In the study in which WE was induced by thiamine deficiency, animals were imaged at baseline, presymptomatic stage (day 10), symptomatic stage (days 12 and 14), and after recovery on days 31 and 87. A decrease in FA in the inferior colliculi was first noted on day 10 but showed recovery on day 87. On the other hand, the FA decrease in the thalamus first noted on day 12 persisted through day 87 (Dror et al. 2010). This model was also used in a pharmacological DTI study in which animals were exposed to rasagiline, a selective monamine oxidase B inhibitor, as a potential protective agent against thiamine-deficiency–induced brain damage (Dror et al. 2014). In addition to reducing ventricular enlargement, rasagiline appeared to ameliorate the effects of thiamine deficiency on the FA decrease in the thalamus (Dror et al. 2014). Histopathology showed that treatment with rasagiline reduced the lesions in thalamus and colliculi observed in the thiamine-deficient brain (Eliash et al. 2009). Rasagiline has not been evaluated in human patients with WE.
