September 23, 2009

The migraine headache

Our recent understanding of the anatomy of headaches could lead to new treatments. One debated scenario is that a spreading depression wave causes the pain by releasing substances that activate pain-sensitive nerve fibers

Today, I ordered a human brain anatomy model. I had to choose from over two dozen models. The simplest version would have sufficed to demonstrate the migraine wave patterns propagating on the surface of the brain. I decided to go for the deluxe brain. Who wouldn't?

While waiting for my new deluxe brain, I thought it is a nice idea to kill time and explain where according to current hypotheses the roots of migraine headaches are. In fact, I really chose the deluxe version, because I need the add-on stuff like the arteries and the opened head base to explain to my physics students the pathway and anatomy of migraine headaches.

Usually, I do not talk about headache although I work in migraine research now for almost 18 years. No wonder, a safe bet is that I will be asked after a conference talk: What about the headache?

Well, I'm interested in pattern formation in brain tissue related to migraine. Neither gray nor white matter can hurt, simply because brain tissue lacks pain-sensitive nerve fibers. So I may open my talk mentioning that headache is a symptom while migraine is a disease and therefore one should not say migraine is a headache, but that is all. Unless being asked explicitly.

But our recent understanding of the anatomy of headaches suggests that these pattern formation processes that I study, that is, a reaction-diffusion wave called spreading depression causes the pain by releasing substances that then activate pain-sensitive nerve fibers in the brainstem. So finally I got interested.

Lithograph plate of the trigeminal nerve. This nerve is sends sensory information from the face to the brainstem. From Henry Gray's Anatomy of the Human Body

All sensory information from the face, that is, also pain, is sent to a sort of relay station, the trigeminal nucleus. It extends throughout the entire brainstem. During a migraine, this nucleus gets abnormally activated, which eventually causes the pain. Firstly, neurotransmitters are released from the spreading depression wave in the cortex. This in turn will activate the trigenimal network. Signals from the trigenimal nucleus will then be send upwards along the remaining pain pathway. They pass through another relay station, the thalamus before they finally reach their destination, the sensory cortex. There, the sensation of pain is created. As a consequence, if we could stop the wave process, which is believed to be at the start of this cascade, we also stop the headache.

A second scenario says that actually the brainstem causes both, the spreading depression wave and the pain. The pain is either activated by the induced spreading depression wave, as described above, or the brainstem could independently trigger the pathway to the sensory cortex.

It remains to be seen in which direction this debate is going. It will probably not be quickly decided. So my physics students have some time to learn anatomy, once my deluxe brain arrived.


  1. Hi, Markus! This is a challenge to understand... So why would the pain start in the face (and we don't feel it there)and move to the nerves in the brain?

    Do we feel the spreading wave - is it part of the prodrome phase and what I call the 'foggy-head'? Is it a pulsating wave that then causes the nerve inflammation and pain?

    I want a new deluxe brain! One without migraine, that is. :)