GC082 Severe Headache: Headache And Neuralgia; Neuro-imaging I
Severe headache encompasses acute, high-intensity cephalalgias—including primary headaches, neuralgias, and secondary causes—requiring neuroimaging to identify or exclude structural, vascular, or other intracranial pathology.
Headache and Neuralgia; Neuro-imaging I
This lecture (GC 082, Dr. K H Chan) is the foundational neurology headache lecture. It covers the entire spectrum of headache and neuralgia from first principles—classification, history-taking, primary headaches (TTH, migraine, cluster/TACs), secondary headaches (temporal arteritis, headaches of sudden onset), and facial neuralgia (trigeminal neuralgia). The lecture also touches on neuro-imaging indications.
Why this matters clinically: Headache is the single most common neurological symptom you will encounter. The core clinical skill is distinguishing primary headaches (benign, recurrent, no structural cause) from secondary headaches (symptomatic of an underlying, potentially life-threatening pathology). The examiner will test your ability to:
- Classify headaches using IHS criteria
- Take a structured headache history
- Recognize red flags for secondary headache
- Know the mechanisms, treatments, and prophylaxis for migraine and TTH
- Diagnose and manage trigeminal neuralgia
- Know when and what neuroimaging to order
- Recognize temporal arteritis as a medical emergency
Exam relevance: This lecture has been directly tested in past papers (2022 Q59 on trigeminal neuralgia investigation, 2023 Q60 and 2024 Q65 on SAH workup, 2025 Q52 on LP after normal CT in thunderclap headache) [1][2][3][4].
IHS Classification of Headache Disorders
The IHS (International Headache Society) Classification is the framework used to classify all headaches. The ICHD-II/III system divides headaches into primary and secondary categories. [5]
This is the organizing schema for the entire lecture. Every headache you encounter should be mentally filed into one of these categories.
| Category | Examples |
|---|---|
| Migraine | With aura, without aura |
| Tension-type headache (TTH) | Episodic, chronic |
| Cluster headache and other TACs | Cluster, paroxysmal hemicrania, SUNCT |
| Other primary headaches | Exertional, orgasmic cephalgia |
These are the dangerous ones. The lecture emphasizes that diagnosis of primary headache requires careful exclusion of secondary causes [5].
The headache history is structured around these key elements: [5]
- Onset (sudden → thunderclap → SAH until proven otherwise)
- Location (unilateral vs bilateral; frontal, temporal, occipital, periorbital)
- Duration of pain
- Attack frequency & timing (circadian pattern → cluster; morning → ↑ICP)
- Pain severity
- Nature of pain (pulsating → migraine; band-like → TTH; lancinating → neuralgia)
- Aggravating or precipitating factors
- Relieving factors
- Drug Hx (analgesic overuse → MOH)
- Social Hx
- Family Hx (FHM is autosomal dominant)
- Past headache Hx
- Impact of headache (disability, days off work)
Clinical Pearl: Red Flags in Headache
Red flags that suggest secondary headache and mandate urgent investigation:
- Thunderclap onset (peak severity within seconds–minutes) → SAH
- New-onset headache after age 50 → temporal arteritis, SOL
- Progressive worsening / change in pattern → SOL, chronic subdural
- Headache worse in morning / with coughing → raised ICP
- Fever + headache + neck stiffness → meningitis
- Focal neurological deficits
- Seizures
- History of cancer or immunodeficiency
- Headache always on the same side → structural lesion
- Headache not responding to treatment
Tension-Type Headache (TTH)
TTH general diagnostic criteria: [5]
Episodic TTH:
- ≥10 episodes of headache, each lasting 30 min – 7 days
- ≥2 of the following:
- Bilateral location
- Pressing/tightening (non-pulsating) quality
- Mild to moderate intensity
- Not aggravated by routine physical activity
- Both of the following:
- No nausea or vomiting
- No more than one of photophobia or phonophobia [6]
Chronic TTH (CTTH):
- ≥15 headache days per month for ≥3 months [6]
The mechanism involves peripheral and central sensitization. The initial trigger is pericranial myofascial tissue (PMT) tenderness—muscle tension in the head and neck generates nociceptive input. In episodic TTH, peripheral mechanisms dominate. In chronic TTH, central sensitization at the level of the spinal horn/trigeminal nucleus caudalis (SH/TNC) takes over, meaning the brain's pain processing becomes dysfunctional even without ongoing peripheral nociceptive input.
