Subject(s)
Hemolysis , Hyperbilirubinemia/cerebrospinal fluid , Subarachnoid Hemorrhage/cerebrospinal fluid , Amoxicillin/adverse effects , Anti-Bacterial Agents/adverse effects , Chemical and Drug Induced Liver Injury/cerebrospinal fluid , Chemical and Drug Induced Liver Injury/etiology , Humans , Male , Middle Aged , Oxyhemoglobins/cerebrospinal fluid , Spinal PunctureABSTRACT
Chronic bilirubin encephalopathy, characterized clinically by extrapyramidal movement abnormalities, vertical gaze abnormalities, and hearing loss, results from neuronal injury after marked hyperbilirubinemia in term and preterm infants. In premature infants, bilirubin staining of specific brain structures has been described at autopsy after only moderate hyperbilirubinemia, but classic chronic bilirubin encephalopathy without marked hyperbilirubinemia has been reported only rarely. We report a case of a 7-year-old, former 29-weeks' gestation, gravely ill premature infant with a peak bilirubin level of 13.3 mg/dL in the neonatal period. We compare this case with a 12-year-old, former term infant with a peak bilirubin level of 49.4 mg/dL on day 10 of life. Both children have dystonia, athetosis, upward gaze palsy, and sensorineural hearing loss, with MRIs showing characteristic abnormal signal in the globus pallidus. We add previously unreported cerebrospinal fluid neurotransmitter levels that show a mild decrease in the dopamine metabolite homovanillic acid in the former premature infant only.
Subject(s)
Infant, Premature, Diseases/cerebrospinal fluid , Kernicterus/cerebrospinal fluid , Neurotransmitter Agents/cerebrospinal fluid , Child , Developmental Disabilities/etiology , Female , Follow-Up Studies , Globus Pallidus/pathology , Homovanillic Acid/cerebrospinal fluid , Humans , Hydroxyindoleacetic Acid/cerebrospinal fluid , Hyperbilirubinemia/cerebrospinal fluid , Infant, Newborn , Infant, Premature , Kernicterus/complications , Kernicterus/pathology , Magnetic Resonance Imaging , Tyrosine/analogs & derivatives , Tyrosine/cerebrospinal fluidABSTRACT
To evaluate the relationship of serum cerebrospinal fluid (CSF) and brain total bilirubin levels in asphyxia, an experiment was designed with 5 to 6-week-old Sprague-Dawley rats. The rats were randomized into control and experimental groups. All rats received intravenously 30 mg/kg of bilirubin. Four hours later the experimental group was asphyxiated. Forty-eight hours after asphyxiation, the bilirubin concentrations in blood, CSF, and brain were measured in both study groups. Mean CSF and brain bilirubin levels were significantly higher in the experimental compared to the control group; however, mean serum bilirubin levels were not different. Moreover, in the experimental group a significant correlation existed between CSF and brain bilirubin concentrations. In conclusion, an asphyxiatic insult resulted in disruption of both the blood-brain and the blood-CSF barriers.
Subject(s)
Asphyxia/cerebrospinal fluid , Bilirubin/cerebrospinal fluid , Blood-Brain Barrier , Hyperbilirubinemia/cerebrospinal fluid , Animals , Animals, Newborn , Asphyxia/metabolism , Bilirubin/analysis , Bilirubin/blood , Brain Chemistry , Disease Models, Animal , Hyperbilirubinemia/metabolism , Random Allocation , Rats , Rats, Inbred StrainsABSTRACT
A spectrophotometric method for semi-quantitative determination of oxyhaemoglobin, methaemoglobin and bilirubin in the cerebrospinal fluid is described and evaluated. The method involves correction for CSF protein. It is based on absorbance registrations on three wavelengths; 400, 420 and 470 nm. Reference values for a healthy control group and a hyperbilirubinaemic group are presented. Evaluation of the method shows that it is well suited to semi-quantitative determination of haem derivatives in the CSF.
