IM17.1-14 | Headache — Graded Quiz

Correct. This is medication-overuse headache (MOH): sumatriptan >=10 days/month and ibuprofen >=15 days/month for >3 months, with transformation of episodic to daily headache. The primary treatment is withdrawal of the overused medication. Adding a prophylactic without first withdrawing the overused agent is ineffective — prophylactics fail in active MOH. Ergotamine causes MOH itself. MRI is not indicated in the absence of red flags when MOH explains the change.

In MOH, prophylaxis added on top of ongoing overuse is ineffective. The essential first step is drug withdrawal. Withdrawal headache peaks at 1–3 days and resolves over 1–2 weeks. After a 2–4 week washout, prophylaxis can be initiated if indicated.

Medication-overuse headache requires withdrawal of the causative agent(s) as the primary intervention. Prophylaxis started without withdrawal will not succeed. Ergotamine is itself a cause of MOH. A change in headache pattern in a patient with established primary headache without new neurological signs does not automatically warrant MRI if MOH adequately explains the change.

Correct. Giant cell arteritis (GCA) with visual symptoms is an ophthalmological emergency. High-dose prednisolone (1 mg/kg/day, up to 60 mg/day; IV methylprednisolone if vision already affected) must be started immediately to prevent permanent visual loss from anterior ischaemic optic neuropathy. Temporal artery biopsy can be performed within 1–2 weeks after starting steroids without significantly reducing diagnostic sensitivity — histological changes persist. Awaiting biopsy risks irreversible blindness.

GCA red flags: age >50, new headache, elevated ESR/CRP, temporal tenderness, jaw claudication, visual symptoms. Treat immediately with high-dose prednisolone — never delay for biopsy. Biopsy remains diagnostic for 1–2 weeks post-steroids. Untreated = irreversible bilateral blindness.

Giant cell arteritis with visual involvement is an emergency. Start high-dose corticosteroids immediately — do not delay for biopsy. Biopsy can still be diagnostic up to 2–4 weeks after starting steroids. Jaw claudication + scalp tenderness + raised ESR + visual symptoms in an older patient = GCA until proven otherwise.

Correct. This presentation — meningism + non-blanching rash + haemodynamic instability — is consistent with meningococcal meningitis/meningococcaemia, a life-threatening emergency. IV ceftriaxone 2 g should be given IMMEDIATELY. The sequence is: blood cultures (30 seconds) → IV ceftriaxone → CT head → LP only if safe (no papilloedema, no focal deficit, not haemodynamically unstable). Antibiotics must not be withheld pending CT or LP — every hour of delay increases mortality. Add IV dexamethasone 0.15 mg/kg for adjunctive anti-inflammatory benefit.

Bacterial meningitis emergency sequence: blood cultures → IV ceftriaxone 2 g IMMEDIATELY → CT head → LP if safe. Dexamethasone adjunctive. Non-blanching rash = meningococcaemia. Do NOT delay antibiotics for LP or CT in a deteriorating patient.

In suspected bacterial meningitis with haemodynamic instability or signs of raised ICP, blood cultures should be taken and IV ceftriaxone given IMMEDIATELY. Never delay antibiotics for LP. LP is safe only if CT shows no mass lesion, no signs of raised ICP, and patient is haemodynamically stable. Add IV dexamethasone as adjunctive therapy.

Correct. Ring-enhancing lesion with mass effect, midline shift, and papilloedema is a clear contraindication to LP (risk of transtentorial herniation). The presence of a secondary headache cause has been established by CT. The differential includes primary brain tumour, cerebral abscess, or metastasis — all requiring urgent neurosurgical assessment. LP is absolutely contraindicated here. Corticosteroids (dexamethasone) reduce vasogenic oedema around the tumour as a temporising measure.

Contraindications to LP: papilloedema, focal neurological deficit, altered consciousness, mass lesion with midline shift, coagulopathy. CT head first if any of these are present. LP in the presence of mass effect risks fatal herniation.

