophyseal joints contribute to central sensitisation; moreover, when considered with the ameliorating effect of anaesthetising40-53 or neurotomy54-57 of the medial branch of the third occipital nerve in humans, animal data provide a compelling argument for cervical zygapophyseal joints as a source of neck pain and/or headache.

Furthermore, a significant body (of animal research) involving noxious intervention of cervical musculature demonstrating sensitisation of the Brainstem/TCN provides additional support for cervical afferent sensitisation of the TCN.58-62

The fact that headache related neurophysiological phenomena result from non-injurious loading of the zygapophyseal joint capsule has significant implications. Not the least is that these findings are incongruent with the biomechanical premise that the degree of symptoms would be proportional to magnitude of soft tissue loading.63,64

Accordingly, there is general agreement that conventional medical imaging lacks sensitivity for capsular and intra-articular injuries of the spine.49,52-54,56,57,63,65,66 Consequently, computed tomography (CT) and magnetic resonance imaging (MRI) are not appropriate tests to rule out pathology.49,56,57,63,65,66 Instead, identifying lesions is likely to require more sophisticated and specialised methods. For example, in a positron emission tomography (PET) study, tracer uptake in proximity to the second cervical vertebra was significantly greater in Chronic Whiplash Associated Headache (CWAH) patients than controls, indicating local persistent peripheral tissue inflammation.67

Secondly, and conspicuously in relation to whiplash (and therefore implicitly cervical) disorders, the inability of customary medical imaging to identify pathology implies that the source of patients’ symptomatology is not always clinically detectable;52-54,56,66,68 i.e. the absence of extensive, conspicuous zygapophyseal joint capsular damage does not rule out nociceptive (symptomatic) relevance.49,52,63

Perhaps this explains why associated cervical symptoms are absent in some with CeH; 25000 hours of the author’s clinical experience suggests associated cervical symptoms are not a pre-requisite for cervical involvement.

Yes… CeH is a Secondary Headache, secondary to disturbed function of structures supplied by C1-3 cervical nerves, which, with rapid advances in technology of medical investigative techniques, are likely to demonstrate…

Just because you cannot see it, does not mean ‘it does not exist’

In the meantime, clinical experience and research would suggest that reproduction and resolution of customary head pain as the examination technique is sustained, remains the most accurate and cost effective determination of CeH or, relevancy of cervical afferents as the source of sensitisation of the TCN in Primary Headache.11


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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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