Tinnitus after head injury: evidence from otoacoustic emissions

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 diYculty 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 clickevoked (TEOAEs) and spontaneous otoacoustic emissions (SOAEs), were recorded, and a test of eVerent 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 eVerent 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". (J Neurol Neurosurg Psychiatry 1998;65:523-529)

Stability of the Medial Olivocochlear Reflex as Measured by Distortion Product Otoacoustic Emissions

“…Altered MOC inhibitions have been reported in individuals with auditory neuropathy (Starr, Picton, Sininger, Hood, & Berlin, 1996), auditory processing disorders (Muchnik et al, 2004;Sanches & Carvallo, 2006), autism (Khalfa, Bruneau, et al, 2001), temporal lobe epilepsy (Khalfa, Bougeard, et al, 2001), learning disability (Garinis, Glattke, & Cone-Wesson, 2008), and tinnitus (Ceranic, Prasher, Raglan, & Luxon, 1998). Likewise, enhanced functioning of the MOC system has been reported in musicians (Micheyl, Khalfa, Perrot, & Collet, 1997;Perrot & Collet, 2014).…”

Increased contralateral suppression of otoacoustic emissions indicates a hyperresponsive medial olivocochlear system in humans with tinnitus and hyperacusis

“…Anomalous MOC function has been hypothesized, and tested for, in a variety of clinical conditions, including tinnitus, a prevalent and often disruptive condition in which sound is perceived in the absence of actual sound (Shargorodsky et al 2010;Stouffer and Tyler 1990). Despite a large number of studies, however, it remains unclear whether or not there is a relationship between MOC function and tinnitus (Attias et al 1996(Attias et al , 2005Ceranic et al 1998;Chéry-Croze et al 1993Fávero et al 2006;Fernandes and Santos 2009;Geven et al 2011Geven et al , 2012Graham and Hazell 1994;Hesse et al 2005Hesse et al , 2008Hsu et al 2013;Lalaki et al 2011;Lind 1996;Paglialonga et al 2010Paglialonga et al , 2011Riga et al 2007;Riga et al in press;Urnau and Tochetto 2012). Results differ even among the more carefully controlled studies of this issue, with some reporting reduced MOC function in tinnitus (Attias et al 1996;Riga et al 2007) and others reporting no difference compared with controls (Geven et al 2011;Lind 1996;Paglialonga et al 2010Paglialonga et al , 2011.…”

Prospective Associations Between Traumatic Brain Injury and Postdeployment Tinnitus in Active-Duty Marines

“…27,[60][61][62][63][64][65] The initial shock wave from a blast leads to shearing of tissues, 25 directly injuring the cochlea and leading to an inflammatory response with subsequent neural degeneration. 26 Animal models of TBI demonstrate loss of ribbon synapses from inner hair cells to the auditory nerve in mild cases and then deterioration of outer hair cells of the cochlea, leading to altered auditory nerve activity.…”