Framing tinnitus-correlated distress as a brain disorder may contribute to the very distress it seeks to explain

Introduction

A recent Nature Reviews Disease Primer by Vanneste and colleagues is an accomplished synthesis of tinnitus research (Vanneste et al., 2026): a state-of-the-field review covering epidemiology, mechanisms, diagnosis, management, quality of life and future directions. It traces the tinnitus percept to cochlear injury and deafferentation followed by maladaptive plasticity, increased central gain and thalamocortical dysrhythmia “modulated by limbic and salience networks,” and distinguishes the symptom from an accompanying “distress component” hypothesised to be encoded by a “medial, extra-lemniscal pathway that projects to the anterior cingulate cortex, the insula and other regions of the limbic system.” Tinnitus accompanied by such distress is termed “bothersome tinnitus” or, in reflection of previous work (De Ridder et al., 2021), “tinnitus disorder.” The Primer recommends de-catastrophising psychoeducation (“counselling”) and cognitive behavioural therapy (CBT) as first-line care, and its Outlook locates future progress in research concerning biomarkers, gene and regenerative therapies, neuromodulation and the digital delivery of psychological treatment.

Contemporaneously, nine of the Primer's ten authors contributed to a Perspective built on the same conceptual framework (De Ridder et al., 2026). Whereas the Primer synthesises the available evidence, the Perspective extends it into a set of more explicit clinical claims, arguing that the currently descriptive, operational definition of “tinnitus disorder” should also be understood as a theoretical one, identifying a distinct disorder entity with its own presumed aetiology and pathophysiology (De Ridder et al., 2026). Neurophysiologically, the Perspective distinguishes three pathways: “a lateral ‘loudness' pathway, a descending ‘inhibitory' pathway, and a medial ‘distress' pathway that is specifically activated in tinnitus disorder, providing a neural basis for tinnitus related suffering.” On this basis, the Perspective argues that tinnitus disorder should be diagnosed and graded as a distinct clinical entity using standardised diagnostic criteria and severity thresholds based on anxiety and depression questionnaire cut-offs.

Taken together, the two publications may be understood as offering a unified account of tinnitus that is likely to shape both research funding and clinical practice, and to determine what the scientific and clinical community might take the field's current position to be.

The account presented in these papers is necessarily broad. Our concern focuses on how tinnitus-correlated distress is defined, described, explained, classified and putatively addressed within this framework.

Both the Primer and Perspective acknowledge psychological stress as a mechanism of symptom chronification including roles of catastrophising, threat magnification, helplessness and rumination as processes linking psychological vulnerability to suffering. In addition, we do not dispute that tinnitus may be accompanied by substantial distress, cognitive difficulties and functional impairment, nor the importance of the reviewed neurophysiological lines of research. Rather, we argue that the framework progressively shifts the explanatory centre of gravity from the psychological context, content and meaning of distress towards its presumed neurophysiological correlates. In this context, meaning denotes for us

“the person-specific significance that an event, sensation, relationship, or symptom holds for a particular individual, given their developmental history, goals/values, identity, and current relational context. It is expressed in appraisals (“what this implies for me”), and in the functions which emotions and behaviours serve (e.g., to protect attachment, preserve control, signal injustice, avoid shame). It can be explicit (verbalisable beliefs) or implicit (felt tendencies, action patterns), and it is context-dependent and revisable” (Boecking et al., 2026b).

This shift proceeds through a series of moves which are cumulatively consequential. First, distress associated with tinnitus is constituted as a disorder in its own right (Perspective; adopted by the Primer under the heading “bothersome tinnitus” and “tinnitus disorder”). Second, domain-general neural correlates of stimulus processing are hypothesised as encoders of that distress (Primer) and subsequently elevated to putative pathophysiological substrates of “tinnitus disorder” (Perspective). Third, those same correlates are proposed as targets for neuromodulation (Primer). Fourth, the distress taken to define the construct is redescribed through psychiatric comorbidity nomenclature (Primer, Perspective) and then used to anchor a proposed severity classification (Perspective). Fifth, psychological interventions, although acknowledged as first-line treatments, risk being recast as transferable packages of techniques suited to standardised or digital delivery (Primer). Throughout these transitions, five conceptual distinctions are repeatedly collapsed: correlation and causation; description and explanation; neural correlation and psychological meaning; the pragmatic function of diagnostic categories and their transformation into explanatory disorder constructs; and standardised symptom-focused treatment protocols vs. individualised psychological formulations that may include, but are not limited to, tinnitus as index symptom.

Table 1 provides a structured reconstruction of this inferential sequence. For each move, we contrast the claims advanced in the Primer or Perspective with what the cited evidence and the texts' own caveats support, and with interpretations that would follow if neurophysiological correlates were not assumed to constitute the primary explanatory level. Overall, we argue that emotional, cognitive, behavioural, interpersonal, and social contexts, as well as biographical experiences, memories, and the meaning which the tinnitus stimulus acquires within these contexts, contribute to clinical presentations in their own right and should not be reduced to mere downstream consequences of neural events. A framework that implies neurophysiological findings to be inherently explanatory risks decontextualising the processes through which distress is experienced and maintained in lived experience and changed in clinical practice.

Table 1. Inferential transitions through which tinnitus-correlated distress is transformed into a neurobiologically framed disorder entity.

