Stress, the Amygdala, and Hyperneuroplasticity

By Dr. Patty Gently on August 18, 2025

Stress, the Amygdala & Hyperneuroplacticity

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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Stress, the Amygdala, and Hyperneuroplasticity

Introduction

When we endure prolonged or repeated stress, the amygdala, the brain’s instinctual threat detector, ramps into overdrive, while the prefrontal cortex (PFC), responsible for nuanced thought, regulation, and emotional reflection, becomes less salient. This imbalance, when combined with hyperneuroplasticity (seen in gifted, autistic, and ADHD neurotypes), helps explain how adaptive survival responses can become entrenched patterns that shape a range of conditions.

Amygdala 'Overactivation' and PFC Downregulation

The prefrontal cortex, a relatively late-evolved structure essential for working memory, planning, and emotional control, is disproportionately vulnerable to stress. Even mild, uncontrollable stress can rapidly impair its function, while chronic stress leads to structural changes such as dendritic atrophy and synaptic spine loss in prefrontal neurons (Arnsten, 2009; McEwen & Morrison, 2013). These stress effects occur on both short- and long-term scales: acutely, elevated norepinephrine and dopamine levels overactivate α1-adrenergic and D1 receptors, triggering intracellular cascades that weaken recurrent synaptic connectivity and effectively take the prefrontal cortex “offline” (Arnsten et al., 2015).

At the same time, stress heightens amygdala activity. The amygdala not only detects threat but also amplifies its own salience signaling under stress, driving hypervigilance and rapid emotional responses. Normally, the prefrontal cortex exerts top-down inhibition of the amygdala, tempering fear and emotional reactivity. When prefrontal control is compromised, this inhibitory brake is lost, allowing the amygdala to dominate (Phelps & LeDoux, 2005). The result is a shift toward bottom-up emotional processing, allowing us to become reactive, impulsive, and narrowed in cognitive flexibility (Liston et al., 2009).

In everyday life, this explains why under stress we may suddenly struggle to retrieve a familiar word, lose perspective in decision-making, or overreact to even minor frustrations. In such situations, the amygdala’s rapid threat appraisal fills the vacuum left by a downregulated prefrontal cortex.

The Amplifying Lens of Hyperneuroplasticity

Neuroplasticity enables the brain to adapt by strengthening or weakening connections between neurons in response to experience. In hyperneuroplastic systems, however, this process can occur with unusual speed and intensity. Research shows that stress hormones such as cortisol, in combination with amygdala-driven norepinephrine release, accelerate the consolidation of emotionally charged associations (McEwen, 2022; Roozendaal, McEwen, & Chattarji, 2009). This means that adaptive and maladaptive responses alike can become rapidly ingrained, sometimes after only a single exposure. Once the amygdala hijacks the system, hyperneuroplastic brains may overlearn threat associations, reinforcing rigid loops of anxiety, avoidance, or compulsive behavior.

Put more plainly: a hyperneuroplastic brain is like a high-speed recorder. It takes a snapshot of stressful or threatening experiences and plays them back on repeat, long after the danger is gone. That rapid wiring can be life-saving in moments of real threat, yet it also explains why stress can leave such deep grooves, making it harder to shake habits of fear, vigilance, or avoidance once they’ve been learned.

Reframing Behavioral Symptoms as Survival Expressions

Many behaviors often labeled as pathological, such as compulsions, avoidance, or emotional outbursts, can be reframed as adaptive survival expressions. In hyperneuroplastic systems, these behaviors form with unusual speed and intensity: associations consolidate rapidly, and survival-driven responses become deeply wired after even brief exposures. From a neurobiological perspective, this reflects the amygdala’s activation of defensive survival circuits under stress (LeDoux & Pine, 2016), combined with hyperneuroplasticity’s tendency to amplify and stabilize whatever is learned (McEwen, 2022).

Clinically, this dynamic is visible in obsessive-compulsive disorder (OCD), Tourette’s syndrome, pathological demand avoidance (PDA), and rejection sensitive dysphoria (RSD). In each case, behaviors that appear disruptive or excessive often begin as adaptive strategies to reduce threat or regain control. Yet because hyperneuroplasticity accelerates the embedding of these responses, the brain can lock into rigid loops more quickly and resist change more strongly. In OCD specifically, maladaptive habit formation illustrates how stress-driven learning can override goal-directed control (Gillan & Robbins, 2014). When the amygdala dominates for extended periods, these adaptations ossify and no longer serve their protective function.

I explored this process in Intersection of Intensity, suggesting that what often looks like pathology in gifted/galvanic and twice-exceptional populations can instead be understood as the brain’s best attempt at survival in environments that overwhelm its regulatory capacity. Hyperneuroplasticity provides the double edge: it fuels extraordinary adaptability and, at the same time, magnifies the risk of maladaptive overlearning.

