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PubMed This is a summary of 86 peer-reviewed journal articles Updated
Neurology · Migraine

Understanding Migraine as a Neurological Disorder

At a Glance

Migraine is a chronic, complex neurological disorder rooted in genetics and brain chemistry, not just a severe headache. It involves measurable biological changes in the brain, including hyperexcitability and the release of pain-signaling proteins like CGRP, which cause debilitating attacks.

It is a common experience: you tell someone you have a migraine, and they respond by suggesting an aspirin or asking if you’ve “tried drinking more water.” This reflects a deep-seated misunderstanding of what you are going through. Migraine is not just a “bad headache” that you can push through with willpower. It is a chronic, complex neurological disorder—a condition where the brain processes sensory information differently, often leading to debilitating attacks that affect every aspect of life [1][2].

A Global Perspective on Migraine

You are not alone in this experience. Migraine is one of the most common medical conditions in the world, affecting approximately 1 in 7 people globally [3][4].

  • Prevalence: Migraine affects about 14.7% of the global population [3].
  • Gender Disparity: Women are disproportionately affected, experiencing migraine 2 to 2.5 times more often than men [3][4]. This is often linked to hormonal shifts, but it also involves distinct biological differences in how the female brain responds to triggers [5].
  • Impact: In 2021, migraine was ranked as a leading cause of Years Lived with Disability (YLDs) worldwide, illustrating the massive impact it has on patients’ ability to function [6].

Moving Beyond “Just a Headache”

Medical research has moved far beyond the old idea that migraine is simply “vascular” (caused by blood vessel expansion). We now know that migraine involves measurable biological changes in the brain [1]:

  • Cortical Excitability: The brains of people with migraine are often “hyperexcitable,” meaning they react more strongly to sensory inputs like light, sound, or smell [7].
  • The Role of CGRP: A key player in migraine is Calcitonin Gene-Related Peptide (CGRP), a small protein that transmits pain signals and dilates blood vessels during an attack [8]. Many modern treatments specifically target this protein [9].
  • Structural Changes: Neuroimaging shows that during and between attacks, there are functional changes in areas like the brainstem (the brain’s “control center” for pain) and the thalamus (which processes sensory information) [10][11].

Common Misconceptions

Because migraine is often an “invisible” illness, many myths persist that can lead to stigma or delayed care.

Myth Reality
Migraine is just a psychological response to stress. While stress is a common trigger, migraine is a biological disease rooted in genetics and brain chemistry [1][12].
If you don’t have an “aura,” it isn’t a migraine. Only about 25-30% of people experience aura (reversible visual or sensory changes) [13]. Most migraine attacks occur without it.
Migraine only happens during the “pain” phase. Migraine is a cycle. Many people experience a prodrome (warning signs) days before the pain, and a postdrome (a “hangover” feeling) after [14].

What Research Still Investigates

While we have made massive strides in understanding migraine, some areas remain uncertain. Doctors are still working to understand exactly why some people transition from episodic migraine (occasional attacks) to chronic migraine (15 or more headache days per month) [15]. Additionally, because migraine is “polygenic”—meaning it involves many different genes—researchers are still mapping out why certain treatments work for some people but not for others [1][16].

Your diagnosis is a recognition of a biological reality. Understanding that your symptoms have a physical basis in your nervous system is the first step toward finding a management plan that treats the disorder, not just the pain.

Explore the Guide:

01

Mapping Your Migraine: Phases, Triggers, and Truths

Learn the 4 phases of a migraine attack: prodrome, aura, headache, and postdrome. Understand the difference between true triggers and early warning signs.

02

The Science of the Storm: Biology and Diagnosis

Understand the biology behind migraine attacks, including CSD and CGRP. Learn how doctors diagnose migraines and recognize important SNOOP red flag symptoms.

03

Defining Your Diagnosis: Subtypes and Classifications

Learn how doctors classify migraine subtypes. Understand the difference between episodic and chronic migraine, auras, and vestibular or hemiplegic migraines.

04

The Modern Toolkit: Treatment Standards and Options

Learn about the latest migraine treatment options, including 2024 AHS guidelines, CGRP therapies, gepants vs. triptans, and ways to prevent medication overuse.

05

Building Your Care Team: Preparing for Success

Learn how to build a migraine care team and find a headache specialist. Discover tips for tracking symptoms, preparing for visits, and discussing 2024 updates.

Common questions in this guide

Is a migraine just a bad headache?
No, a migraine is a complex neurological disorder, not simply a severe headache. It involves measurable biological changes in the brain, such as increased cortical excitability and changes in pain signaling proteins, which affect how sensory information is processed.
Do you have to have an aura to have a migraine?
No, you do not need to experience an aura to have a migraine. Only about 25 to 30 percent of people experience an aura, which can include reversible visual or sensory changes. The majority of migraine attacks occur without an aura.
Are migraines just caused by psychological stress?
While stress is a very common trigger for an attack, it is not the root cause. Migraine is a biological disease driven by genetics and brain chemistry. Having a migraine means your brain physically processes sensory inputs differently.
Are migraines more common in women?
Yes, women experience migraines two to two and a half times more often than men. This is frequently linked to hormonal shifts, but it also involves biological differences in how the female brain responds to migraine triggers.
What is the difference between episodic and chronic migraine?
Episodic migraine involves occasional attacks, while chronic migraine is diagnosed when a person experiences 15 or more headache days per month. Doctors and researchers are actively studying why some people transition from occasional attacks to a chronic condition.

Questions to Ask Your Doctor

Curated prompts to bring to your next appointment.

