GC109 Headache And Loss Of Consciousness Acute Stroke, Subarachnoid Haemorrhage And Vascular Malformation
Acute stroke involves sudden neurological deficit from cerebral ischemia or hemorrhage, subarachnoid haemorrhage is bleeding into the subarachnoid space typically from a ruptured aneurysm, and vascular malformations are abnormal collections of blood vessels that can cause hemorrhage or seizures.
This lecture (GC 109, Prof. Gilberto Leung) is a neurosurgical perspective on cerebrovascular emergencies — the single most important cause of sudden headache with loss of consciousness. It covers four pillars: (1) haemorrhagic stroke (spontaneous ICH), (2) acute ischaemic stroke ("brain attack"), (3) subarachnoid haemorrhage (aneurysmal SAH), and (4) cerebral vascular malformations & related conditions (AVM, Moyamoya, cervical arterial dissection).
Learning Objectives:
- Recognize that sudden headache + deterioration in consciousness = cerebrovascular event until proven otherwise [1]
- Distinguish haemorrhagic from ischaemic stroke, deep from superficial haemorrhage, and traumatic from spontaneous SAH
- Understand time-critical management: IV tPA thrombolysis (3–4.5 hrs), endovascular thrombectomy (6 hrs)
- Know the three key complications of aneurysmal SAH: rebleeding, vasospasm, hydrocephalus
- Classify vascular malformations and understand when to intervene
How this fits into exams: This is one of the highest-yield neurosurgery lectures for the Fourth Summative. Past papers (2020–2025) repeatedly test stroke imaging interpretation, management priorities for SAH (angiography vs intubation vs LP), tPA time windows, dense MCA sign, and the concept of "brain attack." [6][7][8][9]
Part 1: Overview & Consciousness
A slide titled "Causes of Headache" is shown early — reminding that headache has many aetiologies, but in the acute/severe setting, vascular causes dominate. [1]
Two components are required for consciousness: [1]
- Brainstem reticular activating system (RAS) → provides arousal (the "on switch")
- Cerebral cortex → provides awareness (content of consciousness)
Loss of consciousness (LOC) = failure of either or both. [1]
Why this matters: A massive cortical infarct (e.g., MCA territory) can cause LOC by knocking out enough cortex. A brainstem haemorrhage directly destroys the RAS. Understanding this helps you predict which stroke locations cause LOC.
LOC is a spectrum: [1]
- Coma is defined when GCS ≤ 8
- At GCS ≤ 8 the patient is unarousable, cannot protect airway, and has inadequate breathing → this is why GCS ≤ 8 mandates intubation
High Yield Clinical Pearl
When a patient has GCS ≤ 8 from SAH, the MOST APPROPRIATE immediate action is endotracheal intubation (airway protection), NOT cerebral angiography. Angiography is next, but ABC always comes first. This was directly tested in the 2021 Fourth Summative Q61. [7]
Intracranial: Vascular, Trauma, Tumour, Hydrocephalus, Infection/inflammation [1] Extracranial: Metabolic, Drugs & toxin, Respiratory insufficiency, Cardiac insufficiency [1]
Clinical logic: When you see a comatose patient, think "is this a brain problem or a body problem?" Metabolic coma (e.g., hypoglycaemia, hepatic encephalopathy) typically has no focal signs, whereas structural intracranial causes usually produce focal neurological deficits.
Key Lecture Statement — Exam Favourite
"A sudden onset of headache with deterioration in consciousness is a cerebrovascular event until proven otherwise." [1]
Can be ischaemic or haemorrhagic [1] Typically abrupt onset [1] Headache — from raised ICP or meningeal irritation [1] LOC — if brainstem/cortical failure [1] Focal deficits — depending on location [1] Severely disabling or fatal; but potentially reversible [1] Distinct subtypes with different prognoses [1]
Part 2: Haemorrhagic Stroke (Spontaneous ICH)
Often refers to spontaneous intracerebral haemorrhage (ICH) [1] e.g., lenticulostriate arteries of MCA [1]
Why lenticulostriate arteries? These small perforating arteries arise directly from the MCA and supply the basal ganglia/internal capsule. In chronic hypertension, they develop lipohyalinosis and Charcot-Bouchard microaneurysms, which eventually rupture. Because they're small vessels branching from a high-pressure trunk, they're extremely vulnerable.
