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Bilirubin-induced neurologic dysfunction

Ronald van Toorn, Philip Brink, Johan Smith, Christelle Ackermann, Regan Solomons
The clinical expression of bilirubin-induced neurological dysfunction varies according to severity and location of the disease. Definitions have been proposed to describe different bilirubin-induced neurological dysfunction subtypes. Our objective was to describe the severity and clinico-radiological-neurophysiological correlation in 30 consecutive children with bilirubin-induced neurological dysfunction seen over a period of 5 years. Thirty children exposed to acute neonatal bilirubin encephalopathy were included in the study...
September 2, 2016: Journal of Child Neurology
Joel G Hashimoto, Kristine M Wiren, Clare J Wilhelm
Alcohol abuse is associated with neurological dysfunction, brain morphological deficits and frank neurotoxicity. Although these disruptions may be a secondary effect due to hepatic encephalopathy, no clear evidence of causality is available. This study examined whether a 72h period of alcohol intoxication known to induce physical dependence, followed by a single withdrawal, was sufficient to induce signs of hepatic encephalopathy in male and female mice. Animals were continuously intoxicated via alcohol vapor inhalation, a procedure previously shown to induce significant neurotoxicity in female mice...
July 2016: Neurotoxicology and Teratology
Vinod K Bhutani, Ronald J Wong, David K Stevenson
Preterm neonates with increased bilirubin production loads are more likely to sustain adverse outcomes due to either neurotoxicity or overtreatment with phototherapy and/or exchange transfusion. Clinicians should rely on expert consensus opinions to guide timely and effective interventions until there is better evidence to refine bilirubin-induced neurologic dysfunction or benefits of bilirubin. In this article, we review the evolving evidence for bilirubin-induced brain injury in preterm infants and highlight the clinical approaches that minimize the risk of bilirubin neurotoxicity...
June 2016: Clinics in Perinatology
Naser Amini, Nasim Vousooghi, Mahmoudreza Hadjighassem, Mehrdad Bakhtiyari, Neda Mousavi, Hosein Safakheil, Leila Jafari, Arash Sarveazad, Abazar Yari, Sara Ramezani, Faezeh Faghihi, Mohammad Taghi Joghataei
Kernicterus is a neurological syndrome associated with indirect bilirubin accumulation and damages to the basal ganglia, cerebellum and brain stem nuclei particularly the cochlear nucleus. To mimic haemolysis in a rat model such that it was similar to what is observed in a preterm human, we injected phenylhydrazine in 7-day-old rats to induce haemolysis and then infused sulfisoxazole into the same rats at day 9 to block bilirubin binding sites in the albumin. We have investigated the effectiveness of human adiposity-derived stem cells as a therapeutic paradigm for perinatal neuronal repair in a kernicterus animal model...
May 2016: Neurotoxicity Research
Robert D Christensen, Hassan M Yaish, Patrick G Gallagher
Newborn infants who have hereditary spherocytosis (HS) can develop anemia and hyperbilirubinemia. Bilirubin-induced neurologic dysfunction is less likely in these neonates if the diagnosis of HS is recognized and appropriate treatment provided. Among neonates listed in the USA Kernicterus Registry, HS was the third most common underlying hemolytic condition after glucose-6-phosphate dehydrogenase deficiency and ABO hemolytic disease. HS is the leading cause of direct antiglobulin test (direct Coombs) negative hemolytic anemia requiring erythrocyte transfusion in the first months of life...
June 2015: Pediatrics
Bolajoko O Olusanya, Tinuade A Ogunlesi, Praveen Kumar, Nem-Yun Boo, Iman F Iskander, Maria Fernanda B de Almeida, Yvonne E Vaucher, Tina M Slusher
Hyperbilirubinaemia is a ubiquitous transitional morbidity in the vast majority of newborns and a leading cause of hospitalisation in the first week of life worldwide. While timely and effective phototherapy and exchange transfusion are well proven treatments for severe neonatal hyperbilirubinaemia, inappropriate or ineffective treatment of hyperbilirubinaemia, at secondary and tertiary hospitals, still prevails in many poorly-resourced countries accounting for a disproportionately high burden of bilirubin-induced mortality and long-term morbidity...
