Tinnitus after head injury: evidence from otoacoustic emissions
- aInstitute of Laryngology and Otology, University College London, 330 Gray’s Inn Road, London, UK, bThe National Hospital for Neurology and Neurosurgery, Department of Neuro-otology, Queen Square, London, UK
- Dr Borka J Ceranic, Department of Neuro-otology, The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK. Telephone 0044 171 837 3611 ext 3384; fax 0044 171 829 8775.
- Received 10 November 1997
- Revised 26 February 1998
- Accepted 12 March 1998
Abstract
OBJECTIVE Tinnitus may be caused by a lesion or dysfunction at any level of the auditory system. This study explores cochlear mechanics using otoacoustic emissions in patients with tinnitus after head injury, in whom there seems to be evidence to support dysfunction within the CNS.
METHODS The study included 20 patients with tinnitus and other auditory symptoms, such as hyperacusis and difficulty in listening in background noise, after head injury, in the presence of an “intact” auditory periphery (normal or near normal audiometric thresholds). They were compared with 20 normal subjects and 12 subjects with head injury, but without tinnitus, who had similar audiometric thresholds. In all subjects otoacoustic emissions, including transient click-evoked (TEOAEs) and spontaneous otoacoustic emissions (SOAEs), were recorded, and a test of efferent medial olivocochlear suppression, consisting of recording of TEOAEs under contralateral stimulation, was performed.
RESULTS A significantly higher prevalence of SOAEs (100%), higher TEOAE response amplitudes, and reduced medial olivocochlear suppression in patients with tinnitus in comparison with subjects without tinnitus have been found.
CONCLUSION These findings have been interpreted to be an extracochlear phenomenon, in which the reduction in central efferent suppression of cochlear mechanics, leading to an increase in cochlear amplifier gain, was subsequent to head injury. Auditory symptoms in these patients seemed to constitute the “disinhibition syndrome”.
