Vagus Nerve Stimulation and Neuroplasticity

BruceBlaus, CC BY-SA 4.0 , via Wikimedia Commons

How Neuromodulation Supports Learning, Rehabilitation, and Recovery

Recovery after brain injury, neurological illness, or prolonged dysfunction depends fundamentally on the brain’s ability to adapt and reorganise. This adaptive capacity is known as neuroplasticity.

Crucially, this capacity is not fixed. It depends on the integrity of the systems that regulate attention, arousal, learning, salience, and physiological state. In practice, this means that the brain’s ability to change is shaped not only by what has been damaged, but by how effectively the remaining system can support adaptive reorganisation.

Vagus nerve stimulation (VNS) does not create recovery on its own. Rather, it is used to modulate the biological conditions under which neuroplastic change becomes more likely, particularly when stimulation is paired with meaningful experience, rehabilitation, or training.

Change in the brain is not simply driven by activity, but by how effectively that neural activity is regulated and stabilised over time.

This page includes a Frequently Asked Questions section and selected scientific references for readers wishing to explore the neuroscience of VNS and neuroplasticity in greater depth.

Neuroplasticity, Not Neurogenesis, Drives Adult Recovery

Two biological processes are often discussed in relation to recovery after brain injury or neurological dysfunction:

  • Neurogenesis – the formation of new neurons
  • Neuroplasticity – the reorganisation of existing neural circuits

While neurogenesis occurs robustly early in life, it is limited and region-specific in adulthood. In contrast, neuroplasticity remains active throughout life and is the primary mechanism by which adults recover function after brain injury or adapt to new demands.

Neuroplasticity includes:

  • strengthening or weakening of synapses
  • recruitment of alternative neural pathways
  • redistribution of function within and across brain networks
  • refinement of sensory, cognitive, and behavioural processing

For rehabilitation to be effective, plasticity must be selective, context-sensitive, and stabilised over time.

Neuroplasticity Is Experience-Dependent

Neuroplastic change does not occur simply because the brain is stimulated. It occurs when experience, attention, effort, salience, and feedback shape neural activity in a structured way.

This is why passive exposure alone is often insufficient. Neuroplastic change depends on meaningful engagement with experiences that shape behaviour, perception, regulation, or learning in ways that are functionally relevant.


As a result:

  • passive treatments have limited impact
  • repetition alone is insufficient without engagement
  • timing and behavioural context matter
  • adaptive learning depends on salience, relevance, and physiological state

The brain requires neuromodulatory signals to determine which experiences should drive lasting change. These regulatory systems effectively determine whether experience leads to meaningful adaptation or fades without lasting impact (Sara, 2009).

Plasticity Is Regulated, Not Continuously “On”

Neuroplasticity is not a continuously active process. It is gated by systems that regulate arousal, salience, uncertainty, attention, behavioural relevance, and learning rate.

Following stroke, traumatic brain injury, chronic stress exposure, neurological illness, or prolonged dysfunction, the systems that regulate attention, fatigue, arousal, autonomic stability, and learning may themselves become dysregulated. In this context, rehabilitation may fail not simply because of structural damage, but because the physiological conditions required for stable learning and adaptation are impaired.

This distinction is important. Functional outcome is determined not only by the extent of injury, but by whether the nervous system remains capable of adaptive self-reorganisation.

Neuromodulation and Plasticity Gating

A schematic of the neuromodulatory control of neuroplasticity

Plasticity is strongly influenced by neuromodulatory systems that regulate learning and behavioural adaptation.

Key systems include:

  • noradrenergic
  • cholinergic
  • dopaminergic
  • serotonergic

Among these, the noradrenergic locus coeruleus system appears to play a particularly important role in regulating adaptive learning, attentional gain, salience detection, and plasticity thresholds (Sara, 2015).

These systems do not merely “turn plasticity on.” They influence:

  • which experiences are prioritised
  • how strongly learning occurs
  • how rapidly adaptation takes place
  • whether change stabilises over time

Optimal neuroplasticity follows a regulatory balance. Both insufficient and excessive neuromodulatory activation may impair adaptive learning, reflecting an inverted-U relationship between arousal and plasticity (Atzori et al., 2016).

