The upper cervical spine is in the box seat to, at the very least be a major contributor to the over activity in the brainstem, if not to be the underlying cause, but is largely ignored by mainstream medicine.
Through the first 3 parts of this anatomy series we have shown the symptoms of headache and migraine are predominantly related to the trigeminal system. We also learned that the upper 3 cervical nerves intermingle with the trigeminal nerves in the trigemino-cervical nucleus (TCN) – the “relay station” for the information coming in from these nerves to the brain. In the last part we saw clear evidence that this relay station is overactive, not just in migraine, but also tension-type headache, menstrual migraine, cervicogenic headache and cluster headache.
All of this is well understood throughout the neurological community, and the anatomical pathways are accepted. What is a matter of debate is how much contribution the neck makes to headache and migraine. Up until the 1990 International Headache Society (IHS) classification of headache, cervicogenic headache was not recognized as an “official” headache type. At some levels of the neurological world, there is still debate as to whether cervicogenic headache really exists at all.
Since being recognised, the official prevalence rate has been reported as between 0.4-4% of the population, compared to migraine (15%) and tension type headache (30%). We believe cervicogenic headache is under-diagnosed and represents closer to 80% of headache sufferers. We are not alone in this view. Dr Peter Rothbart, director of a large headache treatment facility in Ontario Canada suggest the same rate:
“Approximately 800 new headache patients per year are examined at our clinic. An estimated 80% of these patients are diagnosed with cervicogenic headache. Of these patients, almost none are referred with this diagnosis. Physicians are not taught to consider or explore neck structures when investigation headaches. This results in a rarely diagnosed but common condition” (1)
Is it a coincidence that around the same number, 81% are looking for more effective treatment?
The reason for the difference is that cervicogenic headache is not permitted to exist based on its outward symptoms the way migraine and tension headache do. It can’t. Clinically it often looks exactly the same as tension type headache or migraine. Even the president of the IHS admits:
“Headache of cervical origin and migraine often shows similar clinical presentations” (2)
So migraine is classified and diagnosed on the way it looks.
In the clinic it can look identical to the headaches accepted to come from the cervical spine.
So how can doctors or neurologists know the difference without excluding the cervical spine?
Based on this alone I would argue that is sufficient cause to “Check your neck”.
For cervicogenic headache to prove its existence it must demonstrate clinical signs that implicate a source of pain in the neck (none have been sufficiently validated for the IHS to accept), or the headache is abolished following diagnostic blockade of pain referring structures in the upper cervical spine. Diagnostic blockades are not practical in the clinical setting, and it is extremely difficult to block every pain sensitive structure.
Firstly, each spinal nerve supplies two spinal joints, the segment above and below where it exits the spine. Secondly each joint has sensory nerves that originate from two spinal levels and there can be intermingling of levels for up to 3 spinal levels. It is possible that sensory information including pain can intermingle with the trigeminal nerve from as low as the C7 nerve root. (3)
So unless you block almost all the cervical nerves, this doesn’t appear a valid diagnostic tool for cervicogenic headache either.
Effectively, it becomes impossible to diagnose cervicogenic headache in anything but a laboratory – and even then, it’s debatable whether the methods are valid. Little wonder it barely exists – officially.
Even more confusing is that certain areas of neurology are now treating upper cervical nerves (Greater occipital nerve – branch of C2) with electrical stimulators and having some effect with migraine. In a recent podcast on the ABC Andrew Charles – Professor of Neurology at UCLA explained: (4)
"There is quite intense interest in the occipital nerves because they feed directly into some of these brain pathways we think are responsible for migraine. So there are actually now stimulator devices some people find helpful"
"There is growing recognition that the upper cervical nerve roots may actually be playing an equally important role and many, many migraine sufferers get neck pain before, during or after an attack."
On face value this might seem that the call of Dr Shevel is being heeded and the source of pain is being recognised, but unfortunately Professor Charles then goes on to say:
"This leads many people to seek chiropractic treatment or massage when in fact really this is just a symptom of their migraine, and if you effectively treat the migraine, the neck pain goes away."
