Hyperacusis

My perspective on hyperacusis mechanisms and approach to treatment has evolved over 30 years of clinical experience and neuroscience research – with a focus on the links between auditory, somatic and psychological pathways; and the remarkable similarities and overlap with chronic pain and trauma mechanisms.

My online hyperacusis clinic at DWM Audiology is known world-wide, and most of my patients have been severely impacted by their hyperacusis. Tens of thousands of hours have been spent attentively listening to and documenting the factors described relating to the onset, development and persistence of their hyperacusis, and their associated physical and psychological symptoms.

A process of considered and analytical reflection while evaluating my patients’ histories and shepherding them through a recovery process allowed common, consistent and repeated patterns and themes to emerge. This enabled me to identify the links with tensor tympani syndrome (TTS), revealed TTS pathways/triggers and provided insights into hyperacusis mechanisms.

I became increasingly confident modifying or discarding the available clinical guidance on hyperacusis definitions, mechanisms, classification, assessment and treatment if not congruent with my clinically based observations, analysis and research.

Treatment is carefully curated, delivered in a multidisciplinary setting and personalised, to ensure each patient remains safe from symptom exacerbation. Most of my hyperacusis patients have achieved at least partial desensitisation, both from their hyperacusis as well as the severity of their sound-induced physical symptoms - even those with the most severe degree of hyperacusis.

Now that I have retired from clinical practice, my focus is to expand the understanding of hyperacusis mechanisms to reflect these clinical learnings and ensure authenticity with lived experience. I provide guidance to the hyperacusis community, and education and training to clinicians so they can deliver effective and safe treatment.

What is hyperacusis?

Hyperacusis and misophonia are the terms used to explain significant and dysfunctional intolerance to everyday sounds. Hyperacusis and misophonia can occur concurrently. However, the sounds perceived as intolerable, the subconscious negative evaluation of these sounds and the involuntary neurophysiological and psychological responses following exposure are different, so they are distinctly separate conditions.

Hyperacusis is defined as an abnormal intolerance; a heightened sense of volume and awareness of certain sounds, which other people can comfortably tolerate; and generally aural symptoms of physical discomfort/pain following exposure to these sounds. Sounds that are most intolerable are loud, impulse and impact sounds, particularly when they are unexpected, sudden, sustained and in close proximity to the ears. High frequency (treble) and low frequency (bass) sounds tend to be less well tolerated.

The typical cluster of physical symptoms following exposure to these sounds, including pain in and around the ear, is highly specific and consistent with TTS (Westcott et al 2013, Noreña et al 2018, Fournier et al 2022).

Hyperacusis is a spectrum disorder and can range from mild through to severe to extreme. Sound-induced symptoms consistent with TTS can also range from mild to severe to extreme – with chronic sound-aggravated neuropathic pain from trigeminal nerve inflammation at the extreme end of the spectrum. Often, but not always, the more severe the hyperacusis, the more severe the sound-induced TTS symptoms become.

Hyperacusis can affect one or both ears. If bilateral, hyperacusis severity as well as the range and severity of sound-induced TTS symptoms may differ in each ear.

The physical suffering, emotional impact and lifestyle constraints of hyperacusis can be profound, traumatic and life-altering, particularly for those who experience sound-induced pain.

There is very little understanding of hyperacusis in the community. Sound-induced TTS symptoms are involuntary, not readily objectively measurable and may be delayed. Explaining such an abnormal reaction to sound to other people, including health professionals, is difficult and people with hyperacusis often feel misunderstood and trivialised. The unusual cluster of sound-induced symptoms are frequently misdiagnosed, ignored or not believed. Commonly used evaluation and treatment approaches tend not to personalise assessment or desensitisation strategies to suit individual capacity, with a consequent risk of symptom exacerbation.

When exploring the underlying mechanisms of hyperacusis from a clinical perspective, it becomes apparent that there are no distinct or mutually exclusive boundaries which allow hyperacusis to be neatly subdivided into classification categories or subtypes. There are however a number of predisposing and underlying factors which need to be considered and identified in each patient.

Potential predisposing factors

Tinnitus: large-scale prevalence research has identified secondary hyperacusis in approx. 50% of help-seeking tinnitus patients (Schecklmann et al 2014, Westcott et al 2013). It is my experience that hyperacusis is underdiagnosed, so can be unrecognised and unsupported in tinnitus patients.
Acoustic shock: hyperacusis following acoustic shock can be particularly severe.
Pre-existing TTS
Misophonia has the potential to escalate into hyperacusis. Generally, misophonia precedes hyperacusis.
Abrupt and significant changes in hearing can be a factor towards hyperacusis development, particularly if recruitment develops or is enhanced. Recruitment is a distorted growth of loudness due to cochlear (inner ear) damage from a sensorineural hearing loss, so that loud, impact and impulse sounds are heard with a more grating and jarring quality.
Neurological damage/disorders affecting auditory processing eg concussion, head injury.

Placebo and Nocebo

The mindset (beliefs, expectations, safety/lack of safety) and context are powerful in reinforcing a positive or negative subconscious response to a stimulus or treatment.

