HPHR Paper™ · No. 04
- Author
- Dr. Emmanuel Frantzis, DC, MSc, IFMCP, DACNB, DO(MP)
- Published
- Published September 2026
- Reading time
- 5 min read
- Level
- Intermediate
Executive Summary
One of the defining characteristics of the human nervous system is its remarkable capacity to adapt. This ability, known as neuroplasticity, underlies learning, memory, skill acquisition, and recovery following injury. Throughout life, experience continually modifies neural circuits, allowing the nervous system to respond to changing internal and external demands.¹–⁴
Although neuroplasticity is frequently discussed in the context of rehabilitation and recovery, contemporary neuroscience demonstrates that it is neither inherently beneficial nor harmful. The same biological mechanisms that support learning and recovery also allow the nervous system to reinforce persistent stress responses, inefficient movement strategies, and pain when those patterns are repeatedly experienced. Understanding neuroplasticity therefore requires consideration not only of its extraordinary adaptive capacity, but also of the factors directing that adaptation.
Scientific Foundation
The concept of neuroplasticity has fundamentally transformed modern neuroscience. For much of the twentieth century, the mature nervous system was considered relatively fixed once development had been completed. Subsequent research has demonstrated that this assumption is incorrect. Structural and functional modifications continue to occur throughout life in response to learning, behaviour, environmental demands, injury, and experience.¹²
This remarkable capacity explains why children acquire language with extraordinary efficiency, why musicians refine complex motor skills through years of deliberate practice, why athletes continually improve performance through repetition, and why recovery following neurological injury remains possible. Rather than representing a specialized biological process, neuroplasticity reflects one of the fundamental operating principles of the adaptive nervous system.
Landmark Concepts
Neuroplasticity as an Adaptive Process
Neuroplasticity refers to the nervous system’s capacity to modify its structure and function in response to experience. These adaptations occur across multiple levels of biological organization and include changes in synaptic efficacy, dendritic architecture, neuronal connectivity, neurotransmitter systems, gene expression, and large-scale neural networks.¹²
Importantly, neuroplasticity should not be viewed as inherently beneficial or detrimental. The nervous system continually adapts to the information it receives, becoming progressively more efficient at patterns that are repeatedly activated. Repetition strengthens neural pathways regardless of whether those adaptations ultimately support optimal function or contribute to less desirable physiological or behavioural responses.
This distinction represents an important shift in clinical thinking. Rather than asking whether neuroplasticity is occurring, the more meaningful question becomes: what is the nervous system adapting to?
Brain-Derived Neurotrophic Factor and Nervous System Adaptation
Among the molecular regulators of neuroplasticity, brain-derived neurotrophic factor (BDNF) has emerged as one of the most extensively investigated. BDNF plays essential roles in neuronal survival, synaptic transmission, learning, memory, and activity-dependent plasticity, making it a central mediator of nervous system adaptation.²⁴
Research has also explored the relationship between BDNF and persistent pain. Zanette et al. (2006)¹ reported that individuals with fibromyalgia who exhibited higher circulating concentrations of BDNF also demonstrated lower pressure-pain thresholds, suggesting an association between altered neuroplastic mechanisms and pain sensitivity. Similarly, Salgado and colleagues² reviewed the growing body of evidence linking BDNF with central sensitization and persistent pain while emphasizing its broader role in adaptive nervous system physiology.
These findings should be interpreted within their appropriate biological context. BDNF is not a “pain molecule.” Rather, it is a fundamental regulator of nervous system adaptation whose influence extends across development, learning, recovery, and experience-dependent plasticity. Its association with persistent pain reflects the complexity of neuroplastic mechanisms rather than the action of a single molecular pathway.
Current Evidence
Recent research has continued to expand our understanding of neuroplasticity by integrating molecular neuroscience, neuroimmunology, and systems biology. Contemporary investigations demonstrate that BDNF functions within a highly interconnected regulatory network involving neuroimmune signalling, synaptic plasticity, glial activation, and activity-dependent cortical reorganization rather than acting as an isolated molecular mediator.³
Current evidence also emphasizes that neuroplasticity should be understood as a systems-level process extending well beyond individual synapses or isolated brain regions. Recent reviews describe dynamic interactions among BDNF, inflammatory mediators, neurotransmitter systems, metabolic function, and large-scale neural networks as contributors to adaptive nervous system function across both health and disease.³⁻⁵ These observations reinforce the view that persistent pain cannot be explained by a single molecular mechanism but instead emerges through complex interactions occurring across multiple levels of nervous system organization.
Collectively, the contemporary literature strengthens one of the central themes of this paper: neuroplasticity is neither inherently beneficial nor harmful. It is a fundamental biological property of the nervous system whose effects are determined by the experiences, environments, and physiological conditions that continually shape its adaptation.
Discussion
One of the most important advances in contemporary neuroscience has been the recognition that neuroplasticity is a continuous biological process rather than an event limited to childhood, neurological injury, or formal rehabilitation. Throughout life, the nervous system remains responsive to experience, continually reorganizing itself in response to repeated patterns of sensory input, movement, cognition, emotion, and behaviour.
This understanding has important clinical implications. When most individuals hear the term neuroplasticity, they naturally associate it with recovery, learning, and improvement. Those associations are entirely appropriate, yet they represent only part of the picture. The scientific literature demonstrates that the nervous system does not distinguish between adaptive experiences that enhance function and those that reinforce less desirable physiological patterns. Just as repeated practice strengthens the neural circuits required for athletic performance or musical expertise, repeated exposure to persistent stress responses, protective movement strategies, or ongoing pain-related behaviours may also become increasingly efficient through experience-dependent plasticity.
Importantly, this should not be interpreted as suggesting that persistent pain is “learned” in a simplistic sense. Rather, it highlights the remarkable adaptive capacity of the nervous system and underscores the importance of understanding the biological, psychological, and environmental influences shaping that adaptation. Appreciating neuroplasticity therefore shifts the clinical question away from whether adaptation is occurring and toward understanding the direction in which the nervous system is adapting.
HPHR Clinical Perspective™
If the nervous system becomes progressively more efficient at whatever it repeatedly experiences, what patterns—physical, cognitive, emotional, behavioural, or physiological—might it be adapting to, and how might those adaptations influence long-term health and recovery?
Primary References
Zanette, S. A., et al. (2006). Higher serum brain-derived neurotrophic factor levels are associated with lower pressure-pain thresholds in fibromyalgia.
Salgado, A. S. I., et al. (Review of BDNF, central sensitization, and adaptive nervous system physiology.)
Cordeiro, R., et al. (2024). The role of brain-derived neurotrophic factor in chronic pain: Links to central sensitization and neuroinflammation. Biomolecules, 14(1), 71.
Nijs, J., et al. (2015). Brain-derived neurotrophic factor as a driving force behind neuroplasticity in neuropathic and central sensitization pain: A new therapeutic target? Expert Opinion on Therapeutic Targets, 19(4), 565–576.
(Recent review of systems neuroscience and adaptive neuroplasticity, 2024–2025. Final APA citation to be verified during publication editing.)