Primary destruction of brain tissue with loss of function [1] Haematoma causes raised ICP [1] Rebleeding occurs [1]
Key concept: Unlike ischaemic stroke where you're trying to save penumbra, in ICH the primary damage is done — surgery can decompress but cannot undo the primary injury. This fundamentally shapes management philosophy.
Systemic hypertension — most common cause overall [1] Amyloid angiopathy — classically lobar haemorrhage in elderly [1] Haemorrhagic transformation of infarction [1] Bleeding tendency [1] Tumour bleeding [1] AVM/cavernoma [1] Venous sinus thrombosis [1] Moyamoya disease [1] Arterial dissection [1] Vasculitis [1] Sympathomimetic abuse [1]
| Cause | Typical Location | Key Feature |
|---|---|---|
| Hypertension | Deep (BG, thalamus, pons, cerebellum) | Most common; small vessel disease |
| Amyloid angiopathy | Lobar (peripheral) | Elderly; recurrent; no HTN needed |
| AVM | Any (often lobar in young) | Congenital; associated aneurysm |
| Tumour bleeding | Variable | Look for enhancing mass on contrast CT |
| Anticoagulant-related | Any | Check INR; reverse urgently |
| Cocaine/sympathomimetics | Any | Ask about drug use in young patients |
Patient selection depends on: Age, Co-morbidities, Location of haematoma, Neurological status, Aetiology [1]
Treatment: [1]
- ABC & ICP control
- Mannitol (osmotic diuretic to reduce cerebral oedema)
- Surgical decompression
- CSF drainage (if associated hydrocephalus)
- Clot evacuation
No role for steroids [1]
Why no steroids? Steroids reduce vasogenic oedema (e.g., around tumours), but ICH-associated oedema is primarily cytotoxic. Steroids don't help and increase infection/hyperglycaemia risk. This is a classic exam trap.
Tranexamic acid might help [1]
Why? Tranexamic acid is an antifibrinolytic — it stabilizes clot to reduce haematoma expansion. Evidence is emerging but not definitive.
Reverse bleeding tendency [1] Principles of maintaining CBF apply (i.e., CPP = MAP − ICP) [1]
Location Matters — Deep vs. Superficial
Haemorrhage locations: [1]
- Superficial lobes: Frontal, Parietal, Occipital
- Deep nuclei: Basal ganglia, Thalamus, Internal capsule, Brainstem
Basal ganglia, Thalamic, Brainstem haemorrhage [1] Commonly due to systemic hypertension [1] Poor functional outcome [1] Often managed conservatively unless young [1]
Why poor prognosis? Deep structures (internal capsule, thalamus) contain densely packed motor/sensory tracts. Even a small haemorrhage causes devastating deficits. Surgery to evacuate deep haematomas often causes more damage traversing normal brain to reach the clot. Brainstem haemorrhage destroys the RAS directly.
BG + IVH — shown in imaging: basal ganglia haemorrhage with intraventricular extension (blood tracking into ventricles) [1]
Involves superficial lobes [1] Commonly due to hypertension [1] Other pathology (e.g., tumour, bleeding tendency, vasculitis, AVM) [1] Deep nuclei/brainstem may be compressed but not primarily injured [1] Surgery is life-saving and can have reasonably good functional outcome [1]
Why better outcome with surgery? The clot is superficial and accessible. Removing it relieves mass effect on deep structures that are compressed but not destroyed. Hence, function can recover.
