Clinical phenotype and management of sound-induced pain: Insights from adults with pain hyperacusis
Open accessPublished 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.
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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
- Premisecitation
Adults with pain hyperacusis report receiving less benefit from behavioral interventions such as sound therapy.
“and reduced benefit from behavioral interventions (e.g., sound therapy) 4.”
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
- Interpretationcitation
In many cases, pain hyperacusis appears to be a multifactorial syndrome that also involves some degree of loudness hyperacusis, tinnitus, and other otologic and sensory disturbances.
“In many cases, pain hyperacusis appears to be a multifactorial syndrome that also involves some degree of loudness hyperacusis, tinnitus, and other otologic and sensory disturbances 4,32,35.”
Quote in the paperNot a substantial claim2 of 3 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
- cites [32] Pienkowski, 2014, A review of hyperacusis and future directions: part II. Measurement, mechanisms, and treatment, Am J Audiol source
- cites [35] De Meulemeester, 2023, Comparing tinnitus, pain, psychosocial and cognitive factors between patients with tinnitus and pain: a systematic review, J Psychosom Res source
The Discussion (section 4, around line 389) reports that patients with tinnitus and headache or TMJ pain more often have hyperacusis and vertigo, and that hyperacusis is more severe in patients with both pain and tinnitus than in those with tinnitus alone. It does not study pain hyperacusis as a distinct syndrome, distinguish loudness hyperacusis, or establish that pain hyperacusis is multifactorial. (LLM, conf=0.86)
Experimental — accuracy not yet measured
- Interpretationown data
Our 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.”
Quote in the paperSubstantial claim4 of 6 sources checked- cites [9] Noreña, 2018, An integrative model accounting for the symptom cluster triggered after an acoustic shock, Trends Hear source
- cites [10] Westcott, 2016, Hyperacusis-induced Pain: understanding and management of tonic tensor tympani syndrome (TTTS) symptoms, J Pain Relief source
- 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
The Discussion proposes that type II cochlear afferents could contribute to painful hyperacusis, but it does not identify the trigeminal nerve as involved. A search for trigeminal nerve involvement and pain pathways found no passage addressing that specific claim; the Discussion says whether the described cochlear structures project to central pain pathways remains to be determined. (LLM, conf=0.76)
Experimental — accuracy not yet measured - cites [14] Auerbach, 2014, Central gain control in tinnitus and hyperacusis, Front Neurol source
The Introduction describes hyperacusis as sometimes painful, but it does not link that pain to the trigeminal nerve. Searches for trigeminal nerve involvement and related pain mechanisms found no passage in our copy addressing that proposed involvement. (LLM, conf=0.75)
Experimental — accuracy not yet measured - 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
The Introduction (page unavailable) links cochlear afferent CGRP and nociception to hyperacusis. The Discussion (page unavailable) mentions trigeminal nociceptive neurons only as an analogy for a possible mechanism in type II cochlear afferents; it does not propose trigeminal nerve involvement in pain hyperacusis. (LLM, conf=0.85)
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.
- Premisecitation
Evidence shows that the co-occurrence of tinnitus and pain increases psychosocial distress and hyperacusis severity beyond each symptom alone.
“There is evidence that the co-occurrence of tinnitus and pain increases psychosocial distress and hyperacusis severity above and beyond each symptom alone35.”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [35] De Meulemeester, 2023, Comparing tinnitus, pain, psychosocial and cognitive factors between patients with tinnitus and pain: a systematic review, J Psychosom Res source
The Results (lines 40–46) report higher psychosocial distress and hyperacusis severity in patients with both tinnitus and pain than in patients with tinnitus alone. They do not establish that both outcomes are higher than in patients with pain alone, as 'beyond each symptom alone' implies. The reported evidence is low to moderate. (LLM, conf=0.88)
Experimental — accuracy not yet measured
- Premisecitation
Both Type-II cochlear afferents and C fibers can be activated by adenosine triphosphate, a pain-signaling molecule released by damaged tissue including outer hair cells.
“Specifically, both types of fibers can be activated by adenosine triphosphate, a pain-signaling molecule that is released by damaged tissue, including the outer hair cells 11,12,27.”
