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Role of Neuroplasticity in Neuro-rehabilitation

Original Author - Dinu Dixon

Top Contributors - Oshomoji Olawale, Rucha Gadgil, Dinu Dixon, Candace Goh, Vidya Acharya, Tolulope Adeniji and Alexandra Stead  

Introduction

Neuroplasticity is the brain’s capacity to reorganise neural pathways and form new connections across the lifespan.[1] [2] Plasticity can be both adaptive (leading to improved functional outcomes) and maladaptive (leading to dysfunctional or harmful outcomes).[3] Phantom limb pain has been linked to maladaptive sensorimotor plasticity, which is an important consideration in rehabilitation approaches.[4] [5]

In neurorehabilitation, structured, task-specific practice harnesses these mechanisms to restore function and participation after neurological conditions.[6] Targeted therapies can drive experience-dependent change and support recovery when delivered with adequate dose, intensity, and specificity.[7]

[8]

In the context of neurorehabilitation, this phenomenon becomes particularly significant when addressing conditions such as stroke, traumatic brain injury, or neurodegenerative diseases.[9] Four key processes underpin neuroplasticity-based rehabilitation, each contributing to the structural and functional changes that support recovery:[7][10]

  1. Structural changes
  2. Functional reorganisation
  3. Experience-dependent plasticity
  4. Use dependent (activity-dependent) plasticity

Structural changes

Structural change refers to modification of neural architecture (neurones, synapses, glia, myelin) in response to experience, learning, injury, or rehabilitation.[10] The key aspects of structural changes associated with neuroplasticity are synaptic plasticity, dendritic growth and remodelling, axonal sprouting, neurogenesis, myelination changes, cortical map reorganisation.[1][9]

Synaptic plasticity

Synapses are the junctions between neurones where communication occurs. Structural changes in synaptic connections are a fundamental aspect of neuroplasticity.[11] These changes can involve the growth of new synapses (synaptogenesis), the elimination of existing ones (synaptic pruning), and changes in the strength of connections (synaptic strength).[11]

Dendritic growth and remodelling

Dendrites are the branching extensions of neurones that receive signals from other neurones.[12] Neuroplasticity can lead to the growth of new dendrites or changes in the branching patterns of existing ones. [12] This dendritic growth allows neurones to form new connections and enhance their communication with other neurones.

Axonal sprouting

Axons are the long projections of neurones that transmit signals to other neurones.[13] After injury or in response to learning, axons can undergo sprouting, where new branches emerge.[13] This can facilitate the formation of alternative pathways for signal transmission, bypassing damaged areas and promoting functional recovery.[14]

Neurogenesis

While traditionally believed to be limited in the adult brain,[15] recent research suggests that neurogenesis (the generation of new neurones) can occur in certain regions, such as the hippocampus.[16] Although its extent and functional significance in neurorehabilitation remain topics of active investigation.[16] Some studies report that hippocampal neurogenesis in humans occurs throughout physiological ageing, whilst others indicate it declines to negligible levels by early childhood.[17]

Myelination changes

Myelin is the insulating sheath around axons that facilitates faster signal transmission.[18] [19] Neuroplasticity can involve changes in myelination, such as the formation of new myelin sheaths or alterations in the thickness of existing ones.[19][20] These changes contribute to the efficiency of neural communication.

Cortical map reorganisation

In sensory and motor areas of the brain, cortical maps represent specific body parts or functions.[21] Following injury or changes in sensory or motor input, these maps can undergo reorganisation.[22] For example, following unilateral motor impairment, motor networks may reorganise across both hemispheres, with increased recruitment of contralesional motor regions and use-dependent changes in cortical representations.[23] In a 2021 randomised controlled trial involving 46 hospitalised post-stroke patients, repetitive transcranial magnetic stimulation (rTMS) was associated with improved motor recovery alongside changes in cortical motor network connectivity.[24]

Functional reorganisation

Functional reorganisation refers to the brain's ability to reassign or redistribute tasks and functions to different areas in response to injury, damage, or changes in sensory or motor input.[2] This process is a key aspect of neuroplasticity and is particularly relevant in the context of neurorehabilitation.[7]

Adaptive plasticity

Functional reorganisation is an example of adaptive plasticity, where the brain adapts to challenges by redistributing functions to undamaged areas.[2] This can involve changes in the activation patterns of neurones or the recruitment of additional brain regions to compensate for lost or impaired functions.[11]

