More than just a headache

You have been dealing with headaches for most of your adult life. Sometimes they don’t bother too often, whilst other times it seems to always be in the background, like a rabid dog, just ready to pounce and take you out.

Maybe something happened… an injury,  or a fall. Perhaps increased stress at home or at work…and since then they’ve become insufferable. 

Each episode lasts several hours sometimes for up to days at a time. 

Normal work and activities become much to difficult, and there’s nothing you can do except lay in a corner, or in a closet with a towel over your head waiting for your head to stop feeling like its being pounded by a hammer, about to explode…and you know that even the slightest of moments can cause vomiting and nausea.

Strong medication can sometimes be helpful if you get to it in time. But if you don’t, you simply have to ‘wait it out’.

So why is this happening to YOU? And what can be done about it.

To solve your migraines, we need to answer a few questions

    1. What is a migraine? Is it just a ‘bad headache’?
    2. Why do they keep coming back?
    3. Why are they getting worse?
    4. How do I get rid of them?!

What You Need To Know About Migraines

Migraine is a genetic, neurological condition. The ‘Headache’ is simply one feature of migraine.

Fact #1

1 in 10 people suffer from migraines. Most people THINK that migraines are isolated events - that they just come and go randomly, but once they are gone, they are gone for good….this is not the case!

Fact #2

While most people consider migraines as simply a ‘bad headache’, the reality is that Migraine is NOT ‘just a headache’.

Fact #3

 Even when no headache is present, Migraineures do not function ‘normally’. Migraines may actually be considered a chronic neurological disorder, or ‘illness’.

What Causes Migraines?

Migraines are due to your parents!

No, I don’t mean because they ‘stress you out’ (maybe they do?). Migraines are due to an abnormality excitable brain that is capable of activating the trigeminal system in genetically susceptible people. That means its in your genes (Thanks mom and dad!)…This results in 1) Nasty headaches, but also 2) a slew of autonomic, cognitive, emotional and musculoskeletal issues.

These issues can occur DURING or OUTSIDE of the headache phase.

This is why it is crucial to identify if you have migraine, as it should influence the understanding of your feelings and behaviours even outside of the headache. And it greatly impacts any medical treatment you receive, since migraineures suffer DIFFERENTLY.

You can certainly blame your parents for your Migraine's (they are due to your genetics)...but that doesn't help.
What will help, is understanding WHY they happen, and taking a holistic approach to managing them
Dr. Joe Tanti

Migraineur's Brains are Very Exciting!

The brain of a migraineur is highly excitable.

The majority of neural connections within the brain are inhibitory. They dampen DOWN responses, which helps maintain neurological stability. 

Said another way, we should not over-react or under-react to our environment. Unfortunately this ‘normal’ response does not happen in the migraineur!

Migraine sufferers have alterations in their genetic expression.

This causes unstable brain activity. Meaning that people with migraines tend to both over-react and under-react to environmental conditions. They also have a lower tolerance for sensory stimulus. 

This is even more difficult when you are fatigued and during times of stress. 

Your Neuromodulatory System is Defective if you have Migraine

Some of the lights in my house work on a dimmer switch. The light doesn't just go ‘On’ or ‘off’. I can control how much light is there is. Said another way, I am able to modulate the light. This is similar to how our bodies work…

Normal brain function is greatly dependent upon modulation. We can ramp up, or down the sensitivity of our brain. The major modulatory systems of the brain involve serotonin, dopamine and noradrenaline. The specific groups of neurons (nuclei) in the brainstem for each of these neurotransmitters, and the axons of these neurons travel to multiple areas of the brain and spinal cord to have an influence on the activity of the entire central nervous system. 

In other words, these modulatory pathways determine how responsive our central nervous system is to our environment.

Several modulatory systems have been identified that use serotonin, noradrenaline and dopamine. Serotonin is involved with mood and pain perception. Noradrenaline is involved in selective attention, and dopamine is involved in reward behaviours that determine how we experience pleasure and pain. 

Its important to remember that your genes code for enzymes and receptors that determine how well these systems operate. And we know that these gene products are can be altered in migraineurs. 