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
The Discussion says both somatic C fibers and type II cochlear afferents are sensitive to ATP and can be excited by ATP released during tissue damage. But the Abstract and Results identify nearby supporting cells as a major source of ATP after outer hair cell damage; they do not establish that the damaged outer hair cells themselves release the ATP activating these fibers. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measured - 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
The supplied Abstract (page unavailable) says type II afferents can be excited by ATP released during tissue damage, by analogy to pain-sensing C-fibers. The Introduction (page unavailable) says type II afferents contact outer hair cells, but the passages do not say that damaged outer hair cells release ATP. That specific part of the claim is unsupported by this copy. (LLM, conf=0.78)
Experimental — accuracy not yet measured
- Findingown data
Benzodiazepines were identified as among the most effective analgesic options for pain hyperacusis.
“Benzodiazepines and nerve blockers emerged as the most effective analgesic options while non-pharmaceutical therapies were largely ineffective.”
Quote in the paperSubstantial claim - Findingown data
Nerve blockers were identified as among the most effective analgesic options for pain hyperacusis.
“Benzodiazepines and nerve blockers emerged as the most effective analgesic options while non-pharmaceutical therapies were largely ineffective.”
Quote in the paperSubstantial claim - Findingown data
All 32 participants in the study reported that pain hyperacusis negatively affected their psychosocial and physical functioning.
“All participants endorsed negative effects of pain hyperacusis on psychosocial and physical function.”
Quote in the paperNot a substantial claim - Findingown data
Non-pharmaceutical therapies were mostly ineffective for the participants' sound-induced pain.
“Benzodiazepines and nerve blockers emerged as the most effective analgesic options while non-pharmaceutical therapies were largely ineffective.”
Quote in the paperSubstantial claim - Findingown data
Among the participants, 80.77% reported burning sensations triggered by sound.
“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.”
Quote in the paperNot a substantial claim - Findingown data
Sound-induced pain sensations in this group were located in the ear or in other body areas.
“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.”
Quote in the paperNot a substantial claim - Findingown data
Among the participants, 73.08% reported throbbing sensations triggered by sound.
“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.”
Quote in the paperNot a substantial claim - Findingown data
Among the participants, 76.92% reported stabbing sensations triggered by sound.
“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.”
Quote in the paperNot a substantial claim - Findingown data
Among the participants, 53.85% reported pinching sensations triggered by sound.
“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.”
Quote in the paperNot a substantial claim - Findingown data
46.15% of participants reported referred pain elsewhere in the body outside the head and neck region.
“Many participants reported referred pain in addition to pain in or near the ears, including pain in the face (73.08%), head (side – 57.69%, back – 42.31%, front – 30.77%), throat (34.62%), neck (53.85%), and elsewhere in the body (46.15%; i.e., outside the head and neck region) (Figure 2C).”
Quote in the paperNot a substantial claim - Findingown data
42.31% of participants reported referred pain in the back of the head.
“Many participants reported referred pain in addition to pain in or near the ears, including pain in the face (73.08%), head (side – 57.69%, back – 42.31%, front – 30.77%), throat (34.62%), neck (53.85%), and elsewhere in the body (46.15%; i.e., outside the head and neck region) (Figure 2C).”
Quote in the paperNot a substantial claim - Findingown data
Only a few patients reported >75% pain relief from CBT (n=1), sound therapy (n=2), TMJ-specific treatments (n=2), and chiropractic/massage (n=1).
“Only a few patients reported modest-to-excellent effects (>75% pain relief) of cognitive behavioral therapy (n = 1), sound therapy (n = 2), TMJ-specific treatments (n = 2), and chiropractic or massage therapy (n = 1).”
Quote in the paperSubstantial claim - Findingown data
96.15% of participants experience tinnitus.
“Almost all participants (96.15%) experience tinnitus (perception of phantom sounds), and their tinnitus is often reactive (88.46%) (i.e., exacerbated by the presence of external sounds).”
Quote in the paperNot a substantial claim - Findingown data
73.08% of participants reported referred pain in the face.
“Many participants reported referred pain in addition to pain in or near the ears, including pain in the face (73.08%), head (side – 57.69%, back – 42.31%, front – 30.77%), throat (34.62%), neck (53.85%), and elsewhere in the body (46.15%; i.e., outside the head and neck region) (Figure 2C).”
Quote in the paperNot a substantial claim - Findingown data
Cannabinoids were consistently rated as ineffective for pain relief (n = 9).
“Cannabinoids were consistently rated as ineffective for pain relief (n = 9), with one participant indicating that they made their pain hyperacusis worse.”
