Cited by 10Hearing, Cochlea, Tinnitus, GeneticsPain Mechanisms and TreatmentsHearing Loss and Rehabilitation

Clinical phenotype and management of sound-induced pain: Insights from adults with pain hyperacusis

Open access
Jahn, Kelly N., Kashiwagura, Sean Takamoto, Yousuf, Muhammad Saad·2025·The Journal of Pain

Published version of a preprint

Abstract

Pain hyperacusis, also known as noxacusis, causes physical pain in response to sounds that do not bother most people. How sound causes excruciating pain that can last for weeks or months is not well understood, resulting in a lack of effective treatments. To gain insight into the underlying mechanisms of the condition, 32 adults attended a virtual focus group to describe their sound-induced pain. Focus group data were used to develop three follow-up surveys that aimed to identify the most common symptoms of pain hyperacusis as well as the participants' use of therapies for pain relief. All participants endorsed negative effects of pain hyperacusis on psychosocial and physical function. Most reported sound-induced burning (80.77%), stabbing (76.92%), throbbing (73.08%), and pinching (53.85%) sensations that occur either in the ear or elsewhere in the body. Participants have used numerous pharmaceutical and non-pharmaceutical interventions to alleviate their pain with varying degrees of pain relief. Benzodiazepines and nerve blockers emerged as the most effective analgesic options while non-pharmaceutical therapies were largely ineffective. Symptoms and therapeutic approaches were generally consistent with peripheral mechanistic theories of pain hyperacusis (e.g., trigeminal nerve involvement). An interdisciplinary approach to clinical studies and the development of animal models are needed to identify and treat the pathological mechanisms of pain hyperacusis. PERSPECTIVE: This article presents the physical and psychosocial consequences of debilitating sound-induced pain (i.e., pain hyperacusis) and the interventions that sufferers have sought for pain relief. The results are largely consistent with peripheral mechanistic theories (e.g., trigeminal nerve involvement) and will guide future work to investigate neural mechanisms and effective therapies.

Integrity signals

Registry

Crossref · 10.1016/j.jpain.2024.104741

Cites

38 of 38 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

26 of 46 cited sources checked · 12 supported · 0 flagged · accuracy not yet measured

  • Premisecitation

    Adults with pain hyperacusis often have a relatively severe clinical presentation.

    “Individuals with pain hyperacusis often present with a relatively severe clinical phenotype”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [4] Williams, 2021, A phenotypic comparison of loudness and pain hyperacusis: symptoms, comorbidity, and associated features in a multinational patient registry, Am J Audiol source
  • Premisecitation

    Healthcare professionals have few tools available to diagnose, monitor, and treat pain hyperacusis.

    “healthcare professionals have limited tools to diagnose, monitor, and treat the condition 5”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [5] Baguley, 2018, Hyperacusis: major research questions, Hno source

      The “How to measure hyperacusis” section describes substantial limitations in assessment methods, and “Treatment” identifies unanswered questions about treatment efficacy. The paper also says pain-related categories can be difficult to distinguish in clinical practice. These passages support limited tools for hyperacusis generally, but do not specifically establish the availability of tools to monitor or treat pain hyperacusis. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
  • Premisecitation

    The pain hyperacusis phenotype is not widely recognized by healthcare professionals.

    “they do not widely recognize the pain hyperacusis phenotype 6.”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [6] Jahn, 2023, Hyperacusis diagnosis and management in the United States: clinical audiology practice patterns, Am J Audiol source

      In “Definition of Hyperacusis and Related Conditions” (page not provided), only 20 of 94 surveyed U.S. audiologists mentioned pain when defining hyperacusis, consistent with limited attention to pain in this group. The paper does not establish that healthcare professionals generally fail to recognize pain hyperacusis as a distinct phenotype; its Conclusions say knowledge among professionals outside audiology is unclear. (LLM, conf=0.83)

      Experimental — accuracy not yet measured
  • Premisecitation

    Existing 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.”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites [9] Noreña, 2018, An integrative model accounting for the symptom cluster triggered after an acoustic shock, Trends Hear source

      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 measured
    • cites [10] Westcott, 2016, Hyperacusis-induced Pain: understanding and management of tonic tensor tympani syndrome (TTTS) symptoms, J Pain Relief source
    • cites [13] Wood, 2024, Damage-evoked signals in cochlear neurons and orting cells, Front Neurol source
  • Premisecitation

    Adults with pain hyperacusis frequently report symptom exacerbations, called setbacks, in response to trigger sounds.

