Summary
A study1 in mice offers clues about the neurological events that spark migraines. It suggests that a brief brain ‘blackout’ — when neuronal activity shuts down — changes the content of the cerebrospinal fluid. This altered fluid travels through a previously unknown gap in anatomy to nerves in the skull where it activates pain and inflammatory receptors.
Fluid collected shortly after a CSD increased activity of trigeminal nerve cells. This could be triggered from pain signals sent from these activated cells. But the fluid collected 2.5 hours after CSDs didn’t have the same effect.“Whatever is released in the cerebrospinal fluid is degraded. So, it’s a short-lasting phenomenon,” says Nedergaard.
