Counseling Protocol for a Transitional Intervention for Debilitating Hyperacusis

Abstract

Introduction:

This clinical focus article describes a structured counseling protocol for use with protected sound management and therapeutic sound in a transitional intervention for debilitating hyperacusis. The counseling protocol and its associated visual aids are crafted as a teaching tool to educate affected individuals about hyperacusis and encourage their acceptance of a transitional intervention.

Description of Counseling Components:

The counseling protocol includes five components. First, the patient's audiometric results are reviewed with the patient, and the transitional intervention is introduced. An overview of peripheral auditory structures and central neural pathways and the concept of central gain are covered in the second and third components. Maladaptive hyper-gain processes within the auditory neural pathways, which underlie the hyperacusis condition, and associated connections with nonauditory processes responsible for negative reactions to hyperacusis are covered in the fourth component. Detrimental effects from misused hearing protection devices (HPDs) and the necessity to wean the patient from overuse of HPDs are also discussed. In the fifth component, the importance of therapeutic sound is introduced as a tool to downregulate hyper-gain activity within the auditory pathways; its implementation in uncontrolled and controlled sound environments is described. It is explained that, over the course of the transitional intervention, recalibration of the hyper-gain processes will be ongoing, leading to restoration of normal homeostasis within the auditory pathways. In turn, associated activation of reactive nonauditory processes, which contribute to hyperacusis-related distress, will be reduced or eliminated. As recalibration progresses, there will be less need for protected sound management and sound therapy. Sound tolerance will improve, hyperacusis will subside, and daily activities in typical healthy sound environments will again become routine.

Results and Conclusion:

The combination of counseling with protected sound management and therapeutic sound is highlighted in companion reports, including a summary of the outcomes of a successful trial of the transitional intervention.

This clinical focus article is one in a collection of four companion reports, including Formby, Secor, et al. (2024), Eddins et al. (2024), and Formby, Cherri, et al. (2024), which provides background for and details of the components implemented in a successful field trial of a transitional intervention for classical loudness-based hyperacusis (LH; Tyler et al., 2014). The latter report in this collection describes the outcomes of the field trial. The purpose of this report was to delineate the structured counseling component of the intervention. This counseling protocol is designed with a specific intent to be used together with a progressive strategy of protected sound management and therapeutic sound presentation offered by output-limiting, bilateral, ear-worn devices equipped with sound generators, as detailed by Eddins et al. (2024). The purposes of the counseling in our intervention are multiple. Counseling serves as an instructional and motivational tool to promote the patient's understanding of their LH, the underlying maladaptive hyper-gain processes as the basis for LH, and the goal of the transitional intervention in downregulating these hyper-gain processes. The counseling also plays a key role in encouraging the patient's acceptance and compliance with the treatment. Among other important purposes of our counseling protocol is that of preparing the affected individual to transition from their self-imposed silence, ensured by isolation and overprotection against real or perceived offending sounds, to the starting point for acceptance and use of therapeutic sound in the treatment protocol. This counseling educates the patient about the counterproductive effects of the misuse and overuse of hearing protection devices (HPDs). This point of treatment initiation, which begins with the willingness to accept and use enriched protected therapeutic sound, is promoted with delivery of the structured counseling in a scripted protocol. The structured counseling also is the critical component in the intervention for mitigating negative emotional and physiological reactions associated with LH-related distress.

Preliminary to the detailed presentation of our counseling protocol in this report, we first consider the role of counseling in the treatment of LH and other factors and research results that influenced our crafting of the counseling protocol. This focused review supplements the broader overview of counseling for hyperacusis, including annoyance hyperacusis, fear hyperacusis, and pain-related hyperacusis, that we shared in the presentation of the background and rationale for our full transitional intervention (see Formby, Secor, et al., 2024). The selected literature reviewed here is specifically focused on helping the reader understand and appreciate our motivation and strategy for the design of and the content included in this counseling protocol for LH.

Consideration of the Role of Counseling in the Treatment of LH and Other Factors in Crafting the Counseling Protocol for the Transitional Intervention for Debilitating LH

Notwithstanding the results of a single-site survey in which patients with hyperacusis ranked counseling to be the most effective treatment for their hyperacusis (Aazh et al., 2016), there are only a handful of reports in the hyperacusis literature that provide evidence of benefit from “counseling-only” strategies for hyperacusis (i.e., counseling offered without some form of companion sound therapy; Fackrell et al., 2017). Most of these reports describe protocols based on principles of cognitive behavioral therapy (CBT; Aazh et al., 2019; Beck, 2011). However, as highlighted below, even in CBT, the associated treatment effects may be (and typically are) confounded by desensitization exercises that promote incremental sound exposures over the course of the interventions. CBT is a psychological intervention that has been used successfully in treating problems of anxiety and avoidance behaviors (of the kind encountered in debilitating hyperacusis). The goal of CBT is to modify the patient's dysfunctional cognitions, negative thoughts, and avoidance-seeking behaviors (Aazh et al., 2019). As of 2019, there were only four trials of CBT for hyperacusis reported in the literature (Aazh et al., 2019), and none of these were conducted with an active control group. The most rigorous among these trials is that reported by Jüris et al. (2014). Their intervention consisted of six CBT treatment sessions in which the patients learned new behaviors for dealing with hyperacusis, mainly through exposure to sounds in a controlled and stepwise fashion over a 2-month period. Sound enrichment and exposure exercises were encouraged outside of the counseling sessions. Jüris et al. reported that all their study outcome measures (loudness discomfort levels [LDLs], Hearing Questionnaire, Quality of Life Inventory, and an adapted version of the Tampa Scale of Kinesiophobia), except the Hospital Anxiety and Depression Scale, yielded significant treatment effects in their CBT treatment group relative to a wait-list control group. The wait-list control group subsequently obtained similar treatment effects after receiving CBT. Sound tolerance, as measured by treatment-related LDL change (their primary outcome measure), was improved from baseline (typically just over 70 dB HL) by ~6–9 dB at treatment end. Posttreatment, 32 of 56 (57%) study patients had a positive improvement in their LDL of at least 6 dB in one ear, with 35 of 55 (64%) patients considered positive responders at a 12-month follow-up visit based on changes in their work and social sound-avoidance behaviors.

Our counseling protocol, as described below, differs substantially from CBT. It follows closely after the recalibration counseling approach described by Gold and Formby (2017) for treatment of decreased sound tolerance among persons with hearing loss who self-reported aversion to amplified sound. Their counseling protocol borrowed from principles originally described by P. J. Jastreboff and Jastreboff (2000) and P. J. Jastreboff and Hazell (2004) for treating hyperacusis. In essence, they assume in their treatment model that LH arises from maladaptive neural hyperactivity within the central auditory pathways and that, through gradual exposure to desensitizing sound therapy, this maladaptive hyperactivity can be downregulated to reset normal neural gain function, leading to resolution of LH. We relied on Jastreboff's neurophysiological model, updated for the treatment of LH and other conditions of decreased sound tolerance (P. J. Jastreboff & Jastreboff, 2014, 2016), to account for the negative emotional and physiological reactions that give rise to the associated distress, anxiety, and aversive responses to hyperacusis. In the Jastreboff treatment model, counseling plays an important role in habituating the latter negative reactions to sound, but it is not apparent in their model how counseling could directly affect recalibration or desensitization of the maladaptive neuronal hyperactivity giving rise to LH.

