Neural activity is altered by childhood trauma exposure and varied by sex in typically developing youths during sustained attention-to-response tasks (SART)

Abstract

It is well recognized that adults with exposure to childhood traumas are at risk of developing psychopathology and executive dysfunction. However, how these executive function deficits emerge following trauma exposure has not been widely examined. We hypothesized that children exposed to a higher number of early childhood traumas would show reduced amplitude and longer latency in cortical response in executive brain regions during tasks requiring sustained attention and inhibition, compared to children with fewer or no such experiences. We report data from sixty-five typically developing youths 9–15 years of age who self-reported exposure to childhood traumatic events, not including abuse. Brain signals were recorded with magnetoencephalography (MEG) while the sustained attention-to-response task (SART) task was performed. Task-activated sources were localized, and we investigated brain function by measuring amplitude and latency of task-evoked cortical response in frontal and parietal cortices with repeated-measures analysis of variance. A significant (p < 0.05) main effect revealed higher amplitude in low-trauma compared to high-trauma groups in ventral anterior cingulate cortex and superior parietal cortex. Further, significant three-way interactions (trauma/hemisphere/peaks) were found in amplitude of superior parietal cortex and response latency of precentral cortex during the correct No-Go condition, and simple effect analysis showed significantly shorter latency in the high-trauma group in right precentral cortex at P1. Significant interactions of trauma with sex and hemisphere were revealed in multiple pre-selected regions, such that high exposure to trauma affected cortical processing in male and female groups differently. The results may explain sex-specific vulnerability and risks of exposure to childhood trauma with increased susceptibility to psychopathology in adulthood.

1. Introduction

High rates of exposure to frightening and life-threatening events among children lead to a dynamic interaction between emotion and cognition that may cause increased vulnerability to anxiety, depression, impulsivity, and post-traumatic stress disorder (PTSD) which are major public mental health concerns (Hayes et al., 2012; Morey et al., 2016). Several stress-related events, such as natural disasters, war-related stress, severe accidents, sexual abuse, terrorist attacks, and mental or physical assault can lead to functional alterations in the brain (Shim et al., 2017; Dossi et al., 2020). Stress-related disorders in adolescence are often misdiagnosed or undetermined due to a lack of childhood trauma exposure history, limited diagnostic assessments, or application of adult PTSD criteria (Sheynin et al., 2020). Early childhood psychological trauma requires specific diagnostic markers, early intervention, and effective treatment to prevent secondary disabilities (substance abuse, personality disorder, and PTSD-related psychopathology) (KAMINER et al., 2005). Trauma-related psychological effects are usually demonstrated by clusters of symptoms including re-experiencing through intrusive memories, avoidance of appalling reminders, chronic hyperarousal, and hypervigilance towards potential threats of surroundings (Bremner et al., 2004; Shim et al., 2017). Prior studies demonstrated sex-specific differences in the prevalence of anxiety, and depression in individuals with traumatic experiences that have an association with worsening symptoms of dissociation and experience difficulties in executive or inhibitory control function (Melara et al., 2018; Breslau et al., 1997). Furthermore, trauma exposure may cause an alteration of neuro-cognitive maturation that regulates the response to fear, emotions, memory, attention, and executive functions that affect social interaction, personal intelligence, working skills, and perceptual judgment in daily life (Selemon et al., 2019; Hayes et al., 2012). Youths who are exposed to a range of traumatic events in early life are more susceptible to developing mood disorders or PTSD in adulthood which also may include poor concentration, sleep disturbances, and excessive vigilance to potential threats (Kaminer et al., 2005). Veterans who reported a history of interpersonal early-life trauma showed significant impairments in sustained attention and poor inhibitory control (Fortenbaugh et al., 2017; Falconer et al., 2008). By examining cortical activation patterns in adolescents during a sustained attention and inhibitory control task, our study offers valuable insight into how trauma exposure may disrupt normative neurodevelopment during a critical period of maturation of executive function. In addition, it allows for the early identification and interventions that may reduce the effects of stress and anxiety on the development of cognitive functions, which in turn helps to prevent cognitive and psychological disturbances like poor inhibition, substance abuse, suicidal tendencies, and domestic violence in adult life.

Recent neuroimaging studies in adolescents have demonstrated that cortical maturation during this stage is closely tied to improvements in executive function, yet this developmental trajectory also renders the adolescent brain particularly vulnerable to environmental stressors such as trauma (Son et al., 2023; Fortenbaugh et al., 2017; Lewis et al., 2017). In the present study, we strategically selected brain regions based on prior literature highlighting structural and functional abnormalities associated with trauma exposure and performance of a Go/No-Go task. Specifically, we focused on the anterior cingulate cortex, prefrontal cortex, and parietal cortex, all of which play critical roles in executive function but are also impacted by fear processing, emotional regulation, and stress-related memory formation (Funahashi, 2017; Hampshire et al., 2010; Selemon et al., 2019). Hyperarousal and hypervigilance are the most common features of stress-related disorders and may involve the activation of prefrontal cortex and parietal cortex that control the visuospatial function of stressful memories (Bremner et al., 1999). Functional studies elucidate the cortical network of cognitive processing and demonstrate that stress-related functional changes of the prefrontal, anterior cingulate cortex, and parietal cortex may be responsible for difficulties in inhibitory control, visuospatial memory, and attention processing in individuals with past trauma exposure (Bremner, 2006; Arnsten et al., 2015). Executive control areas play a key role in neural communication of planning of response, inhibition, and preparation of action to potential threatening provocation. Several meta-analysis studies found a positive correlation between general trait impulsivity and childhood maltreatment, which provides evidence of primary deficits in cognition with poor regulatory and adaptive inhibitory functioning in individuals with early life stress (Karl et al., 2006; O’Doherty et al., 2015; Zhai et al., 2019). The limbic region of the brain plays a critical role in regulating the emotions related to traumatic events, which is also involved in the processing and storage of stressful memories as traumatic reminders and causes long-lasting effects on cognition and executive function (Bremner, 2006; Shin et al., 2004). There is controversy about structural deficits associated with trauma exposure, several studies have demonstrated loss of volume in the hippocampus, prefrontal cortex, amygdala, and anterior cingulate cortex associated with PTSD (Karl et al., 2006; O’Doherty et al., 2015) although other studies have not found changes of volume in the hippocampus and other regions (Yehuda et al., 2007; Woodward et al., 2006).

