The list of possibilities for hyperacusis mechanisms is still quite large.
To narrow the discussion, we focus primarily on cases induced by acoustic trauma.
It is natural then to start with the middle ear function for possible models.
The stapedius muscle is responsible for sound attenuation by dampening the vibration of the stapes.
Since many hyperacusis patients appear to have a normal stapedial reflex test (by current testing methods), there are very few works on the topic.
In a work on the "Functional Model of the Middle Ear Ossicles," the authors suggest a mechanism of how paralysis of the stapedius muscle, caused by an injury to the facial nerve, results in hyperacusis.
Further insights might be gained by a deeper analysis and possible advancement of the various acoustic reflex testing methods comparing a hyperacusis population to a control group.
Many possible mechanisms for hyperacusis start in the cochlea. Baguley and Andersson's book references Sahley and Nodar's 2001 article on "A Biochemical Model of Peripheral Tinnitus."
A summary from their abstract states: "Naturally occurring opioid dynorphins are released from lateral efferent axons into the synaptic region beneath the cochlear inner hair cells during stressful episodes.
In the presence of dynorphins, the excitatory neurotransmitter glutamate, released by inner hair cells in response to stimuli or (spontaneously) in silence, is enhanced at cochlear NMDA receptors.
This results in altered neural excitability and/or an altered discharge spectrum in (modiolar-oriented) type I neurons normally characterized by low rates of spontaneous discharge and relatively poor thresholds.
It is also possible that chronic exposure to dynorphins leads to auditory neural excitotoxicity via the same receptor mechanism."
They propose this spontaneous activity leads to the perception of tinnitus and that the perceived intensity of sound may increase resulting in hyperacusis.
This work is an example of where model associations between tinnitus and hyperacusis can be difficult.
It would be far better to have an analysis of similar causal mechanisms purely in relationship to hyperacusis.
There are a wide range of supporting hyperacusis works describing the connections to the cochlea.
The case of a musician who had his cochlea destroyed in a mostly deaf ear to relieve his symptoms is interesting as later works suggest such a radical measure may not impact the problem.
Some works suggest an abnormality of outer hair cell (OHC) function.
In a work entitled "DPOAE in Tinnitus Patients with Cochlear Hearing Loss considering Hyperacusis and Misophonia," the authors promote the model that the OHC's are the most probable place generating tinnitus.
They find that decreasing of otoemission "DPOAE amplitudes in patients with cochlear hearing loss and tinnitus suggests significant role of OHC pathology, unbalanced by IHC injury in generation of tinnitus in patients with hearing loss of cochlear localization.
DPOAE fine structure provides us the additional information about DPOAE amplitude recorded in two points per octave, spreading the amount of frequencies f2, where differences are noticed in comparison of two groups - tinnitus patients and control.
Function growth rate cannot be the only parameter in estimation of DPOAE in tinnitus patients with cochlear hearing loss, also including subjects with hyperacusis and misophony.
Hyperacusis has important influence on DPOAE amplitude, increases essentially amplitude of DPOAE in the examined group of tinnitus patients.
" Another work focused on the OHC's impact from 1996 is entitled "Nonlinearity of mechanoelectrical transduction of outer hair cells as the source of nonlinear basilar-membrane motion and loudness recruitment."
According to the experiment's data and "the feedback concept of outer hair cell action, disruption of the mechanoelectrical transduction of OHC leads to both a reduction of gain and linearizing of the response; that is, to both hearing loss and loudness recruitment.
" Since recruitment and hyperacusis are quite different, this model should not be extented to hyperacusis.
However, since most OHC works were not primarily focused on hyperacusis, it may be useful to have a dedicated project that can conclusively prove OHC function in typical hyperacusis patients.
Dr. J. A. Vernon at the Oregon Health and Science University provided a basic clinical overview in 2002 entitled "Hyperacusis: Testing, Treatments, and a Possible Mechanism." He describes background information on the topic and the pink noise treatment program he has used for patients.
He concludes with a brief summary of the model often accepted for the cause: "It appears that the normal function of the olivocochlear bundle, which supplies efferent innervation to the cochlea, is to exert a suppressive or inhibitor effect upon responses to incoming sounds.
If these efferent nerves are not performing normally it seems somewhat reasonable to propose that all sounds might be perceived as being louder than usual."
One classic work that led to moving beyond the cochlea is a paper from 2000 by Salvi, Wang, and Ding at University of Buffalo entitled: "Auditory plasticity and hyperactivity following cochlear damage."
In it they describe some of the "functional changes that occur in the central auditory pathway after the cochlea is damaged by acoustic overstimulation or by carboplatin, an ototoxic drug that selectively destroys inner hair cells (IHCs).
Acoustic trauma typically impairs the sensitivity and tuning of auditory nerve fibers and reduces the neural output of the cochlea.
Surprisingly, our results show that restricted cochlear damage enhances neural activity in the central auditory pathway.
Despite a reduction in the auditory-nerve compound action potential (CAP), the local field potential from the inferior colliculus (IC) increases at a faster than normal rate and its maximum amplitude is enhanced at frequencies below the region of hearing loss.
To determine if this enhancement was due to loss of sideband inhibition, we recorded from single neurons in the IC and dorsal cochlear nucleus before and after presenting a traumatizing above the unit's characteristic frequency (CF).