A model for pathophysiology of CTTH: PMT → brainstem interneurons (BI) → motor nuclei (MN) → SH/TNC (spinal horn/trigeminal nucleus caudalis). In CTTH, central sensitization at SH/TNC level becomes the driver of pain rather than peripheral muscle tenderness. [5]
This is why amitriptyline works for CTTH—it modulates central pain processing, not peripheral muscle tension.
Aim: prevent TTH from becoming CHRONIC [5]
Acute/Abortive Treatment:
| Drug | Notes |
|---|---|
| NSAIDs (ibuprofen, naproxen, aspirin 500/1000mg) | First-line for acute attacks |
| COX-2 inhibitor (lumiracoxib) | Alternative if GI concerns |
| Paracetamol (500/1000mg) | Weaker but safer |
| Combinations (NSAID + sedative, caffeine, tranquillisers) | More effective but ↑ risk of MOH |
| Topical Tiger Balm or peppermint oil | Mentioned in the lecture—surprisingly evidence-based for mild TTH |
Medication Overuse Headache (MOH)
Using acute analgesics >2-3 days/week can transform episodic TTH into chronic daily headache (medication overuse headache). This is a common exam trap. The treatment of MOH is withdrawal of the offending analgesic, not adding more drugs.
Prophylactic Treatment (for CTTH):
Long-term prophylactic treatments for TTH: [5]
| Category | Drugs |
|---|---|
| Non-pharmacological | Stress management, relaxation therapy, physical therapy |
| Antidepressants | Amitriptyline (first-line prophylaxis), maprotiline, mirtazapine, slow-release venlafaxine |
| Alpha-2 adrenergic agonist | Tizanidine (+ amitriptyline) |
| Anti-epileptic | Topiramate |
Amitriptyline: reduces daily headache duration by 118 hrs [5]. This is the key prophylactic agent for CTTH.
Migraine
Migraine is a neurovascular disorder of the brain; common, chronic, incapacitating. Attacks of (1) severe headache, (2) autonomic nervous system dysfunction, (3) in some, aura involving neurologic symptoms. [5]
Key epidemiological facts: [5]
- 10% general population (6% males, 15% females); 2010 global prevalence 14.7%
- From age 16, 2–3 times more frequent in females
- Peak incidence: age 14-16 for females, age 10-12 for males
- In women ~age 40: highest prevalence (24%)
- 90% onset before age 50 → new headache after 50 is NOT migraine until proven otherwise
Two main types: [5]
Migraine without aura (75%)
Migraine with aura (1/3 of migraineurs)
- Migraine patients defined as having ≥2 attacks with aura or ≥5 attacks without aura
- Up to 33% migraineurs experience both types of attack
- Up to 42% may have migraine aura without headache (acephalgic migraine)
Aura symptoms: one or more transient focal neurological symptoms [5]
Visual (99%) — the classic scintillating scotoma, zigzag lines, fortification spectra
Sensory (31%) — tingling, numbness, typically spreading over minutes
Aphasic (18%) — difficulty with speech
Motor (6%) — rare; when present, consider familial hemiplegic migraine
- Gradual development over >4 min, or several symptoms in succession
- Usually last 5-60 min (motor symptoms may last longer)
- Aura nearly always precedes headache (follows or accompanies aura within 60 min)
Why does aura develop gradually? Because it reflects cortical spreading depression (CSD)—a slowly propagating wave of neuronal/glial depolarization across the cortex (~3 mm/min). The gradual spread of CSD across the visual cortex produces the expanding scotoma. This is fundamentally different from a TIA/stroke, where onset is sudden.
