Skip to content

You are reading 1 of 2 free-access articles allowed for 30 days

Evolving back pain therapy

There has been a significant shift in our perception of inflammatory back disease over the last few decades. This is partly due to the improvements in imaging, allowing an earlier diagnosis of the disease (in its responsive, ie, inflammatory rather than damaged, ie, ankylosed state), reclassification of these conditions and in particular due to the development of efficient pharmaceuticals for treatment.

Early inflammatory arthritis clinics and rapid triaging of peripheral joint inflammatory symptoms are now the norm in rheumatology. The onus lies with us to also find inflammatory back symptoms, knowing how excellent the outcomes are with prompt therapy and management.

The terminology has changed too — just when we were coming to terms with spondyloarthropathy (SpA), it is now divided into axial SpA (axSpA: spine, sacroiliac joints) and peripheral SpA (pSpA: other areas as well as axial disease).

The treatment responsiveness to DMARDs differs between the two, so this is a sensible reclassification. The rest of this article will concentrate on spine-centred disease — axSpA.

What diseases comprise axSpA?

 This is a heterogenous group of overlapping conditions, with ankylosing spondylitis (AS) being the best-recognised, but psoriatic, IBD-related, reactive, undifferentiated and juvenile-onset also well recognised. Careful evaluation can find an overlap of features: ie, asymptomatic colitis on endoscopy in the psoriatic axSpA patient; a history of inflammatory eye disease in the AS patient; or a distant history of diarrhoeal illness triggering the first episode of spinal symptoms.

AxSpA is as prevalent as rheumatoid arthritis, affecting 1-to-2 per cent of the population, with a significant disease burden.

So, as the (typically) young man with back pain enters the consultation room, the challenge is to extract the 10 per cent of cases with inflammatory disease, as the management will differ greatly from the ‘standard’ mechanical back issues.

A few questions to ask:

  1. Is this patient’s back pain inflammatory?
  2. Are there any other clues — ie, are there any associated features?
  3. But the blood tests are normal…?
  4. Should I test for HLA-B27?
  5. Should I image (X-ray or MRI) this patient?
  6. How to diagnose axSpA?
  7. How will I manage axSpA and when should I refer to rheumatology or physiotherapy?

1. Is this patient’s back pain inflammatory?

 In many patients with axSpA, onset of symptoms occurs in the third decade of life, starting with back pain that can be insidious at onset, and mild and non-specific in the early stages of the disease. Although chronic back pain is the primary symptom of axSpA, patients can be pain-free for long periods of time. Similarly, other signs and symptoms of early axSpA are often subtle and can fluctuate over time, which can result in a delayed diagnosis in primary care and also in rheumatology practice.

Inflammatory back pain (IBP) is present if four-out-of-five of the following parameters are evident in an individual with chronic back pain that has been present for more than three months:

  1. Age at onset <40 years.
  2. Insidious onset.
  3. Improvement with exercise.
  4. No improvement with rest.
  5. Pain at night (with improvement upon getting up) (Assessment of SpondyloArthritis International Society (ASAS), Sieper et al, 2009).

 Is that enough of a symptom cluster to diagnose?

IBP is present in 70‑to-80 per cent of patients with axSpA, but also occurs in 20-to-25 per cent of patients with mechani-cal back pain. IBP alone is not sufficient for diagno-sis; the presence of IBP only increases the probability of axSpA from 5 per cent to 14-to-16 per cent.

2. Are there any other clues — ie, are there any associated features?

  •  Sacroiliac disease.

  1. Deep buttock ache/pain, can radiate down back of thigh (mimics sciatica).
  2. Often alternates from one sacroiliac joint to another.
  3. Awakens patient in second half of night, better with exercise (ie, inflammatory).

  • Psoriasis, uveitis, Crohn’s/ulcerative colitis (HLA-B27-associated diseases).
  • Known family history of HLA-B27-associated disease.
  • Peripheral arthritis (typically asymmetrical, large-joint oligoarthritis, eg, knee and opposite ankle).
  • Enthesitis (insertion of tendon into bone — especially plantar fasciitis, Achilles tendinitis).

