Anthony O Ahmed1, Brian Kirkpatrick2, Eric Granholm3,4, Laura M Rowland5, Peter B Barker6,7, James M Gold5, Robert W Buchanan5, Tacina Outram1, Miguel Bernardo8,9,10,11, María Paz García-Portilla10,12,13,14, Anna Mane10,15,16, Emilio Fernandez-Egea17,18, Gregory P Strauss19. 1. Department of Psychiatry, Weill Cornell Medicine, White Plains, NY, USA. 2. Department of Psychiatry, University of Nevada, Reno School of Medicine, Reno, NV, USA. 3. Department of Psychiatry, University of California, San Diego, San Diego, CA, USA. 4. Psychology Service, VA San Diego Healthcare System, San Diego, CA, USA. 5. Department of Psychiatry and Maryland Psychiatric Research Center, University of Maryland School of Medicine, Baltimore, MD, USA. 6. The Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, USA. 7. FM Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, MD, USA. 8. Barcelona Clinic Schizophrenia Unit, Hospital Clinic of Barcelona, Neuroscience Institute, Barcelona, Spain. 9. Department of Medicine, Institut de Neurociències, Universitat de Barcelona, Barcelona, Spain. 10. Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Madrid, Spain. 11. August Pi I Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. 12. Department of Psychiatry, Universidad de Oviedo, Oviedo, Spain. 13. Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Oviedo, Spain. 14. Servicio de Salud del Principado de Asturias (SESPA), Oviedo, Spain. 15. Institut de Neuropsiquiatria i Adiccions, Parc de Salut Mar, Barcelona, Spain. 16. Fundació Hospital del Mar Medical Research Institute (IMIM), Barcelona, Spain. 17. Department of Psychiatry, Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK. 18. Cambridgeshire and Peterborough NHS Foundation Trust, Cambridge, UK. 19. Departments of Psychology and Neuroscience, University of Georgia, Athens, GA, USA.
Abstract
OBJECTIVES: Negative symptom studies frequently use single composite scores as indicators of symptom severity and as primary endpoints in clinical trials. Factor analytic and external validation studies do not support this practice but rather suggest a multidimensional construct. The current study used structural equation modeling (SEM) to compare competing dimensional models of negative symptoms to determine the number of latent dimensions that best capture variance in biological, psychological, and clinical variables known to have associations with negative symptoms. METHODS: Three independent studies (total n = 632) compared unidimensional, two-factor, five-factor, and hierarchical conceptualizations of negative symptoms in relation to cognition, psychopathology, and community functioning (Study 1); trait emotional experience and defeatist performance beliefs (Study 2); and glutamate and gamma-aminobutyric acid levels in the anterior cingulate cortex quantified using proton magnetic resonance spectroscopy (Study 3). RESULTS: SEM favored the five-factor and hierarchical models over the unidimensional and two-factor models regardless of the negative symptom measure or external validator. The five dimensions-anhedonia, asociality, avolition, blunted affect, and alogia-proved vital either as stand-alone domains or as first-order domains influenced by second-order dimensions-motivation and pleasure and emotional expression. The two broader dimensions sometimes masked important associations unique to the five narrower domains. Avolition, anhedonia, and blunted affect showed the most domain-specific associations with external variables across study samples. CONCLUSIONS: Five domains and a hierarchical model reflect the optimal conceptualization of negative symptoms in relation to external variables. Clinical trials should consider using the two dimensions as primary endpoints and the five domains as secondary endpoints.
OBJECTIVES: Negative symptom studies frequently use single composite scores as indicators of symptom severity and as primary endpoints in clinical trials. Factor analytic and external validation studies do not support this practice but rather suggest a multidimensional construct. The current study used structural equation modeling (SEM) to compare competing dimensional models of negative symptoms to determine the number of latent dimensions that best capture variance in biological, psychological, and clinical variables known to have associations with negative symptoms. METHODS: Three independent studies (total n = 632) compared unidimensional, two-factor, five-factor, and hierarchical conceptualizations of negative symptoms in relation to cognition, psychopathology, and community functioning (Study 1); trait emotional experience and defeatist performance beliefs (Study 2); and glutamate and gamma-aminobutyric acid levels in the anterior cingulate cortex quantified using proton magnetic resonance spectroscopy (Study 3). RESULTS: SEM favored the five-factor and hierarchical models over the unidimensional and two-factor models regardless of the negative symptom measure or external validator. The five dimensions-anhedonia, asociality, avolition, blunted affect, and alogia-proved vital either as stand-alone domains or as first-order domains influenced by second-order dimensions-motivation and pleasure and emotional expression. The two broader dimensions sometimes masked important associations unique to the five narrower domains. Avolition, anhedonia, and blunted affect showed the most domain-specific associations with external variables across study samples. CONCLUSIONS: Five domains and a hierarchical model reflect the optimal conceptualization of negative symptoms in relation to external variables. Clinical trials should consider using the two dimensions as primary endpoints and the five domains as secondary endpoints.
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