The placebo/nocebo effect is more than positive or negative thinking, it is a subconscious phenomenon affecting symptoms modulated by the brain, including the perception of pain and the reaction to tinnitus.

A sense of safety induced by a placebo, can trigger the brain's natural pain-relief mechanisms, reducing the perception of pain signals from nociceptors. Tinnitus is known to be highly responsive to the placebo benefit of any positively perceived stimulus or treatment.

Pain expert Prof. Lorimer Moseley “We now know that pain can be turned on, or turned up, by anything at all that provides the brain with credible evidence that the body is in danger and needs protecting.”

We know from chronic pain research that the limbic system will become protective towards stimuli perceived (rightly or wrongly) as a potential threat, and that a nocebo effect occurs when a perceived lack of safety aggravates pain.

Severe tinnitus triggers a powerful subconscious drive to ensure the tinnitus will not be aggravated by any external factors, such as sounds, medications, food, drinks etc, perceived (rightly or wrongly) as potentially aggravating the tinnitus or damaging the hearing.

For some, the combined effects of a belief/expectation of harm + heightened levels of tinnitus vigilance + subconscious protectiveness towards threatening stimuli can trigger tinnitus spikes due to a nocebo effect. This can become further exacerbated by the somatosensory influence on tinnitus of heightened levels of stress held in the jaw muscles.

This subconscious protectiveness can become triggered by daily exposure to loud, unavoidable and unpredictable sounds – setting the scene for hyperacusis development.

Factors underpinning hyperacusis

the sense of hearing in humans and animals evolved as a survival mechanism, providing warning of danger/loss of safety; our brain is hard wired to be vigilant towards the auditory environment
the ear is anatomically open to keep us safe (and alive) - we have not evolved the ability to ‘close our ears’ equivalent to closing our eyes. We cannot control incoming auditory stimuli other than blocking the ears and avoidance strategies.
normal hearing is highly sensitive, allowing us to hear a huge range of sounds – through walls and the ground, from a distance etc. so that our subconscious brain is flooded with auditory input.
generally, only a proportion of the sounds we are capable of hearing will be relayed to the conscious brain for our attention.
sound is therefore pervasive, unavoidable and often unpredictable. Our subconscious brain, where sounds are evaluated for meaning and importance, expects hearing to remain stable and will be deeply disoriented by abrupt and significant changes in hearing.
nocebo effect: the development of a subconscious (primal) threat that certain sounds are unsafe and will aggravate tinnitus; cause harm to the ear/hearing; cause pain

How does hyperacusis develop?

Developing hyperacusis as a secondary reaction to tinnitus is the most common pathway, but not the only pathway, for hyperacusis to develop. Hyperacusis can develop without tinnitus being bothersome or even present.

Tinnitus most commonly develops as a result of a hearing loss or change in hearing, which may be due to noise damage in the cochlea (inner ear). However, hyperacusis is a centrally mediated condition, i.e. hyperacusis originates in the brain, whether it develops secondary to tinnitus or as a result of some other cause. This in turn typically triggers sound-induced symptoms consistent with TTS as an involuntary, nociceptive ‘protective’ response. See the TTS page for details about this pathway.

Hyperacusis makes clinical sense and aligns with lived experience when viewed as a subconscious and involuntary protective nocebo phenomenon, the result of a primal threat strongly influencing auditory processing, triggered by unavoidable everyday sounds subconsciously evaluated as ‘unsafe’ to the ear/hearing/tinnitus.

Once the initial ‘seed’ or triggering event for the subconscious hyperacusis threat has taken place, a vicious cycle can develop due to the inevitability of loud/sudden/unexpected sound exposure triggering TTS and fuelling the threat, leading to a pathway of escalation.

Why do some people have a delayed response in their symptoms following intolerable sound exposure?

A subconscious appraisal of threat in response to intolerable sound exposure may be immediate, particularly if there are sound-related trauma associations (eg acoustic shock), or build up more slowly, which is why some people have a delay or a cumulative effect in their sound-induced pain/aural symptoms.

The danger of incorrect beliefs

A hyperacusis research focus has been to investigate hidden cochlear/auditory nerve damage as a possible trigger for hyperacusis and a source of sound-induced pain. This has been extrapolated into a widely held perspective of hyperacusis as an ongoing sound-induced cochlear damage-related phenomenon.

Understandable, as sound-induced TTS symptoms can include muffled, distorted hearing and a concrete, potentially treatable site-of-lesion holds appeal – but I have found this perspective does not align with clinical and lived experience. Nor is this consistent with the successful desensitisation outcomes experienced by many of my patients.

The effect of promoting this perspective has the potential to reinforce the threat underpinning hyperacusis, locking in a vicious cycle of persistence and escalation.

I consider the following widespread beliefs to be incorrect:

sound-induced pain/aural symptoms indicates sound-induced damage to the inner ear (cochlea) or to the hearing has occurred
the inner ears or hearing status of people with hyperacusis are uniquely vulnerable or fragile, and are being repeatedly damaged by everyday intolerable sound exposure
avoidance of intolerable sounds is needed to avoid ongoing damage.

