Time course of brainstem pathophysiology during first month in term infants after perinatal asphyxia, revealed by MLS BAER latencies and intervals

Dynamic changes in electrophysiology of brainstem auditory neurons during the first month after birth were studied in 51 term infants after perinatal asphyxia using maximum length sequence brainstem auditory evoked responses. The responses were recorded on d 1. 3, 5, 7, 10, 15, and 30 after birth. On d 1, wave III and V latencies and all interpeak intervals increased significantly at all repetition rates of clicks used (91-910/s), especially the higher rates (ANOVA, p < 0.05-0.0001). On d 3. all these latencies and intervals increased further and differed more significantly from the normal control subjects. Thereafter, the latencies and intervals decreased progressively. On d 7, wave V latency and all intervals still differed significantly from the control subjects. These dynamic changes were more significant at higher rates of clicks than at lower rates. On d 10 and 15, all intervals decreased significantly. On d 30, all wave latencies decreased to the values in the normal control subjects on the same day. The intervals also approached normal values, although the III-V and I-V intervals still increased slightly. These results indicate that hypoxic-ischemic brain damage persists during the first week, with a peak on d 3, and recovers progressively thereafter. By 1 mo, the damage has largely returned to normal. Maximum length sequence brainstem auditory evoked responses results correlated well with the stage of hypoxic-ischemic encephalopathy during the first week. The present study revealed a general time course of brainstem pathophysiology after asphyxia, although there were individual variations. Our findings can be used as a reference to monitor cerebral function and help judge the value of neuroprotective or therapeutic interventions. The first week, particularly the first 3 d, is a critical period of hypoxic-ischemic brain damage, and early intervention may prevent or reduce deterioration of the damage.