Corpus callosum size and diffusion tensor anisotropy in adolescents and adults with schizophrenia

Abstract

The corpus callosum has been implicated as a region of dysfunctional connectivity in schizophrenia, but the association between age and callosal pathology is unclear. Magnetic resonance imaging (MRI) and diffusion-tensor imaging (DTI) were performed on adults (n=34) and adolescents (n=17) with schizophrenia and adult (n=33) and adolescent (n=15) age- and sex-matched healthy controls. The corpus callosum was manually traced on each participant’s MRI, and the DTI scan was co-registered to the MRI. The corpus callosum was divided into five anteroposterior segments. Area and anisotropy were calculated for each segment. Both patient groups demonstrated reduced callosal anisotropy; however, the adolescents exhibited reductions mostly in anterior regions while the reductions were more prominent in posterior regions of the adults. The adolescent patients showed greater decreases in absolute area as compared with the adult patients, particularly in the anterior segments. However, the adults showed greater reductions when area was considered relative to whole brain white matter volume. Our results suggest that the initial stages of the illness are characterized by deficiencies in frontal connections, and the chronic phase is characterized by deficits in the posterior corpus callosum; or, alternatively, adolescent-onset schizophrenia may represent a different or more severe form of the illness.

Left-hemisphere lateralization for language and interhemispheric fiber tracking in patients with schizophrenia

“…This suggests that the global severity of illness and the severity of negative symptoms (NS) are associated with a disturbance of WM in the temporal interhemispheric tract. These results were in accordance with previous findings highlighting a negative correlation between FA values in the splenium or the temporal lobe WM and negative PANSS sub-scores (Mitelman et al, 2007;Michael et al, 2008;Balevich et al, 2015). The demonstrated impairment of WM tracts between the posterior temporal regions supports the idea that WM abnormalities are not only located in the tracts connecting the frontal regions as often reported (Wheeler and Voineskos, 2014) but also probably diffuse throughout the brain, particularly in patients with NS.…”

“…This abnormality was indicated by decreased FA and increased RD. In agreement with our findings, neuroimaging studies showed lower callosal integrity (through FA or RD) in either the whole CC (Miyata et al, 2010;Knochel et al, 2012;Freitag et al, 2013) or, more specifically, in the splenium region (Kyriakopoulos et al, 2008;Clemm von et al, 2014;Holleran et al, 2014;Balevich et al, 2015). These results were congruent with the investigated interhemispheric tract, since its projection, connecting homologue temporal cortical regions, crosses the splenium region.…”

Genetic Deletion of Akt3 Induces an Endophenotype Reminiscent of Psychiatric Manifestations in Mice

“…Based on these observations, it is believed that Akt3 could be an important regulator of postnatal brain development (Tschopp et al, 2005). Interestingly, mood disorders such as schizophrenia and major depression showed common and distinct patterns of volumetric alteration relative to healthy individuals in a number of brain areas (Wright et al, 2000; van Tol et al, 2010; Balevich et al, 2015; Wise et al, 2016). The possibility that the observed psychiatric-like behaviors may originate from the reduced brain volume induced by Akt3 deletion is interesting, but highly speculative.…”

WD40-repeat 47, a microtubule-associated protein, is essential for brain development and autophagy

“…The genetics of corpus callosum biology is, however, highly heterogeneous, and despite technological advances in next generation sequencing, 75% of callosal disorders have no identified genetic cause (11). Recent studies have suggested that a smaller corpus callosum is associated with a higher risk for autisms (12), bipolar disorder (13), and schizophrenia (14). Corpus callosum abnormalities are often seen in conjunction with other defects, such as smaller or larger brain size and malformations of cortical development (15).…”