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. Author manuscript; available in PMC: 2025 Aug 22.
Published before final editing as: Clin Psychol Sci. 2025 Jul 27:10.1177/21677026251351850. doi: 10.1177/21677026251351850

Prospective Relations between Cortical Thickness and Change in Internalizing Symptoms are Moderated by Chronic Stress Exposure in Adolescents with Depression and Anxiety

Adrienne L Romer 1,2, Nicholas A Hubbard 3, Randy P Auerbach 4, Anastasia Yendiki 5,6, Satrajit Ghosh 6,7, Aude Henin 6,8, Stefan G Hofmann 9, John D E Gabrieli 10, Susan Whitfield-Gabrieli 7,8,10,11, Diego A Pizzagalli 2,6,12
PMCID: PMC12369654  NIHMSID: NIHMS2088534  PMID: 40852172

Abstract

Brain structural alterations have been associated with internalizing symptoms concurrently. Less is known about whether these alterations relate to change in internalizing psychopathology during adolescence, a sensitive period for the effects of stress on neurodevelopment and internalizing symptoms. We examined whether cortical thickness (CT) was prospectively related to change in an internalizing factor in 203 adolescents (aged 14-17) with depression and/or anxiety diagnoses or no diagnosis from the Boston Adolescent Neuroimaging of Depression and Anxiety study. We conducted residualized change regression models to determine whether baseline CT was associated with one-year change in internalizing factor scores, and whether chronic stress exposure moderated these relations. Lower bilateral temporal pole and left insula CT were associated with one-year increases in internalizing factor scores and were moderated by chronic stress. These novel results identify specific cortical structure features that might contribute to worsening depression and anxiety, particularly in adolescents with high chronic stress.

Keywords: Internalizing, Psychopathology, Brain Structure, Stress, Adolescence

Introduction

Adolescence is a period of heightened risk for the onset of depressive and anxiety disorders (Kessler et al., 2001; Kessler, Berglund, et al., 2005; Solmi et al., 2022), conditions that are highly comorbid across the lifespan (Avenevoli et al., 2015; Kessler, Chiu, et al., 2005; Merikangas et al., 2010). The high rates of comorbidity among depressive and anxiety disorders suggest that there may be shared risk markers that predispose youth to both forms of disorder. Factor-analytic studies have identified a latent internalizing factor, which captures shared variation among depressive and anxiety disorders, accounting for their comorbidity and severity (Achenbach & Edelbrock, 1981; Krueger & Markon, 2006, 2011). Examining the psychological and neurobiological mechanisms underlying this internalizing factor can improve identification of shared risk markers for both depression and anxiety during adolescence, a period characterized by greater risk of onset for these conditions.

Neuroimaging research has identified structural neural alterations in youth with internalizing psychopathology (Ducharme et al., 2014; Gold et al., 2017; Kaczkurkin et al., 2019, 2020; Merz et al., 2018; Mewton et al., 2020; Newman et al., 2016; Parkes et al., 2021; Smolker et al., 2022; Snyder et al., 2017), particularly within ventral and medial prefrontal cortex (PFC) regions, insula, and subcortical regions such as the amygdala and hippocampus. Generally, smaller volume and thinner cortices have been identified in youth with internalizing psychopathology (Kaczkurkin et al., 2019; Merz et al., 2018; Mewton et al., 2020; Newman et al., 2016; Parkes et al., 2021; Snyder et al., 2017); however, some studies find increased thickness or volume associated with greater anxiety symptoms (Gold et al., 2017; Smolker et al., 2022) or no association between internalizing psychopathology and volume or CT (Durham et al., 2021; Schmaal et al., 2017). Discrepancies among studies may be due to differences between subtypes of internalizing symptoms (as in Kaczkurkin et al., 2020) or the use of case-control comparisons (as in Gold et al., 2017; Schmaal et al., 2017) rather than dimensional assessments of symptoms.

Another plausible explanation is that there may be differences in relations between cortical structure and symptoms across developmental stages. For example, one study found that the relation between internalizing symptoms and cortical thickness (CT) reversed from childhood to adolescence such that greater anxious and depressive symptoms were associated with lower ventromedial PFC thickness during childhood (5-8 years old), but higher thickness of this region during adolescence (after 15 years old) (Ducharme et al., 2014). Age-related discrepancies in these relations may be due to the substantial cortical maturation that occurs during youth development. CT increases from birth to early childhood and then decreases linearly throughout childhood and adolescence (Sydnor et al., 2021). Lower-order, unimodal sensorimotor cortices also tend to develop earlier than the higher-order, heteromodal association cortices (i.e., prefrontal and parietal regions) (Sydnor et al., 2021). Thus, the pattern of associations between cortical structure and internalizing symptoms may vary from childhood to adolescence, such that greater CT during adolescence could reflect abnormalities (i.e., possibly delayed or stunted cortical maturation) in the normative cortical thinning that occurs during this developmental stage (e.g., Smolker et al., 2022).

At the same time, most research examining the structural neural correlates of internalizing disorders has been conducted at one point in time, which does not allow for examining changes in cortical structure and psychopathology over youth development or for establishing their temporal precedence. A few exceptions have tested whether internalizing symptoms prospectively predicted changes in cortical structure over time (Ducharme et al., 2014; Taylor et al., 2021; Whittle et al., 2020) or whether changes in cortical structure prospectively predicted future symptom onset (Bos et al., 2018). Results from these studies showed that higher baseline internalizing symptoms (Ducharme et al., 2014; Taylor et al., 2021) or greater increases in internalizing symptoms over time (Whittle et al., 2020) were associated with reductions in the amount of cortical thinning over time. Specifically, Bos et al. (2018) found that accelerated cortical thinning within lateral orbitofrontal and precentral regions prospectively related to the onset of future depression symptoms in adolescents. Additionally, Foland-Ross et al. (2015) found that lower right medial orbitofrontal, right precentral, left anterior cingulate, and bilateral insula CT predicted the future onset of depression over the course of five years in a small sample of adolescent girls (N=33) with an overall accuracy of 70% (Foland-Ross et al., 2015). However, few studies have examined whether cortical structure is associated with future changes in a latent internalizing factor over time, which is important for identifying structural neural risk markers of both depression and anxiety disorders.

