IM17.1-14 | Headache — Glossary

Nucleoside analogue antiviral; drug of choice for herpes simplex encephalitis (HSE) and severe HSV infection; mechanism: selectively phosphorylated by viral thymidine kinase → acyclovir triphosphate inhibits HSV DNA polymerase (chain termination); dose for HSE: 10 mg/kg IV every 8 hours for 14–21 days; must be started empirically in suspected encephalitis without awaiting HSV PCR; adverse effects: nephrotoxicity (crystalline nephropathy — ensure hydration), phlebitis.

Tricyclic antidepressant used as a first-line migraine and tension-type headache preventive at sub-antidepressant doses (10–75 mg nocte); mechanism: serotonin/noradrenaline reuptake inhibition, sodium channel blockade, antihistamine; adverse effects: sedation, dry mouth, constipation, QTc prolongation; particularly useful when migraine is comorbid with depression, anxiety, or insomnia.

The cognitive tendency to over-weight the first diagnosis reached and under-weight subsequent evidence that points to a different diagnosis; in headache practice, a major cause of missed SAH and meningitis in patients previously labelled with migraine or tension headache; prevented by re-evaluating every significant change in headache pattern.

Transient, fully reversible focal neurological symptoms occurring before or during the headache phase of migraine; most commonly visual (scintillating scotoma — zigzag fortification spectra with central scotoma); can also be sensory, language, motor (hemiplegic), brainstem, or retinal.

Turbid/purulent appearance; markedly elevated WBC (500–10,000+ cells/mm³) predominantly neutrophils; markedly elevated protein (>100 mg/dL); markedly low glucose (CSF:serum ratio <0.4); elevated opening pressure; Gram stain positive in 60–80% before antibiotics.

Involuntary flexion of the hips and knees in response to passive flexion of the neck in a supine patient; a sign of meningeal irritation reflecting reflex reduction of meningeal tension; sensitivity similar to Kernig's; high specificity when present.

A vasodilatory neuropeptide released from trigeminal nerve terminals during migraine attacks, causing meningeal vasodilation and neurogenic inflammation; CGRP levels are elevated in migraine attacks and fall with triptan administration; target of the newest preventive migraine therapies (monoclonal antibodies against CGRP or its receptor).

The bundle of L2–S5 nerve roots descending through the lumbar cistern below the conus medullaris (which ends at L1–L2 in adults); floats freely in CSF and deflects away from the LP needle rather than being injured; the anatomical basis for the safety of LP below L2.

Third-generation cephalosporin; first-line treatment for community-acquired bacterial meningitis; dose 2 g IV every 12 hours; excellent CSF penetration (CSF:serum ratio ~20–30% at inflamed meninges); bactericidal via inhibition of cell wall synthesis; covers S. pneumoniae, N. meningitidis, H. influenzae; does NOT cover Listeria monocytogenes — add ampicillin in patients >60 years or immunocompromised.

Thrombosis of the dural venous sinuses or cortical veins causing raised ICP and sometimes cortical venous infarction; risk factors include OCP use, puerperium, dehydration, thrombophilia; presents with progressive headache, papilloedema, seizures; diagnosed by MRI with MR venography; treated with anticoagulation.

Referred pain from upper cervical spine structures (C1–3) transmitted via the trigeminocervical complex to the head; characterised by onset from neck movement, unilateral distribution from occiput to frontal region, reproduction of headache by pressure on cervical structures, and restricted cervical range of motion; classified as secondary headache in ICHD-3.

Migraine occurring on ≥15 days per month for >3 months, with migraine features on ≥8 of those days; often associated with medication-overuse headache; requires preventive pharmacotherapy.

A trigeminal autonomic cephalalgia characterised by severe unilateral periorbital or temporal pain lasting 15–180 minutes with ipsilateral cranial autonomic features (lacrimation, nasal congestion, conjunctival injection, miosis, ptosis); attacks cluster in periods of weeks to months; patients are typically agitated and pace during attacks.

