• Clinical science

Migraine

Abstract

Migraine is characterized by recurrent episodes of typically unilateral, localized headaches that are frequently accompanied by nausea, vomiting, and sensitivity to light and sound. In approximately 25% of cases, patients experience an aura preceding the headache, which involves reversible focal neurologic abnormalities, for example, visual field defects (scotomas) or paresis lasting less than an hour. Migraine is a clinical diagnosis. Treatment of attacks consists of general measures (e.g., bedrest and protection from outer stimuli) together with administration of nonsteroidal anti-inflammatory drugs (e.g., aspirin) and antiemetics (e.g., prochlorperazine) if nausea is present. In severe cases, triptans may be added. Prophylactic treatment (e.g., beta blockers) may be indicated if migraines are especially frequent or long lasting, or if abortive therapy fails or is contraindicated.

Epidemiology

  • Prevalence: ∼18% of females and ∼6% of males
  • Peak incidence: 30–40 years
  • Migraine is the second most common type of headache.

References:[1]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

  • The exact pathophysiology is unclear.
  • Genetic predisposition
  • Potential triggers
    • Emotional stress
    • Weather changes
    • Certain food and beverages: alcohol, nicotine, citrus fruits, dairy products, food containing tyramine (e.g., chocolate, red wine)
    • Poor sleeping habits
    • Hormonal changes in women: menstruation, hormone intake (oral contraceptive pills)

References:[1][2]

Pathophysiology

The pathophysiology of migraine is not fully understood. Different aspects contribute to the development and severity of migraine, such as

  • Vascular dysregulation: vasodilation appears to play a role and there is an association between migraine and disorders with generalized vasospasms
  • Dysregulation of pain sensitization in the trigeminal system
  • Cortical spreading depression: continuously spreading depolarization of neuronal cells in the cortex

References:[3]

Clinical features

Migraine is characterized by recurrent attacks and may occur with aura (∼ 25% of cases; ) or without aura (∼ 75% of cases). A typical migraine attack passes through four stages, with aura (if present) appearing before the headache. However, migraine patterns may differ and not follow the characteristic stages.

  1. Prodrome (facultative , 60% of patients): 24–48 hours before the headache starts
    • Excessive yawning
    • Difficulties writing or reading
    • Sudden hunger or lack of appetite
    • Mood changes
  2. Aura (only present in ∼25% of patients): paroxysmal reversible focal neurologic symptoms
    • Visual disturbances
      • Photopsia (scintillating scotoma): starts centrally and shifts peripherally
      • Central scotoma
      • Flashing lights
      • Distorted color perception
      • Fortification spectra
    • Paresis
    • Impaired sensibility, paresthesia
    • Dizziness
    • Aphasia
  3. Headache
    • Localization: typically unilateral, but bilateral is possible , especially frontal, frontotemporal, retro-orbital
    • Duration: usually 4–24 hours, rarely over 72 hours
    • Course: progression of pulsating, throbbing, or pounding pain
    • Exacerbated by physical activity
    • Accompanying symptoms: photophobia, phonophobia, and nausea/vomiting
  4. Postdrome (facultative)
    • Feeling of exhaustion or euphoria
    • Muscle weakness
    • Anorexia or food cravings

The typical migraine headache is “POUND”: pulsatile, one-day duration, unilateral, nausea, disabling intensity

References:[4]

Subtypes and variants

Silent migraine

  • Clinical presentation: Typical migraine headache is absent. However, aura symptoms are present
  • Clinical course: During the course of the disease, typical migraine symptoms frequently develop.

Basilar migraine

  • Vasospasm of the basilar artery is most likely the underlying cause.
  • Occipital headaches
  • Aura symptoms
    • Bilateral visual field defects or double vision
    • Dysarthria
    • Ataxia
    • Hearing impairment, tinnitus, or dizziness
    • Bilateral paresis or bilateral paresthesia/hypoesthesia
    • Consciousness disturbance

Retinal migraine

  • Clinical presentation
    • Migraine headache
    • Recurring episodes of unilateral vision deficits (scotomas or blind spots, light flashes, or complete monocular blindness)
      • May eventually lead to irreversible vision loss, likely due to migraine-related ischemia

Ophthalmoplegic migraine

Vestibular migraine

  • Epidemiology: most common cause of spontaneous relapsing vertigo attacks in the middle-aged
  • Clinical presentation: headaches; rotational and postural vertigo with signs of peripheral or central vestibular dysfunction
  • Treatment: In addition to migraine treatment, antivertigo agents may be used (e.g., dimenhydrinate).

Diagnostics

  • Diagnosis can be made if there is a history of characteristic migraine attacks
    • With aura: ≥ 2 attacks
    • Without aura: ≥ 5 attacks
  • Physical exam to exclude red flag symptoms, such as :
    • ↑ blood pressure
    • Tenderness of the superficial temporal artery
    • Neck stiffness; fever
    • Severe headache with sudden onset and stiff neck
    • Painful ocular movements
    • Cranial nerve dysfunction
  • Neuroimaging should be used in headaches with an unusual clinical presentation or persistent neurologic or psychopathologic abnormalities.
  • Patients diagnosed with migraines should be screened for cardiovascular disease (especially in smokers and/or if taking oral contraceptives)

Migraine is a clinical diagnosis that is based on patient history and physical examination!

References:[1][4]

Differential diagnoses

References:[5]

The differential diagnoses listed here are not exhaustive.

Treatment

Management consists of abortive and/or preventative therapy and varies according to each individual.

Abortive therapy

Triptans

Agents
Mechanism of action
  • 5‑HT1 receptor agonist Inhibition of perivascular aseptic inflammation within the dural arteries (central effect); vasoconstriction of (dilated) cranial and basilar arteries
  • Most effective if taken at the onset of headache
Indications
Side effects
  • Temporary blood pressure increase (very common)
  • Paresthesia and sensation of cold in the extremities
  • Dizziness, malaise, flashes
  • Frequent intake (≥ 10x/month) can lead to headaches
  • Coronary ischemia (rare)
Contraindications

Prophylactic therapy

References:[1][5][6][7][8]

Complications

  • Status migrainosus:
  • Migrainous infarction
    • Persistent migraine with aura symptoms in combination with infarctions (e.g., clinical focal neurologic impairment)
    • Diagnostic criteria and clinical presentation
      • Aura lasting at least 60 minutes
      • Infarction detection (in the clinically relevant cerebral area) on imaging
      • The ischemic infarction is not due to a different condition.

We list the most important complications. The selection is not exhaustive.