A Common Imbalance Underlying Multiple Conditions

Rather than being entirely distinct, conditions such as complex post-traumatic stress disorder (cPTSD), rejection sensitive dysphoria (RSD), pathological demand avoidance (PDA), obsessive-compulsive disorder (OCD), and Tourette syndrome may reflect unique surface expressions of a shared systemic imbalance. In each of these conditions, symptoms that look very different on the surface, where flashbacks and hyperarousal in cPTSD, compulsions in OCD, 'social defiance' in PDA, or motor tics in Tourette’s, can all be traced back to a common circuitry pattern:

• Overfunctioning amygdala: heightened threat perception and emotional reactivity (Phelps & LeDoux, 2005).

• Hyperneuroplastic wiring: rapid, deeply entrenched adaptation that accelerates the consolidation of both protective and maladaptive responses (Goldfarb & Phelps, 2017).

• Under-supported PFC: reduced capacity for regulation, reflection, and nuanced response, limiting the ability to recalibrate once patterns set in (Arnsten, 2009; McEwen & Morrison, 2013).

Taken together, this framework shows how hyper-reactivity (maybe overexcitablity), repetitive loops, and difficulties with regulation arise across seemingly unrelated diagnostic categories. When viewed through the combined lenses of hyperneuroplasticity and monotropism, (a cognitive style in which attention tends to be intensely focused on a small number of interests or stimuli at a time), these conditions may be understood as different constellations of regulatory dissonance within the same stress-adaptation system (Arnsten, 2009; Gently, 2024).

Supporting Evidence from Neuroscience

Though often identified as a physiological burden, stress can also be understood as a neurological sculptor, actively reshaping emotional and decision-making circuits in ways that reverberate across lived experience (McEwen, 2007). Under chronic load, the prefrontal cortex (PFC) undergoes structural and functional remodeling, with weakened amygdala–PFC connectivity that shifts regulation toward hyper-reactivity (Liston et al., 2009; Maron-Katz et al., 2016). Acute stress further compounds this vulnerability, disrupting PFC function and rapidly impairing working memory and executive control (Arnsten, 2009; Hermans et al., 2014).

More recent evidence confirms that stress consistently biases functional connectivity toward the amygdala, reinforcing bottom-up threat processing at the expense of top-down regulation (Zhang et al., 2022; Goldfarb & Phelps, 2017). Using a hyperneuroplastic framework, these findings suggest that heightened plasticity accelerates both the sculpting and entrenchment of stress-induced patterns, making adaptive circuits more vulnerable to being rewired into maladaptive ones. Gifted and other neurodivergent individuals often experience this dynamic as disproportionate reactivity or exhaustion, when in reality it is the direct consequence of a brain primed for rapid change and deep processing. What looks like fragility may be hyperneuroplastic survival wiring; an adaptation that, when unsupported, becomes self-perpetuating and difficult to unlearn. When celebrated and understood, it may also be optimized for creative growth, flexible problem-solving, and adaptive resilience, allowing individuals to channel stress-shaped circuits in constructive and life-enhancing directions.

References

Arnsten, A. F. T. (2009). Stress signalling pathways that impair prefrontal cortex structure and function. Nature Reviews Neuroscience, 10(6), 410–422. https://doi.org/10.1038/nrn2648

Arnsten, A. F. T., Raskind, M. A., Taylor, F. B., & Connor, D. F. (2015). The effects of stress exposure on prefrontal cortex: Translating basic research into successful treatments for post-traumatic stress disorder. Neurobiology of Stress, 1, 89–99. https://doi.org/10.1016/j.ynstr.2014.10.002

Gently, P. (2024). Intersection of intensity: Exploring giftedness and trauma. Gifted Unlimited, LLC.

Gillan, C. M., & Robbins, T. W. (2014). Goal-directed learning and obsessive–compulsive disorder. Philosophical Transactions of the Royal Society B: Biological Sciences, 369(1655), 20130475. https://doi.org/10.1098/rstb.2013.0475

Goldfarb, E. V., & Phelps, E. A. (2017). Stress and the trade-off between hippocampal and striatal memory. Current Opinion in Behavioral Sciences, 14, 47–53. https://doi.org/10.1016/j.cobeha.2016.11.017

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Liston, C., McEwen, B. S., & Casey, B. J. (2009). Psychosocial stress reversibly disrupts prefrontal processing and attentional control. Proceedings of the National Academy of Sciences, 106(3), 912–917. https://doi.org/10.1073/pnas.0807041106

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McEwen, B. S., & Morrison, J. H. (2013). The brain on stress: Vulnerability and plasticity of the prefrontal cortex over the life course. Neuron, 79(1), 16–29. https://doi.org/10.1016/j.neuron.2013.06.028

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