What We Know About Migraines

Author: Bryan Lang, PT, DPT, MHA, CSCS, Cert.DN: Doctor of Physical Therapy, Business Owner, Associate Professor, and Blog Contributor. Explores common client questions, helps find solutions for every day functional health concerns, and interprets difficult theories in healthcare rehabilitation. Committed to life-long learning and education. Learn more about Bryan on Google+.

There has been a lot of discussion about migraines over the last few years. Quite frankly, the main theory as to how migraines are caused has been turned upside down. Now researchers are looking at different mechanisms that they believe could be the cause of a migraine and are working on new forms of therapies to combat this crippling issue.

The facts:

  • Migraines are the 19th greatest cause of years lived with disability

  • 12% of the US has migraines (equates to 37 million people)

  • Prevalence age is 12-40 years old

  • There are a greater number of whites who experience migraines than blacks.

Definition of migraine headaches without aura:

  • Recurrent headache attacks lasting 4-72 hours. Unilateral location, pulsating quality, moderate or severe pain intensity. Aggravation causing avoidance to physical activity and association with nausea and vomiting, photophobia and phonophobia.

Diagnostic Criteria:

  • At least 5 attacks

  • Headaches lasting 4-72 hours

  • At least two of the following characteristics

    • Unilateral location

    • pulsating quality

    • moderate or severe pain intensity

    • aggravation by or causing avoidance with physical activity (eg, walking or climbing stairs)

  • During headaches at least one of the following

    • Nausea and/or vomiting

    • photophobia and phonophobia

  • Not attributed to another disorder

Definition of migraines with aura:

Recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually develop over a 5-20 minute period and lasts for less than 60 minutes. Headaches with the features of migraines without aura usually follows the aura symptoms. Less commonly, headache lacks migrainous features or is completely absent.

Diagnostic criteria

  • At least 2 attacks

    • lasting 4-72 hours

  • Migraine aura with the following symptoms

    • lasting 4-72 hour

    • Unilateral location

    • pulsating quality

    • moderate or severe pain intensity

    • aggravation by or causing avoidance with physical activity (eg, walking or climbing stairs)

  • Not attributed to another disorder

Why is it so hard to figure out what causes a migraine? Maybe it has to do with the extensive list as to what can cause headaches in the first place. Take a look at the list below and you’ll see that there are actually 13 types of headaches.

Primary headaches


Tension-Type Headache

Cluster headache and other trigeminal autonomic cephalalgias

Secondary headaches

Headaches attributed to head and/or neck trauma

Headaches attributed to cranial or vertical intracranial disorder

Headaches attributed to non-vascular intracranial disorder

Headaches attributed to a substance or its withdrawal

Headaches attributed to infection

Headaches attributed to disorder of homeostasis

Headache or facial pain attributed to disorder of the cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial structures

Headache attributed to psychiatric disorder

Cranial neuralgias, central and primary facial pain and other headaches

Cranial neuralgias and ventral causes for facial pain

Other headache, cranial neuralgia, central or primary facial pain.


For researchers and medical providers, part of the frustration with headaches has been trying delve into not only what causes a migraine, but if the symptoms a person is experiencing are truly caused by a migraine or by one of the other impairments that cause headache symptoms.

What was the old theory of how migraines were caused?

The oldest theory to how migraines develop has to do with meningeal blood vessels. An event (some kind of stress) triggers the blood vessels to change. Either they constrict and produce an aura, or they dilate and produce pain. The major flaw with this theory is that the location where the vessels are dilating or constricting isn't in the same area of the brain that would produce an aura. This has lead researchers to challenge the old theory. Instead, they believe that the change in blood vessels (either constricting or dilating) is something that occurs with a migraine, but does not appear to be the primary mechanism as to why they occur. 

The new theories:

There are two new theories as to how migraines develop. I am going to spend most of my time on the Neurogenic Theory, because I feel it has the most evidence to be the main culprit. 

  • Theory 1 – The Neurogenic Theory (in a nutshell)

Symptoms occur because of something called cortico-spreading depression, which occurs in the occipital cortex of the brain. Cortico-spreading excitation/activation starts everything in the back of the brain (occipital cortex) which then leads to cortico-spreading depression. So, imagine a wave of excitation, followed by a wave of depression going from the back of the brain, to the front. The waves that occur in the brain directly relate to the aura (visual area in the brain). Then the spread goes to the somatosensory cortex which results in the experience of pain. Cortico-spreading depression is behind the wave of activity causes the aura and pain, but excitation starts it.

How is this system activated?

2 primary modes of activation

Nerves start to fire in synchronicity in the occipital cortex which kicks off the depression. It has an effect on the vessels inside, rather than outside, of the brain, dura, pia, arachnoid, and meninges. As the excitation and depression move forward, it starts to add inflammation to the meninges vessels, which causes massive vasodilation. The trigeminal nerve, or more specifically, the trigeminal cervical nucleus (TCN), is responsible for reporting pain associated with the meninges and the meningeal vessels.

