OBJECTIVES: To determine the origin of the acoustically evoked short latency negative response (ASNR), a peculiar V-shaped response at about 3 to 4 milliseconds found during auditory brainstem response recordings. Previous reports demonstrated that the ASNR is present only in ears with profound hearing loss under intense stimulation. It has already been excluded as any kind of artifact. The individuals with ASNR had good vestibular function in spite of their poor hearing, suggesting a relation between the ASNR and the vestibular system. The saccule and vestibular nuclei are hypothesized to be the sense organ and the generator of the response, respectively. The current study tested the saccular function for ears with ASNR and searched for ASNR in ears with a functionless cochlea. STUDY DESIGN: Prospective study. SETTING: Academic tertiary referral center. PATIENTS: Twenty patients with bilateral profound hearing loss, aged 6 to 62 years, including 16 cochlear implant recipients. Twelve healthy participants with normal hearing, aged 23 to 30 years, served as the control group. INTERVENTIONS: Recordings of vestibular evoked myogenic potential (VEMP) and auditory brainstem responses. MAIN OUTCOME MEASURES: The presence or absence of ASNR in ears with cochlear implants. The presence or absence and threshold of VEMP in ears with ASNR versus ears without ASNR. RESULTS: ASNR was recorded by sound stimulation from three ears with unaided cochlear implants, a model of functionless cochlea. VEMP was evoked by sound stimulation to all the nine ASNR ears without threshold difference from normal control ( > 0.05), implying normal saccular function for the ASNR ears. For the ears with profound hearing loss and absence of ASNR, about two thirds were considered to have saccular afunction because of absence of VEMP. The other third displayed VEMPs with higher threshold than normal control ( < 0.01), indicating saccular hypofunction. Furthermore, ASNR and VEMP were elicited from an ear diagnosed with semicircular canal hypofunction. CONCLUSIONS: It is clear that the presence of ASNR is dependent not on residual hearing but on normal saccular function. On the basis of these results, the authors believe ASNR to be saccular in origin.
OBJECTIVES: To determine the origin of the acoustically evoked short latency negative response (ASNR), a peculiar V-shaped response at about 3 to 4 milliseconds found during auditory brainstem response recordings. Previous reports demonstrated that the ASNR is present only in ears with profound hearing loss under intense stimulation. It has already been excluded as any kind of artifact. The individuals with ASNR had good vestibular function in spite of their poor hearing, suggesting a relation between the ASNR and the vestibular system. The saccule and vestibular nuclei are hypothesized to be the sense organ and the generator of the response, respectively. The current study tested the saccular function for ears with ASNR and searched for ASNR in ears with a functionless cochlea. STUDY DESIGN: Prospective study. SETTING: Academic tertiary referral center. PATIENTS: Twenty patients with bilateral profound hearing loss, aged 6 to 62 years, including 16 cochlear implant recipients. Twelve healthy participants with normal hearing, aged 23 to 30 years, served as the control group. INTERVENTIONS: Recordings of vestibular evoked myogenic potential (VEMP) and auditory brainstem responses. MAIN OUTCOME MEASURES: The presence or absence of ASNR in ears with cochlear implants. The presence or absence and threshold of VEMP in ears with ASNR versus ears without ASNR. RESULTS: ASNR was recorded by sound stimulation from three ears with unaided cochlear implants, a model of functionless cochlea. VEMP was evoked by sound stimulation to all the nine ASNR ears without threshold difference from normal control ( > 0.05), implying normal saccular function for the ASNR ears. For the ears with profound hearing loss and absence of ASNR, about two thirds were considered to have saccular afunction because of absence of VEMP. The other third displayed VEMPs with higher threshold than normal control ( < 0.01), indicating saccular hypofunction. Furthermore, ASNR and VEMP were elicited from an ear diagnosed with semicircular canal hypofunction. CONCLUSIONS: It is clear that the presence of ASNR is dependent not on residual hearing but on normal saccular function. On the basis of these results, the authors believe ASNR to be saccular in origin.