Joseph Gonzalez-Heydrich1, Michelle Bosquet Enlow2, Eugene D'Angelo2, Larry J Seidman3, Sarah Gumlak4, April Kim4, Kristen A Woodberry5, Ashley Rober4, Sahil Tembulkar4, Kelsey Graber4, Kyle O'Donnell4, Hesham M Hamoda2, Kara Kimball4, Alexander Rotenberg6, Lindsay M Oberman7, Alvaro Pascual-Leone8, Matcheri S Keshavan5, Frank H Duffy6. 1. Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA; Harvard Medical School, Department of Psychiatry, 401 Park Drive, Boston, MA 02215, USA. Electronic address: Joseph.Gonzalez-Heydrich@childrens.harvard.edu. 2. Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA; Harvard Medical School, Department of Psychiatry, 401 Park Drive, Boston, MA 02215, USA. 3. Harvard Medical School, Department of Psychiatry, 401 Park Drive, Boston, MA 02215, USA; Beth Israel Deaconess Medical Center, Department of Psychiatry, Commonwealth Research Center, 75 Fenwood Road, Boston, MA 02115, USA; Massachusetts General Hospital, Department of Psychiatry, 55 Fruit Street, Boston, MA 02114, USA. 4. Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA. 5. Harvard Medical School, Department of Psychiatry, 401 Park Drive, Boston, MA 02215, USA; Beth Israel Deaconess Medical Center, Department of Psychiatry, Commonwealth Research Center, 75 Fenwood Road, Boston, MA 02115, USA. 6. Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA; Harvard Medical School, Department of Neurology, 25 Shattuck Street, Boston, MA 02115, USA. 7. E.P. Bradley Hospital and Warren Alpert Medical School, Brown University, Neuroplasticity and Autism Spectrum Disorder Program and Department of Psychiatry and Human Behavior, 1011 Veterans Memorial Parkway, East Providence, RI 02915, USA. 8. Harvard Medical School, Department of Neurology, 25 Shattuck Street, Boston, MA 02115, USA; Beth Israel Deaconess Medical Center, Division of Cognitive Neurology and Berenson-Allen Center, 330 Brookline Avenue, Boston, MA 02115, USA.
Abstract
BACKGROUND: The N100 is a negative deflection in the surface EEG approximately 100 ms after an auditory signal. It has been shown to be reduced in individuals with schizophrenia and those at clinical high risk (CHR). N100 blunting may index neural network dysfunction underlying psychotic symptoms. This phenomenon has received little attention in pediatric populations. METHOD: This cross-sectional study compared the N100 response measured via the average EEG response at the left medial frontal position FC1 to 150 sinusoidal tones in participants ages 5 to 17 years with a CHR syndrome (n=29), a psychotic disorder (n=22), or healthy controls (n=17). RESULTS: Linear regression analyses that considered potential covariates (age, gender, handedness, family mental health history, medication usage) revealed decreasing N100 amplitude with increasing severity of psychotic symptomatology from healthy to CHR to psychotic level. CONCLUSIONS: Longitudinal assessment of the N100 in CHR children who do and do not develop psychosis will inform whether it predicts transition to psychosis and if its response to treatment predicts symptom change.
BACKGROUND: The N100 is a negative deflection in the surface EEG approximately 100 ms after an auditory signal. It has been shown to be reduced in individuals with schizophrenia and those at clinical high risk (CHR). N100 blunting may index neural network dysfunction underlying psychotic symptoms. This phenomenon has received little attention in pediatric populations. METHOD: This cross-sectional study compared the N100 response measured via the average EEG response at the left medial frontal position FC1 to 150 sinusoidal tones in participants ages 5 to 17 years with a CHR syndrome (n=29), a psychotic disorder (n=22), or healthy controls (n=17). RESULTS: Linear regression analyses that considered potential covariates (age, gender, handedness, family mental health history, medication usage) revealed decreasing N100 amplitude with increasing severity of psychotic symptomatology from healthy to CHR to psychotic level. CONCLUSIONS: Longitudinal assessment of the N100 in CHR children who do and do not develop psychosis will inform whether it predicts transition to psychosis and if its response to treatment predicts symptom change.
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