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Perinatal complications in children with attention-deficit hyperactivity disorder and their unaffected siblings

Leila Ben Amor1, Natalie Grizenko, George Schwartz

  • 1Department of Psychiatry, Laval University, Québec.

Journal of Psychiatry & Neuroscience : JPN
|March 31, 2005
PubMed

Insights

Neonatal complications are a significant nonshared environmental risk factor for attention-deficit hyperactivity disorder (ADHD). This study found higher rates of these complications in children with ADHD compared to their siblings, suggesting a potential pathogenic role.

Area of Science:

  • Child psychiatry
  • Neurodevelopmental disorders
  • Environmental epidemiology

Background:

  • Attention-deficit hyperactivity disorder (ADHD) is influenced by genetic and nonshared environmental factors.
  • Pregnancy, labor/delivery, and neonatal complications (PLDNC) are associated with ADHD, but their specific role as shared or nonshared factors is unclear.

Purpose of the Study:

  • To identify specific elements of PLDNC that act as nonshared environmental risk factors for ADHD.
  • To investigate the nature of the association between PLDNC and ADHD within families.

Main Methods:

  • An intrafamily study design compared PLDNC history between children with ADHD and their unaffected siblings.
  • Data collected using the Kinney Medical and Gynecological Questionnaire and McNeil-Sjostrom Scale.
  • Seventy children with ADHD and 50 unaffected siblings participated; ADHD symptoms were measured using CBCL, CPT, and RASS.

Main Results:

  • Children with ADHD exhibited significantly higher rates of neonatal complications compared to their unaffected siblings.
  • Neonatal complications in children with ADHD correlated with more severe ADHD symptoms (CBCL scores) and poorer performance on the Continuous Performance Test (CPT).

Conclusions:

  • Neonatal complications appear to be a nonshared environmental risk factor in the development of ADHD.
  • These findings suggest a potentially pathogenic role for neonatal complications in ADHD etiology.
Abstract

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