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Injury to the subcortical white matter of the brain occurs in a variety of neurologic diseases and is typically characterized by increased signal on T2-weighted MRI sequences. In the setting of cerebrovascular disease, accumulation of so-called white matter hyperintensities (WMH) is associated with cognitive decline.1 This type of WMH burden may derive in part from discrete ischemic events such as lacunar strokes or microemboli. However, it can also have a more insidious, covert progression that may not respond to traditional stroke prevention strategies. While the pathophysiology of progressive WMH is not fully understood, it is hypothesized to result from intermittent hypoxia due to poor vasoreactivity in the setting of blood pressure fluctuations.2 In patients with sickle cell disease (SCD), a similar phenotype can occur in a much younger population than those at risk for cerebrovascular disease. In this case, the hypoxia is attributed to the decreased oxygen-carrying capacity of abnormal erythrocytes.
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