Migraines and the Hypothalamus, Part Two: From an Ancient Place

Migraine and Hypothalamus Part TwoSparkling, half moon shaped objects. Expanding radiant blobs. Tingling fingers and lips. Even garbled words and sentences.

This is the stuff of migraine auras, those bizarre, temporary neurological disturbances that often precede your throbbing head pain.

People have been documenting their auras for nearly a millenia, though it’s likely we humans have been experiencing them for even longer. And for most of that time, they remained a great mystery. It’s only been within the last century that we even began to have a clue as to what they were all about.

Cortical spreading depression (or just “spreading depression”). That’s the technical term we now use to describe what’s going on inside the brain during a migraine aura. First described by Aristides Leao in 1944, it’s an expanding area of reduced neuronal activity – it starts small in a remote corner of the brain, then spreads out at a predictable rate to adjacent parts. And that depressed brain activity leads to deficits or distortions in neurological function – a.k.a “auras”.

Fortunately, spreading depression typically burns out in about 20-45 minutes. And it takes the aura with it.

As it turns out, this peculiar phenomenon isn’t just limited to humans. Poke a blunt object at the brain of a rabbit, cat, monkey, or rat, and the same thing happens. In fact, it’s a mechanism that, so far as we can tell, can be elicited in every mammal. As well as in birds and frogs.

This would indicate that it’s a feature of our neurobiology that first evolved a very, very long time ago. Our last common mammalian ancestor is thought to have first appeared around 60 million years ago. If we throw in birds and frogs, we have to go a good bit further back.

Suffice it so say then that spreading depression has been with us for a really long time. But we appear to be the only species in whom it’s regularly elicited in the course of everyday life (i.e. as part of a migraine), and the only species in whom it often leads to excruciating cranial pain.

A few of possibilities as to why it exists in the first place:

One is that it’s a mechanism that serves useful some purpose, still providing us with some type of survival advantage. Given that it occurs in response to injury (as well as in response to other stressors like a lack of oxygen), perhaps it has a protective function.

Another is that it evolved many moons ago in a very distant ancestor, conferring some sort of adaptive benefit to that organism, but that now it’s just a vestigial holdover — a relic of our evolutionary past like our appendix or goose bumps.

Or, maybe it’s an epiphenomenon, an intrinsic feature of nervous system physiology, expressed in particular circumstances but of no adaptive significance whatsoever.

The one thing we can be sure of is that it didn’t come about in the service of screaming head pain. And so when it occurs as part of migraine, it’s an aberration (i.e. – occurring in the wrong context, akin to when our “fight or flight” reaction gets turned on by worrisome thoughts, producing a physiologic response intended to help us respond to a survival threat). It’s an aberration that comes from a very old part of our brain, but that appears to have only begun manifesting itself in humans in this manner in the modern era (thanks to our newfangled diets and lifestyles).

But, if we’re looking towards the origins of migraine, to why we get them in the first place, the presence of spreading depression as a feature of migraine physiology offers up some helpful clues. And while the jury is still out on whether it occurs in the course of every single migraine headache (regardless of whether the affected individual experiences an aura), it’s a feature so tightly linked to migraine that a complete theory of migraine origins must account for it.

So, to summarize, here’s what we know about spreading depression

1.  It’s a very early phenomenon in the course of a migraine.

2.  It stems from an old (evolutionarily speaking) part of the brain.

3.  When occurring in the context of migraine, it’s an aberration.

 

That’s all for now – we’ll pick up where we’ve left off here in part 3!

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