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 thrombolysis within 4.5 hours for eligible disabling stroke, selected advanced-imaging thrombolysis to 9 hours/unknown onset, and endovascular thrombectomy (EVT) for eligible large-vessel occlusion, including selected patients out to 24 hours [14]
- Know the three key complications of aneurysmal SAH: rebleeding, vasospasm, hydrocephalus
- Classify vascular malformations and understand when to intervene
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]
Reading the paired visual: the facial pain map distinguishes common primary/extracranial patterns (TMJ/temporal, sinus/cheek, cluster/periorbital, tension/band-like, neck/occipital and migraine/hemicranial), while the adjacent intracranial pressure–volume curve explains danger. The skull initially compensates for added volume by displacing CSF/venous blood; once that reserve is depleted, a small additional volume produces a steep ICP rise, reduced compliance, impaired perfusion and possible herniation.
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
- A GCS of 8 or less is a major warning for airway failure, but the decision to intubate rests on airway reflexes, oxygenation/ventilation, trajectory and anticipated procedures—not the number alone. In the exam case with GCS 6 after SAH, immediate airway protection is clearly appropriate.
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]
Reading the six CT examples: acute blood is hyperdense (bright). The panel contrasts deep basal-ganglia and thalamic ICH, lobar ICH, cerebellar ICH, basal-cisternal SAH and an ischaemic MCA territory that is initially subtle/hypodense and can later acquire patchy hyperdensity from haemorrhagic transformation. First identify where the blood is—parenchyma, ventricles, subarachnoid space or extra-axial compartment—before naming the cause.
The accompanying compartment diagram separates haemorrhages that are mostly traumatic (epidural and subdural), mostly spontaneous (deep ICH/IVH), and either traumatic or spontaneous (lobar ICH and SAH). This is a probability guide, not a substitute for the history or vascular imaging.
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
- Hyperosmolar rescue when clinically indicated (mannitol or hypertonic saline according to protocol; not routine continuous prophylaxis)
- 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” — lecture-era uncertainty [1]
Tranexamic acid can reduce early haematoma expansion in selected patients, but current evidence has not established improved functional outcome; it is not routine blanket treatment. Priorities are rapid imaging, smooth blood-pressure control, urgent reversal of anticoagulation when present, neurocritical care and selected neurosurgery [15].
Reverse bleeding tendency [1] Principles of maintaining CBF apply (i.e., CPP = MAP − ICP) [1]
Decompresses brain & is life-saving but does not affect primary injury [1] Functional prognosis depends on location & extent of haemorrhage [1]
Reading the operative sequence: the first CT shows a large ICH with mass effect and intraventricular extension; the surgical photograph shows evacuation through a cortical corridor; the postoperative CT shows a smaller residual cavity and reduced mass effect. Evacuation creates space and can prevent herniation, but it cannot restore tissue already destroyed by the initial bleed.
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 without open evacuation; age alone is not the decision rule
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] Hypertension can cause lobar bleeding, but cerebral amyloid angiopathy and structural lesions become important explanations, especially with age or atypical imaging Other pathology (e.g., tumour, bleeding tendency, vasculitis, AVM) [1] Deep nuclei/brainstem may be compressed but not primarily injured [1] Selected surgery may be life-saving; routine open evacuation of every lobar ICH has not shown a general functional benefit [15]
Why might superficial location matter? A lobar clot may be more surgically accessible, with less normal tissue traversed than for a deep clot. That anatomical rationale does not make surgery universally beneficial; deterioration, mass effect, volume, location, cause, premorbid function and patient goals determine selection [15].
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 small, rigid compartment. A haematoma can rapidly compress the brainstem and obstruct the fourth ventricle. Immediate evacuation with or without EVD is recommended for neurological deterioration, brainstem compression, obstructive hydrocephalus or a cerebellar ICH volume of at least 15 mL; this improves survival, while the effect on functional outcome is less certain [15].
Exam Discrimination: When to Operate on ICH
| Operate | Conservative |
|---|---|
| Lobar/subcortical ICH with mass effect | Deep BG/thalamic ICH in elderly |
| Cerebellar ICH with deterioration, brainstem compression, hydrocephalus or volume ≥15 mL | 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."
Time-critical standard treatment for eligible disabling ischaemic stroke [14] Converts plasminogen to plasmin, which lyses clot [1] Routine window: within 4.5 hours from last known well; do not wait until the end of the window [14] Can substantially improve outcome but is not guaranteed to reverse the deficit
Mechanism: thrombolytics such as alteplase and tenecteplase promote conversion of plasminogen to plasmin and fibrin breakdown. The 2026 AHA/ASA guideline endorses either alteplase or tenecteplase within 4.5 hours for eligible disabling stroke. Selected unknown-onset or 4.5–9-hour presentations may receive thrombolysis using MRI DWI–FLAIR or perfusion mismatch; non-disabling deficits are managed differently [14].