So you may be wondering, how does all of this actually lead to the migraine headache? Well, the key to this lies in understanding descending pain inhibition.

Migraines Are Caused By Defective Descending Inhibition of Your Pain System

Migraine sufferers seem to be constantly at the mercy of their own incompetent pain system. I’m not saying that YOUR incompetent…just that your pain system is (sorry to say). 

The periaqueductal grey (PAG) is an area around the central canal of the midbrain (uppermost part of the brainstem just beneath the thalamus). You can think of the PAG as the brain’s pharmacy of endogenous opiates. 

The neurons in this region travel downward to connect onto lower brainstem areas, using opioids as their transmitters. 

This action powerfully stimulates the brain stem regions! Which causes a signal to inhibit the trigeminal nucleus and dorsal horn. 

The result? 

Less pain signals being transferred, and less pain. This is why opioids are so good at inhibiting pain!


The brain keeps a tight control, and our ability to inhibit pain appears to happen in this ‘top down manner’ from the cortex, to the PAG, and then to brainstem nuclei that powerfully restrain the second order neurons from the spinal cord. 

The problem with migraineurs is that they seem to have a dysfunctional opiate system as well, which means that the function of all three levels of that chain are impaired. The result is a state of uncontrolled excitation of the trigeminal nucleus, even in response to normal levels of sensory input.

A water fountain spraying in a lake

Wow this is getting complex! Its easy to see why treating migraines can be so complicated! But there is still more you need to know…

At A Tipping Point

The experience of head pain requires activation of the trigeminal nucleus. This is where the neurons that have sensory inputs from the head and neck are located. 

THIS that is the central deficiency that underpins migraine. When the pain system malfunctions it can wreak havoc. 

Each episode appears to have a point of no return, or tipping point. 

Migraine headaches typically provide an early window during which something can be done to stop the process in its tracks and prevent a more severe episode from winding up. 

However, once this opportunity is missed, even very strong doses of medication seem to have limited effectiveness, and the episode has to run its course. This of course is when an opportune adjustment to the spine in this early window can sometimes stop an attack.

What Is The Tipping Point?

The pain system is doing what it is designed to do - release a load of inflammatory mediators at the site of an assumed tissue injury. However, in migraine there is no tissue injury - but the pain system ‘thinks’ there is one. To understand why, let us review some basics.


Nociception is a protection system that is designed to respond to stimulus that is capable of causing damage. So when there is a threat of tissue injury the nociceptive system needs to activate powerfully to protect you. When enough nociception signals are triggered, this is when we feel pain.

We do not want it active at any other time!  

The key point is that when it comes to any headache, especially migraines 

ALL of the sensory signals from cranial structures (such as meninges and blood cerebral blood vessels) and sensory signals from neck structures converge onto the trigeminal nucleus. 

So, there is a sensory convergence of head and neck inputs onto the trigeminal nucleus (TN)!

When normal pain inhibition from higher brain areas onto the trigeminal nucleus weakens, the second order pain neurons gradually drift closer to firing threshold and the pain pathways become ever more sensitive - a process called central sensitisation

Question Mark person wondering what the answer is

As this weakens further, we reach a point where even normal non-noxious stimulus are enough to generate pain in the head and neck region! 

But it can get even worse…

Once a pain pathway is allowed to activate, the primary sensory neurons respond as if there is tissue injury! 

This causes a release of vasoactive peptides and other mediators of the inflammatory process (such as substance P and calcitonin gene-related peptide CGRP). 

This produces a sterile inflammatory response within the cerebral vasculature, and the vessel wall becomes leaky…provokeing even further sensitisation of the primary afferent neurons and the whole process upregulates even further. 

The sensory neurons start to discharge at even higher rates because they are now truly exposed to local chemical irritation. 

However, the important point to note is that the whole process seems to be initiated by the brain itself in the absence of any peripheral tissue injury.

The origin of the throbbing pain has been the subject of much debate. It is thought that once the trigeminal nucleus starts to discharge strongly up through the thalamus to the cortex, there is a wave-like pattern of firing through thalamic and cortical circuits that produces the throbbing pain quality. This is in contrast to the old theories of vascular pulsation. 

