Migraine

All Diseases

Introduction

Migraine is a neurological disorder characterised by recurrent headaches, often throbbing and one-sided, with nausea, sensitivity to light and sound, and functional disability lasting hours to days.

Some attacks are preceded by aura—reversible visual, sensory, or speech disturbances lasting 5–60 minutes. Migraine without aura is most common. Chronic migraine means headache on 15 or more days per month with migraine features on at least 8 days.

Triggers include hormonal shifts, sleep change, stress, certain foods, and weather. Treatment combines acute pain relief, preventive medication, and lifestyle modification. Most patients manage well with personalised plans.

This page explains types, symptoms, diagnosis, treatment, prevention, and when emergency evaluation is needed.

Overview

Migraine involves abnormal brainstem and trigeminovascular activation with neurogenic inflammation of meningeal vessels. Serotonin (5-HT) fluctuation and CGRP release play key roles in modern treatment targets.

Diagnosis is clinical using International Classification of Headache Disorders criteria. Neuroimaging is reserved for red flags—sudden worst headache, focal neurology, or new headache after age 50.

Women are affected three times more often than men, linked partly to oestrogen fluctuation. Family history is present in most patients. Prognosis improves with appropriate preventive strategy.

  • Recurrent neurological headache disorder
  • With or without aura; chronic form ≥15 headache days/month
  • Symptoms: throbbing pain, nausea, photophobia, phonophobia
  • Triggers: hormones, sleep, stress, foods, weather
  • Acute: triptans, NSAIDs, antiemetics
  • Preventive: beta-blockers, topiramate, CGRP antibodies, Botox
  • Neuroimaging if red flags present
  • Strong genetic component

What happens in the body

Cortical spreading depression may trigger aura. Trigeminal nerve activation releases CGRP and substance P, dilating meningeal vessels and causing neurogenic inflammation perceived as throbbing pain.

Central sensitisation prolongs attacks and increases allodynia. Serotonin receptor changes modulate pain pathways. Hypothalamic dysfunction links migraine to sleep and autonomic symptoms.

  • Trigeminovascular activation and meningeal inflammation
  • CGRP central to modern acute and preventive therapy
  • Cortical spreading depression in aura subtypes
  • Serotonin pathway involvement
  • Central sensitisation prolongs attacks
  • Genetic ion channel and receptor variants in families

Signs and symptoms

Migraine unfolds in phases in many patients:

  • Prodrome: mood change, food craving, neck stiffness, yawning (hours to days before)
  • Aura: visual zigzags, numbness, speech difficulty—reversible, under one hour
  • Headache: throbbing pain, often unilateral, worsened by activity
  • Nausea, vomiting, photophobia, and phonophobia during attack
  • Postdrome: fatigue and cognitive fog for 24–48 hours after
  • Chronic migraine: frequent headache with migraine features most days
  • Abdominal migraine in children—stomach pain without headache
  • Status migrainosus: attack lasting more than 72 hours

Causes and risk factors

Migraine arises from genetic vulnerability plus triggers:

  • Strong family history and polygenic inheritance
  • Hormonal fluctuation—menstruation, pregnancy, menopause
  • Sleep deprivation or oversleeping
  • Stress and post-stress letdown
  • Skipped meals, dehydration, alcohol (especially red wine)
  • Strong smells, bright lights, loud noise
  • Weather and barometric pressure change
  • Not caused by brain tumour in vast majority of cases

Diagnosis and evaluation

Clinical history establishes diagnosis in typical cases:

  • Headache diary documenting frequency, duration, and features
  • ICHD criteria: unilateral pulsating pain, nausea, photophobia, disability
  • Neurological exam normal between attacks
  • MRI or CT when red flags—thunderclap onset, focal signs, new headache over 50
  • Exclude medication-overuse headache if daily analgesic use
  • Identify aura to distinguish from TIA or stroke mimic
  • Cardiovascular risk assessment before triptans

Treatment and management

Acute and preventive strategies are combined:

  • Acute: triptans, NSAIDs, acetaminophen, antiemetics (metoclopramide)
  • Gepants (rimegepant, ubrogepant) and ditans for CGRP pathway—acute options
  • Preventive: propranolol, topiramate, amitriptyline, valproate (non-pregnant)
  • CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab, eptinezumab)
  • OnabotulinumtoxinA for chronic migraine
  • Neuromodulation devices—vagus nerve, single-pulse TMS in selected patients
  • Stop medication overuse—limit triptans and analgesics to avoid rebound
  • Identify and avoid personal triggers; CBT and biofeedback

Prevention, self-care, and lifestyle

Not every condition is fully preventable, but the steps below may lower risk or recurrence:

  • Regular sleep and meal schedule
  • Hydration and moderate caffeine—avoid excess or withdrawal
  • Exercise and stress management
  • Limit known dietary triggers individually documented
  • Preventive medication when attacks frequent or disabling
  • Migraine diary to refine plan

Possible complications

Delay, missed care, or unsafe self-medication can raise the chance of complications in some cases:

  • Chronic migraine and medication-overuse headache
  • Status migrainosus requiring IV treatment
  • Migrainous infarction (rare stroke with aura)
  • Increased cardiovascular risk in migraine with aura (modest)
  • Depression and anxiety comorbidity
  • Work and school absenteeism

When to see a doctor or seek emergency care

Seek prompt medical advice or emergency care if any of the following apply—it is safer not to wait and see:

  • New severe or thunderclap headache—emergency
  • Headache with fever, stiff neck, confusion, or focal weakness—emergency
  • Change in headache pattern or new headache after age 50
  • Migraine more than 4 disabling days per month—discuss prevention
  • Headache during pregnancy—specialist guidance needed

Living with the condition

Keep a headache diary. Take acute treatment early in attack. Discuss realistic preventive goals with your doctor. Many patients reduce attack frequency substantially with modern CGRP therapies.

Frequently asked questions

Are migraines dangerous?

Usually not life-threatening, but severe or changing headaches need evaluation; aura carries a small stroke risk factor that should be discussed with your clinician.

Can migraine be cured?

No permanent cure, but effective acute and preventive treatments control most patients' attacks.

Is migraine just a tension headache?

No. Migraine has distinct features—nausea, photophobia, throbbing quality, and disability—and different treatment pathways.

Important caution

This article is general health education, not neurology prescribing advice.

Sudden worst-ever headache or headache with neurological deficits requires emergency evaluation.

Triptans and preventive drugs should be prescribed with cardiovascular and pregnancy considerations in mind.