Imaging in schizophrenia

INTRODUCTION In the past, evidence was lacking to show that schizophrenia is a brain disease. This notion was mainly based on finding no or little abnormalities in postmortem brains of patients with schizophrenia. (1) This resulted in searching for other supposed causes like failing family interactions. In the 60s and 70s, clinical investigators concluded that faulty interactions between the family members, particularly between mother and child, could cause or worsen schizophrenia. (2) For years, parents had to carry the burden of guilt, as they were to blame for their children’s illness. Through new in vivo neuroimaging techniques, such as computer tomography (CT), enlarged ventricles were found to be present in schizophrenia. (3) This finding consequently offered a new impulse to further explore the neurobiological causes of schizophrenia. Over the years and through technical progress, it was possible to study the brain more extensively in vivo. The use of magnetic resonance imaging (MRI) allowed for the quantification of gray and white matter and for measurement of discrete, cortical and subcortical structures (Figure 10.1). In a meta-analysis of Wright et al., (4) it was convincingly shown that brain-volume abnormalities are present in schizophrenia. The volume of the body of the lateral ventricle was found to be increased (16%) while cerebral volume was reduced (2%). The latter was primarily attributed to a decrease in gray matter volume (2%). Nevertheless, a small but significant reduction was found in white matter (1%) (see also Table 10.1). The improved quality of the MRI scans made it also possible to manually delineate brain areas of interest. Regional pathology indicates larger reductions in temporal and frontal lobe (5) and more specifically in medial temporal structures (hippocampus and amygdale) (6, 7).