Using data from the Adolescent Brain Cognitive Development (ABCD) study, we previously examined prospective relations between baseline CT and subsequent within-person changes in transdiagnostic psychopathology factor scores over the course of two years during preadolescence (ages 9-10 at baseline) (Romer et al., 2023). We found that preadolescents with thinner cortices at the baseline wave, particularly in sensorimotor and temporal brain regions, showed the steepest within-person decreases in internalizing factor scores, compared to those with average or high CT (Romer et al., 2023). This association was specific to the internalizing factor, as baseline CT was unrelated to within-person change in the general ‘p-factor’ or other specific psychopathology factors. As sensorimotor and temporal regions thin more rapidly at an earlier age in childhood than heteromodal association cortices (Sydnor et al., 2021), we hypothesized that the degree of normative age-related cortical thinning in these regions, likely reflective of greater pruning and myelination (Sowell, 2004; Whitaker et al., 2016), may be protective against the development of internalizing symptoms during preadolescence.

Although an initial important step in determining the prospective relations between cortical structure and subsequent changes in internalizing psychopathology, this previous study (Romer et al., 2023) was limited in two ways. First, the ABCD sample included preadolescents aged 9-10 at baseline, which is prior to the onset of many internalizing symptoms (Avenevoli et al., 2015; Kessler, Berglund, et al., 2005). Given the extensive cortical maturation that occurs from childhood to adolescence (Sydnor et al., 2021) and the evidence that relations between internalizing symptoms and cortical structure may differ across childhood and adolescence (e.g., Ducharme et al., 2014), it is important to examine prospective relations between cortical structure and changes in internalizing psychopathology during adolescence, which is a period of heightened risk. Second, only items from a parent-reported measure of symptoms (i.e., Child Behavior Checklist) were included in the factor-analytic models of the structure of psychopathology. Research suggests low-to-moderate correspondence between informants on measures of internalizing symptoms (De Los Reyes et al., 2015). The extent to which parents/guardians are aware of their child’s symptoms may vary by the quality of the parent-child relationship (Curhan et al., 2020; Rescorla et al., 2013). Thus, taking a multi-informant approach in the modeling of adolescent internalizing psychopathology may provide a more nuanced understanding of adolescents’ symptoms across reporters.

Finally, a meaningful next step for this work is to test whether relations between cortical structure and change in adolescent internalizing psychopathology are moderated by environmental factors such as chronic stress. There is robust evidence of associations between greater stress exposure and greater internalizing psychopathology during adolescence (e.g., see Low et al., 2012; March-Llanes et al., 2017 for reviews). One hypothesis is that cortical structural alterations may reflect underlying neural vulnerabilities to internalizing psychopathology that may be amplified under conditions of chronic stress, consistent with a diathesis-stress model. Indeed, prior structural MRI research has demonstrated that relations between life event stress and internalizing symptoms were strongest for adolescents with smaller subcortical volumes (i.e., amygdala and hippocampus), compared to those with larger volumes (Gorka et al., 2014; Weissman et al., 2020). However, less is known about whether associations between cortical structure, rather than subcortical structure, and internalizing psychopathology may be strongest for adolescents with greater exposure to chronic stress. Determining whether chronic stress exposure is a moderator of relations between cortical structure and change in internalizing psychopathology can help to identify adolescents who are particularly at risk for co-occurring depression and anxiety.

Therefore, in the current study, we used two waves of clinical data and the first wave of structural magnetic resonance imaging (MRI) data from the Boston Adolescent Neuroimaging of Depression and Anxiety (BANDA) study to test whether baseline thickness of 68 cortical regions is prospectively related to change in internalizing psychopathology over one year during adolescence, and whether this relation is moderated by chronic stress exposure. The BANDA sample includes 225 adolescents (aged 14-17 at baseline) with at least one depressive and/or anxiety disorder as well as adolescents with no lifetime history of any clinical diagnosis (i.e., healthy controls), allowing us to sample the continua of adolescents’ anxious and depressive symptoms (Hubbard et al., 2023). We addressed the following research questions: 1) Do alterations in baseline CT prospectively relate to one-year change in internalizing symptoms during adolescence?; and 2) Are associations between baseline CT and one-year change in symptoms moderated by chronic stress exposure?

To this end, we employed both adolescent- and parent-reported measures of internalizing symptoms. Using confirmatory factor analyses (CFA), we calculated adolescent- and parent-reported internalizing factor scores from a correlated two-factor model using the same clinical scales at baseline and one-year follow-up waves. As we only had two timepoints of data, we were unable to differentiate between-person from within-person effects using longitudinal multilevel modeling. Thus, we employed residualized change regression models to test whether baseline CT was related to internalizing factor scores at one-year follow-up, controlling for baseline internalizing scores (i.e., to reflect one-year change in internalizing factor scores). We then tested whether this relation was moderated by baseline adolescent-reported chronic stress exposure. Based on previous findings from adolescent neuroimaging studies demonstrating higher CT associated with higher internalizing symptoms (Castagna et al., 2018; Ducharme et al., 2014; Gold et al., 2017; Smolker et al., 2022) and our prior findings from the ABCD study (Romer et al., 2023), we hypothesized that higher baseline CT would be associated with one-year increases in internalizing factor scores. We also hypothesized that the relations between CT and internalizing factor scores would be moderated by chronic stress exposure such that adolescents with greater stress exposure would show a stronger positive relation between CT and change in internalizing factor scores.

Transparency and Openness

Preregistration.

This study was not preregistered.

Data, materials, code, and online resources.

De-identified data are openly available through the National Institutes of Health Data Archive (http://dx.doi.org/10.15154/1528446). Analysis code is available at https://github.com/Ageyr13/BANDA_BrainStructure_INT. Supplemental Material is available online.

Reporting.

We report how we determined our sample size, all data exclusions, all manipulations, and all measures in the study.

Ethical approval.

Parents provided informed consent and adolescents assented to study procedures approved by Mass General Brigham Institutional Review Board (Protocol #P002534).

