Background
Neurocognitive effects of prenatal alcohol exposure in adulthood are not well documented. Questions persist regarding the extent to which there are specific, measurable effects beyond those associated with global ability deficits, whether individuals without the full fetal alcohol syndrome (FAS) demonstrate alcohol-related cognitive impairments and whether observed memory effects are specific to a particular modality, that is, verbal versus visual/spatial domains.
Methods
In this study, verbal and nonverbal selective reminding paradigms were used to assess memory function in 234 young adults (M age: 22.78, SD: 1.79). Alcohol-exposure was quantified prenatally. Alcohol groups included: Individuals with physical effects of alcohol exposure (Dysmorphic Group, n=47); Exposed individuals without such effects (n=74). Contrast groups included: Controls (n=59) matched for ethnicity, socioeconomic status and hospital of birth; Special Education contrast group (n=54) included to control for disability status. Memory outcomes entailed total recall, delayed recall, and measures of encoding and retrieval and learning over trials as indexed by slope.
Results
Results indicated that Dysmorphic individuals were significantly less efficient in memory performance than Controls on all of the outcomes measured but they did not differ from those in the Special Education contrast group. The non-dysmorphic, alcohol-exposed group was intermediate in their performance, suggesting a continuum of effects of prenatal exposure. Evaluation of the encoding and retrieval aspects of memory performance indicated that learning rather than forgetting accounted for the deficits associated with prenatal alcohol exposure. Finally, no interaction was found between modality of presentation (verbal and nonverbal) and effects of alcohol exposure on memory performance.
Conclusion
These findings indicate that prenatal alcohol exposure is associated with persistent and specific effects on memory performance and that these problems result from less efficient encoding of information across both verbal and nonverbal modalities. Education and training efforts with this clinical group should take these characteristics into account.
Polymorphisms in the oxytocin receptor gene are commonly associated with prosocial behaviors in the extant literature, yet their role in antisocial behaviors has rarely been explored, particularly during the transition from adolescence to early adulthood. We examined a prospective cohort (N = 404), collecting youth, mother, and clinician reports of conduct-disordered and antisocial behavior at ages 15 and 20. The oxytocin receptor gene rs53576 polymorphism was hypothesized to interact with social stress to predict antisocial outcomes. Structural equation modeling results revealed a significant main effect at age 15 (p = .025); those with the G allele exhibited higher levels of conduct problems. Structural equation modeling revealed a significant Gene × Environment interaction at age 20 (p = .029); those with the G allele who experienced high social stress exhibited higher levels of antisocial behavior. Heterozygous (AG) grouping models were compared, and parameter estimations supported G dominant groupings. These novel findings suggest that rs53576 polymorphisms may influence social salience and contribute to risk for antisocial outcomes, particularly under conditions of high social stress.
Recent data suggest that up to 11 percent of the United States population uses antidepressants such as Serotonin Reuptake Inhibitors (SRIs; Pratt, Brody, & Gu, 2011). This statistic includes pregnant women, 5 to 10% of whom report antidepressant use during pregnancy (Huybrechts et al., 2013; Austin, 2006; Cooper, Willy, Pont, & Ray, 2007), and this number may be increasing over time (Bérard, Boukhris, & Sheehy, 2016). SRIs are a mainstay treatment for depression and have historically been preferred by depressed pregnant women due to their relative safety profile, a view which emerged following initial reports of low risk for poor health or for congenital malformations (Harrington, Lee, Crum, Zimmerman, & Hertz-Picciotto, 2013; Lattimore et al., 2005). However, more recent research calls this view into more question, with studies suggesting potential increased risk for cardiac malformations among children exposed (Huybrechts, et al., 2014; Bérard, Zhao & Sheehy, 2017). In addition, a large cohort study exploring the association between prenatal SRIs and later child outcomes linked prenatal SRI exposure with slightly greater risk for Autism Spectrum Disorders (ASD; Croen, Grether, Yoshida, Odouli, & Hendrick, 2011), generating new concerns regarding increased risk for neurodevelopmental disorders. This initial report was followed by a plethora of studies and reviews on prenatal SRI exposures and ASD (Andrade, 2017; Freire, de Oliveira, & Pereira Pondé, 2016; Gentile, 2015; Healy, Le Noury, & Mangin, 2016; Kobayashi, Matsuyama, Takeuchi, & Ito, 2016; Mezzacappa et al., 2017; Rai et al., 2017). Similarly, recent studies have found significant associations between prenatal SRI exposure and atypical language development among toddlers and adolescents (Brown et al., 2016; Handal, Skurtveit, Roth, Hernandez-Diaz, & Selmer, 2016; Skurtveit, Selmer, Roth, Hernandez-Diaz, & Handal, 2014).
