Binswanger’s disease

Created 18/02/2022, last revision 07/11/2023

Binswanger’s disease is a progressive neurological disorder characterized by ischemic involvement of 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 in individuals with long-term and poorly corrected 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

Etiology

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)

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typical clinical presentation and imaging findings +vascular risk factors (especially hypertension)

CT: symmetrical hypodensities in deep white matter + lacunar infarcts + atrophy
MRI (FLAIR, T2): extensive periventricular and subcortical white matter lesions + subcortical lacunar infarcts + atrophy
- lesions are more pronounced on MRI compared to CT
- scales to assess the extent of the white matter lesions on MRI:
  - FAZEKAS
  - ARWMC

CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy)
- typical lesions in the external capsule and pole of the temporal lobe
- more pronounced low signal intensities of the basal ganglia and dentate nuclei
normal pressure hydrocephalus (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 follows 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)

the disease is irreversible; therapy may slow down or halt its progression
antiplatelet or anticoagulant therapy may be considered to reduce the risk of thromboembolic events
aggressive treatment of arterial hypertension
aggressive treatment of other vascular risk factors (e.g., diabetes, hyperlipidemia, etc.)

symptomatic psychiatric therapy
- antidepressants
- anxiolytic drugs
- hypnotic drugs
cognitive enhancers – cholinergic deficiency is assumed in VaD (vascular dementia)
- studies have shown some effects of both donepezil and rivastigmine Black, 2003][Birks, 2013]
physical and occupational therapy
- to maintain mobility and reduce the risk of falls
- to help patients adapt to physical limitations and maintain independence for as long as possible