The deficit syndrome in schizophrenia: Associations with hippocampal volume and prefrontal cortical thickness

Background: The deficit syndrome is a subtype of schizophrenia characterized by primary and enduring negative symptoms. Frontal and temporal structural alterations have been associated with this clinical phenotype. The purpose of this study was to test whether a neuroimaging phenotype (e.g. hippocampal volume and prefrontal cortical thickness) could discriminate between the deficit and non-deficit subtype in schizophrenia. Methods: MRI scans were obtained in 89 patients and 87 controls. Hippocampal volume and prefrontal cortical thickness was measured using Freesurfer. The following regions of interest were used: the inferior frontal gyrus (pars triangularis, pars orbitalis and pars opercularis), the frontal pole and the hippocampus. The Schedule for the Deficit Syndrome was used to make deficit versus non-deficit diagnoses, resulting in 25 patients being diagnosed with the deficit syndrome and 64 patients diagnosed as non-deficit. Regression analyses were used to examine associations between region of interest (dependent variable) and the deficit syndrome (independent variable) controlling for age, gender and educational level. Results: A dose-response relationship, indicating the lowest cortical thickness values for the deficit group, intermediate cortical thickness values for the non-deficit schizophrenia group, and the highest cortical thickness values for the control group, was found for the following regions: the left pars triangularis (deficit vs. controls: β = − 0.42 P = 0.00; non-deficit vs. controls: β = − 0.61 P = 0.00; deficit vs. non-deficit: β = − 0.88 P = 0.00), the right pars triangularis (deficit vs. controls: β = − 0.43 P = 0.00; non-deficit vs. controls: β = − 0.76 P = 0.00; deficit vs. non-deficit: β = − 1.05 P = 0.00), the left frontal pole (deficit vs. controls: β = − 0.19 P = 0.00; non-deficit vs. controls: β = − 0.11 P = 0.00; deficit vs. non-deficit: β = − 0.22 P = 0.00) and the right frontal pole (deficit vs. controls: β = − 0.13 P = 0.00; non-deficit vs. controls: β = − 0.09 P = 0.00; deficit vs. non-deficit: β = − 0.17 P = 0.00). In addition, deficit patients were significantly different from non-deficit patients and controls with respect to the following brain regions: the cortical thickness of the right pars orbitalis (deficit vs. controls: β = − 0.08 P = 0.05; non-deficit vs. controls: β = − 0.03 P = 0.23; deficit vs. non-deficit: β = − 0.08 P = 0.01), left hippocampal volume (deficit vs. controls: β = − 240.08 P = 0.01; non-deficit vs. controls: β = − 25.11 P = 0.69; deficit vs. non-deficit: β = − 152.56 P = 0.02) and right hippocampal volume (deficit vs. controls: β = − 247.77 P = 0.01; non-deficit vs. controls: β = − 34.35 P = 0.60; deficit vs. non-deficit: β = − 166.59 P = 0.01).Discussion: The data suggests that the deficit syndrome in schizophrenia might be related to underlying prefrontal and hippocampal pathology. The hippocampus is highly interconnected with the prefrontal cortex.