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.