Møller (2007) and Eggermont
(2007) describe the possible pathophysiology of tinnitus resulting from neural
synchrony in the peripheral auditory system, increase in signal firing rates in
neurons at various locations, and tonotopic map changes in the peripheral
auditory cortex. Møller (2007) stated when the cochlea becomes impaired, both
inhibitory and excitatory signals to the cochlear nucleus may be decreased, but
especially inhibitory signals. Additionally, other nuclei in the auditory
pathway may have increased excitability due to this reduced inhibition.  Perceptions from tonotopic map changes were
compared to those sensations experienced and described as a “phantom limb”
(Eggermont, 2007). Eggermont stated cochlear injury could be correlated with
decreased inhibition in deafferented frequency regions in the primary auditory
cortex, contributing to the perceived sound. Møller (2007) also indicated
tinnitus may arise from neural plasticity and reorganization of the central
nervous system and non-classical pathways, so parts of the nervous system not
usually involved in processing sounds develop a role.

Roberts et al.
(2010) suggest that the interruption of afferent connections to the central auditory
structures of the brain, such as the sensorineural loss of high-frequency
hearing due to inner ear damage by noise exposure or ototoxic agents, causes an
increase of spontaneous firing rates in more central neurons. These increased
firing rates may lay the foundation for neural synchrony leading to tinnitus.

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The focus of this
study will be on Tinnitus Retraining Therapy (TRT), which is based on the
neurophysiological model of tinnitus described by Jastreboff (2011) as the
appearance of clinically relevant, bothersome tinnitus that involves areas of
the brain in addition to the auditory system area, namely the limbic and
sympathetic autonomic nervous systems, in the negative reaction to the
perception of the sounds. The cause of the neural activity producing tinnitus
is proposed to be outer and inner hair cell dysfunction, such as described
above; however, the neurophysiological model for TRT additionally is focused on
the negative reactions from the tinnitus that are perceived by some individuals
when the tinnitus signal spreads to other areas of the brain.

Rosing, Schmidt,
Wedderkopp, and Baguley (2016) conducted a systematic review of literature and
found a large range in tinnitus rates reported by various studies, with
occurrence from 4.7% to 46% in the pediatric population and 23.5% to 62.2% in
children with hearing loss, with the samples being children 5-19 years of age.
The large ranges were contributed to several causes, including differences in
study design and question proposals to the pediatric patients. In any patient,
tinnitus can have a negative impact on the individual with the perception.
According to the American Tinnitus Association (2016), in the general
population, on a scale of 1-10, tinnitus impacts individuals’ daily lives at a
level of 10 in about 5% of the population with the condition. McCormack et al.
(2014) found tinnitus to be bothersome in about 4% of individuals, or 22-26% of
their sample who reported tinnitus. Some of the effects tinnitus can have
include anxiety, sleep problems, and trouble concentrating. How tinnitus
affects children specifically is a topic with limited research. However, Shetye
and Kennedy (2010) report that interference with sleep, difficulty with
concentration at home and school, tiredness, and anxiety are commonly reported
co-occurring symptoms in children with tinnitus.

            Currently,
there are several possible treatments for individuals suffering from tinnitus,
including cognitive behavioral therapy, counseling, sound therapies, and medical
approaches including pharmacological methods to treat associated conditions
such as anxiety (Katz, Chasin, English, Hood, & Tillery, 2015). The focus
of this study is on Tinnitus Retraining Therapy outcomes for children with
tinnitus that impacts their daily lives.