Actually, it’s not a fact. That would suggest there is proof that the neck doesn’t refer headaches. There is no such proof. He also just finished saying treating the occipital nerve (C2 spinal nerve) with a stimulator was helpful for some?
To me this sounds half pregnant.
If you had leg pain and numbness in your foot that coincided with back pain, the first place to look would be your back. If your therapist said “we are going to treat the pain and numbness in the leg, and the back pain will just go” that you may well seek a second opinion.
Yes, it is possible for foot and leg problems to cause back pain, but it is far more common in the other direction – at the very least you wouldn’t rule the back out without checking it. That is exactly what Professor Charles would like you to do………81% continue to search for more effective treatment.
So without any supporting evidence to rule out the neck it is, again, brushed aside as irrelevant. Despite the obvious anatomical links, despite the overwhelming number of pain producing structures in the cervical spine, and despite the tick of approval for "stimulators" treating cervical nerves, any other form of neck treatment should not be considered.
Seriously? This makes no sense to me. If it does to you please post and let me know.
Little wonder we are sitting at under 20% satisfied with their current treatment when such an obvious source of pain referral is ignored.
The evidence is clear.
Check your neck with an expert at a dedicated clinic. The sooner the better.
I would like to note that I don’t believe ALL headache or migraine arises from the neck. I’ll agree with Dr Rothbart and settle for 80%.
(1) Rothbart P. The cervicogenic headache: A pain in the neck. Can J Diagnos 1996; 13: 64–71.
(2) Goadsby PJ, Bartsch T Anatomy and physiology of pain referral patterns in primary and cervicogenic headache disorders. Headache Currents 2005;10:42-48.
(3) Antonaci, F. Cervicogenic Headache: Consideration of pathogenesis. Chapter 11, in Tension Type and Cervicogenic Headache; pathophysiology, diagnosis and management.
The brainstem of chronic headache and migraine sufferers is overactive.
Insights 1 and 2 examined the anatomy of headaches – the trigeminal nerve intermingling with the upper cervical nerves in the brainstem. The scientific evidence for the abnormal physiology (overactivity) involved in all major headache types is clear.
With an unknown aetiology (cause), headaches were historically described according to symptoms. This view persists today with the International Headache Society’s (IHS) current classification system (1). This led to treatments targeting symptoms, and caused researchers and clinicians to speculate about the underlying cause.
Migraine’s typical throbbing pain was assumed to be due to blood vessels constricting and then dilating. This theory gained much support and is still cited by many today, however research in the past two decades has disproven it prompting the president of the IHS to write “The vascular theory of migraine – a great story wrecked by the facts” (2).
The “tightening” quality of tension headache was thought to be increased scalp muscle tension. In 1977 an EMG study (measures muscle activity) showed that the tension of scalp muscles was no different to non-headache sufferers, yet the muscles in the top of the cervical spine significantly increase activity (3).
The two widely accepted theories regarding the underlying aetiology of headache and migraine were effectively dead.
So what then is the underlying problem and how do we know?
Three key areas of research combine to tell the story of an overactive brainstem.
Positron emission tomography (PET) scans show activity in a part of the body. The trigemino-cervical nucleus (TCN) has been shown to have increased activity using PET scans (3-4). This overactivity is present during and after the attack indicating it is not as a result of the attack, but constantly present and fundamentally contributing to the attack.
The triptans (e.g. Imigran, sumatriptan, Zomig, Maxalt) have a strong effect on a form of Serotonin highly specific to the TCN, which as previously described, has a dampening effect on activity in the brainstem and blocks pain signals from going up to the brain (6). Interestingly though, the triptans have demonstrated an effect in migraine, menstrual migraine, tension type headache, cluster headache and cervicogenic headache (7-10). This indicates all of these headache types have a common underlying problem - overactivity of the TCN.
