Abstract
Objectives:
Examine maternal and paternal ADHD and ASD symptoms in relation to very preterm (VPT) and full-term (FT) children’s ADHD and ASD symptoms.
Study Design:
In this longitudinal study, maternal- and teacher-report of child ADHD and ASD symptoms were obtained for 119 children (VPT=79, FT=40) at age 5-years using the Conner’s Rating Scale-Revised (CRS-R) and Social Responsiveness Scale-2 (SRS-2). A biological parent completed self- and observer-report CRS-R and SRS-2, and measures of mood/affect, stress, and social support to assess psychosocial distress. Data were analyzed using mixed-effect models adjusted for covariates.
Results:
Child ADHD symptoms were associated with VPT birth, maternal distress, and maternal ADHD symptoms (p≤.02) and paternal ADHD symptoms (p<.001). Regarding ASD, VPT birth and parental ASD symptoms were associated with child ASD symptoms (p≤.009). Parental symptoms and birth group had no interaction.
Conclusions:
VPT birth and parental psychopathology represent independent risks for ADHD and ASD.
Children born very preterm (VPT, <30 weeks gestational age [GA]) have an increased risk of Attention Deficit Hyperactivity Disorder (ADHD) and Autism Spectrum Disorder (ASD) in childhood, with rates as high as 23% and 7% for these disorders compared to 9% and 2% in full-term (FT) children, respectively (1–5). In addition to ASD and ADHD being highly co-morbid (6,7), these disorders are highly heritable. Prior research has reported heritability estimates of around 88% for ADHD and 83% for ASD between parents and offspring, suggesting that these disorders likely have common heritable influences (8–10). However, maternal and paternal ADHD/ASD symptoms have not been examined in relation to ADHD/ASD symptoms in VPT children. Prior work from our group has examined maternal ASD and ADHD in relation to latent profiles of internalizing and externalizing symptoms in VPT children at age 5-years. The results of this work found maternal ADHD was associated with latent profiles characterized by higher levels of socio-emotional problems in VPT children, but not with lower-risk or typically developing latent profiles. We did not, however, examine domain-specific associations between maternal, paternal, and child ADHD and ASD symptoms (11).
Although ADHD and ASD symptoms are heritable, other family psychosocial factors likely play a role in the development of childhood ADHD and ASD symptoms. Maternal depression, anxiety, and stress are linked with increased ASD and ADHD symptoms in offspring (12–15). Lower socio-economic status (SES) is also associated with higher rates of ADHD, whereas inverse associations have been reported for ASD (16,17). Both maternal psychosocial stress and low SES increase the likelihood of preterm delivery (18,19). However, the extent that parental ADHD and ASD symptoms and family psychosocial factors explain variability in ADHD and ASD symptoms in VPT children is unknown. Study aims were to investigate maternal and paternal ADHD symptoms on child ADHD symptoms, and maternal and paternal ASD symptoms on child ASD symptoms in VPT and FT children at age 5. We also examine maternal psychosocial distress, medical factors associated with preterm birth and social background.
METHODS
A sample of 104 VPT infants (23–30 weeks GA), born 2007–2010, were recruited from the St. Louis Children’s Hospital Level-IV Neonatal Intensive Care Unit. At age 5-years, 85 VPT children returned for a developmental assessment (retention rate: 82%). A second sample of 40 FT singleton children (37–41 weeks GA) were recruited by two mechanisms. Thirty FT children were recruited from the schools, pediatric offices, and local communities of VPT children at age 5-years. An additional 10 FT children were recruited as infants from an adjoining maternity hospital (11). Birth groups were similar in terms of race (p=.51), sex (p=.85), and family income-to-needs ratio (p=.58, Table 1) (20). Exclusion criteria for both groups determined by electronic medical record included congenital/chromosomal abnormalities, suspected/proven congenital infection, and parent unable to give informed consent. Exclusion criteria for FT infants also included acidosis on cord blood gases, known neonatal brain lesions, neonatal seizures, and a positive maternal drug screen (see Appendix 1 for additional Methods details).
Table 1.