A delicate fibrin pellicle that forms when tuberculous meningitis CSF (with its characteristically elevated protein) is left to stand in a test tube; a classic but relatively insensitive sign of TBM; represents the high fibrinogen content of the CSF in this condition.

The tapered lower end of the spinal cord, terminating at approximately L1–L2 in adults (L3 in neonates); structures below the conus are cauda equina nerve roots only; LP below L2 avoids direct cord injury.

A slow wave of electrochemical neuronal depolarisation followed by sustained suppression, propagating at 3–5 mm/min across the cortex; the electrophysiological correlate of migraine aura.

Meningitis caused by Cryptococcus neoformans in HIV patients with CD4 <100 cells/µL; minimal CSF pleocytosis (blunted immune response), mildly elevated protein, mildly low glucose, markedly elevated opening pressure; India ink shows encapsulated yeast (sensitivity ~70–80%); CrAg has sensitivity >95%; serial therapeutic LPs to reduce ICP are critical.

Ratio of CSF glucose to simultaneously measured serum glucose; normal >0.6; reduced in bacterial meningitis (<0.4) and TBM (<0.5); normal (≥0.6) in viral meningitis and SAH; requires simultaneous serum glucose measurement at LP.

The combination of hypertension, bradycardia, and irregular (Cheyne-Stokes) breathing seen as a late sign of massively elevated intracranial pressure indicating impending brainstem herniation; the triad must not be awaited — raised ICP management must begin at first clinical suspicion.

IV dexamethasone 0.15 mg/kg q6h for 4 days, started with or before the first antibiotic dose; reduces mortality and neurological sequelae (especially deafness in pneumococcal meningitis) by attenuating the inflammatory response; not indicated if TBM or cryptococcal meningitis is the primary concern.

IV dexamethasone 0.15 mg/kg every 6 hours for 4 days in bacterial meningitis, started WITH or BEFORE the first antibiotic dose; reduces mortality and neurological sequelae (especially deafness from pneumococcal meningitis) by attenuating the cytokine-mediated inflammatory response to bacterial lysis; also used in TBM (0.3–0.4 mg/kg/day tapering) to reduce meningeal inflammation and improve survival.

Injection of 10–20 mL of autologous blood into the epidural space at the LP site to seal a persistent dural CSF leak; performed by an anaesthetist for refractory post-LP headache (>72 hours, orthostatic); >90% effective.

Non-selective serotonin (5-HT₁) agonists and vasoconstrictors used in acute migraine; ergotamine tartrate 1–2 mg oral; DHE 1 mg IM or IV (useful in emergency department); contraindicated in cardiovascular disease, cerebrovascular disease, peripheral vascular disease; ergotamine overuse (>2 days/week) causes ergotamine-MOH; largely replaced by triptans due to better tolerability.

Automated nucleic acid amplification test for Mycobacterium tuberculosis and rifampicin resistance on CSF or other specimens; results in ~2 hours; sensitivity for TBM ~50–80%; WHO-recommended rapid diagnostic test for TBM, superior to AFB smear.

A granulomatous vasculitis of medium and large vessels typically affecting the temporal artery; presents with new-onset headache in patients >50 years with scalp tenderness, jaw claudication, and elevated ESR (typically >50 mm/hr); ophthalmic artery involvement can cause irreversible blindness; treated with high-dose prednisolone initiated empirically before biopsy.

A structured patient record (paper or app) logging each headache attack with date, time, duration, severity, potential triggers, associated symptoms, medications taken and their effect, and menstrual cycle; establishes attack frequency baseline for preventive therapy decisions, identifies consistent triggers for avoidance, and documents the MOH medication-day count.

A rare migraine subtype characterised by motor weakness as part of the aura; either familial (autosomal dominant mutations in CACNA1A, ATP1A2, SCN1A) or sporadic; triptans and ergotamine are contraindicated.