2015: BMC Pediatrics
Paula G Radmacher, Frank D Groves, Joshua A Owa, Gabriel E Ofovwe, Emmanuel A Amuabunos, Bolajoko O Olusanya, Tina M Slusher
BACKGROUND: Severe neonatal jaundice with associated acute bilirubin encephalopathy occurs frequently in low- and middle-income countries, where advanced diagnostic technology is in short supply. In an effort to facilitate the physical diagnosis of acute bilirubin encephalopathy, we pilot-tested a modified bilirubin induced neurologic dysfunction scoring algorithm in a group of pediatric trainees (residents) and their mentors (consultants) in a resource-constrained setting. METHODS: Jaundiced Nigerian infants were examined by consultant and resident pediatricians...
2015: BMC Pediatrics
Bolajoko O Olusanya, Folasade B Osibanjo, Tina M Slusher
BACKGROUND: Available evidence suggests that low- and middle-income countries (LMICs) bear the greatest burden of severe neonatal hyperbilirubinemia characterized by disproportionately high rates of morbidity, mortality and neurodevelopmental disorders compared to high-income countries. We set out to identify the risk factors that contribute to the burden of severe hyperbilirubinemia in the most developmentally disadvantaged LMICs to highlight areas for action and further research. METHODS: We systematically searched PubMed, Scopus, Ovid EMBASE, Cumulative Index to Nursing and Allied Health Literature (CINAHL), WHO Library Database (WHOLIS), African Index Medicus (AIM), African Journals Online (AJOL), LILACS, and IndMed for reports published between January 1990 and June 2014...
2015: PloS One
Courtney J Wusthoff, Irene M Loe
Bilirubin-induced neurologic dysfunction (BIND) is the constellation of neurologic sequelae following milder degrees of neonatal hyperbilirubinemia than are associated with kernicterus. Clinically, BIND may manifest after the neonatal period as developmental delay, cognitive impairment, disordered executive function, and behavioral and psychiatric disorders. However, there is controversy regarding the relative contribution of neonatal hyperbilirubinemia versus other risk factors to the development of later neurodevelopmental disorders in children with BIND...
February 2015: Seminars in Fetal & Neonatal Medicine
Alvin Zipursky, Vinod K Bhutani
Clinical experience with Rhesus (Rh) disease and its post-icteric sequelae is limited among high-income countries because of nearly over four decades of effective prevention care. We hypothesized that Rh disease is prevalent in other regions of the world because it is likely that protection is limited or non-existent. Following a worldwide study, it has been concluded that Rh hemolytic disease is a significant public health problem resulting in stillbirths and neonatal deaths, and is a major cause of severe hyperbilirubinemia with its sequelae, kernicterus and bilirubin-induced neurologic dysfunction...
February 2015: Seminars in Fetal & Neonatal Medicine
Vinod K Bhutani, Ronald Wong
No abstract text is available yet for this article.
February 2015: Seminars in Fetal & Neonatal Medicine
William V Good, Chuan Hou
This review addresses the question whether elevated levels of total serum/plasma bilirubin (TB) cause measurable neurological effects, specifically to visuocortical functioning. Past research in the area of vision and its relation to jaundice has taken advantage of flash visual-evoked potentials (VEPs). Using a steady state VEP, we developed preliminary data suggesting that children who had jaundice with TB levels between 10 and 25mg/dL, but who did not have kernicterus, have measurable changes in visual function, when compared to control infants who did not have jaundice...
February 2015: Seminars in Fetal & Neonatal Medicine
Vinod K Bhutani, Lois Johnson-Hamerman
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...
February 2015: Seminars in Fetal & Neonatal Medicine
Bolajoko O Olusanya
Infants with bilirubin-induced neurologic dysfunction (BIND) are characterized by several developmental disabilities including auditory impairments. This paper explores the societal impact of bilirubin-induced auditory impairments, inclusive of hearing impairments and auditory neuropathy spectrum disorders, on these infants, their families, and on the community in resource-limited countries (per capita income of US$6,000 or less). Auditory impairments have substantial emotional, social, and economic impact on the affected infants, their families and communities...