Clinical and Social Background Characteristics of Very Preterm and Full-Term Children
| VPT (n=79) | FT (n=40) | p | |
|---|---|---|---|
|
| |||
| Clinical Characteristics | |||
| Gestational age(weeks), m(SD) | 26.61(1.77) | 39.50(.85) | <.001 |
| Birthweight(grams), m(SD) | 948.25(254.61) | 3420.43(516.49) | <.001 |
| Male, n(%) | 36(45.6) | 17(42.5) | .85 |
| Multiple birth, n(%) | 31(39.2) | - | |
| Antenatal steroids not administered, n(%) | 7(8.9) | - | |
| Postnatal dexamethasone administered, n(%) | 7(8.9) | - | |
| Sepsis, n(%) | 25(31.6) | - | |
| Necrotizing enterocolitis, n(%) | 4(5.1) | - | |
| Social Background | |||
| Demographic Stressor index, m(SD)a | 1.48(1.4) | 1.35(1.4) | .62 |
| Young mother at delivery, n(%) | 4(5.1) | 1(2.5) | .51 |
| African American, n(%) | 30(37.9) | 17(42.5) | .51 |
| Mother not a High School graduate, n(%)a | 4(5.1) | 3(7.5) | .69 |
| Single parent household, n(%)a | 35(44.3) | 15(37.5) | .56 |
| Public Health Insurance, n(%)a | 45(57) | 18(45) | .22 |
| Income to Need Ratio, m(SD)a | 1.91(2.0) | 2.21(2.2) | .58 |
| Maternal Psychosocial Distress | |||
| Maternal Distress m(SD)a | .90(1.21) | .72(.89) | .45 |
| Depression n(%)a,b | 8(10.3) | 0(0) | .06 |
| Anxiety n(%)a,b | 10(13.7) | 3(9.4) | .54 |
| Parenting Stress n(%)a,b | 10(14.3) | 2(6.1) | .23 |
| Adverse Life Events n(%)a,b | 16(22.9) | 4(12.1) | .20 |
| Low Social Support n(%)a,b | 21(30.0) | 14(43.8) | .18 |
| Full-Scale IQ | |||
| WPPSI-III T-scores m(SD)a | 42.5(9.1) | 54.5(11.0) | <.001 |
Obtained at age 5-year follow-up.
See Methods for specific measures
Procedure.
At the 5-year assessment, a biological parent completed questionnaires and a structured face-to-face interview to obtain information on children’s ADHD and ASD symptoms. The parent also completed questionnaires to assess parental ADHD and ASD symptoms, socio-demographic background, and maternal psychosocial wellbeing. Teachers completed electronic questionnaires to assess children’s ADHD and ASD symptoms. Study procedures were approved by the Institutional Review Board. Written informed consent was obtained from all parents and teachers.
Children’s ADHD and ASD Outcomes.
Parents and teachers completed the Conner’s Rating Scale-Revised (CRS-R) (21) to obtain a dimensional measure of child ADHD symptoms. The CRS-R assesses inattention/cognitive, oppositional, hyperactivity, and combined ADHD symptoms. Parents completed the semi-structured Preschool Age Psychiatric Assessment (PAPA) clinical interview to assess child ADHD diagnosis and symptom severity (22). Parents and teachers also completed the Social Responsiveness Scale-2 (SRS-2) (23) to obtain a dimensional measure of child ASD symptoms, spanning social-communication interaction impairments and restrictive/ repetitive behaviors. As this study focuses on parent-child ADHD and ASD symptoms, birth-group differences in child outcomes are shown in Figure 1 and Appendix 2 (Tables 1 and 2; online only).
Figure 1.
ADHD and ASD Symptoms Between Children Born Very preterm and Full-Term at Age 5-Years
Parent ADHD Symptoms.
Parental ADHD symptoms were assessed with self- and observer-report versions of Conners Adult ADHD Rating Scale (CAARS) (24). At the 5-year follow-up visit, mothers completed the self-report version (n=102), and also completed observer report version to obtain ADHD symptom ratings on the child’s biological father (n=79).
Parent ASD Symptoms.
Maternal and paternal ASD symptoms were assessed using the self- and observer-report versions of the SRS-2 (25). Mothers completed a self-report version (n=101) and also completed observer report version to obtain ASD ratings on the child’s biological father (n=81).
Demographic Stressor Index.
Socio-demographic adversity was measured using a cumulative index to account for life circumstances that may increase stress (26). Five maternal socio-demographic factors were dichotomized (present=1, absent=0) and summed (0–5): mother ≤18 years at delivery, race (African American, proxy for systemic and individual experiences of racism), public health insurance, single-parent household, and no high school qualification.
Maternal Distress Index.