BDI, Beck Depression Inventory; CBT, Cognitive Behavioural Therapy; DBS, Deep Brain Stimulation; HADS, Hospital Anxiety and Depression Scale; NICE, National Institute for Health and Care Excellence; rdACC, Rostral-to-Dorsal Anterior Cingulate Cortex; rTMS, Repetitive Transcranial Magnetic Stimulation; tDCS, Transcranial Direct Current Stimulation; TES, Transcranial Electrical Stimulation; TFI, Tinnitus Functional Index; tFUS, Transcranial Focused Ultrasound Stimulation; THI, Tinnitus Handicap Inventory; TMS, Transcranial Magnetic Stimulation; TQ, Tinnitus Questionnaire; VA/DoD, U.S. Department of Veterans Affairs/U.S. Department of Defense; VAS, Visual Analog Scale.

Throughout the paper, we use “tinnitus-correlated distress” wherever we advance a claim of our own about the relation between percept and distress, since “related” risks being heard as “caused by,” which is an inference the available evidence does not license. We retain “tinnitus-related distress” only when quoting the source texts verbatim or reporting findings under the label used by their authors.

From distress to disorder: the reification of experience into an illness entity

Both the Primer and Perspective papers distinguish tinnitus as a perceptual symptom from distress and functional impairment that may accompany its perception. For the tinnitus symptom itself, the authors provide a neurophysiological account linking peripheral auditory injury to subsequent changes in central auditory processing. Cochlear damage and deafferentation may trigger compensatory alterations in spontaneous firing, neural synchrony, and thalamocortical dynamics. Whilst the mechanisms linking peripheral injury to central reorganisation, and the reasons why only a minority of individuals with hearing loss develop tinnitus, remain incompletely understood, this account provides a clinically useful framework for understanding how the perceptual phenomenon “tinnitus” may initially emerge.

What makes this percept clinically problematic, however, is explicitly acknowledged in the authors' own material. The Primer states that distress severity is shaped not only by sensory factors but also by “affective and cognitive dimensions, including anxiety, depression, and attentional bias towards the phantom percept” (Vanneste et al., 2026). It further discusses neuroticism [i.e., people's “stable tendencies to respond with negative emotions to threat, frustration, or loss” (Lahey, 2009)], sleep disturbance, and stress as relevant contributors to tinnitus-related suffering, while noting that evidence for treatment efficacy largely rests on self-report measures of tinnitus-related distress and functional impairment (Vanneste et al., 2026). Similarly, the Perspective emphasises that psychoacoustic measures, such as loudness matching, pitch matching, maskability and residual inhibition, bear no consistent relation to the self-reported severity or perceived loudness of tinnitus, and that no brain signature corresponds to tinnitus matching or pitch, whereas subjective numeric and visual analog ratings do correlate with activity in the auditory cortex, parahippocampal area, insula and anterior cingulate cortex (De Ridder et al., 2026). Thus, by the authors' account, the key phenomenon that defines “bothersome tinnitus” (Primer) or “tinnitus disorder” (Perspective) is not the perceptual signal itself, but its appraisal, emotional significance, and functional impact.

Whilst this distinction is clinically useful, it can be easily overread. The fact that the percept and distress can be described separately does not establish that they are separable processes, nor does the available evidence support the causal order implied by the term “tinnitus disorder.” The Primer concedes as much, describing the relationship between tinnitus and its psychological “comorbidities” as complex and often bidirectional, with the temporal sequence frequently unclear, and noting that psychological factors can themselves exacerbate the perception of tinnitus (Vanneste et al., 2026).

Our concern lies with the units in which this reciprocity is stated. Framed as comorbidity, bidirectionality holds between disorder categories (i.e., diagnoses) such as “tinnitus and depression,” or “tinnitus and insomnia” whilst leaving the person's experience of the sound unaddressed. General psychological research, by contrast, locates the relevant influences elsewhere. Here, the correspondence between a bodily sensation and its conscious experience is itself variable and depends on (interactions of) a person's characteristics and context (Van den Bergh et al., 2017). What a sensation comes to mean for a person is established through appraisal against their goals, commitments and prior expectations (Lazarus and Folkman, 1984; Scherer, 2009), enduring beliefs about the self and the world formed biographically (Beck and Haigh, 2014), and is elaborated in an effort to reconcile a stimulus with a global meaning system (Park, 2010). From this perspective, emotional experience is not read off the stimulus but constructed from it in context (Barrett, 2017; Boecking et al., 2026b). The same stimulus may acquire very different clinical significance depending on the psychological circumstances in which it occurs. “Tinnitus disorder” names a condition by its symptom, but defines it by its appraisal. Contrary to much clinical communication, mental-health-related syndrome diagnoses remain descriptive operational constructs that group co-occurring features without committing to a specific aetiology (Zachar and Kendler, 2007; Hyman, 2010; Maung, 2019). Re-labelling tinnitus-correlated distress “tinnitus disorder” thus invites a level-crossing in which a correlation is read as a causal direction and “tinnitus,” rather than aetiologically open “distress,” becomes the treatable subject. The relevant clinical question is consequently not “Why is tinnitus distressing?” but “Why is tinnitus distressing for this particular person?”

From correlate to disorder substrate: the causal elevation of neural correlates

Subsequently, the Primer and Perspective papers conduct a second inferential transition by recasting distress primarily in neural terms. Both papers invoke a medial extra-lemniscal pathway linking auditory structures with regions involved in salience and cognitive-affective processing, including the anterior cingulate cortex, insula, and amygdala. Whilst the Primer states that the “distress component of tinnitus” is “hypothesized to be encoded by the medial, extra-lemniscal pathway” (Vanneste et al., 2026), the Perspective more explicitly presents activation within these structures as providing “a neural basis for tinnitus related suffering” (De Ridder et al., 2026).

