What Is Migraine?

Migraine is a chronic neurological disease characterized by recurrent attacks of moderate to severe headache, generally unilateral and pulsating, accompanied by nausea, vomiting, and hypersensitivity to light and sound. It is not a simple headache — it is a complex neurovascular condition with a genetic basis.

The World Health Organization classifies migraine as the second leading cause of global disability among all neurological diseases. It affects about 15% of the world population and is three times more prevalent in women than in men, suggesting a strong hormonal influence.

Migraine attacks can last from 4 to 72 hours and are frequently debilitating, preventing routine activities. About one-third of patients experience aura — transient neurological symptoms that precede or accompany the pain, such as visual, sensory, or language disturbances.

01

Neurological Disease

Migraine is a brain disease, not just a headache. It involves neurovascular dysfunction, central sensitization, and genetic predisposition.

02

Migraine Aura

About 30% of patients experience transient neurological phenomena (visual, sensory, or language) before or during the attack.

03

High Prevalence

Affects approximately 1 billion people globally, making it the second leading cause of disability among neurological diseases.

Pathophysiology

Understanding of migraine has evolved significantly over recent decades. The purely vascular theory (dilation of blood vessels) has been replaced by a neurovascular model that recognizes migraine as a primarily brain disease.

The process begins with activation of the trigeminovascular system — neurons of the trigeminal nerve that innervate the meninges and cerebral vessels. When activated, these neurons release neuropeptides such as CGRP (calcitonin gene-related peptide), substance P, and neurokinin A, which cause neurogenic inflammation and meningeal vasodilation.

Migraine mechanisms: trigeminovascular activation, cortical spreading depression, the role of CGRP, and central and peripheral sensitization
Migraine mechanisms: trigeminovascular activation, cortical spreading depression, the role of CGRP, and central and peripheral sensitization
Migraine mechanisms: trigeminovascular activation, cortical spreading depression, the role of CGRP, and central and peripheral sensitization

Cortical Spreading Depression

Cortical spreading depression (CSD) is a wave of neuronal depolarization followed by suppression of electrical activity that propagates slowly across the cerebral cortex. It is the mechanism responsible for migraine aura — the wave of visual depolarization perceived as scintillating scotomas or zigzag lines.

CSD activates trigeminal fibers in the meninges, establishing the connection between aura and headache. Even in patients without clinical aura, subliminal forms of CSD may be involved in pain generation.

Visual phenomena of migraine aura: scintillating scotoma, zigzag lines (fortification spectrum), typical progression over 5 to 60 minutes
Visual phenomena of migraine aura: scintillating scotoma, zigzag lines (fortification spectrum), typical progression over 5 to 60 minutes
Visual phenomena of migraine aura: scintillating scotoma, zigzag lines (fortification spectrum), typical progression over 5 to 60 minutes

Sensitization and Chronification

During an attack, peripheral sensitization of meningeal nociceptors occurs (pulsating pain that worsens with head movements) followed by central sensitization in the trigeminal caudal nucleus and thalamus (cutaneous allodynia — pain on touching the scalp).

Frequent attacks can lead to structural and functional changes in the brain, facilitating the transition to chronic migraine (15 or more headache days per month). Excessive use of analgesics is one of the main factors in chronification.

Symptoms

A typical migraine attack evolves through distinct phases, although not all patients experience every phase. Understanding this progression helps with early and adequate treatment.

Phases of the migraine attack: prodrome, aura, headache, and postdrome, with the typical symptoms and duration of each phase
Phases of the migraine attack: prodrome, aura, headache, and postdrome, with the typical symptoms and duration of each phase
Phases of the migraine attack: prodrome, aura, headache, and postdrome, with the typical symptoms and duration of each phase
Prodromal Phase (hours to days before)

Mood changes, excessive yawning, food cravings, fluid retention, neck stiffness, and fatigue. Present in up to 77% of patients.

