When Pain Persists Beyond Infection

Some patients with Lyme disease experience pain that spreads, fluctuates, or intensifies long after the acute infection has been treated. Symptoms may worsen with stress, sleep disruption, or physical exertion and often seem disproportionate to findings on examination or testing. When conventional explanations fall short, it becomes necessary to consider how the central nervous system itself may be contributing.

This pattern is frequently misunderstood, yet it reflects a well-described biologic process. This article focuses on altered pain processing in the nervous system rather than tissue damage or pain tolerance.

What Central Sensitization Means

Central sensitization refers to a state in which the brain and spinal cord amplify sensory input, causing ordinary stimuli to be perceived as painful or overwhelming. Central sensitization reflects altered pain processing, not imagined or exaggerated symptoms.

The nervous system, after prolonged exposure to inflammatory or stress-related signals, may remain in a heightened state of alert. This shift represents neuroplastic change rather than psychological distress.  Pain intensity reflects how signals are processed, not the extent of structural injury.

Why Central Sensitization Can Develop in Lyme Disease

Lyme disease can create conditions that promote sensitization through sustained immune activation, delayed diagnosis, or repeated symptom flares. Over time, the nervous system adapts to repeated inflammatory and stress signals by maintaining increased sensitivity to sensory input.

Even after the infection itself is controlled, these changes in pain processing can persist. This helps explain why symptoms may continue despite appropriate treatment and reassuring test results.

How Patients Experience Central Sensitization

Patients often describe pain that migrates or becomes more widespread, along with heightened sensitivity to touch, sound, or light. Symptoms may flare unpredictably and are frequently influenced by emotional or physical stressors.

This variability can be confusing and discouraging, particularly when symptoms do not follow a linear course or respond to conventional pain treatments. Symptom fluctuation reflects dynamic nervous system signaling, not disease progression.

Central Sensitization and Peripheral Nerve Injury

Central sensitization does not exclude the presence of peripheral nerve injury. Many patients with Lyme disease show features of both sensitization and small fiber neuropathy. Neither mechanism is more “real” than the other, and both may require attention.

Understanding this overlap helps explain why single-diagnosis labels and one-dimensional treatment approaches often fall short.

For a discussion of peripheral nerve involvement, readers may wish to review Can Lyme Disease Lead to Small Fiber Neuropathy?, which addresses how infection-related nerve injury can contribute to chronic pain.

A Broader Perspective on Persistent Pain

Recognizing central sensitization allows clinicians and patients to move beyond overly simplistic explanations. Persistent pain in Lyme disease reflects complex, biologic interactions within the nervous system that are meaningful and potentially modifiable with thoughtful care.

Final Thought

Understanding central sensitization in Lyme disease restores context to symptoms that might otherwise be dismissed. When pain persists, it is not a failure of resilience or mindset but a signal that the nervous system has adapted to prolonged stress. Recognizing and naming this process is often the first step toward meaningful improvement.

Frequently Asked Questions

What is central sensitization in Lyme disease?
Central sensitization in Lyme disease refers to biologic changes in how the brain and spinal cord process pain, leading to amplification of sensory signals even after the initial infection has improved.

Is central sensitization the same as pain being psychological?
No. Central sensitization reflects altered nervous system processing and does not mean symptoms are imagined, exaggerated, or emotional in origin.

Can central sensitization occur along with nerve injury?
Yes. Many patients with Lyme disease have features of both peripheral nerve injury, such as small fiber neuropathy, and central sensitization, which can interact and overlap.

Why does pain move or change locations in Lyme disease?
Central sensitization affects how the brain interprets incoming signals rather than where signals originate. As processing shifts, pain perception may migrate even when tissues are unchanged.

References

Pain Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. 2011;152(3 Suppl):S2–S15. PubMed.

Journal of Neuropsychiatry and Clinical Neurosciences Fallon BA, et al. The neuropsychiatric manifestations of Lyme borreliosis. 2008;20(2):123–135. PubMed.

Frontiers in Neuroscience Bonaz B, Bazin T, Pellissier S. The vagus nerve at the interface of the microbiota–gut–brain axis. 2018. PubMed.

Lancet Neurology Tracey I, Mantyh PW. The cerebral signature for pain perception and its modulation. 2007;6(4):377–391. PubMed.

Related Readings 

Autonomic Dysfunction in Lyme Disease in small fiber neuropathy and Lyme disease

Central sensitization syndrome worsens Lyme disease symptoms