Search

Lactate dehydrogenase isoenzymes in cerebrospinal fluid were measured during the first 24 h of life in 25 asphyctic neonates. The infants were subjected to clinical and developmental examinations for a mean follow-up period of 15.2 months. The mean values for cerebrospinal LDH2(MH3) and LDH3(M2H2) isoenzymes were significantly higher in asphyctic infants who died from hypoxic-ischemic encephalopathy or who survived but suffered neurologic sequelae, than they were in those asphyctic infants who survived and were normal in the follow-up studies. Therefore, the authors conclude that the lactate dehydrogenase isoenzyme pattern in cerebrospinal fluid may be of value when assessing anoxic brain damage.

The prognostic value of cerebrospinal fluid (CSF) lactate concentration after an hypoxic-ischemic brain insult was evaluated. Three groups of neonates were studied and followed. Group 1A included 19 asphyxiated neonates who subsequently developed normally, Group 1B included 6 asphyxiated neonates who died or developed neurologic sequelae, and Group 2 consisted of 20 control (comparison) infants. A CSF sample was obtained within the first day of life for cytochemical analysis, culture, and lactate determination with simultaneous determination of serum lactate. The mean CSF lactate level in Group 1B (4.5 mmol/L) was significantly higher than in Group 1A (2.5 mmol/L) (p less than .001). In comparison to the highest CSF lactate concentrations in the normal range in Group 2 (2.7 mmol/L), all Group 1B neonates had elevated CSF lactate levels, and eight neonates (34%) of Group 1A had increased levels. A correlation was found between blood and CSF lactate levels in asphyxiated infants (r = .42, p less than .05), but its meaning is uncertain. We conclude that CSF lactate determinations may be helpful in the evaluation of perinatal hypoxic-ischemic encephalopathy.

Lumbar CSF eicosanoids were measured in 11 neonates with perinatal asphyxia and 12 neonates with suspected sepsis. In the asphyxia group low levels of thromboxane B2 and prostaglandin F2a were detected in five neonates, all of which had had a lumbar puncture prior to 4 hours of age. In the group with suspected sepsis two infants had positive blood cultures and one had strep meningitis. CSF eicosanoids were nondetectable in all patients in this second group with the exception of the infant with meningitis. With meningitis CSF eicosanoids were markedly elevated. These findings suggest that lumbar CSF eicosanoids do not appear to be a clinically useful tool. The data further suggest that eicosanoids are involved in the inflammatory response to meningitis.

Cerebrospinal fluid (CSF) lactate dehydrogenase (LDH) was measured in 54 neonates with intracranial hemorrhage and compared with 82 control, 27 traumatic lumbar puncture, seven meningitis, and 30 asphyxiated newborns. Hospital data, neonatal outcomes, and long-term neurodevelopmental follow-up results were reviewed. CSF LDH was not significantly affected by traumatic lumbar puncture but was elevated in proportion to the severity of CNS hemorrhage as scored by computerized tomography. LDH was also significantly associated with subsequent seizures and hydrocephalus and abnormal long-term developmental outcome.

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.

During a six-month period, lactate measurements were performed on all samples of CSF obtained by lumbar puncture from infants of varying gestational ages between birth and 32 days of age. The normal levels of lactate in the CSF of newborns were demonstrated to be higher than those previously reported in older children or adults. A steady decrease in CSF lactate levels was demonstrated as postnatal age increased, so that after the first ten days of life, CSF lactate levels were within the range reported for older children and adults. We could not demonstrate that neonatal asphyxia or gestational age significantly altered these values.

gamma-Aminobutyric acid (GABA) concentrations in cerebrospinal fluid (CSF) were measured in 20 neonates with various gestational and postnatal ages. These concentrations varied between 9 and 45 nmol/ml which is approximately 20-100 times the concentrations found in adults. CSF GABA concentrations tended to decrease with advancing gestational age. No apparent alterations were noted with increasing postnatal age (until 6 weeks of age). Asphyxia but not neonatal sepsis was accompanied by an increase in CSF GABA concentrations compared to respective controls.

Forty-one cerebrospinal fluid (CSF) specimens from children were investigated with a radioimmunoassay for their content of myelin basic protein (BP). Eight specimens were regarded as BP-positive (BP is greater than or equal to 1.0 ng/ml). Twenty-nine were BP-negative and 4 could not be analyzed because of an excessive protein content. The BP-positive samples were from 6 children with evidence of severe acute brain damage leading to death in 5 cases: i.e., 2 term newborns with perinatal asphyxia, a 4 week-old child with severe convulsions, a 3 year-old boy with hypoxia due to laryngitis, and a 12 year-old girl with encephalitis. One preterm baby survived severe hypoxia and developed hydrocephalus shortly afterwards. We conclude that BP becomes detectable in CSF of newborns and older children under certain pathological conditions, and that the presence of BP in CSF may be associated with severe brain tissue destruction.