Medical Diagnosis

When Managing Headache and Migraine

A colleague recently sought to question some of my criticism of medical diagnosis in migraine, see Commentary for Health Professionals, ‘Managing Headache and Migraine: Why Treatment Often Fails‘.

My thoughts on my colleague’s comments/queries (in bold italics) follow.

Yes there is no test for migraine so the diagnosis is based on reporting.

Yes, based on (reporting of) a set of un-validated signs and symptoms – it doesn’t tell us what we are dealing with or the reason for the recognised biological entity underpinning migraine – a sensitised trigemino cervical nucleus (TCN).

I continue to agree with, and echo others who are critical of the International Headache Society’s (IHS) classification system.

As mentioned before, the IHS classification system of primary headache lacks biological validity and therefore hampers progress in understanding of headache.1 The IHS system is in disarray hence the multiple revisions, 2-6 and it is still not meeting clinicians’ needs with many receiving multiple diagnoses.7,8

Diagnosing primary headache is ‘hypothesising’.

I agree many of the clients we see have a cervicogenic aspect to their migraine. (Either as a trigger, a post migraine experience, or as part of their presentation).

If the above is suggesting that C1-3 afferents are a mere side-show in the migraine process, then this is unfamiliarity with elementary neuro-anatomy, pain/science, neurophysiology and contemporary research.

Manual therapy professions need to move away from the term cervicogenic headache (CxHA) – until there is universal acceptance that CxHA exists (probably not in my lifetime) and, also the term is an ‘intellectual straitjacket’ – it does disservice to the potential (sensitising of the TCN in primary headache) role of noxious C1-3 afferents.

More comments following…

But there are many who have migraines whom physios don’t see because medication is so effective for them in both acute

Agreed. Some are happy to continue taking heavy duty anti-migraine medication which abort episodes (without changing frequency) or perhaps they are not aware that there is potentially a non-pharmaceutical alternative.

or preventative treatment.

Ditto, and… they take prophylactic medication (SSRIs etc) for the rest of their lives. The (apparent) effectiveness of anti-migraine medication doesn’t rule out noxious C1-3 afferents as the reason for sensitisation of the TCN.

Is the neck involved when someone has a twice a year two day migraine,

Yes, in the same way the lumbar spine is involved with recurrent low back pain and the cervical spine with wry neck twice a year.

or a consistent hormonal related pattern of migraine?

Yes. The research shows quite clearly that hormones are not primarily responsible for Menstrual Migraine (MM) – how can they be in a unilateral headache and in many cases alternating unilateral headache? Hormones do not choose to affect one side of the head. Research has shown that hormonal patterns in those with MM are no different to those not experiencing MM. There has to something else – an underlying disorder in the CNS?9 And so it has to come to pass that those with MM have a sensitised TCN… throughout the cycle10 – not surprisingly then that the triptans abort and are recommended for MM.11-14

or is an eight year old child with no history or signs of neck involvement? 

The existence of CxHA is debated,15,16 (because) and currently there is no identifiable pathology i.e. there no validated lesions for CeH.15,16 Thus, CxHA suffers the same fate as those of Primary Headache conditions, for whilst in theory, the pathophysiology of CxHA 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 CxHA, but also as a sensitising source of the TCN in primary headache?

It is generally agreed that CT and MRI are not appropriate tests to rule out pathology.17-22 Instead, identifying lesions is likely to require more sophisticated and specialised methods. For example, in a PET study, tracer uptake in proximity to the second cervical vertebra was significantly greater in chronic whiplash associated headache patients than controls, indicating local persistent peripheral tissue inflammation.23

Temporary reproduction of familiar head pain alone, because of the bi-directional nature of the TCN, whilst creating suspicion does not confirm cervical relevancy. However, my own research,24 suggests that resolution of the typical head pain as the reproducing technique is sustained is a more powerful demonstration of cervical relevancy.

As in humans, histological studies of zygapophyseal joints in rats and goats have identified nociceptive nerve fibres in the joint’s capsular ligament.25-27 Mechanical hyperalgesia or allodynia represents enhanced nociceptive processing and as such is commonly used as an indicator of pain outcomes in animal studies.28,29

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.28-39 Animal studies indicate that nociceptive afferent information from zygapophyseal joints initiate central sensitisation.40-44   These results imply that zygapophyseal joint25,45,46 mediated spinal hyper excitability, plasticity of dorsal horn neuronal activity and pain,34,35,37 occur in response to abnormal alterations in fibre patterns of the capsule’s collagen matrix during loading occurring at or preceding capsular tolerance;47 nociceptive afferent information from zygapophyseal joints initiates central sensitisation.40-44

Pathophysiological effects identified in mechanistic studies of the zygapophyseal joint in animal studies can be extrapolated to human pain processes.48-50

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.40-44

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.17,51

Macroscopic lesions are not necessary in CxHA or C1-3 afferents in primary headache and I suggest nor are obvious clinical signs.

I agree with the concept that migraine is about hypersensitivity but of what?  

There is widespread acceptance that the underlying disorder in migraine involves sensitisation of the brainstem/TCN52,53 – a biological entity (in summary – trigeminal activity in primary headache syndromes requires assessment of nociceptive processing;54 nociceptive specific neurons are present in the spinal trigeminal nucleus and spinal trigeminal tract;54 nociceptive processing occurs predominantly within the sub-nucleus interpolaris and sub-nucleus caudalis (TCN) of the spinal trigeminal nucleus;54 the sub-nucleus caudalis extends to include C1-C3 dorsal horns – the TCN55-57).

Elementary neuro anatomy58-63 dictates, and substantial evidence24,63-66 demonstrates C1-3 afferents are not only a key player in head pain, but a potential source of sensitisation of the TCN, the underlying disorder in migraine,63,67-69 if not in other primary headache conditions;10,68-70 migraine is one of several primary headache disorders,6 so the basic anatomical principles that are described here may more generally apply to other primary headache syndromes.52

Essentially migraine is considered a ‘sensory processing disorder’;71,72 information from the trigeminal field is amplified/distorted as it passes through a sensitised relay centre – the TCN. The TCN is sensitised and whilst other purported sources – for e.g. biochemical/hormonal/ingestants/stress etc. are candidates, migraine by definition, is a unilateral headache; these potential sources of sensitisation cannot be primarily responsible – they are not going to choose to affect one side of the head and in the cases (80% migraine; 30% cluster headache73,74) of alternating headache, choose the other side. Furthermore, when asked to explain the mechanism of alternating, unilateral headache, the response from the medical model of headache is very, very quiet to non-existent; alternating, unilateral symptoms are characteristic of a musculoskeletal event.

Agreeing high quality studies are needed to investigate the complex physiological and chemical aspects. One study demonstrating one aspect, while contributing to our knowledge, cannot be taken as proof of the whole process.

Thank you for recognising my contribution.

Additionally, migraines can be erratic and disappear and recur for months or years at a time. 

Yes, as with low back pain and wry necks.

Only a long term study with recording of the pattern of the attacks and medication taken will demonstrate if the applied treatment actually produces long term changes. 

Yes, as with any intervention, RCTs are needed to confirm anecdotal reports and clinical observations (of many).


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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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