Fact-sheet: Cerebral microangiopathy - cerebral small vessel disease
  • Chronic white matter ischemia
  • Cerebral small vessel disease


Updated on 04/12/2026 at 12:18 PM

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Definition

Cerebral microangiopathy - cerebral small vessel disease is a generic term referring to brain lesions attributed to disease of the small arteries, arterioles, capillaries, venules, or small veins.

It is characterized by structural changes: tortuous vessel walls, reduced caliber and flow, enlarged Virchow-Robin spaces, and white matter demyelination.

Most common cause of vascular dementia (Binswanger's disease) and a major cause of ischemic and hemorrhagic strokes.

Clinical features

  • Asymptomatic: Often an incidental finding on imaging.
  • Cognitive impairment: Major cause of cognitive deficit and vascular dementia (100% prevalence in some dementia studies).
  • Binswanger's disease: Term used to describe a progressive clinical syndrome of cognitive impairment associated with compatible imaging features (diffuse white matter involvement).
  • Risks: Stroke and overall mortality.

Laboratory findings

Cardiovascular risk factors accelerate the lesions: arterial hypertension, diabetes, hypercholesterolemia, and smoking.

Ultrasound

Doppler ultrasound: used for associated macrovascular assessment

CT

Less sensitive than MRI

  • Non-enhancing white matter hypodensities (leukoaraiosis), predominating around the ventricular trigones and in the subcortical region.
  • Ischemic lacunae: focal hypodensities more pronounced than the areas of diffuse demyelination.

MRI

Reference examination. STRIVE-2 recommendations advocate the following sequences: T1, T2, T2-FLAIR, Diffusion (DWI), GRE or SWI, and TOF MR angiography.

  • White matter hyperintensities on T2 and T2-FLAIR, iso- or hypointense on T1 (leukoaraiosis).
  • Lacunes: Fluid-filled cavities measuring 3 to 15 mm. On T2-FLAIR, they are hypointense (fluid signal), sometimes with a hyperintense rim, distinguishing them from demyelination (which remains hyperintense on T2-FLAIR).
  • Enlarged perivascular spaces: Visible on T2-FLAIR as hypointense lacunar-like images, particularly in the insular and lenticular regions.
  • Microbleeds: Identified on susceptibility-weighted sequences (GRE/SWI), predominating in the basal ganglia: Suggests a hypertensive etiology.
  • Cerebral atrophy (cortical and subcortical).

The combination of leukoaraiosis and microbleeds is a poor prognostic factor for the occurrence of intracerebral hematomas in hypertensive patients.

Classification

Fazekas score (or Fazekas and Schmidt score): assesses periventricular lesions and deep white matter lesions

  • Periventricular hyperintensities, grade: 0= Absent
  • 1= Linear or capping hyperintensity
  • 2= Periventricular halo
  • 3= Irregular periventricular hyperintensities extending into the deep white matter
  • Deep white matter hyperintensities, grade: 0= Absent
  • 1= Punctate hyperintensities
  • 2= Beginning confluence of hyperintensities
  • 3= Large confluent hyperintensities

Fazekas Classification MRI

Wahlund grades of white matter and basal ganglia signal abnormalities related to age and vascular risk factors.

  • White matter lesions Grade 0: no signal abnormality
  • Grade 1: focal abnormalities (hyperintensity on FLAIR and T2)
  • Grade 2: beginning confluence
  • Grade 3: diffuse involvement
  • Basal ganglia lesions Grade 0: no signal abnormality
  • Grade 1: a single focal lesion > 5 mm
  • Grade 2: more than one focal lesion
  • Grade 3: confluent lesions

Differential diagnosis

  • CADASIL - Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leucoencephalopathy
  • Cerebral amyloid angiopathy: Cortico-subcortical microbleeds, cortical superficial siderosis, and convexity subarachnoid hemorrhage suggest cerebral amyloid angiopathy.
  • Ependymitis granularis: Juxtaventricular changes (< 3 mm from the ventricle) related to CSF leakage rather than microangiopathy.
  • Other: CNS vasculitis, post-radiation angiopathy, genetic disorders (Fabry disease, MELAS).
  • Non-vascular causes: Hyperintensities may also reflect an inflammatory condition such as multiple sclerosis or toxic leukoencephalopathy.