Migraine Without Aura:
- A: ≥5 attacks fulfilling B-D
- B: Duration 4-72 hours (untreated)
- C: ≥2 of:
- Unilateral
- Pulsating
- Moderate or severe
- Aggravated by routine physical activity
- D: ≥1 of:
- Nausea ± vomiting
- Photophobia AND phonophobia
- E: Not better accounted for by another diagnosis [6]
Migraine With Aura:
- A: ≥2 attacks
- B: ≥1 fully reversible aura symptom (visual/sensory/motor/speech/brainstem/retinal)
- C: ≥2 of:
- At least one aura symptom spreads gradually over ≥5 min
- Each aura lasts 5-60 min
- At least one is unilateral
- Aura accompanied or followed within 60 min by headache [6]
POUND Mnemonic for Migraine
Pulsating, 4-72 hOurs, Unilateral, Nausea/vomiting, Debilitating (aggravated by activity). If ≥4/5 features present, likelihood ratio for migraine is very high. [7]
Dysfunction of brainstem pathways that normally modulate sensory input: [5]
- Trigeminovascular input from meningeal vessels
- Trigemino-autonomic reflex (exaggerated in TACs)
- Modulation of trigeminovascular nociceptive input from dorsal raphe nucleus, locus ceruleus, magnus raphe nucleus
- Reduced cerebral blood flow (oligemia) during migraine aura, preceded by a phase of focal hyperemia
The full pathophysiological cascade explained from first principles:
-
Trigger phase: Internal or external triggers (stress, hormonal changes, foods) activate genetically susceptible brainstem nuclei (especially the dorsal raphe, locus ceruleus, and trigeminal nucleus).
-
Cortical Spreading Depression (CSD): A wave of neuronal/glial depolarization propagates across the cortex. This is the substrate of the aura. CSD activates trigeminal nociceptive afferents in the meninges.
-
Trigeminovascular system activation: CSD and direct brainstem activation cause trigeminal ganglion neurons to release vasoactive neuropeptides, especially CGRP (calcitonin gene-related peptide).
The main source of CGRP is cell bodies in trigeminal ganglia. [5]
-
Neurogenic inflammation: CGRP release causes meningeal vasodilation, plasma protein extravasation, mast cell degranulation → inflammatory soup around meningeal vessels → headache pain.
-
Central sensitization: Prolonged nociceptive input leads to sensitization of second-order neurons in the trigeminal nucleus caudalis → allodynia (pain from normally innocuous stimuli like touching the scalp), throbbing quality, worsening with movement.
-
Autonomic symptoms: The trigemino-autonomic reflex produces nausea, vomiting, pallor, nasal congestion.
FHM genes cause increased neuronal excitability and susceptibility to cortical spreading depression. All 3 genes are implicated in ION TRANSPORT: [5]
| Type | Gene | Protein | Mechanism |
|---|---|---|---|
| FHM1 | CACNA1A | Voltage-gated Ca²⁺ channel α1 subunit | Gain-of-function → ↑ glutamate release → ↑ CSD susceptibility |
| FHM2 | ATP1A2 | Na⁺/K⁺-ATPase α2 subunit | Loss-of-function → impaired glutamate clearance → ↑ CSD |
| FHM3 | SCN1A | Na⁺ channel (SCN) | Gain-of-function → ↑ neuronal excitability → ↑ CSD |
Why this matters for exams: FHM is the proof-of-concept that migraine is a channelopathy. All three mutations converge on the same final common pathway: increased cortical excitability → lowered threshold for CSD → migraine. The examiner may ask you to name the FHM genes or explain how they relate to CSD.
Treatment of Migraine
Treatment of migraine acute attack: [5]
| Step | Drug/Class | Mechanism & Notes |
|---|---|---|
| 1 | Simple analgesics | Paracetamol, NSAIDs (aspirin, ibuprofen) |
| 2 | Ergot derivatives (ergotamine, dihydroergotamine) | 5-HT receptor agonist, inhibit peptide release; sustained generalized vasoconstrictor → adverse vascular events; high risk of overuse syndromes & rebound headache |
| 3 | Ditan (lasmiditan) | 5-HT1F serotonin receptor agonist — no vasoconstrictive effect (safe in cardiovascular disease) |
| 4 | Gepants (small molecule CGRP receptor antagonist) | For moderate-severe migraine attack; block CGRP at the receptor level |
| 5 | Anti-emetics/prokinetics (metoclopramide) | Treat nausea AND improve GI motility → better absorption of oral analgesics |
| 6 | Triptans | See detailed section below |
Triptans are serotonin 5-HT1B/1D receptor agonists with three potential mechanisms of action: [5]
- Cranial vasoconstriction (5-HT1B on vascular smooth muscle)
- Peripheral neuronal inhibition (5-HT1D on trigeminal nerve terminals → ↓ CGRP release)
- Inhibition of transmission through second-order neurons of the trigeminocervical complex → inhibit effects of activated nociceptive trigeminal afferents
Moderate side effects (vasoconstriction) → contraindicated in vascular disorders: [5]
- Coronary artery disease
- Cerebrovascular disease
- Peripheral vascular disease (PVD)
- Uncontrolled hypertension
Triptans vs Ditans vs Gepants
- Triptans (sumatriptan): 5-HT1B/1D agonists → vasoconstrictive → cannot use in vascular disease
- Ditans (lasmiditan): 5-HT1F agonists → NO vasoconstriction → safe in vascular disease but causes CNS sedation
- Gepants (rimegepant, ubrogepant): CGRP receptor antagonists → NO vasoconstriction → can be used for both acute AND preventive treatment
This is a modern distinction the lecture highlights. Know which class to use when triptans are contraindicated.
