NeurologyTier 1Disease (DEADMAN)

Ischaemic stroke

Description

Sudden focal neurological deficit + imaging/tissue evidence of infarction
TIA = tissue-based definition - transient deficit, no infarct on DWI
- Not a benign event: ~5% stroke at 7 days untreated

Bamford / OCSP syndromes

	Criteria	Cause	1yr mortality
TACS	All 3: higher cortical dysfunction + homonymous hemianopia + motor/sensory deficit in 2 of face/arm/leg	Proximal MCA or ICA occlusion	~60%, only ~5% independent
PACS	2 of 3, or isolated higher cortical dysfunction	MCA branch	~15%
LACS	Pure motor, pure sensory, sensorimotor, ataxic hemiparesis, clumsy-hand dysarthria. No cortical signs, no hemianopia	Small vessel	~10%, best functional outcome, highest recurrence
POCS	CN palsy + contralateral deficit, bilateral deficit, disordered conjugate gaze, cerebellar signs, isolated hemianopia	Vertebrobasilar	~20%

Localisation

ACA - leg > arm, abulia, urinary incontinence, grasp reflex
MCA - face/arm > leg, dysphasia (dominant), neglect (non-dominant), gaze deviation toward lesion
- Homonymous hemianopia + contralateral neglect -> parietal (inferior parietal lobule / temporoparietal junction), classically right
PCA - homonymous hemianopia with macular sparing, alexia without agraphia
Basilar - locked-in, quadriparesis, fluctuating coma. Top-of-basilar: cortical blindness + amnesia
Lateral medullary (PICA/vertebral, Wallenberg) - ipsilateral Horner + facial pain/temp loss + ataxia, contralateral body pain/temp loss, dysphagia, hoarseness
- Crossed sensory findings = brainstem until proven otherwise

Epidemiology

~45,000 strokes/yr in Australia; >440,000 survivors
80-85% ischaemic, 15-20% haemorrhagic
Leading cause of adult disability; 3rd leading cause of death
Incidence doubles each decade after 55; ~1/4 occur under 65
Aboriginal and Torres Strait Islander: ~2x rate, ~10-20 yrs earlier onset
M>F incidence, but F higher lifetime risk + worse outcomes (longevity, AF, isolation)

Aetiopathogenesis

TOAST classification

Large artery atherosclerosis ~20% - carotid bifurcation, vertebral origin, intracranial
- Artery-to-artery embolus > low flow
Cardioembolic ~20-25% - AF commonest; also LV thrombus post-MI, prosthetic valve, endocarditis, dilated cardiomyopathy, atrial myxoma
Small vessel (lacunar) ~25% - lipohyalinosis of penetrating arteries; HTN and diabetes dominate
Other determined ~5%
- Dissection - commonest cause under 40 (carotid or vertebral; neck pain, Horner, preceding trauma/chiropractic)
- Vasculitis, reversible cerebral vasoconstriction, antiphospholipid, thrombophilia, sickle cell, Fabry, CADASIL, vasospasm post-SAH
Undetermined/cryptogenic ~25% - includes ESUS; look hard for occult AF and PFO

Penumbra

Core = irreversibly infarcted (CBF <10 mL/100 g/min)
Penumbra = electrically silent, structurally viable, salvageable
- Sustained by collaterals -> collateral status determines how long the window lasts, not the clock
~1.9 million neurons lost per minute untreated
Cytotoxic oedema peaks days 3-5 -> malignant MCA syndrome

Diagnosis

A. Non-contrast CT - first, always

Purpose is to exclude haemorrhage, not to confirm infarct
Early ischaemic signs: loss of grey-white differentiation, insular ribbon sign, sulcal effacement, hyperdense MCA sign
ASPECTS /10 - <6 = large established core

B. CT angiography

Identifies large vessel occlusion (LVO): ICA terminus, M1, proximal M2, basilar
Extend to arch and neck: dissection, tandem stenosis

C. CT perfusion

Separates core from penumbra -> drives extended-window decisions
Target mismatch (DEFUSE-3 style): core <70 mL, mismatch ratio >=1.8, penumbra >=15 mL
CTP overestimates core in the first ~1 h ("ghost core") - do not deny treatment on CTP alone when early

D. MRI

DWI most sensitive, positive within minutes
DWI/FLAIR mismatch -> infarct likely <4.5 h in wake-up stroke

Aetiological workup

ECG on arrival + >=24 h telemetry; prolonged monitoring (7-30 d loop/implantable) if cryptogenic - yield rises with duration
Carotid imaging in all anterior circulation stroke/TIA
TTE; TOE or bubble study if young, cryptogenic, or suspected endocarditis
Lipids, HbA1c, FBE, ESR/CRP, coagulation
Young stroke: thrombophilia, antiphospholipid, vasculitis screen, drug screen, consider vessel wall MRI

Mimics (~20% of code strokes)

Hypoglycaemia - BSL in every patient before thrombolysis
Seizure with Todd's paresis, migraine with aura, functional, sepsis unmasking old deficit, hypertensive encephalopathy, MS relapse

Management

A. Hyperacute reperfusion

Two independent decisions - thrombolysis and thrombectomy are not alternatives; give both where both are indicated.

