This article includes discussion of white matter abnormalities in the brain, leukoaraiosis, and unidentified bright objects (UBOs). The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
The occurrence of white matter abnormalities in the brains of both symptomatic and asymptomatic subjects has been a controversial entity for over a century. The development of magnetic resonance imaging has led to more sensitive detection of these lesions, perhaps even more sensitive than autopsy inspection. Clinical studies have determined associations with cognitive decline and gait impairment, and perhaps increased relative risk for cerebrovascular disease. An animal model of white matter disease and brain atrophy related to diabetes has been established and may assist in the understanding of the pathophysiology of white matter abnormalities. Further clinical and scientific studies will help us understand the importance of white matter abnormalities in the human brain.
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; Blass et al 1991). Although autopsy demonstrated white matter atrophy, Binswanger did not seem to place much significance on this finding (Schneider and Wieczorek 1991). 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 (Alzheimer 1902; Schorer 1992). 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 (Olszewski 1962).
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 (Bradley et al 1984; Gerard and Weisberg 1986). Today it not yet clear that those asymptomatic patients with imaging-identified white matter abnormalities are at risk for later cognitive changes. However, recognition of these imaging abnormalities may be important in particular patient groups.
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