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The clinical syndrome of bilirubin-induced neurologic dysfunction.
Semin Fetal Neonatal Med. 2015 Feb; 20(1):6-13.SF

Abstract

Clinicians have hypothesized a spectrum of minor neurologic manifestations, consistent with neuroanatomical reports and collectively termed as a "syndrome of bilirubin-induced neurologic dysfunction (BIND)," which can occur in the absence of classical kernicterus. The current review builds on these initial reports with a focus on clinical signs and symptoms that are assessed by standardized tools and manifest from neonatal age to childhood. These clinical manifestations are characterized by the following domains: (i) neuromotor signs; (ii) muscle tone abnormalities; (iii) hyperexcitable neonatal reflexes; (iv) variety of neurobehavior manifestations; (v) speech and language abnormalities; and (vi) evolving array of central processing abnormalities, such as sensorineural audiology and visuomotor dysfunctions. Concerns remain that the most vulnerable infants are likely to acquire BIND, either because their exposure to bilirubin is not identified as severe enough to need treatment or is prolonged but slightly below current threshold levels for intervention. Knowing that a total serum/plasma bilirubin (TB) level is not the most precise indicator of neurotoxicity, the role of expanded biomarkers or a "bilirubin panel" has yet to be validated in prospective studies. Future studies that correlate early "toxic" bilirubin exposure to long-term academic potential of children are needed to explore new insights into bilirubin's effect on the structural and functional maturation of an infant's neural network topology.

Authors+Show Affiliations

Department of Pediatrics, Division of Neonatal and Developmental Medicine, Stanford University School of Medicine, Stanford, CA, USA. Electronic address: bhutani@stanford.edu.University of Pennsylvania School of Medicine, Philadelphia, PA, USA.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

25577653

Citation

Bhutani, Vinod K., and Lois Johnson-Hamerman. "The Clinical Syndrome of Bilirubin-induced Neurologic Dysfunction." Seminars in Fetal & Neonatal Medicine, vol. 20, no. 1, 2015, pp. 6-13.
Bhutani VK, Johnson-Hamerman L. The clinical syndrome of bilirubin-induced neurologic dysfunction. Semin Fetal Neonatal Med. 2015;20(1):6-13.
Bhutani, V. K., & Johnson-Hamerman, L. (2015). The clinical syndrome of bilirubin-induced neurologic dysfunction. Seminars in Fetal & Neonatal Medicine, 20(1), 6-13. https://doi.org/10.1016/j.siny.2014.12.008
Bhutani VK, Johnson-Hamerman L. The Clinical Syndrome of Bilirubin-induced Neurologic Dysfunction. Semin Fetal Neonatal Med. 2015;20(1):6-13. PubMed PMID: 25577653.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The clinical syndrome of bilirubin-induced neurologic dysfunction. AU - Bhutani,Vinod K, AU - Johnson-Hamerman,Lois, Y1 - 2015/01/07/ PY - 2015/1/12/entrez PY - 2015/1/13/pubmed PY - 2016/1/1/medline KW - Bilirubin KW - Bilirubin-induced neurologic dysfunction (BIND) KW - Minor neurologic dysfunction KW - Subtle bilirubin injury SP - 6 EP - 13 JF - Seminars in fetal & neonatal medicine JO - Semin Fetal Neonatal Med VL - 20 IS - 1 N2 - Clinicians have hypothesized a spectrum of minor neurologic manifestations, consistent with neuroanatomical reports and collectively termed as a "syndrome of bilirubin-induced neurologic dysfunction (BIND)," which can occur in the absence of classical kernicterus. The current review builds on these initial reports with a focus on clinical signs and symptoms that are assessed by standardized tools and manifest from neonatal age to childhood. These clinical manifestations are characterized by the following domains: (i) neuromotor signs; (ii) muscle tone abnormalities; (iii) hyperexcitable neonatal reflexes; (iv) variety of neurobehavior manifestations; (v) speech and language abnormalities; and (vi) evolving array of central processing abnormalities, such as sensorineural audiology and visuomotor dysfunctions. Concerns remain that the most vulnerable infants are likely to acquire BIND, either because their exposure to bilirubin is not identified as severe enough to need treatment or is prolonged but slightly below current threshold levels for intervention. Knowing that a total serum/plasma bilirubin (TB) level is not the most precise indicator of neurotoxicity, the role of expanded biomarkers or a "bilirubin panel" has yet to be validated in prospective studies. Future studies that correlate early "toxic" bilirubin exposure to long-term academic potential of children are needed to explore new insights into bilirubin's effect on the structural and functional maturation of an infant's neural network topology. SN - 1878-0946 UR - https://wwww.unboundmedicine.com/medline/citation/25577653/The_clinical_syndrome_of_bilirubin_induced_neurologic_dysfunction_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1744-165X(14)00103-6 DB - PRIME DP - Unbound Medicine ER -