Quote in the paperNot a substantial claim - Findingown data
66.67% (n = 16) of participants tried multiple non-pharmaceutical therapies.
“The average participant reported using 4.88 different therapies (range 0 to 12), with 58.33% (n = 14) trying multiple pharmaceuticals and 66.67% (n = 16) trying multiple non-pharmaceutical therapies (Figure 6).”
Quote in the paperNot a substantial claim - Findingown data
80.77% of participants reported non-pain ear fullness or pressure.
“Most participants reported additional, non-pain sensations in the ear such as fullness or pressure (80.77%), fluttering (80.77%), pulsing (65.38%), and vibrations (57.69%) and other sensory sensitivities (53.85%).”
Quote in the paperNot a substantial claim - Findingown data
76.92% of participants described their sound-induced pain as stabbing.
“The pain was most often described as a burning (80.77%), stabbing (76.92%), throbbing (73.08%), or pinching (53.85%) sensation.”
Quote in the paperNot a substantial claim - Findingown data
One participant reported 100% pain relief from Botox injection into the tensor veli palatini muscle.
“The one participant who tried Botox reported that the excellent effect (100% pain relief) was experienced after injection into the tensor veli palatini muscle.”
Quote in the paperNot a substantial claim - Findingown data
84.62% of participants reported symptoms that are asymmetric in severity.
“although 80.77% of the participants endorsed bilateral sound-related pain, many reported unilateral pain (46.15%) or symptoms that are asymmetric in severity (84.62%) (Table 2, Pain Laterality cluster).”
Quote in the paperNot a substantial claim - Findingown data
3.17% (n = 2) of pharmaceutical effectiveness ratings indicated the treatment made pain hyperacusis worse.
“Out of the 63 effectiveness ratings provided across all pharmaceutical interventions, 55.56% (n = 35) of the ratings indicated that the treatment had no effect on pain hyperacusis (0% pain relief) and 3.17% (n = 2) indicated that the treatment made their pain hyperacusis worse.”
Quote in the paperNot a substantial claim - Findingown data
10.53% (n = 6) of non-pharmaceutical effectiveness ratings indicated the treatment made pain hyperacusis worse.
“Out of the 57 efficacy ratings provided across all non-pharmaceutical interventions, most indicated that these treatments had no effect on pain hyperacusis (0% pain relief) (66.67%, n = 38) or that these interventions made their pain hyperacusis worse (10.53%, n = 6).”
Quote in the paperSubstantial claim - Findingown data
73.08% of participants described their sound-induced pain as throbbing.
“The pain was most often described as a burning (80.77%), stabbing (76.92%), throbbing (73.08%), or pinching (53.85%) sensation.”
Quote in the paperNot a substantial claim - Findingown data
88.46% to 96.15% of participants endorsed statements related to mental health consequences.
“Every participant indicated that their lifestyle has changed significantly since the onset of their hyperacusis, with the vast majority endorsing all statements related to isolation and reduced physical activity (range 84.62% to 100%) and mental health consequences (range 88.46% to 96.15%) (Figure 5A-B; Table 2).”
Quote in the paperNot a substantial claim - Findingown data
55.56% (n = 35) of pharmaceutical effectiveness ratings indicated no effect on pain hyperacusis.
“Out of the 63 effectiveness ratings provided across all pharmaceutical interventions, 55.56% (n = 35) of the ratings indicated that the treatment had no effect on pain hyperacusis (0% pain relief) and 3.17% (n = 2) indicated that the treatment made their pain hyperacusis worse.”
Quote in the paperNot a substantial claim - Findingown data
80.77% of participants described their sound-induced pain as burning.
“The pain was most often described as a burning (80.77%), stabbing (76.92%), throbbing (73.08%), or pinching (53.85%) sensation.”
Quote in the paperNot a substantial claim - Findingown data
One participant reported that cannabinoids made their pain hyperacusis worse.
“Cannabinoids were consistently rated as ineffective for pain relief (n = 9), with one participant indicating that they made their pain hyperacusis worse.”
Quote in the paperNot a substantial claim - Findingown data
53.85% of participants reported referred pain in the neck.
“Many participants reported referred pain in addition to pain in or near the ears, including pain in the face (73.08%), head (side – 57.69%, back – 42.31%, front – 30.77%), throat (34.62%), neck (53.85%), and elsewhere in the body (46.15%; i.e., outside the head and neck region) (Figure 2C).”