Following the exposure, some neurons showed substantial broadening of tuning below CF, less inhibition, and a significant increase in discharge rate, consistent with a model involving loss of sideband inhibition.
Selective IHC loss reduces the amplitude of the CAP without affecting the threshold and tuning of the remaining auditory nerve fibers.
Although the output of the cochlea is reduced in proportion to the amount of IHC loss, the IC response shows only a modest amplitude reduction, and remarkably, the response of the auditory cortex is enhanced.
These results suggest that the gain of the central auditory pathway can be up- or down regulated to compensate for the amount of neural activity from the cochlea."
Although this work is centered on hearing loss, there are some important details which may relate to hyperacusis.
Figure 3 C from their initial experiment where chinchillas were exposed to 105db for 5 days shows the overshoot of the IC amplitude just above the 60dB level which exceeds the pre-exposure levels by a significant amount.
In another experiment where the IHC's only were selectively destroyed resulting in a similar reduction in output of the cochlea (lower CAP), the authors also find an increase in AC amplitude.
Thus they propose that a mechanism for tinnitus could be "the loss of lateral inhibition that unmasks pre-existing neural circuits within the auditory pathway."
Additionally they state that since "neural activity is enhanced and that amplitude grows at an abnormally rapid rate following cochlear damage, it seems plausible that recruitment and hyperacusis originate in the central auditory pathway.}
While the model seems to fit well for recruitment, it does not fit as well for typical hyperacusis patients since they often have normal audiograms and do not have hearing loss in the lower thresholds.
Additionally, the work is entirely based on a scenario created by hair cell damage (either IHC and OHC or both) which further supports the need to establish if typical hyperacusis patients have hair cell damage.
In their book (latest version from 2008) entitled Tinnitus Retraining Therapy, Dr. Jastreboff and Dr. Hazell devote the second chapter to "The neurophysiological model of tinnitus and decreased sound tolerance.
" Their primary theory is called the "discordant dysfunction (damage) theory." They postulate that "the tinnitus signal originates in the inner ear when one type of sensory cell, OHC, is more dysfunctional than the other type of sensory cells, IHC, at the same area of the basilar membrane in the cochlea.
When neurons in the dorsal cochlear nuclei receive excitation from IHC but not from the damaged OHC, then an imbalance occurs at this level of the auditory system.
This, in turn, causes abnormal activity in the form of burst of high-frequency neuronal discharges, which, after amplification within the auditory system are perceived as tinnitus."
It is interesting to contrast the theory here focused on OHC loss compared to Salvi's work that was more focused on IHC loss.
On the issue of detectable hearing loss for tinnitus, they state that "20% of patients with tinnitus have normal hearing.
This is because changes are too small to be detectable on a standard audiogram."
A key point to note here is that there is a wide frequency range above the normal 8000Hz range of standard audiograms that could be explored to help confirm these possibilities. In moving from the model above on tinnitus to the model associated with hyperacusis, Jastreboff is less detailed.
The book simply states that "the model predicts that a relatively high percentage of tinnitus patients should exhibit increased sensitivity to external sound, that is decreased sound tolerance.
This is what one would expect from the increased auditory gain, or the combination of an increased gain and some even minor dysfunction of the inner ear.
" Later it is further explained that in hyperacusis, "the external signal undergoes abnormal enhancement/amplification within the subconscious auditory pathways and only secondarily activates the limbic and autonomic nervous systems.
" The opportunity for further works here is similar to above models: prove the functional capabilities of the OHC's in hyperacusis patients.
In 2003, Formby, Sherlock, and Gold presented a paper focused on proving the central gain control process entitled: "Adaptive plasticity of loudness induced by chronic attenuation and enhancement of the acoustic background."
In it the authors show that "after continuous, 2-week earplugging and low-level noise treatments that listeners become more and less sensitive, respectively, to the loudness of sounds.
This simple demonstration of adaptive plasticity is consistent with modification of a theoretical gain control process, which is the basis for desensitizing sound therapies used in treating hyperacusis and related sound tolerance problems."
The specific mechanism of adaptive plasticity is not proposed. While the loudness judgments using the Contour Test of Loudness Perception in the work is helpful, another key component for direct comparison to hyperacusis would have been actual levels and types of pain the participants experienced when exposed back to everyday loud noises.
More specifically did the participants experience pain for the days following the experiment.
Additional opportunities for research relate to a more detailed assessment of hyperacusis patients' symptoms.
Most surveys are trying to establish whether or not a person has hyperacusis.
Baugley has summarized some of these prevalence surveys which show a wide range of results from 8-9% in a Swedish study to 15% in a Polish study.
He also summarizes the following finding: "Among patients attending tinnitus clinics with a primary complaint of tinnitus the prevalence of hyperacusis is about 40%; and in patients with a primary complaint of hyperacusis the prevalence of tinnitus has been reported as 86%".
Beyond the issue of lack of standardization in questionnaires (one by Khalfa is presented as a possible standard), the more important detail for researches is a detailed guide of symptoms beyond life impacts.
For example, with many neuropathies the Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) Pain Scale is used.
Similarly, in hyperacusis it would be helpful to know the level of pain severity, the type of pain such as throbbing, constant, random, the location of pain, the length of pain and timing after excessive noise exposure.
This may yield possible measurable impacts. These results may add insights to psychological mechanisms and models associated with hyperacusis.