Essential migraine mechanism discovered
Scientists have identified a key factor in migraine attacks. The discovery of the mechanism may pave the way for improved migraine drugs.
Scientists still know very little about the cause of migraine attacks, but they may now have come a step closer to solving the migraine mystery.
A new Danish study shows that a certain neurotransmitter, whose functions include expanding the body’s blood vessels, can cause migraine attacks in a majority of migraine patients.
The substance binds to a special cell receptor, the PAC1-receptor, and expands migraine patients’ blood vessels over many hours, and that can help provoke migraine attacks, the researchers conclude.
”This knowledge enables us to suggest development of new drugs that specifically block the properties of this substance, and thus prevent migraine attacks,” says the lead author of the study, Faisal Mohammad Amin, MD, who is a PhD student at Copenhagen University and Glostrup Hospital.
This knowledge enables us to suggest development of new drugs that specifically block the properties of this substance, and thus prevent migraine attacks.
Faisal Mohammad Amin
Previous studies have suggested that the body’s natural neurotransmitter PACAP38 can cause migraine attacks in migraine patients. It has been suspected that this was caused by the substance’s ability to expand the blood vessels. However, scientists also know that another similar neurotransmitter, VIP, also causes the same blood vessels to expand, does not trigger migraine attacks.
The research team from the Danish Headache Centre and Department of Neurology, Glostrup Hospital and Copenhagen University set out to explore the cause of this difference.
They found that:
- 16 out of 22 patients had migraine attacks within 24 hours of receiving PACAP38.
- 4 out of the 22 participants had migraine attacks after a dose of VIP.
- 3 out of the 4 participants who had migraine attacks after receiving VIP also had migraine attacks after receiving PACAP38.
The researchers also found that both neurotransmitters expanded the patients’ blood vessels to the same extent, but that PACAP38 had a much greater long-term effect on the blood vessels than VIP. This may be crucial, says Amin:
“The results indicate that the duration of the expansion of the blood vessels could play a role in triggering a migraine attack, and that it can vary from one patient to another how long the expansion needs to take place before it triggers an attack,” he says.
“We have previously shown that it is not the expansion itself that causes pain. We therefore believe that a long-term expansion can irritate the nerve cells surrounding the blood vessels, which then become oversensitive.”
Read the Danish version of this article at videnskab.dk
Translated by: Dann Vinther
- "Investigation of the pathophysiological mechanisms of migraine attacks induced by pituitary adenylate cyclase-activating polypeptide-38", Brain (2014), DOI: 10.1093/brain/awt369