Electroencephalogram aperiodic power spectral slope can be reliably measured and predicts ADHD risk in early development.

The aperiodic exponent of the electroencephalogram (EEG) power spectrum has received growing attention as a physiological marker of neurodevelopmental psychopathology, including attention-deficit/hyperactivity disorder (ADHD). However, its use as a marker of ADHD risk across development, and particularly in very young children, is limited by unknown reliability, difficulty in aligning canonical band-based measures across development periods, and unclear effects of treatment in later development. Here, we investigate the internal consistency of the aperiodic EEG power spectrum slope and its association with ADHD risk in both infants (n = 69, 1-month-old) and adolescents (n = 262, ages 11-17 years). Results confirm good to excellent internal consistency in infancy and adolescence. In infancy, a larger aperiodic exponent was associated with greater family history of ADHD. In contrast, in adolescence, ADHD diagnosis was associated with a smaller aperiodic exponent, but only in children with ADHD who had not received stimulant medication treatment. Results suggest that disruptions in cortical development associated with ADHD risk may be detectable shortly after birth via this approach. Together, findings imply a dynamic developmental shift in which the developmentally normative flattening of the EEG power spectrum is exaggerated in ADHD, potentially reflecting imbalances in cortical excitation and inhibition that could contribute to long-lasting differences in brain connectivity.

Maternal mindfulness during pregnancy predicts newborn neurobehavior.

Newborn neurobehavioral competencies portend a young child's abilities to modulate their arousal and attention in response to dynamic environmental cues. Although evidence suggests prenatal contributions to newborn neurobehavioral differences, no study to date has examined wellness-promoting traits, such as a pregnant woman's mindfulness, in this association. We examined whether a mother's mindfulness while pregnant related to neurobehavioral outcomes in her neonate, as well as whether maternal mindfulness moderated the link between prenatal maternal emotion dysregulation and newborn neurobehavior. Mothers (N = 162) reported on their mindfulness and emotion dysregulation while pregnant. Newborn arousal and attention were assessed at least 24 h after birth (M = 3.8 days, SD = 8.3) using the NICU Network Neurobehavioral Scale (NNNS). Highly mindful pregnant women reported lower levels of emotion dysregulation. Newborns of highly mindful mothers exhibited higher levels of arousal (e.g., excitability, motor activity) but did not differ in regards to attention at birth. Maternal emotion dysregulation while pregnant was associated with blunted newborn attention, but only among mothers who were less mindful. Our findings suggest that a mother's mindfulness while pregnant may influence her fetus' neurobehavioral development in ways that are evident at birth.

Behavioral and cognitive correlates of the aperiodic (1/f-like) exponent of the EEG power spectrum in adolescents with and without ADHD.

Efficient information processing facilitates cognition and may be disrupted in a number of neurodevelopmental conditions. And yet, the role of inefficient information processing and its neural underpinnings remains poorly understood. In the current study, we examined the cognitive and behavioral correlates of the aperiodic exponent of the electroencephalogram (EEG) power spectrum, a putative marker of disrupted, inefficient neural communication, in a sample of adolescents with and without ADHD (n = 184 nADHD = 87; Mage = 13.95 years, SD = 1.36). Exponents were calculated via FOOOF (Donoghue et al., 2020a) from EEG data recorded during an 8-minute baseline episode. Reaction time speed and variability, as well as drift diffusion parameters (including the drift rate parameter, a cognitive parameter directly related to inefficient information processing) were calculated. Adolescents with ADHD had smaller aperiodic exponents (a "flattened" EEG power spectrum) relative to their typically-developing peers. After controlling for ADHD, aperiodic exponents were related to reaction time variability and the drift rate parameter, but not in the expected direction. Our findings lend support for the aperiodic exponent as a neural correlate of disrupted information processing, and provide insight into the role of cortical excitation/inhibition imbalance in the pathophysiology of ADHD.

Prenatal substance exposure and maternal hostility from pregnancy to toddlerhood: Associations with temperament profiles at 16 months of age.

We investigated whether infant temperament was predicted by level of and change in maternal hostility, a putative transdiagnostic vulnerability for psychopathology, substance use, and insensitive parenting. A sample of women (N = 247) who were primarily young, low-income, and had varying levels of substance use prenatally (69 nonsmokers, 81 tobacco-only smokers, and 97 tobacco and marijuana smokers) reported their hostility in the third trimester of pregnancy and at 2, 9, and 16 months postpartum, and their toddler's temperament and behavior problems at 16 months. Maternal hostility decreased from late pregnancy to 16 months postpartum. Relative to pregnant women who did not use substances, women who used both marijuana and tobacco prenatally reported higher levels of hostility while pregnant and exhibited less change in hostility over time. Toddlers who were exposed to higher levels of prenatal maternal hostility were more likely to be classified in temperament profiles that resemble either irritability or inhibition, identified via latent profile analysis. These two profiles were each associated with more behavior problems concurrently, though differed in their association with competence. Our results underscore the utility of transdiagnostic vulnerabilities in understanding the intergenerational transmission of psychopathology risk and are discussed in regards to the Research Domain Criteria (RDoC) framework.

