The Primer itself is an impressive synthesis. 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. Crucially, it separates the sound itself from a “distress component,” hypothesised to be encoded by a medial, extra-lemniscal pathway projecting to the anterior cingulate cortex, the insula and other limbic regions. The Perspective goes further, arguing that this operational distinction amounts to a theoretical definition of a disease entity with its own aetiology and pathophysiology, and proposing that “tinnitus disorder” be diagnosed and graded using standardised severity thresholds anchored in anxiety and depression questionnaires. The Berlin authors’ concern is that each step in this sequence, taken alone, seems reasonable, but stacked together they progressively shift the explanatory centre of gravity away from the psychological context, content and meaning of distress and toward its presumed neurophysiological correlates.

The first and most consequential move is the reclassification of distress as disorder. The Perspective reports that suffering accompanies tinnitus in roughly 20 percent of the tinnitus population, and its own figures imply approximately 16 percent. Yet, as the authors point out, the evidence assembled is associative and largely cross-sectional. Psychoacoustic measures such as loudness matching, pitch matching, maskability and residual inhibition bear no consistent relation to self-rated symptom severity, and both distress- and percept-anchored measures are purely subjective. Hearing health predicts whether tinnitus is present, but distress and its progression are additionally determined by neuroticism, mood, sleep and fatigue. On the authors’ own criterion, a theoretical definition requires causal predictions; the data supply none about the direction of the relationship between percept and suffering. The Berlin group argues that “tinnitus disorder” may be useful as a purely descriptive, administrative label that helps patients access care, but that elevating it to a causal disease entity is an inferential leap the evidence does not license.

The second move concerns the brain regions themselves. The anterior cingulate cortex and anterior insula, the structures nominated as the substrate of tinnitus-related suffering, are among the least diagnostically specific in the entire clinical neuroimaging literature. They are core nodes of the salience network, engaged whenever any stimulus acquires behavioural relevance, regardless of modality or content. A meta-analysis of 193 voxel-based morphometry studies in 15,892 individuals found grey matter reductions converging on precisely these regions across six different psychiatric diagnoses, and a meta-analysis of 298 functional imaging experiments in 5,427 patients reported the same areas showing shared, rather than diagnosis-specific, disruption during emotional processing. Strikingly, the Perspective itself concedes these limitations, acknowledging that assigning specific psychological functions to regional activations relies on reverse inference and that most studies are cross-sectional, making it impossible to determine whether brain alterations are predisposing factors, consequences, or mere correlates. Yet in the same text, activation in these regions is described as providing “a neural basis for tinnitus related suffering.”

What differentiates two people with comparable levels of neural activation, the authors argue, is not the circuitry but the content of their appraisal: what the sound means for a person in relation to their goals, expectations, biography and relationships. Here they draw on an analogy the Primer and Perspective themselves invoke: chronic pain. Contemporary pain science, culminating in the revised definition of the International Association for the Study of Pain, treats the affective and evaluative dimensions of pain as constitutive of the experience itself, not as downstream consequences of neural events. Applied to tinnitus, this raises a parallel possibility: that distress is not a reaction added to an otherwise independent percept, but part of what makes the percept persist as a salient, troublesome experience. Threat appraisal may increase attentional monitoring; monitoring enhances salience; salience reinforces perceptual prominence that is then interpreted as threatening. Within predictive-coding accounts, the conscious experience of a symptom arises from the interaction of sensory input with prior expectations, attention and meaning-making.

The critique becomes clinically pointed when the authors turn to framing effects. Leventhal’s Common-Sense Model of illness self-regulation, supported by extensive meta-analytic evidence, holds that patients construct illness representations, beliefs about the identity, cause, consequences, timeline and controllability of their symptoms, and that these beliefs shape emotional responses, coping and outcomes, often independently of underlying pathophysiology. Illness representations marked by low perceived control and biological causation predict poorer coping across chronic conditions. Biological conceptualisations of psychological distress have been shown to reduce clinicians’ empathy, and for some patients, particularly those with catastrophic illness beliefs, they may diminish perceived controllability and hope. For others, such explanations can reduce self-blame. The impact of a biomedical narrative therefore depends on the meanings it conveys and the psychological functions it serves. The bitter irony the authors identify is that the Primer itself warns clinicians against “sensitization to the symptom,” meaning the increased salience of tinnitus produced by repeated monitoring, threat-focused interpretation and heightened emotional arousal, while its broader narrative anchors distress in a brain disorder and treats this framing as psychologically neutral.