The Role of the Locus Coeruleus

The locus coeruleus is a small nucleus located in the brainstem and the brain’s principal source of noradrenaline. Despite its small size, it projects extensively throughout the cortex, limbic system, cerebellum, hippocampus, and spinal cord, giving it widespread influence over brain state and behavioural regulation (Sara, 2009).

Noradrenaline released from the locus coeruleus:

  • modulates synaptic plasticity
  • regulates attentional gain
  • supports learning from salient experience
  • influences behavioural flexibility
  • alters learning rate under changing environmental conditions
  • shapes the persistence and consolidation of memory

Research increasingly suggests that the locus coeruleus plays a central role in determining when the brain should adapt, how strongly it should adapt, and which experiences are important enough to stabilise into long-term change (Silvetti et al., 2013; Hansen, 2017).

The locus coeruleus and the widespread distribution of noradrenergic projections throughout the brain.

Vagus Nerve Stimulation and the Locus Coeruleus

Afferent fibres of the vagus nerve project to brainstem nuclei, particularly the nucleus tractus solitarius, which interacts closely with the locus coeruleus and broader neuromodulatory systems.

Through these pathways, vagus nerve stimulation can influence the regulatory systems involved in:

  • arousal
  • attention
  • salience processing
  • autonomic regulation
  • adaptive learning
  • neuroplasticity
Image showing the locus coeruleus and the distribution of noradrenaline in the brain.
The locus coeruleus and the distribution of noradrenaline in the brain.

When applied conservatively and in context, auricular VNS appears capable of influencing the conditions under which learning and adaptation occur, rather than directly imposing change itself.

This distinction is crucial.

VNS:

  • does not “force” plasticity
  • does not encode specific skills or memories
  • does not replace rehabilitation or learning

Instead, it may increase the brain’s responsiveness to meaningful experience, rehabilitation, and training.

In this sense, VNS acts on the conditions that determine whether learning can occur efficiently, rather than on the content of what is learned.

Cochlear Implants as an Example of Adaptive Neuroplasticity

An important example of this principle comes from cochlear implant research.

Cochlear implants do not simply restore hearing automatically. Rather, they provide a novel pattern of sensory input that the brain must gradually learn to interpret. Successful hearing outcomes therefore depend heavily on adaptive neuroplasticity.

Research has shown that activation of the locus coeruleus can dramatically accelerate this adaptation process in animal models, improving how rapidly the auditory system learns to interpret cochlear implant signals (Glennon et al., 2019).

This finding illustrates a broader principle central to rehabilitation neuroscience:

Recovery depends not only on stimulation or training itself, but on whether the nervous system is in a physiological state that supports adaptive learning.

The same principles are relevant across rehabilitation domains, including:

  • stroke recovery
  • motor rehabilitation
  • cognitive rehabilitation
  • behavioural adaptation
  • autonomic regulation
  • emotional regulation

Evidence from Rehabilitation Research

The strongest clinical evidence for VNS-enhanced neuroplasticity currently comes from stroke rehabilitation.

Randomised controlled trials have shown that VNS paired with task-specific motor rehabilitation leads to better functional outcomes than rehabilitation alone.

These findings provide proof of principle:

  • plasticity can be modulated
  • timing and pairing matter
  • neuromodulation amplifies learning rather than movement itself
  • rehabilitation outcomes depend partly on brain state regulation

Research in rehabilitation settings suggests that VNS may enhance neuroplastic adaptation when stimulation is paired closely with meaningful behavioural activity. However, VNS may also influence autonomic regulation, emotional state, and adaptive functioning more broadly during ordinary daily experience, even outside formal rehabilitation paradigms.

This aligns with broader neuroscience literature suggesting that the locus coeruleus-noradrenergic system regulates learning selectively rather than indiscriminately (Pettigrew, 1978; Sara, 2015).

Timing, Pairing, and Precision Matter

VNS is not simply a matter of increasing stimulation intensity.