Our counseling protocol differs in at least two important respects from Jastreboff's treatment model for hyperacusis. First, as part of their tinnitus retraining therapy (TRT) treatment for primary hyperacusis, P. J. Jastreboff and Hazell (2004) proposed a transitional desensitization protocol with associated counseling, which they combined with sound enrichment therapy delivered bilaterally by low-level broadband sound generators. Exposure to the latter is typically implemented with gradual increases in the output levels of the sound generators per Hazell and Sheldrake (1992). In contrast, we crafted our scripted LH counseling protocol for recalibration rather than desensitization of the hyper-gain LH processes, a distinction in the mechanistic strategies for therapeutic sound delivery proposed by Baguley and Andersson (2007). Our recalibration protocol calls for the therapeutic sound from bilateral sound generators to be set at a constant “soft, but comfortable” output level matched for equal loudness between the ears, which was also implemented in Formby et al. (2015). This therapeutic level is typically unchanged (or little changed) over the course of the intervention period. Depending on the patient's sound environment, we offer the therapeutic sound without protective output-limiting loudness suppression (LS) in safe controlled sound environments and with protective LS in uncontrolled sound environments via bilateral devices (Eddins et al., 2024). The latter output-limiting protection is systematically reduced as the patient's sound tolerance improves and as their dynamic range (DR) for loudness progressively expands over the course of the transitional intervention. Thus, a second difference of our counseling approach from that of P. J. Jastreboff and Hazell and subsequent iterations of their protocols for hyperacusis and decreased sound tolerance (P. J. Jastreboff & Jastreboff, 2014, 2015, 2016) is that their desensitization approach was implemented without transitional protective LS from their bilateral devices or related counseling.

Sound-protective strategies similar to ours (Eddins et al., 2024) have been previously described by Sammeth et al. (2000), Valente et al. (2000), Vernon (2002), Vernon et al. (2002), and Westcott (2006). Their strategies included the implementation of bilateral ear-worn devices offering large amounts of output-limiting LS to limit exposures to potentially offending louder sounds; however, to our knowledge, once the devices were initially set, none of these studies included the adjustment of the output-limiting LS as part of the intervention. Also, none of these protective devices offered therapeutic sound. Moreover, these studies did not report a related counseling protocol or an objective evaluation with systematic follow-up to assess improvements in their patients' LH conditions. The latter information would be needed to adjust the threshold for the output-limiting LS. Among these studies, only Vernon and colleagues (Vernon, 2002; Vernon et al., 2002) reported a companion treatment protocol. The protocol, originally described by Vernon (1987) in a case report, proposed incremental change in pink noise stimulation presented by earphones. The pink noise was set adaptively at a level just below discomfort over the course of the desensitizing intervention for the LH condition. Sammeth et al. and Westcott also suggested the protective sound management approach could potentially be combined for further benefit with a desensitization treatment, albeit neither implemented a companion treatment protocol with the use of their protective devices. All the above studies reported anecdotal evidence and positive reports from some patients relating protective benefits and improved communication in some situations when using their output-limiting devices.

The activation and release of the protective LS over the course of the transitional intervention, as previewed with LH patients in our counseling protocol, was a notable modification of the recalibration counseling protocol originally described by Gold and Formby (2017). Formby et al. (2015) successfully implemented the Gold and Formby counseling protocol in combination with sound therapy from bilateral sound generators to expand (by ~12 dB) the DRs of nine of 11 individuals with hearing impairment; all were problematic hearing-aid users pretreatment because of their reduced sound tolerance and associated limited DR. A notable result reported by Formby et al. (2015) was that counseling, offered with the use of ineffectual placebo sound generators (effectively counseling alone), afforded seven members of an otherwise similar group of nine participants little or no treatment benefit (as measured by negligible change in their loudness judgments) over the course of their (typical) 6-month intervention period. One of the two participants who did benefit from counseling alone had moderately severe LH pretreatment. This participant's posttreatment LDLs approached normal limits, increasing dramatically from 65 dB HL pretreatment to 90 dB HL at the end of the intervention period. This 25-dB change indicates that recalibration counseling may be more effective and important for severely debilitated cases of LH than for mild cases. In other words, counseling is important for those whose negative emotional and physiological reactions are heightened, and thus, counseling-induced habituation of these negative reactions would likely be most beneficial. Interestingly, despite the dramatic increases in the latter participant's posttreatment LDLs, their apparently improved sound tolerance did not translate into improved speech understanding, which occurred only after they received crossover treatment combining counseling with the use of effectual sound generators to expand further their DR (Formby et al., 2017). Here, it is noteworthy that those participants who did not benefit from the “counseling alone” intervention in Formby et al. (2015) all had pretreatment LDLs ≥ 80 dB HL. Their LDLs, although somewhat lower than those of typical listeners, were consistent in that they and most other study participants denied distressing sound tolerance problems and related complaints.

It is worthwhile to reiterate and consider again the synergistic treatment effects above for their group of participants who were assigned to counseling combined in treatment with the use of the conventional bilateral sound generators. These participants who, pretreatment, were averse to amplified sound achieved an average posttreatment increase of ~12 dB in their loudness judgments. This incremental change represented a statistically and clinically significant improvement in their sound tolerance. In contrast, two otherwise comparable groups of sound-averse listeners with hearing impairment, one group assigned to sound generators without counseling and a second group assigned to counseling paired with ineffectual placebo sound generators, achieved average posttreatment increases in their loudness judgments of ~6 and ~2 dB. Thus, recalibration counseling, like that to be described in this clinical focus article, when effectively offered alone with the placebo sound generators, was ineffective but, when offered together with the use of bilateral sound generators, combined for an average treatment effect that was more than additive. We have previously speculated on possible mechanisms by which counseling combines with sound therapy to achieve a synergistic treatment effect beyond the effects of either treatment alone. We refer the interested reader to Formby et al. (2015, 2017) and Gold and Formby (2017) for this conjecture.

This brief review indicates that whatever the mechanism is by which counseling contributes to treatment of LH, its benefit is value added when combined with sound therapy protocols. Accordingly, we crafted the following counseling protocol for use with protected sound management and therapeutic sound in the transitional intervention described by Formby, Cherri, et al. (2024).

