Migraine is the most common neurological disorder worldwide, and the most disabling condition for people aged 15-49, yet it is a poorly understood (by society) and poorly treated condition.

Migraine is so much more than a ‘bad headache’. The characterisation of migraine as a ‘headache disorder’ diminishes the far reaching impact on the ability of the sufferers’ brain to function. Migraine was first recognised for, and is defined by the non-headache or associated features that captured the attention of medical practitioners as far back as Hippocrates (400 B.C.) and Aretaeus of Cappadocia (30-90 A.D.) who first described a number of the non-headache features of migraine including:


flashes of purple on black colours before the sight, or all mixed together, so as to exhibit the appearance of a rainbow expanded in the heavens

Lethargy, Anxiety, Photophobia, Phonophobia, and Osmophobia.

there is much torpor, heaviness of the head, anxiety and weariness. For they flee the light; the darkness soothes their disease; nor can they bear readily to look upon or hear anything disagreeable; their sense of smell is vitiated

Aretaeus cautioned fellow physicians from taking the condition lightly, and carried on the work of Hippocrates in treating migraine as a medical condition:

the pain …… remains in the half of the head. This is called heterocrania, an illness by no means mild, even though it intermits, and although it appears to be slight. For if at any time it set in acutely, it occasions unseemly and dreadful symptoms……nausea; vomiting of bilious matter…..

The Stigma of Migraine

As traditional beliefs surrounding humoral theory started to become challenged by the emergence of anatomical science, causal explanations started to reflect the underlying anatomy. Unfortunately a lack of an obvious pathological cause, combined with a sexist view of the ‘weak female disposition’ combined with stress as a key trigger started to shift views on migraine from a medical condition to a psychosomatic condition brought on by an inability to handle life stress.

“It was a disorder that most obviously affected women and so wasn’t taken as seriously … and it’s a pain disorder. Pain is subjective: we don’t have any way of measuring it, which can make it very hard for people to believe it’s real.”

Elizabeth Loder – Neurologist

The key shift back from a psychological illness to a medical one occurred almost 90 years ago Harold Wolff’s (and colleagues) experiments, not only entrenched the vascular theory of migraine (reproducing temple pain by pulling on the middle cerebral artery of live conscious patients), but also demonstrated the effect of ergotamine as a potent vasoconstrictor, seemingly the mechanism by which ergotamine had been used as a natural remedy for migraine. Finally there appeared to be a mechanical change in blood vessels that medication could impact, bringing migraine back to a medical problem, but the stigma remained significant for decades more, and still lingers in some corners of society today.

Modern Pharmacological Management

Around the same time as Wolff was changing the medical view of migraine, two big events were occurring. The development, effectiveness and commercialisation of insulin, and then penicillin sewed seeds within an emerging pharmaceutical industry.  The outbreak of World War II in 1939 and the subsequent demand for penicillin threw the pharmaceutical industry into overdrive. At the end of the war the paradigm that produced miracle drugs that saved vast amounts of life and limb, was applied broad-brush to every other facet of healthcare.

The market is, of course, very big,” Loder says. “It’s a common disorder, it lasts decades. So, that made pharmaceutical companies sit up and take notice; money poured into the field; it improved and professionalised research.

Elizabeth Loder – Neurologist.

Despite the billions of pharmaceutical industry dollars poured into research, the improvements have only come with safety and tolerability. There is very little improvement seen in the ability of these medications to decrease migraine frequency, severity or duration in significant ways. If you have tried numerous medications and failed, or your body adapted to them and they lost efficacy, or you couldn’t tolerate the side effects – or the medications work great, but you don’t want to stay on them forever, then it’s time to start to ‘unpick the migraine puzzle’.

Medication focusses very heavily on inhibiting pain pathways, and for good reason – one of the most recognisable symptoms of a migraine is a severe headache, and it is often framed in those terms forming a key pillar of the ‘Classification of Headache Disorders’.