In our study, we examined the task-evoked cortical response as measured with magnetoencephalography (MEG) in the prefrontal, anterior cingulate, and parietal cortex during performance of the sustained attention-to-response task (SART). Impairment in sustained attention in PTSD has been reported in previous research, which provides evidence of reduction of frontal cortex activation and abnormal changes of parietal cortex activity during exposure to mimicking stressful psychological trauma (Bremner et al., 2004; Falconer et al., 2008; Dossi et al., 2020). Early life trauma exposure might have an impact on various domains of cognitive behavior, including poor inhibitory control and attention disturbance that may be revealed by abnormal electrophysiological signatures in the frontoparietal cortex as well as alteration of cortical arousal and excitability (Aupperle et al., 2012; Fortenbaugh et al., 2017). There is growing evidence that exposure to traumatic events during a sensitive period of brain development alters neural and cognitive functioning and leads to difficulties in executive performance, inhibition, and attention (Melara et al., 2018). However, there are limited studies specifically examining the effects of trauma, unrelated to abuse or neglect, on cortical alterations in youth populations. Addressing this gap, our study aims to capture trauma-associated neuro-cortical changes during this critical developmental window, with the goal of informing strategies for early identification and intervention.

SART assesses a quantitative subdomain of executive functions requiring participants to inhibit motor responses to infrequent rare targets (No-Go stimuli) and execute motor responses to frequent common targets (‘Go’ stimuli), which are designed to measure the accuracy and repetitive conscious processing of habituation and distraction to stimuli (Wilson et al., 2018). An individual’s ability to sustain attention and maintain inhibitory control is determined by response inhibition errors which are the sum of failures to withhold motor responses to ‘NO-GO’ stimuli (i.e., Commission errors), and attention processing errors which are a failure to continue to respond to repetitive ‘Go’ stimuli (i.e., errors of omission) (Xiao et al., 2015; McMackin et al., 2020). Marshall et al. and Zhai et al. have reported poorer accuracy on inhibition in behavioral performance and significantly altered function of inhibitory control circuits (anterior cingulate cortex) in fMRI during the performance of inhibitory tasks in individuals with a history of childhood traumatic experience (Marshall et al., 2016; Zhai et al., 2019). This study offers valuable insights into the temporal dynamics of cortical activation and processing speed associated with stress sensitivity in the prefrontal, anterior cingulate, and parietal cortices during inhibitory control tasks among individuals with and without childhood trauma exposure. While later components such as the P300 have traditionally been emphasized in studies of inhibitory control (Bourisly and Pothen, 2016; Hart et al., 2012; Luo and Zhang, 2020), emerging evidence underscores the critical role of early sensory processing in modulating attentional engagement and inhibitory functions (Oken et al., 2006; Tan et al., 2024), particularly in adolescent populations (Baijot et al., 2017; Jetha et al., 2021). Informed by prior work on the SART (Pinner et al., 2023; Dang et al., 2018), we employed a broad temporal window to capture three key event-related potential components: P1 (100–200 ms), reflecting early sensory-perceptual and attentional processes; P2 (200–350 ms), associated with early cognitive evaluation; and P3 (350–550 ms), linked to decision-making and response inhibition. This comprehensive temporal framework enhances the interpretability of trauma-related neural differences, shedding light on their timing and functional relevance within core cognitive control regions.

Several published studies documented that females tend to have disproportionately higher rates of mood disorders and experience increased chronicity and severity of psychological symptoms compared to males (Breslau et al., 1997) (Ramikie and Ressler, 2018). Male and female neurophysiology develop under the influence of different hormonal exposures which cause significant changes between males and females in terms of socialized perception and interaction with the world (Birkeland et al., 2017; Ramikie and Ressler, 2018). Females disproportionately experience several psychiatric disorders including anxiety, depression, emotional disorders, and bipolar disorder (Li et al., 2018) relative to males. This potential variation by sex has led us to investigate possible sex differences in cortical function during the performance of the SART in these youths with exposure to traumatic events.

This investigation is among the first to use the high temporal resolution of magnetoencephalography (MEG) to examine whether children with high versus low levels of non abuse-related trauma exposure exhibit different patterns of brain activity during a Go/No-Go task. We hypothesized that children exposed to a greater number of early life traumas would show reduced amplitude and prolonged latency of cortical responses in executive regions during the sustained attention to response task (SART), relative to their low-trauma counterparts. Our approach was informed by previous findings on SART (Pinner et al., 2023) (Gool et al., 2020), which highlight the involvement of early (P1, P2) and late (P3) components in attentional control and inhibitory processing. Accordingly, we focused on executive and inhibitory control networks, including the prefrontal cortex (PFC), anterior cingulate cortex (ACC), pre-central cortex (PCC), and superior parietal cortex (SPC). We further anticipated that these trauma-related effects would differ by sex, potentially reflecting sex-specific neurodevelopmental trajectories following early stress exposure. In line with our hypotheses, we found that children in the high-trauma group exhibited reduced amplitude of neural responses in key executive control regions, the anterior cingulate cortex (ACC), and superior parietal cortex (SPC). Interestingly, we observed significantly faster latencies in the high-trauma group during the early P1 window in precentral cortex, a finding that deviates from the typical neurodevelopmental impairment pattern of delayed latencies and may suggest heightened early sensory reactivity or hypervigilance. Our results provide compelling evidence of trauma-induced alterations in both the amplitude and timing of neural responses during cognitive control. These findings underscore the impact of early adversity on brain function and highlight the critical need for early, trauma-informed intervention strategies in vulnerable youth populations.

2. Materials and methods

2.1. Participants and study group

Typically developing youths in the age range of 9–15 years were enrolled as a part of the Developmental Chronnecto-Genomics (Dev-CoG) study, which is a large multimodal, longitudinal study on the developing brain that recruited 200 participants (Stephen et al., 2021). The goal of the study was to examine data obtained by behavioral and emotional performance scales, MEG, MRI (structural, functional, and diffusion), and neuropsychological assessment of typically developing youths. In this experiment, we processed and reported MEG data from 65 participants among them 31 females and 34 males who returned for the second year of the DevCog study at the New Mexico site and completed the entire visit including the SART. The participants were recruited based on our study inclusion and exclusion criteria from the local communities in Albuquerque, New Mexico through flyer distribution, advertisement, and presentations at different community events. The inclusion criteria were that the participant was between 9 and 14 years of age at study enrollment and typically developing. The exclusion criteria for participants were: unable to consent/assent, history of any known neurological or developmental disorder, current use of any psychotropic medications or substance abuse, failure to meet the MRI screening criteria, or an individual education plan (IEP) for developmental delay. Written informed consent was obtained from a parent of each participant and formal assent was completed by participants before starting the study procedures. All study protocols were approved by an accredited institutional review board (Advarra IRB) and carried out in accordance with the Declaration of Helsinki.