Description of Counseling Components

Overview of the Counseling Protocol for Debilitating LH

Based on our experience with similar counseling strategies and armed with knowledge from our research and related efforts of others delineated above, we crafted a modified version of Gold and Formby's (2017) recalibration counseling protocol for use with protective sound management and therapeutic sound in a transitional intervention for debilitating LH. We have scripted the structured counseling content and added a set of new coordinated visual aids, including anatomical images and model diagrams, to go along with our counseling content. Our basic teaching model, which we use to explain LH and related distress responses to the patient, is based on a set of simplified block diagrams adapted from Jastreboff's neurophysiological model for hyperacusis (P. J. Jastreboff & Jastreboff, 2000, 2014, 2016). These diagrams begin with a depiction of normal and disordered (elevated) central auditory gain processes as well as the recalibration (downregulation) of the latter hyper-gain processes consequent to treatment. Modifications of the block diagrams also illustrate involvement of nonauditory central nervous system processes and treatment effects consistent with remediation of associated negative emotional and physiological reactions to LH. A simplified (theoretical) block diagram of the pain pathway is newly added in the teaching model to denote and represent hypothetical processes underlying pain hyperacusis and associated or concurrent relations with LH (Eggermont, 2018; Flores et al., 2015; Liu et al., 2015).

The counseling protocol, which the counselor typically delivered in a single session over a period of approximately 1 hr, including questions from the patient and discussion, consists of five basic components that help to explain and to educate the LH patient about (a) the transitional intervention strategy, their LH documented by atypically reduced LDLs, and the example of a successfully treated patient (comparing pre- and posttreatment LDLs), which highlight the interventional goal of alleviating LH through a recalibration process; (b) the peripheral auditory system and neural connections; (c) central auditory processes and processing, including the introduction of plastic neuronal gain processes within the central auditory pathways; (d) LH modeled as a hyper-gain process, including contributions and habituation of nonauditory central nervous system processes to LH-related distress (i.e., the negative emotional and physiological reactions to offending louder sounds); and (e) the rationale for transitioning from inappropriate use of HPDs to enriched environmental sound exposure as well as use of controlled and protected therapeutic sound (delivered by bilateral ear-worn devices) to achieve the goal of recalibration of hyper-gain processes. This successful outcome will be signaled by the patient's reduced reliance on sound protection and their unhealthy use of HPDs; acceptance of safe and healthy typical sound levels; improved sound tolerance; and, ultimately, resolution of LH and associated distress responses. The counseling session concludes with review and reinforcement of the counseling principles and the objectives of the transitional intervention for the individual. These components of the counseling protocol are described below in detail and generally follow the topics listed in the checklist shown in Table 1. In our transitional intervention protocol, the counseling was scheduled for delivery on the second day of a 2-day treatment visit (Formby, Cherri, et al., 2024). This scheduling of the counseling protocol followed the day after completion of the fitting protocol during which the initial thresholds for LS activation were set in the protective devices and the therapeutic sound levels from the sound generators were fixed bilaterally as described by Eddins et al. (2024).

Table 1.

Checklist of the five main components covered during the counseling session.

Component 1: Overview of the transitional intervention, audiometric results, and treatment goals

Present the general overview of and rationale for the transitional intervention. Review participant's baseline audiometric results. Review participant's baseline loudness discomfort levels and reduced dynamic range (DR) for pure tones. Present treatment goals of improved sound tolerance, an expanded DR for loudness (illustrated with a case example), and an enhanced ability to use appropriate amplification if the patient has hearing loss.

Component 2: Overview of peripheral auditory anatomy and neurophysiology

Explain the anatomy and physiology of the auditory system. Describe outer, middle, and inner ear components (relate to patient's hearing). Explain that people hear at the brain (auditory system acts as a transformer). Describe the structure and function of inner (IHCs) and outer (OHCs) hair cells with reference to sound tolerance (IHCs: hearing; OHCs: fine tuning and instantaneous gain adjustment). Explain afferent/efferent neural control of peripheral auditory gain. Introduce the gain dial concept: If auditory input is reduced (i.e., earplugs), then the brain will “turn up the gain” in an attempt to enhance the input.

Component 3: Overview of the central auditory system and gain control processes

Explain how the brain handles the input from the peripheral auditory system. Describe subcortical areas: monitoring and filtering; role in adjusting the gain dial. Describe cortical areas: loudness perception following gain dial increase. Discuss that the resulting LH reflects plastic gain processes that are overcompensating for reduced peripheral input to the central auditory pathways. This is represented by the clockwise rotation setting of the gain dial. Controlled sound therapy is designed to turn down (i.e., recalibrate) the gain to restore normal homeostasis within the auditory pathways, leading to resolution of LH.

Component 4: Hyper-gain and nonauditory processes contributing to LH and LH-related distress

Explain the normal-gain system. Explain the hyper-gain system in reference to the normal-gain system using the gain dial diagram. When related to the patent condition, explain pain hyperacusis as a maladaptive hyper-pain–gain process that is plastic and malleable. Explain the associated emotional (limbic system) and physiological (autonomic nervous system) reactions, when these negative reactions are related to the participant's condition, and their roles in giving rise to comorbid conditions of misophonia (i.e., annoyance hyperacusis) and phonophobia (i.e., fear hyperacusis).

Component 5: Recalibration of central gain using sound therapy

Explain the functions of the treatment device, emphasizing the importance of low-level sound therapy as the primary tool in “turning down the gain” within the auditory pathways. Show another example of positive treatment effects for a patient with LH. Explain the secondary role of sound therapy in the process of habituation of emotional responses and physiological reactions to LH, which reduces activation of the limbic and autonomic nervous systems, respectively; the resulting effect is to weaken and disrupt these subconscious neuronal connections with the hyper-gain processes within the central auditory pathways. The associated LH-related distress and negative reactions thus resolve as the hyper-gain processes undergo recalibration. Recalibration of gain within the hyper-gain auditory pathways restores the normal-gain system resulting in resolution of LH. Explain the diagram comparing normal loudness perception in contrast to sound deprivation and LH as a function of treatment device, emphasizing the importance of low-level healthy sounds in the restoration of a full DR. Avoiding silence: Keep a low level of neutral sound on at all times, day and night. Examples are a fan, computer, sound machine, nature tape, humidifier, or fountain set at low volume. Use appropriate noise protection (earplugs only when needed), but not overprotection. Provide a summary sheet for the counseling session and address participant's questions and concerns as relevant to the intervention and their LH condition.

Note. LH = loudness-based hyperacusis.

The First Component: Overview of the Transitional Intervention, Audiometric Results, and Treatment Goals

The first component begins with an overview of the intervention. This component introduces the importance of the counseling and how it, together with therapeutic sound, has been used successfully in the clinic for more than 30 years to treat sound tolerance problems (Gold et al., 2000; P. J. Jastreboff, 2019). This information is followed by a review of the individual's audiometric results, including the audiogram, speech test results (i.e., spondee thresholds, word recognition scores, and speech-in-noise scores), the LDLs, and the auditory DR. Their reduced LDL values and DRs are discussed, which are explained as explicit representations of LH and implicit indices of the underlying elevated auditory gain. After the review and explanation of these results, we briefly explain that, after successful treatment to recalibrate the elevated auditory gain processes (which are plastic and responsive to sound-induced manipulation), affected individuals can expect incremental increases in their LDLs and expansion of their DRs. The resulting improvements in LH will enable them to better tolerate typical sound environments that were intolerable before treatment. To illustrate a successful treatment outcome, we present the example of a patient with LH reported by Formby and Gold (2002), who achieved treatment success with a TRT-based protocol that implemented some of the basic treatment principles used in our intervention. This example presents the patient's audiometric thresholds and the LDLs measured prior to and over the course of their successful treatment. The measurements are characterized by large posttreatment incremental shifts in the patient's LDLs across frequency (without change in the audiometric thresholds), leading to improved sound tolerance and resolution of LH. The results for this exemplar patient serve to illustrate and highlight the goal of our transitional intervention. If the patient has hearing loss and is a hearing aid user, then we explain that a successful treatment may allow them to increase the amount of amplification that they can tolerate comfortably (Formby et al., 2017). That is, a positive treatment outcome will offer them an expanded aided DR with associated benefits for aided listening. This initial introductory component of the counseling concludes with reinforcement of the objectives and goal of the treatment protocol, with counselor responses to patient questions and/or concerns.