Methods

Participants

The BANDA study is part of a larger Human Connectome Project study from the Connectomes Related to Human Diseases initiative. The sample includes 225 adolescents (aged 14-17 at baseline) recruited from the greater Boston area through Boston University, Massachusetts General Hospital, and McLean Hospital. Full recruitment details and relevant procedures within this study can be found elsewhere (Hubbard et al., 2020, 2024; Siless et al., 2020). General inclusion criteria included: adolescents age 14-17 years at the time of scanning; parent and adolescent English fluency; parent and adolescent IQ ≥ 85. Exclusion criteria were: adolescent MR-contraindicators; adolescent premature birth (< 37 weeks or < 34 weeks for twins, or < 5 lbs at birth); history of serious medical condition or head injury; hospitalization of > 2 days for neurological or cardiovascular disease; diagnosis of autism spectrum disorder; use of daily migraine medication. Participants were administered an in-person clinical interview and symptom assessment, and eligible participants then underwent an MRI scanning session. Parents and adolescents were compensated for participation. In the current study, participants with missing demographic information, complete nonresponse on clinical symptom data, or those who did not pass structural MRI quality assurance measures were excluded (baseline Wave 1: n=203; one-year follow-up Wave 2: n=149).

Adolescents were recruited who had at least one current diagnosis of an anxiety or depressive disorder (n=140), or no lifetime psychiatric disorders (n=63). Diagnoses were confirmed via the Kiddie Schedule for Affective Disorders and Schizophrenia Present and Lifetime Version (K-SADS) (Kaufman et al., 2000) adapted for Diagnostic and Statistical Manual of Mental Health Disorders, 5th Edition criteria (DSM-5) (American Psychiatric Association, 2013). The K-SADS was administered to the accompanying parent and adolescent, and diagnoses were confirmed by a licensed clinical psychologist. Notably, 80.6% of the included patients had at least one comorbid diagnosis (see Table S1 in the Supplemental Material for a diagnostic breakdown of the included sample).

Measures

See Supplemental Material available online for additional details on measures.

Adolescent-Reported Internalizing Symptoms.

Current depressive and anxiety symptoms were measured with the Mood and Feelings Questionnaire (MFQ) total score (Messer et al., 1995) and the Revised Child Anxiety and Depression Scale (RCADS) Major Depressive Disorder, Generalized Anxiety, Obsessive-Compulsive Disorder, Panic Disorder, Separation Anxiety Disorder, and Social Phobia subscale scores (de Ross et al., 2002) at baseline and one-year follow-up waves. These scales previously have been shown to demonstrate acceptable to excellent levels of internal consistency in this sample (Cronbach’s α ranged from 0.78 for the RCADS-Separation Anxiety subscale to 0.96 for the MFQ) (Hubbard et al., 2020).

Parent-Reported Internalizing Symptoms.

The Child Behavior Checklist (CBCL; age 6-18 form), a well-established 119-item parent rating scale describing child behaviors and emotions was administered to parents/caregivers at baseline and one-year follow-up (Achenbach, 2009). The CBCL Anxious/Depressed, Withdraw/Depressed, and Somatic Complaints subscale scores were used to measure parent-reported internalizing symptoms. Adolescents’ depression symptoms also were measured using the MFQ-Parent Report total score (Messer et al., 1995). These scales previously have been shown to demonstrate excellent internal consistency in this sample (CBCL Internalizing Cronbach’s α = 0.94; MFQ-PR Cronbach’s α =0.95) (Hubbard et al., 2020).

Stress Exposure Interview.

The Stress and Adversity Inventory for Adolescents (STRAIN) is an automated, computerized, structured interview administered to the adolescent participants at the baseline wave. The STRAIN assesses adolescents’ exposure to and perceptions of 75 different life stressors spanning multiple life domains (e.g., housing, education) and psychosocial characteristics (e.g., interpersonal loss, humiliation) (Slavich et al., 2019). In the current study, we assessed adolescents’ chronic stress exposure using the total count of chronic difficulties score, which is a sum score of the total number of chronic life events endorsed by the adolescents. Here, “chronic” refers to stressors that the adolescents endorsed lasting at least one month (although most were present for longer) rather than the acute life events they reported which may only last a few days. The STRAIN also assesses perceptions of chronic stress with the severity of chronic difficulties score, which was strongly correlated with the total count of chronic difficulties score (r=0.961). We also examined the total number of chronic difficulties for 9 of the 12 life domains (i.e., housing, education, treatment/health, marital/partner, financial, legal/crime, other relationships, parent/guardian, and death) and five social-psychological characteristics (i.e., interpersonal loss, physical danger, humiliation, entrapment, and role change/disruption subscales) for which there was sufficient variability in participant responses (see Table S2 in the Supplemental Material for descriptive statistics and descriptions of the STRAIN measures).

Demographic Covariates

Adolescent age, sex assigned at birth, race, ethnicity, parental education level, and total combined family income over the past year were obtained via parent report, along with data on adolescents’ current psychiatric medication use. We averaged both parent/caregiver reports of their education level. Adolescent participants completed the Tanner Stage Developmental Scale as a measure of relative physical development and primary- and secondary-sex characteristics.

MRI Data Acquisition, Processing, and Quality Control

MRI acquisition and scanning parameters, processing, and quality assurance procedures are described elsewhere (Hubbard et al., 2020, 2024; Siless et al., 2020) and in the Supplemental Materials. Briefly, brain data were collected on a Siemens 3T Prisma whole-body scanner with a 64-channel head coil (Siemens Healthcare, Erlangen, Germany). High-resolution structural data (0.8-mm isotropic voxels) were acquired using a T1-weighted MPRAGE sequence with a duration of 7 min 50 s (in-plane acceleration factor of 2). Scan parameters for TR, TE, TI, and flip angle were 2.4 s, 2.18 ms, 1.04 s, and 8°, respectively. Cortical surface reconstruction and subcortical segmentation were performed based on automated, atlas-based, segmentation procedures in FreeSurfer using the standardized, HCP minimal preprocessing workflow (Glasser et al., 2013). We used post-processed CT data mapped to 34 cortical parcels per hemisphere based on the Desikan–Killiany brain registration atlas (Desikan et al., 2006).