Direct brainstem compression [1] IVH & obstructive hydrocephalus [1] Rapidly fatal if large size [1] Good prognosis if timely surgery [1]
Why is cerebellar haemorrhage special? The posterior fossa is a tiny, rigid compartment. A haematoma there quickly compresses the brainstem (causing coma, respiratory arrest) and blocks CSF flow through the 4th ventricle (causing acute obstructive hydrocephalus). But the cerebellum is not "eloquent cortex" — if you evacuate promptly, patients can do remarkably well. This is a classic indication for emergency surgery. [1][3]
Exam Discrimination: When to Operate on ICH
| Operate | Conservative |
|---|---|
| Lobar/subcortical ICH with mass effect | Deep BG/thalamic ICH in elderly |
| Cerebellar haemorrhage (> 3 cm or with brainstem compression) | Brainstem haemorrhage |
| Young patient with good premorbid status | Devastating primary injury with poor GCS |
| Accessible clot causing obstructive hydrocephalus |
Part 3: Acute Ischaemic Stroke ("Brain Attack")
Causes: [1]
- Cardioembolism (AF, valvular disease, recent MI)
- Critical arterial stenosis (atherosclerosis)
- Arterial dissection
Can be painful without raised ICP [1] +/- LOC depending on location & extent [1] Acute cell death & loss of function [1] Cells in penumbra potentially salvageable [1] Aim at timely restoration of perfusion [1]
The Penumbra Concept — Why Time Matters: When an artery is occluded, there's a core of brain tissue that dies almost immediately (CBF < 10 ml/min/100g). Surrounding this core is the penumbra — tissue that's ischaemic but still viable (CBF 10–20 ml/min/100g). These cells are surviving on collateral blood supply but will die if flow isn't restored. Every minute of ischaemia = more penumbra converts to core. This is why "time is brain."
Standard treatment (but not yet available 24/7 everywhere in HK!) [1] Converts plasminogen to plasmin, which lyses clot [1] Therapeutic window of 3–4.5 hours from symptom onset [1] Can completely reverse deficit [1]
Mechanism: tPA (tissue plasminogen activator, e.g., alteplase) binds fibrin in the clot and converts plasminogen→plasmin locally, dissolving the thrombus. It works best for smaller, more recent clots.
Does not respond well to IV tPA [1]
Why? Large clots (e.g., MCA trunk occlusion) have too much thrombus for systemic tPA to dissolve effectively.
Confirm LVO with urgent CT angiography [1] Standard: Endovascular mechanical thrombectomy (EMT) within 6 hours of symptom onset [1]
Dense MCA Sign — hyperdense MCA on plain CT representing acute thrombus within the artery [1] Acute MCA Occlusion → Potential large infarction [1]
Past Paper Alert — 2022 Q68
"The absence of 'dense MCA sign' does not exclude cerebral ischaemia" — this was the CORRECT answer. The dense MCA sign is a specific but not sensitive sign. Many patients with MCA occlusion don't show it on plain CT. [8]
Also tested: EMT is for large vessel occlusion, NOT small vessel. IV tPA should NOT be delayed to 6 hours — it should be given ASAP within 3–4.5 hrs. Tranexamic acid is for haemorrhagic stroke, NOT ischaemic stroke.
Ischaemic brain has disturbed BBB & vascular reactivity [1] Reperfusion haemorrhage worsens outcome [1] Particularly if delayed reperfusion (hence EMT within 6 hours) [1]
Why does this happen? During ischaemia, capillary endothelial cells die and the blood-brain barrier breaks down. When blood flow is restored (either spontaneously or via treatment), blood leaks through damaged vessels into the infarcted tissue. This is why:
- There's a time limit on thrombolysis/thrombectomy
- CT must exclude haemorrhage BEFORE giving tPA
- Anticoagulants are generally withheld in the acute phase of large infarcts
Size of salvageable penumbra varies with collateral vascular supply [1] Routine CT or MRI cannot tell [1] Advanced imaging can delineate a "mismatch" between truly dead brain and salvageable penumbra tissue [1] Identify who may benefit from treatment > 6 hours post-onset [1]
Clinical context: CT perfusion and MRI diffusion-perfusion mismatch studies are increasingly used. If there's a large mismatch (big penumbra relative to core), the patient may benefit from thrombectomy even beyond 6 hours (e.g., the DAWN and DEFUSE-3 trials extended the window to 24 hours in selected patients).
