An Integrative Model Accounting for the Symptom Cluster Triggered After an Acoustic Shock
Open accessAbstract
Acoustic shocks and traumas sometimes result in a cluster of debilitating symptoms, including tinnitus, hyperacusis, ear fullness and tension, dizziness, and pain in and outside the ear. The mechanisms underlying this large variety of symptoms remain elusive. In this article, we elaborate on the hypothesis that the tensor tympani muscle (TTM), the trigeminal nerve (TGN), and the trigeminal cervical complex (TCC) play a central role in generating these symptoms. We argue that TTM overuse (due to the acoustic shock), TTM overload (due to muscle tension), and ultimately, TTM injury (due to hypoxia and “energy crisis”) lead to inflammation, thereby activating the TGN, TCC, and cortex. The TCC is a crossroad structure integrating sensory inputs coming from the head–neck complex (including the middle ear) and projecting back to it. The multimodal integration of the TCC may then account for referred pain outside the ear when the middle ear is inflamed and activates the TGN. We believe that our model proposes a synthetic and explanatory framework to explain the phenomena occurring postacoustic shock and potentially also after other nonauditory causes. Indeed, due to the bidirectional properties of the TCC, musculoskeletal disorders in the region of the head–neck complex, including neck injury due to whiplash or temporomandibular disorders, may impact the middle ear, thereby leading to otic symptoms. This previously unavailable model type is experimentally testable and must be taken as a starting point for identifying the mechanisms responsible for this particular subtype of tinnitus and its associated symptoms.
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Middle ear theories suggest that tensor tympani muscle overload or damage can cause pain that spreads via inflammation to activate the trigeminal nerve and generate neuropathic pain and other otologic symptoms.
“Middle ear theories of pain hyperacusis suggest that tensor tympani muscle (TTM) overload or damage can lead to pain that spreads via inflammatory processes to activate the trigeminal nerve and generate neuropathic pain and other otologic symptoms 9.”
From Clinical phenotype and management of sound-induced pain: Insights from adults with pain hyperacusis (2025) · cites this paper as [9]
The Abstract and Conclusion propose that tensor tympani overload or injury leads to inflammation, trigeminal activation, pain that can spread, and other otologic symptoms. The Referred Pain section also links injury and chronic inflammation to trigeminal-pathway hyperactivity. The paper does not identify the resulting pain as neuropathic; a search for that term found it only in a reference title. (LLM, conf=0.84)
Experimental — accuracy not yet measuredExisting conceptual frameworks for the biological basis of pain hyperacusis lack strong human empirical evidence and rely mainly on theory or animal models.
“Existing conceptual frameworks of the biological underpinnings of pain hyperacusis lack strong empirical evidence from humans, relying largely on theory 9,10 or animal models 13,14.”
From Clinical phenotype and management of sound-induced pain: Insights from adults with pain hyperacusis (2025) · cites this paper as [9]
The Introduction says the mechanisms of the acoustic-shock symptom cluster remain elusive, and the Pathophysiological Model of TTTS section presents a proposed model influenced by a single well-documented case. This supports characterizing this framework as largely theoretical, but the paper does not establish the broader claim that existing pain-hyperacusis frameworks generally lack strong human evidence or rely mainly on animal models. (LLM, conf=0.82)
Experimental — accuracy not yet measuredOur results could be consistent with trigeminal nerve involvement in pain hyperacusis.
“Taken together with existing theories 9-12,14,27 and other patient surveys4, our results could be consistent with trigeminal nerve involvement in pain hyperacusis9.”
From Clinical phenotype and management of sound-induced pain: Insights from adults with pain hyperacusis (2025) · cites this paper as [9]
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- Authors
- Noreña, A. J., Fournier, P., Londero, A., Ponsot, D., & Charpentier, N.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Hôpital Européen Georges-Pompidou (FR)
- Université de Lyon (FR)
- Université de Lorraine (FR)
- Corresponding author
- Noreña, Arnaud J.
- Venue
- Trends in Hearing
- Publisher
- SAGE Publications
- Published
- 2018-01
- Volume
- 22
- Pages
- 2331216518801725-2331216518801725
- ISSN
- 2331-2165 (ISSN-L)
- PMC
- PMC6156190
- OpenAlex
- W2893606825
- Cited by
- 42
- References
- 154
- Citations by year
- 2026: 4 · 2025: 2 · 2024: 10 · 2023: 4 · 2022: 5 · 2021: 5 · 2020: 9 · 2019: 2 · 2017: 1
- FWCI
- 0.74
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Trends in Hearing (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- HAL AMU (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Aix-Marseille Université
- The supplementary pension institution of Klesia
- Centre National de la Recherche Scientifique
- B2V
- Topics
- Life Sciences › Neuroscience › Sensory Systems › Hearing, Cochlea, Tinnitus, Genetics
- Life Sciences › Neuroscience › Neurology › Vestibular and auditory disorders
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Keywords
- acoustic shocks, tinnitus, hyperacusis, ear fullness, dizziness, referred pain, tensor tympani muscle, trigeminal nerve, otitis media, muscle overuse, hypoxia, energy crisis, multimodal integration, whiplash injury, temporomandibular disorders
- MeSH terms
- Ear, Middle, Earache, Female, Humans, Male, Hyperacusis, Shock, Temporomandibular Joint Disorders, Tensor Tympani, Tinnitus, Trigeminal Nerve, Cluster Analysis
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