Small vessel disease

🧠 Introduction

• Cerebral Small Vessel Disease (SVD) causes ~25% of all ischaemic strokes and >40% of dementia cases.
• It contributes to cognitive decline, gait impairment, mood disturbance, and vascular dementia.
• Common in the elderly on CT/MRI, but imaging–clinical correlation is variable (asymptomatic → gait dyspraxia → dementia).
• Underlying pathology for many deep haemorrhages (see haemorrhagic stroke chapter).
• Strongly linked to hypertension and other vascular risk factors.
• SVD itself cannot be directly imaged - instead, we use markers: lacunes, microbleeds, WMHs.

⚙️ Aetiology & Pathology

• A disease of small penetrating arterioles (<800 µm), branching from the Circle of Willis and vertebrobasilar system.
• Exposed to high pressures → prone to injury.
• Key mechanisms:
  • 🩸 Lipohyalinosis (degenerative, different to atherosclerosis).
  • 🧠 Amyloid angiopathy (elderly, lobar bleeds).
  • 🧬 Inherited genetic defects (CADASIL, Fabry’s, CARASIL).
  • 🦠 Vasculitis (autoimmune/inflammatory).
• End result → white matter demyelination, axonal loss, gliosis, and small deep strokes (lacunes <15 mm).
• Risk factors: age, hypertension, diabetes.

💡 Clinical pearl: Multiple acute lacunar infarcts → think embolism (not pure SVD).

🔬 Imaging Features

• CT: Periventricular hypodensity, often with atrophy.
• MRI T2/FLAIR: White matter hyperintensities (WMHs) in periventricular & deep regions.
• DWI: Detects acute lacunes (≤1.5 cm).
• Gradient echo / SWI: Microbleeds (siderosis).
• Appearance can mimic demyelination (MS).

📏 Fazekas Scale

Grades WMHs severity:
PVWM 0–3 (caps → halo → extension) and DWM 0–3 (punctate → confluent).
Used more in research than routine practice.

🧩 Clinical Spectrum

• Often subclinical, but may present as:
• Classical lacunar syndromes:
  • Pure motor or pure sensory stroke.
  • Sensorimotor stroke.
  • Ataxic hemiparesis.
  • Dysarthria–clumsy hand.
  • Hemichorea / hemiballismus.
• Chronic manifestations: Vascular dementia, gait apraxia, vascular parkinsonism.

📚 Pantoni’s Classification (2010)

SVD is heterogeneous - multiple pathologies converge on small vessels:

• 🩸 Arteriosclerosis: Lipohyalinosis, microaneurysms (HTN, diabetes, age).
• 🧠 Amyloid angiopathy: β-amyloid deposition, lobar bleeds, Alzheimer link.
• 🧬 Inherited: CADASIL, CARASIL, Fabry’s, MELAS, COL4A1 mutations.
• 🦠 Vasculitis/Immune: SLE, RA, ANCA vasculitides, Sneddon’s syndrome.
• Other: post-radiation angiopathy, venous collagenosis.

🩺 Management

• No specific cure - focus is on risk factor modification.
• 🎯 Control hypertension, diabetes, lipids, smoking.
• 💊 Antiplatelet therapy: Aspirin first-line. SPS3 trial: no benefit of dual therapy (aspirin+clopidogrel).
• 🏃 Lifestyle: exercise, diet, vascular prevention.
• 🔍 Consider genetic causes if young onset (e.g. CADASIL, Fabry’s).
• In acute stroke → thrombolysis is not contraindicated in lacunar infarction.

💡 Exam Pearl: SVD is the main cause of lacunar stroke, vascular dementia, gait apraxia, and deep haemorrhage. Think “small deep vessel” whenever you see a lacunar infarct on CT/MRI.