Pre- and Perinatal Risk for Attention-Deficit Hyperactivity Disorder: Does Neuropsychological Weakness Explain the Link?

Abstract

Etiological investigations of attention-deficit hyperactivity disorder (ADHD) and disruptive behavior problems support multiple causal pathways, including involvement of pre- and perinatal risk factors. Because these risks occur early in life, well before observable ADHD and externalizing symptoms emerge, the relation between risk and symptoms may be mediated by neurodevelopmental effects that manifest later in neuropsychological functioning. However, potential dissociable effects of pre/perinatal risk elements on ADHD and familial confounds must also be considered to test alternative hypotheses. 498 youth aged 6–17 years (55.0% male) completed a multi-stage, multi-informant assessment including parent and teacher symptom reports and parent ratings of pre/perinatal health risk indicators. Youth completed a neuropsychological testing battery. Multiple mediation models examined direct effects of pre- and perinatal health risk on ADHD and other disruptive behavior disorder symptoms and indirect effects via neuropsychological functioning. Parental ADHD symptoms and externalizing status was covaried to control for potential familial effects. Effects of prenatal substance exposure on inattention were mediated by memory span and temporal processing deficits. Further, effects of perinatal health risk on inattention, hyperactivity-impulsivity, and ODD were mediated by deficits in response variability and temporal processing. Further, maternal health risks during pregnancy appeared to exert direct rather than indirect effects on outcomes. Results suggest that after controlling for familial relatedness of ADHD between parent and child, early developmental health risks may influence ADHD via effects on neuropsychological processes underpinning the disorder.

Fluid Reasoning Mediates the Association of Birth Weight With ADHD Symptoms in Youth From Multiplex Families With ADHD

“…In contrast, the present study extended hypotheses to a larger sample consisting of siblings from a broad age range with high genetic load for ADHD (although age was controlled in all analyses), and controlled for IQ. Contrary to Morgan et al (2016) as well as the larger literature on birth weight and ADHD, but consistent with other mediational studies of birth weight and ADHD symptoms (e.g., Wiggs et al, 2016), we did not observe a significant total effect of birth weight on ADHD symptoms (i.e., association of birth weight with ADHD symptoms unadjusted for the mediators). This may be attributable to several factors, including higher power to detect indirect effects relative to the total effect (Loeys et al, 2015), or the elevated ADHD symptom severity of this high-risk sample relative to case-control or population-based samples previously used to establish birth weight–ADHD associations.…”

Sex moderates the impact of birth weight on child externalizing psychopathology.

“…The data in this manuscript have been used in previous manuscripts (e.g. Wiggs, Elmore, Nigg, & Nikolas, 2016), but the analyses in previous manuscripts did not specifically examine the moderation of the association between birth weight and Attention-Deficit Hyperactivity Disorder by sex. …”

Sekundäre Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung

“…Da eine mütterliche ADHS das Risiko für Suchterkrankungen und Substanzmissbrauch erhöht, muss davon ausgegangen werden, dass sich bezüglich des mütterlichen Tabak-und Alkoholkonsums in der Schwangerschaft möglicherweise genetische und Umweltfaktoren vermischen [25]. In ihrer Übersichtsarbeit wiesen Sciberras et al [12] daher auf die meist unzureichende Methodik der vorliegenden Literatur hin, da in den meisten Studien nicht konsequent versucht wurde, genetische und Umweltfaktoren zu trennen.…”