The Shared Terrain of Hyperneuroplasticity, the Blood-Brain Barrier, and Functional Neurological Disorder (HNP, BBB, EDS, MCAS, POTS, and FND? WTF!!??)
- Dr. Patty Gently
- Aug 27
- 9 min read
By Dr. Patty Gently on August 27, 2025
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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The Shared Terrain of Hyperneuroplasticity, the Blood-Brain Barrier, and Functional Neurological Disorder (HNP, BBB, EDS, MCAS, POTS, and FND? WTF!!??)
Introduction: A Constellation of Openness
When we talk about brain and body function, we often fall into linear explanations: this causes that, and dysfunction sits at the end of the chain. Medicine and psychology alike have tended to build categories around cause-and-effect thinking. In doing so, neurochemical imbalance explains depression, vascular block explains stroke, and trauma explains PTSD. These models can be useful, yet they can also oversimplify in areas where more holistic realities refuse linearity.
Hyperneuroplasticity (HNP) offers a way to understand these realities differently. I use HNP to describe an unusually high capacity for rapid, deep, whole-system neural reconfiguration. As a systemic profile, HNP includes heightened responsiveness, permeability, and adaptability across multiple domains. This framing shifts us away from reducing neurodifferences such as giftedness, ADHD, autism, or cPTSD solely to diagnoses or defects. And an HNP system doesn’t simply learn more quickly. It adapts in ways that can reshape identity, experience, and physiology. That adaptability can be extraordinary, fueling creativity and growth, and it can also be destabilizing when too much change or input floods the system at once.
In recent years, science has sought to catch up with what many neurodivergent and connective tissue populations already know through lived experience: that the boundaries between body systems are porous. The blood–brain barrier (BBB), long imagined as a fortress wall, turns out to be more of a responsive filter that tightens and loosens in response to inflammation, hormones, stress, and environment (Sweeney et al., 2019; Swissa et al., 2024). At the same time, conditions such as Ehlers–Danlos Syndrome (EDS), mast cell activation syndrome (MCAS), dysautonomia, and Functional Neurological Disorder (FND) reveal patterns of fragility and reactivity that are not limited to one organ system but cascade through the body (Keep, 2023).
Placed side by side, these phenomena are not isolated anomalies, nor are they strictly causal in relation to one another. Instead, they can be understood as parallel expressions of a hyperresponsive system that is adaptive, sensitive, and vulnerable at the same time. This post explores how hyperneuroplasticity, barrier permeability, connective tissue fragility, immune reactivity, autonomic variability, and functional reorganization interlock as a constellation of openness, rather than a pathologized chain of cause and effect.
The Blood–Brain Barrier: Gatekeeper and Conduit
The BBB is often described as the brain’s border patrol. It functions as a living interface that constantly regulates what enters brain tissue from the bloodstream and what is kept out (Sweeney et al., 2019; Brandl et al., 2023). Its structure is made up of several interdependent components that work together seamlessly. Endothelial cells form the thin, specialized lining of blood vessels and act as the primary interface between blood and brain tissue, while tight junctions hold these cells together with protein complexes that prevent unwanted substances from slipping through. Surrounding them are astrocytic end-feet, the terminal projections of astrocytes that wrap around blood vessels, fine-tuning permeability and nutrient exchange. Alongside them, pericytes, the contractile cells embedded in the vessel wall that stabilize capillaries and maintain barrier integrity. In concert, these elements ensure that the BBB is not a static wall but a dynamic gatekeeper: selectively transporting glucose for energy, hormones for signaling, and nutrients for metabolism, while actively blocking pathogens, toxins, and other threats that could destabilize neural networks.
Understanding the BBB helps us further understand what it means to have a “leaky brain."
A what!!?? Yup.