Statistical Analyses

Analyses were conducted in the following steps. First, CFA was used to fit a correlated two-factor measurement model of adolescent- and parent-reported internalizing symptoms. Second, we examined the longitudinal measurement invariance of the factors from this model over the two waves to determine the stability of the factors over time. Third, factor scores at each wave were extracted from the longitudinal measurement invariant model using the standard regression method in Mplus. We tested factor score intercorrelations over the waves to determine their reliability over time. Fourth, residualized change regression models were employed to examine the prospective relations between 68 baseline CT parcels (34 parcels per hemisphere) and one-year change in the factor scores. Fifth, for any significant prospective relations, we examined whether chronic stress exposure moderated the relations between baseline CT and change in the factor scores. Each of these analyses is described in detail below.

Confirmatory Factor Analyses and Longitudinal Measurement Invariance

A correlated two-factor model of internalizing symptoms was fit at baseline and one-year follow-up waves. The six RCADS subscale scores and the MFQ total score loaded on the adolescent-reported internalizing factor and the three CBCL subscale scores and MFQ-PR total score loaded on the parent-reported internalizing factor. The latent adolescent- and parent-reported internalizing factors were allowed to correlate.

We examined the longitudinal measurement invariance of the factors over the two waves to determine whether the factors are equivalently measured over time. We tested models of configural and metric invariance. Configural invariance tests whether the same factor structure can adequately fit the data over time; we tested a model in which the indicators loaded on the same factor at each wave. Metric invariance tests whether the factor loadings are equivalent over time. If metric invariance holds, we can examine change in relative status of participants over time using residualized change regression models. We tested a model in which the factor loadings were equivalent across the two waves. We used likelihood ratio testing to compare the fit of these two models, which tested whether adding additional equality constraints resulted in a significant decrement to model fit. We also examined correlations between the factor scores derived from these latent models as a test of reliability over the waves and the degree of convergence across adolescent- and parent-reporters.

The CFAs and measurement invariance testing were performed in Mplus version 8.4 (Muthen & Muthen, 1998) using maximum likelihood estimation with robust standard errors. We assessed each model’s fit to the data using the chi-square value, comparative fit index (CFI), Tucker-Lewis index (TLI), root-mean square error of approximation (RMSEA), and standardized root mean squared residual (SRMR). Nonsignificant chi-square tests indicate good model fit; nonetheless, generally this test is overpowered in large samples. CFI and TLI>0.90 and SRMR<0.05 indicate adequate fit; RMSEA<0.08 is considered acceptable (Kline, 2015). For the measurement invariance testing, the chi-square difference test was calculated using the Sattora-Bentler scaling correction to better approximate chi-square under non-normality (Satorra & Bentler, 2010). Given that the chi-square value may be overly sensitive to minor deviations from a perfect model in large samples, we also considered change in alternate fit indices >.010 (i.e., RMSEA and CFI) (Putnick & Bornstein, 2016).

Residualized Change Models

We used residualized change regression models to test prospective relations between the thickness of each of the 68 cortical parcels derived from the surface-based atlas procedure (34 parcels per hemisphere) and change in the adolescent- and parent-reported internalizing factor scores over two study waves (one-year timeframe). Specifically, the adolescent- and parent-reported one-year follow-up factor scores were regressed onto each of the 68 baseline CT parcels controlling for the baseline factor scores in separate regressions. Covariates included sex and age (see also Sensitivity Analyses). For any CT parcels that were significantly related to the factor scores, we conducted post-hoc moderation analyses wherein we tested whether total chronic stress exposure and specific domains of stress exposure moderated the association between the CT parcels and factor scores.

Analyses were performed in R version 4.4.0 (http://www.r-project.org/) using the “lm” function (R Core Team, 2024). We corrected for multiple comparisons by using a false discovery rate (FDR) procedure (Benjamini & Hochberg, 1995) (q<0.05) for each set of 68 parcel-wise tests as well as for the set of post-hoc moderation analyses.

Sensitivity Analyses

We conducted four sensitivity analyses to test the robustness of putative associations between baseline CT and one-year change in internalizing factor scores. To do this, for any significant associations, we additionally controlled for the effects of (1) baseline psychotropic medication use, (2) total intracranial volume, (3) Tanner pubertal stage, and (4) parental education and total household family income (last year), each of which might influence both CT and internalizing symptoms.

Results

Descriptive Statistics

Descriptive statistics are summarized in Table 1. We tested baseline differences in all study variables between participants with (N=149) versus without (N=54) available one-year follow-up data. Although there were differences in medication use, Tanner stage, chronic stress exposure, and depression, withdrawn/depressed, and somatic complaints symptoms between those with and without missing follow-up data, none of those differences were significant after FDR correction for the 22 tests (q<0.05). As a result, we used full information maximum likelihood estimation in the confirmatory factor and longitudinal measurement invariance models to estimate missing data for the 26% of the sample who did not have one-year follow-up data available. This procedure is recommended when data are missing at random (Enders, 2022), a condition that was likely given that any differences between participants with or without missing data were not significant after FDR correction for multiple testing. We also performed an additional sensitivity analysis by removing the 54 participants with completely missing follow-up data (n=149) and rerunning the residualized change regression models.

Table 1.

Descriptive Statistics of all Study Variables and Comparisons Between Participants with Complete versus Missing Follow-Up Data.

