Chronic Pain Neuroscience: How Pain Reprocessing Therapy (PRT) Retrains the Brain

Neuropsychologist Ana Laura Utrilla Lack analyzes the neuroscience of chronic pain, central sensitization, and how pain reprocessing therapy (PRT) successfully retrains the brain.

Executive summary of this article’s key points:
1. What neuroplastic chronic pain is, why it persists, and its emotional, cognitive, and social impact.
2. The neuroscientific foundations of chronic pain.
3. What pain reprocessing therapy is and how it works (PRT).
4. How to apply pain reprocessing therapy (PRT) from a neuropsychological perspective.

Introduction

In 2023, nearly one in four adults (24.3%) reported having experienced chronic pain in the previous three months, and approximately 8.5% experienced pain so persistent that it significantly limited their daily life or work (Lucas & Sohi, 2024). 

Everyone has experienced some type of pain at some point in life. Pain acts as an alarm signal that directs our attention to the part of the body requiring care. It also helps us stop behaviors that, if repeated, could cause harm. The problem arises when that “alarm” becomes dysregulated. In such cases, the body remains in a constant state of alert, even though the actual danger is no longer present, resulting in chronic pain. 

What is chronic pain, and why does it persist even without physical injury?

According to the International Association for the Study of Pain (IASP, 2020), pain is an unpleasant experience associated with, or resembling that associated with, actual or potential tissue damage. However, pain is not merely a bodily signal or a direct response to a physical stimulus; it is a complex construction of the brain involving different components, including: 

• Emotional components, since it may be accompanied by fear, distress, or frustration. 
• Cognitive components, such as interpretations, expectations, and memories associated with pain. 

In this sense, pain functions as a protective signal and not necessarily as a direct marker of damage. 

Acute pain or chronic pain?

Acute pain	Chronic pain
Arises after an injury, inflammation, or some type of tissue damage.	Pain that persists for more than three months2. It may continue even when the tissue has healed and there is no active structural injury3.
The function of pain is protective, promoting self-care behaviors1.	The changes are associated with the central nervous system, since pain learning occurs and neuroplasticity acts maladaptively, consolidating hyperactive pain pathways1.
	It may be referred to as neuroplastic or nociplastic pain2, in which the brain generates the pain experience without a current tissue-damage signal.

Emotional, cognitive, and social impact of chronic pain

The emotional sphere is closely linked to chronic pain and the relationship can run in both directions: pain negatively affects emotional state, while emotions in turn influence the experience of pain. Therefore, understanding the emotional impact is highly relevant both to how a person learns to live with pain and to the intervention process aimed at unlearning the way they experience it. 

When pain persists for more than three months, it is expected to affect quality of life and daily activities, directly affecting the emotions and self-esteem of the person experiencing it (Bair et al., 2003). Chronic pain does not only hurt the body; it also causes emotional exhaustion. The following emotional states may be observed most frequently: 

Impact of chronic pain	Description	Consequences
Anticipatory anxiety	Arises when anticipating situations, places, movements, or memories that could trigger pain.	Generates avoidance behaviors and persistent fear, keeping the body in a constant state of alert.
Irritability and low frustration tolerance	Prolonged alertness and irritability associated with the persistence of the painful symptom.	Intense emotional reactions or outbursts in response to situations that were previously tolerable.
Frustration and helplessness	The experience of “doing everything and not improving” when conventional interventions are ineffective because there is no clear tissue damage.	Endless pursuit of treatments (allopathic and alternative) with only temporary relief, reinforcing discouragement.
Persistent sadness or discouragement	Feelings of hopelessness from believing there is no way out of the pain after unsuccessful attempts to improve.	Development of depressive symptoms, reduced pleasurable activities, and a negative impact on social and work relationships.
Interoceptive hypervigilance	The attentional system is trained to continuously monitor the body for signs of threat.	Biased interpretation of neutral stimuli as alarms and severe difficulty concentrating while reading or conversing.
Learned body memory	The brain establishes associations and conditioning between specific contexts and the onset of pain.	Pain activation even without tissue damage and generalization of avoidance behaviors in response to supposedly dangerous situations.
Catastrophic thoughts	Beliefs that the body is “getting worse” or that pain will progressively impair life.	Increased activation of brain threat networks and reinforcement of central sensitization processes.
Cognitive rigidity and rumination	Excessive consumption of executive-function resources focused on distress.	Limited mental flexibility and difficulty shifting attentional focus toward other life experiences.

