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IM17.1-14 | Headache — Practice Quiz
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A 26-year-old woman presents with recurrent headaches for 2 years. Each episode lasts 6–8 hours, is unilateral, pulsating, of moderate-to-severe intensity, and is associated with nausea and photophobia. The headaches are aggravated by climbing stairs. Neurological examination is normal. Which ICHD-3 diagnosis best fits this presentation?
Correct. ICHD-3 criteria for migraine without aura require at least 5 attacks lasting 4–72 hours with at least 2 of: unilateral, pulsating, moderate-to-severe intensity, aggravation by routine physical activity; plus at least 1 of: nausea/vomiting or photophobia and phonophobia. This presentation meets all criteria. No aura is described.
ICHD-3 migraine without aura: at least 5 attacks, 4–72 hours duration, unilateral pulsating moderate-to-severe pain aggravated by activity, plus nausea/vomiting or photophobia and phonophobia. Female-to-male ratio 3:1.
Migraine without aura requires: headache lasting 4–72 hours, unilateral pulsating moderate-to-severe pain aggravated by activity, with nausea or photophobia/phonophobia, occurring in at least 5 attacks. Tension-type headache is bilateral, pressing (non-pulsating), and not aggravated by activity. Cluster headache is strictly unilateral periorbital with autonomic features and lasts 15–180 minutes.
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A 32-year-old man describes attacks of severe, strictly unilateral periorbital pain lasting 45–60 minutes, occurring once or twice daily for 3 weeks, always at night. During attacks he has ipsilateral lacrimation, nasal congestion, and ptosis. Between attacks he is completely well. What is the MOST likely diagnosis?
Correct. Cluster headache is characterised by strictly unilateral periorbital or temporal pain of very severe intensity lasting 15–180 minutes, occurring up to 8 times per day in clusters (typically weeks to months), with ipsilateral cranial autonomic features (lacrimation, rhinorrhoea, conjunctival injection, Horner syndrome). Male predominance, nocturnal attacks are classic.
Cluster headache is a TAC: strictly unilateral severe periorbital pain lasting 15–180 minutes with ipsilateral autonomic features (lacrimation, rhinorrhoea, conjunctival injection, Horner syndrome). Male predominance. Attacks cluster over weeks then remit.
The combination of strictly unilateral severe periorbital pain lasting 15–180 minutes with ipsilateral autonomic features (lacrimation, rhinorrhoea, ptosis/miosis = Horner) in a cluster pattern is diagnostic of cluster headache, a trigeminal autonomic cephalalgia (TAC). Migraine is longer-lasting and lacks prominent ipsilateral autonomic signs. Trigeminal neuralgia produces lancinating electric-shock pain in seconds.
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A 38-year-old woman with known migraine presents to the emergency department after a new headache that reached maximal severity within 30 seconds of onset while exercising. She describes it as the worst headache of her life. The headache is still severe. Which SNNOOP10 red flag does this represent, and what is the FIRST investigation of choice?
Correct. Thunderclap headache — reaching maximal intensity within 1 minute (classically described as seconds) — is the most critical SNNOOP10 red flag because subarachnoid haemorrhage (SAH) must be excluded. CT head (non-contrast) is the first investigation: sensitivity for SAH is approximately 98% within 6 hours of ictus. A prior history of migraine does NOT make thunderclap headache safe to attribute to migraine.
Thunderclap headache (onset to peak within seconds) = SAH until proven otherwise. First step: non-contrast CT head (sensitivity ~98% at 6 hours, falls to ~50% at 1 week). If CT negative with high suspicion: LP at >=12 hours to detect xanthochromia.
A thunderclap onset (peak within seconds to 1 minute) is the premier red flag for subarachnoid haemorrhage (SAH). Non-contrast CT head is the first investigation, with approximately 98% sensitivity within 6 hours. If CT is negative or equivocal and suspicion remains, lumbar puncture at 12 hours or later looks for xanthochromia or elevated red cells. Never attribute thunderclap headache to a pre-existing primary headache disorder without ruling out SAH.
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A 24-year-old woman describes a 20-minute episode of slowly spreading numbness and tingling starting in her right hand, moving up the arm and then involving the face and tongue, followed by a moderate unilateral throbbing headache lasting 8 hours. She has had similar episodes three times. What is the MOST accurate diagnosis?
Correct. Migraine with typical sensory aura is characterised by a gradual spread of sensory disturbance (cheiro-oral march — hand, arm, face) over 5–60 minutes, unilateral, fully reversible, followed within 60 minutes by migraine headache. The slow Jacksonian spread (marching) distinguishes it from TIA (which has abrupt onset). Brainstem aura requires diplopia, dysarthria, tinnitus, ataxia, decreased consciousness. Hemiplegic migraine has motor weakness.
