HYPERACUSIS AND CLOSED HEAD/NECK INJURY
M. A. Johnson, M.S., Director of the Oregon Tinnitus and Hyperacusis Treatment Clinic, Portland, Oregon (est. 1996)
Twenty eight subjects were identified with a primary complaint of hyperacusis following closed head injury and/or cervical injury. Secondary symptoms were tinnitus (60%) and reported cognitive changes (50%). The clinic specializes in the treatment of tinnitus and hyperacusis, and the subjects were referred by physicians or audiologists for evaluation and treatment. Average age for the 28 subjects was 41.8 years. Eighteen subjects were male, ten were female. Primary cause of injury was automobile accident.
Initial intake included a lengthy case history, review of all previous medical records, and examination of any laboratory results requested prior to the first appointment. Evaluation of the subjects included a complex audiologist battery of tests to evaluate both auditory and vestibular function. Subjective questionnaires were completed with regard to degree of sensitivity, degree of annoyance of the primary condition, and negative effect on lifestyle.
Onset of the primary symptom of hyperacusis was described as a period of time following the head injury from immediate to a period of months. Eighty percent of the patients describe changes in hearing following the injury including distortion, muffling, sensitivity to high pitched sounds, a feeling of numbness or loss of sensation, feeling plugged up, or feeling referred pain in adjoining anatomical areas. Patients also complained of ear tenderness, excessive crackling or popping sounds, a sensation of uncomfortable awareness of the area, and a feeling of fluid or pressure in the ear.
Subjects were advised as to the results of the evaluation and a course of treatment was proposed. The subjects were at the clinic for a period of six hours.
Full audiologic battery was completed, including LDLs by pure tone, UCLs using monitored live voice, computerized dynamic posturography, and tinnitus matching/masking protocols
The typical auditory profile of the average subject included a slight asymmetrical hearing loss. In over 60% of the subjects, a distinct pattern of a slight shift in the mid frequencies (1500 4000 Hz) was noted, with an average difference between ears of 12.5 dB at one or more frequencies. Hearing loss, or thresholds below 25 dB, was rare in these subjects, with the exception of the normal presbycusic profile associated with age which tends to be in the high frequencies.
Hyperacusis was present in 100% of the 28 subjects. Severity levels varied from mild (tolerance levels for LDLs by pure tones from 70-90 dB at 3 or more frequencies) to profound (at threshold detection levels to 10 dB SL at 3 or more frequencies). There was a distinct loss of tolerance in the higher frequencies in all subjects. Tests were repeated twice to increase subjective reliability and test-retest values were highly correlated.
Hyperacusis was often more severe in one ear in these subjects. Using the medical records, it was determined that in 70% of the cases, the side of the head or neck that was struck during the injury was identified as the most hyperacusic ear during the testing. Testing supported this identification in 80% of the subjects.
Monitored live voice UCLs were also obtained and used to verify pure tone LDL findings. On average there is a 15 dB difference between UCL averages and LDL averages, reflecting the low frequency energy present in human voices.
A questionnaire regarding the cognitive and balance functioning of the subjects indicated a need for further investigation into these areas for these subjects. Referrals were provided to appropriate service providers.
Hyperacusis following injury is often delayed in its onset, which supports the theory that the once the initial injury has subsided in swelling or congestion, bruising or bleeding, other factors begin to accelerate and manifest into auditory and/or cortical damage. Hyperacusis may well fall into a category more associated with a destructive auto immune response to injury, i.e., akin to injury induced arthritis, rather than a separate trauma outcome. It is often noted that the hyperacusis will emerge in one ear first, but rather quickly be present in both ears, leading to speculation on the probability of involvement of the central nervous system.
The idea of reflected cortical damage is suggested as the injury may be peripheral initially, but the disruption of the signal processing capacity of the afferent and efferent auditory systems will be manifested in a bilaterally pattern rather quickly. The shifts in central processing will be directly related to changes in the cochlear outer and inner hair cells, possible damage to the VIIIth nerve, and shearing and stretching of the nerve roots where they enter the brainstem areas. The disrupted flow of signals to and from the cochlea is possibly reflected in changes of function of the cortical auditory centers, and therefore this could affect the ability of the efferent system to direct the outer hair cells in their ability to enhance or dampen incoming sounds.
Hyperacusis may also be related to auto immune disorder and other inflammatory conditions as many of the subjects reported other varieties of auto immune disorders including skin conditions, allergies, and arthritis (15 subjects).
Hyperacusis and slight shifts in hearing loss were identified in 28 subjects, with symptoms that included changes in hearing acuity and loss of tolerance for normal sound levels. Onset of hyperacusis can vary from immediate to several months. Testing protocol should include LDLs using pure tones and UCLs using monitored live voice.