Quote in the paperNot a substantial claim - Findingown data
65.38% of participants reported non-pain ear pulsing.
“Most participants reported additional, non-pain sensations in the ear such as fullness or pressure (80.77%), fluttering (80.77%), pulsing (65.38%), and vibrations (57.69%) and other sensory sensitivities (53.85%).”
Quote in the paperNot a substantial claim - Findingnone given
The pain often fluctuates in severity, location, and quality.
“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 - Findingown data
46.15% of participants reported unilateral pain.
“although 80.77% of the participants endorsed bilateral sound-related pain, many reported unilateral pain (46.15%) or symptoms that are asymmetric in severity (84.62%) (Table 2, Pain Laterality cluster).”
Quote in the paperNot a substantial claim - Findingown data
Average cluster ratings spanned from 1.66 for the Head Sensations cluster to 4.21 for the Lack of Empathy or Support from Others cluster.
“The average ratings for each cluster ranged from 1.66 for Head Sensations (least common across all participants) to 4.21 for Lack of Empathy or Support from Others (most common across all participants).”
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.
- Findingown data
The average participant reported using 4.88 different therapies (range 0 to 12).
“The average participant reported using 4.88 different therapies (range 0 to 12), with 58.33% (n = 14) trying multiple pharmaceuticals and 66.67% (n = 16) trying multiple non-pharmaceutical therapies (Figure 6).”
Quote in the paperNot a substantial claim - Findingown data
100% of participants indicated that their lifestyle changed significantly since the onset of their hyperacusis.
“Every participant indicated that their lifestyle has changed significantly since the onset of their hyperacusis, with the vast majority endorsing all statements related to isolation and reduced physical activity (range 84.62% to 100%) and mental health consequences (range 88.46% to 96.15%) (Figure 5A-B; Table 2).”
Quote in the paperNot a substantial claim - Findingown data
Participants consistently reported experiencing setbacks after sound exposure.
“participants consistently reported experiencing setbacks after sound exposure (Table 2, Symptom Setback cluster)”
Quote in the paperNot a substantial claim - Findingown data
96.15% of participants wear hearing protection devices to manage their symptoms.
“To manage their symptoms, most of the participants employ control and avoidance behaviors such as wearing hearing protection devices (96.15%) and planning their lifestyle to avoid sound exposure (100%) (Table 2).”
Quote in the paperNot a substantial claim - Findingown data
87.50% (n = 21) of participants tried both pharmaceutical and non-pharmaceutical therapies.
“Participants reported that they have tried a variety of treatments to alleviate sound-induced pain, with most participants (87.50%, n = 21) having tried both pharmaceutical and non-pharmaceutical therapies (Figure 6, Table 3).”
Quote in the paperNot a substantial claim - Findingown data
80.77% of participants endorsed bilateral sound-related pain.
“although 80.77% of the participants endorsed bilateral sound-related pain, many reported unilateral pain (46.15%) or symptoms that are asymmetric in severity (84.62%) (Table 2, Pain Laterality cluster).”
Quote in the paperNot a substantial claim - Findingown data
53.85% of participants described their sound-induced pain as pinching.
“The pain was most often described as a burning (80.77%), stabbing (76.92%), throbbing (73.08%), or pinching (53.85%) sensation.”
Quote in the paperNot a substantial claim - Findingown data
30.77% of participants endorsed migraines associated with sound exposure.
“A smaller, but noteworthy, percentage of participants endorsed symptoms such as inflammation (61.54%), itchiness (73.08%), or redness (30.77%) near the site of their sound-related pain and other head-related sensations such as fullness/pressure (61.54%), migraines (30.77%), dizziness (30.77%), or nausea (26.92%) associated with sound exposure (Table 2).”
Quote in the paperNot a substantial claim - Findingown data
57.69% of participants reported referred pain on the side of the head.
“Many participants reported referred pain in addition to pain in or near the ears, including pain in the face (73.08%), head (side – 57.69%, back – 42.31%, front – 30.77%), throat (34.62%), neck (53.85%), and elsewhere in the body (46.15%; i.e., outside the head and neck region) (Figure 2C).”
Quote in the paperNot a substantial claim - Findingown data
Non-pharmaceutical interventions were largely ineffective at providing relief from pain hyperacusis in this cohort.