International Classification of Headache Disorders, 3rd edition (2018), published by the International Headache Society; provides operationalised diagnostic criteria for over 200 headache diagnoses, organised into primary headaches, secondary headaches, and cranial neuralgias.

Raised intracranial pressure without a structural cause on neuroimaging; typically affects obese young women; presents with daily headache, papilloedema, visual obscurations, and CN VI palsy; diagnosed by elevated opening CSF pressure >25 cmH₂O on LP after MRI/MRV excludes CVT; treated with acetazolamide and weight loss.

Rapid CSF staining in which India ink particles are excluded by the large polysaccharide capsule of Cryptococcus neoformans, producing a clear halo around the dark-stained cell body; sensitivity ~70–80% in AIDS-related cryptococcal meningitis; supplemented by CrAg testing.

Inability to passively extend the knee beyond approximately 135° when the hip is flexed to 90° due to pain from meningeal traction; a sign of meningeal irritation; sensitivity ~5–30% for bacterial meningitis, specificity ~95%; performed with the patient supine and relaxed.

Paradoxical worsening and increased frequency of headache due to regular overuse of acute headache medications; defined as use of simple analgesics/NSAIDs/paracetamol on ≥15 days/month, or triptans/ergotamine/opioids on ≥10 days/month, for >3 months; primary treatment is analgesic detoxification.

Chemoprophylaxis for close contacts of a confirmed meningococcal meningitis case to eradicate nasopharyngeal carriage; options: rifampicin 600 mg twice daily for 2 days; or single-dose oral ciprofloxacin 500 mg (preferred in adults — simpler regimen); or single-dose ceftriaxone 250 mg IM (preferred in pregnancy); meningococcal disease is a notifiable condition requiring immediate public health notification.

Dopamine D2 antagonist; pro-kinetic (promotes gastric emptying) and anti-emetic; used as adjunct to oral analgesics in migraine to improve drug absorption by reversing migraine-related gastric stasis; dose 10 mg oral or IV; adverse effects: extrapyramidal reactions (acute dystonia — particularly in young women with repeated dosing), tardive dyskinesia with prolonged use.

Previously termed classical migraine; migraine preceded by or accompanied by transient, fully reversible focal neurological symptoms (aura) that develop over ≥5 minutes and last <60 minutes; most commonly visual (scintillating scotoma). An absolute contraindication to combined oestrogen-containing contraceptives.

The most common form of migraine (75–80% of cases); characterised by recurrent 4–72-hour attacks of moderate-to-severe pulsating unilateral headache, aggravated by physical activity, with nausea or photophobia and phonophobia; ≥5 attacks required for ICHD-3 diagnosis.

Unilateral or bilateral CN VI (abducens) palsy producing convergent squint and diplopia on lateral gaze, occurring in raised ICP from any cause due to the long intracranial course of the nerve making it susceptible to stretching; does NOT localise the level of pathology.

National TB Elimination Programme anti-TB regimen for tuberculous meningitis: 2HRZE (2-month intensive phase: isoniazid + rifampicin + pyrazinamide + ethambutol daily, weight-band FDC) + 10–12HR (continuation phase: isoniazid + rifampicin daily) = total 12–18 months; plus dexamethasone and pyridoxine; same four drugs as pulmonary TB but extended continuation phase due to slower CNS mycobacterial clearance.

Resistance to passive neck flexion in the supine patient; a sign of meningeal irritation caused by infection (bacterial, viral, tuberculous meningitis), subarachnoid haemorrhage, or carcinomatous meningitis; indicates the CSF space is inflamed and examination of CSF is required.

The hydrostatic pressure of CSF measured by manometer at LP with the patient in lateral decubitus position; normal 10–20 cmH₂O; elevated in raised ICP, meningitis, CVT; very elevated (>30–40 cmH₂O) in cryptococcal meningitis; must be measured in lateral decubitus for accuracy.

Bilateral swelling of the optic disc due to raised intracranial pressure transmitted along the optic nerve sheath; recognised on fundoscopy by blurred disc margins, disc hyperaemia, loss of the optic disc cup, venous engorgement, and elevation of the disc; requires urgent investigation for raised ICP cause.

