Charlie A Davidson1, Danijela Piskulic2, Jean Addington2, Kristen S Cadenhead3, Tyrone D Cannon4, Barbara A Cornblatt5, Thomas H McGlashan6, Diana O Perkins7, Larry J Seidman8, Ming T Tsuang9, Elaine F Walker10, Carrie E Bearden11, Daniel H Mathalon12, Scott W Woods6, Jason K Johannesen13. 1. Department of Psychiatry, Yale University, New Haven, CT, United States. Electronic address: cadavid@emory.edu. 2. Hotchkiss Brain Institute, Department of Psychiatry, University of Calgary, Calgary, Alberta, Canada. 3. Department of Psychiatry, University of California San Diego, La Jolla, CA, United States. 4. Department of Psychology, Yale University, New Haven, CT, United States. 5. Department of Psychiatry, Zucker Hillside Hospital, Queens, NY, United States. 6. Department of Psychiatry, Yale University, New Haven, CT, United States. 7. Department of Psychiatry, University of North Carolina, Chapel Hill, NC, United States. 8. Department of Psychiatry, Harvard Medical School at Beth Israel Deaconess Medical Center, Massachusetts General Hospital, Boston, MA, United States. 9. Department of Psychiatry, University of California San Diego, La Jolla, CA, United States; Institute of Genomic Medicine, University of California, La Jolla, CA, United States. 10. Department of Psychology, Emory University, Atlanta, GA, United States. 11. Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, CA, United States; Department of Psychology, University of California, Los Angeles, Los Angeles, CA, United States. 12. Department of Psychiatry, University of California, San Francisco, San Francisco, United States; Psychiatry Service, San Francisco, CA, United States. 13. Department of Psychiatry, Yale University, New Haven, CT, United States; Psychology Service, VA Connecticut Health Care System, West Haven, CT, United States.
Abstract
BACKGROUND: Clinical high risk (CHR) status is characterized by impairments in social cognition, but questions remain concerning their stability over development. In cross-sectional analysis of a large naturalistic sample, the current study examined whether those at CHR status show deviant trajectories for age-related change in social cognitive ability, and whether these trajectories are influenced by treatment history. METHOD: Emotion perception (EP) and theory of mind (ToM) were assessed in 675 CHR and 263 healthy comparison (HC) participants aged 12-35. Age effects in CHR were modeled against HC age-expected performance. Prior medication status was tested for interactions with age. RESULTS: CHR exhibited normal age trajectory for EP, but significantly lower slopes for ToM from age 17 onward. This effect was specific to stimuli exhibiting sarcasm and not to detection of lies. When treatment history was included in the model, age-trajectory appeared normal in CHR subjects previously prescribed both antipsychotics and antidepressant medication, although the blunted trajectory still characterized 80% of the sample. DISCUSSION: Cross-sectional analyses suggested that blunting of ToM in CHR develops in adolescence, while EP abilities were diminished evenly across the age range. Exploratory analyses of treatment history suggested that ToM was not affected, however, in CHRs with lifetime histories of both antipsychotic and antidepressant medications. Reduction in age-expected ToM ability may impair the ability of individuals at CHR to meet social developmental challenges in adolescence. Medication effects on social cognition deserve further study.
BACKGROUND: Clinical high risk (CHR) status is characterized by impairments in social cognition, but questions remain concerning their stability over development. In cross-sectional analysis of a large naturalistic sample, the current study examined whether those at CHR status show deviant trajectories for age-related change in social cognitive ability, and whether these trajectories are influenced by treatment history. METHOD: Emotion perception (EP) and theory of mind (ToM) were assessed in 675 CHR and 263 healthy comparison (HC) participants aged 12-35. Age effects in CHR were modeled against HC age-expected performance. Prior medication status was tested for interactions with age. RESULTS:CHR exhibited normal age trajectory for EP, but significantly lower slopes for ToM from age 17 onward. This effect was specific to stimuli exhibiting sarcasm and not to detection of lies. When treatment history was included in the model, age-trajectory appeared normal in CHR subjects previously prescribed both antipsychotics and antidepressant medication, although the blunted trajectory still characterized 80% of the sample. DISCUSSION: Cross-sectional analyses suggested that blunting of ToM in CHR develops in adolescence, while EP abilities were diminished evenly across the age range. Exploratory analyses of treatment history suggested that ToM was not affected, however, in CHRs with lifetime histories of both antipsychotic and antidepressant medications. Reduction in age-expected ToM ability may impair the ability of individuals at CHR to meet social developmental challenges in adolescence. Medication effects on social cognition deserve further study.
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