Panelists describe the changes that happen in the brain during the phases of migraine, reinforcing the biology of this disease that culminates in sensory amplification.
Stephen Silberstein, MD; Peter Goadsby, MBBS; David Dodick, MD; and Stewart Tepper, MD
PUBLISHED December 17, 2018
Stephen Silberstein, MD: What happens in the brain during migraine with or without aura?
Peter Goadsby, MBBS: It says something fundamental about how we think about migraines. It’s like saying migraine is a problem in the brain; we should say that that’s what we currently think. I say it to people all the time that neurologists should study and treat migraine.
We’ve learned a lot about what’s happening in the brain and migraine. We know quite a lot about the earliest phase. The premonitory or the prodrome phase is hours or days before the attack when the sufferer can feel cognitive dysfunction: they can get a little bit moody or become lethargic; they could get cravings for sweet or savory things, urinate more frequently and experience neck discomfort. We know that there are changes in the hot thalamic region and brain stem changes in the mid-brain—probably in the peri-optical gray. There’s also variation in the response of the trigeminal nucleolus to a nociceptive stimulus. We know hours to days beforehand that the brain is changing—indeed it’s part of the attack. It’s been illuminated by brain functional imaging and reinforced by the fact that migraines are a neurologic disease that we can understand. It’s exciting to think that in the brain there’s, for example, changes in the hypothalamic region—increased urination, for example. Or we talk about things like the cravings—appetite stimulation. We start to understand where that biology might be. We understand that there are changes in visual cortex with photophobia, which is not going to surprise a neurologist that the cortex changes. But it reinforces how biological this problem is.
And then finally, we’re starting to even look into the end of the attack—the postdrome phase; we’re starting to see widespread brain and cortical dysfunction during the postdrome when patients will say, “For hours or a day I just feel drained.” As if their brain is turned off. Well guess what? The brain is turned off. But it’s marvelous that we get these insights into these complexities; they’re still vague, but that’s because they’re complex; we’re illuminating that now with brain imaging.
David Dodick, MD: What happens in the brain is it amplifies sensory information that’s coming in. It’s as if migraine is a problem with sensory amplification. The light in here all of a sudden becomes too bright for me, sound becomes too loud, odors become too pungent and noxious, and perhaps nociceptive information that’s continuously traveling into the brain is not registering as pain. Spatial equilibrium may be affected as well: Some people get dizzy or vertiginous during their attacks. When you think about it, migraine is a disorder where the brain is amplifying the sensory information that’s coming into it.
Stewart Tepper, MD: It’s interesting that we have this series of functional imaging studies that show us each aspect of brain change before the attack, during the attack and after the attack at the same time that we have the evolution of preventive agents that probably don’t cross into the brain at all. There must be some interaction between the brain and the periphery that these new drugs are stopping. I know trigeminal ganglion counts, but I’m thinking they’re not getting into the brain. If they’re not, then you’re able to stop this process peripherally while the brain itself is changing—presumably, underneath it.
Stephen Silberstein, MD: Why, in a patient with a severe migraine attack, does doing an occipital nerve block turn the process off? Think about it. The occipital nerve is not the distribution of the pain—it’s not part of the trigeminal nerve. I think what David said is correct: There are centers in the brain that amplify noise. If you stimulate the nerve that’s recording from the brain stem and you stimulate to the superior sagittal sinus, you cut information off. The problem is we’re creating a wall between the inside and the outside of the brain when it’s one system that interacts.
David Dodick, MD: Constantly.
Stephen Silberstein, MD: Constantly. And I think we can affect the system at multiple points if we lessen input to the brain. If we modify the way the brain responds, we can’t say it’s A or B—it’s both.