The therapeutic implications follow. The Primer’s outlook proposes biomarkers of “abnormal tinnitus-related brain activity” and neuromodulation to retune “dysfunctional circuits,” yet its own evidence table rates transcranial magnetic stimulation “Against” in three of five guidelines and calls deep brain stimulation, focused ultrasound and transcranial pulse stimulation exploratory. A meta-analysis of 26 randomised trials found pooled effects on tinnitus severity non-significant overall, null for repetitive TMS and borderline for tDCS. An rTMS-specific meta-analysis reported improvements on the Tinnitus Handicap Inventory but no significant effect on loudness matching. The pattern is telling: where benefits appear, they show up on composite measures of tinnitus-correlated distress, not on the perceptual measures the mechanistic rationale targets. Moreover, generalised anxiety and depression improved in parallel with tinnitus-specific distress, and no trial the authors could identify measured psychological mediators such as appraisal, perceived control or expectancy. Adequate blinding remains a recognised challenge in neurostimulation research, leaving expectancy effects as a live alternative explanation. The authors also question the Perspective’s citation of two historical reports of prefrontal leucotomy for tinnitus as evidence that suffering can be dissociated from the percept, noting that a null result on loudness measures the same texts deem uninformative cannot establish separable pathways.

The critique extends to the diagnostic apparatus itself. The Perspective proposes grading “tinnitus disorder” severity using cut-offs on the Hospital Anxiety and Depression Scale, the Beck Depression Inventory and tinnitus-specific questionnaires, describing the psychiatric scales as “tinnitus-unrelated” and their agreement with tinnitus measures as “further confirmation.” The Berlin authors see a jangle fallacy: measures with different labels indexing largely the same distress-related content cannot validate one another. Tinnitus questionnaires are attribution-anchored; the Tinnitus Handicap Inventory asks whether tinnitus makes the respondent angry or impairs concentration, and someone for whom tinnitus has become the organising explanation for broader difficulties may endorse such items regardless of the percept’s actual causal contribution. Psychiatric labels, the authors stress, describe recurring symptom constellations without explaining why a particular individual becomes distressed in a particular way. Treating “comorbid depression” or “comorbid anxiety” as independent causal agents asks descriptive categories to perform explanatory work they were never designed to do.

Even psychological treatment risks being reshaped by the biomedical architecture. The Primer rightly recommends cognitive behavioural therapy and counselling as first-line care, and guided internet-based CBT is non-inferior to face-to-face treatment for tinnitus. But within a framework that treats distress as a brain disorder, CBT risks being recast as a transferable package of standardisable techniques suited to app-based or even AI-driven delivery. The evidence for digital formats derives from guided interventions retaining therapist contact, and meta-analytic work emphasises alliance, empathy and expectancy as crucial to outcome. In a striking recent finding spanning nine studies and more than 6,000 participants, identical empathic responses were rated as less empathic and less supportive when attributed to artificial intelligence rather than to a human, a demonstration that the meaning of a message depends on its perceived source, not just its content. The authors argue that if the bottleneck in tinnitus care is access to relational, formulation-based treatment, the proportionate response is to expand clinician training rather than scale thinner automated substitutes.

The Berlin team closes with a constructive, testable agenda. Future research should examine whether explanatory framing itself shapes illness representations, and whether those representations influence the appraisal, perceived control and distress through which “tinnitus disorder” is defined. Neuromodulation trials should measure psychological mediators alongside neural target engagement, and adequately blinded studies could test whether expectancy-dependent effects attenuate when treatment credibility is controlled. Psychological treatment research should establish when tinnitus itself is the appropriate object of intervention and when broader affective and interpretative processes are. None of this requires abandoning neuroscience; distress is not independent of neural activity, and the authors acknowledge the practical necessity of diagnoses within current healthcare systems. Their demand is subtler and arguably more radical: that neurophysiological accounts be communicated alongside, not instead of, person-centred psychological formulations that preserve context, appraisal and meaning. Until the field tests whether its own explanatory models feed back into the distress they describe, the clinically relevant question, they insist, is not why tinnitus is distressing, but why it is distressing for this particular person.

Subject of Research: Conceptual critique of framing tinnitus-related distress as a neurobiological disorder entity

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

Article References: Boecking, B., Steinmetzger, K., Rose, M., Brueggemann, P., & Mazurek, B. (2026). Framing tinnitus-correlated distress as a brain disorder may contribute to the very distress it seeks to explain. Frontiers in Audiology and Otology, 4, Article 1914013. https://doi.org/10.3389/fauot.2026.1914013

Image Credits: AI Generated

DOI: 10.3389/fauot.2026.1914013

Keywords: tinnitus, tinnitus disorder, distress, neuromodulation, cognitive behavioural therapy, illness representations, salience network, appraisal, predictive coding, psychiatric diagnosis, psychological formulation, brain disorder framing