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Migraines – a pain in the neck!

Neck based headache and migraine cannot be distinguished based on symptoms alone, even in the presence of neurological changes such as aura.

To be officially diagnosed with migraine your neck MUST be excluded as a potential source of symptoms.

This is because migraine is a diagnosis of exclusion based on how the symptoms look. We know the neck can cause identical symptoms to migraine (including with aura). In fact the president of the international headache society (IHS), Professor Peter Goadsby has commented on the difficulty health professionals face in distinguishing between the two, saying that ‘migraine and neck based (cervicogenic) headache often show similar clinical presentations’.

So which do you have, migraine or cervicogenic?

The problem is that current approaches are either inadequately assessing the neck, or ignoring it completely. Imaging (X-ray, CT or MRI) will only show major structural damage such as broken bones, damaged ligaments or space occupying lesions rather than mechanical stresses – often this is reported as NAD (no abnormality detected). In many cases people with neck symptoms will have visited a manual therapist (physiotherapist, chiropractor, osteopath, masseur) who uses the same techniques to assess and treat headache and migraines as they use to treat localised stiffness and pain. In other words the tools are not designed for the job. In some cases this will have an effect in the short term (symptoms either better or worse) and in other cases it will miss the point completely and have no effect.

We use a technique known as the Watson Headache Approach ® which has been developed specifically to test the relationship between your neck and the referral of headache and associated symptoms. Furthermore it is the only hands on technique that has been shown to lower activity in the trigeminal nucleus – the ‘headache centre’ known to be overactive in ALL major headache types.

Based on the similarity of symptom presentation alone, and the fact that our techniques are developed specifically for headache and migraine – that should be enough to warrant an assessment.

Independent research is catching up to what we have known clinically for years, and is overwhelmingly pointing to a cause that has consistently been overlooked. The neck has gone from being considered irrelevant to become the leading suspect, and an area that must be excluded as the source before proceeding on the all too familiar pathway of symptom blocking medications.

The summary of the evidence is:

  1. Migraine symptoms look identical to symptoms produced by problems in the top of the neck. For this reason alone everyone with suspected migraine should have the neck excluded as the source, even in the absence of neck symptoms.
  2. The common underlying problem in all headache types is an over-stimulated brainstem – specifically the trigeminal nucleus housing all the nerves for the head and face.
  3. The 3 nerves from the top of the neck feed directly into this over-stimulated trigeminal nucleus.
  4. Researchers who have performed diagnostic blocks of these upper neck nerves have shown it can temporarily abolish pain in all forms of headache including migraine (and migraine with aura).
  5. Postural research shows migraine sufferers (along with Tension-type headache sufferers) have a more significant head forward posture than those non-headache sufferers
  6. 70% of migraine sufferers experience neck symptoms (tightness, pain) before, during or after their migraine.
  7. The techniques employed by this clinic have been shown to decrease the overstimulation of the trigeminal nucleus – by treating the cause, and previously mis-understood fault in the top part of the neck.

The research has also shed light on what migraines are not. Migraines are not a vascular event, and while small changes in blood flow may serve to trigger a migraine, it is just that, a trigger or a spark……..not the powder keg. The powder keg is the overactive trigeminal nucleus, and there are many potential ‘sparks’ or triggers. Instead of ‘chasing triggers’ (which can be extremely difficult as often they interact and can be inconsistent) we prefer to deal with the powder keg – treat headaches and migraines at the source and treat the overactive trigeminal nucleus.

It is no coincidence that research shows 81% of migraine sufferers are looking for a better solution, and 80% of sufferers are ‘misdiagnosed’ and actually have neck based symptoms.

We believe the reason that there is such a big overlap in symptoms between headache types is because they all originate in the same region – the brainstem.

What exactly IS a migraine?

There is no diagnostic test to prove you have migraine. It is a conclusion drawn based on the clinical presentation (outward signs and symptoms such as throbbing, intense pain, presence of nausea or vomiting, sensitivity to light and sound) and that these symptoms cannot be attributed to other known conditions.

