Hyperbilirubinemia and Language Delay in Premature Infants

Abstract

Objective To evaluate if language delay at three years in premature infants is associated with prior exposure to hyperbilirubinemia during the first two weeks after birth. Patients and Methods We performed retrospective case-control study of infants admitted to the Neonatal Intensive Care Unit between January and October 2003. Inclusion criteria included a birth weight ≤ 1500 grams and follow-up to age three years. Exclusion criteria included genetic disorders and hearing loss or recurrent ear infections. Peak total serum bilirubin (TSB) during the first two weeks and duration of hyperbilirubinemia (days with TSB > 8 mg/dl) were determined. Infants with language delay and receiving speech therapy by three years were identified through developmental clinic charts and tracking program and compared to infants who had normal language development. Results 125 infants with birth weight ≤ 1500 grams were admitted to the Neonatal Intensive Care Unit between January and October 2003. Fifteen infants died and 110 were discharged home. 102/110 (93%) of infants had follow-up to age three years. Four infants were excluded (1 genetic disorder, 3 delayed hearing loss or recurrent ear infections). 24 infants had a language delay and received speech therapy while 74 infants had normal language development. There was no significant difference in peak TSB and duration of hyperbilirubinemia between the two groups. On logistic regression, only bronchopulmonary dysplasia was associated with language delay (Adjusted odds ratio 7.3, 95% confidence interval 2.5 – 22). Conclusions Hyperbilirubinemia defined as peak TSB level or duration of elevated bilirubin in days is not associated with language delay in premature infants. However, this issue deserves investigation since other measures of bilirubin, such as unbound bilirubin may be associated with language delay.

A psychometric study of the Bayley Scales of Infant and Toddler Development – 3rd Edition for term and preterm Taiwanese infants

“…Moreover, no term Taiwanese infants were classified as having cognitive or motor delay, and only few infants had language delay based on the Bayley-III standard. Meanwhile, preterm Taiwanese infants' cognitive and motor performance approached the Bayley-III norms, and their rates of developmental delay were lower than the previously established prevalence estimates (cognitive delay 0-1% vs. 4-30%, language delay 2-9% vs. 8-26%, and motor delay 0-1% vs. 4-11%) (Amin, Prinzing, & Myers, 2009;Jackson, Needelman, Roberts, Willet, & McMorris, 2012;Kaaresen et al, 2008;Maguire et al, 2009aMaguire et al, , 2009bMossabeb, Wade, Finnegan, Sivieri, & Abbasi, 2012;Mukhopadhyay, Malhi, Mahajan, & Narang, 2010;Peters et al, 2009). The finding concerning the underestimation of the rate of developmental delay by the Bayley-III has also been documented in recent studies of term and preterm infants in Western countries (Acton et al, 2011;Anderson et al, 2010;Esteban et al, 2010;Makrides et al, 2010;Moore et al, 2012;Reuner et al, 2013;Robertson et al, 2010;Spittle et al, 2010;Vohr et al, 2012).…”

Sensory Integration, Sensory Processing, and Sensory Modulation Disorders: Putative Functional Neuroanatomic Underpinnings

“…For example, even relatively slight elevations in perinatal bilirubin levels can generate brain abnormalities, particularly within the basal ganglia [213]. BINDS, or bilirubin-induced neurotoxic disorders, are often associated with the development of cognitive deficits, including problems with attention that reflect disturbance within basal ganglia gating mechanisms [214,215]. Based upon the neuroanatomic position and function of the basal ganglia, disturbances in the gating of sensory perceptions might be predicted as well [216].…”

Is Neonatal Jaundice Associated with Autism Spectrum Disorders: A Systematic Review

“…Premature infants are at higher risk of bilirubin-induced neurotoxicity compared to term infants consistent with the findings of increased prevalence of ASD among premature infants compared to term infants (Amin 2004; Burd et al 1999; Eaton et al 2001; Larsson et al 2005; Maimburg and Vaeth 2006). Both autism and bilirubin-induced neurotoxicity may also manifest clinically with abnormal auditory evoked responses and impaired communication further suggesting biological plausibility (Amin 2004; Amin et al 2009; Funato et al 1996; Perlstein 1960; Russo et al 2008; Rosenhall et al 2003; Whitehouse and Bishop 2008). Several investigators have demonstrated prolongation of absolute and interpeak latencies of auditory brainstem evoked response in autistic children (Rosenhall et al 2003; Thivierge et al 1990; Wong and Wong 1991).…”