Migraine aura spreads gradually over 5–60 minutes (cortical spreading depression), distinguishing it from TIA (abrupt) and epilepsy (rapid Jacksonian march in seconds). Typical aura = visual, sensory, or speech/language. Followed by headache within 60 minutes.
The key discriminating feature is the gradual spread (march) of sensory symptoms over 5–60 minutes — this is the hallmark of aura, driven by cortical spreading depression. TIA has abrupt onset without spread. The sensory symptoms are unilateral, fully reversible, and followed by headache. Without motor weakness, hemiplegic migraine is excluded; without brainstem symptoms, brainstem aura is excluded.
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A 45-year-old man presents with a band-like, bilateral, pressing headache of mild-to-moderate severity lasting 4 hours. There is no nausea, vomiting, photophobia, or phonophobia. He has had similar headaches twice a week for the past 3 months. Neurological examination is normal. Which diagnosis is MOST consistent with ICHD-3 criteria?
Correct. ICHD-3 tension-type headache (TTH): bilateral, pressing/tightening (non-pulsating), mild-to-moderate intensity, not aggravated by routine activity, without nausea/vomiting, and photophobia and phonophobia are not both present. Frequent episodic TTH = 1–14 headache days per month on average for >3 months. Chronic TTH requires >=15 days per month. No overuse is mentioned, and daily unremitting onset is not described.
TTH: bilateral, pressing, mild-to-moderate, not aggravated by activity, no nausea, no combined photophobia + phonophobia. Episodic (<15 days/month) vs chronic (>=15 days/month). Most common primary headache globally.
Tension-type headache is bilateral, pressing (non-pulsating), mild-to-moderate, NOT aggravated by routine physical activity, with absent nausea/vomiting and not both photophobia and phonophobia simultaneously. Frequency 1–14 days/month = frequent episodic TTH. Chronic TTH requires >=15 headache days/month. Without documented medication overuse or daily onset from the start, MOH and NDPH are not the primary diagnosis.
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A 30-year-old woman presents with daily headaches for the past 4 months. She previously had episodic migraine (2–3 attacks per month) well controlled on sumatriptan. Over the past 6 months she has been using sumatriptan 3–4 times per week. Now her headaches occur every day, are dull and bilateral in the morning, and worsen with each dose of sumatriptan wearing off. What is the MOST likely diagnosis?
Correct. Medication-overuse headache (MOH) develops in patients with primary headache who use acute medications excessively: triptans or ergotamine on >=10 days per month, simple analgesics on >=15 days per month, for more than 3 months. The paradoxical result is daily or near-daily headache that worsens with repeated dosing. Treatment is withdrawal of the overused medication — the headaches typically worsen transiently then improve.
Medication-overuse headache: prior episodic headache + acute drug use >=10 days/month (triptans/ergots) or >=15 days/month (analgesics) for >3 months = daily headache. Treatment = withdraw the overused medication. Triptans are a common culprit because of their efficacy and frequent use.
Medication-overuse headache (MOH) is triggered by excessive use of acute headache medications (triptans: >=10 days/month; analgesics: >=15 days/month for >3 months). The hallmark is daily headache in a patient who previously had episodic headache, with headache worsening as each dose wears off. Treatment is controlled withdrawal of the overused agent. The key teaching pearl is: if a patient's headaches worsen the more painkillers they take, think MOH.
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A 28-year-old woman is diagnosed with migraine without aura (>4 attacks per month, each lasting 12–24 hours, severely affecting work). She has no cardiovascular disease or hypertension. Which of the following represents appropriate FIRST-LINE ABORTIVE therapy for an individual attack?
Correct. Triptans (5-HT1B/1D agonists) are first-line acute therapy for moderate-to-severe migraine or for attacks that do not respond to simple analgesics. Sumatriptan is the prototype; oral dose 50–100 mg, with a second dose allowed after 2 hours if partial response. NSAIDs (ibuprofen, naproxen) are co-first-line for mild-to-moderate attacks. Amitriptyline and propranolol are prophylactic agents, NOT acute. Opioids (codeine) should be avoided due to MOH risk.
Abortive migraine therapy: NSAIDs/aspirin for mild-to-moderate; triptans (sumatriptan 50–100 mg oral) for moderate-to-severe or NSAID-resistant. Triptans are 5-HT1B/1D agonists — cause intracranial vasoconstriction + inhibit CGRP release. Contraindicated in coronary artery disease, stroke, uncontrolled hypertension.
Acute migraine treatment: mild-to-moderate attacks = NSAIDs or aspirin 900 mg + metoclopramide. Moderate-to-severe or NSAID-resistant attacks = triptans (sumatriptan 50–100 mg oral, or 6 mg subcutaneous for fastest onset). Amitriptyline and propranolol are preventive, not abortive. Opioids are discouraged because of medication-overuse headache risk.
