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White matter hyperintensities: pearls and pitfalls in interpretation of MRI abnormalities.

To the Editor:

Atwood et al acknowledge that the pathophysiology of white matter hyperintensities (WMH) is uncertain and underscore the possibility of ischemic etiology, especially in the elderly.1 These authors regard WMH as an excellent marker of brain aging and emphasize their heritability in patients with negative correlation with cerebrovascular brain injury.

WMH are neither age-specific nor generally heritable, having been found in both sexes in hypertensive encephalopathy, puerperal eclampsia, migraine, and therapy with cyclosporin, interferon-α, and tacrolimus.2,3 Kruit and coworkers found WMH in MRI only in women migraine patients,2 which likely reflects an investigational artifact. Atwood et al did not exclude hypertensive and migraine patients from their analysis, which prominently confounds their interpretation of WMH as indicative of brain aging.

An important pathophysiological clue to the nature of WMH is offered by the characteristic difference in the distribution of infarcts and deep WMH in migraine patients. Predominantly posterior circulation territory (PCT) migrainous infarcts in contrast to anterior circulation infarcts in embolic or atherosclerotic thrombotic strokes in general are likely related to rheological factors. Anatomical vulnerability of the posterior cerebral artery renders it particularly susceptible to vasospastic influences in migraine patients.4 The rare occurrence of neuroanatomically nonlateralizing—in relation to headache or aura—PCT infarcts in younger migraine sufferers might represent an uncommon complication of an adaptive vasospasm that rarely reduces …