Stroke & TIA

Stroke is an acute focal neurological deficit of vascular origin lasting >24 hours (or causing death), while a transient ischaemic attack (TIA) is a transient episode of neurological dysfunction caused by focal ischaemia without acute infarction. "Time is brain" — every minute of large-vessel occlusion destroys ~1.9 million neurons, which is why stroke is a hyperacute emergency on par with STEMI.

Definition & classification

A stroke is sudden-onset focal (occasionally global) neurological deficit due to a vascular cause, persisting >24 hours. A TIA is now defined on a tissue basis — transient symptoms with no infarction on diffusion-weighted MRI (DWI) — rather than the old time-based "<24 hour" definition. Most true TIAs last <1 hour.

Broadly:

Type	Frequency	Core mechanism	Imaging signature
Ischaemic	~80–85%	Thrombosis / embolism → vessel occlusion	CT often normal early; hypodensity later; DWI restriction
Haemorrhagic — intracerebral (ICH)	~10–15%	Vessel rupture (hypertension, amyloid)	Hyperdense (bright) blood on NCCT
Haemorrhagic — subarachnoid (SAH)	~5%	Aneurysm rupture	Blood in basal cisterns/sulci

Ischaemic stroke — TOAST classification (mechanism-based):

1. Large-artery atherosclerosis (e.g., carotid stenosis)
2. Cardio-embolism (atrial fibrillation, prosthetic valves, recent MI)
3. Small-vessel disease / lacunar (lipohyalinosis of penetrating arteries — strongly linked to hypertension & diabetes)
4. Other determined cause (dissection, vasculitis, hypercoagulable states)
5. Undetermined (cryptogenic)

Oxfordshire (Bamford) clinical classification — predicts territory and prognosis:

• TACI (total anterior circulation infarct): all three of — higher cortical dysfunction, homonymous hemianopia, motor/sensory deficit of ≥2 areas. Worst prognosis.
• PACI (partial anterior): two of the three TACI features, or isolated cortical dysfunction.
• LACI (lacunar): pure motor, pure sensory, sensorimotor, or ataxic hemiparesis — no cortical signs. Best prognosis.
• POCI (posterior circulation): brainstem/cerebellar/occipital features.

High-yield: TIA is now a tissue-based diagnosis — transient symptoms with no DWI lesion. If MRI shows infarction despite resolved symptoms, it is a stroke, not a TIA.

Etiology & pathophysiology

The ischaemic cascade and the penumbra

When a vessel occludes, cerebral blood flow (CBF) drops. The core (CBF <10 mL/100 g/min) undergoes rapid, irreversible infarction. Surrounding it is the ischaemic penumbra — tissue with CBF ~10–20 mL/100 g/min that is electrically silent but structurally viable, kept alive by collateral flow. The penumbra is the therapeutic target: reperfusion (thrombolysis/thrombectomy) salvages it, whereas without flow it is recruited into the core over hours.

The mismatch concept underpins extended-window therapy: a large area of hypoperfused-but-viable tissue (penumbra) relative to a small core (seen as perfusion–diffusion mismatch on MRI, or CTP core/penumbra mismatch) means salvageable brain remains.

Mechanistically, ATP depletion → failure of Na⁺/K⁺-ATPase → cytotoxic oedema, glutamate-mediated excitotoxicity, Ca²⁺ influx, free-radical injury and apoptosis.

Haemorrhagic stroke

• Hypertensive ICH: rupture of lenticulostriate microaneurysms (Charcot–Bouchard aneurysms). Classic sites — basal ganglia/putamen (commonest), thalamus, pons, cerebellum.
• Cerebral amyloid angiopathy: β-amyloid deposition in cortical vessels → lobar haemorrhages in the elderly, often recurrent.
• SAH: rupture of a berry (saccular) aneurysm, commonest at the anterior communicating artery.

High-yield: Hypertension is the single most important modifiable risk factor for both ischaemic and haemorrhagic stroke. Atrial fibrillation is the classic source of cardio-embolic stroke.

Clinical features

Onset is abrupt/maximal at onset (embolic) or stuttering (thrombotic). Key territorial syndromes are heavily tested.