Maternal psychosocial distress was assessed using a cumulative index. Five key factors were dichotomized (at-risk=1, low-risk=0) based on validated clinical cut-offs and the poorest tertile of the sample (11) and summed (0–5): depressive symptoms, Beck Depression Inventory-II total >13 (27); anxiety symptoms, State Trait Anxiety Inventory trait subscale >40 (28); parenting stress, Parent Stress Index total ≥260 (29); adverse life events, PSI Life Events total ≥17 (29); and social support, Social Support Questionnaire satisfaction subscale ≤5.17 (30). Established clinical cut-off values were used for all measures besides the Social Support Questionnaire satisfaction subscale, as it does not have a validated clinical cut-off value, so the poorest the poorest tertile of the study sample (≤5.17) was used to create the cut-off value.
Infant Clinical Index.
Clinical data were collected for VPT infants from infant medical records. Factors were dichotomized (present=1, absent=0) and summed (0–10): intrauterine growth restriction, prolonged oxygen supplementation, did not receive antenatal steroids, received dexamethasone, necrotizing enterocolitis, sepsis, patent ductus arteriosus, retinopathy of prematurity, ≥3SD weight-for-height/length, and >75th centile for parenteral nutrition duration (11).
Child Full Scale Intellectual Quotient (FSIQ).
Child FSIQ was assessed using the Wechsler Preschool Primary Scales of Intelligence-III (31). Children completed the Information, Vocabulary, Word Reasoning, Block Design, Matrix Reasoning, Picture Concepts, and Coding subtests.
Data Analysis.
Data analysis was performed in SPSS (version 24, IBM Corp). Missing data (2.5% −15% across measures) was estimated using multiple imputation with aggregate data reported (32). Missing paternal data was not presumed missing-at-random due to non-custodial fathers and was not imputed. In the whole sample, birth group (VPT=1, FT=0), Maternal Distress index, and maternal ADHD and ASD t-scores were fitted to child ADHD and ASD parent-report t-scores using Linear Mixed-effect Models (LMM) adjusted for family clustering, demographic stressor index, and child’s sex (F=2, M=1). PAPA ADHD symptom count was also used as a dependent variable to examine predictors of clinically impairing symptoms assessed with a structured interview. Significant independent variables were tested for interactions and non-significant predictors were removed in order to report the most parsimonious model. LMMs were then performed for children who had paternal ADHD and ASD t-scores to examine the role of paternal background. Next, maternal and paternal ADHD symptoms were added in the same model to examine maternal versus paternal heritable risk. Maternal and paternal ASD symptoms were colinear (r=.69, p<.001) and could not be examined in the same model (see Table 3; Online Only for correlations between parental background factors). Supplementary analysis was performed to adjust findings for child FSIQ (Tables 4 and 5; online only, online Appendix 2) and with teacher ratings as dependent variables (Table 6; online only, Appendix 2). Within-group analysis among VPT children showed that neither birthweight nor infant clinical risk was correlated with ADHD or ASD symptoms (all p>.05; Table 7; online only, Appendix 2). Power analysis for multiple regression with 5 independent variables and sample size n = 119 (the sample size for the majority of the models) would have 99% power to detect small and moderate effect sizes (i.e., R2 =.20-.35), and power analysis for multiple regression with 4 independent variables and sample size n = 80 (sample size for paternal data) would have 95% power to detect small effect sizes (i.e., R2 =.20) and 99% to detect moderate effect sizes (i.e. R2=.35).
RESULTS
Aim 1: Maternal and Paternal Factors associated with Children’s ADHD Symptoms Maternal Psychosocial Distress and ADHD Symptoms.
As shown in Table 2, the covariate factors sex (p=.63) and demographic stressor index (p=.55) were not associated with parent- reported child ADHD symptoms and were removed from further analysis (n=119, see Table 8; online only and Appendix 2 for detailed analysis of demographic stressors). As expected, VPT birth (p=.02), maternal psychosocial distress (p<.001), and maternal ADHD symptoms (p=.007) were independently associated with children’s ADHD symptoms. There were no interactions between VPT birth and maternal ADHD symptoms (Estimate=−3.61, p=.16) or VPT birth and maternal distress (Estimate=−2.88, p=.31).
Table 2.