Aura (5-60 minutes)

Visual phenomena (scintillating scotomas, zigzag lines), sensory (unilateral tingling), or language (dysphasia). Present in 30% of patients.

Headache (4-72 hours)

Unilateral, pulsating, moderate to severe pain, aggravated by physical activity. Accompanied by nausea, photophobia, and phonophobia.

Postdromal Phase (up to 48 hours)

Fatigue, difficulty concentrating, "hangover" sensation. Frequently underestimated but can be as disabling as the pain itself.

Critérios clínicos
08 itens

Symptoms of the Migraine Attack

  1. 01

    Unilateral pulsating headache

    Pain predominantly on one side of the head with a throbbing character, which may alternate sides between attacks.

  2. 02

    Nausea and vomiting

    Present in up to 80% of patients. Vomiting can be so intense that it prevents oral intake of medications.

  3. 03

    Photophobia and phonophobia

    Hypersensitivity to light and sound, leading the patient to seek dark and quiet environments.

  4. 04

    Worsening with physical activity

    Head movements, climbing stairs, or any exertion intensifies the pain.

  5. 05

    Cutaneous allodynia

    Pain on light touch of the scalp, face, or neck — indicates central sensitization.

  6. 06

    Osmophobia

    Hypersensitivity to odors, present in up to 40% of patients — relatively specific to migraine.

  7. 07

    Visual disturbances (aura)

    Bright spots, zigzag lines, scotomas — last 5-60 minutes and precede the pain.

  8. 08

    Autonomic symptoms

    Lacrimation, nasal congestion, and unilateral ptosis can occur, especially in intense unilateral forms.

Diagnosis

Diagnosis of migraine is essentially clinical, based on a detailed history of attacks. There is no laboratory or imaging test that confirms the diagnosis. The criteria of the International Headache Society (ICHD-3) are the gold standard.

Neuroimaging tests (CT or MRI) are indicated when there are red-flag signs suggesting secondary headache, but they are not necessary for the diagnosis of typical migraine.

🏥ICHD-3 Criteria for Migraine without Aura

  • 1.At least 5 attacks meeting the criteria below
  • 2.Headache lasting 4-72 hours (untreated)
  • 3.At least 2 of: unilateral, pulsating, moderate/severe intensity, worsens with physical activity
  • 4.At least 1 of: nausea and/or vomiting, photophobia and phonophobia
  • 5.Not attributed to another condition
50%
OF PATIENTS WITH MIGRAINE ARE NOT DIAGNOSED
4-72h
TYPICAL DURATION OF AN UNTREATED ATTACK
30%
OF PATIENTS PRESENT WITH AURA
2-3%
OF THE POPULATION HAVE CHRONIC MIGRAINE

Differential Diagnosis

The diagnosis of migraine is clinical, but several other conditions can mimic its attacks. The medical acupuncturist should be alert to red flags indicating secondary causes and to the criteria that distinguish migraine from other types of primary headache.

DIAGNÓSTICO DIFERENCIAL

Diagnóstico Diferencial

Tension-Type Headache

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  • Bilateral band/pressure pain
  • No nausea, mild photophobia at most
  • Does not worsen with physical activity

Testes Diagnósticos

  • ICHD-3 criteria
  • Headache diary

Cluster Headache

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  • Unilateral periorbital
  • Duration 15-180 min
  • Ipsilateral autonomic symptoms
Sinais de Alerta
  • Cluster periods with >3 episodes/day = neurological evaluation

Testes Diagnósticos

  • ICHD-3 criteria
  • Headache diary

Subarachnoid Hemorrhage

  • "Worst headache of life"
  • Sudden onset in seconds
  • May have neck stiffness
Sinais de Alerta
  • Thunderclap headache = urgent CT

Testes Diagnósticos

  • Non-contrast head CT
  • Lumbar puncture

Headache from Intracranial Hypertension

  • Worsens when lying down
  • Morning nausea
  • Papilledema
Sinais de Alerta
  • Papilledema = urgent neuroimaging