The Second Component: Overview of Peripheral Auditory Anatomy and Neurophysiology

In the second component, the counselor describes and explains the anatomy and physiology of the outer, middle, and inner ear. The pinna is described as the structure that captures and transmits sound to the eardrum, the window to the middle ear. The middle ear is described as an air-filled space with a chain of three interconnected bones that transmit the sound-induced vibrating motion of the eardrum to the inner ear. The inner ear is described as the organ responsible for hearing and balance. Balance stimuli are conveyed by vestibular structures within the inner ear. Their stimulation provides information to the brain that informs us where our head is in the environment and other information that aids our spatial orientation. The cochlear portion of the inner ear is the sensory organ for hearing. Sound transmission from the middle ear activates the cochlea, which is described as a spiraling fluid-filled tube that contains the sensory structures for hearing, the inner hair cells (IHCs) and outer hair cells (OHCs). These hair cell structures are delineated, along with the concept of electrochemical transduction. The IHCs are described as the primary sensory transducers for hearing. They are innervated by afferent nerve fibers that convey the information from the sound stimulation through complex central auditory pathways to the auditory cortex of the brain. The functions of the OHCs are explained to be those of fine tuning and instantaneous gain adjustment, which boost our sensitivity to low-level sounds. Efferent feedback processes, controlled by the brain, contribute to the latter. Also, we note that constant low-level activity from the hair cells gives rise to spontaneous neuronal activity in the absence of external sound. A cross-sectional view of the cochlea, highlighting the basilar membrane and the hair cells, is displayed when this information is presented. Here, we point out for the patient that the OHCs are more susceptible than the IHCs to acoustic trauma and the effects of aging (Schaette, 2018). The frequency specificity of the basilar membrane is explained as a continuum, with the basal end tuned to high frequencies and the apical end tuned to low-frequency sound stimulation. After having explained the anatomy and function of the auditory inner ear, the counselor clarifies for the patient that the sound stimulation transduced by the ear leads to processing and perception within higher centers of the brain. This concept is elaborated in the third component of the counseling.

The Third Component: Overview of the Central Auditory System and Gain Control Processes

The third component focuses on the central auditory pathways and transmission of sound inputs from the auditory periphery. The counseling begins with an anatomical illustration of the subcortical auditory structures and afferent auditory fiber tracts between these structures and the auditory cortex. Similar to the structured counseling of TRT and the corresponding imagery (e.g., M. M. Jastreboff & Jastreboff, 2002), a simplified block diagram of the auditory periphery and the subcortical auditory pathways then is presented. The diagram includes both afferent input to higher cortical centers and corresponding efferent output representing neural feedback connections back to these lower level peripheral and subcortical auditory structures (see Figure 1). The concept of central auditory gain is introduced and described by a “dial initially set to 0” (i.e., in a typical state of neuronal equilibrium or homeostasis). The turning of the dial clockwise represents an increase in gain that results in an increase in the perceived strength of the auditory signal (i.e., the signal is perceived as louder). Gain control and modification is explained in terms of neuronal plasticity, which the counselor relates as an adaptive compensatory operation within the central auditory pathways. Growing evidence indicates that processes at multiple levels within the central auditory pathways contribute in various ways to auditory gain control (Auerbach et al., 2014; Chen et al., 2015; Eggermont, 2018; Munro et al., 2014; Roberts et al., 2018; Salvi et al., 2021; Wong et al., 2020). Experimental conditions that are believed to induce LH in animals indicate that these neuronal processes may incrementally amplify neural gain at progressively higher levels within the central auditory pathways in response to reduced peripheral input from damaged cochlear processes. The resulting amplification leads to the largest suprathreshold gain response at the level of the auditory cortex (Auerbach et al., 2014, 2019; Salvi et al., 2021); the latter may be further compounded and augmented through neuronal interactions and connections with nonauditory subcortical and cortical processes (Chen et al., 2015; Salvi et al., 2021). Animal studies indicate that the inferior colliculus (IC) may be an especially important neural structure in controlling central gain (Auerbach et al., 2014; Brotherton et al., 2015; Salvi et al., 1990). The IC receives binaural input from the superior olivary complex and lateral lemniscus, which is consistent with LH being a binaural condition.

Figure 1.

Normal-gain system with the “gain dial” setting at 0, representing no increased central gain (i.e., inhibitory and excitatory central neural auditory pathway processes in equilibrium).

The IC and other subcortical auditory mechanisms initiate the processes of isolating and enhancing the auditory signal as it is transmitted to the auditory cortex; this processing may occur in at least three ways (P. J. Jastreboff & Hazell, 2004). The first way is through selective perception of important and unimportant information that is conveyed by the auditory signal via efferent connectivity from the cortex. The important information is passed on to higher auditory centers, whereas the unimportant information is not passed upstream (P. J. Jastreboff & Hazell, 2004). The second way is through sensory contrast. The auditory signal is compared to its neuronal background, and the greater the contrast between the foreground signal and the background, the greater the perceived signal strength (P. J. Jastreboff & Hazell, 2004). The third way is through prioritization, which represents processes that enable us to focus attention on and give importance to some signal inputs over others (P. J. Jastreboff & Hazell, 2004).

The counselor explains to the patient the concept of central auditory pathway plasticity, emphasizing the remarkable adaptive capacity to decrease or increase neuronal gain and modulate loudness perception based on chronic increases or decreases in peripheral sound input to the central auditory system (Formby et al., 2003; Formby, Sherlock, et al., 2007; Fournier et al., 2014; Munro & Blount, 2009; Munro & Merrett, 2013; Munro et al., 2014; Noreña & Chery-Croze, 2007). This component of the counseling establishes the bases for our intervention, which relies on the plasticity of higher auditory centers in response to controlled therapeutic sound (as an input stimulus to the central auditory pathways) to downregulate the elevated central auditory gain processes of the patient with LH. It is this sound-induced recalibration of central gain processes that we represent by the “turning down the gain dial” in the model diagram.