February 2015: Seminars in Fetal & Neonatal Medicine
Ronald J Wong, David K Stevenson
The pathologic phenotype of severe hyperbilirubinemia in the newborn infant is primarily due to excessive bilirubin production and/or impaired conjugation, resulting in an increased bilirubin load. This may, in turn, increase an infant's risk for the development of bilirubin-induced neurologic dysfunction (BIND). The highest-risk infants are those with increased bilirubin production rates due to hemolysis. Several immune and non-immune conditions have been found to cause severe hemolysis, and these are often exacerbated in those infants with perinatal sepsis and genetic predispositions...
February 2015: Seminars in Fetal & Neonatal Medicine
Jon F Watchko, Michael J Painter, Ashok Panigrahy
Investigators have hypothesized a range of subcortical neuropathology in the genesis of bilirubin-induced neurologic dysfunction (BIND). The current review builds on this speculation with a specific focus on the cerebellum and its connections in the development of the subtle neuromotor disabilities of BIND. The focus on the cerebellum derives from the following observations: (i) the cerebellum is vulnerable to bilirubin-induced injury; perhaps the most vulnerable region within the central nervous system; (ii) infants with cerebellar injury exhibit a neuromotor phenotype similar to BIND; and (iii) the cerebellum has extensive bidirectional circuitry projections to motor and non-motor regions of the brainstem and cerebral cortex that impact a variety of neurobehaviors...
February 2015: Seminars in Fetal & Neonatal Medicine
Dora Brites, Adelaide Fernandes
Bilirubin-induced neurologic dysfunction (BIND) and classical kernicterus are clinical manifestations of moderate to severe hyperbilirubinemia whenever bilirubin levels exceed the capacity of the brain defensive mechanisms in preventing its entrance and cytotoxicity. In such circumstances and depending on the associated co-morbidities, bilirubin accumulation may lead to short- or long-term neurodevelopmental disabilities, which may include deficits in auditory, cognitive, and motor processing. Neuronal cell death, astrocytic reactivity, and microglia activation are part of the bilirubin-induced pathogenesis...
February 2015: Seminars in Fetal & Neonatal Medicine
Jessica Rose, Rachel Vassar
Advances in the care of neonatal hyperbilirubinemia have led to a decreased incidence of kernicterus. However, neonatal exposure to high levels of bilirubin continues to cause severe motor symptoms and cerebral palsy (CP). Exposure to moderate levels of unconjugated bilirubin may also cause damage to the developing central nervous system, specifically the basal ganglia and cerebellum. Brain lesions identified using magnetic resonance imaging following extreme hyperbilirubinemia have been linked to dyskinetic CP...
February 2015: Seminars in Fetal & Neonatal Medicine
John A Stanford, Jeffrey M Shuler, Stephen C Fowler, Kimberly G Stanford, Delin Ma, Douglas C Bittel, Jean-Baptiste Le Pichon, Steven M Shapiro
BACKGROUND: Neonatal jaundice resulting from elevated unconjugated bilirubin occurs in 60-80% of newborn infants. Although mild jaundice is generally considered harmless, little is known about its long-term consequences. Recent studies have linked mild bilirubin-induced neurological dysfunction (BIND) with a range of neurological syndromes, including attention-deficit hyperactivity disorder. The goal of this study was to measure BIND across the lifespan in the Gunn rat model of BIND. METHODS: Using a sensitive force plate actometer, we measured locomotor activity and gait in jaundiced (jj) Gunn rats versus their nonjaundiced (Nj) littermates...
March 2015: Pediatric Research
Maria Alexandra Brito, Inês Palmela, Filipa Lourenço Cardoso, Inês Sá-Pereira, Dora Brites
The blood-brain barrier (BBB) is a complex and dynamic structure that plays a key role in central nervous system (CNS) homeostasis. It strictly regulates the entrance of molecules into the brain parenchyma and prevents the access of neurotoxins and pathogens while promoting the efflux of several molecules. The brain microvascular endothelial cells are the anatomical basis of the BBB, which has unique characteristics such as the elaborate junctional complexes that nearly obliterate the intercellular space as well as the presence of influx and efflux transporters...
November 2014: Archives of Medical Research
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