Orthostatic headache after LP (worse upright, relieved lying flat) from ongoing CSF leak through the dural puncture site; incidence 10–30%; prevented by smallest needle gauge with bevel parallel to dural fibres; treated with rest, fluids, caffeine; refractory cases need epidural blood patch.

A headache disorder in which the headache itself constitutes the condition, without any underlying structural, vascular, infective, or metabolic cause; examples include migraine, tension-type headache, and cluster headache. Accounts for >90% of headache presentations.

Non-selective beta-adrenoceptor blocker; first-line preventive therapy for migraine; dose 40–120 mg twice daily; contraindicated in asthma/COPD, heart block >1st degree, decompensated heart failure, Raynaud's, insulin-dependent diabetes; inhibits rizatriptan metabolism (use 5 mg not 10 mg rizatriptan if combined).

Co-prescribed with isoniazid (10–25 mg/day) in TB treatment; prevents isoniazid-induced peripheral neuropathy, which occurs due to isoniazid's competition with pyridoxal kinase impairing pyridoxal phosphate (active B6) synthesis; mandatory in TBM due to the extended duration of isoniazid use.

Elevation of pressure within the rigid skull compartment above the normal range (5–15 mmHg); clinical features include morning headache (worse on waking and with Valsalva), effortless vomiting, papilloedema, visual obscurations, CN VI palsy (non-localising), and eventually altered consciousness and herniation syndromes.

An oral triptan (5-HT₁B/₁D agonist) for acute migraine; dose 10 mg oral (available as oral disintegrating tablet — dissolves on tongue without water, useful in nausea); dose reduced to 5 mg when co-prescribed with propranolol (which inhibits rizatriptan metabolism via MAO-A inhibition, increasing rizatriptan plasma levels).

The characteristic visual aura of migraine — a flickering, crescent-shaped arc of zigzag lines (fortification spectra) surrounding a blind spot that expands and moves across the visual field over 20–30 minutes; caused by cortical spreading depression in the visual cortex.

A headache that is a symptom of an underlying condition such as subarachnoid haemorrhage, meningitis, raised intracranial pressure, or medication overuse; always requires investigation to identify and treat the underlying cause.

A thunderclap or severe headache that precedes a major subarachnoid haemorrhage, often by hours to weeks, caused by a 'warning leak' from an aneurysm; may resolve spontaneously and be mistakenly attributed to tension or migraine; missing a sentinel headache and not performing CT then LP is among the most serious errors in emergency medicine.

A validated clinical mnemonic listing 10 red-flag features that should prompt investigation for secondary headache causes: Systemic symptoms, Neoplasm history, Neurological deficit, Onset sudden/thunderclap, Older age new onset, Pattern change, Positional, precipitated by Exertion, Eye symptoms, Referred, Radiation, Retinal symptoms, Risk factors (immunodeficiency).

First-line migraine preventive; mechanism: GABA-transaminase inhibition, sodium channel blockade, suppression of CSD; dose 500–1500 mg/day; highly teratogenic (neural tube defects, cognitive impairment in offspring); absolutely contraindicated in pregnancy and in women of childbearing potential without reliable contraception; adverse effects include weight gain, tremor, alopecia, thrombocytopaenia.

Optical measurement of CSF supernatant absorbance at wavelengths corresponding to oxyhaemoglobin (415 nm) and bilirubin (450–460 nm) after centrifugation; significantly more sensitive than visual inspection for detecting xanthochromia; NICE-recommended method for suspected SAH.

A migraine attack persisting for >72 hours despite adequate treatment; requires emergency admission for IV hydration, parenteral analgesia and anti-emetics, and monitoring; prolonged attacks increase risk of spreading cortical depression and, rarely, migrainous cerebral infarction.