We do not dispute that distress is associated with neural activity. Rather, we see a difficulty when domain-general correlates of appraisal, salience, and emotional processing are elevated to the status of a pathophysiological substrate of “tinnitus disorder” (De Ridder et al., 2026). The anterior cingulate cortex and the anterior insula are core nodes of a salience network engaged whenever a stimulus acquires subjective relevance, irrespective of its modality or content (Uddin, 2015). Large-scale neuroimaging studies demonstrate that these regions operate non-specifically across multiple cognitive and affective domains (Poldrack, 2011; Yarkoni et al., 2011). This non-specificity extends across heterogeneous clinical populations. For example, a meta-analysis of 193 voxel-based morphometry studies in 15,892 individuals found grey matter reductions converging on the dorsal anterior cingulate and bilateral anterior insula across six psychiatric diagnoses (Goodkind et al., 2015). Moreover, a meta-analysis of 298 functional imaging experiments in 5,427 patients reported the same regions among those showing shared rather than diagnosis-specific disruption during general emotional processing (McTeague et al., 2020). Thus, the structures nominated as the substrate of “tinnitus disorder” are among the least diagnostically specific in the clinical neuroimaging literature. Importantly, the Perspective itself acknowledges both limitations. It notes that “assigning specific psychological functions to regional activations relies, in part, on reverse inference and is, therefore, not specific,” and that neuroimaging findings in regions such as the anterior cingulate, insula, or parahippocampus “are not uniquely diagnostic of ‘suffering' or ‘salience,' but rather are consistent with broader domain-general processes that may contribute to tinnitus-related distress.” At the same time, however, activation in these regions is described as providing “a neural basis for tinnitus related suffering” (De Ridder et al., 2026).

Thus, the medial pathway may appropriately be interpreted as a correlate of context-dependent stimulus evaluation. The inferential difficulty arises, however, when this correlate is reified into an explanatory mechanism: because the disorder is defined descriptively by distress, a neural correlate of that distress is taken to provide an explanation for the disorder and, in turn, becomes a putative target for neuromodulatory or pharmacological intervention. In doing so, the framework risks conflating correlation with mechanism and abstracting neural activity from the psychological and interpersonal contexts through which the stimulus acquires clinical significance.

An alternative may be drawn from the papers' repeated analogy between chronic tinnitus and pain (De Ridder et al., 2026; Vanneste et al., 2026). The comparison is clinically valuable because pain science has confronted a closely related conceptual problem of how to relate sensory influences to the subjective experience which together constitute pain. Rather than conceptualising pain as a sensory signal that may elicit distress downstream, contemporary pain science conceptualises pain as an experience in which sensory, affective and social dimensions are constitutively intertwined. The International Association for the Study of Pain (IASP) defines pain as “an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage” (Raja et al., 2020; italics added). Thereby, this definition includes the affective and evaluative dimensions of sensory information as integral components of the phenomenon itself—and not as a secondary consequence of neural processes.

Applied to chronic distressing tinnitus, this analogy raises a parallel possibility: that distress is not a reaction added to an otherwise independent percept, but constitutive of the clinical experience through which tinnitus becomes problematic. The Perspective's own architecture invites this reading. It distinguishes a lateral pathway that “conveys perceptual aspects of tinnitus” from the “medial distress or suffering pathway” (De Ridder et al., 2026), whilst also identifying the latter with the salience network said to be required for an auditory stimulus to reach conscious awareness. This creates a tension within the model wherein either “suffering” attributes a functional specificity which these structures do not encode, or conscious tinnitus perception already recruits the very mechanisms the model proposes to distinguish suffering from mere perception.

The reciprocity noted earlier can then be specified: stimulus perception, appraisal, attentional monitoring, coping behaviours and relational context influence one another against the backgrounds of personal history and personality. Threat appraisal may increase attentional monitoring; increased monitoring may enhance salience; and enhanced salience may reinforce perceptual prominence that is subsequently interpreted as threatening. Within predictive-coding accounts of symptom perception, the conscious experience of a symptom arises from the interaction of sensory input with prior expectations, attention and meaning-making (Van den Bergh et al., 2017). Notably, the Primer mentions this framework (Vanneste et al., 2026), but applies it exclusively to the generation of the tinnitus symptom and not to the co-determination of perceptual experience through psychological appraisal processes operating within iterative cycles of emotion generation and emotion regulation (Everaert et al., 2021).

Overall, whilst the source texts concede many elements of this critique, they stop short of integrating them at the level of a person's experience, where we argue that psychological meaning and context need to be treated as integral to symptom experience rather than as residual influences.

Neurophysiological framing: when explanatory models may reinforce the phenomena they describe

The clinical implications of the above-described conflation of explanatory levels extend beyond questions of taxonomy or nomenclature. Leventhal's Common-Sense Model of illness self-regulation (Leventhal et al., 1980), which is supported by a large body of meta-analytic evidence (Hagger et al., 2017; Hagger and Orbell, 2022), proposes that individuals actively construct illness representations; i.e., beliefs about the identity, cause, consequences, timeline, and controllability of their symptoms, including mental-health-related difficulties (Cannon et al., 2022). These representations then shape their emotional responses, coping behaviours, treatment engagement, and ultimately clinical outcomes, often independently of any underlying pathophysiology. From this perspective, explanatory frameworks are not psychologically neutral, as they shape how researchers conceptualise a phenomenon such as tinnitus, clinicians communicate it, and patients understand, cope with, and ultimately experience it (Weiner, 1985; Crisson and Keefe, 1988).