When a specific area of the brain is damaged, the surrounding healthy tissue may take on the tasks that were previously handled by the damaged region.[2] This compensatory mechanism allows individuals to regain some level of function, even if the original neural circuitry has been disrupted.[11]

Brain functional networks reorganise in a task-dependent manner, with connectivity patterns varying according to task demands and motor execution.[25]

Cross-modal reorganisation

In cases where one sensory modality is impaired, such as vision or hearing loss, the brain may reorganise to enhance processing in the remaining intact modalities.[26] [27] For instance, following hearing loss, the auditory cortex may become recruited for visual or somatosensory processing, reflecting cross-modal reorganisation.

Time course of reorganisation

The extent of functional reorganisation often depends on the individual's experiences and activities.[25] Rehabilitation interventions that target specific functions or sensory-motor tasks can drive adaptive changes in the brain.[28][29] Repetitive and focused training can enhance the effectiveness of functional reorganisation.[25]

Functional reorganisation can occur over time as the brain continues to adapt to new conditions.[2] Immediate changes may be driven by the recruitment of nearby areas, while longer-term changes may involve more extensive reorganisation as a result of sustained rehabilitation efforts.[2][30]

Experience-dependent plasticity

Experience-dependent plasticity is a fundamental concept in neuroscience that describes the brain's ability to undergo structural and functional changes in response to experiences, sensory input, and learning.[1] [31] This type of neuroplasticity is driven by the specific activities and interactions an individual engages in, and it plays a crucial role in shaping the organisation and function of the nervous system.[31]

Neural activity and learning

Experience-dependent plasticity is closely tied to neural activity.[31] When neurones are repeatedly and consistently activated in response to a particular experience or stimulus, their activity patterns can gradually change, with some becoming more or less responsive over time, reflecting ongoing functional reorganisation of cortical representations.[32]

Learning is a classic example of experience-dependent plasticity.[31] When we acquire new information or skills, neural circuits associated with those activities are modified.[33] This can involve the formation of new synapses, changes in synaptic strength, and the reorganisation of neural networks to support the storage and retrieval of memories.[33]

Sensory cortex plasticity

Experience-dependent plasticity is most extensively characterised in sensory cortices, particularly the visual, somatosensory, and auditory systems, where changes in sensory experience drive robust structural and functional reorganisation of cortical circuits across development and adulthood.[34] For example, the visual cortex in the brain can undergo changes in response to visual experiences, and the auditory cortex can be shaped by auditory input. This plasticity allows the brain to adapt to specific sensory environments and optimise sensory processing.

Use-dependent plasticity

Use-dependent plasticity, also known as activity-dependent plasticity, refers to the phenomenon where neural circuits in the brain undergo structural and functional changes in response to specific patterns of activity or use. This type of neuroplasticity is based on the principle of "use it or lose it" whereby neural connections that are frequently used are strengthened, while those that are seldom used may weaken or be eliminated. Use-dependent plasticity plays a crucial role in learning, memory, and the adaptation of the nervous system to changes in sensory and motor experiences.[35]

Exercise-induced plasticity

Aerobic exercise is one of the most evidence-supported adjuncts to neuroplasticity-based rehabilitation with Brain-derived neurotrophic factor (BDNF) acting as a key mediator of exercise-induced neuroplasticity.[36] [11] BDNF promotes synaptogenesis (formation of new synapses) by binding to Tropomyosin receptor kinase B (TrkB receptors).[11]

Synaptic strength

Use-dependent plasticity is driven by the activity of neurones.[35] When a particular neural pathway is repeatedly activated, either through sensory input or motor output, the synaptic connections within that pathway can be modified.[35]

The strength of synaptic connections between neurones is a key aspect of use-dependent plasticity. Increased activity at a synapse can lead to the strengthening of that connection, a phenomenon known as long-term potentiation (LTP).[37] Conversely, decreased activity can result in long-term depression (LTD), a weakening of synaptic connections.[37]

Learning and skill acquisition

Learning new skills or acquiring new information often involves both use-dependent and experience-dependent plasticity, as there's an overlap in these areas.[38] [39] For example, practising a musical instrument, learning a new language, or mastering a motor task leads to changes in the neural circuits associated with these activities.[40]

Constraint-induced movement therapy (CIMT)