IHS Classification:

Migraine is considered a primary headache type. That is, that it is a neurological event that cannot be associated with a known pathology (e.g. not secondary to a tumour, neck problem etc). So a key element of the diagnosis is to exclude the symptoms as secondary to other pathology known to cause the same symptoms. Medical history is often enough to exclude sinister pathology and in some cases imaging of the brain may be sought to exclude this cause. Given problems from the neck can cause the same symptoms, how is the neck excluded as part of the diagnosis? Rarely with imaging which is almost always clear, and in rare cases where something is present it’s often not relevant to symptoms. Exclusion is often based on failed treatment of the neck, either aggravating symptoms, or providing only short-term relief.

In such cases treating the neck is considered to be only relieving symptoms and not worth pursuing. Odd then, that the approach of medications can only be to relieve symptoms (given they don’t claim to know the cause) yet this is acceptable.

Diagnostic criteria:

  1. At least 5 attacks fulfilling criteria B – D.
  2. Headache attack lasting 4-72 hours (untreated or unsuccessfully treated).
  3. Headache has at least two of the following characteristics:
    1. Unilateral location
    2. Pulsating quality
    3. Moderate or severe pain intensity
    4. Aggravation by or causing avoidance of routine physical activity (e.g. walking or climbing stairs)
  4. During headache at lease one of the following:
    1. Nausea and/or vomiting
    2. Photophobia and phonophobia
  5. Not attributable to another disorder

Frequency and duration

Classic or episodic migraine occurs less than 14 days per month, and in some (very lucky) cases maybe only once or twice per year. Episodes more than 14 days per month are considered to be chronic or retractable migraine sometimes referred to as ‘Status Migrainous’. In the most extreme cases people may have continuous symptoms, 24 hour a day, 7 days per week sometimes referred to as chronic daily migraine or Hemicrania Continua.

This is not to be confused with new daily persistent headache (a chronic form of tension-type headache) in which sufferers lack the nausea, sensitivity to light and sound that forms part of the migraine diagnosis.


Officially, like all other primary headaches (Tension-type headache and Cluster Headache) there is officially ‘no known’ cause for migraines. Triggers or things that ‘set off’ a migraine episode are not considered causes.

What we know about all major headache types is that the baseline activity levels in the trigeminal nucleus are elevated. This key area houses all the nerves for the head and face and receives direct input from the neck via the C1, C2, and C3 spinal nerves. Far from being irrelevant, the neck is the most likely cause of all headache types, and should be considered the cause until it has been excluded – appropriately fulfilling the diagnostic criteria E for primary headache (not attributable to other known causes).


Due to the official causes being unknown it is hard to direct prevention to any specific area. Instead triggers are often targeted, and many migraine sufferers will have attempted to keep a diary over the years trying to tease out consistent triggers. In some cases this can be highly effective, but more often than not triggers are inconsistent, and interact with each other and other parts of the brain whose activity levels may fluctuate


Medical Rx:

Medications to block symptoms:

Analgesic, anti-inflammatory, Abortive (triptans – imigran, relpax, Naramig, Zomig, Maxalt), anti-emetics (anti-nausea – e.g. Maxolon) prophylactics/preventives (sumatriptan, sandimigran, anti-seizure, anti-depressant, anti-anxiety, analgesics, , blood pressure medications (beta blockers).

Botox – the effect in clinical trials is only marginal compared to placebo. In June 2012 the UK’s National institute for health and care excellence (NICE) noted “the large placebo effect seen in the trials. It was also aware that the incremental effect of botulinum toxin type A compared with placebo may have been increased by people in the active treatment arm realising that they were receiving botulinum toxin type A because of its side effects.

The problem is that 70% of people injected with botox guess correctly they were on it. In other words we can expect an enhanced placebo effect leading one eminent Neurologist to comment “Botulinum toxin A used to treat headache evokes prominent placebo effects and it is likely that these effects are solely responsible for its apparent effectiveness”.

Manual Therapy:

At present the only manual therapy technique to show relevance to migraine is the Watson Headache Approach ® (the only technique employed by this clinic). While this might seem surprising, up until the research undertaken by Dean Watson, the neck was considered largely irrelevant, and while diagnostic studies have looked at the neck they are laregley based on anaestheitic blockades of the spinal joints rather than a manual non-invasive assessment using the hands of highly skilled practitioners.