    “wherein they report frequent “setbacks” (i.e., symptom exacerbations in response to trigger sounds)”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [4] Williams, 2021, A phenotypic comparison of loudness and pain hyperacusis: symptoms, comorbidity, and associated features in a multinational patient registry, Am J Audiol source
  • Classified as probably not a substantial claim. 17
  • May combine two claims. 22
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    A recent survey found that 62.5% of adults with hyperacusis experience some degree of sound-induced physical pain.

    “a recent survey demonstrated that 62.5% of adults with hyperacusis experience some amount of sound-induced physical pain 4.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [4] Williams, 2021, A phenotypic comparison of loudness and pain hyperacusis: symptoms, comorbidity, and associated features in a multinational patient registry, Am J Audiol source

      The Method section reports that 152 of 243 adults (62.6%) were classified as having pain hyperacusis, close to the cited 62.5%. But that classification required daily or continuous ear pain; 90.5% reported ear pain at least some of the time. The cited percentage therefore does not describe adults experiencing any amount of pain. (LLM, conf=0.90)

      Experimental — accuracy not yet measured
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    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.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [9] Noreña, 2018, An integrative model accounting for the symptom cluster triggered after an acoustic shock, Trends Hear source

      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 measured
    • Rests on an assumption: The trigeminal nerve carries sensory information from the middle ear to the trigeminocervical complex in the brainstem and then to the cortex.
    • Rests on an assumption: The trigeminocervical complex integrates sensory and nociceptive inputs from the middle ear, head, and neck, and can serve as a node for referred pain and head sensations.
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Inner ear models suggest that Type-II cochlear afferents may be involved in auditory nociception because they share morphologic and neurochemical properties with pain-sensing C fibers.

    “Alternatively, inner ear models of pain hyperacusis suggest that Type-II cochlear afferents may be involved in auditory nociception, as these fibers have similar morphologic and neurochemical properties to pain-sensing C fibers in the somatic nervous system11,12,27.”
    Quote in the paperNot a substantial claim2 of 3 sources checked
    • cites [11] Flores, 2015, A non-canonical pathway from cochlea to brain signals tissue-damaging noise, Curr Biol source
    • cites [12] Liu, 2015, Unmyelinated type II afferent neurons report cochlear damage, Proc Natl Acad Sci source
    • cites [27] Wu, 2018, Opposing expression gradients of calcitonin-related polypeptide alpha (Calca/Cgrpα) and tyrosine hydroxylase (Th) in type II afferent neurons of the mouse cochlea, J Comp Neurol source
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Mechanical stress irritation is a causative factor in trigeminal neuralgia, and surgical relief of mechanical stress is a common treatment for intractable pain.

    “Irritation due to mechanical stress like compression, torsion, and angulation, is a causative factor in the development of trigeminal neuralgia and surgical methods that relieve mechanical stress are common treatment options for intractable pain in these individuals23,24.”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites [23] Chelmis, 2024, Microvascular decompression: an effective approach for trigeminal neuralgia caused by a dolichoectatic basilar artery after multiple treatment failures, J Neurol Surg Rep source

      The Introduction identifies neurovascular compression as a cause of classic trigeminal neuralgia, and the Discussion describes microvascular decompression as a treatment that relieves compression. Our copy does not identify torsion or angulation as causes, so it supports the compression-and-treatment portion but not those specific examples of mechanical stress. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
    • cites [24] Murugesan, 2024, retrospective analysis of medical management strategies for trigeminal neuralgia: an institutional review, Cureus source

      The Introduction (page not provided) describes blood-vessel compression as a proposed mechanism of trigeminal neuralgia and identifies microvascular decompression as an established option when medication fails. It does not mention torsion or angulation, and it presents compression as a theory rather than an established cause. The Discussion (page not provided) also describes surgery as an alternative when medical treatment is ineffective, not the usual first-line approach. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
  • May combine two claims.

    Premisecitation

    Interactions between the auditory and pain pathways may be mediated in part by opioid signaling, consistent with the excellent pain relief from oxycodone reported by one participant.