In the context of rehabilitation, use-dependent plasticity is leveraged to promote recovery after injury or neurological conditions.[35] Therapeutic interventions encourage the repeated and purposeful use of impaired limbs or functions to drive neuroplastic changes and improve motor skills.[29]

This is a rehabilitation technique that takes advantage of use-dependent plasticity.[41] In CIMT, the use of the unaffected limb is constrained, forcing individuals to rely on and intensively use the impaired limb.[42] This promotes the rewiring of neural circuits associated with motor control and coordination.[42] The original CIMT eligibility threshold requires at least 10° of active wrist extension, at least 10° of thumb abduction/extension, and at least 10° of extension in at least two additional digits on the affected hand (the '10 × 10 × 10' criteria).[43] Higher-functioning candidates typically demonstrate ≥20° of wrist extension and ≥10° of extension across all digits.[43][44]

Enriched environments

Exposure to a stimulating and enriched environment can facilitate use-dependent plasticity.[45] Varied sensory stimuli and engagement in cognitively and physically challenging activities contribute to the strengthening of neural connections.

Use-dependent plasticity is relevant in the context of various neurological disorders, including stroke and traumatic brain injury.[9]

Kleim and Jones ten principles

Kleim and Jones ten principles (specificity, repetition matters, intensity matters, time matters, salience matters, age matters, transference, interference, use it or lose it, use it and improve it) are foundational to neuroplasticity.[46] More information can be found here.

[47]

Summary

Neuroplasticity is the brain's capacity to form new connections by reorganising its neural pathways. Neurorehabilitation leverages and enhances neuroplasticity; the relationship is reciprocal. Rehabilitation programmes should embed the core principles outlined by Kleim and Jones to optimise outcomes.[46] Neuroplasticity-based strategies target network dysfunction across neurological conditions and can yield durable functional gains.[2] Additional details on how neuroplasticity can be applied to neurorehabilitation can be found on the neuroplasticity after stroke page.

