A Heads-up on Migraines: What Causes the Throbbing

August 5, 2013

The current study may help create new pathways for better understanding and developing more effective and more specific medications.

In the field of pain, many tenets that once were accepted as fact have since been disproven. For example, it was a given that low back pain with sciatica was primarily caused by irritation of nerve roots as they exited the spine. Unfortunately, many views like this linger and many patients continue to receive treatments based on them.

Generations of physicians have been educated to understand migraine headaches as a vascular phenomenon that involves dilation of cranial arteries-and this view endures. The efficacy of medications specifically prescribed for migraines-including ergotamine and, more recently, the triptans-has long been considered to be based primarily on their vasoconstrictive actions. However, we know that other medications that aren’t vasoconstrictors, such as the NSAIDs, can be beneficial for many migraine sufferers, so this action doesn’t appear to be a requirement for efficacy.

The vascular theory also has been contradicted by studies demonstrating that vasodilation in itself does not produce migraines in those who don’t suffer from these headaches and that even when a triptan provides relief of migraines there is little connection between the onset of analgesia and vascular changes.1

One common component of migraines has continued to linger in the minds of many as still suggesting that there is a significant vascular component: the throbbing nature of the headaches.

But even here research has demonstrated the apparent fallacy of this association.

If the throbbing is vascular in origin, a correlation between arterial pulse rate and the throbbing pain rate could be reasonably expected. Although it was generally believed that such a correlation was accepted fact, there never was clear evidence to support this. And when research was finally done to examine it specifically, no association between the two was uncovered.2

This raises the interesting question: If the throbbing isn’t vascular in origin, then what is its etiology? A newly published study has attempted to determine what this may be.

Mo and colleagues3 studied a patient who had a history of chronic migraines that had resolved but continued to suffer from the throbbing sensation. Once again they found no association between the throbbing and the arterial pulse rate. What they did find was a distinctive pattern on an electroencephalogram (EEG) that indicated a neurologic etiology for the throbbing rather than a vascular one.

Obviously, as this is only a single case study, further studies need to be done to confirm the findings. Also, there are certain limitations regarding the subject.

This person suffered from migraines without aura. Many headache experts think that this type of migraine may be closer to tension-type headaches than to migraines with aura and, furthermore, that there may actually be many types of headaches with different etiologies under these general headings. Even migraines with aura can be subdivided into multiple subtypes. Although the examination of aura was not a goal of this study, it would be interesting to know the results if a similar one was done on a subject who suffered both aura and throbbing.

Also, the throbbing sensation in this patient was separate from the headache, as it continued after the pain itself resolved, so we don’t know whether the same results would be found if, as many migraine sufferers describe, the pain is throbbing in nature.

EEG changes in migraine sufferers are of special interest because certain anticonvulsants, most notably topiramate and divalproex, can be effective for these headaches. How and why these medications exert their effects on the pain and other aspects of migraines is still the subject of conjecture.

What does all this mean for migraine sufferers? As an accompanying editorial noted, the growing evidence that the vascular theory of migraines does not explain many clinical aspects of them indicates that a focus on developing migraine medications based on their ability to cause vasoconstriction is misguided.4

As many patients with migraines receive limited or no benefit from the currently available medications, there is certainly a need for new alternatives. The current study may help create new pathways for better understanding of the etiology of migraines and developing more effective and more specific medications for treating them.

1. Rahmann A, Wienecke, Hansen JM, et al. Vasoactive intestinal peptide causes marked cephalic vasodilation, but does not induce migraine. Cephalalgia. 2008;28:226-236.
2. Ahn AH. On the temporal relationship between throbbing migraine pain and arterial pulse.Headache. 2010;50:1507-1510.
3. Mo J, Maizels M, Ding M, Ahn AH. Does throbbing pain have a brain signature?Pain. 2013;154:1150-1155.
4. Goadsby PJ. All that is obvious is not clear: what is the origin of throbbing pain in migraine?Pain. 2013;154:970-971.