Testes Diagnósticos

  • Fundoscopy
  • MRI/CT

Giant Cell Arteritis

  • Patients >50 years
  • Pain in the temporal artery
  • Very elevated ESR
Sinais de Alerta
  • Risk of blindness from ophthalmic artery ischemia

Testes Diagnósticos

  • ESR
  • CRP
  • Temporal artery biopsy

Migraine vs Tension-Type Headache: The Most Frequent Distinction

Differentiation between migraine and tension-type headache is the most common diagnostic challenge in clinical practice. Migraine presents with typically unilateral and pulsating pain, with nausea and worsening with movement — criteria that tension-type headache does not meet. The headache diary is the most valuable tool for this distinction, since it documents the characteristics of each attack over time.

It is important to remember that the two types of headache can coexist in the same patient. In that case, each attack should be classified separately according to its own criteria. The medical acupuncturist should instruct the patient to record the characteristics of each episode to guide individualized treatment.

Red Flags That Require Urgent Investigation

Certain headache patterns require immediate investigation to rule out serious secondary causes. The so-called "thunderclap headache" — pain of maximum intensity that peaks in seconds — should be investigated as subarachnoid hemorrhage until proven otherwise, even if the patient already has a history of migraine. Any abrupt change in the usual headache pattern also warrants investigation.

The presence of fever, neck stiffness, focal neurological deficit, papilledema, or onset after age 50 are other classic red flags. When in doubt, the physician should always prioritize ruling out secondary causes before confirming a diagnosis of primary headache. This conduct protects the patient and is the foundation of responsible medical practice.

Migraine with Aura vs Vascular Causes

Migraine aura — especially visual phenomena — should be differentiated from transient ischemic attack (TIA). Typical aura spreads slowly (marching in 20-30 minutes), while vascular symptoms tend to have more abrupt onset. In addition, migraine visual aura is typically positive (lights, zigzag), while TIA frequently causes loss of function (dark scotoma, visual field blackout).

Patients with migraine with aura, especially women using combined oral contraceptives or who smoke, present a slightly increased risk of ischemic stroke. In these cases, the choice of preventive treatment and contraceptive method should be discussed with the physician. Evaluation of cardiovascular risk factors is an inseparable part of adequate migraine management.

Treatment

Migraine management involves three pillars: acute treatment (aborting attacks), preventive treatment (reducing frequency and intensity), and lifestyle modifications. The therapeutic choice depends on the frequency, intensity, and functional impact of attacks.

ACUTE VS PREVENTIVE TREATMENT

FEATUREACUTE TREATMENTPREVENTIVE TREATMENT
GoalRelieve the current attackReduce frequency and intensity of attacks
When to useAt the start of the attackDaily (continuous use)
MedicationsTriptans, NSAIDs, gepantsBeta-blockers, anticonvulsants, anti-CGRP
IndicationEvery patient with migraineFrequency >= 4 attacks/month or disabling attacks
Onset of actionMinutes to hoursWeeks to months
CautionsAvoid use > 10 days/monthMaintain for a minimum of 3-6 months

Acute Treatment

Triptans (sumatriptan, rizatriptan, zolmitriptan) are 5-HT1B/1D receptor agonists and represent first-line treatment for moderate to severe attacks. They act by reversing meningeal vasodilation and inhibiting CGRP release. They should be taken early in the attack for maximum efficacy.

Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, naproxen, and acetylsalicylic acid are effective for mild to moderate attacks. The combination of triptan + NSAID is more effective than either alone.

Gepants (rimegepant, ubrogepant) are oral CGRP receptor antagonists, a more recent option for patients who do not tolerate triptans or have cardiovascular contraindications.

Preventive Treatment

Indicated when the patient has 4 or more attacks per month, very disabling attacks, failure of acute treatment, or risk of medication-overuse headache. Options include beta-blockers (propranolol), anticonvulsants (topiramate, valproic acid), antidepressants (amitriptyline, venlafaxine), and onabotulinumtoxinA (for chronic migraine).