Applied to the Primer and Perspective, we are concerned that psychological processes are predominantly conceptualised through a medical-psychiatric or neurophysiological lens. Whilst neural correlates undoubtedly reflect psychological processes, these processes are also shaped by biography, learning, interpersonal relationships, and subjective meaning-making. Clinically, they therefore require simultaneous consideration at neurophysiological and experiential levels, rather than privileging biomedical explanations. Neural descriptions identify correlates of experience; however, they do not replace explanations at the level of lived experience. Framing tinnitus-correlated distress primarily in terms of disrupted medial pathway dynamics, salience network dysfunction, limbic hyperactivity, or altered large-scale connectivity may inadvertently foster illness representations characterised by neurological causation and diminished perceived controllability. For some individuals, such explanations may be experienced as:

“Something in my brain is broken; recovery lies outside myself in the hands of experts expected to repair brain dysfunction or restructure my thoughts.”

Biological conceptualisations of psychological distress have been shown to reduce clinicians' empathy (Lebowitz and Ahn, 2014). For some patients, particularly those with illness anxiety or catastrophic illness beliefs, such conceptualisations may diminish perceived controllability and hope (Kemp et al., 2014; Lebowitz, 2014; Johnstone, 2021) and potentially facilitate progressively more intensive biomedical interventions (Rosendal et al., 2005). For others, however, biological explanations may reduce self-blame, felt responsibility, and fear of personal failure (Haslam and Kvaale, 2015). Similarly, clinicians may use neurophysiological accounts either as heuristic tools that communicate complex psychological processes in a non-stigmatising manner or as literal explanatory models that displace psychological formulation and redirect research and treatment priorities towards biological mechanisms alone. These divergent effects suggest that the clinical impact of biomedical explanations depends not only on their scientific validity, but also on the meanings they convey and the psychological functions they serve.

This distinction may be particularly important in tinnitus, where distress is central to the symptom's clinical significance and perceptual persistence. Communicating meaningful psychological processes primarily through the lens of neurophysiological dysfunction may inadvertently reduce perceived controllability, heighten threat appraisal, and increase attentional monitoring—precisely the cognitive-affective processes most consistently associated with chronic tinnitus-related distress (Trevis et al., 2018; Kleinstäuber and Weise, 2020). Thus, if explanatory frameworks shape illness representations as proposed by Leventhal's model, privileging neurophysiological explanations over context and meaning may inadvertently reinforce the very processes through which an initially benign percept acquires enduring emotional significance. This concern does not imply that neurophysiological accounts should be rejected; however, they should be consistently integrated and communicated alongside person-centred psychological formulations that preserve context, appraisal and meaning.

This suggestion sits in both agreement and tension with the Primer. Discussing physician communication during assessment, the authors caution against inadvertently increasing tinnitus salience through facilitating “repeated monitoring, threat-focused interpretation and heightened emotional arousal, which can reinforce attention to the sound and contribute to distress over time,” and advise clinicians to gather history “without inadvertently amplifying the patient's attention to, and concern about, the tinnitus percept” (Vanneste et al., 2026). Separately, in its account of counselling, the Primer states that patients should be informed “that the perception of tinnitus is not identical to the emotional reaction to it” (Vanneste et al., 2026). Whilst we agree with these recommendations, we are concerned that their broader surrounding narrative (i.e., the characterisation of distressing tinnitus primarily as a disorder of dysfunctional neural circuitry with a predominantly neuromodulatory therapeutic horizon) may inadvertently undermine them.

If clinicians' illness beliefs and the biomedical (as well as psychological) models they communicate can themselves influence patients' threat appraisal, attentional focus, and illness representations, then explanatory frameworks should be understood as clinically active components of care. We advance this as a testable hypothesis warranting empirical investigation.

From correlate to modulation target: the therapeutic repurposing of neural signatures

Despite the Primer's distinction between a hypothesised lateral pathway representing initial symptom generation and a medial pathway hypothesised to encode the “distress component” of stimulus processing, its Outlook section largely links proposed interventions to “tinnitus” as a unitary target, without explicitly specifying whether individual approaches are intended to modify the percept, emotional distress, or both. Whereas regenerative approaches are conceptually aligned with targeting peripheral contributors to the auditory percept (e.g., through hair-cell and cochlear repair), interventions aimed at tinnitus-correlated distress appear to assume that distress can be reduced by modulating presumed pathological neural activity.

For example, biomarkers of “abnormal tinnitus-related brain activity” and neuromodulatory strategies aimed at retuning “dysfunctional circuits,” including aberrant thalamocortical rhythms or “limbic hyperactivity,” are proposed as potential targets without accounting for psychological context and meaning (Vanneste et al., 2026). Importantly, the Primer itself acknowledges no more than “modest to moderate” effectiveness for the non-invasive neuromodulatory approaches it discusses [transcranial magnetic stimulation (TMS), transcranial electrical stimulation (TES), and bimodal stimulation], while categorising emerging approaches [including invasive deep brain stimulation (DBS) and non-invasive techniques such as transcranial focused ultrasound stimulation (tFUS) and transcranial pulse stimulation] as exploratory approaches for “tinnitus” (Vanneste et al., 2026). A systematic review of 24 randomised controlled trials (RCTs) of neuromodulation therapies explicitly hypothesised to desynchronise pathological neural activity reported that, for the acoustic modalities it covered, “evidence for the effectiveness of acoustic neuromodulations [sic] therapies was very limited” (Hoare et al., 2024). A recent meta-analysis of 26 RCTs (n = 1,576) across neuromodulation modalities reported that pooled effects on tinnitus severity did not reach significance, were borderline for transcranial direct current stimulation (tDCS) [eight trials; standardised mean difference (SMD) −0.36, 95% CI −0.75 to 0.02] and null for repetitive TMS (rTMS; five trials; SMD −0.15, 95% CI −0.37 to 0.07) (Kitsis et al., 2026). An rTMS-specific meta-analysis reported improvements on the Tinnitus Handicap Inventory (THI) immediately post-treatment [eleven trials, n = 739; mean difference (MD) −11.54, 95% CI −17.32 to −5.77] and at 1-month follow-up (three trials; MD −10.98, 95% CI −17.42 to −4.54), and on a visual analog scale (VAS) immediately post-treatment (four trials, n = 350; MD −1.85, 95% CI −2.26 to −1.45). No significant immediate effect was observed on Tinnitus Questionnaire (TQ) scores (three trials, n = 218) or on loudness matching (three trials, n = 144) (He et al., 2025).

