Body, Mind, and Brain Lab

Dr. Park’s research program lies at the intersection between clinical, cognitive and social neuroscience. Her lab studies the nature of cognitive and social functioning in individuals with schizophrenia or bipolar disorder and people at elevated risk for psychosis in order to elucidate the etiology and neural basis of psychotic disorders, and understand the complex relationships among clinical symptoms, cognitive deficits, and brain abnormalities.

Sohee Park Ph.D.

Gertrude Conaway Vanderbilt Professor

• Department of Psychology
• Office: Wilson 525
• Lab: Wilson 213
• Email: sohee.park@vanderbilt.edu

Education

• B.A. Honours (Natural Sciences Tripos) University of Cambridge
• M.A. (Psychology) Columbia University
• Ph.D. (Psychology) Harvard University
• Post-Doc. (Psychology) Harvard University

Academic Positions

• Research Scientist, Neurologischeklinik & Psychiatric Hospital (Burghölzli) of University of Zürich
• Assistant Professor, Northwestern University
• Associate Professor, Vanderbilt University
• Professor, Vanderbilt University

Membership

• Fellow of the Association for Psychological Science
• Fellow of the International College of Neuropsychopharmacology
• Executive Board, Society for Research in Psychopathology (elected for the term 2014-2017)
• Executive Board, Schizophrenia International Society (elected for the term 2018-2022)
• Life Member, Association for the Scientific Study of Consciousness
• Member, Society for Research in Psychopathology
• Member, Asian American Psychological Association
• Member, Society for a Science of Clinical Psychology

Executive Board

Contribution to Diversity, Equity and Inclusion

She has selected four areas of her research that have contributed to a better understanding of the underlying mechanisms and the surface manifestation of schizophrenia:

Establishing working memory deficit as a core feature of schizophrenia

During graduate school, I had the good fortune to work with Philip Holzman and Patricia Goldman-Rakic, and together we discovered the presence of working memory deficits in schizophrenia that paralleled single cell recording studies of prefrontal regions in nonhuman primates. A quarter of century ago, such translational collaborations were rare, and even more unusual were my mentors’ enthusiastic support for a relatively high-risk dissertation project. I tested the hypothesis that the core deficit and the most likely endophenotypic marker of schizophrenia was a working memory (i.e., active short term memory) deficit that cascades to all aspects of cognitive and social impairments, and that this deficit arose from abnormal frontoparietal circuitry. We demonstrated that a majority of individuals with schizophrenia and half of their healthy relatives have working memory deficit, and that this problem was specific to the schizophrenia-spectrum but not to bipolar disorder. These findings were published in a series of articles and contributed towards establishing cognitive deficits as core features of schizophrenia (now widely accepted in the field). These early experiments led to a lifelong interest in identifying components of cognitive symptoms, and associated phenotypic markers of schizophrenia.

We now know that working memory deficit is stable in the patients (see Lee & Park, 2005) and found in individuals at elevated risk (for a review see Park & Gooding, 2014). We have also sought to elucidate the etiology of working memory deficits in schizophrenia by examining both the neural correlates (Lee, Folley, Gore & Park, 2008; Kim, Matthews & Park, 2010), and by carefully analyzing the components of encoding and retention mechanisms (e.g., Mayer & Park, 2012; Mayer, Fukuda, Vogel & Park, 2012; Mayer, Kim & Park, 2014). A full specification of cardinal features of schizophrenia could result in the development of effective treatments. Moreover, specification of behavioral markers may help us detect precursors of psychosis in young people at high-risk, which should point to powerful intervention strategies.

Schizophrenia-spectrum is characterized by deficits and enhancements.

Schizophrenia is not only characterized by impairments. There are surprising pockets of intact and enhanced abilities. We found that individuals with schizophrenia and healthy at-risk individuals sometimes benefitted from distributed spatial attention and disinhibition when divergent thinking was required and that during these events, their frontal cortical activity was more bilateral compared with that of control participants (Folley & Park, 2005; Gibson, Folley & Park, 2009). Furthermore, one of the most counterintuitive and intriguing findings that has emerged from our research is the superior visuospatial imagery ability of individuals with schizophrenia and those at risk for schizophrenia. We have shown that schizophrenia-spectrum is associated with enhanced mental imagery generation, inspection and manipulation abilities despite impaired working memory and attention (e.g. Thakkar & Park, 2010, 2012; Benson & Park, 2013; Matthews, Collins, Thakkar & Park, 2014). These results pointed to altered frontoparietal circuitry and opened an avenue toward studying the relationship between the spatial self and the visuospatial environment.

