INS NYC 2024 Program

Poster	Poster Session 04 Program Schedule 02/15/2024 12:00 pm - 01:15 pm Room: Shubert Complex (Posters 1-60) Poster Session 04: Neuroimaging \| Neurostimulation/Neuromodulation \| Teleneuropsychology/Technology Final Abstract #20 Differential Neural Processing of Socially Generated Sounds in Autism Spectrum Disorder and Misophonia Alissa Chen, Icahn School of Medicine at Mount SInai, New York, United States Jeanpierre Tenesaca, Icahn School of Medicine at Mount Sinai, New York, United States Sarah Banker, Icahn School of Medicine at Mount Sinai, New York, United States Jadyn Trayvick, Icahn School of Medicine at Mount Sinai, New York, United States Arabella Peters, Icahn School of Medicine at Mount Sinai, New York, United States Abigaël Thinakaran, Icahn School of Medicine at Mount Sinai, New York, United States Xiaosi Gu, Icahn School of Medicine at Mount Sinai, New York, United States Jennifer Foss-Feig, Icahn School of Medicine at Mount Sinai, New York, United States Daniela Schiller, Icahn School of Medicine at Mount Sinai, New York, United States Category: Neurophysiology/EEG/ERP/fMRI Keyword 1: autism spectrum disorder Keyword 2: neurocognition Keyword 3: auditory processing disorder Objective: Previous research has shown that people tend to suppress neural responses to self-generated sounds versus externally-generated sounds. This phenomenon likely occurs through corollary discharge signals, which allow us to distinguish between events that occur in the environment and those produced by one’s own body (Ford et al., 2001; Crapse and Sommer, 2008). This process may be disrupted in individuals with autism spectrum disorder (ASD) and misophonia, conditions involving altered sensory and social processing. Impaired distinction between self and other could cause an altered sense of agency over socially produced sounds, potentially leading to intolerance of social sounds when a lack of control is experienced. Here, we use a self-agency sound paradigm to test for differences in neural processing of self- and socially- generated sounds in individuals with ASD, misophonia, and typical development (TD). Participants and Methods: High-density electroencephalogram (EEG) was used in adults with ASD (n=59), misophonia (n=36) and TD (n=41) during an agency task, which consisted of 200 trials with four blocks: self-generated, computer-generated, socially-generated, and motor control. In each block, participants heard tones every 2-seconds, produced either by themselves via button-press (self block), by the computer (computer block), or by an adjacent experimenter (social block), and a motor control block. Mean amplitudes of the N1 responses (i.e., negative deflection at 100ms) to tones were extracted from the Cz central electrode for each condition. We hypothesized that individuals with either ASD or misophonia would show altered suppression of self vs social signals. One-way ANOVA investigated group differences in self-suppression of N1 responses (self minus social). Follow-up ANOVAs tested for group differences in N1 response in each block; Tukey post-hoc t-tests were used for significant effects. The broad autism phenotype questionnaire (BAPQ) assessed ASD symptoms, and linear regression investigated the relationship between ASD symptoms and N1 amplitudes. All analyses controlled for age, sex, and perceived socioeconomic status. Results: There was a significant main effect of group on N1 self-suppression (F=5.33, p=0.006), such that individuals with ASD showed decreased self-suppression compared to TD individuals (t=3.26, p=0.004). Follow-up tests by condition showed a significant main effect of group on mean N1 amplitude in the socially-generated block (F=4.58, p=0.013), such that the ASD group showed decreased social N1 responses compared to TD individuals (t=-2.53, p=0.034) and those with misophonia (t=-2.44, p=0.043). Across all groups, decreased social N1 responses correlated with greater ASD symptoms (t=2.39, p=0.019). There were no group differences in N1 amplitude in the self-generated block (F=1.76, p=0.18). Conclusions: These results suggest that early sensory responses to socially-generated sounds are disrupted in ASD but not in misophonia, a clinical control group also characterized by hypersensitivity to social sounds. Specifically, the ASD group showed a decreased differentiation between self- and socially-generated sounds, and reduced N1 responses to social sounds were associated with increased ASD symptoms across all groups. These results support the idea that an altered sense of agency may contribute to impaired social and sensory cognition in ASD and may provide potential neural mechanisms underlying these deficits.