Evidence increasingly suggests that effectiveness depends on:

  • timing
  • behavioural relevance
  • salience
  • tolerability
  • context

VNS appears especially useful when:

  • stimulation is sub-threshold and well tolerated
  • delivered in close temporal association with training or other treatment
  • paired with meaningful, goal-directed activity
  • integrated into broader rehabilitation or behavioural frameworks

High-intensity or indiscriminate stimulation does not necessarily enhance plasticity and may be counterproductive. Precision and restraint are central to clinical benefit.

How We Use VNS to Support Neuroplasticity

At Ormond Neuroscience, VNS is always embedded within a broader rehabilitation framework called Neuroharmonics. It is used to support learning and adaptation, not replace them.

Depending on the individual and clinical context, this may involve:

  • conservative auricular stimulation
  • pairing with rehabilitation, therapy, or structured cognitive work
  • behavioural and lifestyle intervention
  • attention to sleep, autonomic regulation, health, and emotional state
  • cognitive or psychological rehabilitation

The goal is not simply symptom reduction, but improving the physiological conditions that allow adaptive self-organisation and meaningful recovery to occur.

Limits and Expectations

VNS does not:

  • create recovery in the absence of effort
  • replace rehabilitation or therapy
  • bypass the need for repetition and meaningful engagement
  • guarantee functional improvement

Neuroplastic change is gradual and cumulative.

However, modern neuroscience increasingly recognises that meaningful neuroplasticity can remain active years after injury or illness when the appropriate conditions for adaptive learning are present.

In Summary

Neuroplasticity is the biological foundation of recovery, adaptation, and learning in the adult brain.

Vagus nerve stimulation can influence the regulatory systems that gate plasticity, particularly through interactions with the locus coeruleus-noradrenergic system. In this way, VNS may help make the brain more responsive to rehabilitation, experience, and meaningful behavioural change.

Recovery is therefore best understood not simply as a matter of stimulation or exercise, but as a process that depends on how effectively the nervous system can regulate and stabilise adaptive change over time.

When used carefully and in context, VNS is a physiologically grounded intervention that may support the conditions under which meaningful neuroplastic recovery becomes more likely.

Learn More

If you’ve wondered about the terminology, “vagus” is a noun referring to the nerve itself, whereas “vagal” is an adjective referring to things related to the nerve, such as vagal pathways, vagal modulation, or the commonly used (but strictly incorrect) phrase “vagal nerve stimulation.”

For further information about vagus nerve stimulation and its clinical applications, please see the following pages:

Ormond Neuroscience Web Pages

Talks and Interviews

For those interested in a deeper exploration of the neuroscience and clinical application of VNS, the following talks and interviews provide additional context:

Get in Touch

If you would like to explore whether vagus nerve stimulation is appropriate for your situation, please get in touch to arrange an interview.

Frequently Asked Questions

What is neuroplasticity?

Neuroplasticity refers to the brain’s ability to adapt, reorganise, and modify its functioning in response to experience, learning, injury, or environmental change. In adults, neuroplasticity is the primary mechanism through which rehabilitation, learning, and functional recovery occur.

What is the difference between neuroplasticity and neurogenesis?

Neurogenesis refers to the formation of new neurons, whereas neuroplasticity refers to changes in the organisation and functioning of existing neural networks.

Although limited neurogenesis may occur in specific regions of the adult brain, most meaningful recovery after injury or illness depends on neuroplasticity rather than large-scale growth of new neurons.

Does vagus nerve stimulation create neuroplasticity by itself?

No. Vagus nerve stimulation does not “force” neuroplasticity or directly create specific skills, memories, or behaviours.

Rather, VNS appears capable of influencing the physiological systems that regulate attention, salience, autonomic state, and adaptive learning, potentially making the brain more responsive to meaningful experience, rehabilitation, and behavioural change.

Why does VNS need to be used in context?

Neuroplasticity is strongly influenced by behavioural relevance, engagement, salience, and physiological state. This means that meaningful learning and recovery depend not only on stimulation itself, but on the context in which the brain is functioning.