High Yield Exam Point
Exam-era answer: “3–4.5 hours.” Current practice: treat eligible disabling stroke as soon as possible within 4.5 hours, with imaging-selected extensions in defined patients. [14]
Large clots are less likely to recanalise with IV thrombolysis alone, but eligible IVT should still be given without delaying EVT [14]
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 thrombectomy (EVT) as soon as possible for eligible LVO; the slide's fixed 6-hour ceiling is obsolete. Selection extends to 24 hours in defined anterior-circulation cases, and current guidance supports basilar-artery EVT within 24 hours for selected patients [14]
Dense MCA Sign — hyperdense MCA on plain CT representing acute thrombus within the artery [1] Acute MCA Occlusion → Potential large infarction [1]
Reading the LVO/EVT images: a dense MCA on non-contrast CT is an intraluminal-clot clue; the 3-D CTA shows an abrupt MCA cutoff; the follow-up CT demonstrates how a proximal occlusion can evolve into a large territorial infarct. The thrombectomy panel traces femoral/radial arterial access, catheter delivery to the intracranial clot, stent-retriever/aspiration engagement and removal of the red thrombus. DSA before treatment shows absent downstream branches; after reperfusion, the arterial tree refills.
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: EVT targets an amenable arterial occlusion, not a small-vessel lacune. Eligible IV thrombolysis should not be delayed while arranging EVT. Tranexamic acid has no role in reperfusing an ischaemic stroke.
Ischaemic brain has disturbed BBB & vascular reactivity [1] Reperfusion haemorrhage worsens outcome [1] Risk relates to infarct burden, blood-brain-barrier injury, reperfusion and treatment timing—not a universal 6-hour cliff
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] Non-contrast CT establishes haemorrhage and early infarct burden; advanced CT/MR techniques can estimate core–penumbra mismatch 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: the slide labels perfusion/diffusion mismatch “future practice,” but this is now established selection technology. CT perfusion or MR mismatch can identify salvageable tissue for extended-window IV thrombolysis in selected patients and for EVT beyond 6 hours, although not every early-window patient requires perfusion imaging [14].
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 can deterioration be delayed? Cerebral oedema evolves over the first several days. In malignant MCA infarction, hemicraniectomy allows the swollen hemisphere to expand outward rather than herniate downward. It reduces mortality but does not reverse the infarct; disability outcomes, age, premorbid function and the patient's values require urgent shared decision-making. Avoid presenting one historical mortality percentage or “young and fit only” as a universal rule.
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
- Increasing age (the slide's “> 40” is not a screening/treatment threshold)
- 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]
- Superficial parasympathetic fibres are vulnerable → a dilated poorly reactive pupil is a classic clue
- Ptosis and ophthalmoplegia may also occur; preserved eye movement is not required Urgent angiogram & intervention before rupture! [1]
Why does this pattern occur? CN III runs adjacent to the PComA, and its superficial parasympathetic fibres are vulnerable to external compression. A painful acute third-nerve palsy—especially with pupil involvement—requires urgent aneurysm imaging. Pupil sparing makes a microvascular palsy more likely but does not make a new third-nerve palsy automatically benign or non-urgent.
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 | Often impaired; may evolve | Often impaired |
| Pain | Often present | Variable |
| Cause | PComA aneurysm, uncal herniation | Diabetes, HTN microvascular |
| Urgency | Emergency vascular imaging | Prompt clinical evaluation; do not rely on pupil sparing alone |
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]
Fundal image: the sharply demarcated pre-retinal/subhyaloid haemorrhage illustrates Terson syndrome, an intraocular haemorrhage associated with an abrupt ICP rise in SAH. It supports severe intracranial haemorrhage but is not pathognomonic for SAH.
Clinical suspicion. H&E. [1] CT – can be very subtle or even normal [1] LP – selected patients after a negative CT, depending on CT timing and specialist interpretation [16]
- Blood-stained CSF
- SAH vs. traumatic tap!