2.2. Questionnaires for symptoms and history of trauma exposure

To assess the exposure to or experience of past traumatic events, participants were asked to complete a modified version of the UCLA Trauma History Profile (THP) which excluded the physical and sexual abuse history questions on request of the IRB (Hooper et al., 2011; Steinberg et al., 2004). Participants were also asked to complete the self-report Trauma Symptom Checklist for Children (TSCC) which was designed to evaluate the state of posttraumatic stress and severity of psychological symptomatology associated with traumatic experiences in children ages 8–17 years (Brier, 1996). Participants reported the frequency of occurrence of a variety of trauma-related symptoms using a scale ranging from 0 (“never”) to 3 (“often”). This screening questionnaire is composed of six subscales, including anxiety (ANX), depression (DEP), anger (ANG), posttraumatic stress (PTS), overt (DIS-O), and fantasy (DIS-F) dissociation. We used the raw score from each symptom item. A history of experiences with a variety of traumatic events (more than 2 exposures) indicates higher rates of trauma exposure and a score of less than 2 is often considered to represent low trauma exposure (Steinberg et al., 2013).

2.3. Sustained attention to response task (SART)

A Go/No-Go task was designed to test the deficits of attention and inhibitory function related to traumatic experiences in these youth participants. Before initiating the task, the task was explained to each participant. They were allowed to practice the task to ensure they understood the task instructions. The random version of SART was displayed on a screen placed in front of participants, 1 m from the nasion. The required response is to press a button to frequent (Go) stimuli and withhold the response to unexpected, rare target (No-Go) stimuli (Robertson et al., 1997). Digits 1 to 9 were presented in random order and participants were instructed to press a button with their index finger in response to every number except the number ‘3’ (i.e., No-Go stimuli) (Fig. 1). On each trial, a blank fixation screen was presented for 280 ms to hold the participant’s gaze followed by a presentation of a random digit 1–9 for 150 ms, then, a blank screen appeared for 670 ms. The total duration of each trial was 1100 ms. There was an equal probability of presenting each number with an 11 % probability for the frequency of the No-Go stimulus. The task duration was 15 min, resulting in 945 trials (105 trials/digit) for each participant.

Fig. 1.

Random SART paradigm: a blank fixation screen was presented for 280 ms to hold the participant’s gaze towards the presentation screen and the digits 1 to 9 were presented independently in random order for 150 ms and participants were instructed to press a button with their index finger in response to every number except number ‘3’ (i.e., No-Go stimuli). Only for visualization, green circular stimuli represent “press the button” and red colored X indicates “Withhold button press”; the circle and X were not presented on the screen.

2.4. MEG data acquisition

Neuromagnetic data were recorded during the performance of the SART using the whole-cortex 306 channel MEGIN MEG system within a magnetically shielded room (Vacuumschmelze – Ak3B) at the Mind Research Network in Albuquerque, New Mexico. MEG data were collected at a sampling rate of 1000 Hz with an online 0.01 Hz high-pass filter and a 300 Hz anti-aliasing filter. Prior to MEG data collection, two sets of standard bipolar electrodes were placed to capture the electrocardiogram (ECG two-channels-bilaterally on the left and right clavicle) and electrooculogram (EOG two-channels- just above the left eye and lateral to the outer canthus of the right eye) to monitor the artifact from heartbeat and eye blinks/eye movement, respectively. The head position indicator (HPI) coils were placed on both mastoid bones and the fore-head along the hairline to obtain information on head shape/size and head coordinate system relative to the MEG sensors. HPI monitoring enables recordings of head position continuously throughout the MEG scan and is used to correct for head movement during the scan. A three-dimensional Polhemus 3-D tracking device was used to digitize the location of these HPI coils along with three fiducial points (left-right preauricular and nasion) to define the head-centered coordinate system in addition to points around the scalp surface. These points were used to optimize the co-registration of the MEG data to the structural MRI images.

2.5. Magnetic resonance imaging data collection

Structural T1-weighted MRI images were acquired using a Siemens 3T Trio Tim scanner with a 32-channel head coil at the Mind Research Network, Albuquerque, NM. A multi-echo 3-dimensional magnetization-prepared rapid gradient echo (MPRAGE) sequence was used with the following parameters; echo time of 1.9 ms, repetition time 2400ms, 8° flip angle, voxel size 1.0 × 1.0 × 1.0 mm³, the field of view 256 mm and 5 min 46 s for data acquisition time. Structural MRIs were collected from all participants for use in estimating the MEG source locations. We used an auto-analysis pipeline employing Freesurfer (http://surfer.nmr.mgh.harvard.edu) to reconstruct the cortical surface from the MPRAGE sequence for the automatic segmentation of scalp, skull, and cortical surfaces for use in creating subject-specific head models for each participant for MEG source analysis.

2.6. Data analysis

2.6.1. MEG preprocessing and sensor space analysis

MEG raw data were preprocessed using Neuromag Max-Filter Max Move software (Neuromag, 2010) to eliminate the primary artifacts such non-physiological noise and to correct for head motion. After Maxfilter preprocessing, the MEG data were loaded into Brainstorm (https://neuroimage.usc.edu/brainstorm/Tutorials), and eyeblinks and cardiac events were removed from the MEG sensor waveform by using signal space projectors based on the EOG and ECG signals, respectively. The data were notch-filtered at 60 Hz and the harmonics to remove line noise. Epochs were extracted from the continuous recording based on task stimulus and responses from both ‘Go’ and ‘No-Go’ stimuli, which were divided into two separate conditions correct/incorrect depending on accuracy to observe the cortical function during successful or unsuccessful inhibition of response during the Go/No-Go task. Once trials were categorized into the relevant conditions, data were signal averaged to produce the averaged evoked responses for each condition. Epochs were defined as 100 ms prior to the onset of the stimulus to 700 ms after the onset of the stimulus for the signal-averaged waveforms.