Many parts, and often the most disabling parts of migraine are factors other than headache or pain. Lethargy, decreased cognitive function (often referred to as ‘brain fog’), sensitivity to light or sound, aura, dizziness or vertigo, and nausea and vomiting. It is the associated symptoms that made migraine stand out from other headaches, and indicate what it really is:

An inability of parts of the brain to appropriately receive, and/or interpret, and/or respond to sensory input

Migraine would be far better classified as a ‘Brainstem Dysfunction Syndrome‘ or ‘Central sensitisation disorder’.



Migraine and the sensitised brainstem

Recent advances in research with continual brain scanning over a 30-day cycle, have demonstrated that in the earliest beginning (premonitory phase – see Migraine phases below) of a migraine there are significant changes in activity of key brainstem regions:

  1. The Trigemino-Cervical Complex (TCC): brainstem region where trigeminal (head and face) nerves mix with upper 3 neck nerves and key area for the pain of headache, and in a state of constant ‘overstimulation’ in migraineurs.
  2. The hypothalamus; master controller of our homeostasis (internal balance), and controller of our internal body clock.
  3. Dorsal Pons; region that controls our ‘alertness levels and threat response’ activity, and can ‘dial up or down’ the pain response.

The early involvement of the TCC is interesting, as it is the key signalling area for headache, but this ‘uncouples’ from the hypothalamus before headache has even begun. What is happening in the TCC to cause this disruption?

In an overwhelming proportion of sufferers, small muscles under the base of the skull are causing disruption.

So what you say? I don’t have a sore neck, or restriction of movement.

These small muscles are extremely sensitive. Rather than just helping to ‘turn your head’ (in fact they don’t actually help do that at all), the sub-occipital muscles play a critical role in:

  • Vestibular function; they help your head distinguish between ‘looking down’ and falling forwards. In other words, head-on-body versus whole body movement.
  • Cardiovascular function; they signal ahead to blood pressure centres (solitary nucleus – also the centre for nausea) that you are moving from laying down to sitting up. This preempts this system to compensate for the changes in blood pressure as we move against gravity.
  • Visual system; coordinating with the eye muscle at multiple sites they control the direction of our gaze.
  • Headache production; 40% of the nerves coming in from these muscles converge onto the  same nerves that come in from the head and face (trigeminal nerve). Overstimulation sets off the bodies ‘alert’ system, and the focus shifts to the most important structure – the head. Testing this ‘convergence’ or the cross-wires from the neck to the head is a cornerstone of the Watson Headache ® Approach, and also proven to decrease the overactivity in the TCC

Many studies in recent times have demonstrated repeatedly that the small muscles in the top of the neck are dysfunctional in migraineurs. Often not in a way that limits movement or causes pain from the muscles themselves (this would be call a ‘cervicogenic headache’), but in a way that creates a constant underlying ‘noise’ disrupting the normal functioning of multiple brainstem regions including the hypothalamus, dorsal pons and TCC.

Watson Headache® Approach

The most significant non-pharmacological research undertaken has targeted TCC, the brainstem area that is constantly irritated and sets off the hypothalamus when migraines start. This research used the Watson Headache® Approach to decrease the underlying sensitivity of the TCC by very carefully treating the top of the neck..

This highly targeted technique treats the sensitivity, or ‘decreases the noise’, and calms the brainstem down. Treatments that aim to loosen tight muscles and stretch stiff joints can be far too heavy handed, and often are not sustained – resulting in short term relief, or aggravation. At the Melbourne Headache Centre you have access to the most experienced Watson Headache ® Practitioners in the world aside from Dean Watson himself. No drugs and no cracking of the neck. Treatment that gets to the heart of the problem.

Migraine is the outward appearance of an overloaded brainstem. Understanding what causes this overload is critical to successfully achieving control over your condition, rather than continually applying bandaid solutions that attempt to deal with each of the many different brain pathways that can become involved.