Neuroscientific foundations of chronic pain

According to the model of pain reprocessing therapy (PRT), neuroplastic chronic pain is explained as a learned response of the central nervous system, in which the brain keeps pain pathways active as a protective mechanism, even when there is no current tissue damage to justify the signal (Gordon & Alon, 2021).

Neural plasticity and central sensitization: how the brain “learns” to feel pain

Neural plasticity is the brain’s ability to reorganize itself and form new synaptic connections based on experience (Pascual-Leone et al., 2005). Every learning process involves the repeated activation of specific neural circuits; the more they are used, the more efficient and automatic they become, a phenomenon described by the Hebbian principle of learning.

This same principle operates in chronic pain. In many cases, pain begins with an actual injury or inflammatory process. However, when that painful experience is accompanied by intense emotional states —such as fear, distress, or hypervigilance—, the neural circuits associated with pain are repeatedly activated. Even after the body tissue has healed, the pain circuit may become “overtrained,” making it more reactive and easier to activate, even automatically. 

This does not mean that the pain is imaginary. The painful experience is real, but its origin is no longer in the body’s periphery; instead, it lies in the activation of brain networks involved in threat detection, anticipation, and responses to danger. 

In this context, central sensitization refers to a phenomenon in which the central nervous system becomes hypersensitive, interpreting neutral or harmless bodily signals as painful. Daily activities that do not involve tissue damage—such as typing on a computer, walking short distances, or making gentle movements— can become pain triggers when they have previously been associated with discomfort, stress, or aversive experiences. 

In this way, stimuli that were originally neutral can acquire threat value. The brain remains in a sustained “alert mode”, with fear, anticipation, and protection circuits persistently activated, detecting danger where objectively there is none.

Neural networks involved and cognitive changes associated with pain

No single brain region is responsible for pain; rather, it depends on the sustained activation of multiple neural networks that process the sensory signal, as well as its cognitive interpretation and emotional meaning (Wager et al., 2013). In neuroplastic pain, these networks are hyperactive or dysregulated, which is why pain can be experienced even without peripheral damage.

The main structures involved include: 

Brain structure	Function in chronic pain	Impact on the patient
Insula	Increased perception of internal signals.	Constant bodily hypervigilance.
Amygdala	Processing of fear and threat.	Association of pain with danger and anxiety. Avoidance and negative anticipation.
Anterior cingulate cortex (ACC)	Appraisal of suffering and attributed emotional relevance.	Pain perceived as exhausting and emotionally draining.
Salience network	Detection of stimuli relevant to survival.	Pain displaces every other attentional focus.
Default mode network	Self-referential states and rumination.	Repetitive thoughts focused on pain: “Why does it hurt?”.

Together, these changes in the brain’s functional connectivity explain why chronic pain is not merely a sensory experience, but a global brain state involving body perception, emotion, attention, memory, and personal meaning. Pain persistence is reinforced by the interaction between these networks: bodily hypervigilance, fear of pain, attention biased toward internal sensations, and negative beliefs about one’s body keep pain pathways active, consolidating maladaptive learning in the nervous system.

What is pain reprocessing therapy (PRT) according to Alan Gordon?

Pain reprocessing therapy (PRT) is an approach developed by Alan Gordon (2021) and his team, based on findings from pain neuroscience. This model is based on evidence that, in many cases of chronic pain, the source of pain is not an active structural injury but a misinterpretation by the brain, which perceives certain bodily signals as dangerous when they are not. 

From this perspective, neuroplastic pain persists because the central nervous system has learned to associate certain sensations, movements, or contexts with threat. PRT seeks to modify this association, promoting a shift from interpreting “danger” to interpreting “safety.” In other words, the goal is not to ignore pain, but to help the brain recognize that, in the absence of tissue damage, the pain signal does not pose a real risk to the body. 

PRT principles and how it works to retrain the brain

Before beginning pain reprocessing therapy, it is essential to conduct an appropriate medical evaluation to rule out active structural, inflammatory, infectious, or neurological causes that could explain the pain. Pain reprocessing therapy (PRT) is not intended to replace medical care, but to complement it when it has been established that no active injury accounts for the persistent pain. 

Once current tissue damage has been ruled out, PRT is based on the following principles: 

• Pain can be real even without structural damage: the pain experience is genuine, but its source may lie in learned and sensitized brain circuits.
• The brain learns to feel pain and can also unlearn it: through neural plasticity, threat circuits associated with pain can weaken when pain is no longer interpreted as danger. 
• Safety is the central element of change: brain retraining occurs when a person can experience bodily sensations from a state of calm and safety rather than fear or hypervigilance. 
• Attention and the meaning assigned to pain influence its intensity and persistence: changing the internal narrative from threat to safe protection promotes the progressive deactivation of pain networks.

