What We Know (And Don’t Know) About Headaches

Robert Cowan, MD • January 17, 2012

Today we know much more about why we get headaches, how to prevent them, and how to treat them when they break through our defenses than we did twenty years ago. We know that migraine is a genetic disease with a clear (if incompletely understood) biological basis. You inherit migraine from your parents, or someone in an earlier generation. We know that migraine is a chronic condition, which does not mean the patient always has a headache, but that they are always susceptible to getting one, just as an asthmatic is always susceptible to an asthma attack. We know there is more to migraine than just head pain. Because it affects many parts of the brain, it cause all sorts of problems in addition to pain. And we are starting to understand the connections between headache and other symptoms that headache sufferers experience. We also have a much better understanding of what triggers, worsens, improves and treats migraine. We have several good medicines that are not simply painkillers, but that specifically work on the migraine process. And did you know that pain medication is usually not good for migraine, but may well make it worse and increase the frequency of your headaches? That condition is called medication overuse headache, and used to be called rebound headache.
But there is still a lot we don’t know. We don’t know if migraines start in the cortex (the “thinking” part of the brain) or if they start in the back of the brain in the brainstem, where “unconscious” processing of information from the environment takes place. We don’t know if people who have an aura or warning before their migraines have a different condition from those of us whose headaches come on without warning. We don’t know why chocolate triggers headache in one patient but not in the next. And we think we know but are not sure if having migraine places you at increased risk for other medical conditions like heart attack, and particularly neurological ones like stroke. Migraine is a very complicated puzzle. But it is a puzzle that is coming together in an exciting and more understandable way.
From the 1940’s until the 1990’s, the scientific underpinnings of migraine did not change much. With the introduction of sumatriptan in 1993 and the ensuing infusion of money from pharmaceutical companies, an explosion in research funding followed and, as a result, our understanding of and ability to care for migraine changed dramatically.
Today, we have an awareness of the basic pathophysiology or scientific causes of migraine that simply did not exist a generation ago. Drugs currently in development could revolutionize our current rescue and prevention strategies. We are learning about the microenvironment of the brain and its interactions with the outside world and the rest of the body. Even our understanding of migraine pain has become much more sophisticated. We now understand that headache pain proceeds in several distinct phases, each of which can (and should) be addressed differently. Pain begins peripherally in the main nerve that mediates sensation in the head, outside the brain itself , called the trigeminal nerve. It then proceeds deep into into the central nervous system in the brain stem, where, if left unchecked, it eventually becomes a vicious cycle of inflammation and overstimulation. We have a better understanding of how to recognize where in this pain cycle a patient is at any given moment, and how best to break that cycle.
Despite the recent explosion of information, the science of migraine is still in its infancy. Eventually, research will yield information about diet, medication, and genetics that will dramatically improve the lives of those suffering from debilitating migraine.
For example, recent work has shown that migraine has two “stages” and that triptans are effective primarily in the first stage but considerably less so in the second. A phenomenon called “cutaneous allodynia” helps us identify when the first stage is ending and the second stage beginning. Basically, cutaneous allodynia refers to that time in a headache when the skin, scalp, hair and teeth, become very sensitive, and even painful to the touch. For most migraineurs, this occurs between thirty and 120 minutes into a headache and can last for many hours, often beyond the end of the pain phase of the headache. In terms of treatment, this is very helpful information because it:
• Explains why triptans are often not effective if taken late in the headache phase.
• Gives valuable guidance as to when to take a triptan.
• Suggests that other kinds of medications which treat inflammation might be more useful later in a headache.

Another example of recent scientific progress influencing migraine treatment identified a particular prostaglandin found in high concentration in the spinal fluid of migraineurs compared to non-migraineurs. This prostaglandin is associated with sleep. This finding lends insight into the healing magic of sleep for migraineurs and may eventually give us a tool for managing migraine through the manipulation of the prostaglandin pathway. (DO YOU WANT TO MENTION SOME NAMES FOR PEOPLE TO LATCH ON TO?)

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