Baseline Sample (n=203) Non-Missing Sample (n=149) Missing Sample (n=54) X2/t Unadjusted P-value
Min Max Mean (SD) or No. (%) Mean (SD) or No. (%) Mean (SD) or No. (%)
Demographic Variables
Age (years), 13.9 16.9 15.39 (0.85) 15.39 (0.85) 15.40 (0.86) 0.102 0.919
Sex (females) 131 (64.5) 92 (61.7) 39 (72.2) 1.901 0.168
Non-White 45 (22.2) 32 (21.5) 13 (24.1) 0.155 0.694
Hispanic 14 (6.9) 10 (6.7) 4 (7.4) 0.057 0.811
Medication Use 96 (47.3) 63 (42.3) 33 (61.1) 5.637 0.018
Tanner Stage 4.0 22.0 17.36 (2.64) 17.11 (2.75) 18.06 (2.17) 2.254 0.025
Parent Education 2.5 8.0 6.12 (1.25) 6.11 (1.31) 6.16 (1.08) 0.270 0.787
Family Income 0 5 4.32 (1.12) 4.38 (1.10) 4.13 (1.17) 1.380 0.169
Cortical Structure
Mean CT 2.7 3.2 2.97 (0.08) 2.98 (0.08) 2.97 (0.08) 0.394 0.694
Intracranial Volume 1323514.8 1999487.4 1630824.95 (151835.55) 1638021.46 (145324.25) 1610967.94 (168359.09) 1.122 0.263
STRAIN Interview
Chronic Stress 0 31 9.56 (6.59) 8.85 (6.53) 11.47 (6.43) 2.504 0.013
Adolescent-Reported Internalizing Measures
MFQ Total 0 56 18.29 (15.57) 16.46 (14.93) 23.43 (16.31) 2.852 0.005
RCADS Depression 0 29 8.75 (6.83) 8.05 (6.72) 10.72 (6.83) 2.469 0.014
RCADS GAD 0 18 5.49 (4.00) 5.33 (3.95) 5.92 (3.98) 0.941 0.348
RCADS Panic 0 22 5.50 (5.32) 5.11 (5.41) 6.60 (4.97) 1.759 0.080
RCADS Social 0 27 12.39 (7.02) 11.99 (7.20) 13.53 (6.41) 1.376 0.170
RCADS SepAnx 0 14 2.31 (2.63) 2.19 (2.61) 2.62 (2.69) 1.017 0.311
RCADS OCD 0 17 2.87 (3.23) 2.72 (3.23) 3.26 (3.21) 1.045 0.297
Parent-Reported Internalizing Measures
MFQ-PR Total 0 55 12.79 (12.00) 11.82 (12.07) 15.52 (11.47) 1.921 0.056
CBCL Anxious/Depressed 0 25 6.55 (5.49) 6.31 (5.61) 7.21 (5.15) 1.019 0.310
CBCL Withdraw/Depressed 0 15 3.90 (3.36) 3.60 (3.18) 4.75 (3.74) 2.145 0.033
CBCL Somatic Complaints 0 16 2.93 (3.01) 2.60 (2.93) 3.87 (3.09) 2.632 0.009
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Note. Comparisons were made by chi-square tests for categorical variables and independent samples t-tests for continuous variables. None of the p-values survived FDR correction for the 22 tests (q<0.05).Parental education level reflects the average level across both parent/caregiver reports. Mean parental education level of 6 is equivalent to having finished a four-year degree. Mean total combined family income of 4 is equivalent to between $75,000 and $100,000 income over the past year. Chronic Stress reflects the total count of chronic difficulties score.

CT=cortical thickness; MFQ=Mood and Feelings Questionnaire; RCADS=Revised Child Anxiety and Depression Scale; GAD=Generalized Anxiety Disorder; SepAnx=Separation Anxiety; OCD=Obsessive-Compulsive Disorder; MFQ-PR=Mood and Feelings Questionnaire-Parent Report; CBCL=Child Behavior Checklist.

Confirmatory Factor Analysis, Measurement Invariance, and Factor Score Reliability Over Time

To account for biases within the same response mode (i.e., method effects), a correlation between the adolescent- and parent-reported MFQ total scores was included. Based on examination of modification indices and residuals, an additional correlation between the adolescent-reported RCADS Depression subscale and the MFQ total score, two measures of adolescent depressive symptoms, was added to the model. The resulting correlated two-factor model fit the data well (Figure 1; Table S3 in Supplemental Material). All factor loadings were positive and statistically significant (p<0.001).

Figure 1. Confirmatory Factor Model of Adolescent- and Parent-Reported Internalizing Symptoms.

Figure 1.

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Confirmatory factor model is depicted of the correlated two-factor model of adolescent- and parent-reported internalizing measures at baseline. Model fit statistics and standardized loadings are reported. The 7 adolescent-reported measures loaded on the latent Adolescent Internalizing factor (Adol INT) and the 4 parent-reported measures loaded on the latent Parent Internalizing factor (Parent INT), which were allowed to correlate.

Note: Social=Revised Child Anxiety and Depression Scale (RCADS) Social Anxiety Disorder subscale; Panic=RCADS Panic Disorder subscale; SepAnx=RCADS Separation Anxiety Disorder subscale; OCD=RCADS Obsessive-Compulsive Disorder subscale; GAD=RCADS Generalized Anxiety Disorder subscale; MDD=Major Depressive Disorder subscale; MFQ=Mood and Feelings Questionnaire total score; AnxDep=Child Behavior Checklist (CBCL) Anxious/Depressed subscale; Withdrawn=CBCL Withdraw/Depressed subscale; Somat=CBCL Somatic Complaints subscale; MFQ-PR=MFQ-Parent Report total score; X2=chi-square value; df=degrees of freedom; CFI=Comparative Fit Index; TLI=Tucker Lewis Index; RMSEA=Root Mean Square Error of Approximation; SRMR=Standardized Root Mean Squared Residual.

Likelihood ratio tests showed that imposing metric invariance did not result in a significant decrement in model fit relative to configural invariance (Table S4 in Supplemental Material). These findings support the use of residualized change regression models to examine change in relative status of participants over time. Consequently, factor scores were calculated at both waves from our final correlated two-factor model, which imposed metric invariance, using the standard regression method in Mplus. Factor scores were highly correlated with their underlying factors (factor score determinacy all >0.90). We standardized the factor scores to a mean of 100 (SD=15), with higher scores indicating a greater propensity to experience all forms of internalizing symptoms (baseline adolescent-reported internalizing factor score range=78-146; baseline parent-reported internalizing factor score range=78-153).

Bivariate factor-score intercorrelations and correlations with demographic covariates are shown in Table S5 in Supplemental Material. The factor scores were strongly correlated over time (r=0.756 and r=0.767 for adolescent- and parent-reported scores, respectively), indicating high reliability over the waves. Adolescent- and parent-reported factor scores also were moderately correlated at both waves (Baseline: r=0.685; One-Year Follow-Up: r=0.617), indicating agreement between reporters.

Is cortical thickness prospectively related to one-year change in internalizing symptoms?