In this way, PRT acts directly on the mechanisms of learning and central sensitization, helping the nervous system recalibrate its response to bodily sensations that were previously experienced as dangerous. 

Practical exercises and techniques based on PRT

Implementing PRT relies on a solid psychoeducation process designed to help people understand the neuroplastic origin of their pain. Since many people with chronic pain constantly seek a physical or structural cause to explain their discomfort, it is essential to broaden this understanding and introduce the possibility that pain may be mediated by the central nervous system.

Through this process, a person can begin to observe their pain with greater distance and curiosity: 

• In what contexts does it appear? Does it always occur during the same activity, or does it vary depending on emotional state? 
• Does its intensity change depending on the environment, stress, or company? Does the location of the pain change? 

These questions help identify patterns of pain activation that would be difficult to explain solely by tissue damage. Recognizing these variations fosters an understanding that neuroplastic pain does not imply real danger to the body, but rather a learned response of the nervous system. 

One of the core techniques of PRT is somatic tracking, described by Gordon (2021) as a process that integrates three main components:

Main component	Clinical objective	Technique
Mindfulness	Nonjudgmental observation.	Approach the sensation with curiosity, not fear.
Reappraisal from a position of safety	Change the meaning of pain.	“There is no structural damage; my body is safe.”.
Positive affect and a kind tone	Reduce the negative emotional burden.	Use compassionate language, gentle humor, or metaphors.

Initially, somatic tracking is usually guided by a therapist trained in PRT, so that the person learns to practice the technique independently in daily life. Through repeated practice, the brain begins to associate bodily sensations with states of calm and safety, promoting the progressive weakening of learned pain circuits. 

Scientific evidence and recent clinical cases

Pain reprocessing therapy (PRT) has empirical support, particularly from the randomized clinical trial published by Ashar and colleagues (2021), which evaluated the efficacy of this intervention in people with chronic low back pain. The results showed that participants who received PRT experienced:

1. Significant reductions in pain intensity compared with control groups.
2. Changes in the activity of brain regions involved in pain and threat processing. 

These findings support the hypothesis that neuroplastic chronic pain can be modified through interventions aimed at changing the brain’s interpretation of pain rather than focusing exclusively on peripheral treatment. Clinically, multiple case reports and clinical series have documented relevant functional improvements, such as a gradual return to avoided activities, reduced fear of movement, and restored social and work participation. 

Although PRT is not a universal intervention for every type of chronic pain, the available evidence suggests that it is a particularly useful treatment option when no active structural damage is identified and central sensitization and pain-learning mechanisms predominate. 

Practical application of pain reprocessing therapy (PRT) in neuropsychology

Pain reprocessing therapy (PRT) can be naturally integrated into neuropsychological practice for patients with neuroplastic chronic pain by addressing the cognitive, emotional, and behavioral processes that maintain activation of threat circuits. This practice is not limited to a merely symptomatic intervention; neuropsychology can play an important role in the relearning process, which seeks to modify attentional and interpretive patterns that reinforce central sensitization. 

Cognitive, emotional, and behavioral assessment of patients with chronic pain

As part of the neuropsychological assessment of patients with chronic pain, it is clinically relevant to explore the following components: 

1. Cognitive components:
   • Attentional biases toward bodily sensations and threat signals.
   • Catastrophic or hypervigilant interpretive style regarding pain.
   • Dysfunctional beliefs about the body, damage, and disability (“if it hurts, something is wrong,” “movement will hurt me”).
   • Cognitive rigidity and pain-focused rumination.
2. Emotional components:
   • Levels of anticipatory anxiety, fear of movement (kinesiophobia), and fear of injury.
   • Affective states associated with persistent pain, such as frustration, hopelessness, or irritability.
   • Difficulties regulating emotions when pain appears.
3. Behavioral components:
   • Avoidance behaviors and progressive reduction of meaningful activities.
   • Body-checking behaviors and constant searching for signs of pain.
   • Body-protective patterns that reinforce the perception of fragility.

From a PRT perspective, this assessment does not aim only to describe the patient’s profile, but to identify the feedback loops that keep threat circuits active (attention → interpretation → emotion → behavior → increased sensitization). This functional formulation makes it possible to design interventions aimed at interrupting these loops and promoting corrective experiences of bodily safety. 

Integration with physical, occupational, and medical therapies

Working with patients with chronic pain usually requires an interdisciplinary approach, in which coordinating healthcare professionals from different fields is essential so that the messages patients receive from each professional are not contradictory or reinforce the perception of pain as structural damage or bodily fragility. 