The Fourth Component: Hyper-Gain and Nonauditory Processes Contributing to LH and LH-Related Distress

To explain LH, the underlying hyper-gain response within the central auditory pathways, and how this elevated gain response can be manipulated and downregulated, we return to the schematic model of the normal auditory pathways with neural gain processes at equilibrium (i.e., neural excitatory and inhibitory activity in balance), shown in Figure 1. Again, we explain that this homoeostatic state is represented in the model by a “gain” volume control setting at “0.” This model and imagery, adapted conceptually from P. J. Jastreboff and Jastreboff (2000, 2014, 2016) and P. J. Jastreboff and Hazell (2004), consists of representations of an external sound source and its input to the peripheral and central auditory systems. The terminal structure in the block diagram of the normal-gain system is a representation of the cortical mechanisms responsible for hearing. The “hyper-gain” model of LH is then presented with the auditory pathways shown to be like the normal-gain system except for an abnormal increase in suprathreshold sensitivity, or gain, within the subcortical auditory structures (see Figure 2). This augmented gain results in amplification of the sound stimulation within the central auditory pathways, reflecting compensation for reduced sound input from the auditory periphery (or from lower levels of the central auditory pathway). Again, the hyper-gain condition is represented schematically by turning of the gain volume control clockwise to increase the system's sensitivity. It is this hypothetical enhancement of the neuronal response to the auditory signal by hyper-gain processes that we and others believe gives rise to LH (see Auerbach et al., 2014; Brotherton et al., 2015; Eggermont, 2018; Formby, Sherlock, et al., 2007; Hazell & Sheldrake, 1992; Pienkowski et al., 2014; Roberts et al., 2018; Salvi et al., 2021).

Figure 2.

Hyper-gain system with the “gain dial” turned clockwise to represent the increased central gain that gives rise to loudness hyperacusis (LH) and associated activation of neuronal connections that contribute to the subconscious and conscious negative emotional and physiological reactions to LH.

To represent the negative reactions to LH (the associated distress and stress responses) and introduce Jastreboff's concepts of misophonia (annoyance hyperacusis; Tyler et al., 2014) and phonophobia (fear hyperacusis; Tyler et al., 2014; see P. J. Jastreboff & Jastreboff, 2000, 2014, 2015, 2016), and the poorly understood condition of pain hyperacusis (Tyler et al., 2014), we add to the hyper-gain model (shown in Figure 2) the contributions from the limbic and autonomic nervous systems (P. J. Jastreboff & Hazell, 2004). The model for pain hyperacusis presumably includes one or more additional pathways, which are not shown here.

Neuronal connections between the limbic system, which controls emotions, and the hyper-gain central auditory pathways are denoted. It is explained that the relative strength of these subconscious, nonauditory connections increases (or decreases) the distress associated with the LH hyper-gain response, while also determining the annoyance to specific sounds or classes of sounds and the fear of specific sounds or classes of sounds. The autonomic nervous system, which is responsible for our negative physiological responses and related stress reactions to sound (i.e., hypervigilance and hyperarousal), is also shown with corresponding neuronal connections to the limbic and hyper-gain central auditory pathways. The relative strength of the neuronal connections with these subconscious processes, when elevated in LH, augments associated negative reactions to all offending sounds and, when relevant, the annoyance, anxiety, fear responses, or some combination of these to specific offending sounds, giving rise to misophonia and phonophobia. Hence, whenever the affected listener is exposed to emotionally and anxiety-provoking sounds, the resulting responses, or negative reactions, from the limbic and autonomic nervous systems are activated. The activated response may be further magnified when cognitive resources and conscious thoughts (e.g., perseverating worry that the hyperacusis condition will worsen) are involved. Cortical connections then feed into connections with the associated subconscious processes to create a vicious feedback loop. It is at this point in the counseling that the counselor explains passive habituation of LH-related distress responses and other associated negative emotional and physiological reactions to sounds that are offending for the debilitated patient with LH. This passive habituation process is explained in terms of reducing and, ultimately, habituating the neuronal connections between the hyper-gain central auditory pathways, the limbic system, the autonomic nervous system, and other higher neuronal centers of the brain that form the negative feedback loops in the model.

The Fifth Component: Recalibration of the Central Gain System Using Sound Therapy

The focus of the counseling in the last component is to explain the use and role of therapeutic low-level broadband sound in the recalibration (downregulation) of hyper-gain sensitivity within the auditory pathways. In our intervention, this neutral sound therapy is provided by bilateral behind-the-ear sound generators, supplemented by healthy, enriched environmental sound sources within the home. This hyper-gain recalibration process is illustrated schematically in Figure 3 and explained below.

Figure 3.

Normal-gain system following recalibration of central gain (R_G) to ameliorate loudness hyperacusis (LH) and habituation of negative emotional (H_E) and physiological reactions (H_R) associated with LH.

The counselor initially explains that sound therapy plays a secondary role in facilitating habituation of the negative emotional and physiological reactions associated with LH-related distress. As habituation of the LH-related negative reactions progresses, the ongoing exposure to controlled low-level neutral sound leverages the plasticity of the central auditory pathways, downregulating the elevated neuronal sensitivity and hyper-gain processes. This is the recalibration response that is critical for alleviating LH in our intervention. In turn, as the hyper-gain neural response within the central auditory pathways is diminished through sound-induced recalibration, there is less activation of the conscious cortical processes and the nonauditory subconscious processes. In the theoretical model of the hyper-gain system depicted in Figure 2, the former processes interconnect with the latter processes and act to further amplify the negative emotional and physiological reactions to LH. Thus, sound therapy plays a dual role in downregulating the hyper-gain sensitivity within the central auditory pathways, while, along with counseling, also reducing activation of conscious and subconscious processes that contribute to the associated negative reactions (i.e., the related distress, anxiety, and inordinate aversion responses that are comorbid in some hyperacusis cases) to LH (P. J. Jastreboff & Hazell, 2004; Tyler et al., 2014). Accordingly, the habituation and reduction of the negative reactions proceeds as gain recalibration progresses over the course of the intervention. Ultimately, with successful intervention, the neuronal connections between the conscious and subconscious processes, which contribute to the negative reactions associated with LH, will be habituated. In turn, the hyper-gain central auditory pathway response will be recalibrated to a homeostatic state to ameliorate LH. The resulting model, shown in Figure 3, then is identical to the normal-gain model of the auditory pathways with the neural gain processes returned to their equilibrium, as depicted in Figure 1.