“Non-pharmaceutical interventions were largely ineffective at providing relief from pain hyperacusis in our cohort.”
Quote in the paperSubstantial claim - Findingown data
92.31% of participants reported that their sound-induced pain can occur in or near their ears.
“Although 92.31% of participants reported that the pain can occur in or near their ears, less than half of participants (42.31%) indicated that this was “Always” the case.”
Quote in the paperNot a substantial claim - Findingown data
30.77% of participants endorsed dizziness associated with sound exposure.
“A smaller, but noteworthy, percentage of participants endorsed symptoms such as inflammation (61.54%), itchiness (73.08%), or redness (30.77%) near the site of their sound-related pain and other head-related sensations such as fullness/pressure (61.54%), migraines (30.77%), dizziness (30.77%), or nausea (26.92%) associated with sound exposure (Table 2).”
Quote in the paperNot a substantial claim - Findingown data
61.54% of participants endorsed fullness/pressure as a head-related sensation associated with sound exposure.
“A smaller, but noteworthy, percentage of participants endorsed symptoms such as inflammation (61.54%), itchiness (73.08%), or redness (30.77%) near the site of their sound-related pain and other head-related sensations such as fullness/pressure (61.54%), migraines (30.77%), dizziness (30.77%), or nausea (26.92%) associated with sound exposure (Table 2).”
Quote in the paperNot a substantial claim - Findingown data
The most frequently reported non-pharmaceutical treatments were meditation/yoga/mindfulness (n=12), counseling (n=11), CBT (n=9), sound therapy (n=8), and tinnitus retraining therapy (n=5).
“Respondents who tried non-pharmaceutical interventions reported the following treatments, in descending order of frequency: meditation, yoga, or mindfulness therapy (n = 12), counseling (n = 11), cognitive behavioral therapy (n = 9), sound therapy (n = 8), and tinnitus retraining therapy (n = 5).”
Quote in the paperNot a substantial claim - Findingown data
73.08% of participants endorsed itchiness near the site of their sound-related pain.
“A smaller, but noteworthy, percentage of participants endorsed symptoms such as inflammation (61.54%), itchiness (73.08%), or redness (30.77%) near the site of their sound-related pain and other head-related sensations such as fullness/pressure (61.54%), migraines (30.77%), dizziness (30.77%), or nausea (26.92%) associated with sound exposure (Table 2).”
Quote in the paperNot a substantial claim - Findingown data
34.62% of participants reported referred pain in the throat.
“Many participants reported referred pain in addition to pain in or near the ears, including pain in the face (73.08%), head (side – 57.69%, back – 42.31%, front – 30.77%), throat (34.62%), neck (53.85%), and elsewhere in the body (46.15%; i.e., outside the head and neck region) (Figure 2C).”
Quote in the paperNot a substantial claim - Findingown data
80.77% of participants reported non-pain ear fluttering.
“Most participants reported additional, non-pain sensations in the ear such as fullness or pressure (80.77%), fluttering (80.77%), pulsing (65.38%), and vibrations (57.69%) and other sensory sensitivities (53.85%).”
Quote in the paperNot a substantial claim - Findingown data
96.15% of participants reported that medical and healthcare professionals do not understand their symptoms.
“All participants reported that individuals within their social network do not understand their hyperacusis symptoms, with 100% endorsing this concept for family and friends, and 96.15% indicating that medical and healthcare professionals do not understand their symptoms (Figure 4; Table 2).”
Quote in the paperNot a substantial claim - Findingown data
57.69% of participants reported non-pain ear vibrations.
“Most participants reported additional, non-pain sensations in the ear such as fullness or pressure (80.77%), fluttering (80.77%), pulsing (65.38%), and vibrations (57.69%) and other sensory sensitivities (53.85%).”
Quote in the paperNot a substantial claim - Findingown data
42.31% of participants indicated that their sound-induced pain was always in or near their ears.
“Although 92.31% of participants reported that the pain can occur in or near their ears, less than half of participants (42.31%) indicated that this was “Always” the case.”
Quote in the paperNot a substantial claim - Findingown data
30.77% of participants reported referred pain in the front of the head.
“Many participants reported referred pain in addition to pain in or near the ears, including pain in the face (73.08%), head (side – 57.69%, back – 42.31%, front – 30.77%), throat (34.62%), neck (53.85%), and elsewhere in the body (46.15%; i.e., outside the head and neck region) (Figure 2C).”
