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 Ͻ 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. Abbreviations BAER, brainstem auditory evoked response dB nHL, decibel normal hearing level HI, hypoxia-ischemia HIE, hypoxic-ischemic encephalopathy HII, hypoxic-ischemic insult MLS, maximum length sequence There is growing evidence to suggest that HII after asphyxia produces permanent brain damage by processes that continue for many hours after the insult (1-3). The neurotoxic cascade leads to delayed cell death hours, days, or months later. This may provide an opportunity for early therapy aimed at preventing further damage of the brain. However, further study of the pathophysiologic process of HI brain damage, especially during the critical period, is of great importance for planning any intervention with neuroprotective and therapeutic measures (4 -8).A major neuropathologic pattern of HIE in term infants is known to be selective neuronal necrosis. After perinatal asphyxia discrete lesions are very common in the brainstem (9 -11). In acute total asphyxia there is extensive neuronal necrosis. The damage preferentially affects the brainstem, thalamus, and basal ganglia with the cerebral cortex being relat...

Auditory neural responses to acoustic stimuli of different rates were studied by analyzing changes in brainstem auditory evoked responses (BAER) with increasing repetition rate of clicks, or rate-dependent changes, in 62 very preterm babies (gestation 24 -32 wk). None had perinatal asphyxia or major complications at the time of testing (37-42 wk postconceptional age) to exclude their possible effects on the recorded BAER. As the rate of clicks was increased from 21/s to 51/s and 91/s, I-V interpeak interval in these babies increased similarly to that in normal term neonates. The rate-dependent change decreased significantly in I-III interval, but increased significantly in III-V intervals and III-V/ I-III interval ratio (all p Ͻ 0.01). At all three rates of clicks, the I-V interval, the most commonly used BAER variable, tended to increase slightly but did not differ significantly from the term neonates. The I-III interval decreased significantly at higher click rates (ANOVA p Ͻ 0.05 at 51/s and Ͻ 0.001 at 91/s), whereas the III-V interval and III-V/I-III interval ratio increased significantly at all 21/s, 51/s, and particularly 91/s (p Ͻ 0.01-0.001). No abnormalities were found in wave V amplitude at any rates. These results suggest that very preterm babies have an advanced peripheral development of the brainstem auditory pathway but a retarded central development or central impairment. A nearly normal I-V interval does not exclude a possible abnormality in its subcomponents (I-III and III-V intervals). In babies who have a normal BAER at a conventionally used low rate of clicks, we cannot exclude an abnormal BAER at higher rates. Babies who are born very preterm account for a large proportion of perinatal mortality and are at high risk of neurodevelopmental deficits (1-5). Many of the survivors have long-term neurologic disorders or behavior problems, e.g. minimal brain damage and learning disabilities, and visual and hearing deficits. Those who have sensorineural hearing loss develop more neurologic complications than control infants (6). However, there are still controversies regarding early neural development in these babies. Some investigators reported a delay in development (7-9), whereas others found no apparent abnormality (10, 11). Better understanding of the early development and neurophysiology underlying later disability is important for improving the management of these babies.BAERs represent the electrophysiologic activity of a large number of auditory neurons in the brainstem after transient acoustic stimulation. The responses have been widely used to study auditory function and its development in babies (12)(13)(14)(15)(16)(17)(18). Although most of the previous BAER studies in preterm babies reported no significant abnormalities (12, 18), others reported an increase in BAER wave latencies and intervals, suggesting retarded development (16). To date, none of the previous reports were concentrated on the study of BAER central components in very preterm babies.The neonatal BAER is significantly aff...

The results suggest poor myelination and synaptic function of the brainstem in infants with bronchopulmonary dysplasia, resulting in impaired functional integrity. In comparison, peripheral neural function was relatively intact.