Maternal Background Factors and Parent- Reported Child ADHD and ASD Symptoms
| Maternal ADHD Symptoms and Distress on Child ADHD Symptoms (n=119) | ||||
|---|---|---|---|---|
| Estimate (SE) a. | p | Estimate (SE) b. | p | |
| Sex | −.96(2.0) | .63 | - | - |
| Demographic Stressors | .72(1.2) | .55 | - | - |
| VPT Birth | −5.35(2.4) | .03 | −5.40(2.4) | .02 |
| Maternal Distress | 4.64(1.4) | .001 | 4.85(1.3) | <.001 |
| Maternal ADHD Symptoms | 3.57(1.3) | .006 | 3.48(1.3) | .007 |
| Maternal ASD Symptoms and Distress on Child ASD Symptoms (n=119) | ||||
| Estimate (SE) a. | p | Estimate (SE) b. | p | |
| Sex | −1.1(1.8) | .50 | - | - |
| Demographic Stressors | 0.8(1.0) | .43 | - | - |
| VPT Birth | −4.5(1.8) | .01 | −4.59(1.8) | .009 |
| Maternal Distress | 1.5(1.0) | .13 | 1.61(1.0) | .11 |
| Maternal ASD Symptoms | 6.4(1.0) | <.001 | 6.66(1.0) | <.001 |
Model run with all predictors
Model run with significant predictors.
Secondary analysis was undertaken to examine maternal ADHD symptoms and child ADHD symptoms using the PAPA ADHD total symptom count (Table 9; online only). These results suggested male sex (p=.004) was associated with PAPA-identified ADHD symptoms, but VPT birth (p=.29), demographic stressors (p=.71), maternal distress (p=.18), and maternal ADHD (p=.15) were not.
Paternal ADHD Symptoms and Children’s ADHD Symptoms.
In the sample with paternal data (n=80), VPT birth (p=.04) and paternal ADHD symptoms (p<.001) were independently associated with parent-reported children’s ADHD symptoms (Table 3). There was no interaction between VPT birth and paternal ADHD symptoms (Estimate= 1.19, p=.68). Sex (p=.46) and demographic stressors (p=.12) were not significant and were removed from the analysis. A second model was performed using PAPA total ADHD symptom count as the dependent variable (Table 10; online only) and showed that paternal ADHD symptoms (p=.009) was significant, whereas VPT birth (p=.39), sex (p=.43), and demographic stressors (p=.41) were not.
Table 3.
Paternal Background Factors on Parent- Reported Child ADHD and ASD Symptoms
| Paternal ADHD Symptoms on Child ADHD Symptoms (n= 80) | ||||
|---|---|---|---|---|
| Estimate (SE) a. | p | Estimate (SE) b. | p | |
| Sex | 1.0(1.3) | .46 | - | - |
| Demographic Stressors | 2.4(1.6) | .12 | - | - |
| VPT Birth | −5.8 (2.8) | .04 | −5.75(2.8) | .04 |
| Paternal ADHD Symptoms | 5.9 (1.5) | <.001 | 6.35 (1.4) | <.001 |
| Paternal ASD Symptoms on Child ASD Symptoms (n=81) | ||||
| Estimate (SE) a. | p | Estimate (SE) b. | p | |
| Sex | 0.4(1.0) | .69 | - | - |
| Demographic Stressors | 0.9(1.3) | .49 | - | - |
| VPT Birth | −3.9(2.2) | .08 | −3.9(2.2) | .07 |
| Paternal ASD Symptoms | 6.6(1.3) | <.001 | 7.1(1.1) | <.001 |
Model run with all predictors
Model run with significant predictors.
Parental ADHD Symptoms and Children’s ADHD Symptoms.
The effects of both maternal and paternal ADHD symptoms on child ADHD symptoms were examined for children with paternal ADHD data (n=80). Maternal and paternal ADHD symptoms showed a moderate-to-strong correlation in the VPT group (r=.58, p<.001), whereas no association was found in the FT group (r=.17, p=.36). As shown in Table 11; online only, paternal ADHD symptoms (p=.006) and VPT birth (p=.04) were independently associated with parent-reported children’s ADHD symptoms, but maternal ADHD symptoms (p=.38) and maternal distress (p=.09) were not. When multivariate models were extended to include interaction terms, the interaction between VPT birth and maternal distress was significant (Estimate=−6.3, p=.04), but there was no interaction between VPT birth and paternal ADHD (Estimate=2.4, p=.40).
Aim 2: Maternal and Paternal Factors associated with Children’s ASD Symptoms Maternal Psychosocial Distress and ASD Symptoms.
As shown in Table 2 (n=119), the covariate factors sex (p=.50) and demographic stressors (p=.43) were not significant and were removed from subsequent analyses. VPT birth (p=.009) and maternal ASD (p<.001) were associated with parent- reported children’s ASD symptoms (Table 2), but maternal psychosocial distress was not significant (p=.11). There was no interaction between VPT birth and maternal ASD symptoms (Estimate=1.42, p=.48).