Considerable animal research and available human studies suggest that psychological distress experienced by mothers during gestation is associated with later neurodevelopmental deficits in offspring; however, little research has examined potential protective factors that might mitigate this risk. The current study examined the impact of maternal prenatal psychological distress during pregnancy on cognitive outcomes in preschoolers (ages 2.5–5 years) and positive parenting as a potential protective factor. Mother-child dyads (N = 162, mean child age = 44 months, 49 % female) were recruited from a longitudinal cohort of women who had previously participated in a study of maternal mood disorders during pregnancy. Maternal prenatal distress was assessed with multiple measures collected throughout pregnancy. During a follow-up visit, mothers were interviewed about their psychological symptoms since the birth of the child, parenting behaviors were recorded during a parent-child interaction, and children’s cognitive abilities were measured using the Differential Ability Scales, 2nd Edition. Maternal prenatal distress significantly predicted lower general cognitive abilities; however, this relationship was strongest for children whose mothers exhibited low levels of positive engagement and not significant when mothers exhibited high levels of positive engagement. Results suggest that positive parental engagement can protect against the detrimental effects of maternal prenatal distress on preschoolers’ cognitive abilities.
Context: Despite the expanding clinical utility of antipsychotics beyond psychotic disorders to include depressive, bipolar, and anxiety disorders, reproductive safety data regarding the neurodevelopmental sequelae of fetal antipsychotic exposure are scarce.
Objective: To examine whether intrauterine antipsychotic exposure is associated with deficits in neuromotor performance and habituation in 6-month-old infants.
Design, Setting, and Participants: A prospective controlled study was conducted from December 1999 through June 2008 at the Infant Development Laboratory of the Emory Psychological Center examining maternalinfant dyads (N=309) at 6 months postpartum with pregnancy exposure to antipsychotics (n=22), antidepressants (n=202), or no psychotropic agents (n=85). Examiners masked to maternal-infant exposure status administered a standardized neuromotor examination (Infant Neurological International Battery [INFANIB]) that tests posture, tone, reflexes, and motor skills and a visual habituation paradigm using a neutral female face.
Main Outcome Measures: The INFANIB composite score; number of trials required to achieve a 50% decrease in infant fixation during a visual habituation task; and mean time looking at the stimulus across 10 trials.
Results: Infants prenatally exposed to antipsychotics (mean=64.71) showed significantly lower INFANIB scores than those with antidepressant (mean=68.57) or no psychotropic (mean=71.19) exposure, after controlling for significant covariates (F2,281=4.51; P=.01; partial η2=0.033). The INFANIB scores were also significantly associated with maternal psychiatric history, including depression, psychosis, and overall severity/chronicity (P's<.05) and maternal depression during pregnancy was associated with less efficient habituation (r245=0.16; P<.02). There were no significant differences regarding habituation between medication exposure groups.
Conclusions: Among 6-month-old infants, a history of intrauterine antipsychotic exposure, compared with antidepressant or no psychotropic exposure, was associated with significantly lower scores on a standard test of neuromotor performance, highlighting the need for further scrutiny of the reproductive safety and neurodevelopmental sequelae of fetal antipsychotic exposure. Disentangling medication effects from maternal illness effects, which also contributed, remains a critical challenge.
Background: The offspring of mothers with mood disorders may evidence increased behavioral problems as early as preschool; however, no study to date has examined psychophysiological characteristics during infancy, particularly among offspring of mothers diagnosed with bipolar disorder. Elucidating psychobiological mechanisms of risk early in development is critical to inform prevention and early intervention efforts.
Method: This study compared physiological and behavioral responsivity in 6-month-old infants (N = 329) of mothers with lifetime histories of bipolar disorder (BD, n = 44), major depressive disorder (MDD, n = 244), or no history of Axis I disorders (CTL, n = 41). Infant respiratory sinus arrhythmia (RSA) was measured in a laboratory stressor paradigm. Measures of infant affect and behavior during mother-infant interaction, current maternal depressive symptoms, and exposure to stressful life events were examined with respect to diagnostic group and RSA.
Results: Groups did not differ in baseline RSA or infant affect measures. However, during the stressor task, infants of mothers with BD evidenced increases in RSA, while infants of MDD and CTL mothers evidenced decreases in RSA. Though levels of postnatal stress and current levels of maternal depressive symptoms differed among groups, neither of these factors predicted infant psychophysiological responses.
Conclusions: At 6 months of age, infants of mothers with BD show differences in psychophysiological regulation. These differences cannot be accounted for by perinatal outcome, current maternal depressive symptoms, or exposure to stressful life events, and thus may reflect endophenotypic markers of psychopathological risk.
The impact of prenatal alcohol exposure on memory and brain development was investigated in 92 African-American, young adults who were first identified in the prenatal period. Three groups (Control, n=26; Alcohol-related Neurodevelopmental Disorder, n=36; and Dysmorphic, n=30) were imaged using structural MRI with brain volume calculated for multiple regions of interest. Memory was measured using the Verbal Selective Reminding Memory Test and its nonverbal counterpart, the Nonverbal Selective Reminding Memory Test, which each yielding measures of learning and recall. For both Verbal and Nonverbal Recall and Slope, linear trends were observed demonstrating a spectrum of deficits associated with prenatal alcohol exposure. Dysmorphic individuals performed significantly poorer than unexposed controls on 5 of 6 memory outcomes. Alcohol-exposed individuals demonstrated significantly lower total brain volume than controls, as well as lower volume in a number of specific regions including hippocampus. Mediation analyses indicated that memory performance associated with effects of prenatal alcohol exposure was mediated from dysmorphic severity through hippocampal volume, particularly right hippocampus. These results indicate that the association between the physical effects of prenatal alcohol exposure and deficits in memory are mediated by volumetric reduction in specific brain regions.