But migraines are neurological. How could they be neuroplastic?
I think this is one of those questions where two things can sound contradictory when they really aren’t. Migraine is a real neurological disorder with complex biology behind it. We’re talking about changes involving the trigeminal system, brain networks, sensory processing, and other mechanisms that researchers are still working to fully understand. So when I talk about a possible neuroplastic component to migraine, I’m not saying migraines are “just stress,” that you imagined them into existence, or that every migraine could disappear if you simply stopped being afraid of it.
I’m also not speaking about migraines entirely from the outside. Migraines were part of my own years of chronic symptoms, alongside pain, fatigue, and a growing list of diagnoses and things my body supposedly couldn’t handle anymore. At the time, I didn’t divide my symptoms into neat categories of this one is structural, this one is neurological, this one is neuroplastic. They were symptoms. They were miserable. And I wanted them gone. The idea that my brain and nervous system could be contributing to something as physical and consuming as a migraine would once have sounded, at best, confusing.
What I understand differently now is that calling something neurological doesn’t somehow remove the brain and nervous system from the conversation. In fact, migraine research itself has long looked at changes in sensory processing and sensitization. Cutaneous allodynia—the experience of normally harmless things like touching your scalp, brushing your hair, or wearing glasses becoming painful—is common during migraine and is considered a clinical marker of sensitization within the pain-processing system. Research continues to examine central nervous system sensitization in both episodic and chronic migraine.
So I don’t think the most useful question is Are migraines neurological or neuroplastic?
I think it’s: Could neuroplastic processes be contributing to my migraines?
Migraine brains can become very good at anticipating danger
If you’ve had migraines for any length of time, you’ve probably accumulated a mental list of things that are supposedly capable of setting one off. Maybe it’s poor sleep, bright lights, your period, weather changes, stress, exercise, missing a meal, a glass of wine, a particular food, staring at a screen too long, or apparently having the audacity to make plans on a Saturday.
Some of those associations may reflect genuine biological influences on migraine. Hormonal changes, for example, aren’t imaginary because the brain is involved. I would never look at someone’s trigger list and assume that every item on it is simply a learned association.
But I am interested in what happens after you’ve had enough migraines for your brain to start learning the pattern.
Imagine you’ve gotten a migraine after three nights of bad sleep before. You wake up after another terrible night and your first thought is, Oh no. I’m going to get a migraine today. You check your head. Nothing yet. An hour later, there’s a tiny sensation behind your eye. Now you’re really paying attention. Is that pressure? Is the light bothering you more than usual? Should you cancel dinner? Do you have your medication with you? By the time you’ve gotten dressed, a sensation that might otherwise have been background noise has become extremely important.
That doesn’t mean worrying about a migraine simply caused one. Migraine biology is much more complicated than that. But brains are prediction machines, and they learn from repeated experiences. If a particular sensation or circumstance has been followed by a migraine again and again, it makes sense that the brain would start treating that cue as meaningful. A 2025 case series on Pain Reprocessing Therapy and migraine describes this possibility in terms of learned threat associations—harmless internal or external cues, such as hunger, fatigue, or weather changes, becoming associated with danger and potentially contributing to migraine processes.
This is one of the things I find fascinating about neuroplasticity. The brain doesn’t have to consciously decide, Today I shall produce a migraine because the weather app says rain. Learned responses can become automatic. Think about how quickly your mouth waters when you smell something you love cooking, or how your whole body can tense before you’ve even fully registered a sound that startled you. The nervous system is learning and predicting all day long without waiting for our permission.
Pain can become part of that learning too.
Sensitization gives us another piece of the puzzle
If you’ve ever had a migraine where your hair hurt, your glasses suddenly felt unbearable, or touching your face felt painful, you’ve experienced something that pain researchers find particularly interesting. It’s called allodynia, which simply means something that normally wouldn’t hurt is being experienced as painful. Allodynia is common in migraine and is associated with sensitization in the nervous system. One review estimated that cutaneous allodynia occurs in roughly 60% of people with migraine.
I think this is helpful because it demonstrates something that can otherwise be difficult to wrap your head around: the intensity of what we feel isn’t determined only by the intensity of the thing happening to the body. A light touch hasn’t suddenly become physically damaging because you’re having a migraine. The system processing that touch has changed how it responds to it.
So, the sensitivity of the nervous system matters. And once we know that, I become interested in all the other things that can turn that sensitivity up or down.
Does your migraine pattern change when you’re on vacation? Do you tend to get one after a particularly stressful week—or, interestingly, when the stressful week finally ends? Are there triggers that seem incredibly consistent and others that somehow don’t bother you when you’re distracted or having fun? Do you notice a small sensation and immediately know where you believe it’s headed? Have you stopped doing things you enjoy because you’re afraid they’ll trigger an attack?
Those aren’t questions I use to prove someone’s migraines are neuroplastic. They’re questions I use to understand the pattern.
So does PRT work for migraines?
I have personally worked with many clients who have found meaningful relief from migraines using PRT and EAET. As far as research goes, what we have right now is interesting, but early.
In 2025, researchers published the first case series specifically examining PRT for migraine. It followed three people with chronic migraine who had not responded adequately to standard migraine treatments. Their PRT work focused primarily on education about neuroplastic pain and somatic tracking. All three experienced substantial reductions in headache frequency: one went from 18–25 headache days per month to three, another from 30 to five, and the third from 30 migraine days per month to three or four.
What I find especially interesting is that the researchers’ model doesn’t require us to say migraine isn’t neurological. Quite the opposite. They’re asking whether learned threat associations may be one modifiable part of migraine biology. That makes much more sense to me than trying to sort every condition into two boxes labeled REAL MEDICAL PROBLEM and BRAIN THING, as though the brain weren’t part of the body in the first place.