These findings support two competing interpretations with different predictions. A neurophysiological account predicts that benefit scales with verified target engagement and with stimulation parameters. A meaning-based account predicts that reductions in distress track changes in appraisal, perceived control and expectancy, remain largely independent of stimulation site, and diminish under effective blinding. Three features of the available evidence are relevant to distinguishing between these interpretations: whether treatment effects may depend on neural target engagement; which dimension of the tinnitus experience the interventions may be affecting; and whether expectancy and contextual factors may account for the observed improvements.

First, whilst the Primer postulates target engagement as a potential way to optimise modulation outcomes, a systematic review of tDCS parameters (Labree et al., 2022), summarised by Hoare et al. (2024), concluded that “spatial specificity may not be important to treatment effectiveness (and therefore not be a parameter that needs further optimisation).” Similarly, subgroup analyses by target region (such as auditory cortex, left temporoparietal area, or dorsolateral prefrontal cortex) were non-significant in an independent review (Kitsis et al., 2026). Overall, the findings to date are difficult to reconcile with a model in which benefit accrues from engaging a specific neural circuit and leave the possibility open that any observed benefit arises from factors shared across protocols.

Second, the reported trial outcomes are almost exclusively distress-anchored while symptom-level measures rarely appear (Hoare et al., 2024; He et al., 2025). The interventions are thus evaluated on psychological distress, and show little evidence of change on the dimension their mechanistic rationale is intended to target. Where generalised affect was assessed, effect sizes were of a similar magnitude to those observed for tinnitus-related outcomes: pooled improvements in anxiety (SMD −0.44) and depression (SMD −0.40) across four tDCS trials were comparable to the pooled estimate for distress-anchored tinnitus symptom severity (SMD −0.42), an estimate that itself lost significance (SMD −0.38, 95% CI −0.81 to 0.04) once the single trial at highest risk of bias was removed (Hoare et al., 2024). For “depression,” this effect was likewise no longer significant when an alternative instrument was substituted. A protocol that shifts generalised distress and tinnitus-correlated distress in parallel, without demonstrating corresponding changes in perceptual measures, does not necessarily imply selective modulation of tinnitus-specific circuitry and instead warrants investigation of psychological mediators of change. The Primer notes that subjectively perceived loudness “depends on attention and salience” (Vanneste et al., 2026). On that account, a loudness rating is itself an appraisal, made by the same person on the same occasion as the distress rating—rather than an independent index of the percept. Notably, we could identify no trial in either review that reported measuring psychological mediators capable of accounting for the observed treatment effects, such as illness representations, appraisal, perceived controllability, or treatment expectancy.

Third, the observed pattern of short-term self-reported improvement remains compatible with expectancy and contextual effects. Across neurostimulation studies, adequate participant blinding is a recognised challenge in both rTMS and tDCS research, with incomplete blinding frequently acknowledged (Braga et al., 2021; Lefebvre-Demers et al., 2021). This matters because expectancy, appraisal and perceived control co-define the outcome to the extent that tinnitus-correlated distress overlaps with symptom reports. If expectancy, contextual factors, or changes in appraisal contributed substantially to the observed effects, then the operative ingredient would lie less in selective modulation of tinnitus circuitry than in patients' expectation of relief generated by a technologically credible intervention delivered by a trusted clinician within a supportive therapeutic environment.

The same limitations attach to the one neuromodulation intervention the Primer reports as having reached regulatory approval. Here, a pivotal trial of bimodal sound-and-tongue stimulation reported a clinically meaningful benefit of bimodal over sound-only stimulation in a subgroup of participants with moderate-or-worse tinnitus-related distress, as defined by the THI (Boedts et al., 2024). Reflecting our considerations above, the intervention could not be evaluated against a sham condition because, as the authors note, both stimulus components were suprathreshold and therefore detectable by participants. Moreover, the trial's primary and secondary outcome measures reflected tinnitus-correlated distress under conditions in which expectancy could not be separated from treatment. Future trials should therefore systematically assess psychological outcomes and mediators of change using dimensional measures of appraisal, perceived controllability, expectancy, emotion, and related meaning-making processes rather than relying primarily on psychiatric symptom checklists. Respective results should be interpreted in relation to current and biographical contexts in which tinnitus acquires meaning and examined alongside perceptual outcomes. Changes across these domains should be modelled in relation to one another, recognising that perceptual measures such as self-reported tinnitus loudness may themselves be shaped by appraisal and other psychological processes rather than constituting objective or independent indices of the percept.

Taken together, the available evidence does not distinguish whether the reported improvements arise because neuromodulation modifies tinnitus-specific neural mechanisms or because it alters psychological processes such as expectancy, appraisal and perceived control (Rabipour et al., 2018). Under these circumstances, limited efficacy should not be met with the unfalsifiable claim that progressively deeper or more focal targets remain to be found. This is important because the Primer's Outlook appears to advocate for a trajectory towards increasingly invasive target pursuit. For example, it proposes tFUS as a potential route to the focality of DBS, alongside adaptive closed-loop systems designed to detect “limbic hyperactivity” and intervene “only when necessary” (Vanneste et al., 2026) without appropriately weighing the risks linked to such an approach (Grill, 2005; Buhmann et al., 2017). The Perspective appears to similarly extend this trajectory without critical reflection. Among the evidence cited to demonstrate that tinnitus-related suffering can be reduced independently from the percept, it presents two historical reports of prefrontal leucotomy for chronic tinnitus (Elithorn, 1953; Beard, 1965), alongside meta-analyses of CBT and acupuncture as jointly demonstrating the same principle (De Ridder et al., 2026).