Anti-CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab) represent the first therapy developed specifically for migraine. Administered by monthly subcutaneous injection, they reduce attack frequency by 50% or more in about 50% of patients, with a very favorable side-effect profile.

Mechanism of action of anti-CGRP monoclonal antibodies: blocking the CGRP peptide or its receptor in migraine prevention
Mechanism of action of anti-CGRP monoclonal antibodies: blocking the CGRP peptide or its receptor in migraine prevention
Mechanism of action of anti-CGRP monoclonal antibodies: blocking the CGRP peptide or its receptor in migraine prevention

Acupuncture as Treatment

Acupuncture is recognized as a complementary therapeutic option in the prevention of migraine. The 2016 Cochrane review (Linde et al.), involving more than 4,900 patients, concluded that acupuncture can reduce attack frequency compared with placebo or usual care, with an effect similar to preventive pharmacological treatment — although with evidence quality described as low to moderate.

Proposed mechanisms include modulation of trigeminovascular pathways, reduction of CGRP levels, release of endorphins and enkephalins, activation of descending inhibitory pain pathways, and modulation of the autonomic nervous system. Functional neuroimaging studies show that acupuncture activates brain areas involved in pain regulation and autonomic function.

A typical protocol involves weekly sessions for 8-12 weeks, with subsequent monthly maintenance. Results generally appear after 4-6 sessions. Acupuncture can be used alone in patients with contraindications to preventive medications or as an adjuvant to pharmacological treatment.

Prognosis

Migraine is a chronic condition with a variable course over the lifetime. In many patients, the frequency and intensity of attacks decrease with age, especially after the ages of 50-60. In women, improvement frequently occurs after menopause.

With adequate treatment, most patients achieve significant reduction in the frequency and intensity of attacks. Identification and avoidance of individual triggers, combined with preventive treatment when indicated, can substantially improve quality of life.

The main long-term risk is chronification — transition from episodic to chronic migraine. Factors that increase this risk include high attack frequency, excessive use of analgesics, obesity, sleep disorders, depression, and chronic stress. Preventing chronification is a central goal of treatment.

50-70%
ATTACK REDUCTION WITH ADEQUATE PREVENTION
3%
ANNUAL RISK OF CHRONIFICATION WITHOUT TREATMENT
6 months
RECOMMENDED MINIMUM DURATION OF PREVENTIVE TREATMENT
30-40%
OF PATIENTS WITH CHRONIC MIGRAINE REVERT TO EPISODIC WITH TREATMENT

Myths and Facts

Myth vs. Fact

MYTH

Migraine is just a strong headache

FACT

Migraine is a complex neurological disease with a genetic basis, involving neurovascular dysfunction, neurogenic inflammation, and central sensitization. The headache is just one of the symptoms.

MYTH

Migraine is caused by stress — it is an "emotional problem"

FACT

Although stress can trigger attacks, migraine has a well-documented neurobiological basis and a strong genetic component. Neuroimaging studies describe objective structural and functional brain alterations associated with the condition.

MYTH

Chocolate and cheese always trigger attacks

FACT

Triggers are individual and variable. Many foods considered triggers may actually be cravings of the prodromal phase, confusing cause with symptom.

MYTH

Taking an analgesic whenever there is pain is the best approach

FACT

Frequent use of analgesics (more than 10-15 days/month) can cause rebound headache and chronify migraine. Preventive treatment is essential for patients with frequent attacks.

MYTH

Migraine only affects women

FACT

Although more prevalent in women (3:1), migraine also significantly affects men. Before puberty, prevalence is similar between the sexes.

When to Seek Help

Not every headache requires urgent medical evaluation, but some situations demand immediate attention. See a neurologist if your attacks are frequent, disabling, or do not respond to usual treatment.