Phases of a migraine

Most typically migraineurs can be described as being in one of 5 stages, with different symptoms (with different brain region activity) appearing in each stage. Many migraineurs don’t have all 5 phases, and in some cases the aura can appear during or after the onset of headache: (image of stages rather than text)

  1. Premonitory symptoms (or prodrome): First signs of a migraine, present up to 72 hours before aura/pain and include frequent yawning, fatigue/lethargy, food cravings, neck stiffness, disturbed sleep.
  2. Aura:  under 30% of migraineurs get an aura which is a fully reversible neurological deficit – visual, motor or sensory.
  3. Headache and associated symptoms (ictal phase): stereotypically pain is one sided (but can be both) and pulsing or throbbing (can be sharp, pressure, ache). The presence of nausea is a distinguishing feature from Tension-Type Headache.
  4. Postdrome (hangover): the period after pain subsides, but not yet feeling ‘normal’.
  5. Interictal phase: this is the period between episodes, where migraineurs are symptom free. This research describing this phase when migraineurs feel normal shows elevated activity in the TCC with direct implications for the top of the neck.
Find out how we treat


here at the Melbourne Headache Centre

Diagnosis & Symptoms

Migraine can be recognised in Ancient Egyptians texts dating back to 1550 B.C. The word ‘migraine’ is a French derivation of the ancient greek for ‘half’ (hemi) and head/cranium (kranios).

The International Classification of Headache Disorders (ICHD-3) from the International Headache Society (IHS) describes migraine as a recurrent headache disorder manifesting in attacks lasting 4-72 hours, typically unilateral pulsing pain of moderate to severe intensity and aggravated by routine physical activity and associated with nausea and/or photophobia and phonophobia.

Diagnostic Criteria:

A. At least five attacks fulfilling criteria B-D

B. Headache attacks lasting 4-72 hours (untreated or unsuccessfully treated)

C. Headache has at least two of the following four characteristics:

  1. unilateral location
  2. pulsating quality
  3. moderate or severe pain intensity
  4. aggravated by or causing avoidance of routine physical activity (e.g. walking or climbing stairs

D.During the headache at least one of the following:

  1. nausea and/or vomiting
  2. photophobia and phonophobia

E. Not better accounted for by another ICHD-3 diagnosis


In Australia


of people suffer migraine


report an impact on work or home life


are looking for better treatments

Despite significant underfunding for the amount of disability migraine causes, much effort has been put into understanding the depth of the problem across the world.  According to the global burden of disease study, in 2016:

  • 13.97% or 1.04 billion people suffered migraine worldwide in 2016.
  • Migraine is the leading cause of disability in the most productive age group in society (15-49 year olds), and caused 20.3 million years lost to disability (YLD’s). This makes migraine the second leading cause of disability across all ages (after low back pain).
  • Less than 20% of sufferers are seeing a GP in Europe
  • Migraine is estimated to cost the economy:
    • $19.6 billion in the USA
    • €27 billion in Europe
    • $35.7 billion in Australia
  •  Due to low hospitalisation rate the individuals bear the brunt of the cost with respondents to the Migraine in America survey reporting the impact on various aspects of life:
    • 93% report an impact on work
    • 89% report impact on relationships with their partner
    • 87% report an inability to attend school or college
    • 86% report an impact on their relationship with their children

Migraine in Australia

  • 5.3 million sufferers or 22.05% of Australians (28.66% women, 11.96% men)
  • 71% of these sufferers are female
  • 86% of working age
  • 7.6% of migraine sufferers experience 15 or more migraine days per month
  • Migraine is the leading cause of disability from neurological disorders, (stroke is second), and the leading cause of disability from all causes in 15-49 year olds.
  • Annual cost to Australian economy $35.7 billion, $14.3 billion direct healthcare, $16.3 billion lost productivity costs
  • 11.1% of patients sen by a GP are for migraine
  • 81% report searching for a better, more effective treatment
  • 83% don’t expect to improve
  • 60% feel anxious or depressed
  • 40% missed significant family events
  • 21% missed career opportunities

Common Treatments

Migraineurs continue to report a 20-30 % satisfaction rating with treatment options despite an almost doubling on funding in recent years.

This is very reflective of the current ability of medications to manage the problem, and a lack of awareness of legitimate alternatives.

Pharmacological Management of Migraine

Research published in 2017 in America indicates that over 68% of sufferers have inadequate relief of an attack.