Migraine prophylaxis is indicated when: [5]
- Attacks weekly / several times a month
- ≥8 headache days per month
- Attacks less often but very prolonged & debilitating
- Hemiplegic migraine, migraine with brainstem aura
- Frequent, prolonged, uncomfortable aura symptoms
- Migrainous infarction
Most effective prophylactic agent available typically reduces headache frequency by ≥50% in ~50% patients [5]
Proven/Well-Accepted Prophylactic Drugs:
| Drug | Key Side Effects (from lecture) |
|---|---|
| Beta-blockers (propranolol, metoprolol) | Reduced energy, tiredness, depression, postural symptoms; contraindicated in asthma |
| Antidepressants (amitriptyline, other TCAs; venlafaxine) | Drowsiness, anticholinergic S/E, weight gain; serotonin syndrome |
| Calcium channel blockers (flunarizine, verapamil) | Tiredness, weight gain, depression, Parkinsonism |
| Valproate | Drowsiness, weight gain, tremor, alopecia, fetal abnormalities, thrombocytopenia, hepatotoxicity |
| Topiramate | Glaucoma, paraesthesia, weight loss (cf. other drugs cause weight gain), ↑ risk renal stones, contraindicated in pregnancy |
| Gabapentin | Dizziness, sedation |
| Methysergide | Leg cramps, alopecia, retroperitoneal fibrosis, mediastinal fibrosis, cardiac valve fibrosis |
High-Yield Side Effects for Exams
- Valproate → fetal abnormalities (teratogenic; avoid in women of childbearing age)
- Methysergide → retroperitoneal/mediastinal/cardiac valve fibrosis (unique to this drug; classic exam question)
- Topiramate → weight LOSS (opposite of most other prophylactics) + renal stones + glaucoma
- Flunarizine → Parkinsonism (dopamine receptor blocking properties)
Recently Accepted Prophylactic Drugs:
| Drug | Route | Mechanism | Side Effects |
|---|---|---|---|
| OnabotulinumtoxinA (Botox) | IM/SC | Inhibition of neuropeptide/neurotransmitter release | Muscle weakness and atrophy. RCTs show reduced headache frequency, intensity, triptan doses, improved QoL in chronic migraine |
| CGRP or CGRP receptor antagonist monoclonal antibodies (erenumab, fremanezumab, galcanezumab) | SC/IV | Neutralize circulating CGRP or block CGRP receptors | Cautions: hypersensitivity, heart disease, cerebrovascular disease, inflammatory bowel disease |
Neurostimulation devices: [5]
- Transcranial magnetic stimulation (TMS): approved for acute treatment of migraine with aura (2014); now also for acute and prophylactic treatment
- External trigeminal nerve stimulation: approved for acute treatment of migraine with/without aura AND preventive treatment of episodic migraine
Migraine-like symptoms may be caused by: [5]
- Arteriovenous malformations (AVM)
- Internal carotid dissection
- Epilepsy
- MELAS (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes)
- CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarction and leucoencephalopathy)
Why this list matters: If a patient presents with "migraine" plus unusual features (stroke-like episodes, early dementia, maternal inheritance pattern, or young stroke), think of these secondary mimics.
