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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 microbleeds

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 stricking widening of the perivascular spaces in deep grey nuclei representing état criblé.
  • SWI showed exclusively deep microhaemorrhages.

Treatment

  • Primary focus on hypertension management:
    • Strict blood pressure control (target <130/80 mmHg)
    • Lifestyle modifications (diet, exercise, smoking cessation)
  • Management of comorbidities:
    • Diabetes mellitus
    • Hyperlipidaemia
    • Chronic kidney disease
  • Antiplatelet therapy in selected cases:
    • Careful consideration due to increased risk of intracerebral haemorrhage
  • Cognitive rehabilitation and supportive care for patients with cognitive impairment
  • Regular follow-up and monitoring of disease progression with neuroimaging

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