When Pain Persists: How Surgery, Illness, Injury and Trauma Can Lead to Central Sensitization

Pain usually serves an important biological purpose. It alerts us when something is wrong and encourages rest or protection while the body heals. In many cases, once an injury or illness resolves, the pain fades. However, for some individuals the pain does not disappear even after the original medical problem has been treated or the injury has healed. Medical tests may come back normal, tissues may have recovered, yet the pain continues. This can be deeply confusing and often leads people to feel dismissed or misunderstood within the healthcare system. One explanation for this phenomenon is central sensitization, a condition in which the brain and spinal cord become overly responsive, amplifying pain signals and interpreting normal sensations as threatening.

Central sensitization is increasingly understood as a form of nociplastic pain, meaning the pain arises primarily from altered nervous system processing rather than ongoing tissue damage. While central sensitization is a neurophysiological process, it is often shaped and maintained by learned psychological mechanisms such as conditioning and priming, which can reinforce patterns of heightened pain sensitivity over time. The symptoms are very real, but they reflect changes in how the nervous system interprets signals rather than injury in the body itself. This process can develop following surgery, physical injury, autoimmune illness, infection, or prolonged stress, and it often interacts with earlier life experiences that shape how the nervous system responds to threat.

What is central sensitization?

Central sensitization occurs when the central nervous system (the brain and spinal cord), becomes stuck in a heightened state of responsiveness. Under normal circumstances, pain functions like a protective alarm system. When tissue is injured, pain signals travel through the nervous system to alert the brain that something needs attention. As the injury heals, these signals gradually reduce and the system returns to its usual balance. However, when pain signals continue for a long period of time, the nervous system can begin to change. Neural pathways involved in pain transmission become more efficient and more easily activated. As a result, sensations that would normally feel neutral or mildly uncomfortable may begin to feel painful. In effect, the body’s alarm system becomes overly sensitive. Like a smoke detector that continues sounding long after the fire has been extinguished, the nervous system remains on high alert even when the original threat has passed. People experiencing central sensitization often report persistent or widespread pain, heightened sensitivity to touch or pressure, fatigue, brain fog, and symptoms that appear disproportionate to medical findings. This does not mean the pain is imagined or exaggerated. Rather, it reflects real biological changes in how the nervous system processes signals.

Chronic pain after surgery: when the nervous system remains on high alert

One pathway into central sensitization can occur following surgery. For example, some individuals continue to experience abdominal pain even after gallbladder removal, despite the absence of gallstones or ongoing gallbladder disease. This situation is sometimes referred to as post-cholecystectomy syndrome. In these cases, the initial pain may have begun with a genuine problem in the gallbladder. Over time, however, repeated pain signals can lead the nervous system to become sensitized. Even after the organ has been removed and the tissue has healed, the pain pathways remain active. The digestive system is particularly vulnerable to this process because it is closely connected to the nervous system through the gut–brain axis. The nerves that supply the digestive organs communicate constantly with the brain, helping regulate digestion, immune responses, and sensation. When these nerves become sensitized, a condition known as visceral hypersensitivity can develop. Normal digestive sensations may then be interpreted by the brain as painful or threatening. The nervous system effectively retains a memory of the pain, with repeated experiences becoming conditioned patterns that can be automatically reactivated. This makes it easier for discomfort to persist even after the original problem has been addressed.

Injury and the transition from acute to persistent pain

Another common pathway into central sensitization begins with physical injury. This may include events such as musculoskeletal strain, accidents, repetitive use injuries, or even relatively minor injuries that initially heal as expected. In the early stages, pain reflects genuine tissue damage and serves a protective function, encouraging rest and recovery. However, if pain persists beyond the normal healing period, the nervous system can begin to adapt in ways that outlast the injury itself. Prolonged guarding, fear of movement, and repeated attention to pain can reinforce neural pathways associated with threat and discomfort. Over time, the brain may continue to interpret signals from the previously injured area as dangerous, even when the tissue has healed. This can lead to ongoing pain, stiffness, or sensitivity without clear structural cause.

In some cases, the nervous system remains particularly sensitized in that specific location. As a result, a later, minor stimulus such as pressure, movement, or a routine procedure like a blood draw, may reactivate pain in the same area, even months after the original injury. This reflects a form of localized sensitization or pain memory, in which prior threat patterns are more easily re-triggered. In this way, an injury can act as the original trigger, while the persistence or recurrence of pain reflects changes within the nervous system rather than ongoing damage in the body.

Autoimmune disorders and central sensitization

Central sensitization is also frequently observed in autoimmune conditions such as Sjögren’s syndrome. Sjögren’s is a systemic inflammatory disease that primarily affects moisture-producing glands but can also involve the nervous system and other organs. Many individuals with the condition experience symptoms that extend far beyond dryness, including fatigue, widespread pain, and neurological symptoms. Research suggests that a significant proportion of individuals with Sjögren’s experience symptoms consistent with central sensitization. Several mechanisms may contribute to this interaction between the immune system and the nervous system. Inflammation associated with autoimmune disease can influence nerve function directly. Some individuals develop small fiber neuropathy, a condition affecting the tiny sensory nerves responsible for transmitting pain and temperature signals. This can produce burning, tingling, or hypersensitive pain sensations. In addition, many patients with autoimmune illnesses report experiencing pain that seems out of proportion to measurable inflammation levels. This does not mean the symptoms are psychological. Instead, it suggests that the nervous system itself may have become sensitized, amplifying pain signals beyond what inflammation alone would explain. In this way, autoimmune disease and central sensitization can coexist, each influencing the other.