The concept of a leaky brain emerges when this finely tuned barrier becomes more permeable. Under conditions such as systemic inflammation, physical and psychological trauma, chronic stress, autoimmunity, infection, and oxidative stress, the tight junctions between endothelial cells can loosen (Alahmari et al., 2021; Hussain et al., 2021). When that happens, cytokines (small proteins released by immune cells that signal inflammation), immune factors (molecules such as antibodies or complement proteins that modulate immune defense), and excitatory neurotransmitters (chemicals like glutamate that increase neural activity) can cross into neural tissue, amplifying excitability and disrupting signaling balance.
It is important to note, however, that permeability itself is not inherently pathological. The BBB’s flexibility is part of its design. Temporary increases in permeability are sometimes necessary, for example, to allow immune surveillance or molecular signaling to adapt to changing conditions. In this way, barrier permeability can be understood as a double-edged function: it enables responsiveness to challenges, but when sustained or poorly regulated, it exposes the brain to neuroinflammatory stress and instability (Swissa et al., 2024; Cho & Roh, 2025).
The adaptive potential of BBB modulation has become an emerging field of research. Recent findings suggest that permeability shifts are not only markers of disease but may also participate in processes of neural growth, plasticity, and repair (Keep, 2023). This reinforces the broader theme: the systems that keep us most adaptable are often the same systems that leave us most vulnerable when stressors accumulate.
Connective Tissue, Immune Reactivity, and Autonomic Modulation
The integrity of the blood–brain barrier cannot be understood in isolation. It is influenced by the structure of connective tissue, the activity of the immune system, and the regulation of the autonomic nervous system. Each of these domains brings both strengths and vulnerabilities, and together they create a shifting physiological landscape that shapes barrier function.
Ehlers–Danlos Syndrome (EDS) highlights how connective tissue fragility reverberates across systems, shaping both structure and function. Arising from collagen irregularities, EDS makes tissue more flexible but less structurally stable. Blood vessels, joints, and skin all show this paradox of adaptability and fragility. The BBB itself is also collagen-rich: its basement membrane depends on extracellular matrix proteins for stability. In EDS, barrier integrity may therefore be more vulnerable (Severance et al., 2024; Kritas et al., 2020). Moreover, EDS is associated with cerebrospinal fluid leaks and neuroinflammation, further implicating barrier compromise (Severance et al., 2024).
Alongside this connective tissue dimension, many with EDS also experience mast cell activation syndrome (MCAS) and dysautonomia, both of which directly influence barrier dynamics. Mast cells, located at the BBB, release histamine and cytokines when activated, loosening tight junctions and altering permeability (Severance et al., 2024). Dysautonomia, in turn, can disrupt cerebral blood flow, placing stress on vascular stability and BBB regulation (Severance et al., 2024; Raj et al., 2021).
Together, these factors create a fluctuating barrier gate that is more porous in some moments and more restrictive in others. This variability helps explain why individuals may experience periods of neurological clarity one day and disarray the next. It also underscores that connective tissue, immune reactivity, and autonomic regulation are inseparable from the broader conversation about barrier function.
Functional Neurological Disorder: When Reorganization Turns Maladaptive
The conversation about hyperresponsivity and barrier integrity naturally leads to Functional Neurological Disorder (FND). FND is often misunderstood as a psychological issues that is “all in your head.” In reality, it reflects what happens when brain networks misfire or miscommunicate in the absence of structural damage. People with FND may experience seizures, immobilization, involuntary movements, sensory disturbances, or dissociation because regions of the brain fall out of sync with one another (Edwards et al., 2014).
When placed within the HNP–BBB frame, the dynamics of FND begin to make sense beyond the old judgment of feigning injury or illness. A leaky BBB can permit inflammatory molecules, glutamate, or toxins to enter the brain, destabilizing the fine-tuned balance of signaling (Brandl et al., 2023). In a system marked by hyperneuroplasticity, the brain adapts rapidly to such stressors, reorganizing networks in an attempt to maintain function (Marzola et al., 2023). Yet that very capacity for fast reorganization can, under sustained pressure, lead to maladaptive patterns. The result is a nervous system that expresses its instability through real, embodied symptoms, which remain hallmarks of FND.
