Vanessa L Cropley1, Ashleigh Lin2, Barnaby Nelson3, Renate L E P Reniers4, Alison R Yung5, Cali F Bartholomeusz6, Paul Klauser7, Dennis Velakoulis8, Patrick McGorry3, Stephen J Wood9, Christos Pantelis8. 1. Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne and Melbourne Health, Carlton South, Victoria 3053, Australia; Department of Psychiatry, The University of Melbourne, Parkville, Victoria 3052, Australia. Electronic address: vcropley@unimelb.edu.au. 2. Telethon Kids Institute, The University of Western Australia, Perth, Western Australia 6008, Australia. 3. Orygen, The National Centre of Excellence in Youth Mental Health, The University of Melbourne and Melbourne Health, Parkville, Victoria 3052, Australia. 4. School of Psychology,-University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom. 5. Institute of Brain, Behaviour and Mental Health, University of Manchester, Manchester M13 9PL, United Kingdom. 6. Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne and Melbourne Health, Carlton South, Victoria 3053, Australia; Department of Psychiatry, The University of Melbourne, Parkville, Victoria 3052, Australia; Orygen, The National Centre of Excellence in Youth Mental Health, The University of Melbourne and Melbourne Health, Parkville, Victoria 3052, Australia. 7. Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne and Melbourne Health, Carlton South, Victoria 3053, Australia; Monash Clinical and Imaging Neuroscience, Monash University, Clayton, Victoria, Australia. 8. Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne and Melbourne Health, Carlton South, Victoria 3053, Australia; Department of Psychiatry, The University of Melbourne, Parkville, Victoria 3052, Australia. 9. Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne and Melbourne Health, Carlton South, Victoria 3053, Australia; School of Psychology,-University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom.
Abstract
INTRODUCTION: Two thirds of individuals identified as ultra-high risk (UHR) for psychosis do not transition to psychosis over the medium to long-term (non-transition; UHR-NT). Nevertheless, many of these individuals have persistent attenuated psychotic symptoms (APS). The current study examined whether there were differences in baseline grey matter volume (i.e. at initial identification as UHR) in UHR-NT individuals whom had APS compared to those without APS (No-APS) at medium to long-term follow-up. METHODS: Participants were help-seeking individuals who were identified as being at UHR for psychosis between 2 and 12years previously (mean=7.5). The sample consisted of 109 participants who underwent a Magnetic Resonance Imaging scan at baseline and who had not been observed to develop a psychotic disorder over the follow-up period (UHR-NT). Using voxel-based morphometry, baseline grey matter volume (GMV) was compared between participants with (N=30) and without (N=79) APS at follow-up. RESULTS: At baseline, the APS and No-APS groups were clinically indistinguishable. At follow-up, the APS group had significantly worse symptoms and impaired functioning. Individuals with APS had reduced baseline GMV in frontal, temporal, posterior and cingulate regions compared to those without APS at follow-up. Reduced GMV was associated with more severe positive, negative and depressive symptoms and lower global functioning in the combined UHR-NT cohort. These associations were independent of later APS outcome. DISCUSSION: This study found that differences in regional GMV are discernible at an early stage of UHR and may be specific to individuals who have APS and psychopathology at follow-up. Our findings suggest that lower GMV at baseline may confer neurobiological risk for later APS and/or increased psychopathology while the absence of these structural abnormalities might be protective.
INTRODUCTION: Two thirds of individuals identified as ultra-high risk (UHR) for psychosis do not transition to psychosis over the medium to long-term (non-transition; UHR-NT). Nevertheless, many of these individuals have persistent attenuated psychotic symptoms (APS). The current study examined whether there were differences in baseline grey matter volume (i.e. at initial identification as UHR) in UHR-NT individuals whom had APS compared to those without APS (No-APS) at medium to long-term follow-up. METHODS: Participants were help-seeking individuals who were identified as being at UHR for psychosis between 2 and 12years previously (mean=7.5). The sample consisted of 109 participants who underwent a Magnetic Resonance Imaging scan at baseline and who had not been observed to develop a psychotic disorder over the follow-up period (UHR-NT). Using voxel-based morphometry, baseline grey matter volume (GMV) was compared between participants with (N=30) and without (N=79) APS at follow-up. RESULTS: At baseline, the APS and No-APS groups were clinically indistinguishable. At follow-up, the APS group had significantly worse symptoms and impaired functioning. Individuals with APS had reduced baseline GMV in frontal, temporal, posterior and cingulate regions compared to those without APS at follow-up. Reduced GMV was associated with more severe positive, negative and depressive symptoms and lower global functioning in the combined UHR-NT cohort. These associations were independent of later APS outcome. DISCUSSION: This study found that differences in regional GMV are discernible at an early stage of UHR and may be specific to individuals who have APS and psychopathology at follow-up. Our findings suggest that lower GMV at baseline may confer neurobiological risk for later APS and/or increased psychopathology while the absence of these structural abnormalities might be protective.
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