Age and diffusion tensor anisotropy in adolescent and adult patients with schizophrenia

Abstract

Findings of white matter pathology as indicated by diffusion tensor anisotropy values in schizophrenia are well established, but the differences in this measure between the onset of the disease and the chronic state are not well known. To investigate the differences between these states in the progression of the disease of schizophrenia we acquired 1.5 T diffusion tensor anisotropy images on 35 adult patients with schizophrenia and schizoaffective disorder, 23 adolescents having their first psychotic episode, and age and sex matched controls (33 adults and 15 adolescents). Regions of interest in major cortical white matter tracts chosen as salient to the prefrontal executive deficit in schizophrenia were assessed using stereotaxic coordinates from the Talairach and Tournoux atlas. Regions of each tract along anterior-posterior and/or inferior-superior directions in both hemispheres were evaluated in multiway ANOVA. Tracts between the frontal lobe and other brain regions, but not temporal, occipital and interhemispheric tracts, showed a differential aging pattern in normals and patients indicating that the white matter pathology in these regions is not stable between the onset and the chronic state in schizophrenia. This suggests that tracts involved in the connectivity of the temporal lobe white matter deficits were already well in place in adolescent patients, while frontal lobe pathology continues to develop from adolescence to adulthood.

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

“…Adolescent ( n =17) and adult schizophrenia patients ( n =34) and age- and sex-matched healthy controls ( n =15 and n =33, respectively) were recruited as described elsewhere (Schneiderman et al, 2009; see Table-1 for demographic information). Only those adolescents who ultimately received a diagnosis of schizophrenia were included in the current study.…”

“…Studying antipsychotic drug-naïve adolescent patients affords the opportunity to examine potential neurological abnormalities in this patient population without the influence of prolonged exposure to antipsychotic medication and/or hospitalization. To date, only one study has examined corpus callosum abnormalities in antipsychotic drug-naïve adolescent patients using stereotaxically-located regions of interest and reported no differences in anisotropy (Schneiderman et al, 2009). The current study improves on this research by using manually-traced regions-of-interest (the gold standard) and examining the corpus callosum in its near entirety.…”

“…White matter anisotropy data from the participants were described in earlier reports which utilized investigatory methods of stereotaxically-located regions of interest to examine normal aging effects (Schneiderman et al, 2007) and aging effects in the patient groups (Schneiderman et al, 2009). Volume of cortical and subcortical structures and cortical and corpus callosum anisotropy in the adult patients and adult healthy controls have also been previously published by our group (Mitelman et al, 2005a; Mitelman et al, 2005b; Mitelman et al, 2005c; Mitelman et al, 2006; Mitelman et al, 2009; Mitelman et al, 2005d).…”

Diffusion Imaging of White Matter in Schizophrenia: Progress and Future Directions

“…Some cross-sectional studies have found that WM deficits in chronic patients were either absent or less severe than in FE patients (25, 33, 34), and a meta-analysis of FE and multi-episode studies showed that longer duration of illness was associated with more severe WM abnormalities (35). Similarly, research comparing patients with either adolescent or adult onset psychosis has shown that age of onset may impact the degree of WM impairment (36–38). …”

White matter development in the early stages of psychosis

“…Furthermore, genetic analyses in COS patients have shown that carriers of a neuregulin-1 risk allele had a steeper rate of decline in WM volume during adolescence, compared to patients without the risk allele (Addington et al, 2007). Studies comparing adolescent and chronic patients identified effects of age of onset, and suggest that prefrontal FA deficits develop when illness onset occurs at a later age (Kyriakopoulos et al, 2009; Schneiderman et al, 2009). …”