All prospective relations between baseline CT and one-year change in factor scores are shown in Figure 2A and Table S6 in the Supplemental Material. Of the 68 baseline CT parcels, none of the parcels were significantly associated with one-year increases in adolescent-reported internalizing factor scores after FDR correction. Of the 68 baseline CT parcels, three parcels were significantly associated with one-year change in parent-reported internalizing factor scores after FDR correction. Specifically, lower thickness within the left (Std. B=−0.161; 95% CI [−0.244, −0.078]) and right temporal pole (Std. B=−0.145; 95% CI [−0.229, −0.061]) and left insula (Std. B=−0.166; 95% CI [−0.248, −0.083]) were associated with one-year increases in parent-reported internalizing factor scores (all adjusted p<0.05; Figure 2B).

Figure 2. Prospective Relations between Cortical Thickness Parcels and One-Year Change in Adolescent- and Parent-Reported Internalizing Factor Scores.

Figure 2.

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(A) Statistical parametric maps from parcel-wise analyses are shown to illustrate associations between each of the 68 cortical thickness (CT) parcels and one-year change in adolescent-reported (top) and parent-reported (bottom) internalizing factor scores. Color bars reflect effect sizes (standardized betas). Covariates included age and sex. (B) Effect scatterplots of the three associations between the CT parcels (in the left and right temporal pole and left insula) and one-year change in parent-reported internalizing factor scores significant after false discovery rate correction (q<0.05) are shown.

Results from sensitivity analyses demonstrated that these relations were robust to the inclusion of baseline psychotropic medication use, total intracranial volume, Tanner stage, as well as parental education and family income as additional covariates (see Table S7 in Supplemental Material). Relations also remained stable after excluding participants with missing follow-up data (included sample n=149; Table S7 in Supplemental Material). Although relations between the CT parcels and one-year change in adolescent-reported internalizing factor scores were not significant after FDR correction (right temporal pole: Std. B=−0.118; 95% CI [−0.205, −0.031]; left temporal pole: Std. B=−0.080; 95% CI [−0.168, 0.007]; left insula: Std. B=−0.084; 95% CI [−0.171, 0.003]), these relations showed a similar pattern of findings across reporters. Also, of note, lower thickness within a broader array of CT parcels was associated with higher internalizing factor scores (when not examining one-year change), including within the left rostral middle frontal, caudal middle frontal, frontal pole, pars opercularis, fusiform, and supramarginal gyri, and bilateral superior temporal gyri and temporal poles (all p<0.01; see Table S5 in Supplemental Material).

Are relations between cortical thickness and one-year change in internalizing symptoms moderated by chronic stress exposure?

We conducted post-hoc moderation analyses to determine whether the relations between CT in left and right temporal pole and left insula and one-year change in parent-reported internalizing factor scores were moderated by chronic stress exposure. We found that each of these relations was significantly moderated by chronic stress (left temporal pole: Std. B=−0.115, 95% CI [−0.192, −0.039], p=0.004; right temporal pole: Std. B=−0.088, 95% CI [−0.169, −0.008], p=0.033; left insula: Std. B=−0.088, 95% CI [−0.169, −0.007], p=0.033). We estimated simple slopes at 1 standard deviation (SD) below the mean, the mean, and 1 SD above the mean of chronic stress exposure using the interactions package (v1.1.0; Long, n.d.) to illustrate these interactions. In adolescents with high and average levels of chronic stress exposure, lower CT within these parcels was associated with one-year increases in parent-reported internalizing factor scores (all p<0.001). In adolescents with low chronic stress exposure, there was no relation between CT of these parcels and parent-reported internalizing factor scores (all p>0.40). Figure 3A shows this interaction effect for the left temporal pole as an example of this effect; very similar patterns also were found for the right temporal pole and left insula (Figure S1 in Supplemental Material).

Figure 3. Chronic Stress Exposure as a Moderator of Relations between Cortical Thickness and One-Year Change in Internalizing Factor Scores.

Figure 3.

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(A) The interaction between left temporal pole CT and total chronic stress exposure on one-year change in parent-reported internalizing factor scores are shown. The interactions between the right temporal pole and left insula CT parcels and total chronic stress exposure on one-year change in internalizing factor scores are not shown here (see Figure S1 in the Supplemental Material), but also were significant and showed a very similar pattern. Simple slopes analysis revealed that the adolescents with high (1 SD above the mean) and average (mean) total number of chronic stressors and lower left temporal pole CT showed one-year increases in parent-reported internalizing factor scores. There was no relation between left temporal pole CT and parent-reported internalizing factor scores in adolescents with a low total number of chronic stress exposures (1 SD below the mean). (B) Bar charts are shown to depict the interactions between the 14 types of chronic stressors and the 3 CT parcels (left and right temporal pole and left insula) on one-year change in parent-reported internalizing factor scores. Bars with an asterisk depict interaction effects that are significant after FDR correction for the 65 tests (q<0.05). For both (A) and (B), covariates included age and sex and standardized estimates are shown. INT=internalizing; SD=Standard Deviation.

These moderation analyses largely were driven by specific domains of chronic stress (Figure 3B, Table S8 in Supplemental Material). After FDR correction, chronic housing stress moderated the relations between all three CT parcels and one-year change in parent-reported internalizing factor scores. Chronic stress exposure relating to other social relationships and physical danger moderated the relations between bilateral temporal pole CT and one-year change in internalizing factor scores. Education stress exposure moderated the relation between left insula CT and one-year internalizing change. Stress exposure relating to financial, legal/crime, interpersonal loss, entrapment, and role change/disruption also moderated the relation between left temporal pole CT and one-year internalizing change. For each of these interactions, in adolescents with high and average chronic stress exposure, lower CT was associated with one-year increases in the factor scores (all p<0.001). In adolescents with low stress exposure, there was no relation between CT and one-year internalizing change (all p>0.40). Chronic stress exposure relating to treatment/health, marital/partner, parent/guardian, death, and humiliation domains did not significantly moderate any of the associations.

