Timothy C. Hain, MD
Please read our disclaimer Return to Index. Search this site Page last modified: December 5, 2003
Acoustic reflexes measure the stapedius and tensor tympani reflex generated eardrum movement in response to intense sound. They can be helpful in corroborating particular types of hearing loss in situations where patient reliability is questionable. They also occasionally point to central nervous system pathology. Reflexes are ordinarily present for fairly loud sounds, relative to hearing ability. Reflexes that are present at abnormally low sound input levels suggest recruitment with a cochlear site of lesion. Reflexes that decay rapidly suggest a retrocochlear lesion. Reflexes that are bilaterally absent contralaterally suggest a midline brainstem lesion.
A typical setup to measure the stapedius reflex is a tympanometer having a method of delivering both a sound to either ear as well as measuring the admittance of the tympanic membrane. Reflexes may be elicited at 500, 1000 and 2000 hz, using 110 db HL. The amplitude of the reflex, latency, and timing (sustained or rapidly decaying) can be quantified. Typical reflex latencies in noral subjects are 107 msec, ranging from 40-180(Bosatra and Russolo, 1976). Normally the reflex does not decay.
The stapedius reflex consists of a contraction of the stapedius muscle in response to a loud noise. The simplest stapedius reflex arc involving the fewest possible neurons would involve spiral ganglion neurons, the auditory nerve, the cochlear nucleus, the superior olive, the facial nerve nucleus, the facial nerve, and the stapedius muscle. In the brainstem, commisures connect to the other side so an ipsilateral sound can generate a contralateral response.
Because the stapedius reflex involves several nerves and brainstem connections, it can be abnormal in a variety of situations that may not necessarily impair hearing. Cantrell and others reported abnormalities in neurological disorders (Cantrell, 1979).
Central case example: A 40 year old man was well until he was involved in an auto accident. Two days later he developed diplopia and a rotatory type vertigo. On physical examination he had clear spontaneous nystagmus, a fourth nerve palsy, and mildly decreased hearing on the left side. Audiometry documented mildly impaired hearing on the left, but acoustic reflexes were abnormal with very rapid decay on the left side. BAER responses were also very abnormal on the left. An MRI scan documented a lesion resembling an MS placque in his left cerebellar peduncle area, just behind the 8th nerve (see figure to right). His symptoms resolved spontaneously and he has had not further neurological complaints in 5 years of followup. COMMENT: This was most likely a demyelinative lesion resembling transverse myelitis. The abnormal reflex decay pointed towards a central lesion.