2.6.2. Source analysis

Source localization was performed using dSPM as implemented in the Brainstorm toolbox (Tadel et al., 2019). The overlapping spheres head model based on the inner skull surface was generated using the co-registration of MEG to the individual MRI. The local curvature of the skull was determined based on the Freesurfer-extracted skull. The minimum norm estimate was applied to estimate brain-evoked fields separately for the correct and incorrect, Go and No-Go trials. Noise covariance was estimated from baseline (−100–0ms) data. After source localization using each subject’s head model, the source data were low-pass filtered at 32 Hz and the cortical activation maps were z-transformed relative to baseline and converted to absolute values to minimize cancellation across participants. These cortical maps were then transformed to a simplified version of the ICBM152 MNI template and spatial smoothing of 3 mm was applied. Regions of interest (ROI), including left and right medial orbitofrontal cortex (MOFC), lateral orbitofrontal cortex (LOFC), superior parietal cortex (SPC), precentral cortex (primary motor cortex), pars opercularis, and anterior cingulate cortex (dorsal and ventral), were selected from Desikan -Killiany atlas based on prior evidence of source activation during SART (Gool et al., 2020; Falconer et al., 2008; Pinner et al., 2023), (Fig. 2). We selected three distinct time windows—P1 (100–200 ms), P2 (200–350 ms), and P3 (350–550 ms) to extract peak latency and amplitude measures based on our prior study examining children in a similar age range of 8–12 years (Pinner et al., 2023). We confirmed that the time windows from the prior sample matched well with the current sample by inspecting the prominent peaks in the group-averaged time courses for each region of interest (ROI), which were obtained using Brainstorm. The average time courses were computed across all participants and task conditions, and custom MATLAB scripts were used to systematically identify the most prominent peaks within physiologically relevant temporal ranges.

Fig. 2. Regions of interest (ROIs) were chosen a priori from the Desikan-Killiany atlas and the peak amplitude and latency were extracted based on the source analyzed dSPM estimate;

Left and right medial orbitofrontal cortex (MOFC), lateral orbitofrontal cortex (LOFC), superior parietal cortex (SPC), precentral cortex (PCC), parsopercularis, caudal anterior cingulate cortex (dorsal ACC) and rostral anterior cingulate cortex (ventral ACC).

2.6.3. Classification of high and low trauma group based on traumatic events

For our analysis, all youths who reported exposure to 2 or more traumas (n = 38) composed the high trauma group, and all youths who reported no exposure or exposure to 1 trauma (n = 27) composed the low trauma group (Rodriguez et al., 2025). TSCC scores of PTSD-related symptoms and trauma history of high/low trauma groups are provided in Table 1, with significant group differences noted.

Table 1.

TSCC scores of PTSD-related symptoms and trauma history profile between high/low trauma groups.

Variables for TSCC and THP	Low Trauma (Mean ± SD) (N = 27)	High Trauma (Mean ± SD) (N = 38)	P-value
ANX (TSCC)	4.59 ± 2.89	7.21 ± 4.20	0.006*
DEP (TSCC)	3.11 ± 2.11	5.84 ± 3.60	0.0008*
ANG (TSCC)	3.03 ± 3.01	8.28 ± 5.16	0.000002*
PTS (TSCC)	4.48 ± 2.80	10.02 ± 6.23	0.000003*
DIS (TSCC)	4.81 ± 2.90	9.052 ± 5.13	0.0002*
DIS-O (TSCC)	2.77 ± 2.04	5.736 ± 3.64	0.00035*
DIS-F (TSCC)	2.03 ± 1.60	3.31 ± 1.96	0.0066*
Under-Reporting (TSCC)	3.59 ± 2.46	1.79 ± 2.04	0.065
Hyper-Reporting (TSCC)	0.07 ± 0.00	0.29 ± 0.56	0.072
Trauma categories (THP)	0.481 ± 0.50	3.73 ± 0.50	0.00005*

Anxiety (ANX), depression (DEP), anger (ANG), posttraumatic stress (PTS), and dissociation (DIS): overt dissociation (DIS -O) and fantasy (DIS-F).

^*p < 0.05.

2.6.4. Statistical analysis

To address our primary objective—examining how early trauma exposure influences cortical responses during sustained attention and inhibition—we categorized participants into low- and high-trauma groups based on the number of trauma experiences reported (Rodriguez et al., 2025). We conducted independent samples t-tests on demographic variables (e.g., age, socioeconomic status) to assess group differences.

For our main analysis, we used repeated-measures ANCOVA (RM-ANCOVA) to examine differences in cortical responses during SART performance. While trauma exposure and sex were included as between-subject factors in line with our study aims, hemisphere and peak were modeled as within-subject factors to capture potential lateralization effects and temporal dynamics in cortical activation patterns. Age was included as a covariate to account for developmental variability in brain function, which is critical in pediatric samples (Tan et al., 2024). Peak amplitude and latency were extracted from three predefined time windows—P1 (100–200 ms), P2 (200–350 ms), and P3 (350–550 ms)—from each participant’s time course within each region of interest (ROI). To assess the main effects and interactions of trauma exposure and sex on SART-related neural activity across hemispheres and time windows, we conducted a series of three-way repeated-measures ANCOVAs with the following factors: trauma group (low vs. high), hemisphere (left vs. right), and time window (P1, P2, P3). To explore interaction effects between trauma and sex across hemispheres, we conducted additional three-way ANCOVAs (trauma × sex × hemisphere) separately for each time window and ROI. Significant group differences are reported individually by time window.

Finally, we performed Pearson correlation analyses to evaluate the relationship between socioeconomic status (SES) and task-related cortical responses. We adjusted the significant p-values for multiple comparisons by the false discovery rate (FDR) correction (Pike, 2011). Significant group differences were assessed via the chi-square test for significant contrasts in proportions between groups for gender and trauma. IBM SPSS version 28 software was used to perform all statistical analyses and the significant alpha level was set at corrected p < 0.05.

3. Result

3.1. Participant demographics

We collected MEG data during the SART task from 88 participants who returned for the second year of the DevCog study. However, we were not able to report and process data from all participants due to missing MRI data (N = 8), a recent diagnosis of ADHD (N = 4), an incomplete MEG scan (N = 4), extreme motion artifacts (N = 5) or poor MEG data quality (N = 2). The final sample of sixty-five participants was divided into two groups based on trauma exposure. Statistical chi-square analysis revealed groups were well matched in gender (p = 0.78) and the t-tests revealed there were no significant group differences in age (p = 0.612) or SES (p = 0.678) between high and low trauma-exposed groups. We also performed analyses with age and SES as covariates but we did not observe any significant association of these covariates with the cortical response or any factors of interest. Participants’ demographic information and statistical results are described in Table 2.

