Hyperneuroplasticity, Dissociation, and Tinnitus. Oh My.

By Dr. Patty Gently on August 12, 2025

A Man with Headphones

Bright Insight Support Network founder and president Dr. Patricia Gently supports gifted and twice-exceptional adults in their own autopsychotherapy through identity exploration, structured reflection, and alignment with inner values. A writer, educator, and 2e adult, Dr. Patty centers depth, integrity, and complexity in all aspects of her work.

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Introduction: Why These Three Belong in the Same Conversation

Brains are never still. They are living, shifting networks that respond to everything we do, think, and experience. Most of the time, these changes are gradual and balanced. For some, though, the brain’s capacity for change is amplified. Connections strengthen and weaken more quickly, networks reorganize more broadly, and the usual checks on rewiring are looser. This is what I refer to as hyperneuroplasticity, and I see manifestations of it in so many of my gifted neurodivergent clients and friends. 

Heightened adaptability can be a gift or a liability, depending on context. When it meets stress, trauma, or persistent sensory input, the outcomes can diverge sharply. For some, hyperneuroplacticity supports rapid recovery and creative adaptation. For others, it hardens maladaptive patterns, including chronic dissociation or persistent tinnitus. These three phenomena may seem unrelated at first glance, yet they share underlying biological threads. Understanding those links can help us steer neuroplasticity toward healing rather than entrenchment.

Definition and Scope

Neuroplasticity is the brain’s capacity to physically and functionally rewire itself based on experience, learning, or injury. In practical terms, it means that connections between neurons can be strengthened, weakened, or entirely reorganized. These changes may involve subtle shifts in how efficiently existing pathways transmit signals, known as changes in synaptic efficacy, or more dramatic remodeling of entire networks. Hyperneuroplasticity refers to cases where these processes are unusually strong, happen more quickly than average, affect multiple brain systems at once, or continue without the usual regulatory “brakes” in place. This heightened plasticity can drive profound and long-lasting changes, for better or worse. The main drivers include:

Long-term potentiation (LTP): a durable boost in connection strength between neurons, often summed up in the phrase “cells that fire together wire together.” In everyday terms, it’s how repeated activation can make a pathway more efficient.

Long-term depression (LTD): the opposite of LTP, this is a persistent reduction in connection strength, which can help prune or weaken unused or unhelpful pathways.

Metaplasticity: a sort of “plasticity of plasticity,” meaning the brain changes how easily future plastic changes can occur based on past activity.

Homeostatic plasticity: the brain’s balancing act, scaling connection strengths up or down to keep overall activity within a healthy range (Abraham & Bear, 1996; Abraham, 2008; Turrigiano & Nelson, 2011).

Together, these processes form the foundation for both adaptive reorganization, like we witness sometimes in recovery after stroke, and maladaptive reorganization, such as when unhelpful patterns become entrenched.

Hyperneuroplasticity and Dissociation

Dissociation is a disruption in the integration of thoughts, feelings, memories, and identity. It often emerges as a neural adaptation to overwhelming stress, providing a temporary buffer against sensory or emotional overload. It can take several forms, including the following:

Depersonalization: feeling detached from oneself as though watching from the outside.

Derealization: perceiving the world as unreal or dreamlike.

Identity fragmentation: shifts in the sense of self or the emergence of distinct identity states.

Amnesia: gaps in memory for everyday or traumatic events.

Absorption: becoming so focused on an experience that awareness of surroundings fades.

Emotional numbing: dampened emotional responsiveness as a protective measure.

From a network perspective, dissociation reflects coordinated changes in brain regions that regulate perception, memory, and emotion, often involving the interplay between limbic and prefrontal systems. In individuals with hyperneuroplasticity, these shifts can move in different directions. Heightened plasticity in limbic–prefrontal circuits can reinforce dissociative coping patterns, stabilizing them through rapid sensory pathway reweighting and altered connectivity between the default mode and salience networks (Lanius et al., 2015; Daniels et al., 2012). In others, the same adaptability can shorten dissociative episodes by reorganizing memory networks, restoring grounded sensory integration, and strengthening prefrontal regulation over limbic reactivity (van der Kolk, 2014; Roydeva & Reinders, 2021). Environmental enrichment, therapeutic methods such as EMDR and somatic approaches, and neuromodulatory states can bias these outcomes toward recovery rather than entrenchment (Shapiro, 2018; Payne et al., 2015). Those with high neuroplastic potential may respond particularly well to interventions that integrate sensory processing, bilateral stimulation, or targeted emotional processing (Gently, 2025; van den Heuvel & Sporns, 2019; Thomaes et al., 2014).

Hyperneuroplasticity, Low-Dissociation Profiles, and Tinnitus

In clinical observation, a curious pattern emerges. Among hyperneuroplastic individuals, those who rarely or never dissociate seem more likely to have noticeable and often debilitating tinnitus. This is not to imply that dissociation shields against tinnitus entirely, since many who dissociate experience it as well. What stands out, rather, is that in low-dissociation profiles, the absence of this regulatory “circuit breaker” seems to leave the auditory and attentional systems in continuous engagement.