Large infarct can swell with mass effect & raise ICP [1] Maybe initially conscious but then deteriorates in next 24–48 hrs [1] Does not respond well to medical therapy [1] Surgical decompression saves lives but does not reverse deficits [1] For young & fit patient. Ethical issues. [1]
Why 24–48 hours? Cerebral oedema peaks at 3–5 days post-infarction. A massive MCA territory infarct ("malignant MCA syndrome") causes enough swelling to herniate the brain. Craniectomy removes part of the skull to allow the swollen brain to expand outward rather than downward (uncal herniation). RCTs show it reduces mortality from ~70% to ~20%, but many survivors have significant disability — hence the ethical discussion, especially in older patients. [1][3]
Part 4: Subarachnoid Haemorrhage (SAH)
Commonest cause overall is trauma [1] Spontaneous (atraumatic) SAH: [1]
- Saccular or dissecting aneurysm
- "Mycotic" aneurysm (actually infectious — from infective endocarditis)
- Vascular malformation
- Cocaine
If no history of trauma, SAH is aneurysmal in origin until proven otherwise [1]
Critical Clinical Trap
BEWARE: spontaneous SAH then LOC, fall & head injury [1]
A patient may have an aneurysm rupture → SAH → LOC → falls → hits head → comes to ED with "head injury." If you assume it's traumatic SAH, you'll miss the aneurysm.
Always ask: "Headache before or after LOC?" [1]
If headache came FIRST → the SAH caused the fall (spontaneous). If the fall came FIRST → may be traumatic SAH (but still consider aneurysm).
Commonly Circle of Willis [1] Predisposing factors: [1]
- Smoking
- Hypertension
- Age > 40
- Family history
- Female
- CTD: Ehlers-Danlos syndrome, AD polycystic kidney disease, Marfan syndrome, fibromuscular dysplasia
Can be forever asymptomatic [1] Unpredictable spontaneous rupture [1]
Most common aneurysm locations (from senior notes [2]): AComA (35%) = PComA (35%) > MCA (20%)
↑ Size, ↑ Risk of rupture [1] Pseudoaneurysm due to arterial dissection or mycotic aneurysm more unstable [1] Large aneurysms can cause mass effect (e.g., CN palsy) or thromboembolism [1]
An enlarging PComA aneurysm compresses on CN III [1] "Surgical" third nerve palsy: [1]
- Peripheral parasympathetic fibres affected → Dilated pupil and ptosis
- Central fibres intact → preserved eye movement Urgent angiogram & intervention before rupture! [1]
Why does this pattern occur? CN III runs adjacent to the PComA. The parasympathetic fibres (controlling pupil constriction) travel on the outside (periphery) of the nerve. An expanding aneurysm compresses these outer fibres first → fixed dilated pupil (mydriasis) + ptosis. The somatic motor fibres (controlling eye movements) are deeper within the nerve and are initially spared. This is the opposite of a "medical" third nerve palsy (e.g., from diabetes) where microangiopathy affects the central vasa nervorum → spares the pupil.
High Yield Discrimination: Surgical vs Medical CN III Palsy
| Feature | Surgical (compressive) | Medical (ischaemic/diabetic) |
|---|---|---|
| Pupil | Dilated, fixed | Spared (normal) |
| Ptosis | Present | Present |
| Eye movements | Initially preserved, later affected | Affected early |
| Pain | Often present | Variable |
| Cause | PComA aneurysm, uncal herniation | Diabetes, HTN microvascular |
| Urgency | URGENT — angiogram NOW | Non-urgent |
Sudden severe headache — "Worst headache in my life" / "Like being clubbed on my head" [1] Meningism [1] Photophobia [1] +/- LOC [1] Focal neurological deficit [1] Cardiac arrest & out-of-hospital death [1] Fundi — subhyaloid haemorrhage [1] DDx meningitis [1]
Why meningism? Blood in the subarachnoid space irritates the meninges, producing neck stiffness, photophobia, and Kernig's sign — identical to meningitis. But SAH meningism develops after the acute headache, and there's typically no fever (unless later complication). [1][4]
Subhyaloid haemorrhage: Blood tracks along the optic nerve sheath and causes haemorrhage between the retina and vitreous. Pathognomonic for SAH if seen on fundoscopy.
Clinical suspicion. H&E. [1] CT – can be very subtle or even normal [1] LP – only if CT negative [1]
- Blood-stained CSF
- SAH vs. traumatic tap!
