- Clinical science
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.
- The exact pathophysiology is unclear.
- Genetic predisposition
- Potential triggers
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
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.
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
Aura (only present in ∼25% of patients): paroxysmal reversible focal neurologic symptoms
- Visual disturbances
- Impaired sensibility, paresthesia
- 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
- 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
- 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.
- Vasospasm of the basilar artery is most likely the underlying cause.
- Occipital headaches
- Bilateral visual field defects or double vision
- Hearing impairment, tinnitus, or dizziness
- Bilateral paresis or bilateral paresthesia/hypoesthesia
- Consciousness disturbance
- Clinical presentation
- Epidemiology: mostly affects children
- Clinical presentation
- 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).
- Diagnosis can be made if there is a history of characteristic migraine attacks
- Physical exam to exclude red flag symptoms, such as :
- 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!
Medication overuse headache
- Definition: secondary headache disorder caused by frequent use of analgesics
- Unclear pathophysiology, presumably genetic predisposition
- Sex: ♀ > ♂
- Clinical presentation
- Complete discontinuation of all analgesic medications, potentially in an inpatient setting
- In the case of nausea → metoclopramide or domperidone
- Headaches may be relieved with glucocorticoids or antipsychotics.
- Behavioral therapy
- Consider prophylactic treatment of primary headache disorder
The differential diagnoses listed here are not exhaustive.
Management consists of abortive and/or preventative therapy and varies according to each individual.
- General measures: limit stimuli (i.e., light, loud noises) and activity (bed rest)
- Mild to moderate attacks: NSAIDs (e.g., aspirin or ibuprofen)
- Severe attacks: triptans (e.g., sumatriptan) or ergotamine (do not combine these agents!)
- Initial therapy if nausea/vomiting is present: antiemetics (e.g., prochlorperazine, chlorpromazine)
- Children: ibuprofen and family counseling
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- Lifestyle changes: exercise; in moderation ), avoid potential triggers
- Frequent attacks (e.g., ≥ 3 attacks/month)
- Long-lasting attacks (e.g., > 12–24 hours) or aura
- Abortive therapy fails or is contraindicated
- Status migrainosus:
- Persistent migraine with aura symptoms in combination with infarctions (e.g., clinical focal neurologic impairment)
- Diagnostic criteria and clinical presentation
We list the most important complications. The selection is not exhaustive.