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...

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Pain is considered a multidimensional conscious experience that includes a sensory component and a negative affective-motivational component. The negative affective-motivational component of pain is different from the sensory component and amplifies the pain experience. Nowadays, a significant number of preclinical research groups have focused their attention on the affective symptoms of pain. In the present study, we investigated the pain aversion and anxiety-like behavior of the complete Freund’s adjuvant (CFA)-induced chronic pain model. CFA rats experienced spontaneous pain during pain-paired conditioning (pain aversion) and spontaneous pain produces an affective response (anxiety-like behavior). Moreover, pain aversion was gradually attenuated, while the anxiety-like behavior increased in 4 weeks. Therefore, although the negative effect (including pain aversion and anxiety) is always associated with hyperalgesia, the manifestations of negative effect may follow different time courses, which may influence the progress of primary disease. The findings illustrate that targeted therapy should focus on a specific aspect in different stages of pain. Our study emphasizes the necessity of using multiple tests to study pain comorbidities.