Publication Details
Abstract
We used cerebrocortical electrical activity as a measure of bilirubin neurotoxicity in our investigation. Particularly impacted by elevated bilirubin levels are the cerebral hemispheres and thalamic cortex. The connection between the thalamus and the cortex of the cerebral hemispheres produces the rhythmic waves in the EEG, which increases the electrophysiological influence of bilirubin on the brain's bioelectric potential in the long term postnatal age on rhythmic oscillations. examined. The development of the brain's bioelectrical activity, as well as the waves' aberrant characteristics and quantitative power spectrum analysis, were investigated. 25 full-term newborns with bilirubin encephalopathy and 40 healthy infants provided 195 EEG recordings for this purpose (the first assessment was in the first week, the second examination was at 3 months, and the third examination was at 6 months). Delta and theta frequencies make up the primary frequency component in all recordings for both groups. In the initial recordings, the group with hyperbilirubinemia had a greater delta frequency than the control group, but their theta, alpha, and beta frequencies as well as amplitude levels were lower (p < 0.001). The amount of bilirubin was found to be substantially correlated with these changes (p < 0.001). The hyperbilirubinemia group's wave amplitude grew to a level comparable to the control group during the second assessment. Delta and theta frequency bands showed substantial alterations associated to postnatal age (p < 0.001). As we age, the frequency of theta rises while the frequency of delta falls in all regions of the cerebral hemispheres. Additionally, we detected abnormal bielectric activity and recorded epileptiform waves in newborns with bilirubin encephalopathy. This shift in bioelectric activity is particularly indicative of encephalopathy. Despite the disparities in all brain regions, there were differences in delta frequency and theta frequency between children in the hyperbilirubinemia group and those with moderate bilirubin encephalopathy. These differences vanished by the third month. In the third month, there was no difference between the two groups in terms of vertex, K complex, and sleep spindles (p>0.05). We discovered that the amount of bilirubin in the blood, the permeability of the blood-brain barrier, and the clinical course of bilirubin encephalopathy all influence the effects of hyperbilirubinemia on cerebrocortical electrical activity.