Discussion

In the BANDA study of healthy adolescents and their peers with internalizing disorders, we examined prospective relations between baseline CT and between-person change in internalizing symptoms over a one-year period. Lower thickness specifically within the bilateral temporal poles and left insular cortex was prospectively associated with one-year increases in parent-reported internalizing factor scores independent of sex, age, psychotropic medication use, total intracranial volume, pubertal stage, and socioeconomic status. Those prospective relations were significantly moderated by chronic stress exposure, particularly in the context of housing-, social relationships-, and physical danger-related life events. Compared to adolescents with low chronic stress exposure, adolescents with high and average chronic stress and thinner bilateral temporal pole and left insula regions at baseline showed greater increases in parent-reported internalizing symptoms over the course of one year.

Our previous research in 9 and 10 year-old children from the ABCD study showed that lower baseline CT within sensorimotor and temporal cortical regions was associated with within-person decreases in parent-reported internalizing, but not general psychopathology, factor scores over two years (Romer et al., 2023). Those findings supported the hypothesis that lower sensorimotor and temporal CT might be protective against the development of internalizing psychopathology prior to adolescence. Although cross-sectional structural MRI studies in children and adults often find a negative association between CT and internalizing symptoms (Kaczkurkin et al., 2019; Merz et al., 2018; Mewton et al., 2020; Newman et al., 2016; Parkes et al., 2021; Romer et al., 2021), some studies in adolescent samples find the opposite pattern of higher CT associated with greater internalizing symptoms (e.g., Castagna et al., 2018; Ducharme et al., 2014; Gold et al., 2017; Smolker et al., 2022). As typical adolescent neurodevelopment is characterized by extensive synaptic pruning and myelination (Sydnor et al., 2021), this positive association between CT and internalizing symptoms may result from abnormally slowed or stunted synaptic pruning in cortical regions important for cognitive and emotion function (e.g., Smolker et al., 2022).

However, contrary to this prior adolescent research (Castagna et al., 2018; Ducharme et al., 2014; Gold et al., 2017; Romer et al., 2023; Smolker et al., 2022) and our hypotheses, the current results suggest that having thinner temporal pole and insular cortices may indicate risk, rather than protective markers, for subsequent worsening of internalizing symptoms during adolescence, more consistent with the associations typically found in childhood and adulthood. One explanation for these findings is that the adolescents whose symptoms worsened over the one-year period may have experienced excessive synaptic pruning in the temporal pole and insula, regions that may be particularly important for social cognitive and emotional functions (Olson et al., 2013; Uddin et al., 2017). This explanation would be consistent with the Stress Acceleration Hypothesis, which posits that early life stress exposure accelerates maturation of brain regions involved in emotional processing, associative learning, and memory, leading to long-term consequences for neural development and increased risk for affective disorders (e.g., Callaghan & Tottenham, 2016; McLaughlin et al., 2014). It is also possible that the adolescents who experienced worsening symptoms may have undergone a slower rate of normative early childhood thickening in these regions, leading to the lower thickness in adolescence. Because our imaging data were cross-sectional, future research is needed to adjudicate between these two explanations. Specifically, future work should address this question by examining dynamic relations between CT developmental trajectories and internalizing symptoms throughout childhood and adolescence. Alternatively, the discrepancy may be due to a difference in the examination of within-person change in internalizing symptoms (as in Romer et al., 2023) vs. between-person change in symptoms (as in the current study).

Out of all 68 CT parcels tested, lower baseline CT specifically within the bilateral temporal pole and left insula prospectively related to one-year increases in internalizing factor scores. These findings are consistent with prior structural MRI studies that found cortical volume and thickness alterations in the temporal pole (Castagna et al., 2018; Suñol et al., 2018) and insula (Foland-Ross et al., 2015; Snyder et al., 2017) associated with depression and anxiety symptoms. The temporal pole and insula have varied functions involving sensorimotor, socio-emotional, and higher-order cognitive processing (Olson et al., 2013; Uddin et al., 2017). Interestingly, both of these paralimbic regions are involved in social cognitive processes such as theory of mind, empathy, moral judgments, as well as socio-emotional memory, and both are posited to be part of the “social brain network” (Binney & Ramsey, 2020; Frith & Frith, 2010). Transdiagnostic meta-analyses also have identified smaller insula volume as a common feature across adult internalizing, externalizing, and thought disorders (Goodkind et al., 2015; McTeague et al., 2016). The anterior insula is involved in empathy and has been shown to be activated in response to others’ pain and emotional facial expressions (Fan et al., 2011; Uddin et al., 2017). Lesion studies have further shown that left insula lesion specifically is associated with difficulty recognizing facial expressions of emotions (Knutson et al., 2014; Uddin et al., 2017).

Similarly, non-human primate and human lesion findings have underscored causal links between the temporal pole and social behavior (Olson et al., 2013). Olson and colleagues (2013) posit that the temporal pole may be important for encoding and retrieving social concepts such as people’s names, personality traits, and biographical information. Social cognitive dysfunctions have been found across a range of mental disorders (Cotter et al., 2018), including depressive and anxiety disorders (Weightman et al., 2014). One hypothesis is that deficits in higher-order social cognitive processes, particularly difficulties with recognizing emotional facial expressions (supported by the left insula) and difficulties with social semantic memory (i.e., memory about people, traits, and social concepts supported by the temporal pole) may be associated with risk for worsening internalizing symptoms during adolescence.

Our results also clarified that adolescents with high and moderate levels of chronic stress exposure and lower CT within the bilateral temporal poles and left insula showed the greatest one-year increases in internalizing symptoms, compared to their peers with low stress exposure. These cortical findings are consistent with prior subcortical MRI studies, which found that associations between greater life event stress and worsening depression and anxiety were strongest among adolescents with smaller amygdala and hippocampal volumes, compared to those with larger volumes (Gorka et al., 2014; Weissman et al., 2020). Adolescence is thought to be a sensitive period when stress may have greater influence on neurodevelopment compared to other developmental stages (e.g., Gee & Casey, 2015). Greater exposure to chronic stress combined with having thinner temporal pole and insular cortices may confer heightened risk for worsening internalizing symptoms during adolescence. Childhood adversity and stress have been found to be associated with lower CT and volume of the temporal pole, insula, and other salience network regions (Gold et al., 2016; Lim et al., 2014; Peverill et al., 2023; Teicher et al., 2014). Thus, the temporal pole and insula may be especially sensitive to the effects of chronic stress, leading to subsequent increases in co-occurring depression and anxiety symptoms during adolescence. According to the Accelerated Stress Hypothesis (e.g., Callaghan & Tottenham, 2016), it is possible that greater chronic stress exposure leads to accelerated thinning of the temporal pole and insular cortices, which could increase risk for subsequent worsening of internalizing symptoms. Future studies with multiple timepoints of structural MRI and clinical data should test this hypothesis.

