Research recommendations and priorities

• Identify the causes/mechanisms behind setbacks, identify how they could be prevented and how recovery time can be accelerated 

• Coin a new term for setbacks which better encompasses the decline in tolerance (and as such quality of life) and/or worse symptoms after a triggering sound exposure. A similar term in patients with ME/CFS is post-exertional malaise, which describes a worsening of symptoms after exertion. 

• Find out if there are subtypes of pain hyperacusis based on experienced symptoms between patients: 

  • The pain starts immediately during noise exposure: here, the pain intensity decreases as soon as the noise stopts

  • The pain is lasting: it starts during the noise exposure, but even when the noise stopts the pain lasts for hours or even days.

  • The pain is delayed: the patient experiences no pain during a sound exposure, but the pain starts hours or sometives even days later.

  • Any combination of the three.

  • Some improve from CBT and sound therapy; others do not or even worsen from exposure.

  • Some improve from certain antidepressants such as clomipramine, but not everyone reports improvement from these drugs. 

    Certain sufferers improve naturally over time, others do not

  • The pain can be limited to the ear but can also be experienced in other parts of the head, neck and throat. 

• What is the role of central sensitization in hyperacusis? 

• Can pain hyperacusis in certain cases be a form of nociplastic pain? 

• Identify or develop medications which do not have tinnitus or visual issues as a side effect 

• What is the role of jaw, neck and shoulder complaints in hyperacusis? 

• What is the connection between hyperacusis, tensor tympany syndrome, tinnitus, reactive tinnitus, visual snow and light sensitivity? 

• Proper identification and definitions of pain hyperacusis, loudness hyperacusis, tensor tympani syndrome and reactive tinnitus 

• Does the cause of pain hyperacusis primarily lie in the middle ear/trigeminal nerve, inner ear or brain?  

• Developing biomarkers for the various forms of hyperacusis 

• Identify the role between the various hyperacusis subtypes and genes 

• Differentiate between the different forms, severity and duration of hyperacusis and noise sensitivity. 

• Following on this, differentiate between the symptom cluster shown by patients. Do they show loudness, pain, fullness, fluttering of the ear drum, … 

• Include severe patients in your research, who have a too low of a tolerance to leave their homes (e.g. written questionnaires, virtual meetings with captions and text replies, home to lab saliva or blood tests, visiting severe patients at home to learn from them, …) 

• Clinical studies with placebo and control groups, when possible, during testing of the efficacy of cognitive behavioral therapy, sound and exposure therapy, botox injections of the tensor veli palatini muscle and antidepressants such as clomipramine and duloxetine (Cymbalta) 

• What is the role of jaw, neck and shoulder complaints and reactive tinnitus? 

• What is the connection between reactive tinnitus, (stable) tinnitus, hyperacusis and tensor tympany syndrome? 

• What is the connection between serotonin and (reactive) tinnitus? 

• Proper identification and definitions of stable tinnitus, reactive tinnitus and sound-sensitive tinnitus 

• Developing biomarkers for reactive tinnitus to distinguish it from stable tinnitus 

• Is reactive tinnitus a form of central sensitization? 

• Identify the similarities and differences between reactive tinnitus and loudness hyperacusis. 

• Identify the role between reactive tinnitus and genes. 

• Conduct a study about the lived experiences of reactive tinnitus patients similar to Jahn et al. (2025) for pain hyperacusis. Greenbergh & Leigh (2018) provide a good foundation from which to build from 

• Properly distinguish reactive, sound-sensitive tinnitus and stable tinnitus in the literature 

• When testing treatments for tinnitus, inquire whether the patient’s tinnitus is reactive and/or sound-sensitive and whether the treatment also has an effect on the reactivity. 

• Assess the sound/frequencies which cause reactivity in a patient. Is there a link with the frequency of their stable tinnitus and/or their audiogram? 

• Placebo controlled studies for the various used treatment options for reactive tinnitus 

Greenberg, B., Leigh, K. (2018). Loss, Meaning Making, and Reconstruction of Narratives in Adults Enduring Tinnitus Exacerbated by Exposure to Sound. The Practitioner Scholar: Journal of Counseling and Professional Psychology, 7. 

Jahn, K. N., Kashiwagura, S. T., & Yousuf, M. S. (2025). Clinical phenotype and management of sound-induced pain: Insights from adults with pain hyperacusis. The journal of pain, 27, 104741.