White Matter Metabolite Relaxation and Diffusion Abnormalities in First-Episode Psychosis: A Longitudinal Study

Microstructural abnormalities in the white matter (WM) are implicated in the pathophysiology of psychosis. In vivo magnetic resonance spectroscopy (MRS) can probe the brain's intracellular microenvironment through the measurement of transverse relaxation and diffusion of neurometabolites and possibly provide cell-specific information. In our previous studies, we observed differential metabolite signal abnormalities in first episode and chronic stages of psychosis. In the present work, longitudinal data were presented for the first time on white matter cell-type specific abnormalities using a combination of diffusion tensor spectroscopy (DTS), T2 MRS, and diffusion tensor imaging (DTI) from a group of 25 first episode psychosis patients and nine matched controls scanned at baseline and one and two years of follow-up. We observed significantly reduced choline ADC in the year 1 of follow-up (0.194 mu m(2)/ms) compared to baseline (0.229 mu m(2)/ms), followed by a significant increase in NAA ADC in the year 2 follow-up (0.258 mu m(2)/ms) from baseline (0.222 mu m(2)/ms) and year 1 follow-up (0.217 mu m(2)/ms). In contrast, NAA T2 relaxation, reflecting a related but different aspect of microenvironment from diffusion, was reduced at year 1 follow-up (257 ms) compared to baseline (278 ms). These abnormalities were observed in the absence of any abnormalities in water relaxation and diffusion at any timepoint. These findings indicate that abnormalities are seen in in glial-enriched (choline) signals in early stages of psychosis, followed by the subsequent emergence of neuronal-enriched (NAA) diffusion abnormalities, all in the absence of nonspecific water signal abnormalities.

Automated summary

This study used various imaging techniques to observe abnormalities in metabolite signals in white matter cells during the early and chronic stages of psychosis. These abnormalities suggest specific changes in the pathophysiology of psychosis.