Frequently Asked Questions

FREQUENTLY ASKED QUESTIONS · 10

Frequently Asked Questions

Migraine is a neurological disease with a typically unilateral, pulsating attack of moderate to severe intensity, accompanied by nausea, photophobia, and phonophobia, that worsens with physical activity. The common tension-type headache is bilateral, pressure-like, milder, and without these associated symptoms. Migraine also has prodromal, aura (in 30% of cases), and postdromal phases, constituting a more complex experience than a simple headache.

Migraine has no definitive cure, but it is highly treatable. With adequate treatment — preventive when indicated, abortive for attacks, and lifestyle modifications — most patients achieve a 50% or greater reduction in attack frequency and intensity. In some patients, migraine improves spontaneously with age, especially after the ages of 50-60. In women, menopause frequently brings improvement.

Preventive options with the strongest evidence include beta-blockers (propranolol, metoprolol), anticonvulsants (topiramate, valproate), antidepressants (amitriptyline, venlafaxine), and onabotulinumtoxinA (for chronic migraine). Anti-CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab) are the most modern preventives, developed specifically for migraine, with excellent efficacy and few side effects. The choice should be individualized by the physician.

Triptans are indicated for moderate to severe attacks, especially when the patient knows the attack will be debilitating. Simple analgesics (ibuprofen, ASA, acetaminophen) may suffice for mild attacks. The triptan + NSAID combination is more effective than either alone. The crucial point is taking the medication as early as possible in the attack — efficacy decreases significantly if treatment is delayed. More than 10 days/month of abortives raises the risk of rebound headache.

Acupuncture is a therapeutic option with evidence of efficacy comparable to preventive pharmacological treatment in reducing the frequency of migraine attacks (Cochrane review, 2016). In patients who do not tolerate the side effects of oral preventives or prefer to reduce the medication burden, acupuncture can be used as an alternative or in combination with pharmacotherapy. The decision should be made together with the medical acupuncturist, evaluating the individual characteristics of the patient.

The typical protocol for migraine involves 8-12 weekly sessions, followed by monthly maintenance. Results usually appear after 4-6 sessions, although adequate efficacy assessment recommends completing at least 8 sessions. The benefit of acupuncture in migraine tends to be sustained for at least 6 months after the end of treatment, which is an advantage over drugs whose effect ceases on discontinuation.

Migraine has a genetic and neurobiological basis — triggers do not cause the disease but can set off attacks in predisposed individuals. Common triggers include sleep deprivation or excess, prolonged fasting, stress, hormonal variation (menstrual cycle), alcohol (especially red wine), caffeine, intense lights, and strong perfumes. Identifying individual triggers through a headache diary is fundamental — triggers vary widely between patients.

In rare cases, migraine aura — especially motor aura (hemiplegia) — can mimic stroke symptoms. Differentiation is based on typical aura progression (slow, in 20-30 minutes), complete reversibility, and history of similar attacks. "Thunderclap headache" (pain of maximum intensity in seconds) associated with neck stiffness or new neurological deficit should be investigated as subarachnoid hemorrhage or stroke — it should not be attributed to migraine without ruling out a vascular cause.

Yes. Migraine can begin in childhood, and before puberty prevalence is similar between boys and girls. In children, attacks are usually shorter (2-4 hours), bilateral, and with prominent nausea and vomiting. Some children present with migraine equivalents such as recurrent abdominal pain, benign paroxysmal vertigo, or paroxysmal torticollis, which are recognized as migraine manifestations by the ICHD-3 classification. Adequate diagnosis and treatment in children prevents academic and social impact.

Chronic migraine is defined as 15 or more headache days per month, with at least 8 having migraine features, for more than 3 months. The main cause of chronification is excessive use of analgesics (more than 10-15 days/month), which generates rebound headache and maintains the cycle. Other factors include obesity, sleep apnea, depression, anxiety, and high levels of chronic stress. Treatment of chronic migraine requires withdrawal of overused analgesics and introduction of adequate prevention.