Neurologist Messoud Ashina debunks the biggest myth about migraines after 25 years of research… and explains why they can knock you out for 72 hours: “It’s not just a headache”

Migraine can crash into a normal day without warning. One moment you are in class, at work, or stuck in traffic, and the next you are dealing with head pain, nausea, and light sensitivity that can last for days.

A longtime migraine scientist in Copenhagen is urging people to drop one stubborn myth. Professor of neurology Messoud Ashina, who leads the Center for Discoveries in Migraine at the Danish Headache Center and has studied migraine biology for more than 25 years, says the condition is driven by processes deep in the nervous system, not a lack of willpower.

Migraine is not “just a headache”

Many people picture migraine as one-sided head pain with vomiting. He says that stereotype leaves out common symptoms, including light and sound sensitivity and the urge to isolate in a quiet, dark room.

He also points to a detail that can surprise people who have never had an attack. “Just walking to the kitchen for a glass of water or going up the stairs can make it worse,” he said, adding that many attacks force people to lie down and sleep for two or three days.

Old rules can also get in the way of diagnosis. “It can be on both sides,” he said, and nausea or vomiting is not required for it to be migraine.

Why the same “trigger” can fail the next day

Migraine can start on its own, but it can also be linked to internal and external factors, he explains. Hormone shifts are a good example, since some people get attacks around menstruation, but not every cycle.

Alcohol is another familiar story. A glass of wine might be followed by migraine one night, then nothing the next time, even for the same person. So what is going on?

He uses a simple picture. Imagine two buttons that regulate migraine, one that starts an attack and one that shuts it off, while stress, bright light, and other outside factors only matter when the body’s “threshold” is low enough.

The bigger message about blame and lifestyle

That threshold idea matters because it changes how people think about control. Migraine is often framed as a stress problem or a sign of personal weakness, but research keeps pointing back to brain biology that patients cannot simply “snap out of.”

Avoiding every possible trigger can also backfire in real life. “If you tell me all your triggers and I answer ‘don’t do this, don’t eat that, don’t drink that,’ what quality of life do you have left,” he said, “and do I have evidence it works, no.”

Some research suggests the trigger list is not as reliable as it feels in the moment. A 2013 provocation report tested bright or flickering light and strenuous exercise in people who believed those factors reliably caused attacks, yet only a small minority developed migraine afterward.

What today’s treatments actually target

For years, treatment often meant trying general painkillers first and hoping for the best. He describes the arrival of triptans in the early 1990s as a turning point because they were designed to act on migraine mechanisms, not just dull pain.

But he warns that using triptans too often can create a different problem, sometimes called medication overuse headache. When attacks become frequent, clinicians often shift the focus toward prevention, especially for people getting more than a few attacks each month.

That is where newer medicines come in. Some preventive drugs block CGRP, short for calcitonin gene-related peptide, a natural signal that helps carry pain messages and can rise during an attack, and the first of these CGRP-targeting antibodies was reviewed by the U.S. Food and Drug Administration in 2018.

Injections, pills, and what “50 percent” really means

CGRP medicines come in different forms, including lab-made antibodies given as injections and smaller drugs known as gepants that block CGRP signals in another way. In practical terms, the goal is to raise that threshold so attacks are less likely to start.

He says the long-lasting antibodies are part of the appeal. Some doses can work for about four weeks, and in some cases longer, which can matter for people balancing school deadlines, jobs, and family routines.

He also offers a realistic view of results. Preventive treatments can cut attack frequency by about half in just under half of patients, he says, which is meaningful but also a reminder that not everyone responds.

PACAP and the next wave of migraine drugs

CGRP is not the only messenger under the microscope. He has also studied PACAP, another natural signal in the brain that can trigger migraine in some people.

One example is the PACAP-blocking antibody Lu AG09222, which appears in ongoing migraine prevention research on ClinicalTrials.gov. The trial description focuses on adults whose migraines have not been helped enough by other preventive treatments.

He says PACAP medicines are still in clinical testing, and he expects that if studies go well, they could arrive around 2027 or later. The hope is simple, more options for people who did not respond to CGRP medicines or who stop responding over time.

What this could mean for everyday patients

At the end of the day, the shift is about taking migraine seriously as a neurological condition. A 2025 analysis in The Lancet Neurology estimated migraine affects about 14 percent of the global population, which helps explain why it shows up in so many homes and classrooms.

Migraine is also a major driver of disability worldwide, meaning it can steal time from school, work, and relationships even when it is not visible to others.

The core message is that people should not have to carry the blame alone. Migraine may be unpredictable, but understanding the biology behind it is steadily opening new doors for prevention and more individualized care.

The main interview has been published in Illustrerad Vetenskap.