Tinnitus causes an individual to hear sounds that do not have any external sources. These patients experience difficulty in understanding speech in noisy environments. Tinnitus is a common problem in patients with sensorineural hearing loss (SNHL).
Around 10–15% of the global adult population experiences tinnitus. It must be noted that approximately 3% of people with tinnitus experience sleep deprivation, depression, social isolation, and anxiety that affects their professional life, and an overall decrease in quality of life occurs.
Several therapies have been formulated, such as sound maskers, cognitive behavioral-based therapies, and tinnitus-retraining therapy, to alleviate the distress caused by tinnitus. However, to date, there has been no cure for this issue. To effectively silence tinnitus, it is important to uncover its biological origin.
A common hypothesis of tinnitus generation involves a decreased neural activity from an impaired cochlea that induces hyperactivity in the central nervous system. The mechanism behind tinnitus generation has been investigated using animal models of SNHL.
These studies revealed a loss of synaptic connection to inner hair cells, leaving many surviving spiral ganglion neurons unable to respond spontaneously to sound. However, an elevated spontaneous and/or sound-evoked firing occurs in central auditory circuits, manifesting tinnitus symptoms.
Aging and acoustic overexposure cause permanent impairment of the cochlear nerve. Cochlear nerve damage could also occur when the sensory cells remain intact, indicating the possibility of tinnitus in patients with normal hearing.
However, this cochlear neural degeneration (CND) does not increase beyond thresholds until the sound intensity becomes extreme. It must be noted that most vulnerable neurons have high thresholds and low spontaneous rates (SRs). These neurons do not aid in noise detection in quiet environments.
Common underlying pathologies linked to tinnitus are significant CND that occurs in patients with neurofibromatosis of type II, Ménière’s disease, sudden SNHL, and vestibular schwannoma. However, contradictory results have been published regarding the manifestation of tinnitus in CND patients with normal hearing.
About the study
All participants recruited in this study were healthy, between 18 and 72 years of age, and English-speaking. None of the participants had hearing problems or somatic/objective tinnitus history. At baseline, participants presented normal middle-ear function and unremarkable otoscopic examinations.
The study cohort was divided into three groups. The first group included individuals without any history of tinnitus. This group also included individuals who infrequently heard phantom sounds that emerged and resolved within minutes. It was considered as the control group.
The second group included participants who experienced at least one temporary/intermittent tinnitus episode in less than six months. The third group included participants who had experienced continuous tinnitus percept for over six months.
Study findings
A total of 294 individuals were recruited, including 140 female and 154 male participants. The mean thresholds at extended high frequencies (EHFs) were ≤ 20 dB hearing loss (HL).
201 participants reported no experience with tinnitus. It were assigned to the control “no tinnitus” group, and 64 participants experienced temporary/intermittent tinnitus and were assigned to the second “intermittent tinnitus” group. The third “chronic tinnitus” group included 29 participants.
The incidence of CND in participants was estimated using a test battery that assessed different stages of the auditory system. This study observed an association between chronic subjective tinnitus (self-reports) and cochlear neural deficits.
A weaker acoustic middle-ear-muscle reflex (MEMR) and stronger medial olivocochlear reflex (MOCR) circuit were found even when sex and thresholds at standard frequencies were matched. A weaker MEMR strength and higher MEMR thresholds represent chronic tinnitus.
Most participants in the chronic tinnitus group were male, exhibited poor audiometric thresholds, particularly above 3 kHz, and were in noisy environments. In line with previous studies, chronic tinnitus participants had a history of anxiety, depression, and concussion. These conditions were not present in the control group.
The peripheral neural responses of “normal-hearing” participants were compared with those with chronic tinnitus. This assessment revealed tinnitus status to be a significant predictor of cochlear neural responses. The current study revealed that tinnitus sustainability could depend on the degree of peripheral neural damage.
The low- and medium-SR group was more resistant to sound masking compared to the control group. This could be because CND induces difficulties in hearing noise, which is commonly found in SNHL.
It must be noted that the control or no-tinnitus group exhibited a significant reduction in cochlear neural response in the presence of an EHF masker. A similar occurrence was not noted in the chronic tinnitus group.
The EcochG findings strongly indicated a loss of cochlear neurons in the chronic tinnitus group and in the low- and medium-SR fiber population.
Article originally appeared on Medical Life Science News