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A 35-year-old woman has migraine without aura with 5 attacks per month, each lasting >12 hours. She requests preventive therapy. Which of the following agents is evidence-based FIRST-LINE for migraine prophylaxis?
Correct. First-line preventive agents for migraine include: beta-blockers (propranolol 40–160 mg/day, metoprolol), antiepileptics (topiramate 25–100 mg/day, valproate), and tricyclics (amitriptyline 10–75 mg at night). Propranolol has the strongest evidence. Preventive therapy is indicated when attacks occur >=4 days/month, significantly impair function, or do not respond well to abortive therapy. Sumatriptan is abortive only. Carbamazepine is used for trigeminal neuralgia, not migraine prophylaxis.
Migraine prevention (>=4 attacks/month or functional impairment): first-line = propranolol, topiramate, amitriptyline. Second-line = valproate, candesartan, flunarizine. Assess efficacy after 8–12 weeks. Contraindications: propranolol in asthma; valproate in women of childbearing age.
Migraine prophylaxis first-line options: propranolol (beta-blocker), topiramate (antiepileptic), amitriptyline (TCA), valproate. Indication: >=4 attacks/month or significant functional impairment. Sumatriptan is an abortive agent only. Carbamazepine is NOT used in migraine. Each preventive needs 8–12 weeks to assess efficacy.
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A 50-year-old man presents with fever (38.8°C), severe headache, neck stiffness, and photophobia for 18 hours. He is drowsy with a GCS of 13/15. CSF analysis shows: opening pressure 280 mmH2O, white cells 3200/mm3 (90% neutrophils), protein 280 mg/dL, glucose 28 mg/dL (blood glucose 90 mg/dL). Which CSF pattern is this?
Correct. The CSF pattern is classic for bacterial meningitis: markedly elevated neutrophilic pleocytosis (>1000/mm3, predominantly neutrophils), high protein (>100 mg/dL), very low CSF:blood glucose ratio (28/90 = 0.31; normal >0.6). The CSF:blood glucose ratio below 0.4 is characteristic of bacterial (and TB) meningitis, distinguishing it from viral meningitis (normal glucose).
Bacterial meningitis CSF: turbid, neutrophilic pleocytosis (>1000/mm3), protein >100 mg/dL, glucose very low (CSF:blood ratio <0.4). Viral: clear, lymphocytic <500/mm3, mildly elevated protein, normal glucose. TBM: lymphocytic, very high protein, very low glucose, often fibrin web.
Bacterial meningitis CSF: elevated neutrophilic pleocytosis (>500–1000/mm3), high protein (>100 mg/dL), low glucose (CSF:blood ratio <0.4). Viral meningitis has lymphocytic pleocytosis, mildly elevated protein, and normal glucose. TBM has lymphocytic pleocytosis, very high protein, very low glucose, often with a pellicle; opening pressure elevated. Xanthochromia and high red cells characterise SAH.
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A 29-year-old HIV-positive man (CD4 count 45 cells/mcL) presents with 3 weeks of gradually worsening headache, neck stiffness, and confusion. LP is performed: opening pressure 380 mmH2O, lymphocytic pleocytosis, elevated protein, very low glucose. India ink preparation shows encapsulated yeast. What is the MOST appropriate first-line treatment?
Correct. India ink showing encapsulated yeast plus the clinical context (HIV, CD4 <100, subacute onset, very high opening pressure) confirms cryptococcal meningitis. Treatment follows a 3-phase protocol: Induction (2 weeks) = IV liposomal amphotericin B 3–4 mg/kg/day plus flucytosine 100 mg/kg/day; Consolidation (8 weeks) = oral fluconazole 400 mg/day; Maintenance = fluconazole 200 mg/day until immune reconstitution. Serial therapeutic lumbar punctures are required if opening pressure remains >250 mmH2O.
Cryptococcal meningitis (AIDS, CD4 <100): India ink positive, elevated ICP. Treatment: induction = amphotericin B + flucytosine x2 weeks; consolidation = fluconazole 400 mg x8 weeks; maintenance = fluconazole 200 mg. Manage elevated ICP with serial therapeutic LPs.
Cryptococcal meningitis in HIV: confirmed by India ink (encapsulated budding yeast) or cryptococcal antigen. Treatment: Induction = amphotericin B plus flucytosine for 2 weeks; Consolidation = fluconazole 400 mg/day for 8 weeks; Maintenance = fluconazole 200 mg/day. Fluconazole alone is NOT adequate for induction in severe or HIV-associated disease. Raised intracranial pressure (>250 mmH2O) is managed by therapeutic LP.
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