Psychedelic Therapy for Tinnitus and Hearing Disorders

The term “neuroplasticity” is widely used to describe any change in the brain, but a new theoretical paper argues this is a scientific misstep that muddies our understanding of mental health and treatment. Researchers Robin Carhart-Harris, Richard Zeifman, and Lorenzo Pasquini propose a critical distinction, suggesting that many so-called markers of brain plasticity actually measure processes that make behavior *less* flexible, not more.

The Core Problem: Plasticity Is Not Always Plastic

The authors start with a simple definition. True “plasticity proper” is the inherent capacity of a material—or a system—to be shaped, molded, and changed. In neuroscience, however, “neuroplasticity” has become a catch-all term for any induced change in brain function or structure. The paper points out a major paradox: many popular biomarkers of neuroplasticity, such as long-term potentiation (LTP) linked to learning, are part of processes that lead to phenotypic canalization.

Canalization is the development of fixed, stable traits or behaviors—essentially, the brain becoming more rigid and habitual. This is the functional opposite of plasticity proper. Calling a process that solidifies a fear memory or an automatic negative reaction “plasticity” is, the authors argue, a conceptual error. This custom creates an “overgeneralization fallacy,” where all brain changes are seen as inherently adaptive and flexible, which is not the case.

From Measurement to Meaning: Questioning the Health Link

This conceptual fuzziness has practical consequences. The paper explicitly questions the common practice of extrapolating from a biomarker of neuroplastic change directly to assumed improvements in mental health. A brain change measured in a scanner is not automatically therapeutic. The relationship is “logically, context dependent.” For instance, strengthening neural connections in a circuit that perpetuates tinnitus distress or misophonic reactivity would be a change, but a maladaptive one. This underscores why treatments must aim for the right kind of change in the right networks.

A New Framework: Mediational and Recalibrative Plasticity (MR-P)

As a resolution, Carhart-Harris and colleagues introduce a new construct: “Mediational and Recalibrative Plasticity” (MR-P). Unlike broad neuroplasticity, MR-P is specifically aligned with plasticity proper. It describes brain changes that mediate a recalibration of perception, emotion, or behavior toward greater flexibility and adaptability.

The authors demonstrate how markers of MR-P can better describe and predict true phenotypic plasticity—where the “phenotype” is a mental health-relevant state or trait. For example, a successful therapy for hyperacusis might work by inducing MR-P in auditory-limbic networks, recalibrating the brain’s threat response to sound from rigid and reactive to more moderated and context-aware. This moves beyond simply noting “brain change” to specifying the quality and direction of that change.

Implications for Hearing and Sound Sensitivity Disorders

This refined framework has direct relevance for tinnitus, hyperacusis, and misophonia research. These conditions are often characterized by maladaptive, canalized brain states—fixed patterns of heightened auditory salience and negative emotional response. Many existing neuromodulation or behavioral therapies aim to alter these patterns.

The paper suggests we should be cautious about labeling any observed brain change after therapy as “positive neuroplasticity.” Instead, the focus should shift to seeking evidence of MR-P: changes that mediate a genuine recalibration. For instance, research into novel psychedelic-assisted therapy is directly interested in inducing a temporary state of high brain plasticity (or MR-P) to help break rigid pathological networks. Similarly, effective sound therapy for hyperacusis likely works through gradual recalibration, not just passive change.

Furthermore, the context-dependent nature of plasticity explains why stress, such as that documented during the COVID-19 pandemic, can worsen these conditions. Stress often promotes canalizing processes, reinforcing negative loops and reducing the brain’s capacity for adaptive MR-P, which can affect broader mental health as noted in research on CBT-I outcomes.

Sharpening Our Tools for Future Research

The proposal by Carhart-Harris, Zeifman, and Pasquini is a call for greater precision. By distinguishing canalizing neural changes from those representing genuine mediational and recalibrative plasticity (MR-P), researchers can develop clearer hypotheses and better biomarkers. This can help identify which therapeutic agents or procedures are truly inducing a flexible, adaptive brain state conducive to recovery, rather than just any change.

For patients and clinicians, the takeaway is that “promoting neuroplasticity” is an incomplete goal. The objective must be more specific: to support brain changes that recalibrate and mediate improved adaptation. As the field progresses, this nuanced understanding could lead to more targeted and effective interventions for the rigid brain states underlying chronic tinnitus, misophonia, and hyperacusis.

Source: Carhart-Harris, R., Zeifman, R., & Pasquini, L. (2026). Plasticity Proper vs. Neuroplasticity: A Critical Distinction with Implications for Mental Health Science. Frontiers in Neuroscience, 10.3389/fnins.2026.1875339.