Abstract
each MRSI voxel was also analyzed for amounts of gray matter, white matter, hyperintense white matter, and CSF using in-house software (SICORE) in order to obtain tissue volume corrected NAA concentration estimates. Repeated measures ANOVA revealed that compared to the control group, the patients with bipolar I disorder demonstrated: 1) decreased DLPFC NAA bilaterally (p 5 0.0004), 2) decreased prefrontal white matter NAA bilaterally (p 5 0.0014), 3) increased thalamic NAA bilaterally (p 5 0.01), and 4) no significant group or lateralized differences in voxel tissue composition for any of the regions studied. Thus, the NAA alterations in the bipolar group were not due to any differences in voxel tissue heterogeneity between groups. The DLFPC reduction in NAA suggests neuronal loss/dysfunction whereas the observed prefrontal white matter NAA reduction is evidence for compromised axonal integrity that may result in functional disconnection of prefrontal-thalamic pathways. Increased thalamic NAA may represent neuronal hypertrophy, neuronal hyperplasia, or abnormal synaptic/dendritic pruning. The results definitely suggest that neuronal/axonal integrity of DLFPC-thalamic pathways is abnormal in bipolar I disorder.
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