Bilirubin and the Auditory System

Shapiro, Steven M.; Nakamura, Hajime

doi:10.1038/sj.jp.7210635

Cited by 107 publications

(84 citation statements)

References 25 publications

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“…These bilirubin-related changes in electrocerebral activity were time limited; most had disappeared during the second week of life. This transient bilirubin-related depression of neuronal activity has also been demonstrated using brainstem auditory, visual and somatosensory potentials [18,19,20]. …”

Section: Discussionmentioning

confidence: 99%

Moderate Unconjugated Hyperbilirubinemia Causes a Transient but Delayed Suppression of Amplitude-Integrated Electroencephalographic Activity in Preterm Infants

Horst¹,

Bos²,

Duijvendijk³

et al. 2012

Neonatology

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Background: Unconjugated hyperbilirubinemia occurs frequently in preterm infants and may result in bilirubin encephalopathy. Amplitude-integrated electroencephalography (aEEG) is used to evaluate brain function in newborns. Objectives: To investigate the influence of total serum bilirubin (TSB) on the aEEG amplitude of preterm infants and to evaluate aEEG as a noninvasive method to identify acute bilirubin encephalopathy. Methods: We performed a prospective observational study of 34 infants with a gestational age (GA) of 26–31 6/7 weeks. Infants had aEEG recordings on the 1st–5th, 8th and 15th day after birth. Infants with asphyxia, intraventricular hemorrhage >grade I or circulatory insufficiency were excluded. aEEG was evaluated by calculating the mean 5th, 50th and 95th centiles of the aEEG amplitudes. Results: TSB peaked on the 4th day after birth. There was no synchronous relationship between TSB and aEEG amplitudes. The 5th, 50th, and 95th aEEG amplitude centiles on the 8th day correlated negatively with the TSB peak value (r = –0.37, p = 0.048; r = –0.60, p = 0.001; r = –0.44, p = 0.017, respectively), irrespective of GA. The 5th and 50th aEEG amplitude centiles increased with increasing GA (r = 0.45, p < 0.001, and r = 0.26, p < 0.001, respectively) and postnatal age (r = 0.25, p < 0.001, and r = 0.16, p = 0.023, respectively). Conclusions: TSB had no direct effect on aEEG amplitudes in preterm infants. There is, however, a delayed effect on electrocerebral activity in the 2nd week after birth.

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Section: Discussionmentioning

confidence: 99%

Moderate Unconjugated Hyperbilirubinemia Causes a Transient but Delayed Suppression of Amplitude-Integrated Electroencephalographic Activity in Preterm Infants

Horst¹,

Bos²,

Duijvendijk³

et al. 2012

Neonatology

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“…Several theories centering on metabolic-related issues have been proposed to account for the cellular and neurotoxic mechanisms associated with hyperbilirubinemia [Hansen et al, 2001], and these issues are particularly relevant to AN [McDonald et al, 1998;Shapiro and Nakamura, 2001]. Indeed, associations with mitochondrial (dys)function are noteworthy because during the neonatal period, high energy demands are requisite for sustaining life and promoting growth; thus, the importance of bioenergetics for maintaining complex life forms cannot be overstated [Wallace, 2007].…”

Section: Hyperbilirubinemia: Evidence For Mitochondrial Toxicity Effementioning

confidence: 99%

The Mitochondrial Connection in Auditory Neuropathy

Cacace

Pinheiro

2011

Audiol Neurotol

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‘Auditory neuropathy’ (AN), the term used to codify a primary degeneration of the auditory nerve, can be linked directly or indirectly to mitochondrial dysfunction. These observations are based on the expression of AN in known mitochondrial-based neurological diseases (Friedreich’s ataxia, Mohr-Tranebjærg syndrome), in conditions where defects in axonal transport, protein trafficking, and fusion processes perturb and/or disrupt mitochondrial dynamics (Charcot-Marie-Tooth disease, autosomal dominant optic atrophy), in a common neonatal condition known to be toxic to mitochondria (hyperbilirubinemia), and where respiratory chain deficiencies produce reductions in oxidative phosphorylation that adversely affect peripheral auditory mechanisms. This body of evidence is solidified by data derived from temporal bone and genetic studies, biochemical, molecular biologic, behavioral, electroacoustic, and electrophysiological investigations.

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“…[1][2][3] The auditory system is particularly sensitive to the toxic effects of bilirubin. 2 Bilirubin, at high levels, can damage retrocochlear structures such as the brainstem auditory nuclei, inferior colliculi, spiral ganglion neurons, and auditory nerve fibers. 4 The effect of hyperbilirubinemia on auditory dysfunction is generally dose dependent, with greater dysfunction noted at higher total serum bilirubin (TSB) levels.…”

Section: What This Study Adds: In This Northernmentioning

confidence: 99%