What would I actually do with someone who has migraines?
I wouldn’t start by taking away your migraine medication or announcing that every trigger you’ve identified is fake. I wouldn’t tell you to stare into a bright light while skipping lunch just to prove a point. And I wouldn’t assume that because PRT helped me, your migraine history must work exactly like mine.
I’d want to get curious about your particular pattern.
When did the migraines begin? What was happening around that time? Have they changed over the years? What are you afraid will trigger them? Are there things you used to do without thinking that you now approach very carefully? What happens when you first notice the tiniest sign of one coming? Are there times when a supposed trigger doesn’t trigger anything at all? What does your medical evaluation show, and what has your physician recommended?
We might make an Evidence List, looking at what supports a neuroplastic contribution and what doesn’t. If the evidence makes sense, we can begin working with some of those learned danger associations rather than simply trying to convince you that your head is safe.
Somatic tracking might mean noticing a sensation in your head with curiosity rather than immediately jumping ten steps ahead to I’m getting a migraine, there goes my day. If you’ve become frightened of a particular activity because you believe it triggers migraines, we may eventually explore that association through gradual real-life or imaginative exposure. We might work on the constant body checking that can happen when you’re waiting to see whether a migraine is coming, or practice responding differently to the first little sensation that normally sends your brain into high alert.
And importantly, success wouldn’t mean I did somatic tracking and the sensation disappeared, therefore I did it right. That can very quickly become another form of checking.
Maybe you notice the sensation and it stays. Maybe it gets stronger. Maybe it goes away.
The work is in giving the brain a different experience with it: I can feel this without immediately treating it as proof that something terrible is about to happen.
For some people, I might also become curious about emotions and stress. That doesn’t mean “your migraines are caused by stress.” Stress is one of those words that can become so broad it stops meaning much of anything. I’m more interested in specifics. What happens in your body when you’re angry but don’t feel like you can say anything? When you’re under enormous pressure? When you’re trying to keep everyone else happy? When you’ve been holding everything together for so long that you don’t realize how much effort it’s taking?
Those patterns won’t matter for everyone. If they matter for you, we can work with them. If they don’t, we don’t need to force them into the story.
That’s one of the reasons I like doing this work individually. I’m not treating “migraine.” I’m trying to understand the nervous system of the person sitting in front of me.
You don’t have to choose between neurology and neuroplasticity
I think this is ultimately the distinction I want someone with migraines to leave with.
Migraine is a neurological disorder. You can have a family history of migraine, experience aura, have hormonal influences, respond to migraine medication, and still have neuroplastic processes contributing to the frequency, intensity, or persistence of your symptoms. Those ideas don’t cancel each other out.
And the opposite is important too: having a migraine that gets worse with stress, improves on vacation, or responds to nervous-system work doesn’t prove that every migraine you will ever experience is entirely neuroplastic. New or changing headaches still deserve appropriate medical attention, and there are headache symptoms that absolutely shouldn’t be assumed to be benign or neuroplastic.
What neuroplasticity gives us is another place to look.
For years, when my own body was producing symptom after symptom, I thought my job was to figure out what was wrong with each individual part of me. There was always another symptom to analyze, another possible explanation to chase, another reason to be afraid of what my body was doing. Learning about neuroplasticity eventually gave me a completely different question: What if my body isn’t as damaged as it feels? What if my brain has become really, really good at protecting me?
That question changed a lot for me.
It won’t be the answer to every person’s migraines. But for some people—especially those whose migraines have become chronic, whose medical workup hasn’t revealed another explanation, or whose symptoms show strong patterns of fear, prediction, sensitization, and learned triggers—I think it’s a question worth asking.
If you’re wondering whether your migraines or other symptoms show patterns consistent with neuroplasticity, my Neuroplastic Symptoms Self-Assessment is a good place to start. You may also want to read How Do I Know If My Symptoms Are Neuroplastic?, or What Is Somatic Tracking?.
And if you want help looking at your own migraine history and figuring out whether PRT might make sense as part of your approach, I offer a free 15-minute connect call. You don’t have to come in convinced that your migraines are neuroplastic. Honestly, I’d rather you didn’t force yourself to believe anything. We can look at the evidence together and see what your particular pattern tells us.
Research & Further Reading
Fishbein JN, et al. (2025). Pain Reprocessing Therapy for Migraine: A Case Series. Headache. This is the first published case series specifically examining PRT for chronic migraine.
Read the articleMínguez-Olaondo A, et al. (2022). Cutaneous Allodynia in Migraine: A Narrative Review. Frontiers in Neurology. Reviews allodynia and sensitization in migraine, including evidence of central sensitization.
Read the articleCnockaert E, et al. (2026). Human Assumed Central Sensitization in Interictal Migraine: A Systematic Review and Meta-Analysis. Neurological Sciences. This is the newer systematic review/meta-analysis examining evidence for central sensitization between migraine attacks.
Read the articleCoppola G, et al. (2020). Cortical Pain Processing in Migraine. Journal of Neural Transmission. Reviews neurophysiological and neuroimaging evidence related to pain processing, sensitization, and plastic changes in migraine.
Read the article
About the Author
Amberleigh Maida, ICF-ACC, is an Advanced Pain Reprocessing Practitioner and life coach with training in Emotional Awareness and Expression Therapy (EAET). She also holds a master’s degree in creative writing with a focus on nonfiction. Drawing on both professional training and personal experience with chronic pain, she writes about neuroplastic symptoms, the brain-body connection, and approaches to chronic pain and other persistent symptoms.