Migraine headache is often described as having a 'tipping point' - aboundary that defines whether the episode can be easily aborted or not. It seems that if analgesic or anti-inflammatory medication is taken during the early windup stage, it may be enough to prevent the central sensitisation of the trigeminal nucleus, and the release of the vasoactive peptides that amplify the process sharply. 

As such, early intervention is the key to acute migraine management.

This needs to be said again…

EARLY intervention is the key to acute migraine management.

The 4 Phases of Migraine Headache



This consists of vague symptoms that may precede a migraine attack by several hours or even days. Symptoms include: malaise, mood changes, food cravings, fatigue and yawning, sensitivity to light and sound, and changes in appetite (to name a few). It is thought that most of these symptoms are associated with increased dopamine activity. If you can identify their prodromal characteristics it you are then able to initiate treatment early and with a greater likelihood of success.


Migraine Headache

This is the part most people are aware of. The migraine headache is typically said to be a unilateral, throbbing head pain lasting 4-72 hours. However, we now know that the headache is commonly not just on one side. The head pain is usually worsened by physical activity (although there are exceptions), and is often accompanied by nausea and sometimes vomiting, sensitivity to light and sound.


Aura (within an hour before attack)

A sensory disturbance occurring just before the headache in around 20% of people. A migraine aura involves focal neurological symptoms that are reversible within approximately one hour of the attack.  These can be visual, include speech disturbances, paraesthesia, numbness or weakness in an arm or leg and confusion.

Spreading cortical depression reduces blood flow in the corresponding neurons and is thought to be responsible for the symptoms of aura. Once the spreading cortical depression has run its course over about 60 minutes, the next phase of migraine begins.



After the headache comes the postdrome. You may feel exhausted and ‘foggy’ for a day or so, and experience many of the symptoms that characterized your initial prodrome. This is also known as the ‘migraine hangover’- Similar to a hangover without the fun part.

How Does The Neck Fit In?

So far I have emphasized the central role of trigeminal sensitisation in migraine, while also introducing the principle of sensory convergence of neck and cranial structures. These two features make it easy to understand how your neck could create a background level of noxious input to your trigeminal system, sufficient to push you closer to the tipping point for a full-blown migraine attack. 

In this way its easy to see that a neck problem may reduce your brains tolerance for other environmental factors, such as stress and tiredness. It could also explain why sometimes migraines can be more intense and frequent after a neck injury, or neck pain.

Interestingly, sometimes neck pain even occur in the absence of a neck injury. In fact, it is thought that for some, neck pain is one of the symptoms of migraine.

This is significant in terms of management. So much so, that studies have shown that this pattern is more likely to respond positively to manual treatment than if the neck pain develops later in the headache process.


Remember, migraineurs do not possess adequate modulatory systems in the brain. This has important implications, as a major system that is also under constant modulation is the autonomic nervous system. One of the structures that plays such a regulatory role is the hypothalamus, which maintains homeostasis by coordinating the endocrine and autonomic nervous systems with behavioural needs. 

Autonomic control also has an important influence upon circadian rhythms, the regulation of arousal and in pain processing. In fact, the hypothalamus has direct connections with the trigeminal nucleus and is known to play a direct role in pain inhibition.

Many patients experience vague symptoms like hunger, thirst, mental weariness, tiredness, yawning and, on some occasions, a sense of oppression, or even a desire to go pee, etc. Given the central role of the hypothalamus in maintaining homeostasis, it is easy to see why it is thought that hypothalamic dysfunction often precedes a migraine attack. 

This could explain vague symptoms in the lead up to a migraine, such as mood changes and food cravings. It could also account for a tendency to suffer from orthostatic hypotension when getting up quickly. 

Remember, those with migraine have functional impairments in neurological function during and between headache episodes.

Unfortunately many people with migraine do not recognize their prodromal symptoms as an early sign of their descent into migraine, largely because they are so vague. 

However, if YOU DO take note a pattern in behaviour or symptoms that reliably indicates the onset of your prodrome …well now you have an opportunity to intervene early and prevent a full-blown episode.

