Info

Figure 3.4 Meta-analysis of absolute regional brain volumes in schizophrenic patients and controls, from a total of 58 studies. This figure shows how the mean volumes of different brain regions from people with schizophrenia differ from those of controls. Figure reproduced with permission from Wright IC, Rabe-Hesketh S, Woodruff PW, et al. Meta-analysis of regional brain volumes in schizophrenia. Am J Psychiatry 2000;157:16-25

Figure 3.5 Some structural brain abnormalities possibly implicated in the pathogenesis of schizophrenia. Structural abnormalities have been described in many brain areas, and at a variety of anatomical levels, from gross macroscopic changes in whole brain volume, through to subtle cellular displacement or disorganization in the cortex. Increasingly, interest has focused on the distribution of abnormalities, and their structural connectivity: thus, white matter myelination, as well as cortical abnormalities, are targets of investigation

Figure 3.5 Some structural brain abnormalities possibly implicated in the pathogenesis of schizophrenia. Structural abnormalities have been described in many brain areas, and at a variety of anatomical levels, from gross macroscopic changes in whole brain volume, through to subtle cellular displacement or disorganization in the cortex. Increasingly, interest has focused on the distribution of abnormalities, and their structural connectivity: thus, white matter myelination, as well as cortical abnormalities, are targets of investigation hamartomas and arteriovenous malformations occur with increased frequency in schizophrenia.

At the cellular level, various abnormalities in cytoarchitecture have been reported in several brain regions, although not all of these findings have proved robust. However, evidence of neuronal displacement (Figure 3.7) suggests the possibility of some failure in neuronal migration, a process that occurs mainly during the second trimester of fetal development4.

Several findings weigh against the most likely alternative of a neurodegenerative process. The balance of evidence is that most of the brain abnormalities seen in schizophrenia are present at first onset and are non-progressive. Furthermore, markers of neurodegeneration, such as proteins associated with glial response are largely absent, although there may be a small degree of periventricular gliosis. Extracerebral markers of abnormal fetal development provide indirect support for the idea that aberrant neurodevelopment is implicated in schizophrenia. Dermato-glyphic abnormalities are thought to reflect fetal maldevelopment and appear to be more common in schizophrenia (Figure 3.8). Minor physical anomalies also occur with greater frequency in

Figure 3.6 Agenesis of the corpus callosum. This midline sagittal magnetic resonance image shows an absent corpus callosum, a dramatic example of a neurodevelopmental anomaly which, while extremely rare, is thought to have an increased incidence in people with schizophrenia

Figure 3.7 These camera lucida drawings compare the distribution of nicotinamide-adenine dinucleotide phosphate-diaphorase-stained neurons (squares) in sections through the superior frontal gyrus of a control and schizophrenic brain. There is a significant shift in the direction of the white matter in the schizophrenic brain. Numbers 1 through 8 indicate compartments of the brain; Roman numerals indicate cortical layers. Figure reproduced with permission from Akbarian S, Bunney WE, Jr, Potkin SG, et al. Altered distribution of nicotinamide-adenine dinucleotide phosphate-diaphorase cells in frontal lobe of schizophrenics implies disturbances of cortical development. Arch Gen Psychiatry 1993:50:169-77

schizophrenic patients compared with normal controls.

Was this article helpful?

0 0

Post a comment