  • 49% have inadequate symptom relief at 2 hours
  • 38%have a recurrence of symptoms within 24 hours requiring further dosing

Preventive therapy (prophylaxis) fairs even worse. Pooled data on a broad rage of medications including antidepressants, serotonergics, anti-seizure and blood pressure medications indicate:

  • 12% of sufferers people will achieve a 50% reduction in headache days
  • More than 30% are unable to tolerate medications due to side-effects

New age medications promise better side effect profiles and efficacy, however the improvement is in percentage points, and they are still less effective than injecting saline (placebo). You of course will have heard reporting that they are superior to placebo and the reported numbers support this. For example, Emgality (Galcanezumab) is a new age CGRP-monoclonal antibody for migraine prevention;

  • 36 % of patients getting placebo achieved 50% reduction in headache days.
  • 59.3% of the Emgality 120mg group achieved 50% or greater reduction.

It’s better right? Well, maybe. What none of the trials report is that, of course there is also an equivalent placebo effect from receiving Emgality. So the ‘true effect’ of the CGRP-mAb (minus placebo) is 23.3%. This is the reason why both in the United Kingdom and Australia CGRP-mAbs have been rejected for listing under government medication schemes, and that the pharmaceutical companies are supplying them at massively discounted rates (down from the $700-800 single dose, $1400-1600 full dose price-tag per month).

There is a very large unmet need for treatment.

Non-Pharmacological Management of Migraine

There is a lot of ‘noise’ in this space, as many treatments preach avoiding triggers. While in the short term this can be helpful, especially if it is easy to avoid (i.e. drinking wine) then do so. Unfortunately trigger avoidance tends to create an aversion and ‘anticipatory anxiety’ can then replace the trigger – i.e. being worried about the trigger (like a thunderstorm when you see the forecast) can make you just as prone to an attack as the trigger itself.

From a physiological point of view it makes more sense to try to normalise the part of the brainstem that are ‘dysfunctional’ in the lead up to an attack.

This means targeting problems impacting on the TCC and the hypothalamus.

Hypothalamus – the main regulator of the body maintaining our homeostasis.

  • Start with tuning your circadian clock
  • Regulate your meal intake
  • Maintain adequate hydration
  • Develop a healthier relationship to stress
  • Exercise regularly

Targeting the TCC – The Watson Headache® Approach

Overactivity in the TCC is believed to be the key event impacting on the hypothalamus. The Watson Headache® Approach isn’t a ‘regular’ neck treatment, and doesn’t aim to stretch or strengthen muscles. It is a progressive desensitisation technique that very selectively targets the key ‘noise makers’ in the top of the neck and decreases the noise and calms the TCC. This has been demonstrated in the response to blink reflex activity in both migraineurs and tension-type headache sufferers.

This means rather than just ‘stretching or massaging’ the neck and hoping something might help, we are actually treating the one irritating factor that is constantly present, even between attacks – it deals directly with the powder keg, aiming to prevent triggers (sparks) from ‘blowing it up’.


Here it is important to distinguish between the Pathophysiology or changes in the brain function, and Triggers and that lead to migraine.

Pathophysiology of Migraine

Over the centuries this has, and continues to be a topic of much debate. Arguments are often a mix of partial facts supporting deeply entrenched beliefs, and published as science, usually with the purpose of developing a ‘therapeutic target’ – molecules that medications can target.

Prior to Hippocrates (460-370 B.C.) headaches were considered to be ‘evil spirits’ in the head or a ‘visitations from the gods’. With humoral theory (the interaction of 4 fluids -Flem, yellow bile, black bile, and blood) inside the body as the cause of all medical maladies. Anatomical exploration from the 1600’s led to theories espousing blood vessels (blood boiling up in the head) and ‘nerve storms’ akin to epilepsy as likely causes.

Modern imaging methods have disproven ‘vasodilation’ as a cause, and while there are brain activity changes, it is far from the ‘electrical storm’ associated with epilepsy. The divide between blood vessels and nerves still more or less exists with vascular theory is now best represented by the ‘Trigeminovascular theory’ and nerve storm giving way to ‘Brainstem cycling theory’

The Trigeminovascular Theory of Migraine

This theory claims that some underlying irritation causes hyper-excitability of trigeminal nerves, causing inflammatory proteins (neuropeptides) to be released, of which CGRP is currently the most widely known. It is widely accepted (rather than consistently proven) that CGRP is elevated during a migraine attack, and this can be experimentally induced by noxious stimulation of meningeal blood vessels and the trigeminal ganglion (cell bodies of pain nerves from the head and face).

