April 16, 2013
Editor’s Note: This article was provided by our partner, ScienceNordic. The original is here.
Danish researchers have taken a crucial step toward a new explanation of where and why it hurts when we have a migraine.
This throbbing pain in the head, which is usually accompanied by other symptoms such as nausea and sensitivity to light and sound, has been puzzling scientists for centuries.
The new discovery represents a break with the prevailing theory in recent decades:
“This turns on the head our existing ideas of the mechanisms behinds migraines. For many years it was thought that the pain was caused by expanded blood vessels outside the skull,” says Professor Jes Olesen, of The Danish Headache Center (DHC), Glostrup Hospital, Denmark, who co-authored the new study, published in The Lancet Neurology.
“When scans show that the blood vessels do not expand, there must be another reason why the patients get headaches.”
Less Arterial Expansion than Expected
The article is based on experiments designed to identify which arteries expanded during a migraine attack, headed by Faisal Mohammad Amin, a doctor and a PhD student at the DHC.
Using the latest MRI scan technology, Amin examined the inside and outside of the brain and looked at small arteries during natural attacks.
A total of 19 healthy women with migraine took part in the experiment. Their brains were scanned while they suffered a severe migraine headache without aura, headaches that are limited to one side of the head. The scans enabled the researchers to compare the expansions of the blood vessels on the side where the pain was felt with the side where no pain was felt.
“Contrary to what has previously been believed, we found that the arteries on the outside of the skull did not expand during migraine attacks,” says Amin.
“Arteries inside the skull were only slightly expanded on the side where the headache was felt, compared to the other side where no pain was felt.”
Migraine Drugs Don’t Work Like We Thought They Did
The pain-ridden women were then given a popular migraine drug to determine how it affected the arteries.
“We treated the attacks with sumatriptan, which is the most popular migraine drug on the market. And then we made another MRI scan of the brain,” explains Amin.
“Here we observed that the arteries inside the brain remained expanded even after the migraine headache had passed.”
This suggests that the old theory that sumatriptan works by narrowing the arteries may not be right after all. The new findings prepare the ground for studies into why sumatriptan still works even though the beneficial effect does not appear to be linked to the narrowing of arteries.
New Theory: Pain Caused by Extra-Sensitive Nerve Fibres
The new discovery has paved the way for a new theory: migraine pain occurs because the nerve fibres around the blood vessels become extra sensitive.
This means that the blood’s normal pulsation in an artery feels like an intense, throbbing pain. If this is the case, it is as yet uncertain why it is so.
“Our findings are of great importance to our understanding of migraine headaches and future research on migraines,” says Amin.
“At the same time, the findings can also be used to reassure migraine sufferers who worry that their arteries are about to explode during an attack. They’re not.”
Magnetic resonance angiography of intracranial and extracranial arteries in patients with spontaneous migraine without aura: a cross-sectional study
The Lancet Neurology, Volume 12, Issue 5, Pages 454 – 461, May 2013 doi:10.1016/S1474-4422(13)70067-X
Background
Extracranial arterial dilatation has been hypothesised to be the cause of pain in patients who have migraine without aura. To test that hypothesis, we aimed to measure extracranial and intracranial arteries during attacks of migraine without aura.
Methods
In this cross-sectional study, we recruited patients aged 18—60 years from the Danish Headache Centre and via announcements on a Danish website. We did magnetic resonance angiography during spontaneous unilateral migraine attacks. Primary endpoints were difference in circumference of extracranial and intracranial arterial segments comparing attack and attack-free days and the pain and the non-pain side. The extracranial arterial segments measured were the external carotid (ECA), the superficial temporal (STA), the middle meningeal (MMA), and the cervical part of the internal carotid (ICAcervical) arteries. The intracranial arterial segments were the cavernous (ICAcavernous) and cerebral (ICAcerebral) parts of the internal carotid, the middle cerebral (MCA), and the basilar (BA) arteries. This study is registered at Clinicaltrials.gov, number NCT01471314.
Findings
Between Oct 12, 2010, and Feb 8, 2012, we recruited 78 patients, of whom 19 women had a scan during migraine and were included in the final analysis. On migraine compared with non-migraine days, we detected no statistically significant dilatation of the extracranial arteries on the pain side (ECA, mean difference 1·2% [95% CI −5·7 to 8·2] p=0·985, STA 3·6% [—3·7 to 11·0] p=0·532, MMA 1·7% [—1·7 to 5·2] p=0·341, and ICAcervical 2·3% [—0·3 to 4·9] p=0·093); the intracranial arteries were more dilated during attacks (MCA, 13·0% [6·4 to 19·6] p=0·001, ICAcerebral 11·5% [5·6 to 17·3] p=0·0004, and ICAcavernous 11·4% [5·3 to 17·5] p=0·001), except for the BA (1·6% [—2·7 to 5·9] p=0·621). Compared with the non-pain side, during attacks we detected dilatation on the pain side of the intracranial arteries (MCA, mean difference 10·5% [0·7—20·3] p=0·044, ICAcerebral (14·4% [4·6—24·1] p=0·013), and ICAcavernous (9·1% [3·9—14·4] p=0·003) but not of the extracranial arteries (ECA, 2·1% [—3·8 to 9·2] p=0·238, STA, 3·6% [—3·7 to 10·8] p=0·525, MMA, 2·7% [—1·3 to 5·6] p=0·531, and ICAcervical, 5·0% [—0·5 to 10·4] p=0·119).
Interpretation
Migraine pain was not accompanied by extracranial arterial dilatation, and by only slight intracranial dilatation. Future migraine research should focus on the peripheral and central pain pathways rather than simple arterial dilatation.
Funding
University of Copenhagen, the Lundbeck Foundation, the Research Foundation of the Capital Region of Denmark, Danish Council for Independent Research-Medical Sciences, and the Novo Nordisk Foundation.