Binswanger’s disease

David Goldemund M.D.
Updated on 08/03/2024, published on 18/02/2022

  • Binswanger’s disease is a progressive neurological disorder characterized by ischemic damage to the white matter and deep brain structures (basal ganglia and thalamus)
  • usually can be seen in individuals over 50 years of age and is caused by small vessel disease and branch artery atherosclerosis
    • typically observed in individuals with long-term and poorly controlled hypertension and other vascular risk factors
  • clinically characterized by a progressive motor impairment and vascular cognitive deficit (VCI)
  • synonyms used in the literature:
    • Binswanger’s encephalopathy
    • subcortical leukoencephalopathy
    • multi-infarct or vascular dementia of the Binswanger type
    • subcortical ischemic vascular disease
    • subcortical arteriosclerotic encephalopathy (SAE)
    • small vessel dementia


  • arteriolopathy, atherosclerosis, thromboembolism
    • mostly small penetrating artery disease
  • lesions are relatively symmetrical and diffuse – deep periventricular white matter lesions + lacunar infarcts in basal ganglia, thalamus, and brainstem (pons)

Clinical presentation

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Diagnostic evaluation

Imaging methods

  • CT:  symmetrical hypodensities in the deep white matter + lacunar infarcts + brain atrophy
  • MRI (FLAIR, T2): extensive periventricular and subcortical white matter lesions + subcortical lacunar infarcts + brain atrophy
    • lesions are better visualized on MRI compared to CT
    • scales have been developed to assess the extent of white matter lesions on MRI:
Binswanger's disease

Binswanger´s disease (FLAIR, coronary plane)

Extensive leukoencephalopathy in Binswanger´s disease (FLAIR)
Binswanger´s disease (CT and FLAIR)

Differential diagnosis

  • CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy)
    • typical lesions in the external capsule and pole of the temporal lobe   CADASIL with typical temporal pole involvement CADASIL with typical external capsule involvement
    • more pronounced low signal intensity in the basal ganglia and dentate nuclei
  • normal pressure hydrocephalus (NPH)   MRI findings in NPH
    • triad of symptoms: gait disturbance, sphincter insufficiency, and cognitive deterioration (similar to Binswanger’s disease)
    • a rather fluent, gradual progression (whereas Binswanger’s disease usually has a stepwise course)
    • ventricular dilatation in NPH x convexal atrophy in Binswanger’s disease
  • CNS vasculitis
  • Alzheimer’s disease (AD)
  • Dementia with Lewy bodies (DLB)
  • Frontotemporal dementia (FTD)


Prevention of cerebrovascular disease

Symptomatic therapy

  • symptomatic psychiatric therapy
    • antidepressants
      • high prevalence of depression in individuals with Binswanger’s disease
      • selective serotonin reuptake inhibitors (SSRIs) are preferred
    • anxiolytic drugs
      • choose medications that have minimal sedative effects to avoid exacerbating cognitive impairment
    • hypnotic drugs
  • cognitive enhancers – cholinergic deficiency is assumed in VaD (vascular dementia)
    • studies have shown some effects of both donepezil and rivastigmine (acetylcholinesterase inhibitors) Black, 2003][Birks, 2013]
  • physical and occupational therapy aims to:
    • maintain mobility and reduce the risk of falls
    • help patients adapt to physical limitations and learn techniques to maintain independence in daily activities for as long as possible

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Binswanger's disease