Secondary Headache: Temporal Arteritis (Giant Cell Arteritis)
Temporal arteritis (TA), typically elderly [5]
This is a medical emergency because of the risk of permanent visual loss from anterior ischemic optic neuropathy (AION). Treatment must NOT be delayed for biopsy results.
| Symptom | Prevalence |
|---|---|
| Headache (typically bitemporal) | 72% |
| Polymyalgia rheumatica | 58% |
| Malaise, fatigue | 56% |
| Jaw claudication | 40% |
| Fever | 35% |
| Cough | 17% |
| Neuropathy | 14% |
| Sore throat, dysphagia | 11% |
| Amaurosis fugax | 10% |
| TIA/stroke | 7% |
| Permanent visual loss | 8% (opthalmological complications, mostly optic neuropathy, ~20%) |
| Limb claudication | 8% |
| Neuro-otological disorder | 7% |
| Scintillating scotoma | 5% |
| Tongue claudication | 4% |
| Depression | 3% |
| Diplopia | 2% |
| Myelopathy | 0.6% |
3 or more criteria → diagnosis of TA with 91.2% specificity & 93.5% sensitivity: [5]
- Age at onset ≥50 years
- New headaches
- Abnormalities of temporal artery at clinical examination (tenderness, decreased pulsation, nodularity)
- Raised ESR (≥50 mm/hr)*
- Abnormal findings on biopsy of temporal artery (granulomatous inflammation with giant cells)
*Raised CRP ( > 5 mg/L) is another, currently used, clinically useful laboratory parameter [5]
High-Yield: Temporal Arteritis Management
- Do NOT wait for biopsy results before starting treatment
- Start high-dose prednisolone (1 mg/kg/day) immediately upon clinical suspicion
- Temporal artery biopsy should be done within 2 weeks of starting steroids (inflammation persists for weeks on histology)
- Dramatic response to steroids within 24-72 hours supports the diagnosis [8]
- ESR can be characteristically very high (even >100 mm/h)
The lecture classifies headache of sudden onset into primary and secondary causes: [5]
| Primary Headache Disorders | Secondary Headache Disorders |
|---|---|
| Crash migraine | Vascular: unruptured saccular aneurysm, SAH, internal carotid artery dissection, cerebral venous thrombosis, acute hypertension (pressor response, phaeochromocytoma) |
| Cluster headache | Non-vascular intracranial: intermittent hydrocephalus, benign intracranial hypertension, pituitary apoplexy, infection (meningoencephalitis, acute sinusitis), acute mountain sickness |
| Benign exertional headache | Disorders of eyes: acute optic neuritis, acute glaucoma |
| Benign orgasmic cephalgia |
Thunderclap Headache = SAH Until Proven Otherwise
Any headache reaching maximum intensity within seconds to minutes ("worst headache of my life") is SAH until excluded by:
Definition
Neuralgia: [5]
- Sudden, intense, sharp, aching, lancinating, burning, stabbing pain lasting seconds to < 2 min
- Recurring repeatedly within short periods
- Triggered by sensory/mechanical stimuli
Trigeminal Neuralgia (TN)
Most frequent facial neuralgia, prevalence: 3-6 per 100,000 [5]
- Incidence ↑ with age, ~70% patients >60 yrs at onset
- Clinical hallmark: paroxysms of pain, very intensive, almost exclusively unilateral in a trigeminal distribution
- Typical: in second or third division (~5% first division)
- ~3% bilateral → suggesting a secondary origin
Trigger spots and typical triggers: [5]
- Touching/washing face, shaving, brushing teeth, chewing
- Sensory stimulation of cheek, chin, lip, tongue
- Stereotypic pain attacks usually many times per day, for weeks or months, then suddenly stop
- Subsequent pain-free periods for months or years
- Disease course: pain attacks tend to become more frequent over years, & remission periods shorter
Why the pain is paroxysmal: TN pain results from ectopic impulse generation in demyelinated trigeminal nerve fibers. The demyelination (often at the root entry zone where peripheral myelin transitions to central myelin) allows ephaptic transmission—one nerve fiber "short-circuits" to adjacent fibers, creating a burst of synchronized activity perceived as excruciating pain. Touch triggers fire Aβ fibers that cross-excite pain-carrying fibers through these ephaptic contacts.