Inside the trigeminal nucleus, release of  calcitonin gene-related peptide (CGRP) and substance P gets the trigeminal nucleus excited, which goes to the thalamus and the somatosensory cortex that tells you that you have pain.

  • Theory 2 - Periaqueductal grey, nucleus raphe magnum, and locus coeruleus hypoactivation

 This theory  involves three areas of the brain: the periaqueductal gray,  nucleus raphe magnum, and locus coeruleus. When these are hypoactive, it kicks off the cortico-sensory excitation and depression in the occiput. This system creates the cascade that then produces pain. 

What medications help with migraines?

The primary migraine medication used is Triptans, which are serotonin agonist. They have an effect on the meningeal blood vessels and both the peptides CGRP and substance P discussed earlier. Triptans cause massive vasoconstriction of meninges vessels and block CGRP production in the trigeminal cervical nucleus (TCN). 

Other medications that are used block neurons in the brain that connect with glial cells. They also block calcium flow to restrict the excitation discussed in Theory 1 - The Neurogenic Theory. 

The main problem with these medications is that they do not fix the underlying problem. They only help with the secondary processes that occur after the problem has already occurred. That's why migraine medication isn't always effective and also why it can take awhile before medical professionals can find the right medication for each person. In the Neurogenic Theory of how migraines start, it's the cortico-spreading depression that kicks off the whole episode. Until a medication is created to address this first response, medication will not be able to cure migraines for good. 

How can physical therapy help?

I’m going to try to make this very simple; physical therapy will NOT cure migraines. If it could, migraines would be a thing of the past. However, it can cure a headache that has migraine-like symptoms (that could have been diagnosed as a migraine but really isn’t), or it could decrease the frequency of headaches for someone who has migraines. The way PT can help has to do with the fact that issues coming from the neck can send pain signals into the head that can mimic a headache.

The exact mechanism is a little tricky. In our brain-stem, we have something called the Trigeminal Cervical Nucleus or TCN. All of the sensory information from the face, including touch-position and pain-temperature, is sent to this trigeminal nucleus. It extends from the brain-stem, into the mid-brain, to the medulla, and eventually crosses into the cervical spinal cord. Once in the cervical spinal cord, the TCN blends in with the dorsal horn cells of the spinal cord.

Let’s break that down a little. Imagine the TCN as a red string. This red string is responsible for collecting all sensory information from the face and sending it to the brain. The string starts at the bottom of the brain, and goes downward into the spinal cord. When it hits the spinal cord, imagine a white string is now woven into the red string. This is how the TCN merges into the dorsal horn cells of the spinal cord. This white string represents dorsal horn cells.


What do dorsal horn cells do? The dorsal horns are responsible for pain information from the periphery to the central nervous system. In other words, when pain receptors go off in areas distant to the spinal cord or brain, it’s the dorsal horn (the white string) that relays the information to the brain so it can process whether to tell your body that there is truly pain or not in that area.


What do the dorsal horn cells and the TCN have to do with each other? The dorsal horn cells (white string) tells your body about pain from places other than along the spinal cord. The TCN (red string) collects pain sensations from the face. Remember that the two strings wrap around each other in the spinal cord. Where do they come together? They come together at C1-C3 in your cervical vertebrae (the upper part of your neck).


What does all of this mean? It means that, if there is something off in your upper neck that is causing pain, the dorsal horn cells will pick it up, however it will also relay the information into the TCN. If the response is strong enough, your brain will not only send a response back that makes you feel neck pain, but it can also give you a headache. A headache that seems extremely similar to a migraine. It’s similar because a migraine goes into the same sensory pathway as pain coming from your neck (the TCN).


What nerves are part of this process? There are many nerves that innervate the neck and face, but there are some in particular that we believe play a greater role in the sensation of facial pain. The trigeminal nerve is responsible for most of the sensory information in the face. However, afferents (the part of your nerves that send messages up into your brain) from the facial, glossopharengeal, and vegas nerves send sensations from the mouth, ear, and meninges to the TCN.


Back to the first question, how can physical therapy help? We know that the TCN plays a big role in sensory processing and is a factor with neck pain and headaches. Physical therapy, through the use of massage, manipulation, exercise, and dry needling, can help relieve structures in the neck and face that could be sending excessive sensory signals to the TCN. Once the sensation is less in this area of the brain, headaches and neck pain will start to dissipate. Remember, if a headache is truly from a migraine, physical therapy will not cure it. However, with all other headaches caused by an accumulation of neck and face pain from stiff joints, tight muscles, and muscle weakness, physical therapy can be extremely helpful.


In summary...

We are learning much more about how migraines originate, but we're still not at a point where we can actually focus treatments on preventing migraines from happening. We're still trying to treat migraines after they have already started. Physical therapy can help with decreasing the frequency of migraines through treating secondary factors that can create a cascade that facilitates a migraine.