Migraine and Other Primary Headache Disorders¶
Chapter 441 | Part 13: Neurologic Disorders
KEY CLINICAL POINTS¶
- Migraine is the second most common cause of headache and the most common neurologic cause of disability, affecting ~15% of women and 6% of men.
- Pathophysiology involves dysfunction of monoaminergic systems, trigeminovascular activation, and CGRP-mediated mechanisms.
- Treatment includes acute therapies (triptans, NSAIDs, CGRP antagonists) and preventive strategies (beta-blockers, anticonvulsants, neuromodulation).
1. DEFINITION & OVERVIEW¶
Migraine is a primary headache disorder characterized by recurrent attacks of headache with associated neurologic features. Tension-type headache (TTH) and trigeminal autonomic cephalalgias (TACs) are other primary headache disorders. The International Classification of Headache Disorders (ICHD-3) provides diagnostic criteria for these conditions.
Table 441-1: Primary Headache Disorders¶
| Category | Subtypes |
|---|---|
| Migraine | 1.1 Migraine without aura, 1.2 Migraine with aura, 1.3 Chronic migraine |
| Tension-Type Headache | 2.1 Infrequent, 2.2 Frequent, 2.3 Chronic |
| Trigeminal Autonomic Cephalalgias | 3.1 Cluster headache, 3.2 Paroxysmal hemicrania, 3.3 SUNCT/SUNA |
1.1 Primary Headache Disorders¶
Migraine, TTH, and TACs (e.g., cluster headache) are classified as primary headaches. Migraine has subtypes including migraine with/without aura, chronic migraine, and hemiplegic migraine.
1.2 Diagnostic Criteria¶
Migraine diagnosis requires recurrent attacks with unilateral, pulsating headache, moderate/severe intensity, aggravation by activity, and associated symptoms (nausea, photophobia, phonophobia).
2. EPIDEMIOLOGY¶
Migraine affects ~15% of women and 6% of men globally. It is more common in women, with prevalence peaking in reproductive years. Chronic migraine is defined as ≥ 15 headache days/month for ≥ 3 months.
2.1 Risk Factors¶
Genetic predisposition, hormonal fluctuations, environmental triggers (stress, sleep changes, dietary factors), and family history of migraine.
2.2 Demographics¶
Women are 2–3 times more likely to have migraine than men. Age of onset varies, with episodic migraine common in adolescents and chronic migraine increasing with age.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Migraine involves complex interactions between genetic, environmental, and neurobiological factors. Key mechanisms include cortical spreading depression, trigeminovascular activation, and dysregulation of 5-HT and CGRP pathways.
Table 441-2: Migraine Symptoms by Attack Phase¶
| Phase | Symptoms |
|---|---|
| Premonitory (Prodromal) | Neck discomfort, fatigue, yawning, polyuria, food cravings |
| Aura | Scintillating scotoma, visual disturbances |
| Headache Phase | Pain, nausea, photophobia, phonophobia, allodynia |
| Postdrome | Tiredness, concentration impairment |
3.1 Neurotransmitter Involvement¶
5-HT (serotonin) and dopamine play critical roles. Dopamine receptor antagonists (e.g., metoclopramide) are effective in acute treatment. CGRP (calcitonin gene-related peptide) is a key mediator of pain.
3.2 Genetic Mutations¶
Familial hemiplegic migraine (FHM) is linked to mutations in CACNA1A (FHM1), ATP1A2 (FHM2), and SCN1A (FHM3).
4. CLINICAL FEATURES¶
Migraine attacks are characterized by unilateral, pulsating pain with associated neurologic symptoms. Tension-type headache is typically bilateral, non-pulsating, and without associated features.
4.1 Migraine Features¶
Unilateral, throbbing pain; nausea/vomiting; photophobia/phonophobia; aura (visual/brainstem symptoms).
4,2 Tension-Type Headache¶
Bilateral, pressing/pressure-like pain without associated neurologic features. Often featureless compared to migraine.
5. DIFFERENTIAL DIAGNOSIS¶
Distinguish migraine from TTH, cluster headache, and secondary headaches (e.g., sinusitis, brain tumors). Key differentiators include aura, duration, and associated autonomic symptoms.
5.1 Red Flags for Secondary Headache¶
Sudden severe headache (thunderclap), neurological deficits, fever, or history of trauma.
6. INVESTIGATIONS & DIAGNOSIS¶
Diagnosis is based on clinical criteria (ICHD-3). Imaging (MRI) is used to exclude secondary causes, especially in atypical presentations or chronic cases.
Table 441-3: Simplified Diagnostic Criteria for Migraine¶
| Criteria | Details |
|---|---|
| Attack Duration | 4–72 hours |
| Features | Unilateral pain, nausea/vomiting, photophobia, phonophobia |
| Exclusion | No other cause for headache |
6.1 Diagnostic Criteria¶
Table 441-3 outlines simplified diagnostic criteria for migraine, including attack duration, features, and associated symptoms.
7. MANAGEMENT & TREATMENT¶
Acute treatment includes triptans, NSAIDs, and CGRP antagonists. Preventive therapy targets underlying mechanisms with beta-blockers, anticonvulsants, and neuromodulation.
Table 441-4: Acute Migraine Treatment¶
| Drug | Dosage | Route |
|---|---|---|
| Sumatriptan | 50–100 mg PO | Oral |
| Zolmitriptan | 2.5 mg PO | Oral |
| Rimegepant | 75 mg PO | Oral |
| Dihydroergotamine | 1 mg IV/SC | Parenteral |
7.1 Acute Attack Therapies¶
Triptans (e.g., sumatriptan, rizatriptan), NSAIDs (ibuprofen, naproxen), and gepants (rimegepant, ubrogepant) are first-line options. Oxygen and non-invasive vagus nerve stimulation (nVNS) are also used.
7.2 Preventive Therapy¶
Beta-blockers (propranolol), anticonvulsants (topiramate), CGRP inhibitors (erenumab), and neuromodulation (sTMS, nVNS) are recommended for chronic migraine.
8. PROGNOSIS & COMPLICATIONS¶
Migraine is generally benign but can significantly impact quality of life. Complications include status migrainosus, persistent aura without infarction, and migrainous infarction.
8.1 Chronic Migraine¶
Defined as ≥ 15 headache days/month for ≥ 3 months. Risk factors include medication overuse and frequent acute attacks.
9. SPECIAL CONSIDERATIONS¶
Pregnancy, pediatric, and elderly populations require tailored management. Medication overuse headache is a common complication of frequent acute treatment.
9.1 Pregnancy¶
Avoid NSAIDs in late pregnancy. Paracetamol is preferred. Triptans are generally contraindicated.
9.2 Medication Overuse¶
Chronic use of analgesics (e.g., NSAIDs, triptans) can lead to medication-overuse headache. Discontinuation is often required for prevention.
10. KEY POINTS & CLINICAL PEARLS¶
Use the MIDAS score to assess migraine disability. Prioritize triptans for acute attacks and CGRP inhibitors for prevention. Avoid NSAIDs in patients with cardiovascular risk. Neuromodulation (sTMS, nVNS) is effective for acute and preventive treatment.