For many debilitated patients with LH, the willingness to accept and use therapeutic sound is diminished by their use of protective earplugs, earmuffs, or both. Here, the counselor explains that the use of HPDs can be counterproductive to the objectives of sound therapy and the treatment intervention (Formby et al., 2003; Formby, Sherlock, et al., 2007). Furthermore, it is explained that the long-term overuse of sound protection limits exposure to healthy louder sounds that are important for maintaining the typical DR for loudness (i.e., for most persons with normal hearing, the typical DR between their audibility thresholds and LDLs is 95–100 dB; Sherlock & Formby, 2005). To facilitate the transition from HPDs to acceptance of sound therapy, the counselor encourages the patient to use safe neutral sound sources (fans, recordings of nature sounds, etc.), under controlled conditions within the home, without the use of HPDs. Additionally, each patient is provided with the neutral low-level broadband noise stimulation from their bilateral sound generators. The counselor encourages sound generator use as much as possible throughout the waking day. The device may be fit with open domes or with an occluding custom earpiece (see Eddins et al., 2024), and the patient is instructed on how to change the earpiece as part of the initial orientation to device use. The counselor encourages the patient's use of the open domes as much as possible in situations that they deem no risk or low risk for offending sounds (i.e., situations for which they would normally not wear earplugs). When the patient is in uncontrolled sound environments, or environments where offending sound levels are encountered, they are encouraged to use the custom occluding earpiece. This earplug-like earpiece will provide hearing protection against offending louder sounds without sacrificing audibility. The custom earpiece functions like a very good HPD. When coupled to the behind-the-ear devices, the attenuating effects of the custom earpiece are offset by unity-gain amplification, which allows transparent passage of healthy, comfortable sounds without reduction in the sound level. A secondary sound protection feature afforded by the device attenuates only high-level sounds. The custom earpiece also affords delivery of therapeutic sound from a sound generator built into the treatment device. As treatment progresses and sound tolerance improves, the patient with LH is encouraged to use the open domes increasingly more outside of the home under safe conditions. This use of the open domes allows for more natural sound input, facilitating the recalibration process without the need for the occluding earpieces. This recommendation is increasingly emphasized as treatment progresses, especially near treatment end as the LH condition resolves over the course of a successful intervention.

At this point in the counseling, the counselor presents a new diagram, shown in Figure 4. The counselor uses this figure to compare and contrast the counterproductive effects of sound-attenuating HPDs with the protective component of our intervention implemented together with therapeutic sound enrichment. The counselor also uses this visual aid to compare hypothetical loudness responses for very soft, comfortable, loud but OK, and uncomfortably loud sounds for individuals with normal sound sensitivity and with LH as well as when they are using sound-depriving earplugs or our protective treatment devices. The counselor explains that earplugs attenuate all sound levels by a constant amount. Consequently, sound levels that are judged to be very soft for a typical ear may be inaudible for the patient with LH when earplugs are used. The loudness for higher level sounds also is systematically reduced for all listeners when earplugs are used, but the loudness for these higher level sounds is relatively much greater for the patient with LH than for the typical listener (either with or without the use of earplugs). Accordingly, the resulting auditory DR (for loudness) for patients with LH, which is already reduced by the effects of LH, is further reduced and is even more limited by the use of earplugs. Moreover, the counselor reiterates that overuse of sound-attenuating earplugs may exacerbate hyper-gain processes, ultimately making the LH problem even worse (Formby et al., 2003; Formby, Sherlock, et al., 2007). Thus, the counterproductive effects from earplug use compound an already difficult listening problem for individuals with LH, while hindering and retarding treatment.

Figure 4.

Schematic illustration of sound environments and associated loudness perception for individuals with normal loudness sensitivity (Column 2), hyperacusis (Column 3), sound-attenuating earplugs (Column 4), and treatment devices (Column 5). Waveforms in blue represent normal loudness perception to each associated sound environment (in dB HL), whereas waveforms in red represent abnormal or undesirable loudness perception due to either hyperacusis (at high-level sound environments; Column 3) or the use of earplugs (at low-level sound environments; Column 4). Waveforms in black represent the altered loudness perception that both earplugs (Column 4) and treatment devices (Column 5) provide for high-level sounds (also emphasized by the thick black border).

The counselor then explains our solution to overcoming the limiting and counterproductive effects of sound-depriving earplugs. Our intervention approach is to use a protective treatment that we achieve with special hearing devices used bilaterally. Each of the pair of devices incorporates a therapeutic sound generator in combination with digital output limiting to limit exposures to potentially offending loud sounds. Per Sammeth et al.'s (2000) previous nomenclature, we refer to this application in which high amounts of output limiting are used to limit a hyperacusis patient's exposure to potentially offending sound levels as LS (see Eddins et al., 2024). The counselor uses the diagram to illustrate and explain that this device limits offending louder sounds so that these sounds never become uncomfortable. The device includes a snugly fitting earmold. The resulting sound-attenuating effects are offset by unity-gain amplification, which restores typical audibility for low-level sounds. The counselor, using the diagram, points out that the loudness for all sound levels between the audibility threshold and the LS activation threshold set in the protective treatment instrument will be heard in a similar way to those with normal sensitivity and loudness. Thus, over this range, the operation of the protective treatment device will be “transparent.” The counselor concludes the use of the diagram by emphasizing that the loudness of typical environmental sound levels that exceed the LS activation threshold of the protective device will be suppressed and restricted to acceptable limits; these higher sound levels therefore will remain tolerable (i.e., loud but OK) when using the protective device. As treatment with therapeutic sound progresses and the affected individual with LH gradually becomes more tolerant of higher sound levels, the LS activation threshold set in the protective treatment device will be released, and thus increased, systematically. The resulting progressively higher threshold settings will allow for increased exposure to safe and healthy higher sound levels consistent with recalibration and downregulation of the hyper-gain system and improvements in the patient's LH condition over the course of the intervention. The counselor explains that the systematic release from the protective LS is a gradual process allowing the patient to be exposed progressively to safe healthy higher sound levels. This controlled sound exposure is ultimately essential in our intervention for restoring typical sound tolerance and sustaining a normal wide DR for loudness. Otherwise, the ongoing use of the LS set in the protective treatment device at the start of the intervention (which produces the most sound-limiting compression in our intervention) would continue to restrict exposure to the reduced sound levels that we measured pretreatment. Accordingly, the controlled and systematic release of the protective LS over the course of the intervention is necessary to overcome detrimental effects that otherwise would be counterproductive to the recalibration response, treatment-related improvements in sound tolerance with associated expansion of the DR, and resolution of LH.

The counseling session is ended by contrasting the ideas of protection versus overprotection, emphasizing the detrimental impact on the auditory system of prolonged silence and isolation from typical healthy sound exposures. This overprotection, either with or without HPDs, is counterproductive and can adversely increase auditory system gain. The resulting elevated gain, in turn, exacerbates the severity of the hyperacusis condition, making LH more challenging to treat while prolonging the debilitating condition. Accordingly, it is critical for an individual with LH to transition expeditiously from conditions of overprotection to those that allow for exposure to healthy environmental sounds. This objective can be achieved with sensible and judicious use of sound protection, including controlled use of our protective treatment device as part of the transitional intervention in uncontrolled sound environments. The importance of exposure to safe healthy sounds at all times is emphasized, along with avoidance of silence. The counselor reiterates the past success of this basic intervention approach by highlighting again the positive treatment results achieved by successfully treated persons with LH. It is noted that the passive intervention process is patient dependent and gradual, taking advantage of the natural plasticity of the auditory system. Finally, patient questions and concerns are addressed. A summary sheet of the information provided in the counseling and a set of recommendations are provided for the patient to take home and review. This latter information is shown in the Appendix.

