Migraine

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.)¹  who first described a number of the non-headache features of migraine including:

Aura:

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 – Neurologist² 

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 – Neurologist² .

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.³ .

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 aura⁴  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.