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Neuroplastic symptoms · Spine, back and neck

Ankylosing spondylitis: when the inflammation is treated and the pain stays.

Your bloodwork is calmer, the scan is stable, the biologic is working. So why does your back still hurt the way it did?

Karuna LabsUpdated 2026-10-146 min read
The short answer

Ankylosing spondylitis (AS), now often grouped under axial spondyloarthritis, is an inflammatory arthritis of the spine and large joints that usually begins in early adulthood and can stiffen the spine over time. It is a genuine disease with real inflammation, and it is not caused by neuroplastic symptoms. The ATNS Index of Neuroplastic Symptoms is clear on that, and equally clear that when the symptoms, the course over time or the response to treatment do not match what AS should produce, assessing for neuroplastic symptoms is reasonable. Neuroplastic symptoms are real symptoms generated by a sensitized nervous system rather than by active damage. Research now shows that a large share of people with AS carry this extra layer, and an approach exists that addresses it.

This page is about understanding the condition and the role the brain and nervous system can play in it. It is not a diagnosis. Your own clinicians know your case.

What ankylosing spondylitis is

Ankylosing spondylitis is an inflammatory arthritis that targets the spine, the sacroiliac joints where the spine meets the pelvis, and sometimes the hips, shoulders and knees. It tends to start between the late teens and mid thirties, with deep, dull back pain and morning stiffness that eases with movement rather than rest. Over years, inflammation can lead to new bone forming between vertebrae, which reduces flexibility and, in some people, produces a stooped posture.

Doctors increasingly use the umbrella term axial spondyloarthritis, with AS as the form that shows clear changes on X-ray. Diagnosis rests on symptoms, imaging, inflammatory markers and often the HLA-B27 gene. Treatment with anti-inflammatory drugs, exercise and biologic medications that block TNF or IL-17 has changed what living with AS looks like.

This is a structural, immune-driven disease. Nothing in this article suggests otherwise. The question is what else can be happening alongside it.

The neuroplastic contribution

The ATNS Index of Neuroplastic Symptoms states that ankylosing spondylitis is not caused by neuroplastic symptoms. It adds a practical caveat: if the symptoms, the way they change over time, or the response to treatment are not what AS would be expected to produce, an assessment for neuroplastic symptoms is reasonable.

Neuroplastic symptoms are real, physical symptoms produced by learned pathways in the brain and nervous system, a kind of alarm system that has become sensitized, rather than by ongoing damage in the body. They are not imaginary and not a sign of weakness. Because they are learned, they can be unlearned.

In AS, the two can coexist. Years of genuine inflammatory pain give the nervous system plenty of reason to turn its alarm up. Fear of flares, bracing against movement, poor sleep and the stress of a lifelong diagnosis all feed that process. The result is pain that outlasts or outsizes the inflammation that started it. Signs that suggest this layer include:

What the research shows

The evidence for a sensitized nervous system in AS is stronger than many patients are told. A 2026 study of people with axial spondyloarthritis found higher central sensitization scores than in healthy controls, and those who also met fibromyalgia criteria scored higher on central sensitization, pain catastrophizing and sleep disturbance. The authors concluded that these factors contribute to disease burden on their own, independent of inflammation.

A Brazilian study of 52 patients with radiographic axial spondyloarthritis at a tertiary hospital reported features of central sensitization in roughly six in ten. About a third of those who did not meet fibromyalgia criteria still showed it, which means this is not only a story about people with two diagnoses.

A nationwide Korean cohort study found that people with AS had a higher risk of going on to develop fibromyalgia than people without AS, and the authors pointed to central sensitization as the shared mechanism. These are observational studies, so they show association rather than cause, and none tested a treatment aimed at the nervous system in AS specifically. Taken together, though, they explain a familiar clinical picture: controlled inflammation and persistent pain. You can read more about the mechanism in why chronic pain persists.