- 3-bottle test (in traumatic tap, RBC count decreases across sequential bottles; in SAH, it remains constant)
- Xanthochromia after several hours (yellow discolouration from bilirubin — breakdown of haemoglobin in CSF; takes ~6–12 hours to develop, persists up to 2 weeks) MRI – can be false-negative at acute stage [1] Once diagnosed, give tranexamic acid, anticonvulsant & call neurosurgeon [1]
CT sensitivity for SAH: ~95% within 6 hours of onset, drops to ~50% by day 7. This is why a negative CT does NOT exclude SAH — you need LP. [1][2]
Past Paper Alert — 2020 Q62
A 55-year-old man with sudden severe headache, vomiting, neck stiffness, no motor weakness, normal CT within 1 hour. Most likely diagnosis = Aneurysmal rupture (SAH). Even though CT is normal, the clinical picture is classic. The next step would be LP. [6]
Past Paper Alert — 2023 Q60
A 55-year-old man with sudden severe headache, vomiting, neck stiffness. No trauma. Fully conscious, stable vitals. Plain CT shows diffuse SAH. Most appropriate action = CT angiography (to identify the aneurysm). NOT LP (SAH already confirmed on CT), NOT intubation (GCS is normal), NOT dexamethasone (steroids have no role). [9]
No/substandard H&E and poor documentation [1] Head injury & SAH on CT — maybe SAH first then LOC then TBI; maybe LOC/TBI first then traumatic SAH [1] Dismiss headache as migraine, stress, psychological, or part of URI [1] Leave it until tomorrow/grand round [1] Radiologist refuses angiogram [1]
Clinical lesson: SAH is one of the most commonly missed diagnoses in emergency medicine. The lecture explicitly warns against dismissing thunderclap headache. If in doubt, investigate.
Key issues: [1]
- Rebleeding — Day 1: 4%; Day 14: 20%
- Vasospasm
- Hydrocephalus
Cannot undo injury caused by the initial haemorrhage [1] ABC, optimize ICP & CBF [1] Prevent secondary injury and further bleeding [1] Identify & obliterate aneurysm [1]
Rebleeding risk: 4% on Day 1, then ~1-2% per day, cumulative 20% by Day 14. Rebleeding carries ~40% mortality. This is why you want to secure the aneurysm as soon as is feasible — to eliminate the rebleeding risk. [1]
CTA non-invasive but can be false-negative [1] Proceed to DSA ("Gold standard") if CTA negative [1] DSA has 1% stroke risk [1]
| Modality | Pros | Cons |
|---|---|---|
| CTA | Non-invasive, fast, widely available | Can miss small aneurysms |
| MRA | No radiation, no contrast (TOF) | Takes longer, motion artefact |
| DSA | Gold standard, therapeutic capability | Invasive, 1% stroke risk |
Three methods: [1]
- Microsurgical clipping — open craniotomy, clip placed across aneurysm neck
- Endovascular embolization — Guglielmi detachable coils packed into aneurysm via catheter
- Flow diverter — stent-like device placed in parent artery redirecting flow away from aneurysm
Aim for complete obliteration to prevent re-rupture "as soon as is feasible" [1] Method and patient selection depends on age, premorbid status, neurological prognosis and technical feasibility [1]
Microsurgical clipping: Risk of intra-operative rupture & occlusion of parent artery [1]
From senior notes [3]: Endovascular coiling is generally first-line; clipping reserved for wide-necked or anatomically unfavourable aneurysms.
Delayed cerebral ischaemia [1] Starts ~D4, peaks D7–10 [1] High mortality & morbidity [1] Treatment: [1]
- Nimodipine (calcium channel blocker — only drug proven to reduce poor outcomes from vasospasm)
- Maintain good perfusion
- Chemical/Mechanical angioplasty (balloon angioplasty or intra-arterial vasodilators for refractory spasm)
Why vasospasm? Blood breakdown products (oxyhemoglobin, bilirubin oxidation products) in the subarachnoid space trigger arterial smooth muscle contraction and endothelial dysfunction. This leads to narrowing of cerebral arteries → ischaemia. The Fisher grade (amount of blood on initial CT) predicts vasospasm risk.
Nimodipine 60mg Q4h PO (from senior notes [3]) — started on admission and continued for 21 days.
