William Carpenter

Professor at the University of Maryland
Dr. Carpenter's major professional interest has been severe mental illness, especially schizophrenia. His approach to the care and study of patients is within the context of a broad medical model integrating biological, psychological and social data as they pertain to diagnosis, treatment and etiology. He has made original and fundamental contributions in psychopathology, assessment methodology, testing of new treatments and research ethics. He has authored over 400 clinical and scientific articles, book chapters and books. Dr. Carpenter has served on the editorial boards of the Archives of General Psychiatry, Biological Psychiatry, the Journal of Nervous and Mental Disease, Neuropsychopharmacology, Psychiatry Research, Schizophrenia Research, and is Editor-in-Chief of the Schizophrenia Bulletin.  He chaired the Psychosis Work Group for DSM-5, served as director of the Maryland Psychiatric Research Center for 36 years, and is a member of the Institute of Medicine of the National Academies of Science.

Avolition in schizophrenia: A failure to translate reward information into motivated behavior

Avolition has been at the core of the schizophrenia construct since the earliest clinical conceptualizations of the disorder, and is a principal determinant of poor functional outcome that limits social and occupational success. Currently, there are no FDA approved treatments for avolition in schizophrenia, potentially because the cognitive and neural basis of this pathology is not well understood. The current presentation discusses recent developments in the etiology, assessment, and treatment of negative symptoms of schizophrenia, taking a translational neuroscience approach to explaining avolitional pathology. We begin by providing a historical overview of avolition in schizophrenia, highlighting early clinical conceptualizations proposed by Kraepelin, Bleuler, and Rado. These early descriptions are contrasted with modern views of negative symptoms originating in the 1970’s that were further refined in the 2000’s with the NIMH Consensus Conference on Negative Symptoms. Current issues in conceptualizing and measuring negative symptom pathology are discussed, including the primary vs. secondary distinction, whether the latent structure is continuous or categorical, evidence for the multi-dimensionality and 2 separable negative symptom domains, and recent developments in negative symptom assessment. Research on reward processing will also be reviewed, which has begun to provide important insights into the cognitive and neural mechanisms associated with motivational impairments in schizophrenia. Specifically, data will be presented on several aspects of reward processing that are impaired in schizophrenia, including: (1) dopamine-mediated basal ganglia systems that support reinforcement learning and the ability to predict cues that lead to rewarding outcomes; (2) orbitofrontal cortex-driven deficits in generating, updating, and maintaining value representations; (3) aberrant effort-value computations, which may be mediated by disrupted anterior cingulate cortex and midbrain dopamine functioning; and (4) altered activation of the prefrontal cortex, which is important for action selection and generating exploratory behaviors in environments where reward outcomes are uncertain. A new translational affective neuroscience model for understanding avolition is discussed, which proposes that aberrant cortico-striatal interactions may be a common factor underlying these various reward processing abnormalities that manifest clinically as avolition.