Additional Evidence for White Matter Damage in Never-Medicated Adults with Schizophrenia and Schizophreniform Disorder (P02.034)

Abstract

Objective: This study investigates the intrinsic structural abnormalities of brain white matter (WM) in never-medicated adult patients with schizophrenia (SZ) and schizophreniform disorder (SZD). Background Some imaging studies suggested structural WM abnormalities in SZ patients compared with healthy controls (HC). However, the findings are not consistent among studies, probably due to the effect of antipsychotic treatment of the patients enrolled. Furthermore, previous studies did not involve SZD patients, who represent patients at high risk for developing SZ. Design/Methods: Eighteen never-medicated SZ patients, 25 never-medicated SZD patients, and 17 age-matched HC were studied. All participants underwent diffusion tensor (DT) MRI scans. Tract-based spatial statistics was used to compare mean diffusivity (MD) and fractional anisotropy (FA) between groups. Results: Compared with HC, SZ patients showed a decreased MD in the brainstem, internal capsule, genu of the corpus callosum, and main long-associative WM tracts, with a right-side predominance, and an increased FA in the right superior longitudinal fasciculus. Compared with HC, SZD patients showed a decreased MD and an increased FA in the brainstem, bilaterally. Compared with SZD, SZ patients showed a decreased MD and an increased FA in the main long-associative WM tracts and genu of corpus callosum, bilaterally. In all patients, decreased MD and increased FA in the brainstem and main long-associative WM tracts bilaterally were significantly related with a longer time period without medication. Conclusions: Never-medicated SZ and SZD patients present with a similar pattern of DT MRI alterations in the brainstem structures. Furthermore, SZ patients showed additional abnormalities of the main long-associative WM tracts and corpus callosum. This study increases our knowledge on the neural networks involved in the pathophysiology of SZ and may provide information on the critical window of time before treatment initiation. Disclosure: Dr. Canu has nothing to disclose. Dr. Gasparotti has nothing to disclose. Dr. Agosta received personal compensation for activities with Bayer-Schering AG as a speaker. Dr. Valsecchi has nothing to disclose. Dr. Pagani has nothing to disclose. Dr. Comi has received personal compensation for activities with Novartis, Teva Neuroscience, Sanofi-Aventis Pharmaceuticals, Inc., Merck Serono, Bayer Schering, and Biogen Dompe. Dr. Sacchetti has nothing to disclose. Dr. Filippi has received personal compensation for activities with ECTRIMS, MSIF, MS Ireland, US NMSS, Bayer-Schering, Biogen-Dompe AG, Genmab, Merck Serono, Pepgen Corporation, Teva, and Sanofi-Aventis. Dr. Filippi has received research support from Teva, Bayer-Schering and Genmab.