SA66. A Combined 7T Stroop fMRI and MRS Study in First-Episode Schizophrenia

Abstract

Background: Patients with schizophrenia (SZ) consistently perform worse than healthy controls (HC) on cognitive control tasks, and it is thought that this represents a core deficit that may underlie other cognitive symptoms. Previous functional magnetic resonance imaging studies (fMRI) studies have linked this deficit to abnormal activation in the dorsal anterior cingulate cortex (dACC) and the dorsal lateral prefrontal cortex (DLPFC), key regions within the executive network. Moreover, multimodal neuroimaging studies have linked cortical neural activity to concentrations of certain neurochemicals involved in the inhibition/excitation balance—namely, GABA, glutamate (Glu), and glutamine (Gln). The present study compared activation within the executive network during a cognitive control task to dACC resting state concentrations of these neurochemicals. It was predicted that an aberrant relationship would be found in SZ. Our experiment used 7T fMRI and proton magnetic resonance spectroscopy (H-MRS) for data acquisition, and this has certain advantages over lower field strengths including the ability to obtain separate concentrations for Glu and Gln as opposed to a combined estimate (Glx), the determination of GABA concentrations without the use of extensive editing techniques, and a higher BOLD signal-to-noise ratio. Methods: Data from 21 minimally treated first-episode SZ and 21 HC matched for age, gender, and family socioeconomic status were recruited. Subjects completed a Stroop color-naming task in a 7T fMRI scanner. For each individual, the BOLD response to incongruent trials relative to congruent trials was calculated in 3 anatomically defined regions of interest within the executive network: the left and right DLPFC and the dACC. Resting-state neurochemical levels were obtained from the bilateral dACC using 7T H-MRS with an ultra-short echo time (5 ms) STEAM sequence, and referenced to water. Results: The dACC concentrations of both Glu and N-acetylaspartate (NAA) were significantly lower in SZ than HC, Glu: t(40) = 2.3, P < .05, NAA: t(40)= 2.5, P < .05. GABA and Gln concentrations were not different between the groups, but HC Gln concentrations were negatively correlated with dACC BOLD activation, r(20) = −.524, P < .05, a pattern not seen in SZ. Additionally, while HC only displayed a trend-level negative correlation between glutamine and right DLPFC activation, this relationship was significant in SZ, r(16) = −.611, P < .01. An additional analysis revealed that HC choline concentrations positively correlated with activation in the dACC, r(20) = .482, P < .05. This trend was apparent but not significant in SZ. Conclusion: An aberrant relationship between the executive network and dACC concentrations of neurochemicals involved in the inhibition/excitation balance, particularly Gln, may underlie cognitive control deficits in SZ. Additional 7T multimodal neuroimaging studies may have further elucidated these interactions.