    “Moreover, interactions between the auditory and pain pathways may be mediated, in part, by opioid signaling34, consistent with the excellent pain relief from oxycodone that one participant reported (Table 3).”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [34] Manohar, 2020, Interaction of auditory and pain pathways: effects of stimulus intensity, hearing loss and opioid signaling, Hear Res source
  • May combine two claims.

    Premisecitation

    A recent study demonstrated inconsistent clinical practices and insufficient education regarding hyperacusis among audiologists.

    “This is consistent with a recent study that demonstrated inconsistent clinical practices and insufficient education regarding hyperacusis amongst audiologists6.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [6] Jahn, 2023, Hyperacusis diagnosis and management in the United States: clinical audiology practice patterns, Am J Audiol source
  • May combine two claims.

    Premisecitation

    Few studies have focused on the unique considerations of pain hyperacusis, and none have invited participants to self-report the areas of greatest concern and impact.

    “While the psychosocial consequences of hyperacusis are often acknowledged36, few studies have focused on the unique considerations of pain hyperacusis 4, and none have invited participants to self-report the areas of greatest concern and impact.”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [36] Jüris, 2013, Psychiatric comorbidity and personality traits in patients with hyperacusis, Int J Audiol source
    • cites [4] Williams, 2021, A phenotypic comparison of loudness and pain hyperacusis: symptoms, comorbidity, and associated features in a multinational patient registry, Am J Audiol source
  • May combine two claims.

    Premisecitation

    Rodent models show that acoustic overexposure and ototoxicity increase sound-evoked and spontaneous neural activity in the central auditory system, which is believed to underlie hyperacusis.

    “Rodent models demonstrate that acoustic overexposure and ototoxicity facilitate a paradoxical increase in sound-evoked and spontaneous neural activity in the central auditory system, which is believed to underlie the generation of hyperacusis14.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [14] Auerbach, 2014, Central gain control in tinnitus and hyperacusis, Front Neurol source
  • May combine two claims.

    Findingown data

    Participants had tried many pharmaceutical and non-pharmaceutical interventions for pain relief, and the degree of relief varied.

    “Participants have used numerous pharmaceutical and non-pharmaceutical interventions to alleviate their pain with varying degrees of pain relief.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Findingown data

    Other non-pharmaceutical treatments reported were round/oval window reinforcement surgery (n=1), low-level laser therapy (n=1), pranic/energy healing (n=1), TMJ-specific splints/PT (n=3), chiropractic/massage (n=2), dry needling/acupuncture (n=1), and prayer (n=1).

    “The respondents who selected “Other” reported round and oval window reinforcement surgery (n = 1), low-level laser therapy (n = 1), pranic healing and energy healing (n = 1), TMJ-specific splints or physical therapy (n = 3), chiropractic or massage therapy (n = 2), dry needling and acupuncture (n = 1), and prayer (n = 1).”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Findingown data

    The most frequently reported pharmaceuticals were cannabinoids (n=10), benzodiazepines (n=10), antidepressants (n=9), NSAIDs (n=8), muscle relaxants (n=6), anticonvulsants (n=6), nerve blockers (n=4), oxycodone (n=1), and Botox (n=1).

    “Those who use pharmaceuticals reported the following drugs, in descending order of frequency: oral or inhaled cannabinoids (e.g., marijuana, THC, and/or CBD) (n = 10), benzodiazepines (e.g., clonazepam, alprazolam) (n = 10), antidepressants (e.g., clomipramine, amitriptyline, duloxetine) (n = 9), non-steroidal anti-inflammatory drugs (NSAIDS; e.g., ibuprofen, naproxen) (n = 8), muscle relaxants (e”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    Nine participants self-administered at least one non-pharmaceutical treatment instead of following a prescribed protocol.

    “It was noted that nine participants self-administered at least one of these non-pharmaceutical treatments instead of following a protocol that was prescribed by a professional.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    Two participants are currently seeking off-label Botox injections for pain hyperacusis.

    “Two other participants reported that they are currently seeking off-label Botox injections for pain hyperacusis.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    That participant had limited effect from prior Botox injections in the masseter, occipital, and temporal muscles.