LP is absolutely contraindicated with papilloedema plus a mass lesion with midline shift — risk of coning (transtentorial herniation). CT has already established a secondary headache cause. The next step is urgent neurosurgical referral. Dexamethasone reduces perilesional oedema as a bridge to definitive management.

Correct. CT sensitivity for SAH falls from ~98% at 6 hours to approximately 85% at 24 hours and ~50% at 1 week. A normal CT at 13 hours post-ictus does NOT exclude SAH. LP at >=12 hours after ictus should be performed to look for xanthochromia (bilirubin from haemoglobin breakdown, detected by spectrophotometry) and/or a uniformly elevated red cell count that does not decrease between tubes 1 and 4. Xanthochromia peaks at 12 hours and persists for up to 2 weeks.

SAH investigation: CT head first (sensitivity ~98% at 6 hours). If CT normal and suspicion high, LP at >=12 hours for xanthochromia (spectrophotometry) and uniform RBC count. CT-negative/LP-positive SAH diagnosis then triggers CTA to locate aneurysm.

A normal CT at 13 hours after thunderclap headache does not exclude SAH. CT sensitivity for SAH falls with time — by 24 hours it is ~85%. LP at >=12 hours is mandatory: look for xanthochromia (yellow colour from bilirubin, detected by spectrophotometry) and uniformly elevated RBCs. A traumatic tap shows falling RBC count between tubes; true SAH shows uniform count.

Correct. Viral (aseptic) meningitis: clear CSF, lymphocytic pleocytosis (typically <500/mm3), mildly elevated protein (<100 mg/dL), NORMAL glucose (CSF:blood ratio >0.6), negative Gram stain. The parotid swelling prodrome suggests mumps virus as the aetiology. Management is supportive. TBM would show very low glucose, very high protein, and lymphocytic pleocytosis with a longer prodrome and often fibrin clot. Cryptococcal meningitis is associated with immunosuppression and high opening pressure.

Viral meningitis: CSF clear, lymphocytic pleocytosis, mildly elevated protein, NORMAL glucose (CSF:blood ratio >0.6). No treatment needed beyond supportive care. Contrast with TBM: very low glucose + very high protein + lymphocytic + pellicle. India ink/crypto antigen for suspected fungal.

Viral meningitis CSF: clear, lymphocytic pleocytosis (<500/mm3), protein mildly elevated, glucose NORMAL (ratio >0.6). TBM has very low glucose (<2.2 mmol/L), very high protein, low lymphocytic count, often fibrin web. Bacterial meningitis has neutrophilic pleocytosis and very low glucose. Normal glucose ratio + lymphocytic pleocytosis + parotid prodrome = mumps viral meningitis.

Correct. Hypertensive encephalopathy is caused by failure of cerebrovascular autoregulation leading to cerebral oedema. Features: severe hypertension (usually >180/120) + encephalopathy + papilloedema + flame haemorrhages. Management: IV antihypertensive (labetalol, nicardipine, sodium nitroprusside) targeting a 20–25% reduction in mean arterial pressure (MAP) over the first hour; avoid rapid normalisation which risks cerebral hypoperfusion. This is a SNNOOP10 red flag headache (secondary cause: hypertension).

Hypertensive encephalopathy: severe hypertension + confusion + papilloedema + fundal haemorrhages. Manage with IV antihypertensives; reduce MAP by 20–25% over first hour. Rapid normalisation risks cerebral hypoperfusion. A secondary headache requiring emergency admission (SNNOOP10 red flag).

Hypertensive encephalopathy (BP >180/120 + encephalopathy + papilloedema) requires controlled IV antihypertensive therapy. The target is 20–25% MAP reduction in the first hour — NOT rapid normalisation to normal range, which risks ischaemic stroke from impaired autoregulation. This is a secondary headache requiring emergency admission.

Correct. LP in adults is performed between L3–L4 or L4–L5 (below the conus medullaris which ends at L1–L2) to avoid spinal cord injury. The lateral decubitus (left lateral) position with maximal spine flexion (knees drawn to chest, chin tucked) opens the interspinous spaces maximally and is the standard position for measuring opening pressure. The sitting position opens the spaces but does not allow accurate opening pressure measurement.

