Pinpointing the Origins of Migraine in the Brain

By Neuroskeptic | May 22, 2016 4:51 am

Migraines are a very unpleasant variety of headaches, often associated with other symptoms such as nausea, vomiting, photophobia (aversion to light) and visual disturbances. Hundreds of millions of people around the world suffer regular migraines, but their brain basis remains largely unclear.

Now a new paper reports that the origin of migraines may have been pinpointed – in the brain of one sufferer, at least. German neuroscientists Laura H. Schulte and Arne May used fMRI to record brain activity in one migraine sufferer, a woman, who was scanned once per day for 30 days straight.

During the month of the study, the patient suffered three migraines, lasting one or two days each. She chose not to take any medications during the study period. To evoke brain activity, Schulte and May exposed the patient to a small amount of ammonia vapor, a painful and unpleasant stimulus.

Schulte and May found that on the day before a migraine struck (i.e. the ‘preictal’ or prodromal phase) evoked neural activity in the hypothalmus was higher, and functional connectivity between the hypothalamus and the brainstem was increased. During the migraine itself (the ‘ictal’ phase), hyperactivity was seen in an area of the brainstem called the dorsal pons.

These results are interesting because the dorsal pons has previously been found to be hyperactive during migraine. It’s been dubbed the brain’s “migraine generator”. Schulte and May’s data suggest that this is not entirely true – rather, it looks like the hypothalamus may be the true generator of migraine, while the brainstem could be a downstream mediator of the disorder.

migraine_fmriSchulte and May say that a hypothalamic origin of migraines would help to explain some of the symptoms of the disorder, such as changes in appetite, that often accompany the headaches. This is because the hypothalamus is well known for its role in regulation of eating and drinking.

This is a unique study in the field because of its intensive scanning schedule of a single individual (although it’s not quite as many scans as Russ Poldrack had). That’s also it’s weakness, though: it remains to be seen whether these results hold up in other migraineurs.

The authors conclude that

The main finding of this study is that the hypothalamus, depending on the state of the migraine cycle, exhibits an altered functional coupling with the spinal trigeminal nuclei and the region of the dorsal rostral pons.

More specifically, the hypothalamus is significantly more active within the last 24 hours preceding the onset of migraine pain and shows the greatest functional coupling with the spinal trigeminal nuclei, whereas during the ictal state, the hypothalamus is functionally coupled with the dorsal rostral pons, an area that was previously coined ‘the migraine generator’…

In conclusion, our data suggest the hypothalamus to be the primary generator of migraine attacks which, due to specific interactions with specific areas in the higher and lower brainstem, could alter the activity levels of the key regions of migraine pathophysiology.

Then again, Schulte and May don’t address the question of why the hypothalamus triggers migraines in some people, or what causes migraines to occur on particular days and not others.

ResearchBlogging.orgSchulte LH, & May A (2016). The migraine generator revisited: continuous scanning of the migraine cycle over 30 days and three spontaneous attacks. Brain : a journal of neurology PMID: 27190019

CATEGORIZED UNDER: fMRI, papers, select, Top Posts
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  • JDavidP

    This is all well and good as far as it goes. The research’s full worth cannot be assessed until it leads to reliable available preventive treatment. It might be invaluable. It might be worthless. Continue the work.

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  • Dane Parker

    As a migraineur myself, I’m a little skeptical (even if my skepticism is not insurmountable) with this proposed day-before initialization hypothesis. I have identified a common denominator with virtually all my migraines in the form of a drop (but not increase) in barometric pressure of more than 5 hPa in well *under* a 24-hour period–that is, in far less than a day’s time (i.e., 6-12 hours). Again, one could propose workarounds–like, some people’s hypothalamic hyperactivity doesn’t HAVE to take that long (perhaps no time at all?) to trigger a migraine; or, perhaps my hypothalamus in fact has been active prior to the drops in barometric pressure triggering my migraines and I just don’t know that this is what’s happening. But even in the latter case, it seems a rather odd thing to say that hypothalamic activity of a certain type is triggering my migraines, but not if there isn’t a drop in barometric pressure. Such an exception feels like a loss of fidelity in seeking a neurological explanation of migraines.

    • Regret

      As I cannot read the paper at the link, and no reference is made in this blog post, I don’t know if data other than the fMRI scans, such as environmental triggers, were also captured in this study. It would be interesting to know, if anyone has access to the study. [I had migraines from my mid-teens to my mid-thirties and concur that changes in the weather were one of my triggers. I also saw a pattern of food triggers, as have been reported by other sufferers. My teenage son now has migraines.]

      • http://blogs.discovermagazine.com/neuroskeptic/ Neuroskeptic

        In this paper they didn’t examine any environmental factors.

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  • J. Kevin Dix

    Most of the migraine sufferers I know mention a change in the weather (such as a drop in barometric pressure) as a trigger, but I wonder if every pressure drop leads to a migraine or only those which coincide with this hypothalamic activity. The triggers that sufferers are aware of may be necessary, but not sufficient, to cause an attack.

    • Dane Parker

      That’s certainly possible. Again, I’d stress my use of the term “common denominator” for the BP factor. After all, whatever is or isn’t happening neurologically, there are typically other environmental factors involved in triggering my migraines. Namely, a change in temperature as well as weather conditions (other than BP). Allergens are also frequently involved. But these other factors are additive and need not be present in every migraine.The drop in BP seems to be the only pervasive one, AFAIK.

      Having said that, I can only speak for my own migraines, which are highly episodic and sharply acute in both duration and pain; they are not chronic. So I also have to wonder, given there are significant differences in how migraines are often experienced by different migraineurs (and not just with regard to pain–but in the presence or absence of auras and other visual or bodily disturbances) might it be significant that researchers also account for the type and nature of the migraines that are being studied and about which such conclusions are being drawn?

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Neuroskeptic is a British neuroscientist who takes a skeptical look at his own field, and beyond. His blog offers a look at the latest developments in neuroscience, psychiatry and psychology through a critical lens.

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