Impairment of perinatal hypoxia-ischemia to the preterm brainstem.

Hypoxia-ischemia is a major perinatal problem that results in severe damage to the newborn brain. This study assessed functional integrity of the brainstem at term in preterm infants after perinatal hypoxia-ischemia to shed light on the influence of hypoxia-ischemia on the preterm brainstem. We recruited sixty-eight preterm infants after perinatal hypoxia-ischemia, ranging in gestation 28-35 weeks. Brainstem evoked response was studied at term age (37-42 weeks postconceptional age) with 91-910/s clicks using the maximum length sequence technique. Compared with healthy preterm infants, the preterm infants after perinatal hypoxia-ischemia showed a significant increase in I-V interval at very high rates 455 and 910/s of clicks (P<0.05, 0.05). III-V interval and III-V/I-III interval ratio also increased significantly at 455 and 910/s (P<0.05-0.01). The slope of III-V interval-rate function was significantly steeper than in the healthy preterm infants (P<0.05). Compared with normal term controls, the preterm infants after hypoxia-ischemia showed similar, but slightly more significant, abnormalities. The differences between the preterm infants after hypoxia-ischemia and the healthy preterm and term infants generally increased with increasing click rate. These results demonstrated that central components of brainstem auditory evoked response were abnormal at very high click rates in the preterm infants after perinatal hypoxia-ischemia. Click rate-dependent change in the more central part of the brainstem is also abnormal. Apparently, functional integrity of the brainstem, mainly in the more central part, is impaired. Hypoxic-ischemic damage to the preterm brainstem is unlikely to completely recover within a relatively short period after the insult, which is of clinical importance.

Brainstem response amplitudes in neonatal chronic lung disease and differences from perinatal asphyxia.

OBJECTIVE: To examine neuronal function of the auditory brainstem in neonatal chronic lung disease (CLD) and detect any differences from perinatal asphyxia. METHODS: Infants with CLD and infants after perinatal asphyxia were studied at term (37-42 weeks postconceptional age). Wave amplitudes of maximum length sequence brainstem auditory evoked response (MLS BAER) were recorded and compared between CLD and asphyxia. RESULTS: The amplitudes of waves I, III and V, and V/I and V/III amplitude ratios in CLD infants did not differ from those in normal term controls at all click rates 21-910/s. The slopes of amplitude-rate functions were all similar to those in the controls. In infants after asphyxia, however, wave III and V amplitudes were smaller than those in both the controls and CLD infants, particularly at high-rate stimulation. The intercepts of amplitude-rate functions for waves III and V were smaller than in both the controls and CLD infants, although there were no significant differences in the slopes of these functions. CONCLUSIONS: No abnormalities in MLS BAER amplitudes were found in CLD infants but the amplitudes were significantly reduced in asphyxiated infants, resulting in major differences between CLD and perinatal asphyxia. SIGNIFICANCE: There is no major neuronal impairment in the auditory brainstem in CLD but there is in perinatal asphyxia. This difference may be, at least partly, related to the difference in the nature of hypoxia associated with the two problems; the hypoxia is chronic and sublethal in CLD, but is often acute, lethal and associated with ischaemia in perinatal asphyxia.

Sustained depression of brainstem auditory electrophysiology during the first months in term infants after perinatal asphyxia.

OBJECTIVE: To gain further insights into the pathophysiological processes of neuronal impairment in neonatal brainstem after perinatal asphyxia. METHODS: Maximum-length sequence brainstem auditory-evoked response (MLS BAER) was recorded with clicks at 91, 227, 455 and 910/s on days 1, 3, 5, 7, 10, 15 and 30 after birth in 108 term infants who suffered perinatal asphyxia. Wave amplitude variables in the MLS BAER were analysed in detail at 40 dB above BAER threshold in 86 infants who had no peripheral hearing impairment. RESULTS: On day 1 the amplitudes of MLS BAER waves I, III and V were all reduced significantly at all click rates, especially at higher ones (91-910/s, ANOVA P<0.05-0.001). On day 3 these amplitudes were reduced further. On days 5 and 7, the amplitude reduction persisted and did not show any significant further changes. On days 10 and 15 the reduced amplitudes were increased slightly. On day 30 all amplitudes were still reduced significantly (P<0.05-0.0001). During the first month, the reduction of wave amplitudes was more significant for the later MLS BAER components than for the earlier ones, and occurred most significantly at 455 and 910/s clicks. By comparison, the amplitude reduction in conventional BAER was much less significant. CONCLUSIONS: During the first month after perinatal asphyxia the amplitudes of MLS BAER waves were reduced significantly and persistently, which was more significant at higher rates of clicks than at lower rates. The reduction is much more persistent than the increase in wave latencies and intervals we previously reported. SIGNIFICANCE: There is sustained depression of brainstem auditory electrophysiology, indicating neuronal damage of the auditory brainstem, in infants after perinatal asphyxia. This may have important clinical implications.

Sub-optimal function of the auditory brainstem in term infants with transient low Apgar scores.

OBJECTIVES: To assess functional integrity of the auditory brainstem in neonates with transient low Apgar scores. METHODS: Forty-two term infants were studied with brainstem auditory evoked response (BAER) using the maximum length sequence during the first month of life. All had transient low Apgar scores but no clinical signs of hypoxic-ischaemic encephalopathy (HIE). RESULTS: The latencies of BAER waves I and III in these infants were similar to those of age-matched normal controls at all click rates (91/s, 227/s, 455/s and 910/s) during the period studied. Wave V latency was increased at 910/s on day 1 (P<0.01), but did not differ from that in the controls on any other days. I-V interval was increased significantly at 455/s and 910/s on day 1 (P<0.01 and 0.001) and day 3 (P<0.05 and 0.01). On days 5 and 7, BAER wave latencies and intervals were similar to those in the controls. On day 30, all latencies and intervals reached the values in the controls. No abnormalities were seen in BAER wave amplitude variables on any days. CONCLUSIONS: Neonates with transient low Apgar scores but without HIE had a significant increase in I-V interval at very high click rates on the first three days of life. SIGNIFICANCE: Brainstem auditory function is sub-optimal during the first few days in neonates with transient low Apgar scores.