Quote in the paperNot a substantial claim - Findingown data
88.46% of participants have reactive tinnitus that is exacerbated by external sounds.
“Almost all participants (96.15%) experience tinnitus (perception of phantom sounds), and their tinnitus is often reactive (88.46%) (i.e., exacerbated by the presence of external sounds).”
Quote in the paperNot a substantial claim - Findingown data
65.38% of participants indicated that their sound-related pain can change locations.
“More than half of participants indicated that their sound-related pain can change locations (65.38%) and that the quality and severity of the sound-related pain can fluctuate (Table 2, Fluctuating Severity cluster).”
Quote in the paperNot a substantial claim - Findingown data
26.92% of participants endorsed nausea associated with sound exposure.
“A smaller, but noteworthy, percentage of participants endorsed symptoms such as inflammation (61.54%), itchiness (73.08%), or redness (30.77%) near the site of their sound-related pain and other head-related sensations such as fullness/pressure (61.54%), migraines (30.77%), dizziness (30.77%), or nausea (26.92%) associated with sound exposure (Table 2).”
Quote in the paperNot a substantial claim - Findingown data
Lack of empathy or support from others was the highest-rated cluster.
“Figure 4 shows the percentage of participants who endorsed a lack of empathy or support from others, which was the highest-rated cluster.”
Quote in the paperNot a substantial claim - Findingown data
30.77% of participants endorsed redness near the site of their sound-related pain.
“A smaller, but noteworthy, percentage of participants endorsed symptoms such as inflammation (61.54%), itchiness (73.08%), or redness (30.77%) near the site of their sound-related pain and other head-related sensations such as fullness/pressure (61.54%), migraines (30.77%), dizziness (30.77%), or nausea (26.92%) associated with sound exposure (Table 2).”
Quote in the paperNot a substantial claim - Findingown data
100% of participants reported that family and friends do not understand their hyperacusis symptoms.
“All participants reported that individuals within their social network do not understand their hyperacusis symptoms, with 100% endorsing this concept for family and friends, and 96.15% indicating that medical and healthcare professionals do not understand their symptoms (Figure 4; Table 2).”
Quote in the paperNot a substantial claim - Findingown data
All six participants who experienced worsening of pain hyperacusis reported it after therapies involving a sound exposure component.
“All six participants who experienced a worsening of their pain hyperacusis indicated that this occurred after therapies that involved a sound exposure component (i.e., sound therapy or tinnitus retraining therapy).”
Quote in the paperSubstantial claim - Findingown data
58.33% (n = 14) of participants tried multiple pharmaceuticals.
“The average participant reported using 4.88 different therapies (range 0 to 12), with 58.33% (n = 14) trying multiple pharmaceuticals and 66.67% (n = 16) trying multiple non-pharmaceutical therapies (Figure 6).”
Quote in the paperNot a substantial claim - Findingown data
100% of participants plan their lifestyle to avoid sound exposure.
“To manage their symptoms, most of the participants employ control and avoidance behaviors such as wearing hearing protection devices (96.15%) and planning their lifestyle to avoid sound exposure (100%) (Table 2).”
Quote in the paperNot a substantial claim - Findingown data
More than half of participants indicated that the quality and severity of their sound-related pain can fluctuate.
“More than half of participants indicated that their sound-related pain can change locations (65.38%) and that the quality and severity of the sound-related pain can fluctuate (Table 2, Fluctuating Severity cluster).”
Quote in the paperNot a substantial claim - Findingown data
61.54% of participants endorsed inflammation near the site of their sound-related pain.
“A smaller, but noteworthy, percentage of participants endorsed symptoms such as inflammation (61.54%), itchiness (73.08%), or redness (30.77%) near the site of their sound-related pain and other head-related sensations such as fullness/pressure (61.54%), migraines (30.77%), dizziness (30.77%), or nausea (26.92%) associated with sound exposure (Table 2).”
Quote in the paperNot a substantial claim - Findingown data
66.67% (n = 38) of non-pharmaceutical effectiveness ratings indicated no effect on pain hyperacusis.
“Out of the 57 efficacy ratings provided across all non-pharmaceutical interventions, most indicated that these treatments had no effect on pain hyperacusis (0% pain relief) (66.67%, n = 38) or that these interventions made their pain hyperacusis worse (10.53%, n = 6).”