The evidential implications of this comparison are, however, not straightforward. First, an ablative psychosurgical procedure appears within an evidential series alongside psychological and non-invasive interventions, without explicit acknowledgment of the profound differences in mechanism, risk, and interpretability between these approaches. Second, the proposed dissociation between percept and distress rests primarily on the absence of change in loudness. However, the same Perspective argues that psychoacoustic measures “cannot be used as outcome measures in tinnitus management or clinical trials” (De Ridder et al., 2026), and the Primer emphasises that both tinnitus perception and its impact are purely subjective experiences (Vanneste et al., 2026). A null result on a measure the authors themselves regard as uninformative cannot establish that two pathways are separable. This concern is particularly relevant clinically. Severe distress, combined with a predominantly biomedical explanatory framework, may increase demand for increasingly invasive biomedical interventions, a dynamic well-described in persistent physical symptoms (PPS), where medical framing, repeated investigations, and escalating interventions can reinforce illness identity, somatic fixation, and iatrogenic harm (Rosendal et al., 2005; Löwe et al., 2024).

From distress to comorbidity: diagnostic labels and the circular construction of disorder

Where the evidence remains inconclusive as to whether neural targets account for tinnitus-correlated distress, the framework turns to a second conceptual resource: psychiatric nomenclature to account for so-called “comorbidities.” This introduces a different problem—not correlation mistaken for causation, but description mistaken for explanation.

Whilst the Primer acknowledges bidirectional relationships between tinnitus and accompanying psychiatric phenomena, it discusses depression, anxiety, sleep disturbance, cognitive impairment and suicidal ideation largely as separate entities. However, even within the logic of psychiatric nosology, these phenomena are neither conceptually nor clinically independent. Sleep disturbance, impaired concentration, hopelessness, and suicidal ideation are all recognised features of depressive syndromes (Kennedy, 2008), while substantial overlap exists across anxiety and depressive symptom networks more generally (Jacobson and Newman, 2017; Snyder et al., 2023). At the same time, the substantial heterogeneity of symptom profiles among individuals meeting criteria for major depressive disorder has long raised concerns about the validity of depression as a specific and consistent syndrome (Fried and Nesse, 2015).

Rather than either proliferating diagnostic labels or regrouping heterogeneous experiences under a single syndrome label, each phenomenon may be better understood as a meaningful expression of distress requiring formulation in relation to its psychological function, individual determinants, and current and biographical contexts. Treating these phenomena as decontextualised and separate (or separable) explanatory variables risks multiplying descriptive labels without adding explanatory depth. In doing so, the Primer risks importing the descriptive logic of categorical psychiatric nosology into an already medicalised account.

As we have noted elsewhere (Boecking et al., 2026b), and others have argued in detail (Hyman, 2010; Maung, 2019), psychiatric diagnoses describe recurring constellations of cognitive, affective and behavioural symptoms rather than explain why a particular individual becomes distressed in a particular way. Referring to “comorbid depression” or “comorbid anxiety” therefore re-describes aspects of a person's distress in psychiatric terminology without accounting for the person-specific processes through which it developed (e.g., threat appraisal, interpersonal context, learning history, autobiographically shaped meaning and perceived controllability). The difficulty arises when such labels are then treated as independent causal agents (“depression causes tinnitus disorder,” “anxiety exacerbates tinnitus disorder”), at which point descriptive labels are asked to perform an explanatory function they were never designed to provide.

The Perspective goes further, proposing anxiety and depression measures as corroborating criteria for grading the severity of “tinnitus disorder”; its proposed grading table assigns cut-offs for the HADS anxiety and depression subscales and the BDI alongside the TQ, THI and TFI (De Ridder et al., 2026). Here, the Perspective describes the HADS and BDI as “tinnitus-unrelated questionnaires” and presents their agreement with the TQ and THI as “further confirmation” of the proposed grading (De Ridder et al., 2026). This risks a jangle fallacy, whereby measures with different labels are interpreted as indexing distinct constructs despite substantial overlap in the phenomena they capture (Hanfstingl et al., 2024). A related difficulty concerns the interpretation of the tinnitus-specific questionnaires themselves. These instruments measure distress that respondents attribute to tinnitus (for example, the THI asks “Does your tinnitus make you angry?” or “Because of your tinnitus, is it difficult for you to concentrate?”; Newman et al., 1996). A respondent for whom tinnitus has become the organising explanation for broader emotional or functional difficulties may endorse these items, irrespective of the extent to which the percept itself contributes to those difficulties (Duddu et al., 2006). These instruments are therefore attribution-anchored and cannot, on their own, establish the extent to which the auditory percept contributes causally to experienced distress. Agreement between measures therefore provides only limited evidence that “depression” constitutes a distinct contributor to tinnitus-related suffering; rather, it may primarily reflect shared variance in distress-related content that the differing labels obscure.

The clinical significance of this becomes apparent once attribution is understood as a psychological process in its own right. Attributing distress to a bodily phenomenon represents an understandable and often adaptive attempt to make suffering intelligible, legitimate, and communicable within a medical context, where psychological explanations may be less readily available or accepted. The literature on PPS describes this process in detail, highlighting how medical framing, repeated investigation, and diagnostic practices can reinforce illness identity and illness behaviour (Duddu et al., 2006; Kube et al., 2020; Kitselaar et al., 2023). In the companion Perspective (De Ridder et al., 2026), the authors argue in favour of a categorical, psychiatrically anchored rather than dimensional, psychological approach, on the grounds that it is “easy for diagnosis and communication,” “easy for clinical decision-making,” and “in keeping with traditional medical thinking.” At the same time, they recognise that this strategy introduces artificial boundaries, excludes patients who do not fit the categories, and fails to capture graded variation in symptom severity, limitations they regard as acceptable pragmatic trade-offs.