  1. 1.What criteria from the ICHD-3 are you using to confirm my migraine diagnosis?
  2. 2.Based on my symptoms, do I have migraine with or without aura, and how does that change my treatment plan?
  3. 3.How does my migraine frequency and intensity compare to the threshold for 'chronic' migraine?
  4. 4.What biological mechanisms, such as CGRP levels, might be contributing to my specific attacks?
  5. 5.Given my other health conditions, what are the safest preventive options available to me?

Questions For You

Tap a prompt to share your answer — we'll use it plus this page's context to start a tailored conversation.

References

References (16)
  1. 1

    Migraine in monogenic disorders: Shedding light on new therapeutic targets.

    Mascarella D, Zhuang ZA, Gliga O, et al.

    Cephalalgia : an international journal of headache 2025; (45(10)):3331024251389241 doi:10.1177/03331024251389241.

    PMID: 41147997
  2. 2

    Polygenic risk provides biological validity for the ICHD-3 criteria among Finnish migraine families.

    Häppölä P, Gormley P, Nuottamo ME, et al.

    Cephalalgia : an international journal of headache 2022; (42(4-5)):345-356 doi:10.1177/03331024211045651.

    PMID: 34648375
  3. 3

    Headache disorders and public ill-health in India: prevalence estimates in Karnataka State.

    Kulkarni GB, Rao GN, Gururaj G, et al.

    The journal of headache and pain 2015; (16()):67 doi:10.1186/s10194-015-0549-x.

    PMID: 26197976
  4. 4

    Prevalence, Treatment, and Unmet Needs of Migraine in the Middle East: A Systematic Review.

    Alsaadi T, Al Madani A, Alhatou M, et al.

    Pain and therapy 2025; (14(1)):145-183 doi:10.1007/s40122-024-00686-3.

    PMID: 39738973
  5. 5

    Type and Severity of Migraine Determines Risk of Atrial Fibrillation in Women.

    Rhee TM, Choi EK, Han KD, et al.

    Frontiers in cardiovascular medicine 2022; (9()):910225 doi:10.3389/fcvm.2022.910225.

    PMID: 35711356
  6. 6

    The incremental burden and healthcare resource utilization among people with migraine in Europe: Insights from the 2020 European National Health and Wellness Survey.

    Gendolla A, Brown JD, Mercadante AR, et al.

    Cephalalgia : an international journal of headache 2024; (44(12)):3331024241276415 doi:10.1177/03331024241276415.

    PMID: 39633516
  7. 7

    Evoked potential studies in migraine: A systematic review of neurophysiological patterns across migraine subtypes.

    Ulutas S, Özçelik EU, Dabó LG, et al.

    Cephalalgia : an international journal of headache 2025; (45(12)):3331024251398792 doi:10.1177/03331024251398792.

    PMID: 41364425
  8. 8

    CGRP as the target of new migraine therapies - successful translation from bench to clinic.

    Edvinsson L, Haanes KA, Warfvinge K, Krause DN

    Nature reviews. Neurology 2018; (14(6)):338-350 doi:10.1038/s41582-018-0003-1.

    PMID: 29691490
  9. 9

    CROATIAN GUIDELINES FOR SPECIFIC PREVENTIVE TREATMENT OF MIGRAINE WITH MONOCLONAL ANTIBODIES TARGETING CALCITONIN GENE-RELATED PEPTIDE (CGRP) (EPTINEZUMAB, FREMANEZUMAB, AND GALCANEZUMAB) OR THE CGRP RECEPTOR (ERENUMAB).

    Jančuljak D, Petravić D, Mahović Lakušić D, et al.

    Acta clinica Croatica 2024; (63(2)):436-450 doi:10.20471/acc.2024.63.02.22.

    PMID: 40104234
  10. 10

    The brain structure and function abnormalities of migraineurs: A systematic review and neuroimaging meta-analysis.

    Chen ZH, Cui YL, Sun JT, et al.

    Frontiers in neurology 2022; (13()):1022793 doi:10.3389/fneur.2022.1022793.

    PMID: 36419535
  11. 11

    Magnetic resonance spectroscopy studies in migraine.

    Nikolova S, Schwedt TJ

    Neurobiology of pain (Cambridge, Mass.) 2022; (12()):100102 doi:10.1016/j.ynpai.2022.100102.

    PMID: 36531616
  12. 12

    Visual evoked potentials in subgroups of migraine with aura patients.

    Coppola G, Bracaglia M, Di Lenola D, et al.

    The journal of headache and pain 2015; (16()):92 doi:10.1186/s10194-015-0577-6.

    PMID: 26527348
  13. 13

    How Well Does the ICHD 3 (Beta) Help in Real-Life Migraine Diagnosis and Management?

    Ashina S, Olesen J, Lipton RB

    Current pain and headache reports 2016; (20(12)):66 doi:10.1007/s11916-016-0599-z.

    PMID: 27873122
  14. 14

    The chronobiology of migraine: a systematic review.

    Poulsen AH, Younis S, Thuraiaiyah J, Ashina M

    The journal of headache and pain 2021; (22(1)):76 doi:10.1186/s10194-021-01276-w.

    PMID: 34281500
  15. 15

    Chronic migraine: Genetics or environment?

    Chalmer MA, Rasmussen AH, , et al.

    European journal of neurology 2021; (28(5)):1726-1736 doi:10.1111/ene.14724.

    PMID: 33428804
  16. 16

    Dural Immune Cells, CGRP, and Migraine.

    Balcziak LK, Russo AF

    Frontiers in neurology 2022; (13()):874193 doi:10.3389/fneur.2022.874193.

    PMID: 35432179

This information is for educational purposes to help you understand the biology of migraine. It does not replace professional medical advice. Always consult a neurologist or healthcare provider for an accurate diagnosis and treatment plan.

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