Table 2.

Participant demographic information.

Subjects/variables	Low trauma (N = 27)	High trauma (N = 38)	P-value
Age (mean)	13.05 years (SD = 1.69)	12.82 years (SD = 1.94)	0.612
Male (34)\Female (31) (% male)	16M\11F (59.4 % male)	18M\20F (47.36 % male)	0.58
SES (mean)	42.64 (out of 66)	44.03 (out of 66)	0.678
Race	White (21)\Native American (6)	White (33)\ Native American (3)\African American (2)
Ethnicity	Non-Hispanic (17)\ Hispanic or Latino (10)	Non-Hispanic (23)\ Hispanic or Latino (15)

SES (socioeconomic status), (P > 0.05).

3.2. Behavioral performance of SART

We measured each participant’s behavioral performance for reaction time (RT), Go/No-Go correct and incorrect hit, and error rate. Behavioral outcomes were compared between the high/low trauma groups and male/female participants using an independent t-test including Pearson correlation to potential associations between RT and error rate with cortical responses.

There were no significant group differences observed in behavioral performance of SART between trauma groups, although the high trauma group showed a higher number of commission errors for correct responses compared to the low trauma group (Table 3). Behavioral data between female and male participants showed significant differences in the performance of SART in overall reaction times (RT) (Table 3). There were significantly shorter reaction times in females compared to male participants in both trauma groups (Fig. 3) and fewer omission errors (hit rate), but no significant difference in commission errors between males/females (Table 3).

Table 3.

Differences in SART Behavioral performance by trauma group and sex.

Variables	Low Trauma (N = 27)	High trauma (N = 38)	P-value
Correct Go (Hit rate in percentiles)	77.5 %	80.23 %	0.52
Commission Errors (percentile)	58.68 %	62.42 %	0.2
Overall RT (Mean ± SD)	397 ± 98ms	394 ± 70ms	0.9
Variables	Female (N = 30)	Male (N = 35)	P-value
Correct Go (Hit rate in percentiles) (Mean ± SD)	83.21 %	75.47 %	0.05*
Commission Errors (percentile)	62.68 %	60.42 %	0.3
Overall RT (Mean ± SD)	368 ± 74ms	419 ± 84ms	0.01*

RT = reaction time (ms) for Correct Go trial, SD = standard deviation.

Fig. 3.

Reaction time differences (in milliseconds) during SART performance by sex (F = female, M = male) and trauma group (high vs. low). Females demonstrated significantly shorter reaction times than males (p = 0.01), independent of trauma exposure. Error bars represent the standard error of the mean (SEM).

3.3. Changes in task-based cortical activation between high and low trauma groups

We measured the effects of trauma exposure on cortical processing during the performance of SART by examining evoked response peak amplitude and peak latency in the right/left prefrontal, precentral cortex, anterior cingulate cortex, and superior parietal cortex for each condition (Go correct, No-Go correct, and No-Go incorrect) including 3 peaks from selected time windows as between subjects’ factors. We calculated the maximum prominent peaks of the P1 (100–200ms), P2 (200–350ms), and P3 (350–550ms) complex for each region of interest (Fig. 4).

Fig. 4. A and C show activation of cortical areas during performance of SART:

A. left ventral ACC and left medial orbitofrontal cortex; C. lateral and medial orbitofrontal cortex. (prominent red color denoting higher activation relative to pre-stimulus baseline) and B. and D. exhibit simple main effect of trauma on the response time course of 65 participants (Blue = averaged time course from 27 participants of low trauma group, Shaded blue = SEM (standard error of the mean) of the time course of low trauma group and red = averaged timecourse from 38 participants of high trauma group, shaded red = SEM of the time course of high trauma group) from left ventral ACC (B.) and right medial orbitofrontal cortex (D.) during Correct Go trials. In each condition, the peak latency (S) was determined as the time when the response amplitude (arbitrary units) was maximal within the specified time windows P1 (100–200ms), P2 (200–350ms), and P3 (350–550ms) for each participant.

3.4. The main effect of trauma on cortical responses

In line with our a priori hypothesis, we observed a significant main effect of trauma exposure on cortical activation patterns across hemispheres (left, right) and time windows (P1: 100–200 ms, P2: 200–350 ms, P3: 350–550 ms). A three-way repeated-measures ANCOVA was conducted to examine the influence of trauma exposure on peak latency and amplitude, with hemisphere and peak time window as within-subject factors and trauma group as a between-subject factor for each region of interest (ROI). Cortical amplitude from the ventral anterior cingulate cortex (vACC) showed a significant main effect of trauma during Go-Correct trials. Post hoc analysis revealed significantly reduced amplitude in the high-trauma group (7.34 ± 0.7, Mean ± SEM) compared to the low-trauma group (10.27 ± 0.8, Mean ± SEM), F (1,63) = 6.44, η² = 0.093, adjusted p = 0.027* (FDR corrected; Fig. 5). Additionally, the superior parietal cortex showed a significant main effect of trauma during incorrect No-Go trials. Participants in the low-trauma group displayed significantly higher cortical amplitudes (4.9 ± 0.2, Mean ± SEM) compared to those in the high-trauma group (3.61 ± 0.2, Mean ± SEM), F (1,62) = 4.66, η² = 0.083, adjusted p = 0.041* (FDR corrected; Fig. 5). No other post hoc comparisons from the repeated-measures ANCOVA survived FDR correction.

Fig. 5.

Significant main effects (ANCOVA) of trauma exposure on cortical amplitude across hemispheres (left, right) and time windows (P1: 100–200 ms, P2: 200–350 ms, P3: 350–550 ms) during the SART task. The ventral anterior cingulate cortex (vACC) showed significantly reduced cortical amplitude in the high-trauma group during Go-Correct trials. Similarly, the superior parietal cortex exhibited significantly lower activation in the high-trauma group during incorrect No-Go trials. Group differences were significant at p < 0.05 (FDR-corrected). Error bars represent standard error of the mean (SEM).