Acute increase in ICP [1] CSF drainage helps but might provoke re-bleeding if aneurysm not yet secured! [1] Delayed — poor absorption & usually communicating — for shunting [1] Beware of new symptoms several months post-SAH [1]
Why hydrocephalus?
- Acute: Blood clots block CSF outflow (e.g., at aqueduct or 4th ventricle foramina) → obstructive hydrocephalus
- Chronic: Blood products clog arachnoid granulations → impaired CSF absorption → communicating hydrocephalus. May present weeks to months later with gait disturbance, cognitive decline, urinary incontinence (mimicking NPH).
SAH Management Flowchart from Lecture Slide
Clinical Suspicion → Diagnosis of SAH (CT Scan → LP if CT negative) → Identify Aneurysm (DSA/CTA/MRA) → Secure Aneurysm (Clip/Coil) → ICU Care/Angioplasty for Vasospasm → CSF Shunting for Hydrocephalus [1]
From lecture [1] and senior notes [2][3]:
| Complication | Timing | Mechanism | Management |
|---|---|---|---|
| Rebleeding | Day 1 (4%), Day 14 (20%) | Unsecured aneurysm | Secure aneurysm ASAP; tranexamic acid bridge |
| Vasospasm | D4–D14, peaks D7–10 | Blood products → arterial spasm | Nimodipine, maintain perfusion, angioplasty |
| Hydrocephalus | Acute or delayed (months) | Acute obstructive or chronic communicating | EVD acutely; VP shunt if chronic |
| Hyponatraemia | Days to weeks | SIADH or cerebral salt wasting | Fluid management; differentiate CSW vs SIADH |
| Seizures | Any time | Cortical irritation by blood | Anticonvulsant |
| Cardiac arrhythmia | Acute | Catecholamine surge, hypothalamic irritation | Monitoring, supportive |
Part 5: Cerebral Vascular Malformations & Other Conditions
1. Arteriovenous Malformation (AVM) [1] 2. Cavernous Angioma [1] 3. Venous Angioma [1] 4. Capillary Telangiectasia [1]
Most likely congenital [1] Different bleeding risks — highest with AVM [1] Balance between treatment and harm for AVM and CA [1] Manage VA and CT conservatively [1]
| Type | Bleeding Risk | Key Feature | Management |
|---|---|---|---|
| AVM | ~3%/year | AV shunting, flow voids on MRI | Surgery/embolization/radiosurgery |
| Cavernous Angioma | ~1%/year | "Popcorn" appearance on MRI, DSA-negative | Surgery only if symptomatic |
| Venous Angioma | Very low | Normal variant essentially | Conservative |
| Capillary Telangiectasia | Very low | Incidental | Conservative |
Abnormal development of arteries and vein [1] No intervening capillary between artery and vein [1] AV shunting & arterialization of cerebral veins [1] Unstable high-pressure system [1] Prone to rupture [1] Disturbs normal cerebral perfusion ("vascular steal") [1] Associated with aneurysm [1]
Why "vascular steal"? The AVM is a low-resistance shunt — blood preferentially flows through it rather than through normal brain capillaries. This diverts flow from adjacent brain tissue, potentially causing ischaemia.
Clinical Presentation: [1]
- Haemorrhage (~3%/yr) — Deep, IVH, Lobar
- Seizure
- Ischaemia ("vascular steal")
- Headache
- Others: Bruit, Hydrocephalus, Heart failure (high-output from AV shunting, especially in large AVMs or neonatal vein of Galen malformations)
Imaging: CT + contrast, Flow Voids on MRI [1]
Treatment of AVM: [1]
- Mainly to prevent bleeding
- Risk-Benefit balance
- Modality: Surgical excision, Embolization, Radiosurgery, Combination
Spetzler-Martin Grading (from senior notes [5]): Based on size (< 3cm=1, 3-6cm=2, > 6cm=3), eloquence of adjacent brain (eloquent=1, non-eloquent=0), venous drainage pattern (deep=1, superficial=0). Lower grade = better surgical outcome.