Why pain can spread: chronic overlapping pain conditions

A common feature of central sensitization is that pain does not always remain confined to the original site of injury or illness. Instead, symptoms may gradually appear in other areas of the body. This occurs because nerves serving different organs often share pathways within the spinal cord. When these pathways become sensitized, signals from one organ can influence another. This phenomenon is sometimes referred to as cross-sensitization or cross-talk between organs. For example, individuals who initially develop gastrointestinal pain may later begin experiencing urinary or pelvic pain, even though these organs are structurally separate. The nervous system pathways that carry signals from the gut and the bladder interact within the spinal cord, allowing pain signals to spread across systems. This mechanism helps explain why certain conditions frequently occur together, including irritable bowel syndrome, interstitial cystitis or bladder pain syndrome, chronic pelvic pain, fibromyalgia, and persistent fatigue with cognitive fog. These disorders are sometimes described as Chronic Overlapping Pain Conditions (COPCs) because they share a common underlying mechanism: an overly sensitized nervous system.

How early life trauma can increase vulnerability to chronic pain

Research has also shown that early life stress and developmental trauma can increase the risk of central sensitization later in life (you can read more about developmental trauma here and here). The nervous system develops in response to the environments we grow up in. When a child experiences chronic stress, neglect, or trauma, the body’s stress-response systems may become calibrated toward constant vigilance and threat detection. These adaptations may be protective in the short term, but over time they can influence biological systems involved in pain processing. Studies suggest that early adversity can affect stress hormone regulation, immune system activity, and nervous system sensitivity. Together, these changes may make the body more reactive to physical stressors such as illness, surgery, or injury later in life. This does not mean trauma causes pain in a simplistic psychological sense. Rather, it may prime the nervous system, increasing its sensitivity and making persistent pain responses more likely when other medical events occur.

How central sensitization develops

Although each person’s experience is unique, the development of central sensitization often follows a similar pattern. It typically begins with an initial trigger, such as surgery, infection, autoimmune illness, injury, or prolonged stress. These events generate pain signals that activate the nervous system’s protective responses. If the pain signals persist for long enough, the nervous system begins to adapt to this constant stimulation. Pain pathways become more efficient, and the threshold for activating those pathways becomes lower. Over time, symptoms may begin to spread to other areas of the body and may be accompanied by fatigue, sleep disturbances, and cognitive difficulties. Eventually, the pain becomes centralized, meaning the nervous system itself is maintaining the pain response even when the original tissue damage has healed.

Treating central sensitization

Because central sensitization reflects changes in nervous system functioning, treatment often focuses on helping the nervous system return to a more regulated state. Medications that calm nerve signaling, such as gabapentin or related medications, may sometimes be used to reduce pain sensitivity. Increasingly, clinicians also incorporate pain neuroscience education, which helps individuals understand how pain is processed in the brain and why symptoms can persist even after physical healing. Psychological therapies also play an important role. Approaches such as Pain Reprocessing Therapy and trauma-informed somatic and psychotherapy aim to help the nervous system reduce fear responses associated with pain signals and gradually relearn patterns of safety and regulation. Lifestyle factors such as improved sleep, gentle physical activity, stress reduction, and supportive relationships can also contribute to calming the nervous system over time. The goal of these approaches is not to dismiss physical symptoms, but to address the underlying nervous system dysregulation that may be maintaining them.

A more complete understanding of chronic pain

Central sensitization challenges the traditional assumption that pain always reflects ongoing tissue damage. In many cases, chronic pain begins with a genuine physical illness or injury but later becomes sustained by changes in how the nervous system processes signals. Recognizing this allows clinicians and patients to move beyond a purely structural search for damage and toward a more comprehensive understanding of chronic pain. Surgery, autoimmune disease, trauma, and stress can all influence the nervous system in ways that shape how pain is experienced. Over time, the nervous system may learn patterns of heightened threat detection. Yet the nervous system is also capable of change. With appropriate support and treatment, it can gradually relearn patterns of safety and regulation, allowing pain responses to settle. For many people living with persistent symptoms, this understanding offers an important message of hope: while the nervous system may have learned pain, it also retains the capacity to learn recovery.

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Dr. Ingela Thuné-Boyle is a licensed Practitioner Health Psychologist and a Doctor in Behavioural Medicine who specializes in improving the quality of life of people struggling with long-term health problems, chronic pain and trauma. She runs a private online (telehealth) practice at www.ingelathuneboyle.com. You can find out more about her background [here], and more about her approach to therapy [here].

📩 Contact: For therapy or other enquiries, you can contact her at info@ingelathuneboyle.com.

Please note: Advice given in this blog is not meant to take the place of therapy or any other professional advice. The opinions and views offered by the author is not intended to treat or diagnose, nor is it intended to replace the treatment and care that you may be receiving from a licensed physician or mental health provider. The author is not responsible for the outcome or results following their information and advice on this blog.