We would weigh this trade-off differently. Not only does a psychiatric-descriptive account of distress leave psychological mechanisms and experiential content insufficiently examined; it may also introduce an additional layer of medical categorisation for the same underlying experience, with potentially mixed consequences for illness representations as outlined above. Of course, a person's mood, apprehension, or disturbed sleep may well precede tinnitus or shape its perceptual course. However, these experiences represent meaningful thoughts, feelings, and reactions embedded within an individual's history and circumstances, and their importance is precisely a reason to understand them in such terms. In our view, psychiatric nomenclature is not neutral: when a person's response to tinnitus is rendered as a “disorder” or framed as “multimorbidity,” there is a risk that the content that makes that response intelligible becomes obscured, while the terminology may encourage an interpretation of these experiences as discrete internal medical entities rather than as processes emerging through the interaction of individual, psychological, and contextual factors (Veldmeijer et al., 2025).

Although the authors acknowledge that a dimensional, individualised approach may be superior from a patient perspective, citing our own work (Boecking et al., 2026a), they proceed to render this approach contingent upon identifying dimensions corresponding to specific brain correlates amenable to neuromodulation (“The dimensional model may outperform a categorical approach if patient management is shifted from a clinical to a neurobiological approach” [De Ridder et al., 2026]). By equating dimensionality with neurophysiological decomposability, the Perspective omits that the dimensional case we make is a psychometric and clinical one, resting on the structure of psychopathology and its implications for individualised psychological formulation, not a claim that each dimension corresponds to separable brain circuitry. Descriptive dimensional accounts of distress can be highly useful without each requiring a corresponding neural substrate (e.g., Kotov et al., 2021)—yet continue to leave explanation of experience and behaviour open to idiographic formulation.

In closing, we acknowledge the practical necessity of medical or mental health diagnoses within current healthcare systems. However, this necessity should not be mistaken for evidence that psychiatric labels provide adequate explanations of the processes through which distress develops. The same distinction applies to psychological treatment provision. Where a diagnostic category is treated as an explanation rather than an entry point, it may shape not only how distress is conceptualised but also how interventions are designed and delivered.

From psychological therapy to digital protocol: the standardisation of individual meaning-making

The Primer rightly positions CBT and tinnitus-focused counselling as first-line interventions, acknowledging the central, well-evidenced role of psychological treatment in tinnitus care (Vanneste et al., 2026). Indeed, CBT is the only intervention consistently recommended by numerous available treatment guidelines (Langguth et al., 2023). Regarding digital delivery formats, guided internet-based CBT has been shown to be effective for tinnitus-related distress (Beukes et al., 2019), and the Cochrane review the Primer cites reports comparable efficacy for internet- and smartphone-delivered formats (Fuller et al., 2020). Given that specialist psychological provision for tinnitus is scarce in most healthcare systems, the Primer makes a strong case for extending access to psychological interventions.

However, within the Primer's surrounding biomedical architecture, these interventions risk being conceptualised primarily as transferable packages of therapeutic techniques (e.g., cognitive restructuring, behavioural activation, relaxation and attentional training) whose active ingredients are assumed to be sufficiently procedural to allow increasingly standardised delivery through internet-based programmes, smartphone applications and potentially conversational artificial intelligence (AI).

Several assumptions underlying this position warrant closer examination. First, a symptom-focused biomedical perspective sets the index-symptom tinnitus as the organising object of therapy: tinnitus-related cognitions are modified, tinnitus-related avoidance is reduced, habituation to the tinnitus-perception is promoted, and tinnitus-related distress is expected to diminish accordingly. This can be appropriate, but it may disregard the possibility that tinnitus-correlated distress is shaped by broader influences that are expressed through the meaning the percept acquires for an individual. That meaning is informed by biographical experience, underlying assumptions, current life circumstances, and interpersonal contexts, as well as by associations evoked by the symptom itself, potentially reactivating latent themes of emotional vulnerability (Boecking et al., 2026b). In this case, an initial clinical task would be to establish whether and to what extent tinnitus is the appropriate object of intervention at all. A standardised psychological treatment protocol organised around tinnitus assumes that this question has been answered; however, this might need to be tested, as the available evidence shows that the perceptual features of the tinnitus symptom do not predict its appraisal or emotional impact (Westin et al., 2008; De Ridder et al., 2026). Ecological momentary assessment data likewise indicate that emotional states (which are highly context and person-dependent) mediate between perceived tinnitus loudness and tinnitus distress in daily life (Probst et al., 2016). More broadly, meta-analytic evidence establishes systematic associations between cognitive appraisals and emotional responses (Yeo and Ong, 2024) thereby highlighting the distinct possibility of broadening treatment foci and domains beyond tinnitus as index-symptom of care.

Overall, contemporary CBT should routinely involve collaborative case formulation, functional analysis of avoidance and safety behaviours, attention to ambivalence, and case-specific adaptation; however, our concern is that an underlying biomedical architecture may invite a reading of CBT as a standardisable technique package rather than a contextual, formulation-driven intervention tailored to the individual.