Sympathetic vs Parasympathetic Hypo-Function

The majority of studies seem to indicat a reduced sympathetic responsiveness in those with migraine

Evidence for this includes pupillary hypofunction, orthostatic hypotension, a decreased overshoot in the Valsalva manoeuvre, a low level of plasma norepinephrine and increases pain sensitivity.

Altered parasympathetic activity is also a feature, which can go either way - hyperfunction or hypofunction - depending upon the person. Most commonly there is parasympathetic hyperfunction such as tearing of the eye, yawning and a slow heart rate. The evidence also tends to support hyperactivity of cranial parasympathetic nerves, via the trigeminal-parasympathetic reflex. 

Parasympathetic symptoms such as facial flushing, lacrimation and nasal stuffiness may accompany migraine attacks. The involvement of the parasympathetic system may also cause the well-known vasodilation of meningeal blood vessels. This may be due to activation of different brain areas, especially limbic and hypothalamic regions, that then influence different elements of this system. 


Going for a run would is likely the last thing that you would want to do at the onset of a migraine! BUT.for some this actually helps prevent the episode from developing into a full-blown attack!


  • Exercise is a powerful stimulant for the sympathetic nervous system! It might even be useful in those who demonstrates hypo-sympathetic and hyper-parasympathetic function.
  • I’ve had many headache-suffering patients who comment that drinking water can often help to prevent a mild headache from progressing, presumably because they are 'dehydrated'. 
  • However, we should also note that drinking a large quantity of water will also stimulate the hypothalamus, increasing its activity. It may be that other hypothalamic functions, such as its role in descending inhibition of the trigeminal system, will also improve as a consequence. Perhaps we might therefore advise our patients to drink water at the earliest sign of headache onset.


I have already emphasized that migraineurs have a lower tolerance for environmental stressors, because of central nervous system instability. 

Imagine a 'trigger' as potentially any stimulus that interacts with the nervous system's receptors. This might involve smell, sound, visual stimuli (such as glare or flickering lights), ingested chemicals from food/drink/medicine, emotional stimuli, temperature change and a host of other environmental cues. A well-adapted nervous system will detect, respond and adapt to such change, but migraineurs tend to under or over-react. 

If the stimulus is too great, or there are too many triggers at the same time, then neurological integrity is lost and a migraine episode will ensue. Most individuals will only experience a headache when they have accumulated a number of triggers within a certain timeframe - with only the most sensitive individuals reacting to a single stimulus. 

Therefore, a key part of managing your migraine process is identifying and reducing migraine trigger factors.


When approaching a complex management problem like migraine it is useful to have a very simple principle to guide decision-making. If there was one, it might be this. We could consider all forms of migraine management as either attempting to:

Increase Descending Inhibition of the Trigeminal Nucleus

Migraineurs exhibit poor descending inhibitory control of their trigeminal nucleus. Therefore treatment strategies that assist inhibition can be very useful. These might include the use of chiropractic adjustments, and other manual forces that activate the brainstem pain control pathways. You might also benefit from a multitude of other ancillary management strategies that help to stabilize the brain and maintain effective descending inhibition.

Reduce Noxious Input to the Trigeminal Nucleus

A central aim of migraine management is to identify and reduce triggers that activate the pain pathways. Noxious input from your neck can play such a role, as it drives greater activity in the trigeminal nucleus and can bring you closer to threshold. Manual treatment methods can be helpful in decreasing pain inputs from musculoskeletal tissues and in moving the you further away from this threshold point.


In terms of the migraine headache there is one thing that is very clear. The success of treatment depends on early intervention. Unfortunately, prodromal symptoms may not always be obvious. You may simply feel tired or depressed for a day or two prior to your headache. Maybe you are simply “aware” that you are bordering on a headache episode. If this is the case, then a migraine process may well underpin your problem and you should act early to ensure that the smallest intervention has the greatest effect. 

For example, aspirin or acetaminophen may relieve your headache if you take it early on in the process. This is a keystone of migraine management. 

In addition, a well place adjustment could also achieve enough of an inhibitory burst onto the trigeminal system to do stop the episode, before the headache fully develops. Most often I find using both strategies to be advisable.