This framing shows that “leaky brain” and “FND” are not competing explanations but rather complementary facets. The permeability of the barrier represents the substrate (the biological foundation or underlying physical conditions that set the stage for functional outcomes), while the clinical symptoms of FND represent the expression (the outward manifestation of those biological foundations, showing up as lived symptoms and functional experiences). Seen together, they illustrate how systemic openness and heightened adaptability can sometimes transform into vulnerability, underscoring the paradox at the core of hyperneuroplastic systems (Williams et al., 2021).
Hyperneuroplasticity, FND, and Shared Terrain
The framing of Functional Neurological Disorder leads directly into the broader picture of hyperneuroplasticity (HNP). HNP is not caused by a leaky BBB nor by connective tissue fragility, yet it exists alongside them as an expression of heightened systemic responsiveness. In this sense, FND can be seen as one way hyperneuroplasticity becomes destabilized under stress, while EDS, MCAS, and dysautonomia reveal parallel vulnerabilities in connective, immune, and autonomic systems.
Viewed narratively, these domains echo one another. Connective tissue in EDS bends and stretches more easily; mast cells in MCAS spring into reactivity quickly; autonomic instability in dysautonomia disrupts blood–brain balance; and the hyperneuroplastic brain and nervous system reorganizes with unusual speed. Each represents a form of systemic openness that remains flexible, adaptive, and fragile. Just as these systems embody responsiveness, the HNP system is more plastic and capable of dramatic reorganization when challenged (Marzola et al., 2023).
Taken together, permeability in barriers such as in the brain, gut, and vessels; connective tissue laxity; immune system reactivity; autonomic variability; hyperneuroplasticity; and functional expressions like FND can be understood as members of the same family of functions. Each operates with greater openness, giving rise to faster adaptation and also increased vulnerability. They are hyperresponsive systems. Seemingly adaptive and unstable, porous and transformative, the theme repeated across these domains is clear: openness may lead to both responsiveness and risk.
Toward Integration of a Shared Terrain
Zooming out, a broader pattern emerges. Structural fragility in EDS contributes to barrier vulnerability, immune reactivity in MCAS leads to frequent disruption, autonomic instability in dysautonomia adds variable stress to the brain, and hyperneuroplasticity presumably shapes brains that are unusually receptive to rewiring. Functional Neurological Disorder then appears as a lived expression of these destabilized systems (Severance et al., 2024; Marzola et al., 2023; Edwards et al., 2014).
These phenomena are not isolated, nor do they compete for explanatory power. They are parallel expressions of a hyperresponsive systemic profile, with each embodying permeability, adaptability, and heightened sensitivity in its own way. Within this frame, biology and function are not adversaries. They are partners in an ongoing dialogue. Recognizing this integrated reality allows people to validate the biological contributors, such as barrier fragility, immune activation, and vascular stress, while also acknowledging the functional outcomes that manifest as REAL seizures, fatigue, or pain. To see oneself in this light is to understand oneself as both hyperadaptive and hypervulnerable, rather than broken and beyond help.
Taken together, hyperneuroplasticity, the blood–brain barrier, EDS, MCAS, dysautonomia, and FND form a constellation of overlapping expressions of a body and brain that are open, sensitive, and dynamic. This reframing points toward interventions that aim to stabilize barriers, modulate immune activity, regulate autonomic flow, and most importantly, harness hyperneuroplasticity constructively through learning, creativity, and self-directed adaptation.
References
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Brandl, S., Lischke, V., Menger, M. D., & Relja, B. (2023). Blood–Brain Barrier Breakdown in Neuroinflammation. International Journal of Molecular Sciences, 24(16), 12699. https://doi.org/10.3390/ijms241612699
Cho, S.-Y., & Roh, H.-T. (2025). Combined Effects of Particulate Matter Exposure and Exercise Training on Neuroplasticity-Related Growth Factors and Blood–Brain Barrier Integrity. Atmosphere, 16(2), 220. https://doi.org/10.3390/atmos16020220
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