Erin A Hazlett1, Ethan G Rothstein2, Rui Ferreira2, Jeremy M Silverman3, Larry J Siever4, Ann Olincy5. 1. Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Research and Development, James J. Peters Veterans Affairs Medical Center, Bronx, NY, United States; Mental Illness Research, Education, and Clinical Center (VISN3), James J. Peters Veterans Affairs Medical Center, Bronx, NY, United States. Electronic address: erin.hazlett@mssm.edu. 2. Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, United States. 3. Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Research and Development, James J. Peters Veterans Affairs Medical Center, Bronx, NY, United States. 4. Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Research and Development, James J. Peters Veterans Affairs Medical Center, Bronx, NY, United States; Mental Illness Research, Education, and Clinical Center (VISN3), James J. Peters Veterans Affairs Medical Center, Bronx, NY, United States. 5. Department of Psychiatry, University of Colorado, Denver, CO, United States.
Abstract
BACKGROUND: DSM-5 places schizophrenia on a continuum from severe, chronic schizophrenia to the attenuated schizophrenia-like traits of schizotypal personality disorder (SPD), the prototypic schizophrenia-related personality disorder. SPD shares common genetic and neurobiological substrates with schizophrenia, including information processing abnormalities, although they are less marked. This is the first study to directly compare the P50 evoked electroencephalographic response-a measure of sensory gating and a neurophysiological endophenotype-between schizophrenia-spectrum groups. Two hypotheses were tested: (1) Compared with healthy controls (HCs), schizophrenia patients show reduced P50 suppression and SPD patients resemble schizophrenia but exhibit less marked deficits; and (2) Deficient P50 suppression in SPD is associated with greater clinical symptom severity. METHODS: P50 was assessed in 32 schizophrenia-spectrum disorder patients (12 SPD, 20 schizophrenia patients) and 25 demographically-matched HCs. The standard conditioning (C)-testing (T) paradigm was used and P50 suppression was quantified using the T-C difference and the T/C ratio. RESULTS: All P50 measures showed a linear, stepwise pattern with the SPD group intermediate between the HC and schizophrenia groups. Compared with HCs, both patient groups had lower conditioning and T-C difference values. Among the SPD group, greater clinical symptom severity was associated with greater conditioning-response amplitude deficits. CONCLUSION: These findings: (1) are novel in showing that P50 deficits in SPD resemble those observed in schizophrenia, albeit less marked; (2) support the concept that the phenomenological link between SPD and schizophrenia lies in shared neurocognitive/neurophysiological pathologies; and (3) provide evidence that P50 is a neurophysiological endophenotype for schizophrenia-spectrum disorders. Published by Elsevier B.V.
BACKGROUND: DSM-5 places schizophrenia on a continuum from severe, chronic schizophrenia to the attenuated schizophrenia-like traits of schizotypal personality disorder (SPD), the prototypic schizophrenia-related personality disorder. SPD shares common genetic and neurobiological substrates with schizophrenia, including information processing abnormalities, although they are less marked. This is the first study to directly compare the P50 evoked electroencephalographic response-a measure of sensory gating and a neurophysiological endophenotype-between schizophrenia-spectrum groups. Two hypotheses were tested: (1) Compared with healthy controls (HCs), schizophreniapatients show reduced P50 suppression and SPD patients resemble schizophrenia but exhibit less marked deficits; and (2) Deficient P50 suppression in SPD is associated with greater clinical symptom severity. METHODS:P50 was assessed in 32 schizophrenia-spectrum disorderpatients (12 SPD, 20 schizophreniapatients) and 25 demographically-matched HCs. The standard conditioning (C)-testing (T) paradigm was used and P50 suppression was quantified using the T-C difference and the T/C ratio. RESULTS: All P50 measures showed a linear, stepwise pattern with the SPD group intermediate between the HC and schizophrenia groups. Compared with HCs, both patient groups had lower conditioning and T-C difference values. Among the SPD group, greater clinical symptom severity was associated with greater conditioning-response amplitude deficits. CONCLUSION: These findings: (1) are novel in showing that P50 deficits in SPD resemble those observed in schizophrenia, albeit less marked; (2) support the concept that the phenomenological link between SPD and schizophrenia lies in shared neurocognitive/neurophysiological pathologies; and (3) provide evidence that P50 is a neurophysiological endophenotype for schizophrenia-spectrum disorders. Published by Elsevier B.V.
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