In 1996, Starr et al. named a group of auditory dysfunctions characterized by absent or severely abnormal auditory brainstem responses (ABR) and normal otoacoustic emissions (OAE) as auditory neuropathy. AN). It usually starts in adolescence and has bilateral onset and presents with bilateral symmetrical and progressive hearing loss and difficulty recognizing speech, especially in noisy environments. Because auditory neuropathy is rare and newly named, many primary care physicians are still unaware of this disease and often miss or misdiagnose it. Male, 19 years old, from the countryside, had passed the physical examination of grassroots recruits. He was in good general health, denied history of acute and chronic diseases and infectious diseases, and had no history of trauma or surgery. Denies family history of deafness, denies history of ototoxic drug use and noise exposure. The initial physical examination was normal, and the initial hearing test in a quiet environment was fair, with no significant communication impairment. After joining the military, the captain found that he had some degree of communication impairment in daily life, especially in noisy environments. He went to the local outpatient clinic for retesting and was found to have reduced hearing in both ears. In order to further confirm the diagnosis, he was referred to our hospital. Examination: general condition was good, both tympanic membranes were normal, gross hearing was acceptable, and there were no other neurological symptoms. The pure tone hearing threshold test showed: bilaterally symmetrical low-frequency ascending audiogram, the average air-conduction pure tone hearing threshold at low frequency 0.25-1.0 kHz was 55 dB HL bilaterally, and the air- and bone-conduction pure tone hearing threshold at 2.0-4.0 kHz was below 20 dB HL bilaterally (normal), which was moderate sensorineural low-frequency hearing loss. ABR showed that all waves I-V were not elicited in both ears (>110 dB SPL). The distortion product otoacoustic emissions (DPOAE) and transiently evoked otoacoustic emissions (TEOAE) were normal in both ears. High-resolution thin-section CT of the temporal bone showed no abnormalities. The diagnosis was: idiopathic auditory neuropathy (bilateral). The absence or severe abnormality of ABR and the normal OAE are the most important audiological features of auditory neuropathy. The hearing neuropathy mostly starts in adolescents and presents with bilateral symmetrical and progressive hearing loss and inaudible speech. In this case, although “no hearing loss” was the main complaint, the patient’s medical history showed that he had “difficulty recognizing speech in a noisy environment” in the past 3 years, and he felt that it was gradually increasing. The audiological test showed the same audiological characteristics as bilateral auditory neuropathy, and the CT of temporal bone also excluded posterior cochlea occupying lesions, no other neurological disorders, and no family history of genetic predisposition. Because of the insidious onset of auditory neuropathy and its recent naming, it is relatively rare, and many primary care physicians still lack a comprehensive understanding of it, so the diagnosis is often missed. Therefore, a comprehensive audiological test, especially OAE test, should be performed when available for patients with sensorineural deafness, and it has an important significance in its differential diagnosis. In our case, the ABR was not elicited from wave I, while the DPOAE and TEOAE were elicited normally, and the stapedius muscle acoustic reflex was not elicited on the same side, suggesting that the outer hair cells were in normal functional state, and the lesion might be in the inner hair cells, synaptic connections between inner hair cells and auditory nerve fibers, spiral ganglia, cochlear nerve fibers, cranial nerve VIII, and the parts related to the above. Whether the auditory neuropathy eventually involves the outer hair cells is subject to further observation and follow-up.