Relations between CT and internalizing symptom change was driven by greater exposure to specific types of chronic stress, most consistently events related to environmental (e.g., frequent moves, unsafe neighborhood, poor housing conditions, maltreatment, ongoing physical or sexual abuse), and interpersonal contexts (e.g., discrimination or exclusion, dissolution of friendships, peer bullying). Exposure to education-related life events (e.g., overwhelming workload, failing a class) was a specific moderator of relations between lower CT in the left insula and one-year increases in internalizing psychopathology. These results suggest that adolescents with exposure to life events involving physical and social threats may be particularly vulnerable to increases in internalizing symptoms if they have thinner temporal pole and insular cortices.

We also found discrepancies in results across reporters. Specifically, associations between CT and internalizing symptoms did not reach the corrected significance threshold for adolescent-reported factor scores. As adolescents may be less likely to share their inner thoughts and feelings with their parents/caregivers (Curhan et al., 2020; Rescorla et al., 2013), this discrepancy in results based on reporter could indicate that our findings may not be as valid to the adolescents’ experiences themselves. Importantly, however, the pattern of associations was consistent across reporters, with discrepancies only observed regarding statistical significance, suggesting the relations with CT were similar across reporters.

Our findings should be considered in the context of several limitations. First, 26% of the included sample had missing one-year follow-up data. However, sensitivity analyses that removed participants with missing follow-up data further supported our results. Second, there were only two timepoints of clinical data available, which limited our analysis approach to tests of between-person changes in internalizing factor scores over time, and limited the amount of internalizing symptom change possible during only a one-year timeframe. Third, we only had one timepoint of structural MRI data available, which did not allow us to determine whether changes in CT prospectively related to changes in symptoms. This is especially important given that we were unable to determine whether lower thickness at the baseline wave was due to an abnormally faster rate of thinning during adolescence or slowed increases in CT that typically occur during earlier development. Fourth, chronic stress exposure was ascertained via retrospective reporting by the adolescents only and we do not know exactly when the stress exposure occurred during their lifetime. It is possible that adolescents who reported greater symptom severity may be more likely to also report greater exposure to chronic stress. Additionally, the total count of chronic difficulties score is limited in that it treats all stressful events as equivalent, even though exposure to different types of events may confer varying levels of stress on the adolescents (e.g., failing a class vs. the loss of a parent). Future studies should ascertain information about the timing and impact of stress exposure and incorporate other non-self-report measures of stress exposure (e.g., parent/caregiver-report, child protective/medical records).

Despite these limitations, this study identified specific cortical structures important for understanding the development of new or worsening internalizing psychopathology development during adolescence. Lower CT within the bilateral temporal pole and left insula may be risk markers for future worsening of internalizing symptoms during adolescence. Adolescents with high and moderate exposure to chronic stress, particularly those related to environmental and interpersonal events, and lower temporal pole and insula CT may be especially vulnerable to increases in internalizing symptoms. As both the temporal pole and insula have been implicated in social cognition, specific deficits in emotional face processing and social semantic memory may be associated with risk for future internalizing symptoms during adolescence, although this should be directly tested in future research.

Supplementary Material

1

Funding

This project was supported by the National Institute of Mental Health, U01MH108168 (JDEG, SWG) and was made possible by the resources provided by Shared Instrumentation Grants 1S10RR023401, 1S10RR019307, and 1S10RR023043. The authors were partially supported by the National Institute of Mental Health: Dr. Romer (grant F32 MH124409); Dr. Auerbach (grant R01 MH119771); and Dr. Pizzagalli (grant R37 MH068376). Dr. Hubbard and Dr. Romer were partially supported by the Brain and Behavior Research Foundation (Hubbard: #27970; Romer: #32880) and Dr. Romer was partially supported by the Virginia Tech College of Science Dean’s Discovery Fund (#452018). The content is solely the responsibility of the author and does not necessarily represent the official views of the National Institutes of Health or of any other sponsor.

Conflicts of Interest

Dr. Auerbach is an unpaid scientific advisor for Ksana Health, and he is a paid scientific advisor for Get Sonar, Inc. He also has received research funding from Brain and Behavior Research Foundation, Klingenstein Third Generation Foundation, Morgan Stanley Foundation, NIMH, and the Tommy Fuss Fund. Dr. Henin receives royalties from Oxford University Press. Dr. Hofmann receives financial support by the Alexander von Humboldt Foundation (as part of the Alexander von Humboldt Professur), the Hessische Ministerium für Wissenschaft und Kunst (as part of the LOEWE Spitzenprofessur), and the DYNAMIC center, funded by the LOEWE program of the Hessian Ministry of Science and Arts (Grant Number: LOEWE1/16/519/03/09.001(0009)/98), and the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) – Project-ID 521379614 – TRR 393SFB/Transregio 393. He also receives compensation for his work as editor from SpringerNature and royalties and payments for his work from various publishers. Over the past 3 years, Dr. Pizzagalli has received consulting fees from Arrowhead Pharmaceuticals, Boehringer Ingelheim, Compass Pathways, Engrail Therapeutics, Karla Therapeutics, Neumora Therapeutics (former BlackThorn Therapeutics), Neurocrine Biosciences, Neuroscience Software, Sage Therapeutics, Sama Therapeutics, and Takeda Pharmaceuticals; honoraria from the American Psychological Association, Psychonomic Society and Springer (for editorial work) and Alkermes, and research funding from BIRD Foundation, Brain and Behavior Research Foundation, Dana Foundation, DARPA, Millennium Pharmaceuticals, NIMH, and Wellcome Leap. In addition, he has received stock options from Compass Pathways, Engrail Therapeutics, Neumora Therapeutics, and Neuroscience Software. All other authors declare that there were no conflicts of interest with respect to the authorship or the publication of this article. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or of any other sponsor.

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