LP level: L3–L4 or L4–L5 (below conus at L1–L2). Position: lateral decubitus, maximally flexed (fetal position) for accurate opening pressure. Needle tip: subarachnoid space. Withdraw stylet to check for CSF flow before any injection.

LP is performed at L3–L4 or L4–L5 to stay below the conus medullaris (ends at L1–L2 in adults). The left lateral decubitus position with maximal flexion (fetal position) opens the interspinous spaces and permits accurate measurement of CSF opening pressure. Sitting position increases the measured opening pressure artefactually.

Correct. Sodium valproate is absolutely contraindicated in pregnancy (teratogen: neural tube defects, INTEND data showing cognitive impairment in exposed children — highest-risk preventive agent). Topiramate carries significant teratogenic risk (oral clefts). Among standard prophylactics, propranolol (low-dose) and amitriptyline have the relatively better safety profiles in pregnancy and are used when the benefit clearly outweighs risk. Triptans are not preventive agents.

Migraine prophylaxis in pregnancy: valproate absolutely contraindicated (teratogen). Topiramate also teratogenic. Propranolol and amitriptyline have relatively better safety profiles and are used with caution. Non-pharmacological strategies (trigger avoidance, biofeedback) preferred first.

Valproate is the MOST dangerous preventive in pregnancy (neural tube defects, neurodevelopmental harm; absolutely contraindicated). Topiramate also has significant teratogenic risk (cleft palate). Propranolol and amitriptyline are used cautiously in pregnancy when prophylaxis is essential. Sumatriptan is an abortive agent, not preventive.

Correct. Triptans are contraindicated in established coronary artery disease, prior MI or stroke, uncontrolled hypertension, and peripheral vascular disease. This patient has multiple cardiovascular risk factors: smoking, obesity (BMI >30), family history of premature CAD (<55 in first-degree male relative), and COCP use. No single factor is an absolute contraindication, but the constellation warrants formal cardiovascular risk assessment before prescribing. Sumatriptan causes vasoconstriction via 5-HT1B receptors; in the setting of underlying coronary artery disease this can precipitate myocardial ischaemia.

Triptans: absolute contraindication in established coronary artery disease, prior stroke/TIA, uncontrolled hypertension, Prinzmetal angina. Multiple cardiovascular risk factors warrant formal assessment before prescribing. Mechanism: 5-HT1B agonism causes intracranial vasoconstriction but also has mild coronary vasoconstrictive effect.

Triptan contraindications: established CAD, prior MI/stroke, peripheral vascular disease, uncontrolled HTN, Prinzmetal angina, pregnancy. The cumulative cardiovascular risk from smoking + obesity + family history of premature CAD + COCP use in this patient requires formal risk stratification before triptan prescribing, even in the absence of known disease. Triptans are not contraindicated in migraine itself.

Correct. Giant cell arteritis (GCA) is diagnosed clinically in this setting: new headache in a patient >50 years, scalp/temporal tenderness, jaw claudication, dramatically elevated ESR and CRP, weight loss. LP is neither indicated nor helpful here — GCA is not a meningeal disease. The clinical priority is IMMEDIATE high-dose corticosteroids to prevent ischaemic optic neuropathy and visual loss. Temporal artery biopsy confirms the diagnosis but steroids must not await it.

Giant cell arteritis is a large-vessel vasculitis, not meningitis. LP is not indicated. Temporal artery biopsy is the gold standard but steroids must be started immediately in suspected GCA with visual symptoms. Skip LP; start steroids.

Giant cell arteritis does not produce meningitis; LP is not part of the diagnostic pathway. The urgent action is to start high-dose corticosteroids immediately to prevent irreversible visual loss from anterior ischaemic optic neuropathy. Biopsy within 1–2 weeks can still confirm the diagnosis after steroid initiation.