Idiopathic TN (primary TN): normal neurological & MRI examination, no cause detectable [5]
Most common identifiable cause: compression of trigeminal nerve root by an aberrant loop of a blood vessel (60-90%) in neurosurgical and neuroradiological series [5]
MRI for detection of neurovascular contact: [5]
- Sensitivity (50-95%)
- Specificity (65-100%)
- False +ve (7-15%)
- False -ve (10%)
Up to 15% patients: an underlying cause can be identified (symptomatic TN): [5]
- Multiple sclerosis — especially young patients, bilateral
- Structural lesions mainly in pontine region:
- Vestibular/trigeminal schwannoma, meningiomas
- Epidermoid or other cysts
- Vascular brainstem lesions: pontine infarctions, angiomas, AVM
Features more common in symptomatic TN:
- Bilateral involvement
- Abnormal trigeminal reflex
- Trigeminal sensory deficits
When to Suspect Symptomatic TN
If any of these are present, the TN is likely secondary to a structural lesion:
- Young patient (esp. < 40)
- Bilateral pain
- Sensory loss in trigeminal distribution (classic TN has NO sensory loss between attacks)
- Abnormal trigeminal reflex on electrophysiology
- Other cranial nerve deficits → Must investigate with MRI brain
MRI brain scan is the investigation of choice for trigeminal neuralgia [5].
This was directly tested in the 2022 Fourth Summative MCQ Q59: A 79-year-old woman with short-lasting sharp lightning pain over her right cheek, multiple daily attacks lasting 30-40 seconds → Answer: MRI brain scan (not CT, not PET, not SPECT) [1].
Why MRI, not CT? MRI provides superior soft tissue resolution to:
- Detect neurovascular contact/compression at the trigeminal root entry zone
- Exclude MS plaques in the pons
- Exclude CPA tumours (schwannoma, meningioma)
- CT cannot reliably visualize the trigeminal nerve or vascular loops
Treatment of TN
TN due to focal lesion compressing sensory root of V nerve → surgical decompression [5] Primary TN → medical or surgical [5]
Carbamazepine (CBZ): most effective drug, ~75% respond, first-line drug [5]
- Risk of severe allergic reaction (Stevens-Johnson syndrome) → check HLA-B1502 before starting (especially in Southeast Asian/Chinese populations where the allele is prevalent)
- Vertigo, drowsiness, ataxia are common side effects, especially in elderly
- Once pain controlled completely, dose tapered every few weeks to determine whether remission has developed
- Regular blood counts in first few months, then yearly for agranulocytosis
HLA-B*15:02 Screening Before Carbamazepine
In Hong Kong (and Southeast Asian populations), HLA-B15:02 prevalence is ~8%. This allele is strongly associated with carbamazepine-induced Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). **Always check HLA-B15:02 before prescribing carbamazepine.** If positive → use an alternative drug.
Second-line drugs (when CBZ not helpful or tolerated): [5]
- Gabapentin (benign side effects, beneficial in neuropathic pain)
- Pregabalin, Phenytoin, Baclofen, Valproate, Clonazepam, Lamotrigine, Oxcarbazepine, Topiramate
Non-medical treatment options: [5]
| Procedure | Details | Patient Selection |
|---|---|---|
| Alcohol block | Of peripheral branch of V nerve | Temporary relief |
| Microvascular decompression (MVD) | Separation of V nerve from compressing vessel; mortality 1-2%, risk of damage to other cranial nerves | YOUNG patients |
| Percutaneous radiofrequency thermocoagulation | Of V nerve sensory root; corneal sensory loss → serious eye complications; anesthesia dolorosa (painful sensation in numb area) occurs occasionally | ELDERLY patients |
| Section of sensory root | Surgical; used less often now | - |
Why MVD for young, thermocoagulation for elderly? MVD is a major craniotomy with 1-2% mortality but offers the best long-term cure by addressing the root cause (vascular compression). Young patients can tolerate the surgical risk and benefit from decades of relief. Elderly patients have higher surgical risk, so less invasive percutaneous procedures are preferred despite higher recurrence rates and sensory side effects.