Reflexes provide information about activity in the central nervous system (CNS). If a reflex is weak or absent, it is indicative of decreased CNS activity. If a reflex is heightened it is indicative of an overactive CNS. There are two reflexes (nociceptive blink reflex and trigeminocervical reflex) that relate directly to the TCN in the brainstem.
Both of these reflexes are overactive in migraine, menstrual migraine, tension type headache, and cluster headache (11-14).
Remember from insights 1 and 2 all the areas the TCN relays information to the brain from. An overactive TCN could cause you to feel throbbing or tightening pains, get blocked ears, or pain in the teeth or sinuses, when in fact it is just the brainstem fooling the brain. The blood vessels, muscles and ears are fine as demonstrated in earlier studies.
The evidence is clear. Increased TCN activity is a central part of the headache and migraine story. The current dispute in the neurological community is about “what causes this overactivity?”
In the final part of the insights series (part 4) we examine the key area that can cause the brainstem to be overactive, and it is an area that has been largely ignored in headache and migraine - the upper cervical spine.
(1) IHS Classification ICHD-II. International Headache Society. http://ihs-classification.org/en/ Accessed 3/2/13.
(2) Goadsby, P (2009) The vascular theory of migraine – a great story wrecked by the facts. Scientific Commentary. Brain: A Journal of Neurology, 132; pp. 6-7.
(3) Bakal, D.A. and Kaganov J.A. (1977) Muscle contraction and migraine headache: psychophysiologic comparison. Headache 17; pp. 208-15.
(4) Weiller, C. et al (1995) Brain stem activation in spontaneous human migraine attacks. Nature Medicine, July; 1 (7); pp 658-660.
(5) Afridi et al (2005) A positron emission tomographic study in spontaneous migraine. Archives of Neurology, 62 (8); pp 1270-1275.
(6) Goadsbay, P.J. and Hoskin, K.L. (1998) Serotonin inhibits trigeminal nucleus activity evoked by craniovascular stimulation through a 5HT1B/1D receptor: a central action in migraine? Annals of Neurology, 43 (6), pp 711-718.
(7) Ekbom, K. and Hardebo, J.E. (2002) Cluster headache: aetiology, diagnosis and management. Drugs, 62 (1), 61-9.
(8) Siow, H.C. et al (2004) Frovatriptan for the treatment of cluster headaches. Cephalalgia, Dec, 24 (12), pp. 1045-8
(9) Cady, R.K. et al (1997) Responsiveness of non-IHS migraine and tension-type headache to sumaptriptan. Cephalalgia, Aug, 17 (5), pp 588-90.
(10) Pavese N, Bibbiani F, Nuti A, Bonuccelli U. (1994) Sumatriptan in cervicogenic headache. Proceedings European Headache Federation 2nd International Conference; Abstract 131
(11) Nardone et al (2008) Trigemino-Cervical Reflex Abnormalities in Patients With Migraine and Cluster Headache. Headache, 48; pp 578-585.
(12) Nardone, R. and Tezzon, F. (2003) The trigemino-cervical reflex in tension-type headache. European Journal of Neurology, 10 (3), pp 307-312.
The anatomical pathway described in parts 1, 2 and 3 of this series have been known and recorded for several decades. To attribute credit to a single source for the information provided would do a disservice to some that have contributed to my knowledge over the years. Suffice to say that Professor Nikolai Bogduk from the University of Newcastle has produced a body of work over 30 years, which has greatly expanded our knowledge in this area and those that have taught me have undoubtedly drawn upon his publications.
(13) Gantenbein, A.R. and Sandor, P.S. (2006) Physiological parameters as biomarkers of migraine. Headache, 48 (7); pp 1069-74.
(14) Varlibas, A. and Erdemoglu, A.K. (2009) Altered trigeminal system excitability in menstrual migraine patients. Journal of Headache and Pain, 10; pp 277-282.
Roger O'Toole is the Director and Senior Clinician of the Melbourne Headache Clinic and has over 10 years experience as a physiotherapist.