medwireNews: Counter to a common hypothesis for the cause of migraine, a study finds that extracranial dilation of arteries is not associated with spontaneous migraine attacks.
Furthermore, sumatriptan relieves migraine pain in parallel with constriction of normal caliber extracerebral arteries while having no effect on dilated cerebral arteries.
"We detected no evidence of dilation of extracranial arteries on the pain side. We know of no other study to provide stronger evidence that extracranial arterial vasodilation might not be a major source of head pain in migraine," write Messoud Ashina (University of Copenhagen, Denmark) and colleagues in The Lancet Neurology.
Ashina and team conducted magnetic resonance angiography on 19 women during spontaneous unilateral migraine attacks without aura at the Danish Headache Center. The patients had a median age of 33 years, median disease duration of 16 years, and median attack frequency of three per month. The majority (79%) had exclusively unilateral pain.
The researchers tested for differences in arterial circumferences between attack and attack-free days, and between the side that experienced migraines versus the other that remained painless.
There was no significant dilation of the extracranial arteries - the external carotid, superficial temporal, and the middle meningeal - on the painful side during an attack versus attack-free days.
Nor were there any side-to-side differences on attack-free days. Additionally, there were no differences in respiratory frequency or end-tidal tension of carbon dioxide between attack days and attack-free days between during the attack scan and after sumatriptan administration.
With regard to intracranial arteries, a significant bilateral increase in the circumference of the middle cerebral artery (MCA) and the cavernous part of the internal carotid artery (ICA) occurred during an attack, compared with attack-free days. The circumference of the cerebral part of the ICA significantly increased only on the pain side in this instance while basilar artery circumference did not change.
Furthermore, a significantly larger MCA, cerebral ICA, and cavernous ICA circumference occurred in the pain side during a migraine attack.
Sumatriptan caused large circumference reductions in all the exracranial arteries and extracerebral cavernous ICA on both sides.
"Our findings indicate that extracranial arterial dilatation is not a clinically relevant cause of lateralized migraine pain, but suggest that the pain is associated with an ipsilateral intracranial arterial dilatation," conclude the authors.
"Future migraine research should focus on the peripheral and central pain pathways rather than simple arterial dilatation."
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