References

  1. ↑ 1.0 1.1 1.2 Joshua AM. Neuroplasticity. InPhysiotherapy for adult neurological conditions 2022 Jun 21 (pp. 1-30). Singapore: Springer Nature Singapore.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Gazerani P. The neuroplastic brain: current breakthroughs and emerging frontiers. Brain research. 2025 Jul 1;1858:149643.
  3. ↑ Nava E, Röder B. Adaptation and maladaptation: insights from brain plasticity. Progress in brain research. 2011 Jan 1;191:177-94.
  4. ↑ Kikkert S, Johansen-Berg H, Tracey I, Makin TR. Reaffirming the link between chronic phantom limb pain and maintained missing hand representation. cortex. 2018 Sep 1;106:174-84.
  5. ↑ Makin TR, Scholz J, Filippini N, Henderson Slater D, Tracey I, Johansen-Berg H. Phantom pain is associated with preserved structure and function in the former hand area. Nature communications. 2013 Mar 5;4(1):1570.
  6. ↑ Reddy KJ. Introduction to Neurocognitive Rehabilitation. InInnovations in Neurocognitive Rehabilitation: Harnessing Technology for Effective Therapy 2025 Apr 27 (pp. 1-18). Cham: Springer Nature Switzerland.
  7. ↑ 7.0 7.1 7.2 Cramer SC, Sur M, Dobkin BH, O'Brien C, Sanger TD, Trojanowski JQ, Rumsey JM, Hicks R, Cameron J, Chen D, Chen WG. Harnessing neuroplasticity for clinical applications. Brain. 2011 Jun 1;134(6):1591-609.
  8. ↑ William Yan. Neuroplasticity
  9. ↑ 9.0 9.1 9.2 Shichita T, Ooboshi H, Yoshimura A. Neuroimmune mechanisms and therapies mediating post-ischaemic brain injury and repair. Nature Reviews Neuroscience. 2023 May;24(5):299-312.
  10. ↑ 10.0 10.1 Dzyubenko E, Hermann DM. Role of glia and extracellular matrix in controlling neuroplasticity in the central nervous system. InSeminars in Immunopathology 2023 May (Vol. 45, No. 3, pp. 377-387). Berlin/Heidelberg: Springer Berlin Heidelberg.
  11. ↑ 11.0 11.1 11.2 11.3 11.4 11.5 Marzola P, Melzer T, Pavesi E, Gil-Mohapel J, Brocardo PS. Exploring the role of neuroplasticity in development, aging, and neurodegeneration. Brain sciences. 2023 Nov 21;13(12):1610.
  12. ↑ 12.0 12.1 Stingl M, Draguhn A, Both M. A dendrite is a dendrite is a dendrite? Dendritic signal integration beyond the “antenna” model. Pflügers Archiv-European Journal of Physiology. 2025 Jan;477(1):9-16.
  13. ↑ 13.0 13.1 Richards LJ, Huang C, Bauer AQ, Lee JM. Long-range axon branching: contributions to brain network plasticity and repair. Nature Reviews Neuroscience. 2026 Jan 2:1-7.
  14. ↑ Tomé D, Almeida RD. The injured axon: intrinsic mechanisms driving axonal regeneration. Trends in Neurosciences. 2024 Nov 1;47(11):875-91.
  15. ↑ Sorrells SF, Paredes MF, Cebrian-Silla A, Sandoval K, Qi D, Kelley KW, James D, Mayer S, Chang J, Auguste KI, Chang EF. Human hippocampal neurogenesis drops sharply in children to undetectable levels in adults. Nature. 2018 Mar 15;555(7696):377-81.
  16. ↑ 16.0 16.1 Kempermann G. Adult neurogenesis. InNeuroscience in the 21st century: from basic to clinical 2022 Oct 18 (pp. 321-339). Cham: Springer International Publishing.
  17. ↑ Simard S, Matosin N, Mechawar N. Adult hippocampal neurogenesis in the human brain: updates, challenges, and perspectives. The Neuroscientist. 2025 Apr;31(2):141-58.
  18. ↑ Saab AS, Nave KA. Myelin dynamics: protecting and shaping neuronal functions. Current opinion in neurobiology. 2017 Dec 1;47:104-12.
  19. ↑ 19.0 19.1 Flower G, Vorthmann S, Fulton D, Hamilton NB. Plasticity of myelination. Physiology and Pathophysiology of Oligodendroglia. 2025 Jun 12:181-204.
  20. ↑ Chang KJ, Redmond SA, Chan JR. Remodeling myelination: implications for mechanisms of neural plasticity. Nature neuroscience. 2016 Feb;19(2):190-7.
  21. ↑ Brewer AA, Barton B. Cortical field maps across human sensory cortex. Frontiers in Computational Neuroscience. 2023 Dec 15;17:1232005.
  22. ↑ Moreno-López Y, Hollis ER. Sensory circuit remodeling and movement recovery after spinal cord injury. Frontiers in Neuroscience. 2021 Dec 8;15:787690.
  23. ↑ Kerr AL. Contralesional plasticity following constraint-induced movement therapy benefits outcome: contributions of the intact hemisphere to functional recovery. Reviews in the Neurosciences. 2022 Apr 26;33(3):269-83.
  24. ↑ Du J, Yao W, Li J, Yang F, Hu J, Xu Q, Liu L, Lv Q, Liu R, Ye R, Ma M. Motor network reorganization after repetitive transcranial magnetic stimulation in early stroke patients: a resting state fMRI study. Neurorehabilitation and neural repair. 2022 Jan;36(1):61-8.