- Do not rely on a “3-bottle test” alone: falling RBC counts can occur in SAH and persistently bloody tubes can occur after a traumatic tap
- When LP is indicated, allow at least 12 hours from onset and use spectrophotometric bilirubin/xanthochromia according to laboratory protocol [16] MRI – can be false-negative at acute stage [1] Once diagnosed: stabilise, transfer urgently to an expert neurovascular centre, start enteral nimodipine, and secure the culprit aneurysm preferably within 24 hours [17]
Modern CT–LP pathway: obtain urgent non-contrast CT. If a high-quality CT is performed within 6 hours and reported by an appropriately experienced radiologist as negative, NICE advises not routinely offering LP; consider alternatives and specialist advice. If CT is negative more than 6 hours after onset, consider LP at least 12 hours after onset and assess bilirubin spectrophotometrically [16].
Past Paper Alert — 2020 Q62
A 55-year-old man with sudden severe headache, vomiting, neck stiffness, no motor weakness and an early normal CT still has a classic SAH syndrome. The historical paper may expect LP; current next steps depend on scan timing/quality and expert interpretation, and a routine LP after a high-quality CT within 6 hours is no longer automatic [16].
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 is front-loaded: the slide's day-specific percentages are historical teaching estimates. The actionable point is urgent culprit identification and complete aneurysm obliteration, preferably within 24 hours. Maintain careful, low-variability haemodynamics while awaiting treatment [17]. Routine antifibrinolytic therapy has not improved functional outcome, and routine antiseizure prophylaxis is not indicated for everyone; treat new-onset seizures and consider short prophylaxis only in selected high-risk patients [17].
CTA non-invasive but can be false-negative [1] If CTA is negative but an aneurysmal source remains suspected, seek specialist review and consider DSA or MRA [16] DSA is invasive; its risk is centre- and patient-dependent, not a fixed universal 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 | Highest spatial/temporal resolution; therapeutic planning capability | Invasive procedural stroke/vascular risks |
Reading the angiography panel: CTA depicts the aneurysm within a 3-D arterial reconstruction; DSA isolates vascular anatomy with high resolution; MRA can show an aneurysm without ionising radiation. A negative CTA is not an automatic order for DSA in every headache—it triggers specialist review when confirmed SAH pattern or other features leave an aneurysm suspected [16].
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]
Reading the treatment images: clipping closes the aneurysm neck while preserving the parent artery, confirmed by pre/post angiography. Coiling packs the sac from within to promote thrombosis. A flow diverter reconstructs the parent artery and redirects flow, but because it usually requires antiplatelet therapy it is not a routine interchangeable choice for every acutely ruptured aneurysm. Modality selection is multidisciplinary and anatomy-specific [17].
The senior-note rule “coiling first, clipping for wide-necked lesions” is too simple. Endovascular and microsurgical teams select the approach from aneurysm location/neck/branch anatomy, age, haemorrhage pattern, need for antiplatelet therapy, durability and centre expertise [17].
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.
Early enteral nimodipine improves outcomes after aneurysmal SAH and should be started according to protocol; dose modification may be needed if hypotension limits delivery. Treat symptomatic delayed cerebral ischaemia with euvolaemia and induced hypertension when appropriate; avoid prophylactic hypervolaemia/hemodynamic augmentation. Refractory cases may need endovascular vasodilator therapy or angioplasty [17].
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 → urgent non-contrast CT → timing-dependent LP only when indicated → if SAH confirmed, CTA without delay → specialist DSA/MRA if the culprit remains suspected → secure the aneurysm (coil/clip, preferably within 24 hours) → neurocritical care with nimodipine and complication surveillance → EVD/shunt or DCI-directed intervention when indicated [16][17]
From lecture [1] and senior notes [2][3]:
| Complication | Timing | Mechanism | Management |
|---|---|---|---|
| Rebleeding | Highest early, especially before securement | Unsecured aneurysm | Complete obliteration preferably within 24 h; routine antifibrinolysis is not outcome-improving |
| Delayed cerebral ischaemia/vasospasm | Commonly days 4–14 | Multifactorial DCI; angiographic vasospasm is one component | Early enteral nimodipine; euvolaemia; treat symptomatic DCI, selected endovascular rescue |
| 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 | Treat new-onset seizures; no routine blanket long-term prophylaxis |
| 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 | Variable; prior rupture is a major risk modifier | AV shunting, flow voids on MRI | Individualised observation, surgery, embolisation, radiosurgery or combination |
| Cavernous Angioma | Variable by prior haemorrhage and location | “Popcorn”/haemosiderin appearance on susceptibility MRI, often DSA-negative | Usually observe; selected symptomatic/accessible lesions may be treated |
| 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]
Reading the malformation panel: an AVM is a compact vascular nidus with enlarged feeding arteries and draining veins on angiography. A cavernous malformation has a mixed-signal “popcorn” core and haemosiderin rim on MRI. A developmental venous anomaly appears as radially converging medullary veins, while capillary telangiectasia is a faint, usually incidental lesion. These have very different natural histories and must not be grouped as one “bleeding-risk ladder.”