Reinforcement of Counseling Concepts at Follow-Up Visits

The counseling principles described above were reinforced at monthly follow-up visits over the course of the six-visit (spaced by approximately 1 month each) intervention period of our trial (Formby, Cherri, et al., 2024). The counselor discussed with each study participant their progress and provided a printed summary of the initial counseling session (see the Appendix). At each follow-up visit, the study participants were reminded of the importance of their diligent use of low-level therapeutic sounds at all times for promoting “auditory gain” recalibration. The usage of the open domes, which are fitted to the treatment devices, was encouraged as the participant evidenced improvement in the LH condition. Open-dome use was again explained in terms of allowing more natural sound input in controlled, healthy sound environments in combination with the delivery of therapeutic low-level sounds from their ear-level devices (without the use of protective LS). The counselor also reinforced the ongoing usage of neutral, low-level, enriched environmental sounds (e.g., fan, sound machine, or television at low volume) in the home to facilitate the recalibration process. The counselor concluded each follow-up visit by addressing relevant questions and concerns, while offering ongoing encouragement to foster a successful intervention.

Discussion

Our counseling protocol, when used together with protective sound management and therapeutic sound, yielded statistically and clinically positive treatment effects and outcomes in a 6-month intervention for debilitating LH (see Formby, Cherri, et al., 2024). It is not, however, without limitations. These shortcomings stem in large part from the limited understanding of hyperacusis (and the related abnormal perceptual conditions associated with LH). Also, absent controlled studies, we can now only speculate on the mechanisms of the counseling effects separate from those of the protective sound management and therapeutic sound components of our intervention, and the contributions of the individual counseling components to the transitional intervention are uncertain.

The content of the scripted counseling in our transitional intervention was distilled and streamlined to facilitate delivery of essential concepts and principles at a level appropriate for most adults. Some of the more challenging, speculative, and difficult concepts to present were simplified or eliminated from the protocol based on previous experiences in providing this and related information in the clinic (Gold et al., 2000), in our previous studies (Formby et al., 2015; Gold & Formby, 2017; Gold et al., 2021; Scherer & Formby, 2019; Scherer et al., 2020), and in practice to become facile with delivery of the counseling content preliminary to trial initiation. Also, some of the concepts introduced in our counseling, although clearly relevant and prominent in the literature, are at this time not well understood or fully developed. This incomplete understanding includes limited knowledge of the physiological mechanisms and processes by which neutral low-level noise stimulation induces gain recalibration and amelioration of LH (Henry, 2022; Sheppard et al., 2017), notwithstanding clear evidence for positive treatment effects from enriched sound therapy presented above and throughout this report. Another thorny issue in the theoretical component of our counseling is why the chronic reduction in sound input consequent to sensorineural hearing loss does not routinely result in clinical evidence of hyper-gain responses and a much higher prevalence of LH in the literature. We would expect ample evidence of both since all forms of hearing loss reduce the peripheral input to the central auditory pathways and, therefore, should affect compensatory increases in central auditory gain. Perhaps because the deleterious effects of presbycusis and many common forms of recreational and occupational noise-induced hearing loss are gradual, the auditory system may be able to adapt to the gradual reduction in audibility to maintain a relative state of balance between the inhibitory and excitatory central neural auditory processes. This ongoing compensation for subtle auditory damage would contrast with an inability or lesser ability of affected auditory neurological processes to offset more dramatic effects of an unexpected and sudden one-time event such as an acoustic shock (Westcott, 2006), blast, or concussion (Theodoroff et al., 2022) incident. These are the kinds of insults that are most readily ascribed to an obvious causal association with hyperacusis. One can appreciate that these latter deleterious “black swan” incidents are immediately disruptive, both neurologically and emotionally, and are much more catastrophic and distressing than most common forms of sensorineural hearing loss, whose effects tend to be subtle and ongoing over relatively long periods. However, this discrepancy continues to be a conundrum that we do not address in our counseling (see Pienkowski et al., 2014, for their attempts to address this issue).

Another perplexing issue is why some persons with decreased sound tolerance, consistent with LH, suffer associated disabling pain whereas others do not. In a retrospective analysis of the records of patients treated with TRT in a leading specialty clinic for tinnitus and hyperacusis, we determined that only about half of the patients who reported or exhibited evidence of decreased sound tolerance, consistent with LH, complained of sound-induced pain sensations (Formby, Gold, et al., 2007). Accordingly, we included a separate model diagram with a separate pathway to represent pain hyperacusis in our current counseling protocol. At this time, although there is considerable interest in pain hyperacusis, this disabling condition remains poorly understood and may represent one or more conditions with different origins and neural circuitry (Colucci, 2021; Pollard, 2019; Salvi et al., 2022; Suhnan et al., 2017; Tyler et al., 2014). This circuitry may involve nontraditional auditory neural pathways that combine with neural tracts from other sensory systems, most notably the somatosensory system. The latter mediates classical pain sensations. Møller et al. (2005) note that polysensory neurons in the nonclassical (extralemniscal) pathways are broadly tuned and project from the dorsal and medial thalamus directly to the amygdala, other brain structures, and the secondary and association cortices. These nonclassical neural pathways bypass processing in the primary auditory cortex and other primary sensory cortices, which receive their projections from the ventral thalamic nuclei (the classical auditory and primary sensory pathways). Whereas the nonclassical pathways convey neural information to the amygdala that has undergone little processing by the primary sensory centers of the brain, the classical sensory pathways, including the primary auditory pathways, carry highly processed information that is sharply tuned and specific to each sensory system. Thus, the nonclassical neural pathways provide a substrate for cross-modality interactions between the auditory and somatosensory systems. These somatosensory connections with nontraditional auditory fiber tracts could contribute through maladaptive neuroplastic changes to auditory pain sensations and to the related undue distress (mediated by the amygdala) that some individuals with hyperacusis report. Here, it is worth mentioning that Møller et al. suggested TRT represents one example of therapeutic sensory stimulation for reversing such maladaptive neural plasticity. Nociceptive pain processes, which operate through neural feedback within the central nervous system to detect and signal avoidance of potentially damaging and dangerous stimulation, have also been proposed as a mechanism for pain hyperacusis (Colucci, 2021; Flores et al., 2015).

Also mentioned and represented in our various model diagrams, but not considered in detail in our counseling, is a possible role of the efferent system in regulating gain processes within the auditory pathways. Early on, Hazell and Sheldrake (1992) speculated that their positive sound therapy effects for tinnitus patients with hyperacusis may have been mediated through efferent neural activity operating at the cochlear level. We have previously considered this role and dismissed it because of the relatively small and short-term nature of these efferent effects (Formby & Gold, 2002). Efferent fiber tracts, however, run parallel to the afferent neural circuitry throughout the auditory pathways, including corticofugal tracts from the auditory cortex that project back to the medial geniculate body of the thalamus, the IC, and subcollicular auditory nuclei. Corticofugal activation has been established as a mechanism by which auditory gain processes can be controlled and manipulated, including gain plasticity elicited by auditory fear conditioning through the amygdala (see Suga & Ma, 2003). Corticofugal modulation of cochlear processes also may be mediated through activation of olivocochlear neurons in the superior olivary complex. Thus, an efferent role in LH and in the treatment of hyperacusis cannot be ruled out as a significant contributing process (Schaette, 2018).