3.5. Three-way interaction with trauma group, hemisphere, and time window (P1-P2-P3)

We assessed three-way interaction in SART response latency and amplitude for trauma consisting of 2 groups (low and high trauma) X hemisphere (right and left) X peak time windows with three levels (P1, P2, P3 time-windows) for each condition and ROI. We found a significant interaction of the trauma group with hemispheres and peak time windows in cortical amplitude from the superior parietal cortex during correct NoGo condition, F (1,62) = 4.87,η2 = 0.133 p = 0.027* (FDR corrected) (Fig. 6). Simple main effect analysis revealed multiple statistical group differences in peak latency and amplitude of cortical activities throughout the cognitive and inhibitory cortical network across the selected time windows. Therefore, all reported p values are adjusted with false discovery rate (FDR) for multiple comparison correction and most of the p-values did not survive FDR correction. The simple effect analysis (independent t-test) revealed no significant differences between the trauma group in amplitude from the right and left superior parietal cortex. Furthermore, a three-way interaction was found for response latency for the trauma group, hemisphere, and peak time windows in the precentral cortex during correct NoGo condition, F (1,62) = 4.92,η² = 0.133, p = 0.038*, (FDR corrected) (Fig. 7). In the time windows 100–200 ms, the simple main effect analysis showed significant differences in response latency in the low trauma group (Mean = 178, SEM = 5.2) compared to the high trauma group (Mean = 161, SEM = 5.2), p* = 0.026 in the right hemisphere, where high trauma group showed shorter latency compared to low trauma group and P1 did not reveal significant differences in left hemisphere between high trauma (Mean = 170, SEM = 4.9) and low trauma (Mean = 175, SEM = 4.9), p = 0.44) (Fig. 7A). We did not identify significant group differences in simple effect analysis at time windows P2 (200–350 ms) or P3 (350–550 ms) in response latency from the superior parietal cortex between high and low trauma groups in the right and left hemispheres.

Fig. 6.

A Significant F (1,62) = 4.87, η² = 0.133, adjusted p = 0.027* three-way interaction (ANCOVA) with trauma, hemisphere, and peak (P1, P2, P3) time windows were identified in cortical amplitude from superior parietal cortex during correct No-Go condition. A, B, and C present the cortical amplitude of high and low trauma groups in left and right hemispheres from P1, P2, and P3 time windows respectively. T-test revealed no significant group differences between high vs low trauma from the left and right hemispheres.

Fig. 7.

A Significant F (1,62) = 4.92, η² = 0.133, adjusted p* = 0.038 three-way interaction (ANCOVA) with trauma, hemisphere, and peak (P1, P2, P3) time windows were identified in cortical response latency from precentral cortex during correct No-Go condition. A, B, and C represent the response latency (s) of high and low trauma groups in the left and right hemispheres from P1, P2, and P3 time windows respectively. p-value *<0.05 = significant. T-test revealed only significant group (low vs high) differences in response latency at P1 time windows in the right hemisphere, high trauma showed significant (p = 0.026) faster latency compared to low trauma group.

3.6. ANCOVA three-way interaction with trauma group, sex, and hemisphere

RM- ANCOVA tests for each peak revealed a significant three-way interaction (trauma group, sex, and hemispheres) for amplitude in the medial orbitofrontal cortex during correct Go condition for the P2 time window F (1,61) = 5.58, η² = 0.089,p = 0.037* (FDR corrected) and the P3 time window F (1,61) = 10.78, η² = 0.15, p = 0.0032* (FDR corrected) (Fig. 8). The male and female youths in our high trauma group tended to have reduced amplitude compared to the low trauma group which was consistent with our initial findings of amplitude differences by trauma group. However, no significant differences are identified between males and females in low trauma and high trauma groups separately (Fig. 8A & b). Additionally, our result also showed a significant interaction with amplitude changes in the superior parietal cortex during correct Go conditions at P1 time window, F (1,61) = 6.29. η² = 0.09, p = 0.040*(FDR corrected), the t-test between males and females of low trauma group showed significant (p = 0.019*) amplitude differences in the left superior parietal cortex (males showed significantly lower amplitude than females). (Fig. 8C).

Fig. 8.

Significant 3-way interaction of trauma, sex, and hemispheres in A. Cortical amplitude from medial orbitofrontal cortex during correct Go P2 time window, B. Cortical amplitude from medial orbitofrontal cortex during correct Go P3 time window, C. Cortical amplitude from Superior parietal cortex during correct Go P1 time window, the T-test between males and females of low trauma showed significant (P = 0.019*) amplitude changes in the left superior parietal cortex (males showed significantly lower amplitude than females). D. Cortical response amplitude from dorsal anterior cingulate cortex during correct Go P3 time window, the male group of high trauma group showed a significantly (p = 0.009*) delayed latency compared to the female group in the right dorsal anterior cingulate cortex. *p< 0.05 significant.

Significant interaction with trauma, sex, and hemisphere was also observed on response latency in the dorsal ACC during the correct Go condition at the P3 time window, where F (1,61) = 5.76, η² = 0.091, p = 0.042* (FDR corrected). The simple effects t-test revealed significant (p* = 0.009) differences of response latency between males and females in the high trauma group in the right dorsal ACC where males showed significantly longer latency compared to females (Fig. 8D).

4. Discussion

Amplitude and latency of evoked responses are the main components that describe event-related fields (ERF) and a reliable measure of cortical activity in perception, attention, inhibition, and cognitive processing during development (Jetha et al., 2021; Sur and Sinha, 2009). Our study investigated the patterns of cortical response in typically developing youths with trauma exposure and identified sex effects on this outcome. Our overall results demonstrated the effect of trauma exposure on cortical network systems that vary by sex and provide evidence of significant alteration in response latency and amplitude in trauma-exposed youths in the frontal and parietal cortex during the performance of SART. Given prior studies (Mahjoory et al., 2019; Ramchurn et al., 2014), we identified the left and right frontal cortex and parietal cortex as our primary regions of interest because the prefrontal and parietal cortex are involved in the processing of cue recognition, selective attention, response inhibition, and implementation of action (Zhou et al., 2016; Selemon et al., 2019). Changes in activity in these cortical areas often result in an impaired ability to control reflexive actions or impulsive behavior (Miller and Cohen, 2001) (Chafee and Goldman-Rakic, 2000).

Our findings that youths with high trauma exposure have decreased neural activation in ACC and superior parietal cortex during Go trials and incorrect No-Go trials compared to low trauma group perhaps indicate that these individuals not only have difficulties with action outcomes but also with the interpretation of real-time inhibition although this was not reflected in a behavioral change. Our study also identified a significant interaction of trauma with hemisphere and peak time windows in response amplitude from the superior parietal cortex and response latency in the dorsal ACC cortex during correct No-Go conditions. In addition, significant latency differences were observed between the trauma group. Follow-up analysis on the interaction with trauma, sex, and hemispheres revealed a significant interaction between trauma and sex on amplitude and latency changes in the prefrontal and superior parietal cortex. This outcome provides evidence that brain responses differ by sex in youths with exposure to traumatic events.