Quote in the paperSubstantial claim - Findingown data
Hierarchical cluster analysis produced a 17-cluster solution describing the most salient characteristics and consequences of sound-induced pain from the focus group.
“Hierarchical cluster analyses revealed a 17-cluster solution that described the most salient characteristics and consequences of sound-induced pain generated during the focus group (Table 2).”
Quote in the paperSubstantial 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.
- Findingown data
84.62% to 100% of participants endorsed statements related to isolation and reduced physical activity.
“Every participant indicated that their lifestyle has changed significantly since the onset of their hyperacusis, with the vast majority endorsing all statements related to isolation and reduced physical activity (range 84.62% to 100%) and mental health consequences (range 88.46% to 96.15%) (Figure 5A-B; Table 2).”
Quote in the paperNot a substantial claim - Findingown data
Some patients reported 75-100% pain relief from benzodiazepines (n=3), nerve blockers (n=2), anticonvulsants (n=2), Tylenol (n=1), oxycodone (n=1), and Botox (n=1).
“Some patients reported modest-to-excellent effects (75-100% pain relief) from benzodiazepines (n = 3), nerve blockers (n = 2), anticonvulsants (n = 2), Tylenol (n = 1), oxycodone (n = 1), and Botox (n = 1).”
Quote in the paperNot a substantial claim - Findingown data
53.85% of participants reported other sensory sensitivities.
“Most participants reported additional, non-pain sensations in the ear such as fullness or pressure (80.77%), fluttering (80.77%), pulsing (65.38%), and vibrations (57.69%) and other sensory sensitivities (53.85%).”
Quote in the paperNot a substantial claim - Findingown data
One participant reported >90% pain relief from Botox injections in the tensor veli palatini muscle.
“Another participant indicated that Botox injections in the tensor veli palatini muscle had an excellent effect on their pain hyperacusis (>90% pain relief).”
Quote in the paperNot a substantial claim - Findingown data
Most participants attributed the onset of their pain hyperacusis to high-intensity noise exposure or ototoxic substances.
“Most of our participants attributed the onset of their pain hyperacusis to high-intensity noise exposure or ototoxic substances (Table 2).”
Quote in the paperNot a substantial claim - Findingown data
Two participants reported >90% pain relief from nerve blockers.
“Two participants in the present study reported that nerve blockers (e.g., lidocaine, ambroxol) had an excellent effect (>90% pain relief) on their pain hyperacusis.”
Quote in the paperSubstantial claim - Interpretationown data
The reported symptoms and treatment patterns generally aligned with peripheral mechanistic theories of pain hyperacusis, such as trigeminal nerve involvement.
“Symptoms and therapeutic approaches were generally consistent with peripheral mechanistic theories of pain hyperacusis (e.g., trigeminal nerve involvement).”
Quote in the paperSubstantial claim - Premisecitation
The mechanisms by which sound produces severe, long-lasting pain in pain hyperacusis are poorly understood.
“How sound causes excruciating pain that can last for weeks or months is not well understood, resulting in a lack of effective treatments.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [1] Jahn, 2022, Clinical and investigational tools for monitoring noise-induced hyperacusis, J Acoust Soc Am source
- Interpretationreasoning
The poor understanding of pain hyperacusis mechanisms contributes to a shortage of effective treatments.
“How sound causes excruciating pain that can last for weeks or months is not well understood, resulting in a lack of effective treatments.”
Quote in the paperSubstantial claim - Interpretationown data
The reported physical sensations are consistent with neuropathic pain.
“Most participants reported physical sensations consistent with neuropathic pain (i.e., burning, stabbing, throbbing, pinching) that can be induced by nerve irritation (e.g. compression, torsion, or angulation) or inflammation near the pain site.”
Quote in the paperSubstantial claim - Interpretationown data
Emotional and psychosocial symptom clusters were highly rated, suggesting these experiences may be more consistent than the physical manifestation of pain.
“Clusters related to emotional and psychosocial symptoms were highly rated across participants, suggesting that these experiences may be more consistent than the physical manifestation of the pain itself.”
Quote in the paperNot a substantial claim - Interpretationreasoning
The symptoms suggest that the origin of pain hyperacusis may be peripherally mediated, at least in part.
“These symptoms suggest that the origin of pain hyperacusis may be peripherally mediated, at least in part (Figure 1).”