Sound-induced TTS can dampen the transmission of low frequency sounds through the middle ear to the inner ear, resulting in fluctuating symptoms of muffled or distorted hearing. This is not damaging to the middle or inner ear structures.

These incorrect beliefs have no clinical validity. They contribute to keeping people stuck and unable to recover.

The role of anxiety in hyperacusis

ANXIETY DOES NOT CAUSE HYPERACUSIS.

Fear is a fundamental emotion necessary for survival, and exists well below the conscious level in the cerebellum (Batsikadze, G et al, 2024). It is important to distinguish between anxiety and subconscious fear/threat – they are separate. The threat underpinning hyperacusis stems from a primal survival response, out of conscious control. That threat can produce anxiety and will be fuelled by anxiety.

My hyperacusis patients have often been initially bewildered rather than anxious by the onset/escalation of their hyperacusis, for many anxiety has come later.

Anxiety and auditory vigilance are common in people experiencing severe hyperacusis and sound-induced pain because of their lack of control over the auditory environment and the degree of suffering involved.

It is important to distinguish between reasonable alertness and hypervigilance. Monitoring and vigilance towards the auditory environment is an intuitive, natural reaction. This can however perpetuate the subconscious evaluation of intolerable sounds as unsafe.

With correct understanding of hyperacusis and effective support, anxiety and hypervigilance can be managed to minimise any ongoing contribution towards hyperacusis persistence and escalation.

Sound avoidance

In situations where people with hyperacusis feel highly vulnerable to intolerable sound exposure, it is reasonable to use ear plugs/earmuffs, noise cancelling headphones or avoidance behaviour.

This is not needed to avoid damage, but reinforces auditory safety, helping to reassure the subconscious brain and to maintain reasonable lifestyle horizons.

Hyperacusis evaluation and treatment

Outcomes – what to expect?

The factors resulting in hyperacusis are complex and outside conscious control, so a guided desensitisation process is slow, requires correct understanding, determination and belief in the prospect of change - in addition to self-management of personalised strategies and effective treatment of TTS symptoms.

Complete desensitisation may be difficult to achieve and an unrealistic expectation. However, partial desensitisation can make a big difference to the suffering and lifestyle constraints of hyperacusis.

The combined effects of the desensitisation therapy program I developed + effective TTS-focussed treatment have achieved uniquely successful outcomes in treating both hyperacusis and sound-induced pain in my patients.

Sound-induced pain

For hyperacusis patients suffering chronic, severe sound-induced pain, effective medical treatment of pain is the first priority. Their brain has become sensitised: has learnt to associate sound with pain; to anticipate and fear sound-induced pain. A hyperacusis desensitisation therapy program will not be effective until their pain is treated. These patients can be referred to a pain physician, assessed for neuropathic pain and treated for TTS-related trigeminal neuralgia. See the TTS page for treatment details.

A newly formed group, the Hyperacusis Collaborative Research Network (HCRN), consisting of neuroscientists, clinicians (including myself) and patients, has been established to investigate treatments that will provide tangible benefit to people with hyperacusis, particularly those suffering with sound-induced pain. The patients, who initiated the group, and clinicians involved in HCRN have all found that TTS - focussed treatment approaches have achieved uniquely successful outcomes in treating this pain. These approaches arose from TTS research carried out in these patients by myself and by neuroscientist Arnaud Noreña and his team. HCRN aims to take a deep dive to explore, research and obtain evidence on these TTS-related treatment approaches, while remaining open to other treatments that have been effective.

Hyperacusis desensitisation therapy

Hyperacusis desensitisation therapy is based on developing a strong sense of safety: both from any actual risk of inner ear/hearing damage AND from threat, while being aware of, and being able to recognise, the difference between these two issues.

This requires a personalised and multidisciplinary approach aimed at retraining the brain to feel safe in the presence of sounds that are not harmful to the ears, and combines effective treatment of TTS symptoms (including chronic pain) as well as a range of perceptual and psychological strategies. The boundaries of auditory safety/lack of safety need to be carefully determined for each individual to triage and personalise strategies so that symptom exacerbation is avoided.

Once patients know how the brain processes sound subconsciously; have been helped to identify the initial threat ‘seeding’ their hyperacusis onset; and understand their unique auditory, psychological, neural and somatic pathways underpinning their hyperacusis and TTS development - there is potential for reversal. If a patient doesn’t acknowledge the underlying threat or know their pathways or understand the powerful effect of nocebo, they don’t know what/why/how they need to unravel.

So the first and most important step in a hyperacusis treatment process has to be thorough history taking, evaluation and analysis with an experienced, TTS-informed clinician to explore, reveal, evaluate and explain. The explanation provided needs to be free of inadvertently stirring up additional threat. This understanding provides insight, reassurance and a personalised and targeted framework for treatment. Importantly, this understanding is of therapeutic benefit by limiting, and often halting, further escalation.

It should be noted that hyperacusis can be evaluated on the basis of history taking and questionnaires. I recommend against sound-based assessments, in particular loudness discomfort levels, which cause unnecessary suffering, additional threat and frequently aggravate both the hyperacusis and the associated TTS symptoms.