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Hypertensive Microangiopathy

Summary

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  • Chronic hypertension-induced damage to small blood vessels in the brain
  • Characterised by arteriolar wall thickening, luminal narrowing, and white matter changes
  • Imaging findings include white matter hyperintensities, lacunar infarcts, and microbleeds1

Pathophysiology

  • Sustained hypertension leads to:
    • Arteriolar wall thickening and remodelling
    • Endothelial dysfunction and blood-brain barrier disruption
    • Impaired cerebral autoregulation
  • Consequences include:
    • Chronic hypoperfusion of deep white matter
    • Ischaemic damage to small penetrating arteries
    • Increased risk of lacunar infarcts and microbleeds

Demographics

  • Prevalence increases with age and duration of hypertension
  • More common in:
    • Elderly population (>65 years)
    • Individuals with poorly controlled hypertension
    • Patients with diabetes mellitus or chronic kidney disease

Diagnosis

  • Clinical presentation:
    • Often asymptomatic in early stages
    • Cognitive decline, gait disturbances, and mood changes in advanced cases
  • Neurological examination may reveal:
    • Subtle cognitive deficits
    • Mild parkinsonian features
    • Pseudobulbar palsy in severe cases
  • Neuropsychological testing can detect early cognitive impairment

Imaging

  • MRI is the modality of choice:
    • T2-weighted and FLAIR sequences:
    • Periventricular and deep white matter hyperintensities
    • Lacunar infarcts in basal ganglia, thalamus, and pons
    • Gradient-echo or susceptibility-weighted imaging:
    • Microbleeds, typically in basal ganglia and thalamus
    • Diffusion tensor imaging:
    • Reduced fractional anisotropy in affected white matter
  • CT may show:
    • Hypodense areas in white matter
    • Lacunar infarcts
    • Limited sensitivity for microbleeds

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  • A 60-year-old patient with chronic kidney disease and poorly controlled hypertension presented after a TIA.
  • MRI showed hyperintensity of the deep grey nuclei and deep subcortical white matter, consistent with severe small vessel disease.
  • The pattern of microhaemorrhages, exclusively involving the deep white matter and pons, are consistent with hypertensive microangiopathy.

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  • A 50-year-old patient with poorly controlled hypertension had an MRI for headache.
  • T2-weighted imaging showed striking widening of the perivascular spaces in deep grey nuclei representing état criblé.
  • SWI showed exclusively deep microhaemorrhages.

Treatment

  • Blood-pressure control. The deep (basal ganglia, thalamus, pons) distribution of microbleeds distinguishes it from the lobar pattern of amyloid angiopathy

Differential diagnosis

Differential Diagnosis Differentiating Feature
Cerebral Amyloid Angiopathy Lobar and cortical-subcortical microbleeds on GRE/SWI; posterior predominance; superficial siderosis
Multiple Sclerosis Ovoid periventricular lesions; calloso-septal interface ("Dawson's fingers"); no deep microbleeds
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) Anterior temporal pole and external capsule FLAIR hyperintensity; subcortical lacunar infarcts; microbleeds
Vasculitis Beaded appearance of vessels on angiography; vessel wall enhancement on high-resolution MRI; multifocal cortical and subcortical infarcts

  1. Wardlaw et al. Small vessel disease: mechanisms and clinical implications. 2019. The Lancet. Neurology - Open in new tab. ↩