When the brain remains locked into sensory monitoring without relief, auditory networks are more exposed to persistent input and stress-related arousal. Over time, this can encourage maladaptive cortical reorganization (Eggermont & Roberts, 2012). In hyperneuroplastic systems, such reorganization can happen rapidly, reinforcing looped activity in auditory cortex and thalamocortical circuits that produces phantom sound perception (De Ridder et al., 2014). Without dissociation to dampen stress responses, elevated noradrenaline, cortisol, and glutamate further bias plasticity toward persistence (McEwen, 2007; Joëls & Baram, 2009). High sensory precision and rapid pattern recognition can accelerate the process, leading subtle auditory anomalies to be quickly encoded, reinforced, and repeatedly brought into attention (De Ridder et al., 2014).

Mechanistic Insights from Tinnitus Research

Key findings from recent research include a synthesis of structural, functional, and neurochemical evidence, which matters because it clarifies the specific mechanisms by which maladaptive hyperneuroplastic processes lock in and amplify tinnitus perception, helping to explain why it persists, why it remains salient, and where targeted interventions might most effectively disrupt these feedback loops.

Altered auditory–limbic connectivity: This means the brain’s hearing areas are talking more strongly or differently with regions that handle emotion and memory, like the hippocampus, amygdala, and anterior cingulate cortex. That altered communication is linked to ongoing awareness of the sound and the distress it causes (Leaver et al., 2021; Chen et al., 2023).

Limbic gating dysfunction: Normally, emotional circuits can help “turn down” or ignore irrelevant sensations. Here, the amygdala–cingulate system struggles to regulate how important or noticeable the tinnitus signal feels, so it remains front and center (Langguth et al., 2023).

Spontaneous hyperactivity: After hearing nerve damage, certain auditory neurons fire more often than they should, creating phantom sound signals even without external noise (Shore et al., 2016).

Homeostatic plasticity misfires: The brain tries to boost its internal volume after hearing loss to make up for missing input, but in this case that gain boost mimics tinnitus activity, reinforcing the phantom sound (Schultheiβ et al., 2023).

Neurochemical changes: Levels of brain chemicals that calm activity (like GABA) drop early in the anterior cingulate, while stimulating ones (like glutamate) rise later. This chemical shift can make sound-related brain circuits more excitable (Vanneste et al., 2025).

BDNF and inflammatory markers: Elevated markers related to brain plasticity and inflammation, such as brain-derived neurotrophic factor (BDNF), are tied to both sensory–emotional processing problems and entrenched tinnitus (Martinez-Devesa et al., 2025).

Structural remodeling: The support structure around neurons in the primary auditory cortex changes after loud-sound injury, which can lock in new, maladaptive wiring (Holt et al., 2024).

Neuromodulation advances: Techniques like repetitive transcranial magnetic stimulation (rTMS) and combined sound–tongue stimulation show promise in “retuning” brain activity patterns and reducing tinnitus symptoms (Hoare et al., 2024; Conlon et al., 2025).

Shared Neurobiological Features

Hyperneuroplasticity, dissociation, and tinnitus intersect through a set of overlapping brain mechanisms that help explain why these experiences can feel so persistent, why they may arise together in some people, and why targeted interventions have the potential to change them. Understanding these links matters for the reader because it connects the dots between how the brain adapts, how it can sometimes over-adapt in unhelpful ways, and how those same pathways can be harnessed to promote recovery and symptom reduction:

High adaptability in hippocampal–amygdala–prefrontal circuits: In simpler terms, these are deep emotional and memory-related brain regions working with the decision-making centers. When these pathways are highly adaptable, they can quickly set up coping patterns like dissociation during stress, but that same flexibility can also lock in unhelpful sound patterns, as in tinnitus (Lanius et al., 2015; Daniels et al., 2012; De Ridder et al., 2014).

Shifts in sensory processing: This refers to changes in how the brain balances activity between excitatory and inhibitory signals, and how it recruits different senses to work together. Such changes can alter how reality feels and can create phantom perceptions like hearing sounds that aren’t there (Roydeva & Reinders, 2021; Eggermont & Roberts, 2012).

State-to-trait shifts from repeated stress: Here, a temporary brain state—such as dissociation or heightened sound sensitivity—can, through repeated activation, become a long-lasting trait. Conversely, with the right conditions, that same brain flexibility can help reverse the pattern (van der Kolk, 2014; McEwen, 2007).

Research Gaps and Future Directions

Despite advances in understanding plasticity’s role in trauma recovery, maladaptation, and tinnitus generation, research directly linking hyperneuroplasticity with dissociation profiles and sensory phantom conditions remains rare. Longitudinal neuroimaging studies, molecular analyses of plasticity mediators such as BDNF, GABA, and glutamate, and clinical trials targeting specific network recalibration processes would help clarify causality and guide treatment development.

Conclusion and Clinical Implications

Hyperneuroplasticity is a double-edged capacity. For those with low dissociation, the same adaptability that fosters learning and resilience can also lock maladaptive sensory patterns in place. A deeper understanding of auditory–limbic connectivity, limbic gating, spontaneous activity patterns, and homeostatic plasticity can inform more precise interventions. Combining targeted neuromodulation with therapies that integrate sensory and emotional processing offers a promising route. Early identification of individuals at risk may allow clinicians to guide neuroplasticity toward adaptation before maladaptive circuits take hold. The more clearly we can see how plasticity, sensory processing, and coping styles interact, the more effectively we can harness the brain’s natural capacity for change in service of recovery rather than chronic disruption.

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