As noted above, our counseling protocol was based on principles and concepts proposed in Jastreboff's neurophysiological model of hyperacusis (P. J. Jastreboff & Hazell, 2004; P. J. Jastreboff & Jastreboff, 2014, 2016). The early strength of the Jastreboff model was his recognition of the contributions of nonauditory processes, specifically the activation of the limbic and autonomic nervous systems, in the development of the negative reactions and distress response secondary to the activation of the hyper-gain auditory processes responsible for LH. Chen et al. (2015) and Salvi et al. (2021) have proposed a more complex model of hyperacusis based on updated experimental evidence and imaging studies. Their model of hyperacusis implicates key central auditory centers and a broader constellation of nonauditory processes. Specifically, they model hyperacusis as enhanced functional connectivity between the hyper-gain auditory neural network and hyperactive nonauditory neural processes responsible for emotions (amygdala), arousal (reticular formation), -and spatial navigation (hippocampus), motor planning (cerebellum), and motor control (caudate putamen). This enhanced functional connectivity and associated nonauditory neural hyperactivity contributes in their model to further exacerbation of the hyperacusis condition, with associated negative reactions, in a manner like that originally proposed in the simpler Jastreboff model. Accordingly, this additional level of detail and neurological involvement, although important knowledge, would not appear to appreciably enhance the presentation of these basic concepts in our treatment model and the intervention outcome.

Given the issues and considerations above and their theoretical nature, as they relate to the content of our counseling protocol, it is not clear that additional information and level of detail (such as that represented in more complex models of hyperacusis), even if presented, would appreciably improve this counseling protocol in a meaningful way that augments the transitional intervention outcome. In fact, it is not obvious now which components of our counseling protocol are necessary for achieving a positive treatment effect beyond those of convincing the patient that the intervention is potentially worthwhile and merits a trial. Indeed, perhaps some other sensible scientifically based counseling protocol, devoid of elements of the counseling that we deemed important in our transitional intervention, may be combined with our protective sound management and therapeutic sound protocol to achieve comparable, or possibly even better, treatment effects and outcomes than we obtained (Formby, Cherri, et al., 2024). Randomized clinical trials with comparison control assignments of the kind used by Formby et al. (2015), Formby et al. (2022), and Scherer and Formby (2019) would be needed to tease out the mechanisms and key contributions from the counseling to the effects of our transitional intervention. In the future, current and other content information may be expanded or adjusted in our counseling protocol as new evidence indicates the need to revise. For now, the structured counseling protocol described in this clinical focus article presents the necessary concepts and principles, at an appropriate level of detail, for most adult patients to achieve success with our transitional intervention for LH. We note, however, that to date, we have not formally evaluated the counseling content and related counseling materials for patient accessibility. Based on our experience with and our use of these and related counseling protocols and materials in prior randomized controlled trials (Formby et al., 2015, 2022; Gold & Formby, 2017; Gold et al., 2021; Scherer & Formby, 2019; Scherer et al., 2020) and in a clinical setting (Gold et al., 2000), we are confident that our content level is appropriate and applicable for use with most adult patients having at least a high school education when delivered by a competent and knowledgeable counselor in an interactive counseling session.

Conclusions

This clinical focus article has presented the background and motivation for, and a detailed presentation of, a structured counseling protocol. The protocol is a narrative script with associated visual aids to be used with a companion protected sound management and therapeutic sound protocol (Eddins et al., 2024), implemented in a patented transitional intervention for debilitating LH (Eddins et al., 2020). The structured counseling protocol was crafted to educate the patient about the auditory system and its function; their LH condition and associated negative reactions that contribute to related distress and stress responses; and corresponding models of auditory and nonauditory processes representing hyper-gain, emotional, and physiological processing associated with LH. The counseling introduces the rationale for and goal of the transitional intervention leading to recalibration of the hyper-gain processes; habituation of the negative reactions; and, ultimately, resolution of LH and the associated distress. It is emphasized in the counseling that self-isolation from sound as well as misuse and overreliance on HPDs are known barriers to resolution of LH and a successful intervention.

We show in a companion report that this counseling protocol in combination with therapeutic sound and protected sound management can be implemented successfully in a progressive intervention to transition debilitated patients with hyperacusis from inappropriate or overuse of counterproductive sound-attenuating HPDs, or both (Formby, Cherri, et al., 2024). Moreover, we document that, over the course of the transitional intervention, the LH condition is substantially improved for 11 of 12 study participants as their sound tolerance progressively increases with corresponding return to daily activities not previously possible without the use of sound-depriving HPDs. Patient reports posttreatment highlight perceived benefit from counseling in the transitional intervention.

Appendix

Summary of the Counseling Session

• This counseling and sound-therapy treatment has been used successfully in the clinic for at least 25 years. This study has been designed to evaluate an enhanced sound therapy protocol with protective sound management implemented with a special device for treating your debilitating hyperacusis.

• Hyperacusis is an abnormally strong reaction to sounds within the auditory system. It is manifested by inordinate discomfort to sounds that would not evoke a similar reaction in the average listener.

• Lower-than-normal loudness discomfort levels (LDLs), typically less than 75 dB HL, are consistent with problematic primary hyperacusis.

• Our goal is to restore your loudness tolerance to within normal limits. It will be a slow and gradual process, so you should be patient with the treatment.

• The sound therapy treatment involves specialized counseling and controlled exposure to low-level sound from ear-worn devices.

• Primary hyperacusis is a central auditory pathway problem, reflecting an abnormally high-gain setting that makes you more sensitive than normal-to-louder sounds.

• Some people with primary hyperacusis may also develop undue emotional distress (misophonia) and maladaptive physiological reactions (phonophobia) when exposed to sounds.

• The ongoing use of low-level therapeutic sound from sound generators in our intervention, supplemented by enriched neutral environmental sound, normalizes the gain in your auditory system through the process of recalibration. The counseling you received facilitates the habituation of any negative emotional and physiological reactions to offending sounds. Posttreatment, you should be able to perceive most, if not all, sounds similarly to a typical listener.

• The study device also includes an output limiter, or loudness suppression mechanism, that restricts your exposure to potentially loud offending sounds in uncontrolled sound environments. The limiter offers you protection against loud sounds that may be uncomfortable for you. Over time, you should be able to reduce your reliance on the limiter as your sound tolerance improves over the course of treatment.

• Many patients who have successfully completed treatment with a similar sound therapy protocol have achieved the goal of resolving their hyperacusis.

• You should be exposed to healthy sounds as much as possible throughout the day. Try to avoid silence day and night. The therapeutic sound from your sound generators should be reinforced by exposure to healthy environmental sound from other sources such as fans, air conditioners, or sound machines.

Recommendations for You

• Sound-attenuating earplugs and earmuffs can be counterproductive to your treatment. Only use earplugs/earmuffs when you expect to be exposed to loud sounds that may harm your hearing.

• Our goal is for you to be comfortable with all kinds of sounds posttreatment, as was the case prior to your hyperacusis condition.

• Please feel free to contact us whenever you have questions or concerns.

Funding Statement

The development of the counseling protocol described in this clinical focus article was supported by National Institute on Deafness and Other Communication Disorders Grant R21DC015054, awarded to C. Formby and D. A. Eddins.