Congenital ICA stenosis [1] Compensatory proliferation of vascular collaterals ('puff of smoke') — appearance on angiogram [1] Young → Ischaemic symptoms [1] Older → Bleeding (fragile collaterals) [1] Revascularisation surgery might help [1]
Why the age difference? In children, the ICA stenosis causes hypoperfusion → ischaemic strokes/TIAs. Over decades, fragile collateral vessels develop. In adulthood, these thin-walled collaterals rupture → haemorrhagic stroke.
Spontaneous — connective tissue disorder [1] Traumatic — fall, sports, chiropractic [1] ICA dissection — retroorbital pain, Horner's syndrome [1] VA dissection — occipital pain & vertebrobasilar symptoms [1] Ischaemia from arterial occlusion or embolism [1] Dissecting aneurysm can rupture and cause SAH intracranially [1] Anticoagulation if no bleeding [1] Endovascular or bypass surgery [1]
Why Horner's with ICA dissection? The sympathetic fibres ascending to the eye travel along the ICA wall. Dissection damages these fibres → ipsilateral miosis, ptosis, anhidrosis (Horner's syndrome). Combined with ipsilateral headache/retroorbital pain in a young patient with neck trauma → think ICA dissection.
The final slide shows six CT images for identification — a classic exam format:
1. Basal Ganglia ICH — deep hyperdense lesion in BG region [1] 2. SAH — hyperdensity in basal cisterns/sylvian fissures [1] 3. Lobar ICH — peripheral hyperdense haematoma in a lobe [1] 4. MCA Infarction + Haemorrhagic Transformation — hypodense MCA territory with areas of hyperdensity [1] 5. Cerebellar Haemorrhage — posterior fossa hyperdense lesion [1] 6. Dense MCA Sign — hyperdense MCA on plain CT indicating acute thrombus [1]
1. Sudden headache and LOC is cerebrovascular in origin until proven otherwise [1] 2. Haemorrhagic stroke — deep vs. superficial — surgery in selected patients [1] 3. Acute ischaemic stroke ("Brain Attack"): [1]
- IV tPA thrombolysis within 3–4.5 hrs
- Endovascular mechanical thrombectomy within 6 hrs 4. Aneurysmal SAH — rebleeding, hydrocephalus, vasospasm — surgical clipping & endovascular treatment [1] 5. Cerebral AVM — headache, bleeding, seizure, vascular steal [1] 6. Moyamoya disease — ischaemia when young; haemorrhage when older [1] 7. Cervical artery dissection — ischaemia or dissecting aneurysm SAH [1]
Integration with Related Material
The differential for sudden-onset headache includes both primary (crash migraine, cluster headache, benign exertional headache) and secondary causes (SAH, carotid dissection, cerebral venous thrombosis, pituitary apoplexy, acute hypertensive crisis). In the exam, if the question says "thunderclap headache," SAH must be excluded first.
TLOC differential: SAH is listed under "vascular" causes of non-traumatic TLOC — alongside vertebrobasilar TIA. Remember that SAH can present as syncope/collapse, not just headache.
Acute stroke defined as "rapidly developing clinical symptoms and/or signs of focal, and at times global, loss of brain function, lasting > 24 hours or leading to death, no apparent cause other than vascular origin." Ischaemic ~80%, Haemorrhagic ~20%.
- Raised ICP signs: headache worse lying down, morning vomiting, papilloedema, CN VI palsy, Cushing's triad (late)
- CPP = MAP − ICP; target CPP ≥ 70 mmHg, ICP ≤ 20 mmHg
1. MCQ stem: A 48-year-old woman presents with sudden right hemiplegia, right lower facial weakness, conscious, CT brain within 2 hours is normal. Most appropriate next action? → CT angiogram (to look for LVO amenable to thrombectomy) — NOT LP (no suspicion of SAH), NOT tranexamic acid (no haemorrhage), NOT ICP monitoring (conscious, no mass effect). [6]
2. MCQ stem: Patient with SAH, GCS 6. Most appropriate FIRST step? → Endotracheal intubation (GCS ≤ 8 = protect airway). Angiography comes AFTER stabilization. [7]
3. SAQ: Describe the key complications of aneurysmal SAH and their management. → Rebleeding (secure aneurysm), vasospasm (nimodipine, maintain perfusion, angioplasty), hydrocephalus (EVD acutely, VP shunt if chronic). Also mention hyponatraemia, seizures.