Paternal ASD Symptoms and Children’s ASD Symptoms.
In the sample with paternal ASD data (n=81), paternal ASD symptoms (p<.001) were independently associated with parent-reported children’s ASD symptoms (Table 3). Sex (p=.69) and demographic stressors (p=.49) were not significant covariates. There was no interaction between VPT birth and paternal ASD symptoms (Estimate= 1.92, p=.40).
DISCUSSION
This study examines the independent contribution of maternal and paternal ADHD and ASD symptoms on ADHD and ASD symptoms in VPT and FT children. Maternal psychosocial distress and sociodemographic stressors were also examined as risk factors for ADHD and ASD symptoms. Findings suggest VPT birth, maternal distress, and parental ADHD symptoms were associated with increased child ADHD symptoms. The interaction between VPT birth and maternal distress suggested that maternal distress was more strongly associated with child ADHD symptoms in the VPT group. In contrast, the association between maternal and paternal ADHD symptoms on child ADHD symptoms was similar across both groups of children. Risk factors associated with child ASD symptoms included VPT birth and parental ASD symptoms, with no interactions between these risk factors. Parental ASD symptoms were associated with child ASD symptoms in both VPT and FT children. While it could have been hypothesized that the higher rates of ASD and ADHD in VPT children may be due to increased heritability, these findings suggest VPT birth and parental symptoms confer independent risks for child ASD and ADHD. Findings warrant early screening of parental psychiatric symptoms in newborn nurseries, and especially for children born VPT as they are at an additional risk, in order to identify children who are at risk for ADHD and ASD in childhood. These screenings could be added to existing efforts, as many NICUs are now screening parents for mental health issues with many publishing the results demonstrating the feasibility and importance of their screening protocols (33,34).
Parental Factors Associated with Children’s ADHD Symptoms
Consistent with previous research (3,9,13,15), VPT birth, maternal and paternal ADHD symptoms, and maternal distress explained variability in child ADHD symptoms at age 5-years. Specifically, in addition to VPT birth, maternal and paternal ADHD symptoms were associated with CRS-R t-scores. This suggests that family heritability of ADHD may be an important predisposing risk factor for the increased rates of childhood ADHD observed among children born VPT. The heritable transmission of increased ADHD symptoms could occur through genetic or socio-environmental mechanisms. For example, the association between maternal ADHD and child ADHD symptoms could be transmitted through higher levels of negative and intrusive parenting among mothers with psychopathology (35). Of note, previous evidence suggests mothers with ADHD rate offspring on measures of ADHD symptomatology in a similar manner as fathers with ADHD and parents with no ADHD, and associations between maternal depression and child ADHD persist after accounting for any reporting bias among mothers with depression (36,37). Interaction terms between VPT birth, maternal ADHD, and paternal ADHD were not significant, suggesting these risk factors all have independent effects that do not vary as a function of preterm status, and therefore represent independent mechanisms for childhood ADHD.
However, we did find that the effect of maternal distress on child ADHD symptoms varied as function of prematurity. Among the group of children that had paternal data collected, a significant interaction term suggested that maternal psychosocial distress had a stronger relationship with child CRS-R t-scores in the VPT group than the FT group. This finding could reflect the fact that distressed mothers are more likely to deliver preterm or the challenges associated with parenting VPT children who have more complex neurodevelopmental needs than FT children. Prior work has shown that mothers of children with ADHD have higher levels of stress, parental depression and anxiety, and family dysfunction, and that the degree of stress experienced by the parent affects the severity of child symptoms (38,39). While the specific etiology is unclear, our findings suggest parental ADHD symptoms and maternal distress, including depression and anxiety, should be screened for in order to identify infants with higher risk of developing ADHD in later childhood.
Paternal ADHD symptoms was the only significant predictor of child ADHD diagnosis assessed with the PAPA symptom count, suggesting paternal ADHD symptoms is a stronger risk factor for clinically significant ADHD symptoms in offspring. Sex was the only significant predictor when maternal ADHD symptoms were examined in relation to child ADHD using the PAPA, potentially due to known higher rates of ADHD diagnoses in males (40). The differing pattern of risk factors identified are potentially due to the PAPA being a measure of diagnosis, whereas CRS-R looks at a continuum of symptoms.