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 risk is individual, not a fixed 3%/year — prior rupture, deep location/drainage and associated aneurysm matter
- 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
Reading the treatment images: microsurgical resection removes the nidus while preserving feeding/draining anatomy until safe disconnection; embolisation occludes selected feeders/nidus through a catheter; stereotactic radiosurgery aims for delayed obliteration, so haemorrhage risk persists during the latency period. For an unruptured AVM, intervention can itself cause stroke or death; counsel about natural-history risk, life expectancy and procedural risk rather than treating every lesion [18].
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.
Progressive stenosis/occlusion at the terminal intracranial ICA and proximal branches Compensatory proliferation of vascular collaterals ('puff of smoke') — appearance on angiogram [1] Children more often present with ischaemia and adults can present with ischaemia or haemorrhage; this is a tendency, not an age rule Revascularisation surgery is the main disease-directed treatment for selected symptomatic patients [19]
Reading the angiogram: basal collateral networks develop around progressive terminal ICA stenosis, producing the “puff of smoke” appearance. Children commonly present with hypoperfusion/TIA or stroke; adults may also have ischaemia, while fragile collaterals/choroidal pathways can cause haemorrhage. Moyamoya disease is idiopathic; moyamoya syndrome occurs with an associated condition.
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] Antithrombotic treatment is individualised: antiplatelet or anticoagulation strategies are generally used for 3–6 months when appropriate; one is not universally superior [20] Stenting/bypass is reserved for selected recurrent ischaemia or specific anatomy, not routine first-line treatment
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]
- Eligible disabling stroke: alteplase or tenecteplase as soon as possible within 4.5 hours; advanced-imaging extension for selected unknown-onset/4.5–9-hour cases [14]
- LVO: EVT as soon as possible, with imaging/clinical selection up to 24 hours in defined patients [14] 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
High Yield Summary
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The ONE sentence
- Sudden headache + LOC = cerebrovascular until proven otherwise.
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Haemorrhagic stroke
- Deep BG/thalamic/brainstem haemorrhage is often hypertensive and generally not amenable to routine open evacuation. Lobar haemorrhage requires aetiologic evaluation and selected—not automatic—surgery. Cerebellar ICH with deterioration, compression, hydrocephalus or volume ≥15 mL needs immediate evacuation. No prophylactic steroids or routine continuous hyperosmolar therapy.
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Ischaemic stroke ("Brain Attack")
- Eligible disabling stroke: IV alteplase or tenecteplase as soon as possible within 4.5 hours; selected imaging-based extensions exist.
- CT angiography for LVO → EVT urgently; selected patients benefit out to 24 hours.
- 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).
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SAH
- Aneurysmal until proven otherwise (if no trauma).
- Thunderclap headache + meningism.
- Urgent CT; if negative within 6 hours and expertly reported, do not routinely LP. If CT is negative after 6 hours, consider LP at least 12 hours after onset with bilirubin spectrophotometry.
- Three killers: rebleeding (secure aneurysm preferably within 24 hours), delayed cerebral ischaemia (early enteral nimodipine) and hydrocephalus (EVD/shunt when indicated).
- Coil or clip according to aneurysm/patient factors; routine TXA and routine anticonvulsant prophylaxis are not blanket answers.
- Surgical CN III palsy (dilated pupil, ptosis) = PComA aneurysm → urgent angiogram.
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Vascular malformations
- AVM haemorrhage risk and treatment are individualised; surgery, embolisation and radiosurgery each carry trade-offs. Developmental venous anomaly/capillary telangiectasia are usually conservative. Moyamoya produces terminal ICA stenosis with “puff-of-smoke” collaterals and may need revascularisation. Cervical dissection can produce painful partial Horner syndrome or posterior-circulation symptoms; choose antithrombotic therapy individually.
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)
[14] AHA/ASA. 2026 Guideline for the Early Management of Patients With Acute Ischaemic Stroke.
[15] AHA/ASA. 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Haemorrhage.
[16] NICE NG228. Subarachnoid haemorrhage caused by a ruptured aneurysm: diagnosis and management (2022).
[17] AHA/ASA. 2023 Guideline for the Management of Patients With Aneurysmal Subarachnoid Haemorrhage.
[18] AHA/ASA. Management of Brain Arteriovenous Malformations (scientific statement and current hub).
[19] AHA/ASA. Adult Moyamoya Disease and Syndrome: Current Perspectives and Future Directions (scientific statement slide set, 2023/2024).
[20] AHA. Treatment and Outcomes of Cervical Artery Dissection in Adults (2024 scientific statement).
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