Editing Hyperacusis (section)

== Possible mechanisms ==

=== Loudness hyperacusis ===
As one possible mechanism, adaptation processes in the auditory brain that influence the dynamic range of neural responses are assumed to be distorted by irregular input from the inner ear. This is mainly caused by hearing loss related damage in the inner ear.<ref name="pmid26139435">{{cite journal | vauthors = Brotherton H, Plack CJ, Maslin M, Schaette R, Munro KJ | title = Pump up the volume: could excessive neural gain explain tinnitus and hyperacusis? | journal = Audiology & Neuro-Otology | volume = 20 | issue = 4 | pages = 273–82 | year = 2015 | pmid = 26139435 | doi = 10.1159/000430459 | s2cid = 32159259}}</ref> The mechanism behind hyperacusis is not currently known, but it is suspected to be caused by damage to the inner ear and [[cochlea]].

=== Noxacusis ===

==== Inner ear theory ====
Type II afferent fibers of the cochlear nerve are not responsible for hearing like the type I afferent fibers. They are thought to be cochlear pain neurons.  Gain of function of these type II afferent fibers may be caused by a flood of ATP after hair cell damage.<ref name="Liu-2015" /><ref name= "Flores-2015" /> Now sensitized, they react to the small amount of ATP released during the normal process of hearing. This may result in pain.<ref name="Liu-2015">{{cite journal | vauthors = Liu C, Glowatzki E, Fuchs PA | title = Unmyelinated type II afferent neurons report cochlear damage | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 112 | issue = 47 | pages = 14723–27 | date = November 2015 | pmid = 26553995 | pmc = 4664349 | doi = 10.1073/pnas.1515228112 | doi-access = free | bibcode = 2015PNAS..11214723L }}</ref><ref name= "Flores-2015">{{Cite journal |last1=Flores |first1=Emma N. |last2=Duggan |first2= Anne |last3= Madathany |first3=Thomas |last4= Hogan |first4=Ann K. |last5=Márquez |first5=Freddie |last6=Kumar |first6= Gagan |last7=Seal |first7=Rebecca |last8=Edwards |first8= Robert |last9=Liberman |first9=M. Charles |last10=García-Añoveros |first10=Jaime |date=2015-03-02 |title=A Non-canonical Pathway from Cochlea to Brain Signals Tissue-damaging Noise |journal=Current Biology |volume=25 |issue=5 |pages= 606–12 |doi= 10.1016/j.cub.2015.01.009 |issn=0960-9822 |pmc=4348215 |pmid=25639244|bibcode=2015CBio...25..606F }}</ref>

==== Middle ear theory ====
Noreña et al. (2018) propose a model that may account for sound-induced pain and a constellation of other symptoms often experienced after an [[acoustic shock]], [[acoustic trauma]], and potentially other mechanisms of auditory damage.  Symptoms may include a sense of fullness in the ear, [[tinnitus]], and [[dizziness]].<ref name="Noreña 20182"/><ref name="Fournier-2022a">{{Cite journal |last1= Fournier |first1= Philippe |last2=Paleressompoulle |first2=Dany |last3=Esteve Fraysse |first3= Marie-José |last4= Paolino |first4=Fabien |last5=Devèze |first5=Arnaud |last6=Venail |first6= Frédéric |last7=Noreña |first7= Arnaud |date= 2022-09-01 |title=Exploring the middle ear function in patients with a cluster of symptoms including tinnitus, hyperacusis, ear fullness and/or pain |journal=Hearing Research |volume= 422 |page =108519 |doi=10.1016/j.heares.2022.108519 |issn= 1878-5891 |pmid= 35644108 |doi-access= free}}</ref>

The model details how symptoms may be initiated by [[tensor tympani muscle]] damage or overload due to acoustic shock or trauma. Hypercontraction or hyperactivity of the muscle may cause an "[[Adenosine triphosphate |ATP]] energy crisis." The muscle is then forced to create energy without sufficient oxygen, which results in the release of lactic acid into the middle ear space. This acidity can activate pain-sensing neurons. Muscle relaxation requires energy in the form of ATP. In the setting of low ATP, it is more difficult for the muscle to relax, which causes the cycle to continue. Via a cascade of events, the activated pain neurons can cause [[neurogenic inflammation]], which may lead to additional pain. In this way, a "vicious circle" is created.<ref name= "Noreña 20182" /><ref name= "Fournier-2022b">{{Cite journal |last1=Fournier |first1=Philippe |last2=Paquette |first2=Sébastien |last3= Paleressompoulle |first3=Dany |last4=Paolino |first4=Fabien |last5=Devèze |first5=Arnaud |last6= Noreña |first6=Arnaud |date= July 2022 |title=Contraction of the stapedius and tensor tympani muscles explored by tympanometry and pressure measurement in the external auditory canal |journal=Hearing Research |volume=420 |page =108509 |doi=10.1016/j.heares.2022.108509 |issn=1878-5891 |pmid=35568596|doi-access=free}}</ref>

Pain from sound sometimes radiates to the face, scalp, and neck. This may be due to the trigeminocervical complex in the brainstem, which integrates input from and output to various regions of the head and neck, including the middle ear. Of note, the tensor tympani muscle is innervated by the trigeminal nerve. The model also explains how [[Whiplash (medicine)|whiplash]] injuries, [[temporomandibular joint dysfunction]], and other conditions affecting the head and neck regions may influence the function of the tensor tympani muscle and contribute to ear symptoms such as pain hyperacusis.<ref name="Noreña 20182" /><ref name= "Fournier-2022a" /><ref name="Fournier-2022b" />