Different Patterns of Hearing Loss among Tinnitus Patients: A Latent Class Analysis of a Large Sample

Tinnitus is the perception of sound in the absence of a corresponding external acoustic stimulus. With prevalence ranging from 10% to 15%, tinnitus is a common disorder. Many people habituate to the phantom sound, but tinnitus severely impairs quality of life of about 1-2% of all people. Tinnitus has traditionally been regarded as an otological disorder, but advances in neuroimaging methods and development of animal models have increasingly shifted the perspective towards its neuronal correlates. Increased neuronal firing rate, enhanced neuronal synchrony, and changes in the tonotopic organisation are recorded in central auditory pathways in reaction to deprived auditory input and represent--together with changes in non-auditory brain areas--the neuronal correlate of tinnitus. Assessment of patients includes a detailed case history, measurement of hearing function, quantification of tinnitus severity, and identification of causal factors, associated symptoms, and comorbidities. Most widely used treatments for tinnitus involve counselling, and best evidence is available for cognitive behavioural therapy. New pathophysiological insights have prompted the development of innovative brain-based treatment approaches to directly target the neuronal correlates of tinnitus. Copyright © 2013 Elsevier Ltd. All rights reserved.

The classic view of sensorineural hearing loss (SNHL) is that the "primary" targets are hair cells, and that cochlear-nerve loss is "secondary" to hair cell degeneration. Our recent work in mouse and guinea pig has challenged that view. In noise-induced hearing loss, exposures causing only reversible threshold shifts (and no hair cell loss) nevertheless cause permanent loss of >50% of cochlear-nerve/hair-cell synapses. Similarly, in age-related hearing loss, degeneration of cochlear synapses precedes both hair cell loss and threshold elevation. This primary neural degeneration has remained hidden for three reasons: 1) the spiral ganglion cells, the cochlear neural elements commonly assessed in studies of SNHL, survive for years despite loss of synaptic connection with hair cells, 2) the synaptic terminals of cochlear nerve fibers are unmyelinated and difficult to see in the light microscope, and 3) the degeneration is selective for cochlear-nerve fibers with high thresholds. Although not required for threshold detection in quiet (e.g. threshold audiometry or auditory brainstem response threshold), these high-threshold fibers are critical for hearing in noisy environments. Our research suggests that 1) primary neural degeneration is an important contributor to the perceptual handicap in SNHL, and 2) in cases where the hair cells survive, neurotrophin therapies can elicit neurite outgrowth from spiral ganglion neurons and re-establishment of their peripheral synapses. This article is part of a Special Issue entitled .

Tinnitus is an auditory phantom sensation (ringing of the ears) experienced when no external sound is present. Most but not all cases are associated with hearing loss induced by noise exposure or aging. Neuroscience research has begun to reveal how tinnitus is generated by the brain when hearing loss occurs, and to suggest new avenues for management and prevention of tinnitus following hearing injuries. Downregulation of intracortical inhibition induced by damage to the cochlea or to auditory projection pathways highlights neural processes that underlie the sensation of phantom sound.