There are significant gaps in the theory:

  • No broadly applicable hypothesis regarding how this hyper-excitability occurs in the absence of ‘noxious stimulation’ in migraine suffers.
  • Absence of substance P – Stimulation via experimental means increases substance P, which is not elevated in migraineurs.
  • Absence of vasodilatation – CGRP is a potent vasodilator. Functional imaging as well as doppler studies investigated blood flow during migraine and found no significant changes.
  • Injecting CGRP stimulates mild to moderate headache within minutes to hours, and therefore cannot account for the premonitory phase – i.e. migraine starts up to 2 days before the headache.

This model lends itself very heavily to pharmacological intervention. As the cause is ‘unknown’, prevention isn’t possible, but instead they develop ‘therapeutic targets’ (drugs) to block pain signalling pathways. This isn’t a new approach, but one with plenty of mileage left. Anti-histamine and substance-P blocking medications have been trialed with little success in the past. CGRP is currently the hot favourite but in coming years you will hear more about PACAP-38, VIP and adrenomedullin.

Even assuming that the levels were consistently elevated – What is the cause?

If you sprain your ankle you will have elevated levels of inflammatory chemicals to increase pain, make blood vessels leaky to promote healing,  and cause vasodilatation to get more blood into the area, abut also to perfuse healthy tissue surrounding the damage.

A blood test in this situation might conclude that the problem is raised inflammatory markers, when in fact, they are the solution. What is the source of irritation? Functional imaging before an attack begins provides the best insight.

Brainstem Cycling Theory

In more recent years functional imaging that has been conducted continuously over 30 day cycles has shed light on the changes that occur well before headache occurs, and provides the best hope in preventing attacks, and unravelling the migraine puzzle.

This imaging has shown that activity in the hypothalamus altered during the 24h prior to pain onset in response to trigeminocervical nociceptive stimulation. It decreases its coupling to the trigeminocervical complex and increase coupling with the dorsal rostral pons during the pre-headache day and the pain phase of native human migraine attacks.

Could this be from increasing CGRP? Not according to the time to headache from CGRP injections, which is minutes and hours, not a day. What could the source of noxious input be?

The TCC is the key to unlocking the functional changes, and whilst medications offer short term relief, dealing with ‘why’ the TCC is causing noxious inputs into the hypothalamus is clearly an import problem. Neck pain is the most common symptoms associated with headache and migraine, yet rather than look to it as a cause (which suggests manual rather than pharmaceutical intervention) the prevailing wisdom suggest we should ignore it as ‘part of the migraine’.

Upper Cervical Spine Afferents (sensory nerves)

The upper cervical spine is an extremely sensitive area, and is critical to:

  • Balance and vestibular function
  • Pre-empting changes in blood pressure with big postural changes
  • Startle response and initiating fight/flight reactions (coordinating head and eye position)
  • Protection of the head (pain induced reflexes and propagation of head-pain)
  • Mechanical tensioning of the dura in the top of the neck during neck movement.

Is there evidence of neck dysfunction in migraine? Overwhelmingly yes:

  • Neck pain
    • 76.2% of migraineurs report neck pain. This increase to 89.3% when TTH is included. Only 56% of non-headache sufferers report neck pain in the general population.
  • Neck weakness
    • Decreased neck muscle strength and endurance in women with migraine compared to controls.
  • Upper cervical spine dysfunction
    • Increased EMG activity measured in sub-occipital region in migraine (and TTH) compared to controls as far back as 1977.
    • 93% of migraineurs test positive on at least 3 (of 6) standard tests for upper cervical neck dysfunction.

Reflex testing and PET scans have previously indicated that the TCC is overactive before the headache starts. It is ‘overstimulated’ and causing dysregulation of the brainstem.

The Watson Headache® Approach, used exclusively at The Melbourne Headache Centre has been proven to decrease the ‘noise’ or irritation of the trigemino-cervical complex. The reflex activity normalises.