The main effect of trauma exhibits significantly reduced amplitude in our high trauma group compared to the low trauma group in the ventral ACC and superior parietal cortex during processing of both Go and No-Go stimuli. These amplitude differences may be a result of event-related desynchronization of neuronal activation in youths with high trauma exposure, indicating that these youths not only have differences in processing their response outcome itself but also show reduced monitoring of stimuli compared to the age-matched low trauma group (Siems and Siegel, 2020). These analyses also included both hemispheres as components of representing incentive and effortful implementation from the right and left side of the brain, which have been well-defined to study pathological traits of cortical processing and the development of psychological behavior related to trauma exposure (Kostyrka-Allchorne et al., 2019). This reduction of amplitude to target and non-target stimuli is consistent with the results of (Wise et al., 2009; Zhai et al., 2019), which indicated early traumatic experiences may contribute to greater impulsivity and impaired ability to appropriately activate or allocate the neuronal resources to maintain selective attention over processing cognition. Reduced cortical activation in the anterior cingulate cortex (ACC) and superior parietal cortex is consistent with previous studies linking these regions to exposure to stressful life events (Koechlin and Jubault, 2006) (Rae et al., 2015) (Zhai et al., 2019). This association likely reflects their critical roles in inhibitory control, action selection, and error monitoring functions, which are essential for higher-order executive performance. ACC maintains reciprocal connections with the ventrolateral and medial thalamic nuclei, and it also receives signals from the hippocampus, amygdala, and hypothalamus which explains the involvement of ACC in processing inhibitory function and emotions in context with exposure to stressful life events (Karl et al., 2006; Mahjoory et al., 2019; Dossi et al., 2020). Previous studies have demonstrated that ACC is not only engaged in the processing of emotions or attention but also involved in updating action plans and stopping prepotent responses (Aghamohammadi-Sereshki et al., 2022; Crespo-García et al., 2022). Recent studies have introduced the superior parietal cortex as an integral part of action understanding, space perception, and conflict processing and it is also implicated as a key area of attentional monitoring to inhibit selective motor responses during the Go/No-Go task (Zhou et al., 2016, 2021; Mahjoory et al., 2019). In conjunction with these studies, our findings in adolescents provide evidence of changes in brain activity related to exposure to early childhood trauma that may be caused by stress-related alteration of noradrenergic neurotransmitters (De Bellis and Zisk, 2014; Smith and Pollak, 2020; Bremner, 2006); which result in long-term changes of the cortical circuit and provide negative feedback on signal transmission and changes the intraneuronal synaptic efficacy (Lin et al., 2018; Chafee and Goldman-Rakic, 2000).

These findings are also consistent with several recent studies that reported reduced cortical activity and variation of neural processing in inhibitory control networks as a direct result of traumatic events in the adult population (Popescu et al., 2021). In adult studies, Ramchurn et al. noted that fluctuations in amplitude arise from event-related synchronization of cortical activation toward the execution of an accurate response that plays an integral part in communicating with different cortical areas (Ramchurn et al., 2014). High-order executive function, including deliberate actions over selective attention and processing of abstract concepts, requires integrity of cortical activation and fluency of neuro-cortical communication through the cognitive networking system (Cabral et al., 2014; Weeda et al., 2012; Osada et al., 2008), which may be affected by high trauma exposure. Sheynin et al. (2020) provided evidence of decreased cortical connectivity in adolescents with trauma exposure at the medial fronto-parietal network involved in attention processing (Sheynin et al., 2020). Prior research (Pinner et al., 2023) has shown reduced cortical amplitude in ACC in children with Fetal Alcohol Spectrum Disorder during SART in early adolescence, a period recognized as a critical period for frontal lobe maturation, particularly this population is also known to experience comparatively greater amount of trauma in early life (Rockhold et al., 2023). Our findings in typically developing children align with this evidence, suggesting that early trauma may interfere with the normative development of neural circuits involved in attention and cognitive control. Frontal and parietal neurons are activated by the visual stimuli presented in SART for target detection, attentional processing, and planning a movement to withhold the response toward non-target stimuli (Kostyrka-Allchorne et al., 2019; Gool et al., 2020; McTeague et al., 2020).

The significant three-way interaction of trauma X hemisphere X peak in both response amplitude and latency during correct No-Go conditions from the superior parietal cortex and precentral cortex reveals additional complexity in the effects of trauma exposure during performance of the SART. This suggests youths with high exposure to trauma also show irregularity in temporal features of sequential cortical activity along with the time-to-peak response (Lin et al., 2018). Previous studies have determined that latency delay in cortical areas could occur by variation in neural signal propagation or differences in conduction velocity of responses which are regulated by the integrity of activated neurons and the length of the synaptic pathway (Lin et al., 2018; Takemura et al., 2020; Phillips, 1998). In addition, according to our post hoc analysis, youths with high trauma exposure exhibited significant delays in response latency in the precentral cortex during the Correct No-Go condition. The motor response in the SART was performed by the participant’s index finger, which triggers activation of the primary motor area for executive control of predominant motor action toward response selection and inhibition during the Go/No-Go signaling process. It is possible that our significant interaction of trauma with hemisphere and peak time windows in precentral cortex, can elucidate the neurological underpinnings of the signal processing stream related to trauma exposure. Abnormal signal processing in these cortical areas often results in impaired abilities to maintain perceptual judgment and control time-sensitive reflexive actions that can be associated with stress-related behavioral deficiencies (Zhou et al., 2016; Luchicchi et al., 2016). Our simple effect result showed a faster response latency with high trauma exposure in each of those areas compared to our low trauma group. Our findings partially contradict the latency delay often reported in developmental disorders (Sanfratello et al., 2018) (Moore et al., 2014) (Pervin et al., 2022). Since the participants in this study were typically developing, they are not expected to have delayed responses. However, the facilitation of latency in cortical response might be a representation of hyperarousal and hypervigilance behavior, critical for dealing with potential threats, which are features of PTSD and have contributed to the clarification of neuro-behavioral mechanisms underlying stress-related trauma exposure. Furthermore, our results also match Wise et al., and Hanatani et al. (Wise et al., 2009; Hanatani et al., 2005), who found shorter latencies of event-related potentials in panic disorder, which manifests across multiple cortical areas in the processing of attention (Centonze et al., 2005). Altered latency to infrequent targets represents the abnormality of signal transmission and the inability to process the attentive sensory information to discriminate the target stimuli from non-selected stimuli (Bourisly and Shuaib, 2018) (Bourisly and Pothen, 2016). These accelerated neural responses are believed to reflect an adaptive mechanism that enables the brain to quickly detect and react to potential threats (Jovanovic et al., 2013) (Liberzon and Abelson, 2016). While such heightened sensitivity may be beneficial in immediate or high-risk situations, it can become maladaptive over time, leading to persistent disruptions in attentional control and emotional regulation (Wise et al., 2009) (Wu et al., 2012). Our findings of shortened response latencies in trauma-exposed youth may represent a neurophysiological marker of chronic hypervigilance, providing insight into the neuro-behavioral mechanisms shaped by stress-related trauma exposure during critical periods of neurodevelopment.

