My business partner for years has suffered from migraines.  From that situation alone, I could attest to the debilitating effects of the malady.  The fact that 10% of Americans (some 36 million people) also suffer means that many, many days of productive life are affected.   And, most of those folks- and more importantly- most of everyone else has the wrong impressions about migraine.

It is NOT a bad headache- at least in the terms of the way we think about headaches.  Oh, yes, it hurts.  Oh, yes, it’s in the head, but the causes and how it operates is vastly different from the occasional headache that most of us encounter.  (Here’s my blog about headaches.)  Migraines have nothing to do with tyramine.

Migraines are brain disorders; they are not a disorder of the blood vessels.  But, it was considered a headache because the pain can be on one side- or both lateral portions- of the brain.  And, because migraines were previously (for some three centuries) considered disorders of the blood vessels, the wrong drugs (or at least drugs inappropriate for the true causes) were offered to the sufferers; which led to haphazard relief, at best.   Those suffering migraines are thrice as likely to suffer depression, anxiety or bipolar illness, 6-16 times more likely to develop brain lesions, and twice as likely to suffer an ischemic stroke as non-sufferers.

Migraines are genetically inherited (at least 5 different mutations, about a dozen genetic variants).   They are not stress-related (even though many trained neurologists will so state.) Migraines are caused by sensitizations within the brain or hyperexcitability of various neural networks.  These facts mean that while there is a pain in the head, there are various neurological abnormalities occurring as part of the migraine experience, that the headache- while severe- may be the least important biological effect.   Saying the pain is the most important thing is akin to treating the pain one feels from a severed artery with an aspirin, without attempting to repair the artery.

Those suffering from migraines demonstrate a panoply of symptoms- they can’t speak, they can’t understand concepts like they did yesterday, they can’t remember, they can’t concentrate.  But, while they are suffering these symptoms, a standard MRI (magnetic resonance imaging) scan will not typically detect any disorder from the day before.  Because the malady is related to the abnormal function or structure within the brain, both an anatomy and chemistry exists that describes migraines.

No, it takes a functional MRI or PET (Positron Emission Tomography) scan to discern the migraine malady. A series (called a cascade) of neurotransmitter changes activate the pain centers of the body.  The brain centers (light, noise, pain, emotion) that deal with and process sensory information are those that are activated during migraines.  But, more importantly, these centers are activated when there is NO migraine attack.  The brain of one who suffers migraines does not routinely process sensory data in a “normal” fashion.  The networks are abnormally excited- even between attacks.

There can be up to four phases of a migraine.  The premonitory or prodome phase, aurae (not always present), the attack itself, and the postdome phase. One of the differing characteristics of migraine from a “normal” head ache (note how I used two different words there) is the premonitory phase, the inkling that a migraine is coming, exists a day or two prior to the arrival of the migraine.  It can be excessive yawning, a shift in moods, changes in appetite (decreased appetite, food cravings), excessive sensitivity to light or sound, fatigue (drowsiness) or thirst.  The aurae occur in some 20% of sufferers, bright or shimmering lights or shapes at the vision periphery (called positive aurae) or dark holes, blind spots, tunnel vision (negative aurae). The attack can last from 4 hours to three days, with headache, physical pain in the body, nausea, and extreme sensitivity to the environment all potential maladies.  And, then, after the pain subsides, the patient is exhausted and/or “foggy” for a while (the postdome stage).

From:  Dodick & Gargus.  Why Migraines Strike. Scientific American.  August 2008

Migraine pain can be considered cortical or brain stem related.   The cortical version involves hypersensitive neurons in the cortex that induces aurae and pain; this depression releases neurotransmitters that activate the trigeminal nerves, that send pain signals to the sensory cortex and brain stem. The brain-stem scenario involves the raphe nucleus, locus coeruleus, and periaqueductal gray portions of the brain stem behaving abnormally that triggers depression in the cortex (which then follows the pathway above); the brain stem can also activate the sensory cortex itself.

There are a few treatments.  One of the more radical ones is the administration of botulism toxin to the scalp, the temple, the eyebrows.  Which seems to deaden the sensory portions of the nerves.  This process (which acts on the trigeminal nerve) lasts about 3 months.  Another approach is to administer triptans (tryptamine-based drugs) for the acute treatment of migraine pain, the single class of drugs developed over the last half-century to treat migraines (but not approved until 1991).  While they were thought to constrict blood vessels, they actually act by binding to the nerve endings and may even enter the brain, shutting the transmissions of pain down.   A newer approach is to administer Verapamil, a calcium channel blocker.  (It has been reported that using over-the-counter medications like vitamin B2 and magnesium- in way higher than normal dosages- works for some migraine sufferers.)

For those interested in more information, I recommend reading this (technical) document (American Headache Society/American Academy of Neurology)  with updated (2012) guidelines for migraine sufferers.   You should at least glance at the tables and graphs in the document; you will glean much useful tidbits.

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