    “That participant previously received Botox injections in the masseter, occipital muscles, and temporal muscles with limited effect for pain hyperacusis.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Findingown data

    Among respondents who selected 'Other', two used Tylenol, one used Tramadol, one used flunarizine, and one used valacyclovir.

    “Of the respondents who selected “Other”, two reported using Tylenol, one reported Tramadol (opioid), one reported flunarizine, and one reported valacyclovir.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Findingown data

    The 17 clusters were ordered from highest to lowest average rating, with Lack of Empathy or Support from Others ranked highest and Head Sensations ranked lowest.

    “The 17 clusters arranged in order from highest-to-lowest average rating are: Lack of Empathy or Support from Others; Isolation and Reduced Physical Activity; Symptom Setbacks; Mental Health Consequences; Pain Triggers, Severity, and Time Course; Control and Avoidance Behaviors; Pain Laterality; Emotional Reactions to Sound; Symptom Onset; Neuropathic Pain; Fluctuating Severity; Otologic Symptoms (”
    Quote in the paperNot a substantial claim
    • The authors state this as an assumption: Higher average ratings for clusters or statements indicate that the experience is more common among people with pain hyperacusis.
  • May combine two claims.

    Findingnone given

    The pain can occur immediately after sound exposure or be delayed by several hours.

    “The pain often fluctuates in severity, location, and quality, and it can occur immediately after a sound exposure, or it can be delayed by several hours.”
    Quote in the paperNot a substantial claim
  • Classified as probably not a substantial claim.

    Premisecitation

    Pain hyperacusis, also called noxacusis, is a condition in which sounds that are not bothersome to most people cause physical pain.

    “Pain hyperacusis, also known as noxacusis, causes physical pain in response to sounds that do not bother most people.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [3] Tyler, 2014, A review of hyperacusis and future directions: Part I. Definitions and manifestations, Am J Audiol source
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductown data

    The focus group responses were condensed into 92 statements that covered all unique ideas generated during the session.

    “We eliminated redundant ideas and condensed the responses into a set of 92 statements that encompassed all unique ideas generated during the focus group (Table 2).”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    Two authors reached consensus that a 17-cluster solution gave a reasonable level of specificity for the subjective content.

    “After examining five possible cluster solutions, two of the authors (KNJ and STK) reached a consensus that 17 clusters provided a reasonable level of specificity based on the subjective content matter.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Premisecitation

    Loud noises can trigger painful episodes in individuals with trigeminal neuralgia, suggesting that the auditory and trigeminal pathways share anatomy.

    “Moreover, loud noises can trigger painful episodes in individuals with trigeminal neuralgia suggesting that the auditory and trigeminal pathways share anatomy 21.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [21] Love, 2001, Coakham HB. Trigeminal neuralgia: pathology and pathogenesis, Brain source
    • Rests on an assumption: The trigeminal nerve carries sensory information from the middle ear to the trigeminocervical complex in the brainstem and then to the cortex.
    • Rests on an assumption: The trigeminocervical complex integrates sensory and nociceptive inputs from the middle ear, head, and neck, and can serve as a node for referred pain and head sensations.
  • May combine two claims.

    Interpretationreasoning

    Current therapies for pain hyperacusis are inadequate, and the condition is still poorly managed.

    “Consequently, pain hyperacusis remains poorly treated and responds inadequately to existing therapies”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductcitation

    A sample of 15 people is adequate for the sorting phase in concept mapping research.

    “Note that 15 is a sufficient sample size for the sorting stage of a concept mapping study, as the goal of this task is primarily to guide the experimenters in identifying conceptual themes in the data 18.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [18] Trochim, 1989, An introduction to concept mapping for planning and evaluation, Eval Program Plann source
  • May combine two claims.

    Interpretationnone given

    There is little evidence that enhanced central gain is associated with sound-induced pain or that CNS therapies are effective for pain hyperacusis, but there are also no data to the contrary.

    “While there is little evidence showing that enhanced central gain is associated with sound-induced pain nor that CNS therapies are effective for those with pain hyperacusis, there are also no data to the contrary.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Interpretationreasoning

    While many symptoms of pain hyperacusis are consistent with a peripheral etiology, these qualitative data do not rule out a central component.