4. MCQ: Which statement about ischaemic stroke management is correct? → "Absence of dense MCA sign does not exclude cerebral ischaemia" (TRUE). EMT is for LVO not small vessels. tPA given within 3–4.5 hrs, not after 6 hrs observation. [8]
5. SAQ: A young patient presents with a dilated pupil, ptosis, but preserved eye movements. What is the diagnosis and mechanism? → Surgical CN III palsy from PComA aneurysm compressing peripheral parasympathetic fibres. Urgent angiogram needed.
6. MCQ: Deep basal ganglia haemorrhage in an elderly hypertensive patient. Best management? → Conservative (poor functional outcome with surgery in deep ICH in elderly). Surgery only if young or accessible lobar/cerebellar location.
7. SAQ: How do you differentiate SAH from traumatic tap on LP? → 3-bottle test (constant RBC in SAH vs decreasing in traumatic tap), xanthochromia (present in SAH after several hours, absent in traumatic tap).
8. MCQ: Post-SAH vasospasm peaks at what time? → D7–10 (starts ~D4).
High Yield Summary
The ONE sentence: Sudden headache + LOC = cerebrovascular until proven otherwise.
Haemorrhagic stroke: Deep (BG/thalamus/brainstem) = hypertensive, poor outcome, often conservative. Superficial (lobar) = surgery helps. Cerebellar = emergency surgery. No steroids. Tranexamic acid may help.
Ischaemic stroke ("Brain Attack"): IV tPA within 3–4.5 hrs. CT angiogram for LVO → EMT within 6 hrs. Dense MCA sign = thrombus but its absence doesn't exclude ischaemia. Haemorrhagic transformation risk with delayed reperfusion. Decompressive craniectomy for malignant MCA syndrome (saves lives, doesn't reverse deficits).
SAH: Aneurysmal until proven otherwise (if no trauma). Thunderclap headache + meningism. CT → LP if CT negative (xanthochromia, 3-bottle test). Three killers: rebleeding (secure aneurysm), vasospasm (nimodipine, peaks D7–10), hydrocephalus (EVD/shunt). Clip or coil ASAP. Surgical CN III palsy (dilated pupil, ptosis) = PComA aneurysm → urgent angiogram.
Vascular malformations: AVM = highest bleed risk (3%/yr), vascular steal, seizures; treat with surgery/embolization/radiosurgery. Cavernous angioma and venous angioma = lower risk, mostly conservative. Moyamoya = ischaemia in young, haemorrhage in old. Cervical dissection = Horner's (ICA) or vertebrobasilar symptoms (VA); anticoagulate if no bleeding.
Active Recall - Lecture Notes
[1] Lecture slides: GC 109. Headache and loss of consciousness Acute stroke, subarachnoid haemorrhage and vascular malformation.pdf (all pages/slides) [2] Senior notes: Maksim Medicine Notes.pdf (Neurology section, p.245 — SAH, ICH) [3] Senior notes: Maksim Surgery Notes.pdf (p.357–358 — SAH management, ICH, decompressive craniectomy) [4] Senior notes: Adrian Lui Pediatrics Notes.pdf (p.108 — headache differentials including SAH) [5] Senior notes: Ryan Ho Neurology.pdf (p.74, p.88 — cerebrovascular diseases, AVM, Moyamoya) [6] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q61, Q62) [7] Past papers: 2021 Fourth Summative Assessment MCQ.pdf (Q60, Q61) [8] Past papers: 2022 Fourth Summative MCQ.pdf (Q68) [9] Past papers: 2023 Fourth Summative MCQ.pdf (Q60) [10] Lecture slides: GC 082. Severe headache_headache and neuralgia; neuro-imaging I.pdf (p.45 — sudden onset headache differentials) [11] Lecture slides: GC 089. Syncope and irregular heart beat.pdf (p.9 — TLOC classification) [12] Lecture slides: GCBA_Fundamentals_Neuro_Introduction to Neurological Investigations and Emergencies_Prof KC Teo.pdf (p.68 — acute stroke definition)