Parental Factors Associated with Children’s ASD Symptoms
VPT birth, maternal ASD symptoms, and paternal ASD symptoms were associated with child ASD symptoms. While the association between parental and child ASD has been demonstrated in children born FT, current study findings extends previous research demonstrating an association between parental ASD and child ASD in a VPT population (3,15,41). Sex was not a significant predictor of child ASD symptoms, which could be due to the fact that VPT birth has been found to moderate the relationship between sex and ASD (42). While the demographic stressor index was correlated with ASD symptoms, it did not explain variance over and above parental ASD symptoms, potentially due to heritability more directly relating to child ASD than the exposure to demographic stress (16). Maternal and Paternal ASD and ADHD symptoms were highly correlated, which could reflect reporter bias or assortative mating (43,44). In prior work, we found that maternal reports of children’s ASD symptoms were consistent with direct observational ratings of ASD symptoms using a standardized clinical assessment (11), suggesting maternal report bias is unlikely to account for the association between maternal and child ASD symptoms. Taken together, current study findings suggest that VPT birth poses risk independent of heritability of ASD symptoms, and parental psychopathology may place both children born VPT and children born FT at similar risk of poor outcome. Thus, parental ASD is a key family background factor that should be screened in order to identify VPT children that may have compounded risk for ASD.
Strengths and Limitations
Strengths of the study include the high retention rate of the VPT cohort (82%), multi-informant ratings from parents and teachers, and a recruited FT group with similar demographics as the VPT group. Other existing studies of VPT children have fewer families with single parent households, from racial and ethnic minority groups, and with lower SES (3), making current findings generalizable to socially disadvantaged samples of VPT children. Study limitations include the modest sample size, which may have resulted in a lack of statistical power to detect small effect sizes in outcomes in subgroup analyses with smaller sample size. However, the current study sample size is comparable to other studies of children born VPT (45). There was a higher rate of missing paternal ADHD and ASD data due to non-custodial fathers. We also acknowledge that parental ADHD/ASD data for the secondary parent was obtained via the primary caregiver (95% biological mother, 5% biological father) reporting on the other biological parent using validated, observer-report questionnaires. Furthermore, this study did not assess parental ADHD or ASD with a semi-structured clinical interview to obtain psychiatric diagnoses in either parent (24,25). Therefore, future research should focus on larger samples and use clinical interviews for both biological parents in order to further delineate the influence of clinically significant parental ADHD and ASD on ADHD and ASD outcomes in children born VPT.
Conclusions
In addition to VPT birth, maternal and paternal ADHD symptoms, and maternal distress were associated with children’s ADHD symptoms at age 5-years. Similarly, risk factors for increased ASD symptoms included VPT birth and maternal and paternal ASD symptoms. The association between parental ADHD/ASD and child outcomes did not vary as a function of birth group, suggesting that heritability of these disorders is equivalent across birth groups of children. Furthermore, maternal distress spanning high levels of depression, anxiety, parenting stress, poor social support, and adverse life events also contributes to increased ADHD symptoms in children born VPT. When taken together, these collective findings highlight that screening for maternal and paternal ADHD and ASD symptoms, as well as maternal distress, as early as the nursery or NICU stay is important to identify and refer families to early prevention interventions most notably addressing parental mental and caregiving practices as well as providing parental psychoeducation in order to modify the risk trajectory for these children. Further, findings indicate the need for interventions that address parental psychosocial functioning as part of follow-up care of infants born VPT.
Supplementary Material
Disclosures
Study funding was provided by the National Institutes of Health (R01-HD057098, R01-MH113570, R01-MH113883, R01-DA046224, R34-DA050272, K02-NS089852, UL1-TR000448, K23-MH105179, K01-MH122735), Intellectual and Developmental Disabilities Research Center at Washington University (U54-HD087011), Office of Medical Student Research at Washington University (NIK T35 NHLBI Training Grant), Cerebral Palsy International Research Foundation, The Dana Foundation, March of Dimes, The Child Neurology Foundation, The Doris Duke Charitable Foundation, and A NARSAD Young Investigator Award from the Brain and Behavior Research Foundation. Study sponsors played no role in study design, data collection or analysis, writing of the report, or the decision to submit this paper for publication. We thank members of the Washington University Neonatal Developmental Research Group and the IDDRC at Washington University in St. Louis for study coordination and assistance with data collection. Thank you to the children and families involved with this study.
Footnotes
Conflict of Interest The authors have no conflicts of interest to disclose.
Data Availability
Not applicable
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