Poster

02/15/2024
12:00 pm - 01:15 pm
Room: Shubert Complex (Posters 1-60)

Poster Session 04: Neuroimaging | Neurostimulation/Neuromodulation | Teleneuropsychology/Technology

Final Abstract #20

Differential Neural Processing of Socially Generated Sounds in Autism Spectrum Disorder and Misophonia

Alissa Chen, Icahn School of Medicine at Mount SInai, New York, United States
Jeanpierre Tenesaca, Icahn School of Medicine at Mount Sinai, New York, United States
Sarah Banker, Icahn School of Medicine at Mount Sinai, New York, United States
Jadyn Trayvick, Icahn School of Medicine at Mount Sinai, New York, United States
Arabella Peters, Icahn School of Medicine at Mount Sinai, New York, United States
Abigaël Thinakaran, Icahn School of Medicine at Mount Sinai, New York, United States
Xiaosi Gu, Icahn School of Medicine at Mount Sinai, New York, United States
Jennifer Foss-Feig, Icahn School of Medicine at Mount Sinai, New York, United States
Daniela Schiller, Icahn School of Medicine at Mount Sinai, New York, United States

Category: Neurophysiology/EEG/ERP/fMRI

Keyword 1: autism spectrum disorder
Keyword 2: neurocognition
Keyword 3: auditory processing disorder

Objective:

Previous research has shown that people tend to suppress neural responses to self-generated sounds versus externally-generated sounds. This phenomenon likely occurs through corollary discharge signals, which allow us to distinguish between events that occur in the environment and those produced by one’s own body (Ford et al., 2001; Crapse and Sommer, 2008). This process may be disrupted in individuals with autism spectrum disorder (ASD) and misophonia, conditions involving altered sensory and social processing. Impaired distinction between self and other could cause an altered sense of agency over socially produced sounds, potentially leading to intolerance of social sounds when a lack of control is experienced. Here, we use a self-agency sound paradigm to test for differences in neural processing of self- and socially- generated sounds in individuals with ASD, misophonia, and typical development (TD).

Participants and Methods:

High-density electroencephalogram (EEG) was used in adults with ASD (n=59), misophonia (n=36) and TD (n=41) during an agency task, which consisted of 200 trials with four blocks: self-generated, computer-generated, socially-generated, and motor control. In each block, participants heard tones every 2-seconds, produced either by themselves via button-press (self block), by the computer (computer block), or by an adjacent experimenter (social block), and a motor control block. Mean amplitudes of the N1 responses (i.e., negative deflection at 100ms) to tones were extracted from the Cz central electrode for each condition. We hypothesized that individuals with either ASD or misophonia would show altered suppression of self vs social signals. One-way ANOVA investigated group differences in self-suppression of N1 responses (self minus social). Follow-up ANOVAs tested for group differences in N1 response in each block; Tukey post-hoc t-tests were used for significant effects. The broad autism phenotype questionnaire (BAPQ) assessed ASD symptoms, and linear regression investigated the relationship between ASD symptoms and N1 amplitudes. All analyses controlled for age, sex, and perceived socioeconomic status.

Results:

There was a significant main effect of group on N1 self-suppression (F=5.33, p=0.006), such that individuals with ASD showed decreased self-suppression compared to TD individuals (t=3.26, p=0.004). Follow-up tests by condition showed a significant main effect of group on mean N1 amplitude in the socially-generated block (F=4.58, p=0.013), such that the ASD group showed decreased social N1 responses compared to TD individuals (t=-2.53, p=0.034) and those with misophonia (t=-2.44, p=0.043). Across all groups, decreased social N1 responses correlated with greater ASD symptoms (t=2.39, p=0.019). There were no group differences in N1 amplitude in the self-generated block (F=1.76, p=0.18).

Conclusions:

These results suggest that early sensory responses to socially-generated sounds are disrupted in ASD but not in misophonia, a clinical control group also characterized by hypersensitivity to social sounds. Specifically, the ASD group showed a decreased differentiation between self- and socially-generated sounds, and reduced N1 responses to social sounds were associated with increased ASD symptoms across all groups. These results support the idea that an altered sense of agency may contribute to impaired social and sensory cognition in ASD and may provide potential neural mechanisms underlying these deficits.