Epidemiology, (Prevalence, Demographics)

10-15% of the population are affected by migraine. Migraine affects women more than men by 3:2, whereas TTH is closer to even and Cluster headache affects men more than women. The reasons for this are unclear, but we do know that these different headaches take different paths through the brain. They all begin in the trigeminal nucleus, like trains waiting at a major train station. As this activity pushes up into higher parts of the brain each headache types takes a slightly different track. This is likely to be the reason we see different types of headache presenting with different symptoms and presenting with marked gender differences.


Under the current medical model there is a 20% success rate. We believe this is largely due to 80% having the source of their problem ignored or poorly treated.

Data from the Melbourne Headache Centre shows that of the 80% of people assessed to have a neck disorder related to their symptoms, 90% have significant changes with the initial treatment period (2 weeks).


Relevant Research:


  1. Bartsch T,  Goadsby PJ (2005) Anatomy and physiology of pain referral patterns in primary and cervicogenic headache disorders.  Headache Currents 10:42-48.
  2. Watson, D.H, and Drummond, P.D. (2014) Cervical Referral of Head Pain in Migraineurs: Effect on the Nociceptive Blink Reflex. Headache: Journal of Head and Face Pain, June, 1035-1045
  3. The International Classification of Headache Disorders, 3rd Edition (2013), Cephalalgia, 33 (9), 629-808

Overactive brainstem:

  1. Nardone et al (2008) Trigemino-Cervical Reflex Abnormalities in Patients With Migraine and Cluster Headache. Headache, 48; pp 578-585.
  2. Nardone, R. and Tezzon, F. (2003) The trigemino-cervical reflex in tension-type headache. European Journal of Neurology, 10 (3), pp 307-312.
  3. Gantenbein, A.R. and Sandor, P.S. (2006) Physiological parameters as biomarkers of migraine. Headache, 48 (7); pp 1069-74.
  4. Varlibas, A. and Erdemoglu, A.K. (2009) Altered trigeminal system excitability in menstrual migraine patients. Journal of Headache and Pain, 10; pp 277-282.
  5. De Marinis, M. (2007) Blink reflex in cervicogenic headache. Cephalalgia, 27 (7); p 860.
  6. Sand, T. Moll-Nilsen, B. Zwart, J.A. (2006) Blink reflex R2 amplitudes in cervicogenic headache, chronic tension-type headache and migraine. 26 (10); p.1186.

Diagnostic Blockades:

  1. Afridi S, Shields K, Bhola R, Goadsby P (2006) Greater occipital nerve injection in primary headache syndromes: Prolonged effects from a single injection. 122; 126-129.
  2. Anthony M. (2000) Cervicogenic headache: Prevalence and response to local steroid therapy. Cli & Experimental Neurology; 18: S59-S64.
  3. Rozen T, (2007) Cessation of Hemiplegic Migraine Auras with Greater Occipital Nerve Blockade. Headache, 47, 6, 917-919.
  4. Fishbain, D., Cutler R, Cole B, et al (2001) International Headache Society headache diagnostic patterns in pain facility patients. Clin J Pain; 17: 78-93

Postural research:

  1. Biondi D, Report #2 Cervicogenic headache: Diagnostic evaluation and treatment strategies. Pain Management Rounds-Harvard Medical School & Massachusetts General Hospital 2004; vol. 1, issue 8.
  2. Goadsby, P.J. (2009) The Vascular Theory of Migraine – a great story wrecked by the facts. Brain, 132: 6-7.
  3. ‘MIA – Migraine Impact in Australia– survey by Stollznow Research, via national online panel, conducted in April 2011 amongst 507 Australians with migraine aged 18-64. The MIA survey was developed as a partnership initiative between Headache Australia and MSD. The survey was funded by MSD.
  4. NICE (2012) Botulinum toxin type A for the prevention of headaches in adults with chronic migraine: Consideration of the evidence.
  6. Solomon, Seymour (2011) Botulinum toxin for the treatment of Chronic Migraine: The Placebo Effect. Headache, 51, 6, 980-984.