One of the compelling outcomes of our data is a significant interaction between trauma, sex, and hemisphere on both amplitude and latency in the processing of both target and non-target stimuli in the frontal and parietal cortex. There is evidence of sex differences in psychological behavior and neurocognitive disorders (Bourisly and Shuaib, 2018). Females disproportionately have chronic, and higher rates of psychological symptoms but males showed more severe outcomes in stress-related disorders (Breslau et al., 1997) (Olff, 2017). Understanding the effects of traumatic experiences in childhood remains under-studied and conflicting evidence also exists for sexual dimorphism in brain structure (Badura-Brack et al., 2020). Surprisingly, we found significant interactions of trauma and sex in amplitude and latency in multiple regions during both target and non-target stimuli, indicating that cortical processing in individuals with different levels of trauma exposure also differs by sex in detecting and processing stimuli in recognition of response inhibition (Bremner et al., 1999). These differences could result from hormonal influences in functional network connectivity or signal propagation through the nerve fiber with or without structural changes (Gregori et al., 2006) (Liu et al., 2013). Furthermore, our analysis of cortical response between males and females in low and high trauma showed significantly reduced amplitude (low trauma) and delayed latency (high trauma) in males compared to females during Correct Go condition from left superior parietal cortex and right dorsal ACC cortex respectively. Several prior research studies provided evidence of sex differences in event-related potentials (Bourisly and Shuaib, 2018; Bourisly and Pothen, 2016; Gregori et al., 2006); Bourisly et al. (2018) showed larger amplitude and shorter latency in males compared to females with no stress-related exposure, in accordance with our findings. Trauma exposure could be affecting the neural activity differently by sex, showing that reduced peak amplitude tends to occur in males and females with high trauma but the male group may have a higher chance to be affected at multiple time windows across the cortical response in both right and left hemisphere (Ramikie and Ressler, 2018; Bourisly and Shuaib, 2018). These findings may indicate that males are overly alert or quickly startled by potential threats or unusual surroundings compared to females, who may have experienced challenges in executing the response accurately due to variations of neural activation throughout the cortical network (Breslau et al., 1997). Trauma-related electrophysiological changes may lead to changes in the perception of stimuli and cognitive performance by sex (Steffensen et al., 2008) (Jetha et al., 2021). In addition, this combination of latency differences and reduced amplitude within the context of very basic attention and inhibitory discrimination tasks may contribute to the increased negativity and excessive reactivity of trauma-exposed individuals to accommodate challenging, high sensory load environments such as crowds or unfamiliar surroundings (Sheynin et al., 2020; Hayes et al., 2012; Zhai et al., 2019).

5. Limitations

Regarding limitations, participants in this study were not clinically assessed for psychopathology. We studied the effects of trauma exposure in typically developing youths who self-reported exposure to traumatic events during childhood, which limited our ability to directly link neurophysiological findings to clinical outcomes or formal diagnoses.

Second, we also did not capture information regarding childhood maltreatment, including the type, severity, or chronicity of traumatic experiences. As such, some forms of trauma may not have been reflected in self-report measures, and undetected maltreatment may have influenced the results. Without this additional context, we cannot fully differentiate the effects of trauma exposure from other psychosocial or environmental factors that may contribute to observed group differences.

Third, although the high and low trauma groups were well matched on age, sex, and socioeconomic status, there may still be unmeasured confounding factors influencing cognitive or neural development. Importantly, the trauma history profile used in this study did not include information about the timing, duration, or age of exposure to trauma. While we observed medium-to-large effect sizes (η² = 0.089 to 0.15) in several outcomes, we acknowledge that this alone does not allow us to definitively conclude that trauma exposure is the causal driver of the reported neurophysiological and behavioral differences. As highlighted in prior work (Gelman and Carlin, 2014) (Lakens, 2022), large effect sizes in observational studies may be inflated due to sampling variability and should be interpreted with caution. Future research is needed to replicate these findings in larger, independent samples. In particular, longitudinal studies that capture the timing, severity, and frequency of traumatic experiences are essential to more fully understand the causal impact of trauma exposure on brain development in children and adolescents.

Additionally, our cognitive task (SART) was only collected during MEG acquisition, limiting opportunities to compare across modalities. Future studies may benefit from using multimodal imaging (e.g., concurrent fMRI and MEG) to better characterize the spatiotemporal dynamics of trauma-related brain activity.

Finally, adolescence is a critical period of brain development; the prefrontal cortex, a key region of interest in this study, is still maturing during this stage (Selemon et al., 2019). Therefore, the observed trauma-related cortical activation differences may reflect ongoing neurodevelopmental adaptations rather than permanent deficits. Future studies would benefit from longitudinal designs that track trauma-exposed individuals over time to better understand the evolving impact of early trauma on brain function and to distinguish between transient developmental alterations and lasting neurobiological effects.

6. Conclusion

Despite these limitations, this is the first MEG study that identifies impairment in task-evoked neural activation during a Go/No-Go task in youths with high vs. low trauma exposure. Disturbance of neural amplitude and latency in a network of regions (parietal and prefrontal cortex) established evidence of neural differences that may in turn, result in future deficits in attention and poor adaptive inhibitory control in youths with exposure to childhood traumatic experiences. The high trauma group exhibited faster cortical latency during cue recognition, discrimination, and implementation of subsequent goal-directed processes and decreased selective attention capacity during critical processing periods. Identification of the neural effects of trauma in adolescence is important for determining the optimal targets for early intervention to minimize the long-term effects of trauma exposure that can support executive function and improve inhibitory mechanisms before developing secondary disabilities in adulthood.

Data availability

Data will be made available on request.