1. IV thrombolysis

Alteplase 0.9 mg/kg (max 90 mg), 10% bolus then 60 min - within 4.5 h of onset
Tenecteplase 0.25 mg/kg single bolus - alternative within 4.5 h, preferred where LVO present and transfer for thrombectomy planned
Extended window to 9 h (or to mid-point of sleep in wake-up stroke) if advanced imaging shows salvageable tissue - perfusion mismatch or DWI/FLAIR mismatch
- Tenecteplase beyond 4.5 h is outside TGA approval - stroke-physician decision
Absolute contraindications: haemorrhage, recent intracranial surgery/bleed, BP >185/110 unresponsive to treatment, platelets <100, INR >1.7, therapeutic DOAC within 48 h, BSL not corrected
Post-lysis: no antithrombotic for 24 h, repeat CT at 24 h, neuro obs, BP <180/105

2. Endovascular thrombectomy

LVO (ICA, M1, proximal M2, basilar) with disabling deficit
0-6 h - on CTA + non-contrast CT alone
6-24 h - with perfusion or clinical-core mismatch selection (DAWN, DEFUSE-3)
Now also offered with large established core (ASPECTS 3-5) - SELECT2/ANGEL-ASPECT show benefit despite big infarct
Basilar occlusion: benefit out to 24 h (ATTENTION, BAOCHE)
Do not delay thrombolysis while arranging thrombectomy

B. Acute care - everyone, reperfused or not

Stroke unit admission is the single intervention with the largest population benefit
BP: permissive HTN, treat only if >220/120 (or >185/110 if lysed). Rapid lowering extends the infarct
Aspirin 300 mg once haemorrhage excluded (24 h delay if thrombolysed)
Swallow screen before any oral intake - aspiration pneumonia is the commonest early complication
Glucose 6-10 mmol/L; treat fever; avoid hypoxia (O2 only if SpO2 <93%)
VTE prophylaxis: intermittent pneumatic compression (CLOTS-3); no graduated stockings
Early mobilisation, but not very-early high-dose (AVERT)
Decompressive hemicraniectomy for malignant MCA infarction - within 48 h, greatest benefit age <60

C. Secondary prevention

Non-cardioembolic - antiplatelet
- Minor stroke (NIHSS <=3) or high-risk TIA (ABCD2 >=4): aspirin + clopidogrel for 21 days, then single agent
- Longer DAPT increases bleeding without further benefit
Cardioembolic (AF) - DOAC over warfarin (warfarin if mechanical valve or moderate-severe mitral stenosis)
- Timing by infarct size: TIA ~day 1, small ~day 3, moderate ~day 6, large ~day 12 (ELAN supports earlier start than the old 1-3-6-12)
Lipids - high-intensity statin, LDL target <1.8 mmol/L; add ezetimibe if not met
BP - target <130/80, the largest single modifiable contributor to recurrence
Carotid endarterectomy if symptomatic stenosis 70-99% - ideally within 2 weeks; benefit falls sharply after that
- 50-69% - benefit smaller, men > women
PFO closure if cryptogenic stroke, age <60, high-risk PFO anatomy
Smoking cessation, HbA1c, alcohol, exercise, weight

D. Rehabilitation and recovery

MDT: physio, OT, speech, neuropsych, social work
Screen for mood, spasticity, pain, cognition, dysphagia at each review
Driving - no private driving for 4 weeks post-stroke (commercial 3 months), subject to Assessing Fitness to Drive

Avoid

Anticoagulating for large infarct early - haemorrhagic transformation
Nimodipine (SAH only), routine steroids, routine osmotherapy, aggressive acute BP lowering

Associations

AF - 5x risk; commonest treatable cause
HTN, diabetes, smoking, dyslipidaemia, obesity, physical inactivity
Obstructive sleep apnoea - both cause and consequence
CKD - risk factor and limits thrombolysis/anticoagulation decisions
Migraine with aura - modest risk increase, amplified by smoking + COCP
Antiphospholipid syndrome, sickle cell, active malignancy (Trousseau)
Post-stroke depression ~1/3; vascular cognitive impairment
Infective endocarditis - stroke may be the presenting feature; thrombolysis contraindicated

Natural history & complications

~1/3 die or remain dependent, ~1/3 recover with deficit, ~1/3 good recovery
Recovery fastest in first 3 months, continues to 6-12 months
Recurrence ~5% at 1 yr, ~25% at 5 yrs - risk highest in the first days after TIA

Early complications

Haemorrhagic transformation (higher with large infarct, thrombolysis, anticoagulation)
Malignant MCA oedema - days 3-5, young patients with poor atrophy reserve
Aspiration pneumonia, UTI, VTE
Seizures (~5%), post-stroke epilepsy

Late complications

Spasticity and contracture, shoulder subluxation, central post-stroke pain
Depression (~1/3), emotional lability, fatigue
Vascular cognitive impairment and dementia
Falls, pressure injury, malnutrition

Deficits that plateau then worsen = look for a new event, hydrocephalus, seizure, infection or depression - not "natural decline"

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