At Ormond Neuroscience, VNS is therefore used within a broader framework that may include rehabilitation, behavioural intervention, psychotherapy, lifestyle modification, and attention to autonomic regulation and health.

Does VNS have to be paired with rehabilitation or training?

Not necessarily.

Research in stroke rehabilitation and perceptual learning often emphasises close pairing between VNS and structured training because this allows neuroplastic changes to be measured more clearly.

However, VNS may also influence autonomic regulation, emotional processing, stress physiology, and adaptive functioning more broadly during ordinary daily life, even outside formal rehabilitation paradigms.

Can neuroplasticity still occur years after injury?

Yes. Although neuroplasticity is often greatest early after injury, modern neuroscience increasingly recognises that adaptive neuroplastic change can continue for many years.

Meaningful improvement depends not only on time since injury, but on whether the nervous system remains capable of adaptive learning and functional reorganisation.

How does the locus coeruleus relate to VNS and neuroplasticity?

The locus coeruleus is a small brainstem nucleus that releases noradrenaline throughout much of the brain. It plays an important role in regulating attention, salience, arousal, behavioural flexibility, and adaptive learning.

The vagus nerve communicates with brainstem regulatory systems that interact closely with the locus coeruleus. Through these pathways, VNS may influence the conditions under which neuroplasticity and adaptive learning occur.

Selected References and Further Reading

Atzori, M., Cuevas-Olguin, R., Esquivel-Rendon, E., Garcia-Oscos, F., Salgado-Delgado, R. C., Saderi, N., Miranda-Morales, M., Treviño, M., Pineda, J. C., & Salgado, H. (2016). Locus ceruleus norepinephrine release: A central regulator of CNS spatio-temporal activation? Frontiers in Synaptic Neuroscience, 8, 25.
Frontiers in Synaptic Neuroscience

Engineer, N. D., Kimberley, T. J., Prudente, C. N., Dawson, J., Tarver, W. B., & Kilgard, M. P. (2019). Targeted vagus nerve stimulation for rehabilitation after stroke. Frontiers in Neuroscience, 13, 280.
Frontiers in Neuroscience

Glennon, E., Carcea, I., Martins, A. R. O., Multani, J., Shehu, I., Svirsky, M. A., & Froemke, R. C. (2019). Locus coeruleus activation accelerates perceptual learning. Brain Research, 1709, 39–49.
Brain Research

Glennon, E., Zhu, A. Y., Garcia, C., Wadghiri, Y. Z., Valtcheva, S., Svirsky, M. A., & Froemke, R. C. (2022). Locus coeruleus activity improves cochlear implant performance. Nature, 611(7935), 360–366.
Nature

Hansen, N. (2017). The longevity of hippocampus-dependent memory is orchestrated by the locus coeruleus-noradrenergic system. Neural Plasticity, 2017, 2727602.
Neural Plasticity

Kilgard, M. P., & Hays, S. A. (2021). The neuroscience of vagus nerve stimulation. Brain Stimulation, 14(2), 214–238.
Brain Stimulation

Pettigrew, J. D. (1978). The locus coeruleus and cortical plasticity. Trends in Neurosciences, 1, 53–57.
Trends in Neurosciences

Sara, S. J. (2009). The locus coeruleus and noradrenergic modulation of cognition. Nature Reviews Neuroscience, 10(3), 211–223.
Nature Reviews Neuroscience

Sara, S. J. (2015). Locus coeruleus in time with the making of memories. Current Opinion in Neurobiology, 35, 87–94.
Current Opinion in Neurobiology

Silvetti, M., Seurinck, R., van Bochove, M. E., & Verguts, T. (2013). The influence of the noradrenergic system on optimal control of neural plasticity. Frontiers in Behavioral Neuroscience, 7, 160.
Frontiers in Behavioral Neuroscience

Toussay, X., Basu, K., Lacoste, B., & Hamel, E. (2013). Locus coeruleus stimulation recruits a broad cortical neuronal network and increases cortical perfusion. The Journal of Neuroscience, 33(8), 3390–3401.
The Journal of Neuroscience

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