A selective review of volumetric and morphometric imaging in schizophrenia.

Brain imaging studies have long supported that schizophrenia is a disorder of the brain, involving many discrete and widely spread regions. Generally, studies have shown decreases in cortical gray matter (GM) volume. Here, we selectively review recent papers studying GM volume changes in schizophrenia subjects, both first-episode (FE) and chronic, in an attempt to quantify and better understand differences between healthy and patient groups. We focused on the cortical GM of the prefrontal cortex, limbic and paralimbic structures, temporal lobe, and one subcortical structure (the caudate nucleus). We performed a search of the electronic journal database PsycINFO using the keywords "schizophrenia" and "MRI," and selected for papers published between 2001 and 2008. We then screened for only those studies utilizing manual or manually edited tracing methodologies for determining regions of interest (ROIs). Each region of interest was indexed independently; thus, one paper might yield results for numerous brain regions. Our review found that in almost all ROIs, cortical GM volume was decreased in the patient populations. The only exception was the caudate nucleus - most studies reviewed showed no change, while one study showed an increase in volume; this region, however, is particularly sensitive to medication effects. The reductions were seen in both FE and chronic schizophrenia. These results clearly support that schizophrenia is an anatomical disorder of the brain, and specifically that schizophrenia patients tend to have decreased cortical GM in regions involved in higher cognition and emotional processing. That these reductions were found in both FE and chronic subjects supports that brain abnormalities are present at the onset of illness, and are not simply a consequence of chronicity. Additional studies assessing morphometry at different phases of the illness, including prodromal stages, together with longitudinal studies will elucidate further the role of progression in this disorder.