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  • Updated 03.04.2021
  • Released 02.18.2005
  • Expires For CME 03.04.2024

White matter abnormalities in the brain



The occurrence of white matter abnormalities in the brains of both symptomatic and asymptomatic individuals has been a source of interest for over a century. The development of magnetic resonance imaging has led to more sensitive detection of these lesions, even more sensitive than autopsy inspection. Clinical studies have determined associations with cognitive decline, gait impairment, and increased relative risk for cerebrovascular disease. White matter disease is a heterogeneous disorder with mechanisms varying among those with cerebrovascular disease (eg, chronic hypertension vs. CADASIL) and those with demyelinating disorders. This chapter will focus on cerebrovascular disease primarily.

Key points

• White matter disease is present in at least 10% of individuals older than 65 years of age.

• White matter disease correlates with an increased risk of cognitive impairment.

• The cause of white matter disease is not fully understood and has heterogeneous mechanisms.

Historical note and terminology

The introduction of CT in the 1970s followed by the subsequent introduction of MRI for imaging of the brain led to the discovery of largely unexpected changes within the cerebral white matter for both asymptomatic and cognitively impaired individuals. Since that time, the pathogenesis, clinical significance, and pathological correlate of these white matter abnormalities has not been well understood. These changes have been described using numerous terms including white matter abnormalities, cerebral white matter changes, unidentified bright objects (UBOs), or leukoaraiosis—used to refer to all white matter changes visible on neuroimaging studies.

In 1894, Binswanger described the case of a male with syphilis who suffered from a progressive decline in mental functioning, including speech and memory disorders, depression, and personality changes, along with lower extremity weakness and upper extremity tremor (Binswanger 1894; 15). Although autopsy demonstrated white matter atrophy, Binswanger did not seem to place much significance on this finding (165). Then, in 1902, Alzheimer described an analogous case in which he attributed the white matter changes to be due to arteriosclerosis of the long penetrating vessels (03; 166). It was not until 1962 that Olszewski diagnosed Binswanger's earlier case as syphilis, and he proposed the term “subcortical arteriosclerotic encephalopathy” to describe cerebral arteriosclerosis with predominant pathology affecting vessels of the white matter and subcortical grey matter (144).

Although the introduction of modern imaging led to pre-mortem diagnosis of Binswanger disease, it later became obvious that such imaging-detected alterations could occur in both symptomatic and asymptomatic subjects (22; 68). White matter disease is now considered a contributor to cognitive decline (187).

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