The auditory transmission pathway consists of 3 main levels of neurons. The level 1 neurons are bipolar cells whose cytosol is located in the cochlea within the cochlear (spiral) ganglion. The peripheral branch goes to the spiral apparatus (Corti apparatus) of the inner ear; while the central branch forms the cochlear nerve and enters the cerebral bridge to the cochlear nucleus. The cell bodies of the level 2 neurons are in the nucleus of the cochlear nerve. They emit fibers that form part of the rhomboid that crosses to the opposite side and travels upward, and part that travels upward on the same side. The superior fibers form the lateral thalamus tract and most of their fibers end in the medial geniculate body. The cell bodies of the level 3 neurons are within the medial geniculate body. Its axons form the auditory radiation and travel through the occipital part of the internal capsule to the transverse temporal gyrus (the central part of the cerebral cortex, equivalent to the human head above the temples on both sides; this part of the brain is called the temporal lobe, and a raised one in the middle of the collar lobe is called the transverse temporal gyrus, which is a dense concentration of auditory nerve cells and plays a precise role in the analysis and synthesis of external sounds). Brainstem auditory evoked potential (BAEP) is a more sensitive objective indicator of brainstem damage, which is the electrical activity of nerve impulses induced by acoustic stimulation in the auditory conduction pathway of the brainstem, and can objectively and sensitively reflect the function of the central nervous system. The BAEP is often changed when the brainstem is slightly damaged and there are no clinical signs or symptoms. BAEP is a series of 6-7 positive waves recorded within 10 ms after short acoustic stimuli are delivered by headphones. It is possible that these waves have a multi-locus compound origin, but it can also be simply assumed that wave I is an auditory nerve action potential, wave II originates from the cochlear nucleus, wave III comes from the superior olivary complex nucleus of the pons and the rhomboid, waves IV and V represent the lateral thalamic system and the midbrain hypothalamic nucleus, respectively, and waves VI and VII are action potential waveforms of the geniculate body and auditory radiation in the thalamus. Therefore, waves Ⅰ and Ⅱ actually represent the peripheral wave groups of the auditory afferent pathway, and the subsequent waves represent the central segment action potentials. The first 5 waves, wave I to wave V, are the most stable, with wave V having the highest amplitude, and can be used as a marker to identify the BAEP waves. Under normal conditions, wave Ⅱ and wave Ⅰ, or wave VI and wave Ⅶ often fuse to form a composite waveform. The wave Ⅰ latency represents the peripheral conduction time of the auditory pathway, while the wave Ⅰ to wave Ⅴ interwave latency (IPL) is the central auditory conduction time of the brainstem segment, which also represents the integrity of the brainstem function. The brainstem auditory conduction pathway is basically consistent with the development of other brainstem structures, so BAEP testing can reflect not only the development of brainstem auditory function but also the developmental status of the entire brainstem function to a certain extent [some data show that the abnormal BAEP rate is 64.3% in children with ischemic-hypoxic encephalopathy, 56.6% in children with language development disorders, 52.6% in children with hyperbilirubinemia The abnormal BAEP rate was 52.6% in children with hyperbilirubinemia and 52.4% in children with cerebral palsy. If the BAEP is not induced, a serious injury to the proximal cochlear segment of the auditory nerve can be considered; if wave I or waves I and II disappear, a serious injury to the intracranial segment of the auditory nerve or the brainstem can be considered; if the absolute latency (PL) of all BAEP waves is prolonged and bilaterally symmetrical, if the I-V latency (IPL) is not prolonged, conductive deafness or injury to the proximal cochlear segment of the auditory nerve can be considered; if the I-V IPL is prolonged If the I-V IPL is prolonged, it may indicate involvement of the brainstem auditory pathway. If wave I cannot be elicited, but subsequent waves are present and the PL is prolonged, clinical judgments can be made as follows: first, if the III-V IPL is normal, the lesion may be in the lower segment of the brainstem auditory pathway or in the nerve; second, measuring the conduction time from the negative peak before wave II to the peak of wave V or between negative peaks can help distinguish snail lesions from post-snail lesions; third, if waves I and III cannot be elicited, the PL of wave V can be observed. If the corrected PL of wave V still exceeds the upper limit of the normal value, it will reveal a posterior cochlear lesion. The interaural latency difference (ILD) between the PL and IPL of the right and left ears is clinically significant if the ILD values of PL and IPL exceed 0.4 ms, and the change in this parameter suggests a posterior cochlear lesion. I-III or III-VIPL may be analyzed progressively. Prolongation of I-III IPL suggests that the lesion may involve the ipsilateral auditory nerve to the brainstem segment; prolongation of III-V IPL suggests that the lesion may affect the auditory transmission pathway in the brainstem. If the ILD of I-V IPL is significant, the lesion may be on the longer side of the I-VIPL. An abnormal V/I amplitude ratio, which is 1.0 with normal hearing, is the result of a relatively prolonged III-V IPL. If the audiology is normal, the abnormality of this covariate suggests an early brainstem lesion (cerebral bridge to lower midbrain).