A systematic history-taking approach for headache covering onset mode, temporal pattern, SQOTIA characteristics (Site, Quality, Onset, Timing, Intensity, Aggravating/relieving factors), aura, associated symptoms, precipitants, analgesic use, functional impact, family history, and SNNOOP10 red-flag screen.

Bleeding into the subarachnoid space, most commonly from rupture of an intracranial aneurysm; the classic presentation is thunderclap headache; diagnosis by non-contrast CT head (98% sensitive within 6 hours) followed by lumbar puncture if CT is negative (xanthochromia on spectrophotometry).

The prototypical triptan (5-HT₁B/₁D agonist) for acute migraine; available as oral 50–100 mg, subcutaneous 6 mg (fastest onset, 10–20 min — drug of choice when vomiting prevents oral intake), and nasal spray 10–20 mg; maximum 200 mg/24 hours orally; absolute contraindications include ischaemic heart disease and uncontrolled hypertension.

The most prevalent primary headache disorder globally (up to 70% of adults); characterised by bilateral, pressing or tightening, mild-to-moderate headache that is NOT pulsating and NOT aggravated by physical activity; no nausea; differentiated from migraine by these negative features.

A headache reaching maximum intensity within 60 seconds of onset, often described as 'the worst headache of my life'; requires immediate investigation for subarachnoid haemorrhage — protocol is non-contrast CT head followed by lumbar puncture at ≥12 hours if CT is negative.

First-line migraine preventive; broad mechanism: sodium channel blockade, calcium channel blockade, GABA potentiation, glutamate inhibition, carbonic anhydrase inhibition; dose 25–100 mg/day; key adverse effects: cognitive impairment (word-finding, memory — most clinically significant, dose-dependent), paraesthesiae, weight loss, kidney stones, teratogenic (neural tube defects) — contraceptive counselling mandatory in women of reproductive age.

Inadvertent puncture of an epidural or subdural vessel during LP, introducing blood into the CSF sample; distinguished from true SAH by progressive clearing of blood from tube 1 to tube 4 and a clear non-xanthochromic spun supernatant.

A group of primary headache disorders characterised by strictly unilateral pain with ipsilateral cranial autonomic features (lacrimation, rhinorrhoea, nasal congestion, conjunctival injection, ptosis, miosis); cluster headache is the most important TAC.

The nociceptive pathway consisting of trigeminal sensory nerve terminals innervating meningeal blood vessels, which, when activated, release CGRP and other neuropeptides causing neurogenic inflammation and pain; the final common pathway for migraine headache.

A class of selective 5-HT₁B/₁D receptor agonists used for acute migraine treatment; cause constriction of intracranial vessels (5-HT₁B) and inhibit trigeminal nociceptor CGRP release and signal transmission (5-HT₁D); include sumatriptan, rizatriptan, zolmitriptan, naratriptan; contraindicated in ischaemic heart disease, uncontrolled hypertension, cerebrovascular disease, hemiplegic migraine, and brainstem aura migraine.

Clear or opalescent appearance (cobweb clot on standing); lymphocytic pleocytosis 50–500 cells/mm³; markedly elevated protein (100–500 mg/dL); low glucose (CSF:serum ratio <0.5); AFB smear positive in only 10–40%; GeneXpert MTB/RIF on CSF has sensitivity ~50–80% with results in 2 hours.

The line connecting the two posterior superior iliac crests, crossing the lumbar vertebral column at the L4 spinous process or L4–L5 interspace; primary surface landmark for identifying the LP site.

Clear or slightly turbid appearance; moderately elevated WBC (10–500 cells/mm³) predominantly lymphocytes; mildly elevated protein (50–200 mg/dL); NORMAL glucose (CSF:serum ratio ≥0.6); Gram stain and culture negative; the normal glucose is the key distinguishing feature from bacterial meningitis.

Yellow discolouration of CSF due to degradation of haemoglobin (oxyhaemoglobin → bilirubin) after subarachnoid haemorrhage; detectable by spectrophotometry from ≥12 hours up to 2 weeks after the bleed; a key diagnostic finding in SAH when CT is negative.