LAUSR

We read the article by Phyu et al.1 that confirmed increased perfusion in the brain of patients with Fabry disease (FD), essentially involving white matter (WM), mainly at the splenium of the corpus callosum (SCC), correlating with WM hyperintensity (WMH) load. The authors hypothesized a causal role of hyperperfusion in determining WM damage, supporting a causative chain linking hyperperfusion, increased interstitial pressure, and demyelination, resulting in WMH.1 However, this chain of events does not completely fit with the currently available diffusion tensor imaging data in FD that indicate that microstructural alterations do not correlate with WMH load,2–4 and are lacking in the structure with the highest hyperperfusion (i.e., the SCC).