Migraine Triggers

The advice to avoid triggers seems sensible enough. However there is evidence that by reducing normal exposure to things such as light (constantly wearing sunglasses) and sound may in fact make you more sensitive to them and actually increase the frequency of your episodes:

The findings are consistent with the proposition that one etiological pathway to suffering from frequent headaches is via trying to avoid, or escape from potential trigger factors. These results suggest that the traditional clinical advice to headache patients, that the best way to prevent migraine/headache is to avoid the triggers, runs the risk of establishing an insidious sensitisation process thereby increasing headache frequency.

Professor Paul Martin, Psychologist10 


A systematic review of the many studies into migraine trigger factors found:

  • 76% of migraineurs reported triggered attacks.
  • Only 9% very frequent and 27% frequent, 40% were only occasionally related to triggers.

Immediately this paints a picture diminishing the role of triggers for most migraineurs.

Individual triggers occurred in 95% of patients, and the top causes indicated were:

  • 80% stress (triggering 33% of attacks)
  • 65% hormones (triggering 25% of attacks)
  • 57% missed meals
  • 53% weather changes
  • 50% sleep disturbance
  • 44% odours
  • 38% alcohol
  • 30% heat
  • 27% foods

So even the top two, stress and hormones, people could only attribute 25-33% of attacks to these.

Differential Diagnosis

Due to the highly variable presentation of  migraine differentiating it from cervicogenic headache an tension type headache is very challenging. Whilst the classification makes them look like distinctly different, which they need to be for research, in reality there’s significant overlap – many start with TTH and might stay that way or progress and become migraine. If your cervicogenic headache is ‘unilateral on both sides’ there is nothing that will distinguish it from tension type headache.

The only way to know is to test the upper cervical spine for sources of pain. Can we reproduce familiar headpain with palpation of structures in the upper cervical spine, and does treating these structures result in a significant and lasting change in headache presentation.

Migraine consist of recurrent attacks. The first presentations, or sudden changes in ‘typical presentation’ can be very concerning and require medical assessment to rule out sinister pathology such as:

Dissecting aneurysm – vertebral and internal carotid arteries

Important to exclude with acute onset headache with a severe neck pain that will be described like a tearing/fearful pain unlike any neck pain they have experienced before. Inappropriate treatment (spinal manipulation) of these patients can be catastrophic, whereas early diagnosis and detection can avert development of cerebrovascular symptoms.

Brain Tumour

Headache and nausea can be an early and sometimes only symptom which is why any new presentation of headache or migraine should always be investigated. By their nature these are progressive and as different parts of the brain become affected we see seizures, loss of strength and sensation. As a collective with a deteriorating picture these symptoms are cause for concern. Primary headache will tend to present in a very similar way for long periods of time, with a natural history of becoming more intense and more frequent over time. Any sudden change in symptoms with your headache should be investigated (new onset vomiting, numbness, weakness).

Posterior fossa lesions

this incorporates things like tumours, meningiomas, astrocytomas, medulloblastomas etc. Space occupying lesions of the posterior fossa will compress the dura which in the posterior fossa is innervated by the upper cervical nerves. Symptoms occur very early and can include drowsiness, headache, imbalance, ataxia (due to cerebellar involvement), nausea and neck pain.


the onset of a sudden high fever with a stiff neck and severe headache that is different to any headache they have experienced before, nausea and or vomiting, seizures, sleepiness, confusion.

Sub-Arachnoid Haemorrhage (SAH)

Rapid onset escalating to severe extremely quickly. For most migraineurs and primary headache suffers, unless they wake with pain there is a build up from mild/moderate pain to more intense, and a familiar quality, location and associated symptoms. Any ‘new’ pain or sudden deviation from your ‘usual pattern’ either in pain location, intensity or duration should be investigated by your doctor.

Temporal (Giant Cell) Arteritis

Important to exclude with an onset of new headache above the age of 40 years old, unilateral and side-locked pain in the temple with the temporal artery palpable and sore. Constitutes an emergency as blood flow can be impacted to the retina and permanent vision loss can occur.

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