Anterior circulation

• Middle cerebral artery (MCA) — the most commonly affected territory:
  • Contralateral hemiparesis & hemisensory loss, face + arm > leg.
  • Contralateral homonymous hemianopia.
  • Dominant (usually left) hemisphere → aphasia; non-dominant → neglect, anosognosia, constructional apraxia.
  • Gaze deviation towards the lesion (away from the hemiparesis).
• Anterior cerebral artery (ACA): contralateral weakness/sensory loss leg > arm/face, abulia, urinary incontinence, grasp reflex.

Posterior circulation

• Posterior cerebral artery (PCA): contralateral homonymous hemianopia with macular sparing, alexia without agraphia (dominant), visual agnosia.
• Lateral medullary syndrome (Wallenberg) — occlusion of PICA or vertebral artery:
  • Ipsilateral — facial pain/temperature loss (CN V spinal nucleus), Horner syndrome, ataxia, dysphagia/hoarseness (CN IX, X — nucleus ambiguus), vertigo, nystagmus.
  • Contralateral — loss of pain & temperature in the body (spinothalamic tract).
  • Classically NO limb weakness (corticospinal tract is spared — it lies ventrally).
• Medial medullary syndrome (anterior spinal/vertebral): contralateral hemiparesis (sparing face), contralateral proprioception loss, ipsilateral tongue deviation (CN XII).
• Basilar artery occlusion: quadriplegia, coma, cranial nerve palsies; "locked-in" syndrome (preserved consciousness & vertical eye movements only) with ventral pontine lesions.

Lacunar syndromes

Pure motor hemiparesis (posterior limb of internal capsule/pons — commonest), pure sensory stroke (thalamus), ataxic hemiparesis, dysarthria–clumsy hand. No cortical signs (no aphasia, no neglect).

High-yield: Wallenberg (lateral medullary) syndrome = ipsilateral face + contralateral body sensory loss, with no limb weakness. PICA is the eponymous vessel.

Mnemonic for Wallenberg — "DANVAH": Dysphagia, Ataxia, Nystagmus, Vertigo, Anaesthesia (crossed), Horner.

NIHSS — severity scoring

The National Institutes of Health Stroke Scale (NIHSS) quantifies deficit severity (range 0–42), guides treatment decisions and predicts outcome.

NIHSS score	Severity
0	No stroke
1–4	Minor
5–15	Moderate
16–20	Moderate–severe
21–42	Severe

Higher scores correlate with larger infarcts and worse outcome. NIHSS ≥ 6 with a proven large-vessel occlusion is a typical threshold favouring mechanical thrombectomy.

Diagnosis & investigation of choice

Stepwise hyperacute approach: Recognise symptoms (FAST) → confirm time of onset/last-known-well → urgent non-contrast CT (NCCT) head to exclude haemorrhage → check thrombolysis eligibility → CT angiography ± CT perfusion for large-vessel occlusion/thrombectomy planning → reperfusion therapy → stroke-unit admission → workup for cause.

• First / immediate investigation: Non-contrast CT head. Its primary job is to rule out haemorrhage before thrombolysis. Acute ischaemia may be invisible for several hours; early subtle signs include the hyperdense MCA sign (thrombus), loss of insular ribbon, and effacement of sulci. The ASPECTS score (0–10) grades early ischaemic change on CT — lower score = larger established infarct = less benefit/more risk from reperfusion.
• Most sensitive for early ischaemia: MRI Diffusion-Weighted Imaging (DWI) — shows restricted diffusion within minutes. Investigation of choice for confirming small/posterior-fossa infarcts and for TIA.
• CT angiography (CTA): identifies large-vessel occlusion (LVO) — the key gate to thrombectomy.
• CT/MR perfusion: defines core vs penumbra (mismatch) for extended-window thrombectomy.
• Cause workup: ECG and prolonged monitoring (paroxysmal AF), echocardiography, carotid Doppler, lipids, HbA1c, and — in young patients — thrombophilia/vasculitis screen, dissection imaging.

High-yield: The single most important reason to do an immediate NCCT is to distinguish ischaemic from haemorrhagic stroke — because thrombolysis is lethal in haemorrhage.

