This article focuses on hyperacusis is, how it works, and the different treatment approaches based on what is currently known. Hyperacusis is defined as “ unusual tolerance to ordinary environmental sounds and, more pejoratively, as consistently exaggerated or inappropriate responses to sounds that are neither threatening nor uncomfortable loud to a typical person,” (Baguley 2003) I learned in class that due to cochlear hearing loss caused by the loss of outer hair cells, patients have a smaller dynamic range.
In addition, individuals with cochlear hearing loss experience perceived loudness to increase rapidly called loudness recruitment. However, those with hyperacusis have a lower tolerance for loudness than those with normal hearing loss. The article states that loudness recruitment and hyperacusis are distinguishable phenomenons but are not mutually exclusive. When this concept was brought up in class, I was instantly intrigued. I found the lack of knowledge regarding this disorder and the disorder itself fascinating.
The lack of research or epidemiological data makes it increasingly difficult to study. There have been no incidence studies conducted regarding hyperacusis and often the studies are comprised. However, there is a large coincidence rate between tinnitus and hyperacusis. ” Among patients attending tinnitus clinics with a primary complaint of tinnitus the prevalence of hyperacusis is about 40% and in patients with a primary compliant of hyperacusis the prevalence of tinnitus has ben reported as 86%,” (Baguley 2003).
These coincidence rates leads researchers to believe that there is a common mechanism linking the two disorders. Now, there are two instruments that can aid in quantifying the handicap of hyperacusis. Both instruments are questionnaires. The first questionnaire indicated three factors that caused variance. These three are attentional, social and emotional. The second questionnaire examined that more than half of their variance were de to cognitive reactions, somatic behavior and emotional factors. The second questionnaire that is only available in German has shown to be sensitive to treatments.
Another issue with studying hyperacusis is that there is no underlying medical condition that can be found. Hyperacusis is most commonly reported as a symptom of a condition. One commonality of the conditions where hyperacusis has been reported as a symptom, the conditions involve facial nerve dysfunction. ” Since the facial nerve innervates the stapiedial reflex, which is a mechanism for reducing the perceived intensity of impulse sound, these conditions may reduce the efficacy of that reflex and hence increase the perceived intensity of sound,” (Baguley 2003).
However, this does not meet the strict definition of hyperacusis. Some cases of Lyme disease disrupts the peripheral and central nervous system. This disruption can result in a facial palsy, weakness in the muscle and can also result in a disruption of the stapedial reflex. In addition, there are other conditions such as Lyme disease, Williams syndrome, middle cerebral aneurysm, multiple sclerosis and migrainous cerebral infraction, that identify hyperacusis as a symptom without facial nerve dysfunction. A startling 90% of patients with Williams syndrome report hyperacusis.
In regard to Williams syndrome, there is a high prevalence of hyperacusis which led researchers to hypothesize that there is a 5-hydroxytryptamine disturbance. Besides Williams syndrome, conditions with 5-HT disturbances such as migraines, depression, and post-traumatic stress disorder also report symptoms of hyperacusis. Unfortunately, there is no evidence supporting this notion. Another potential mechanism is that hyperacusis may result from a high incidence of otis media with effusion and the associated conductive hearing loss (Baguley 2003).
Researchers Sahley and Nodar hypothesize that stress causes endogenous dynorphins to be released beneath the inner hair cells which may potentiate the neurotransmitter glutamate which causes sound to be perceived with excessive loudness (Baguley 2003). However, there has yet to be any empirical evidence that supports this hypothesis. Another hypothesis suggests that auditory efferent dysfunction is a potential mechanism. In the medial system of the auditory efferent system, the function of this system is to modulate auditory gain and the behavioral response to sound (Baguley 2003).
There is a disturbance of the ability to modulate ce gain which may result in persistent sensitivity (Baguley 2003). Medial disturbances may contribute to both hyperacusis and tinnitus. Yet, there is evidence against this hypothesis. Patients who underwent surgery vertigo do not report increase tinnitus or loudness intolerance and testing reveals no decrease in auditory performance (Baguley 2003). The last hypothesis suggest that hyperexictability is a potential mechanism for hyperacusis and that the central auditory system has a role in establishing auditory gain.
Links have been found which connect the central auditory system and the amygdalae. The anxiety or fear that hyperacusis patients experience may cause this hyperexcitability which could potentially lead to a persistent state of tinnitus. In addition to potential mechanisms for hyperacusis, therapy techniques were also discussed in the article. Patient’s first reaction to hyperacusis may be to protect their ears with devices; however, this may increase the central gain and worsen their condition.
Audiologists can make minor modifications to Tinnitus Retraining Therapy to make it applicable to hyperacusis. The idea behind the treatment is that if the sound intensity is increased form a a low level gradually over time, the patient will become desensitized (Baguley 2003). Another therapy technique used to lessen the psychological distress is Cognitive Behavioral Therapy. However, there is no evidence of the effectiveness of the treatment and CBT therapists seem uninterested in tinnitus or hyperacusis.
There is some controversy between advocates of TRT and CBT, however, the article suggests that patients most likely would benefit from both therapy techniques. Prior to reading this article, I knew very little about hyperacusis and only knew what is was and that those with hyperacusis had a smaller, limited dynamic range. After reading the article, I understand the extent to the lack of research or knowledge about hyperacusis. I found it interesting that a potential mechanism is the disruption of the stapedial reflex, a reflex I learned in class. I remain intrigued regarding this topic and will continue to research more.
