Superior temporal gyrus volume in antipsychotic-naive people at risk of psychosis
Morphological abnormalities of the superior temporal gyrus have been consistently reported in schizophrenia, but the timing of their occurrence remains unclear.
To determine whether individuals exhibit superior temporal gyral changes before the onset of psychosis.
We used magnetic resonance imaging to examine grey matter volumes of the superior temporal gyrus and its subregions (planum polare, Heschl's gyrus, planum temporale, and rostral and caudal regions) in 97 antipsychotic-naive individuals at ultra-high risk of psychosis, of whom 31 subsequently developed psychosis and 66 did not, and 42 controls.
Those at risk of psychosis had significantly smaller superior temporal gyri at baseline compared with controls bilaterally, without any prominent subregional effect; however, there was no difference between those who did and did not subsequently develop psychosis.
Our findings indicate that grey matter reductions of the superior temporal gyrus are present before psychosis onset, and are not due to medication, but these baseline changes are not predictive of transition to psychosis.
Available from: Paolo Fusar-Poli
- "Research in younger relatives has also highlighted the superior temporal gyrus as an important region with reduced volume of both the right and left superior temporal gyrus on ROI tracing (Rajarethinam et al., 2004). Findings consistent with this have also been demonstrated in those at high clinical risk for developing schizophrenia (Crossley et al., 2009; Fusar-Poli et al., 2011b), including abnormalities in the planum temporale (Takahashi et al., 2010). Subjects with an established diagnosis of schizophrenia have also shown functional and structural abnormalities in this region, suggesting this area is important in those who are considered to be at familial high risk, those considered to be at clinical high risk and those with schizophrenia (Gur et al., 2007; Crossley et al., 2009; Nejad et al., 2011). "
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ABSTRACT: Computational brain-imaging studies of individuals at familial high risk for psychosis have provided interesting results, but interpreting these findings can be a challenge due to a number of factors. We searched the literature for studies reporting whole brain voxel-based morphometry (VBM) or functional magnetic resonance imaging (fMRI) findings in people at familial high risk for schizophrenia compared with a control group. A voxel-wise meta-analysis with the effect-size version of Signed Differential Mapping (ES-SDM) identified regional abnormalities of functional brain response. Similarly, an ES-SDM meta-analysis was conducted on VBM studies. A multi-modal imaging meta-analysis was used to highlight brain regions with both structural and functional abnormalities. Nineteen studies met the inclusion criteria, in which a total of 815 familial high-risk individuals were compared to 685 controls. Our fMRI results revealed a number of regions of altered activation. VBM findings demonstrated both increases and decreases in grey matter density of relatives in a variety of brain regions. The multimodal analysis revealed relatives had decreased grey matter with hyper-activation in the left inferior frontal gyrus/amygdala, and decreased grey matter with hypo-activation in the thalamus. We found several regions of altered activation or structure in familial high-risk individuals. Reliable fMRI findings in the right posterior superior temporal gyrus further confirm that alteration in this area is a potential marker of risk.
Available from: Benjamin K Brent
- "Cross-sectional Smaller hippocampal volume bilaterally in CHR Larger L hippocampal volume in CHR-t vs CHR-n, but no differences compared with controls Pantelis et al, 76 2003 Longitudinal Smaller GM in R medial temporal, lateral temporal, and inferior frontal and bilateral cingulate cortices at baseline CHR-t showed reduced GM in L parahippocampal, fusiform, orbitofrontal, and cerebellar cortices and cingulate gyri over time CHR-n showed reduced cerebellar GM Yucel et al, 90 2003 Cross-sectional Interrupted L anterior cingulate sulcus in CHR vs controls, but no differences between CHR-t and CHR-n Garner et al, 105 2005 Cross-sectional Larger baseline pituitary volume in CHR-t vs CHR-n Wood et al, 87 2005 Cross-sectional Smaller hippocampal volume and less L anterior cingulate folding in CHR with GHR vs CHR without GHR Velakoulis et al, 100 2006 Cross-sectional Normal baseline hippocampal and amygdala volume in CHR Smaller whole-brain volumes in CHR vs controls Fornito et al, 89 2008 Longitudinal Bilateral thinning of anterior cingulate in CHR-t also associated with negative symptoms Baseline anterior cingulate differences in CHR-t vs CHR-n predicted time to psychosis onset Takahashi