Intergenerational transmission of emotion dysregulation: Part II. Developmental origins of newborn neurobehavior.

We investigated whether neurobehavioral markers of risk for emotion dysregulation were evident among newborns, as well as whether the identified markers were associated with prenatal exposure to maternal emotion dysregulation. Pregnant women (N = 162) reported on their emotion dysregulation prior to a laboratory assessment. The women were then invited to the laboratory to assess baseline respiratory sinus arrhythmia (RSA) and RSA in response to an infant cry. Newborns were assessed after birth via the NICU Network Neurobehavioral Scale. We identified two newborn neurobehavioral factors-arousal and attention-via exploratory factor analysis. Low arousal was characterized by less irritability, excitability, and motor agitation, while low attention was related to a lower threshold for auditory and visual stimulation, less sustained attention, and poorer visual tracking abilities. Pregnant women who reported higher levels of emotion dysregulation had newborns with low arousal levels and less attention. Larger decreases in maternal RSA in response to cry were also related to lower newborn arousal. We provide the first evidence that a woman's emotion dysregulation while pregnant is associated with risks for dysregulation in her newborn. Implications for intergenerational transmission of emotion dysregulation are discussed.

Testing the programming of temperament and psychopathology in two independent samples of children with prenatal substance exposure.

Prenatal programming models have rarely been applied to research on children with prenatal substance exposure, despite evidence suggesting that prenatal drug exposure is a form of stress that impacts neurodevelopmental outcomes and risk for psychopathology. Utilizing data from two longitudinal multisite studies comprising children prenatally exposed to substances as well as a nonexposed comparison group (Maternal Lifestyle Study, n = 1,388; Infant Development, Environment, and Lifestyle study, n = 412), we tested whether early phenotypic indicators of hypothesized programming effects, indexed by growth parameters at birth and infant temperament, served as a link between prenatal substance exposure and internalizing and externalizing behavior at age 5. Latent profile analysis indicated that individual differences in reactivity and regulation for infants prenatally exposed to substances was best characterized by four temperament profiles. These profiles were virtually identical across two independent samples, and demonstrated unique associations with adjustment difficulties nearly 5 years later. Results of path analysis using structural equation modeling also showed that increased prenatal substance exposure was linked to poorer growth parameters at birth, profiles of temperamental reactivity in infancy, and internalizing and externalizing behavior at age 5. This pathway was partially replicated across samples. This study was among the first to link known individual-level correlates of prenatal substance exposure into a specific pathway to childhood problem behavior. Implications for the developmental origins of a child's susceptibility to psychopathology as a result of intrauterine substance exposure are discussed.

Shaping emotion regulation: attunement, symptomatology, and stress recovery within mother-infant dyads.

The foundations of emotion regulation are organized, in part, through repeated interactions with one's caregiver in infancy. Less is known about how stress physiology covaries between a mother and her infant within these interactions, leaving a gap in our understanding of how the biological basis of emotion regulation develops. This study investigated physiological attunement between mothers and their 5-month-old infants, as well as the influence of maternal depression and anxiety, during stress recovery. During the reengagement phase of the Still Face Paradigm, mother-infant dyads exhibited negative attunement, as measured by inverse covariation of respiratory sinus arrhythmia (RSA). Increases in maternal RSA corresponded to decreases in infant RSA, underscoring dyadic adjustment during recovery. Moreover, infant regulation differed as a function of maternal anxiety, with more anxious mothers having infants with higher RSA during reengagement. Implications for the consolidation of regulatory capabilities within the context of the early caregiving relationship are discussed.

Prenatal Stress, Fearfulness, and the Epigenome: Exploratory Analysis of Sex Differences in DNA Methylation of the Glucocorticoid Receptor Gene.

Exposure to stress in utero is a risk factor for the development of problem behavior in the offspring, though precise pathways are unknown. We examined whether DNA methylation of the glucocorticoid receptor gene, NR3C1, was associated with experiences of stress by an expectant mother and fearfulness in her infant. Mothers reported on prenatal stress and infant temperament when infants were 5 months old (n = 68). Buccal cells for methylation analysis were collected from each infant. Prenatal stress was not related to infant fearfulness or NR3C1 methylation in the sample as a whole. Exploratory sex-specific analysis revealed a trend-level association between prenatal stress and increased methylation of NR3C1 exon 1F for female, but not male, infants. In addition, increased methylation was significantly associated with greater fearfulness for females. Results suggest an experience-dependent pathway to fearfulness for female infants via epigenetic modification of the glucocorticoid receptor gene. Future studies should examine prenatal stress in a comprehensive fashion while considering sex differences in epigenetic processes underlying infant temperament.