Clinically, integration with other disciplines makes it possible to:

• With the medical team: Align clinical communication with a biopsychosocial model of pain, avoiding alarmist explanations that reinforce the interpretation of danger. Medical validation that there is no active damage facilitates the work of reconceptualizing neuroplastic pain.
• With physical therapy and rehabilitation: Promote gradual exposure to movement within a framework of safety, reducing behavioral avoidance and fear of movement. PRT addresses the cognitive interpretation of movement as safe, thereby enhancing the effects of physical intervention.

Consistency across disciplines helps patients receive consistent safety messages, reducing activation of threat circuits and promoting neuroplastic relearning. 

Conclusion

In conclusion, addressing chronic pain through the pain reprocessing therapy (PRT) model proposes a paradigm shift in understanding pain through pain neuroscience: from a signal exclusively associated with tissue damage to a learned nervous-system response that can persist even in the absence of active injury. From the perspective of chronic pain neuropsychology, this approach makes it possible to conceptualize pain as a dynamic phenomenon that can be modulated through experience, learning, and the cognitive-emotional reframing of bodily signals.

Neuroplasticity, understood as the brain’s ability to reorganize its circuits based on experience, is the neuroscientific foundation that explains both pain chronification and the possibility of reversing it. From current research on the brain and chronic pain, we know that just as threat circuits can become overtrained through repeated painful experiences associated with fear, bodily hypervigilance, and central sensitization, these circuits can weaken when the body learns through experience that it is safe and that pain does not represent a real danger. 

Beyond pain reduction, this approach promotes a change in the patient’s relationship with their body, supporting the recovery of function, autonomy, and participation in meaningful activities. Therefore, the intervention is not limited to “controlling the symptom,” but facilitates a process of neurofunctional relearning of pain in which the brain can modify the circuits involved in chronic pain and reduce the persistent activation of threat networks. 

From this perspective, treatment of neuroplastic chronic pain aims to help the nervous system leave its sustained alert mode and return to a state of regulation and safety, drawing on the principles of pain neuroscience and interventions such as pain reprocessing therapy, which seek to retrain the brain to interpret bodily signals within a framework of safety rather than danger. 

References

• Ashar, Y. K., Gordon, A., Schubiner, H., Uipi, C., Knight, K., Anderson, Z., Carlisle, J., Polisky, L., Geuter, S., Flood, T. F., Kragel, P. A., Dimidjian, S., Lumley, M. A., & Wager, T. D. (2021). Effect of pain reprocessing therapy vs placebo and usual care for patients with chronic back pain: A randomized clinical trial. JAMA Psychiatry, 78(1), 13–23. https://doi.org/10.1001/jamapsychiatry.2021.2669
• Bair, M. J., Robinson, R. L., Katon, W., & Kroenke, K. (2003). Depression and pain comorbidity: A literature review. Archives of Internal Medicine, 163(20), 2433–2445. https://doi.org/10.1001/archinte.163.20.2433
• Butler, D. S., & Moseley, G. L. (2013). Explain pain (2nd ed.). Noigroup Publications.
• Gordon, A., & Alon, A. (2021). The way out: A revolutionary, scientifically proven approach to healing chronic pain. Avery.
• International Association for the Study of Pain. (2017). IASP terminology.
• Lucas, J. W., & Sohi, I. (2024). Chronic pain and high-impact chronic pain in U.S. adults, 2023 (NCHS Data Brief No. 518). National Center for Health Statistics.
• Pascual-Leone, A., Amedi, A., Fregni, F., & Merabet, L. B. (2005). The plastic human brain cortex. Annual Review of Neuroscience, 28, 377–401. https://doi.org/10.1146/annurev.neuro.27.070203.144216
• Raja, S. N., Carr, D. B., Cohen, M., Finnerup, N. B., Flor, H., Gibson, S., et al. (2020). The revised International Association for the Study of Pain definition of pain: Concepts, challenges, and compromises. Pain, 161(9), 1976–1982.
• Sluka, K. A., Song, X.-J., Stevens, B., Sullivan, M. D., Tutelman, P. R., Ushida, T., & Vader, K. (2020). The revised IASP definition of pain: Concepts, challenges, and compromises. PAIN, 161(9), 1976–1982.
• Wager, T. D., Atlas, L. Y., Lindquist, M. A., Roy, M., Woo, C.-W., & Kross, E. (2013). An fMRI-based neurologic signature of physical pain. New England Journal of Medicine, 368(15), 1388–1397. https://doi.org/10.1056/NEJMoa1204471

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