TACs include: [5]
- Cluster headache
- Paroxysmal hemicrania
- SUNCT (Short-lasting Unilateral Neuralgiform headaches with Conjunctival injection and Tearing)
- Probable TAC
- Refractory TAC
Cluster Headache
Diagnostic criteria (ICHD-II): [5]
- Severe unilateral orbital/supraorbital/temporal pain lasting 15-180 min
- Frequency: 1 every other day to 8 per day
- Associated with ≥1 ipsilateral autonomic feature:
- Conjunctival injection and/or lacrimation
- Nasal congestion and/or rhinorrhoea
- Eyelid oedema
- Forehead/facial sweating
- Miosis and/or ptosis (Horner's syndrome)
- Restlessness/agitation
Functional MRI during cluster headache attack reveals activation of hypothalamus [5]
Why hypothalamic activation matters: This explains the striking circadian periodicity of cluster headache (attacks at the same time daily, often nocturnal). The hypothalamus is the master circadian clock (suprachiasmatic nucleus). This is also why cluster headache responds to drugs that act on the hypothalamus.
| Feature | Cluster Headache | Migraine | TTH |
|---|---|---|---|
| Duration | 15-180 min | 4-72 hours | 30 min - 7 days |
| Side | Always unilateral | Usually unilateral | Bilateral |
| Character | Excruciating, boring | Pulsating | Pressing/tightening |
| Behaviour during attack | Agitated, restless (paces around) | Lies still in dark room | Remains active |
| Autonomic features | Prominent ipsilateral | Mild (nausea) | Absent |
| Gender | Male predominance | Female predominance | Equal/slight F |
| Acute Rx | High-flow O₂, SC sumatriptan | Triptans, simple analgesics | Analgesics |
The lecture title includes "neuro-imaging I." Based on the lecture content and supporting sources:
When to Image
| Indication | Modality | Why |
|---|---|---|
| Thunderclap headache | NCCT brain (urgent) | Exclude SAH (hyperdense blood in basal cisterns/sulci) |
| CT negative + thunderclap | LP | Xanthochromia confirms SAH missed by CT |
| SAH confirmed | CTA → DSA | Identify aneurysm for treatment |
| Trigeminal neuralgia | MRI brain | Detect neurovascular contact, exclude MS/CPA tumour |
| New headache after age 50 | CT or MRI | Exclude SOL, temporal arteritis workup |
| Headache + focal neurology | MRI (preferred) or CT | Exclude SOL, stroke, abscess |
| Headache + papilloedema | CT (to exclude SOL before LP) → LP | Raised ICP workup |
| Progressive/worsening headache | MRI | Exclude SOL |
| Headache + fever + neck stiffness | CT (if focal signs/↓GCS) → LP | Rule out abscess before LP |
Integration with Related Material
- CNS infection imaging indications: altered mental state + fever, acute severe headache, first seizure with fever, immunocompromised + new neurological signs [12]
- ICA dissection → retroorbital pain + Horner's syndrome
- VA dissection → occipital pain + vertebrobasilar symptoms
- Can cause SAH intracranially if dissecting aneurysm ruptures [9]
Based on past paper themes and lecture content:
-
MCQ: A 79-year-old woman with recurrent brief (30-second) sharp lightning-like pain over her right cheek, triggered by chewing. What is the most appropriate investigation?
- Answer: MRI brain scan (to detect neurovascular contact, exclude CPA lesion/MS) [1]
-
MCQ: A 55-year-old man with sudden severe headache, vomiting, and neck stiffness. CT brain shows diffuse SAH. What is the most appropriate next step?
- Answer: CT angiography (to identify the source aneurysm) [2]
-
MCQ: A 38-year-old woman with sudden severe headache and vomiting. CT brain is normal. What is the most appropriate next step?
- Answer: Lumbar puncture (to look for xanthochromia / blood-stained CSF to exclude SAH) [4]
-
SAQ: Name 3 drugs used for migraine prophylaxis and their key side effects.
- Answer: Propranolol (fatigue, contraindicated in asthma), topiramate (weight loss, renal stones, glaucoma), valproate (teratogenic, hepatotoxicity, weight gain)
-
SAQ: What is the first-line drug for trigeminal neuralgia? What must be checked before starting it?
- Answer: Carbamazepine. Check HLA-B*15:02 (risk of Stevens-Johnson syndrome).
-
SAQ: List the diagnostic criteria for temporal arteritis. How many criteria are needed?