Moreover, the question of why psychological therapies work remains highly debated. Proponents of contextual models emphasise meta-analytic evidence for alliance, empathy, expectancy and therapist effects (Wampold, 2015) whereas critics note that factor–outcome correlations cannot establish causal contribution, and that component studies remain methodologically weak (Cuijpers et al., 2019). The largest synthesis of the alliance–outcome association included 295 studies and more than 30,000 patients. It reported a robust association between alliance and outcome that held across treatment approaches and setting (Flückiger et al., 2018). In tinnitus research, most trials that established the efficacy of internet-delivered CBT for tinnitus evaluated guided interventions, i.e., interventions wherein “therapist or trained personnel was involved during intervention to ensure direct comparability of effects with the […] CBT administered by psychologists” (Sattel et al., 2025). Thus, the available evidence largely reflects formats that retain human attunement. Whether the observed effects extend to digital therapeutics with fully autonomous delivery remains an open empirical question.

The prospect of AI delivering psychological interventions further sharpens this question. For example, Rubin et al. (2025) showed across nine studies with more than 6,000 participants, that AI-generated empathic responses were rated as less empathic, less supportive, and elicited fewer positive and more negative emotions, when attributed to AI than when the identical responses were attributed to a human. This finding is instructive because it reflects our argument that the meaning of a stimulus does not follow from its characteristics. Participants' belief that AI had generated a response was itself sufficient to reduce perceived empathy and support. As multidisciplinary services expand access, often by training non-psychologists in protocolised CBT skills, the corresponding risk is that psychological competence comes to be equated with manualised (or digital) delivery. If the principal constraint in tinnitus care was access to relational, formulation-based psychological treatment capable of addressing the idiographic structure of distress, the proportionate response would be to expand clinician training and service capacity at that very level. Scaling technologically and mechanistically thinner substitutes should not become the default solution while evidence for durable, mechanism-specific effects remains limited.

Conclusion

A recent Nature Reviews Disease Primer on Tinnitus provides an authoritative and likely influential synthesis of current tinnitus-related lines of research (Vanneste et al., 2026). A contemporaneously published Perspective paper by nine of the Primer's ten authors states the clinical and research implications of the outlined framework more explicitly (De Ridder et al., 2026).

Overall, we recognise the potential value of neuroscientific research into mechanisms of tinnitus symptom generation or distress-related experiences. However, we are concerned about the framework's general conceptual architecture which, through a series of steps, privileges a biomedical perspective over psychosocial context and meaning as outlined above and summarised in Table 1.

Notably, the source texts already acknowledge several premises underlying our argument. The Primer recognises that communication can influence symptom salience and threat appraisal, emphasises stress-related processes and patient-centred treatment planning, and notes that intervention should be guided by the patient's primary source of distress. The Perspective similarly acknowledges limitations of neurobiological inference, reports that psychoacoustic measures do not correspond with self-rated symptom severity, recognises the pragmatic rather than empirical basis of categorical nomenclature, and discusses catastrophising, threat magnification, helplessness and rumination as possible mechanisms linking psychological vulnerability to tinnitus-related suffering. However, these observations are not integrated into the subsequently outlined framework in a way that treats psychological processes as meaningful explanatory phenomena in their own right. Of course, distress experiences are not independent of neural activity; nor are the processes we have emphasised (appraisal, attentional monitoring, personal meaning, perceived control, emotions and coping behaviours). However, the clinically relevant difference between two people with comparable symptoms and different emotional responses does not lie simply in the neural systems implementing these processes, but in the content of their evaluations, which are highly subjective, biographically anchored, relationally formed and context-dependent. This content is not determined by the properties of the stimulus itself, and perceptual features of tinnitus repeatedly fail to predict appraisal or emotional impact (Probst et al., 2016; De Ridder et al., 2026). Accordingly, psychological and multidisciplinary care may be better served by formulation-based approaches that address appraisal, expectation, perceived control and personal meaning alongside interventions targeting somatic contributors such as hearing loss.

Much of what we propose is empirically testable. First, future research should examine whether explanatory framing shapes illness representations, and whether these representations subsequently influence the appraisal, perceived controllability and distress through which the authors define “tinnitus disorder.” Such work could establish whether explanatory models themselves contribute to maintaining the phenomena they seek to describe.

Second, neuromodulation research should distinguish explicitly and consistently between neurophysiological and psychological targets, as well as between neurophysiological and psychological mechanisms of change. Measuring psychological mediators alongside target engagement is essential for determining whether observed benefits are mediated by changes in the targeted neural processes, by changes in appraisal, perceived control, treatment expectancy, or contextual factors, or by some combination thereof. Neural target engagement does not resolve this distinction on its own: although neural activity may covary with psychological processes, the content or meaning of those processes cannot be inferred from the neural correlate itself. Likewise, adequately blinded studies could test the prediction that expectancy-dependent effects attenuate when treatment credibility is controlled. Beyond mediation, the outcomes themselves require more disciplined interpretation. Improvements on the THI, TFI, and TQ reflect changes in appraisal-laden self-report (Vanneste et al., 2026) and should therefore not be reinterpreted as evidence of change at the level of the percept or successful circuit modulation.

Finally, psychological treatment research should examine whether tinnitus-specific appraisals explain distress beyond broader affective and interpretative processes, while recognising that these processes themselves may be meaningful determinants of symptom experience. Studies should also examine whether baseline appraisal or illness representations moderate response to standardised versus formulation-based interventions at differing levels of human involvement and relational quality. Such findings would help clarify when tinnitus itself should constitute the primary object of intervention and when broader psychological processes provide more appropriate therapeutic targets.

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Footnotes

Edited by: Ann Perreau, Augustana College, United States

Reviewed by: Juan M. Espinosa-Sanchez, Hospital Universitario Virgen de las Nieves, Spain

Yinfei Liang, Third Affiliated Hospital of Sun Yat-sen University, China