    “Thus, while many symptoms of pain hyperacusis are consistent with a peripheral etiology, these qualitative data do not rule out a central component and experimental studies remain critical to pinpoint the underlying mechanisms.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    The treatment responses discussed in this study are anecdotal rather than verified via randomized controlled trials.

    “It is important to note that the treatment responses discussed in this study are anecdotal rather than verified via randomized controlled trials.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S2 (checkable), S4 (based).

    Interpretationnone given

    It is likely that there are multiple subtypes and mechanisms of pain hyperacusis that may interact idiosyncratically with patient-specific variables to influence treatment response.

    “It is also likely that there are multiple subtypes and mechanisms of pain hyperacusis that may interact idiosyncratically with patient-specific variables to influence treatment response.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Premisenone given

    Sound therapy and CBT are widely used for general hyperacusis, but no literature evaluates their efficacy for individuals with sound-induced pain.

    “Although sound therapy approaches and CBT are widely used to treat general hyperacusis32,33, there is no literature that evaluates the efficacy of these therapies for individuals who specifically experience sound-induced pain.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [32] Pienkowski, 2014, A review of hyperacusis and future directions: part II. Measurement, mechanisms, and treatment, Am J Audiol source
    • cites [33] Potgieter, 2017, Clinical interventions for hyperacusis in adults: a scoping review to assess the current position and determine priorities for research, BioMed Res Int

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Premisecitation

    The tensor veli palatini is innervated by the trigeminal motor root and may form a functional unit with the TTM to control middle ear pressure.

    “The tensor veli palatini is innervated by the trigeminal motor root and may form a functional unit with the TTM to control middle ear pressure 26.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [26] Kierner, 2002, Do the tensor tympani and tensor veli palatini muscles of man form a functional unit?: a histochemical investigation of their putative connections, Hear Res source
  • May combine two claims.

    Study design and conductown data

    The study could not quantify exact dosages, timing, or duration of treatment administration, and many participants followed self-prescribed treatment protocols.

    “We could not quantify the exact dosages, timing, or duration of treatment administration, and many participants followed self-prescribed treatment protocols.”
    Quote in the paperSubstantial claim
  • Classified as probably not a substantial claim.

    Study design and conductnone given

    This work allowed participants to self-generate the most pertinent features of pain hyperacusis that have the greatest impact on their quality of life.

    “Despite these limitations, this work allowed participants to self-generate the most pertinent features of pain hyperacusis that have the greatest impact on their quality of life, and which should serve as primary treatment endpoints in future studies.”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Premisecitation

    The symptoms are consistent with tonic tensor tympani syndrome, in which TTM myoclonus triggers pain and otologic symptoms by irritating the trigeminal nerve, increasing tympanic membrane tension, or altering middle ear ventilation.

    “These symptoms are also consistent with the related tonic tensor tympani syndrome, wherein TTM myoclonus triggers pain within and around the ear and other otologic symptoms by irritating the trigeminal nerve, increasing tympanic membrane tension, or altering middle ear ventilation 10,22.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [10] Westcott, 2016, Hyperacusis-induced Pain: understanding and management of tonic tensor tympani syndrome (TTTS) symptoms, J Pain Relief source
    • cites [22] Fournier, 2022, Exploring the middle ear function in patients with a cluster of symptoms including tinnitus, hyperacusis, ear fullness and/or pain, Hear Res source
    • Rests on an assumption: The trigeminal nerve carries sensory information from the middle ear to the trigeminocervical complex in the brainstem and then to the cortex.
    • Rests on an assumption: The trigeminocervical complex integrates sensory and nociceptive inputs from the middle ear, head, and neck, and can serve as a node for referred pain and head sensations.
  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

    Interpretationreasoning

    Even if pain hyperacusis originates in the periphery, chronic painful irritation of peripheral nerves can lead to central pain sensitization, possibly generating elevated CNS gain.

    “Even if pain hyperacusis originates in the periphery, chronic and painful irritation of peripheral nerves can lead to central pain sensitization, possibly generating elevated CNS gain.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Lidocaine has been proposed as a possible treatment for tinnitus, Meniere's disease, and pain secondary to acute otitis media.