- Answer: Age ≥50, new headache, temporal artery abnormality, ESR ≥50, abnormal temporal artery biopsy. ≥3 of 5 criteria (91.2% specificity, 93.5% sensitivity).
-
MCQ: Which migraine prophylactic drug is associated with retroperitoneal fibrosis?
- Answer: Methysergide
-
SAQ: Explain the pathophysiology of migraine aura.
- Answer: Cortical spreading depression (CSD)—a self-propagating wave of neuronal/glial depolarization spreading across the cortex, which activates trigeminal nociceptive afferents and produces the gradual expansion of visual/sensory symptoms over >5 minutes.
High Yield Summary
Primary Headaches:
- TTH: Bilateral, pressing, mild-moderate, not aggravated by activity. Prevent chronification. Acute: NSAIDs/paracetamol. Prophylaxis: amitriptyline.
- Migraine: Unilateral, pulsating, 4-72h, N/V, photophobia/phonophobia. ≥5 attacks without aura, ≥2 with aura. Mechanism: CSD → trigeminovascular activation → CGRP release → neurogenic inflammation. Acute: triptans (contraindicated in vascular disease), gepants, ditans. Prophylaxis: propranolol, topiramate, valproate, amitriptyline, CGRP mAbs, Botox. Limit acute Rx to 2-3 days/week to avoid MOH. Avoid opioids.
- Cluster/TACs: Unilateral periorbital, 15-180 min, ipsilateral autonomic features, agitation. Hypothalamic activation. Acute: high-flow O₂ + SC sumatriptan.
Secondary Headaches:
- Thunderclap → SAH until proven otherwise: NCCT → LP if CT negative → CTA/DSA
- Temporal arteritis: Age ≥50 + new headache + ↑ESR + jaw claudication → start prednisolone IMMEDIATELY → temporal artery biopsy. Visual loss in ~8-20%.
Trigeminal Neuralgia:
- V2/V3, lancinating seconds, trigger spots. Investigation: MRI brain. First-line: carbamazepine (check HLA-B*15:02). Surgery: MVD (young), radiofrequency thermocoagulation (elderly). Suspect symptomatic TN if: young, bilateral, sensory loss, MS.
FHM Genes: CACNA1A (Ca²⁺ channel), ATP1A2 (Na⁺/K⁺-ATPase), SCN1A (Na⁺ channel) → all ion transport → ↑CSD susceptibility.
Active Recall - Headache and Neuralgia
[1] Past papers: 2022 Fourth Summative MCQ (Q59) [2] Past papers: 2023 Fourth Summative MCQ (Q60) [3] Past papers: 2024 Fourth Summative MCQ (Q65) [4] Past papers: 2025 Fourth Summative MCQ (Q52) [5] Lecture slides: GC 082. Severe headache_headache and neuralgia; neuro-imaging I.pdf [6] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (CNS Diseases - Headache sections) [7] Senior notes: Ryan Ho Neurology.pdf (Headache and Neuralgia chapter) [8] Senior notes: Ryan Ho Rheumatology.pdf (Giant Cell Arteritis section) [9] Lecture slides: GC 109. Headache and loss of consciousness Acute stroke, subarachnoid haemorrhage and vascular malformation.pdf [10] Senior notes: Maksim Surgery Notes.pdf (Neurosurgery - SAH section) [11] Senior notes: Ryan Ho Radiology.pdf (Neuroradiology section) [12] Lecture slides: GC 013. Emergency radiology.pdf
GC081 Seizure And Loss Of Consciousness Delirium And Encephalopathy; Epilepsy; Coma And Brain Death; Care Of Unconscious Patients; Electrophysiology I
A clinical spectrum encompassing seizures, epilepsy, delirium, encephalopathy, coma, and brain death, representing varying degrees of altered consciousness due to abnormal cerebral electrical activity or diffuse brain dysfunction, assessed and characterized through electrophysiological studies such as electroencephalography (EEG).
GC083 Shortness Of Breath In A Construction Site Worker
Acute or subacute dyspnea in a construction worker, typically prompting evaluation for occupational lung diseases such as asbestosis, silicosis, hypersensitivity pneumonitis, or occupational asthma caused by workplace dust and chemical exposures.