  25. ↑ 25.0 25.1 25.2 Cheng HJ, Ng KK, Qian X, Ji F, Lu ZK, Teo WP, Hong X, Nasrallah FA, Ang KK, Chuang KH, Guan C. Task-related brain functional network reconfigurations relate to motor recovery in chronic subcortical stroke. Scientific Reports. 2021 Apr 19;11(1):8442.
  26. ↑ Alzaher M, Vannson N, Deguine O, Marx M, Barone P, Strelnikov K. Brain plasticity and hearing disorders. Revue neurologique. 2021 Nov 1;177(9):1121-32.
  27. ↑ Lucchesi M, Maya-Vetencourt JF, Rusciano D. Multisensory integration, brain plasticity and optogenetics in visual rehabilitation. Frontiers in neurology. 2025 Jul 10;16:1590305.
  28. ↑ Takeuchi N, Izumi SI. Rehabilitation with poststroke motor recovery: a review with a focus on neural plasticity. Stroke research and treatment. 2013;2013(1):128641.
  29. ↑ 29.0 29.1 Winterbottom L, Nilsen DM. Motor learning following stroke: mechanisms of learning and techniques to augment neuroplasticity. Physical Medicine and Rehabilitation Clinics. 2024 May 1;35(2):277-91.
  30. ↑ Sahrizan NS, Yahya N, Law ZK, Wan Zaidi WA, Nabilah Ismail U, Afifah NH, Azri A, Abdul Manan H. A systematic review of alterations in sensorimotor networks following stroke: implications for integration and functional outcomes across recovery stages. Frontiers in Neurology. 2025 May 27;16:1456146.
  31. ↑ 31.0 31.1 31.2 31.3 Lawal O, Ulloa Severino FP, Eroglu C. The role of astrocyte structural plasticity in regulating neural circuit function and behavior. Glia. 2022 Aug;70(8):1467-83.
  32. ↑ Nguyen ND, Lutas A, Amsalem O, Fernando J, Ahn AY, Hakim R, Vergara J, McMahon J, Dimidschstein J, Sabatini BL, Andermann ML. Cortical reactivations predict future sensory responses. Nature. 2024 Jan 4;625(7993):110-8.
  33. ↑ 33.0 33.1 Ma S, Zuo Y. Synaptic modifications in learning and memory–a dendritic spine story. InSeminars in cell & developmental biology 2022 May 1 (Vol. 125, pp. 84-90). Academic Press.
  34. ↑ Jamal T, Yan X, da Silva Lantyer A, Ter Horst JG, Celikel T. Experience-dependent regulation of dopaminergic signaling in the somatosensory cortex. Progress in Neurobiology. 2024 Aug 1;239:102630.
  35. ↑ 35.0 35.1 35.2 35.3 Tataranu LG, Rizea RE. Neuroplasticity and nervous system recovery: cellular mechanisms, therapeutic advances, and future prospects. Brain Sciences. 2025 Apr 15;15(4):400.
  36. ↑ Ashcroft SK, Ironside DD, Johnson L, Kuys SS, Thompson-Butel AG. Effect of exercise on brain-derived neurotrophic factor in stroke survivors: a systematic review and meta-analysis. Stroke. 2022 Dec;53(12):3706-16.
  37. ↑ 37.0 37.1 Bliss TV, Cooke SF. Long-term potentiation and long-term depression: a clinical perspective. Clinics. 2011 Jan 1;66:3-17.
  38. ↑ Fandakova Y, Wenger E. Skill learning in the developing brain: Interactions of control and representation systems. InPsychology of Learning and Motivation 2024 Jan 1 (Vol. 81, pp. 1-40). Academic Press.
  39. ↑ Leech KA, Roemmich RT, Gordon J, Reisman DS, Cherry-Allen KM. Updates in motor learning: implications for physical therapist practice and education. Physical therapy. 2022 Jan 1;102(1):pzab250.
  40. ↑ Olszewska AM, Gaca M, Herman AM, Jednoróg K, Marchewka A. How musical training shapes the adult brain: Predispositions and neuroplasticity. Frontiers in neuroscience. 2021 Mar 10;15:630829.
  41. ↑ Karaganova I, Mindova S. Neuroplasticity after stroke: Adaptive and maladaptive mechanisms in evidence-based rehabilitation. Journal of Stroke and Cerebrovascular Diseases. 2026 Jun 1;35(6):108634.
  42. ↑ 42.0 42.1 Choi H, Kim HJ. The Effect of Constraint-Induced Movement Therapy on Arm Function and Activities of Daily Living in Post-stroke Patients: A Systematic Review and Meta-Analysis. Brain & NeuroRehabilitation. 2024 Nov 21;17(3):e19.
  43. ↑ 43.0 43.1 Kwakkel G, Veerbeek JM, van Wegen EE, Wolf SL. Constraint-induced movement therapy after stroke. The Lancet Neurology. 2015 Feb 1;14(2):224-34.
  44. ↑ Singh P, Pradhan B. Study to assess the effectiveness of modified constraint-induced movement therapy in stroke subjects: A randomized controlled trial. Annals of Indian Academy of Neurology. 2013 Apr 1;16(2):180-4.
  45. ↑ Han Y, Yuan M, Guo YS, Shen XY, Gao ZK, Bi X. The role of enriched environment in neural development and repair. Frontiers in cellular neuroscience. 2022 Jul 21;16:890666.
  46. ↑ 46.0 46.1 Kleim JA, Jones TA. Principles of experience-dependent neural plasticity: implications for rehabilitation after brain damage. Journal of speech, language, and hearing research. 2008;51(1):S225-39.
  47. ↑ Neuro Nation Physical Therapy and Wellness. Understanding the 10 Principles of Neuroplasticity
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