Feature	Ischaemic	Haemorrhagic (ICH)
Onset	Often on waking / sudden	Sudden, often during activity
Headache / vomiting	Less common	More common, early
↓ Consciousness early	Less common	Common
NCCT appearance	Early normal/hypodense	Hyperdense (bright) blood
Antithrombotics	Indicated	Contraindicated

Management & drug of choice

Ischaemic stroke — reperfusion

1. Intravenous thrombolysis — IV alteplase (rt-PA), drug of choice, dose 0.9 mg/kg (max 90 mg), 10% bolus then infusion over 1 hour. Window: within 4.5 hours of symptom onset. (Tenecteplase is increasingly used as a single-bolus alternative.)

Absolute/major contraindications to thrombolysis:

• Any intracranial haemorrhage (current or prior ICH).
• BP >185/110 mmHg uncontrolled.
• Active internal bleeding, recent major surgery/trauma, recent stroke or serious head trauma (≤3 months).
• Platelets <100,000, INR >1.7, therapeutic heparin/DOAC use.
• Blood glucose <50 mg/dL (treat & reassess — a stroke mimic).
• Known intracranial neoplasm/AVM/aneurysm.

2. Mechanical thrombectomy (endovascular clot retrieval) for large-vessel occlusion of the anterior circulation (ICA, proximal MCA-M1):

• Standard window within 6 hours of onset.
• Extended window up to 24 hours in selected patients with favourable imaging mismatch (per DAWN and DEFUSE-3 trials) — small core, large salvageable penumbra.
• Performed in addition to IV thrombolysis when eligible.

3. Antiplatelet therapy: Aspirin 300 mg within 24–48 hours (and after excluding haemorrhage / 24 h after thrombolysis). For minor stroke (NIHSS ≤3) or high-risk TIA, short-term dual antiplatelet (aspirin + clopidogrel for 21 days, per CHANCE/POINT trials) reduces early recurrence, then single agent.

4. Supportive — "permissive hypertension": in non-thrombolysed ischaemic stroke, BP is not aggressively lowered (only treat if >220/120 mmHg) to preserve penumbral perfusion. If thrombolysing, keep BP <185/110. Manage glucose, temperature, swallow assessment (aspiration risk), DVT prophylaxis, and stroke-unit care.

Haemorrhagic stroke

Reverse anticoagulation, control BP (target SBP ~140 mmHg), manage raised ICP; neurosurgical evacuation for cerebellar haematoma >3 cm or with brainstem compression/hydrocephalus. No antithrombotics. SAH: secure aneurysm (coiling/clipping) + nimodipine to prevent vasospasm.

Secondary prevention

• Non-cardioembolic: antiplatelet (aspirin, clopidogrel, or aspirin–dipyridamole) + high-intensity statin + BP control + lifestyle.
• Cardio-embolic (AF): oral anticoagulation — a DOAC (apixaban/rivaroxaban/dabigatran) preferred over warfarin (target INR 2–3 for warfarin). Decision guided by CHA₂DS₂-VASc (risk of stroke) vs HAS-BLED (bleeding risk). Anticoagulation is usually started days after the acute event (delay larger infarcts to reduce haemorrhagic transformation).
• Symptomatic carotid stenosis 70–99%: carotid endarterectomy (CEA) within 2 weeks.

High-yield: Thrombolysis window = 4.5 h; thrombectomy standard window = 6 h, extendable to 24 h with imaging-selected penumbra (DAWN/DEFUSE-3). Aspirin starts 24 h after thrombolysis.

TIA & the ABCD² score

A TIA is a warning — up to ~10% of patients have a stroke within 90 days, many within 48 hours. The ABCD² score stratifies early stroke risk:

Factor	Points
Age ≥60 years	1
Blood pressure ≥140/90 mmHg	1
Clinical features: unilateral weakness = 2; speech disturbance without weakness = 1	1–2
Duration: ≥60 min = 2; 10–59 min = 1	1–2
Diabetes	1

Total 0–7: score ≥4 = high risk (urgent specialist assessment, imaging, and antiplatelet). Current practice favours rapid specialist evaluation of all TIAs regardless of score, with dual antiplatelet for high-risk TIA (CHANCE/POINT) and a search for carotid/cardiac source.