Signs the brain may be part of the picture

Try this today

Separate the two kinds of pain

For one week, keep a two-column note on your phone. In the first column, log morning stiffness: how long it lasts and whether movement eases it, which is the classic inflammatory pattern. In the second, log pain that appears during the day, where it is, and what was happening in your mind and life just before: a tense meeting, a bad night, a worried thought about your spine. At the end of the week, look at the second column. If much of your pain lives there, that is useful information, not bad news. It points to a layer you can work on directly.

A solution that addresses it

Alongside your rheumatology care, there is an approach that addresses the nervous system's contribution: pain and symptom reprocessing. It begins with education about neuroplastic symptoms, so that pain beyond the inflammation makes sense rather than feeling like a mystery or a failure. It uses somatic tracking (observing sensations with curiosity instead of alarm), work to reduce fear and threat, a paced and graded return to movement, emotional awareness and expression, and acceptance and commitment skills. Trained clinicians deliver it, and digital programs increasingly make daily practice possible.

Cindra is a daily AI companion built around these approaches, with daily check-ins, short practices and plain-language lessons for people whose symptoms have a neuroplastic component. If your AS is treated but your pain has not followed, you can join the waitlist.

What to do next

Keep your rheumatology care exactly as it is. Do not change or stop medication without your doctor. AS needs ongoing monitoring, and new symptoms such as eye pain or redness, sudden severe back pain after a fall, bowel changes or chest pain need prompt medical attention, since AS can affect the eyes, gut and heart.

Then ask a direct question at your next appointment: given my markers and imaging, how much of my pain do you think is inflammation? If the honest answer is not all of it, ask whether your pattern fits central sensitization or neuroplastic symptoms. If it might, start learning. Understanding why hurt is not always harm is the first step, and gentle, consistent movement is both AS treatment and nervous-system retraining at once.

Questions people ask

Is ankylosing spondylitis a neuroplastic condition?

No. The ATNS index states it is not caused by neuroplastic symptoms. It does note that when symptoms, course or treatment response are not what AS should produce, assessing for neuroplastic symptoms is reasonable, and research shows a sensitized nervous system is common in people with AS.

Why do I still hurt when my biologic is working?

Biologics reduce inflammation, which is one source of pain. They do not retrain a nervous system that has learned to amplify signals after years of pain. Studies find central sensitization in a large share of people with axial spondyloarthritis, which helps explain pain that persists when markers are quiet.

Does this mean my pain is in my head?

No. Neuroplastic pain is produced by real changes in how the brain and spinal cord process signals. It hurts as much as any other pain. The difference is the cause, and a learned cause is one that can change.

Should I still exercise?

Yes, with your care team's guidance. Exercise is a core AS treatment and also one of the best ways to teach a sensitized nervous system that movement is safe. Start where you are and build gradually rather than pushing through and crashing.

References

  1. Multidimensional contributors to disease burden in axial spondyloarthritis: role of central sensitization, catastrophizing and sleep disturbance. 2026. PMID 41526946
  2. Evaluation of the presence of neuropathic pain and/or central sensitization in patients with radiographic axial spondyloarthritis followed at a tertiary hospital. PMC13488830
  3. Patients With Ankylosing Spondylitis Are Associated With High Risk of Fibromyalgia: A Nationwide Population-Based Cohort Study. PMC7993057
Source: the definition and neuroplastic-contribution framing on this page summarise, in our own words, the entry “Ankylosing Spondylitis” in the Index of Neuroplastic Symptoms (2026) published by the Association for the Treatment of Neuroplastic Symptoms (ATNS, neuroplastic.org). The research summary cites the PubMed records listed above.
Cindra

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Cindra is an AI companion from Karuna Labs built around acceptance and commitment therapy and the science of neuroplastic symptoms. It checks in with you each day, helps you notice what your symptoms are pulling you away from, and nudges you back toward the things that matter. Cindra is invite-only while we build it with early members.

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This article is for general education and is not medical advice, and it does not diagnose or treat any condition. Persistent symptoms deserve a proper medical assessment to rule out disease or injury before a neuroplastic explanation is considered. If your symptoms are new, changing, or come with red-flag signs such as fever, unexplained weight loss, numbness or weakness, chest pain, or loss of bladder or bowel control, see a clinician promptly.