et al, 99 2008 Cross-sectional No increased prevalence of cavum septi pellucidi enlargement in CHR Walterfang et al, 108 2008 Cross-sectional Smaller anterior corpus callosum in CHR-t vs CHR-n Sun et al, 103 2009 Longitudinal Greater brain contraction in R PFC in CHR-t vs CHR over time Takahashi et al, 94 2009 Longitudinal Smaller baseline insula bilaterally in CHR-t vs CHR-n, and in R insula vs controls Reduced GM of bilateral insula in CHR-t vs CHR-n and controls Hannan et al, 96 2010 Cross-sectional No differences in caudate volume in CHR at baseline vs controls or in CHR-t vs CHR-n Takahashi et al, 79 2010 Cross-sectional Smaller STG bilaterally at baseline in CHR vs controls Wood et al, 86 2010 Cross-sectional Smaller L hippocampal volume in CHR vs controls Dazzan et al, 81 2012 Longitudinal Smaller frontal cortex volume in CHR-t vs CHR-n at baseline Reduced parietal cortex and temporal cortex (trend) in CHR-t vs CHR-n Whitford et al, 95 2012 Cross-sectional Smaller cuneus in CHR-HSV-11 vs CHR-HSV-1– and controls Basel Borgwardt et al, 69 2007 Cross-sectional Smaller GM at baseline in posterior cingulate and precuneus bilaterally and L superior parietal lobule in CHR-t vs controls Borgwardt et al, 88 2007 Longitudinal Smaller L insula, STG, cingulate gyrus, and precuneus in CHR vs controls Reduced R insula, inferior frontal and STG in CHR-t vs CHR-n Borgwardt et al, 102 2008 Longitudinal Reduced orbitofrontal, superior frontal, inferior temporal, parietal cortex, and cerebellum in CHR-t vs controls over time Haller et al, 92 2009 Cross-sectional Whole-brain cortical thickness asymmetry in CHR vs controls Koutsouleris et al, 73 2009 Cross "
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ABSTRACT: This article reviews the literature on structural magnetic resonance imaging findings in pediatric and young adult populations at clinical or genetic high-risk for schizophrenia and early-onset schizophrenia. The implications of this research are discussed for understanding the pathophysiology of schizophrenia and for early intervention strategies. The evidence linking brain structural changes in prepsychosis development and early-onset schizophrenia with disruptions of normal neurodevelopmental processes during childhood or adolescence is described. Future directions are outlined for research to address knowledge gaps regarding the neurobiological basis of brain structural abnormalities in schizophrenia and to improve the usefulness of these abnormalities for preventative interventions.
Available from: Stefan Borgwardt
- "Cross-sectional studies indicate that, relative to healthy controls, UHR subjects have reduced grey matter (GM) volume in frontal (Meisenzahl et al.
2008; Mechelli et al.
2011), lateral and medial temporal regions (Meisenzahl et al.
2008). Studies that used a region of interest (ROI) approach reported GM volume increases (Buehlmann et al.
2010) but also reductions (Phillips et al.
2002) in the hippocampus, reductions in the planum polare/temporale, insula and superior temporal gyrus (Takahashi et al.
2009, 2010), increases in the pituitary volume (Büschlen et al.
2011), and reductions in the anterior cingulate cortex (ACC) (Röthlisberger et al.
2012) in the UHR group compared with healthy controls. "
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Grey matter volume and cortical thickness represent two complementary aspects of brain structure. Several studies have described reductions in grey matter volume in people at ultra-high risk (UHR) of psychosis; however, little is known about cortical thickness in this group. The aim of the present study was to investigate cortical thickness alterations in UHR subjects and compare individuals who subsequently did and did not develop psychosis.
We examined magnetic resonance imaging data collected at four different scanning sites. The UHR subjects were followed up for at least 2 years. Subsequent to scanning, 50 UHR subjects developed psychosis and 117 did not. Cortical thickness was examined in regions previously identified as sites of neuroanatomical alterations in UHR subjects, using voxel-based cortical thickness.
At baseline UHR subjects, compared with controls, showed reduced cortical thickness in the right parahippocampal gyrus (p < 0.05, familywise error corrected). There were no significant differences in cortical thickness between the UHR subjects who later developed psychosis and those who did not.
These data suggest that UHR symptomatology is characterized by alterations in the thickness of the medial temporal cortex. We did not find evidence that the later progression to psychosis was linked to additional alterations in cortical thickness, although we cannot exclude the possibility that the study lacked sufficient power to detect such differences.
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