Anterior Choroidal Artery Ischaemic Stroke

Related Subjects: |Acute Stroke Assessment (ROSIER&NIHSS) |Atrial Fibrillation |Atrial Myxoma |Anterior Choroidal Artery Ischaemic Stroke |Causes of Stroke |Ischaemic Stroke |Cancer and Stroke |Hypertension |Small Vessel Disease |CADASIL |CARASIL

🧠 Anterior choroidal artery (AChA) stroke is a rare but clinically important lacunar syndrome. It accounts for ~0.6–2.5% of all ischaemic strokes and ~8–10% of small-vessel (lacunar) infarcts in large registries. Classic presentation: contralateral hemiplegia + hemisensory loss + homonymous hemianopia (complete triad in only ~10–25% of cases). Most cases present as incomplete syndromes (pure motor or sensorimotor). Early recognition on MRI helps confirm diagnosis and guide secondary prevention.

🧬 Vascular Anatomy & Territory

• Origin: arises from supraclinoid internal carotid artery (ICA), usually just distal to posterior communicating artery (PCoA).
• Course: cisternal segment → choroidal fissure → intraventricular segment.
• Supplied structures (variable but classic):
  • Posterior limb of internal capsule (corticospinal & corticobulbar tracts)
  • Ventral posterolateral (VPL) thalamus (sensory relay)
  • Lateral geniculate body (visual pathway)
  • Globus pallidus (pars externa)
  • Optic tract & part of cerebral peduncle
  • Choroid plexus, hippocampus tail, uncus (variable)
• Collateral flow: limited; distal AChA branches have poor anastomoses → vulnerable to isolated occlusion.

📊 Classic vs Real-World Clinical Presentation

🩺 Clinical Features – High-Yield Summary

• Onset: Usually acute (minutes to hours); can be stuttering or progressive in some cases.
• Most frequent syndromes:
  • Pure motor hemiparesis (capsular involvement).
  • Sensorimotor stroke (capsule + thalamus).
  • Ataxic hemiparesis (peduncle/thalamus).
• Less common: dysarthria-clumsy hand, hemineglect, aphasia (if dominant), visual field defects (often incomplete), seizures (rare at onset).
• Red flags for poor prognosis: altered consciousness, complete triad, large infarct volume, cardioembolic source.

🔍 Investigations – Stepwise Approach

1. Urgent brain imaging:
   • Non-contrast CT: often normal early; subtle hypodensity in posterior capsule/thalamus after 12–24 h.
   • MRI brain (gold standard): DWI restriction in posterior limb internal capsule ± thalamus ± lateral geniculate ± cerebral peduncle; T2/FLAIR hyperintensity evolves later.
2. Vascular imaging: CTA/MRA neck & intracranial — assess ICA stenosis, dissection, or embolus source.
3. Cardiac workup: ECG, 24–72 h Holter, transthoracic ± transoesophageal echo.
4. Bloods: FBC, U&Es, glucose/HbA1c, lipids, ESR/CRP, thrombophilia screen (young patients), homocysteine, B12/folate.
5. Other if indicated: 24 h ABPM (hypertension), carotid duplex, prolonged rhythm monitoring.

💊 Management & Secondary Prevention

• Acute phase:
  • Standard stroke protocol: thrombolysis if within window and no contraindications (rarely given in pure small-vessel disease).
  • Mechanical thrombectomy not indicated (distal territory).
  • Antiplatelet therapy: aspirin 300 mg stat → 75 mg daily (or clopidogrel if aspirin intolerant).
  • Supportive care: swallow assessment, DVT prophylaxis, early mobilisation/rehabilitation.
• Secondary prevention (NICE / ESO 2025–2026):
  • Antiplatelet: aspirin monotherapy (or clopidogrel) long-term.
  • Intensive risk factor control:
    • BP target <130/80 mmHg (or <125/75 if diabetic/proteinuria).
    • Statin: high-intensity (atorvastatin 40–80 mg or rosuvastatin 20–40 mg); target LDL <1.8 mmol/L.
    • Glycaemic control (HbA1c <48 mmol/mol if diabetic).
    • Smoking cessation, alcohol moderation, diet/exercise.
  • Anticoagulation only if cardioembolic source (AF, valve disease).
• Rehabilitation: physiotherapy, occupational therapy, speech therapy if dysarthria/aphasia.

📊 Prognosis & Outcome Data

🚩 Red Flags & Do-Not-Miss OSCE Points

• Young patient (<50) + no obvious risk factors → consider dissection, cardioembolism, thrombophilia.
• Complete triad + altered consciousness → large AChA infarct → poorer prognosis.
• Recurrent lacunar events → consider CADASIL or other small-vessel disease.
• Isolated hemianopia without motor/sensory deficit → consider differential (posterior cerebral artery territory).

📌 Key Exam & Viva Pearls

• Most common presentation: pure motor or sensorimotor lacunar stroke — not the full triad.
• MRI hallmark: DWI restriction in posterior limb internal capsule ± thalamus ± lateral geniculate body.
• Always ask about vascular risk factors (hypertension, diabetes, smoking) and cardioembolic sources.
• Secondary prevention = antiplatelet + intensive BP/lipid control (same as other lacunar strokes).
• Differentiate from posterior cerebral artery infarct (more visual field loss, less motor involvement).

📚 References (Feb 2026)

• Radiopaedia: Anterior choroidal artery infarct (updated 2025).
• UpToDate: Anterior choroidal artery territory infarction (2026).
• Arboix A et al. Acute anterior choroidal artery territory infarction. J Neurol Sci 2023–2025 series.
• NICE / ESO Stroke Guidelines (2025–2026): Lacunar & small vessel disease.