Quote in the paperSubstantial claim - Premisecitation
Extensive evidence supports the use of ambroxol to treat neuropathic pain secondary to trigeminal neuralgia, fibromyalgia, and complex regional pain syndrome.
“There is extensive evidence supporting the use of ambroxol to treat neuropathic pain secondary to trigeminal neuralgia, fibromyalgia, and complex regional pain syndrome 25.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [25] Russo, 2023, Ambroxol for neuropathic pain: hiding in plain sight?, PAIN source
- Study design and conductreasoning
The wide variety of treatments and unstructured approach to managing pain hyperacusis precluded systematic analyses of interrelationships between health-related variables, symptom severity, and treatment outcomes.
“The wide variety of treatments and unstructured approach to managing pain hyperacusis precludes systematic analyses of the interrelationships between individual health-related variables, symptom severity, and treatment outcomes.”
Quote in the paperNot a substantial claim - Interpretationnone given
There is little-to-no empirical evidence to support elevated central auditory gain as the underlying cause of sound-induced pain per se.
“However, there is little-to-no empirical evidence to support elevated central auditory gain as the underlying cause of sound-induced pain per se.”
Quote in the paperSubstantial claim - Study design and conductnone given
By design, the participants were a subset of individuals with relatively severe pain hyperacusis.
“By design, our participants were a subset of individuals with relatively severe pain hyperacusis, and future work will survey a broader and more diverse group.”
Quote in the paperSubstantial claim
- Classified as probably not a substantial claim. 17
- May combine two claims. 22
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationA 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).
PremisecitationMiddle 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).
PremisecitationInner 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.
PremisecitationMechanical 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.
PremisecitationInteractions 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.
PremisecitationA 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.
PremisecitationFew 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.
PremisecitationRodent 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 dataParticipants 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 claimMay combine two claims.
Findingown dataOther 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 claimMay combine two claims.
Findingown dataThe 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 claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown dataNine 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 claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown dataTwo 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 claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown dataThat 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 claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Findingown dataAmong 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 claimMay combine two claims.
Findingown dataThe 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 givenThe 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 claimClassified as probably not a substantial claim.
PremisecitationPain 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 dataThe 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 claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductown dataTwo 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 claimMay combine two claims.
PremisecitationLoud 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.
InterpretationreasoningCurrent 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 claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductcitationA 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 givenThere 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 claimMay combine two claims.
InterpretationreasoningWhile 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 claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenThe 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 claimProbably not a substantial claim: may not pass S2 (checkable), S4 (based).
Interpretationnone givenIt 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 claimMay combine two claims.
Premisenone givenSound 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.
PremisecitationThe 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 dataThe 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 claimClassified as probably not a substantial claim.
Study design and conductnone givenThis 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 claimMay combine two claims.
PremisecitationThe 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).
InterpretationreasoningEven 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 claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationLidocaine 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.
InterpretationreasoningDamage-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
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.”
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
MinorThe 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.
“32 adults attended a virtual focus group to describe their sound-induced pain.”
“In the present study, participants (n = 26) joined a 60-minute virtual focus group”
The stated relief threshold excludes the paper's modest-effect category
MinorThe methods define a modest effect as 75% pain relief, but the results describe modest-to-excellent effects as greater than 75% relief.
“Only a few patients reported modest-to-excellent effects (>75% pain relief)”
“Modest effect (75% pain relief)”
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Flagged first, then by citations
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Sorted by citations
Transdiagnostic mechanisms of decreased sound tolerance
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Sound hypersensitivity phenotypes and sound hypersensitivity disorder
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Self-citationJahn, K. N., & Joshi, S. (2026) · Ear and Hearing · doi:10.1097/aud.0000000000001817
Self-citation
- Authors
- Jahn, K. N., Kashiwagura, S. T., & Yousuf, M. S.
- Affiliations
- The University of Texas at Dallas (US)
- Corresponding author
- Jahn, Kelly N.
- ORCID
- Jahn, Kelly N.
- Venue
- The Journal of Pain
- Publisher
- Elsevier BV
- Published
- 2025-02
- Volume
- 27
- Pages
- 104741
- ISSN
- 1526-5900 (ISSN-L)
- PMC
- PMC11807742
- 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
- hybrid
- doi.org
- Licence
- 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.
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