Splitting of the Self and the Body is Central to Schizophrenia

What we learned from our studies of mental imagery was that visual perspective-taking ability is enhanced in individuals with schizophrenia; they are able to mentally rotate their body representation to another person’s viewpoint with ease. Mental imagery and perspective taking are associated with the multisensory temporoparietal regions. Interestingly anomalous sense of the body and self (self-disturbances) can be induced by stimulating these brain areas. Out-of-Body Experience (a feeling of leaving one’s own body) and Felt Presence ( also known as Sensed Presence) are two of the autoscopic hallucinatory experiences that are experienced across a wide range of conditions.

These anomalous experiences of the bodily self are were very important to Bleuler’s conceptualization of schizophrenia, and a distorted, even loss of a sense of self appears to be a core feature of the disorder beginning early during the premorbid and prodromal stages. Furthermore, aberrant self-experiences are highly salient to those diagnosed with schizophrenia throughout the course of illness. Individuals with schizophrenia are very susceptible to experimental manipulation of self faces, body ownership, agency and proprioception (e.g., Lee, Kwon, Shin, Lee & Park, 2007; Thakkar, Nichols, McIntosh & Park, 2011; Hur, Kwon, Lee & Park, 2014; Yun, Hur, Jung, Jang, Youn, Kang, Park & Kwon, 2014; Thakkar, Schall, Heckers & Park, 2015). Thus, understanding neural and psychological mechanisms underlying self-disturbances would have significant implications for implementing treatments, but self-disorder is not a prominent feature of the current DSM-5 criteria. To begin to address this gap, I edited a special issue of Schizophrenia Research in 2014 to showcase theoretical and empirical studies of self and body disturbances in schizophrenia (see Park & Nasrallah, 2014). Our own studies indicate that dissociative bodily experiences (out-of-body experiences, feeling-of-presence) affect as many as 40% of patients and prodromal individuals. Such dissociative experiences are exacerbated by perceived social isolation (loneliness). In turn, social disconnection appears to increase self-disturbance and social delusions. Social isolation and reduced social functioning in schizophrenia present a very difficult barrier that prevents good prognosis and outcome.

Schizophrenia as a Disorder of the Social Brain.

Social impairments are central features of schizophrenia from prodromal phase of the illness to chronic states. Social deficits reduce quality of life and increase relapse rate. Successful social interactions depend on fast and accurate interpretation of actions, intentions and emotions of others. Our work in this area indicates that individuals with schizophrenia are impaired in rapidly extracting task-relevant information and evaluating them to guide action in real time.

With respect to social perception, one of the most prominent problems appears to be a tendency to falsely detect social meaning (e.g. people, intentions, social actions) when there is none. For example, upon seeing random dots moving, schizophrenia patients are likely to perceive a person engaged in an action and this false detection of living agents is accompanied by increased activity of the superior temporal sulcus (e.g., Kim, Doop, Blake & Park, 2005; Kim, Park & Blake, 2011). Both behavioral and neuroimaging results suggest that the patients with schizophrenia are not necessarily impaired in perceiving the ‘signal’ but there may be an increased background ‘noise’ is

Abnormal perception of agency, intentions, actions and emotions are manifested across multiple domains. Patients with schizophrenia and high-risk individuals have difficulty with emotion perception regardless of the types of stimuli (faces, gazes, bodies, gaits, scenes)(Hooker & Park, 2002; Hooker & Park, 2005; Doop & Park, 2009; Peterman, Christensen, Giese, Park, 2013). Interestingly, they seem unable to use physiological and interoceptive cues to guide their social decisions (Peterman, Bekele, Bian, Sarkar & Park, 2015; Aaron, Benson & Park, 2014), and make abnormal social trait judgments (McIntosh & Park, 2014). With respect to social interactions and prosocial behavior, they have difficulty learning from past mistakes to generate appropriate social behavior (Hooker, Roese & Park, 2000; Roese, Park, Smallman & Gibson, 2008).

One of the reasons for social interactional difficulty may be that individuals with schizophrenia are impaired in mental simulation, a process by which internal representations of external events such as movements and actions of others are generated and utilized. Simulation of the external world may provide a mechanism by which we model behaviors of others, supporting rapid action understanding and deficits in mental simulation could lead to misunderstanding of actions of others. Social understanding may be supported by mirror-mechanism that bridges perception and action, self and other. We have shown that imitation and simulation of other people’s behavior are impaired in schizophrenia and that this simulation impairment may indicate abnormal activation of the social brain network that includes the inferior frontal cortex, superior temporal sulcus and the inferior temporal lobule (Park, Matthew & Gibson, 2008; Matthews, Gold, Sekuler & Park, 2013; Thakkar, Peterman & Park, 2014). However, we also found that practice improved simulation over time and therefore, social skills training via simulation might provide an effective method for improving social outcome in schizophrenia.