    “Lidocaine has been proposed as a possible treatment for tinnitus28,29, Meniere’s disease30, and pain secondary to acute otitis media 31.”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [28] Langguth, 2019, Therapeutic approaches to the treatment of tinnitus, Annu Rev Pharmacol Toxicol source
    • cites [29] Zhang, 2024, Intratympanic lidocaine as a potent remedy for tinnitus in sudden sensorineural hearing loss: a double-blind, randomized clinical trial, Otol Neurotol source
    • cites [30] Bertlich, 2021, Intratympanal administration of lidocaine in the management of Ménière’s Disease, Acta Otolaryngol ((Stockh)) source
  • May combine two claims.

    Interpretationreasoning

    Damage-evoked activity in Type-II cochlear afferents has not been linked to perceptual outcomes, and it is unclear how this mechanism alone would account for referred pain and non-pain sensations.

    “Although it is possible that Type-II cochlear afferents could signal tissue damage within the cochlea, damage-evoked activity in these neurons has yet to be linked to perceptual outcomes and it is unclear how this mechanism alone would account for the referred pain and non-pain sensations (e.g., aural fullness, fluttering, muscle spasms) described by many of our participants.”
    Quote in the paperSubstantial claim
35 of 35
  • The authors state this as an assumption.

    Higher average ratings for clusters or statements indicate that the experience is more common among people with pain hyperacusis.

    “Clusters with higher average ratings were interpreted as more common to the lived experience of pain hyperacusis than clusters with lower average ratings.”
  • The authors state this as an assumption.

    A higher percentage of participant endorsement indicates that a symptom is more common among people with pain hyperacusis.

    “Statements that were endorsed by a higher percentage of participants were interpreted as more common to the lived experience of pain hyperacusis than statements that were endorsed by a lower percentage of participants.”
  • The paper relies on this without support.

    The self-reported experiences of the study participants accurately represent the clinical phenotype of pain hyperacusis.

    “Here, we used a participatory research method to generate a conceptual framework for understanding the most salient symptoms of pain hyperacusis from the perspective of individuals who suffer from the condition.”
  • The paper relies on this without support.

    The trigeminal nerve carries sensory information from the middle ear to the trigeminocervical complex in the brainstem and then to the cortex.

    “The trigeminal nerve transmits sensory information from the middle ear to the trigeminocervical complex (TCC) in the brainstem and then to the cortex.”
  • The paper relies on this without support.

    The trigeminocervical complex integrates sensory and nociceptive inputs from the middle ear, head, and neck, and can serve as a node for referred pain and head sensations.

    “The TCC integrates a variety of sensory and nociceptive inputs from the middle ear, head, and neck regions, providing a possible node for the generation of referred pain and head sensations.”
5 of 5

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Focus-group attendance is reported as both 32 and 26

    Minor

    The abstract says 32 adults attended the focus group, while the methods say 26 attended. The discussion also says 32 adults were interviewed, although the focus group is the only interview-like session described.

  • The stated relief threshold excludes the paper's modest-effect category

    Minor

    The methods define a modest effect as 75% pain relief, but the results describe modest-to-excellent effects as greater than 75% relief.

2 of 2

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Authors
Jahn, K. N., Kashiwagura, S. T., & Yousuf, M. S.
Affiliations
The University of Texas at Dallas (US)
Corresponding author
Jahn, Kelly N.
Venue
The Journal of Pain
Publisher
Elsevier BV
Published
2025-02
Volume
27
Pages
104741
ISSN
1526-5900 (ISSN-L)
OpenAlex
W4404645852
Cited by
10
References
38
Citations by year
2026: 6 · 2025: 3 · 2024: 1
FWCI
2.77
Type
journal article
Language
en
Open access
Locations
  • Journal of Pain (publishedVersion, cc-by-nc-nd)
  • medRxiv (acceptedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • PubMed Central (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (submittedVersion, cc-by-nc-nd)
Funders
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK134893)
  • National Institute on Deafness and Other Communication Disorders (K01 DC019647)
Topics
  • Life Sciences › Neuroscience › Sensory Systems › Hearing, Cochlea, Tinnitus, Genetics
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Hearing Loss and Rehabilitation
Keywords
Noxa, psychosocial impact, physical function, benzodiazepines, nerve block, peripheral pain mechanisms, trigeminal nerve, animal models, patient-reported symptoms

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read under definition version 3 (extract-v3) on 2026-09-28.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-09-28.

Cited sources are checked by gpt-6-sol.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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