High-yield: ABCD² is the classic TIA risk score; ≥4 marks high short-term stroke risk. Start aspirin immediately once haemorrhage and a bleed-equivalent are excluded.

Complications

• Haemorrhagic transformation of an infarct (especially large infarcts, post-thrombolysis, post-thrombectomy).
• Malignant MCA infarction — massive cytotoxic oedema → herniation; may need decompressive hemicraniectomy (life-saving, especially age <60).
• Raised ICP, seizures, aspiration pneumonia, DVT/PE, pressure sores, depression.
• Post-stroke spasticity & contractures, central post-stroke (thalamic, Dejerine–Roussy) pain.
• SAH-specific: rebleeding, vasospasm/delayed cerebral ischaemia (peak day 4–14, prevented by nimodipine), hydrocephalus, hyponatraemia (cerebral salt wasting/SIADH).

Key differentials (stroke mimics)

• Hypoglycaemia — always check capillary glucose first; can perfectly mimic focal deficit.
• Todd's paresis (post-ictal focal weakness after a seizure).
• Hemiplegic migraine / migraine with aura.
• Space-occupying lesion — tumour, abscess (subacute onset).
• Functional (conversion) weakness.
• Bell's palsy vs stroke: forehead sparing in stroke (UMN VII), forehead involved in Bell's (LMN).
• Demyelination (MS), Wernicke encephalopathy, hypertensive encephalopathy, subdural haematoma.

High-yield: "Sudden focal deficit" with forehead-sparing facial weakness = central (stroke); whole-face including forehead = peripheral (Bell's palsy).

Recently asked / exam angle

• PICA occlusion → lateral medullary (Wallenberg) syndrome; identify the crossed sensory pattern and absence of limb weakness. Repeatedly asked.
• Drug of choice for acute ischaemic stroke within window = IV alteplase (tPA); dose 0.9 mg/kg; know the 4.5-hour figure and key contraindications (BP >185/110, INR >1.7, recent haemorrhage).
• Thrombectomy windows (6 h → 24 h with DAWN/DEFUSE-3 mismatch) — favourite single-best-answer.
• First investigation in suspected stroke = non-contrast CT (to exclude bleed); most sensitive early test = DWI-MRI.
• Commonest site of hypertensive ICH = putamen/basal ganglia; Charcot–Bouchard aneurysm as the rupturing lesion.
• ABCD² components and the ≥4 high-risk cut-off.
• MCA stroke = face + arm > leg; ACA = leg > arm; gaze deviates towards the lesion.
• AF + stroke → anticoagulate, guided by CHA₂DS₂-VASc; DOAC preferred.
• Hyperdense MCA sign and ASPECTS on CT.
• Locked-in syndrome localises to the ventral pons (basilar artery).

Rapid revision

1. Ischaemic stroke ~80–85%; haemorrhagic ~15–20%. NCCT first to exclude bleed.
2. IV alteplase 0.9 mg/kg within 4.5 h; thrombectomy ≤6 h, up to 24 h with penumbral mismatch.
3. Thrombolysis contraindicated if BP >185/110, INR >1.7, recent ICH/major surgery, glucose <50.
4. Aspirin 300 mg within 48 h — but wait 24 h after thrombolysis.
5. DWI-MRI = most sensitive for acute/posterior infarcts and defines true TIA (no infarct).
6. MCA: face+arm>leg, aphasia (dominant), neglect (non-dominant). ACA: leg>arm.
7. Wallenberg (PICA): ipsilateral face + contralateral body pain/temp loss, no weakness.
8. Lacunar strokes have no cortical signs; commonest = pure motor (internal capsule).
9. Hypertensive ICH commonest in putamen; lobar bleed in elderly → amyloid angiopathy.
10. ABCD² ≥4 = high early stroke risk after TIA; assess urgently, dual antiplatelet (21 days) for high-risk minor stroke/TIA.
11. AF stroke → anticoagulate (DOAC preferred); CHA₂DS₂-VASc guides it; symptomatic carotid 70–99% → endarterectomy.
12. Malignant MCA oedema → decompressive hemicraniectomy; SAH → nimodipine for vasospasm + secure aneurysm.