3. But the blood tests are normal…?

 This is not uncommon in the absence of peripheral arthritis, inflammatory bowel disease or other non-spinal inflammatory disease. Erythrocyte sedimentation rate or especially C-reactive protein can be mildly raised (latter rarely over 15-to-20mg/dl). If higher, it can be suggestive of infection (eg, septic discitis or sacroiliitis). Rheumatoid factor negativity is to be expected; ANA has no role here.

4. Should I do a HLA-B27 test?

 This disease group shows familial clustering and is associated with HLA‑B27 positivity to differing degrees between subtypes. The strongest association is with the symmetrical disease of AS. The link between AS and HLA-B27 holds in all populations.

In comparison with other diagnostic tests for SpA, HLA‑B27 positivity has a high sensitivity and specific-ity, although the performance depends on the prevalence of HLA‑B27 in a particular population. In AS, 75-to-95 per cent of the patients are HLA‑B27-positive, whereas in undif-ferentiated and non-radiographic axSpA (X-rays normal but MRI showing inflammation), the prevalence is much lower (42-to-75 per cent). Absence of HLA‑B27 does not preclude a diagnosis of SpA and is associated with a longer delay in diagnosis. So for earlier disease (what we are aiming to pick up), especially in asymmetric disease, in individuals with a personal or family history of psoriasis or colitis, and in Caucasian populations, the value of testing is unclear. [Figure 1]


Figure 1: Possible screening approach for axial Spa among patients

with chronic lower back pain

5. Should I X-ray or MRI the pelvis/sacroiliac joints/lumbar spine?

 Plain films are the traditional standard for the diagnosis of chronic sacroiliitis and can be graded from 0 (normal) to 4 (ankylosis). However, the key is that they will only detect struc-tural changes such as erosions and sclerosis — the end result of inflammation rather than inflammation itself.

AxSpA can be divided into AS and non-radiographic axial SpA (nraxSpA) where the X-rays are normal (though the MRI shows inflammation). AS is diagnosed using the modified New York criteria, which combine clinical IBP and X-ray changes in the sacroiliitis (Van der Linden S et al). However, in early disease, X-rays are often normal — non-radiographic disease — making these criteria defunct.

In attempting to catch the disease early in its course, MRI is increasingly being used, as inflammatory lesions of nrSpA can be detected with techniques of fat suppression (STIR) and the use of contrast (gadolinium). Bone marrow oedema is considered the most sensitive early change found in axSpA, typically found in the cartilaginous portion of the SI joint. MRI-detected active inflammation has been shown to predict subsequent occurrence of radiographic sacroiliitis.

Importantly, patients with nr-axSpA have similar levels of pain, disease activity and treatment response to those with definite AS. Several ongoing trials in nr-axSpA have shown a good response to biologic agents, with a similar or increased proportion of responders observed in early axSpA compared with trials in established AS.

An important practice point is that the SI joints are not imaged to any useful degree on lumbar spine MR scans and a normal image cannot exclude sacroiliitis — dedicated SI views are required.

It is important to note that expensive MR imaging and genetic testing cannot supplant thoughtful history-taking and examination, and should be reserved only for patients with other features of SpA or back pain starting before the age of 45 years.

6. How to diagnose axSpA?

Diagnostic criteria have evolved. Ultimately, the key is clinical suspicion, possibly supported with imaging or genetic testing and clinical experience with the disease.

7. How will I manage axSpA and when should I refer onwards to rheumatology or physiotherapy?

 All such patients need physiotherapy. I would encourage that all relevant patients, or individuals in whom there is a suspicion, be referred to a rheumatologist for assessment, in the presence of inflammatory back pain or MRI evidence or HLA-B27 positivity (although the latter applies in the relevant clinical setting, eg, arthritis, IBP).

Education is the key — particularly focusing on patients’ self-management. Daily exercise is the best ‘drug’ for symptom control and prevention of stiffness and spinal fusion. Core muscle-strengthening is critical, via swimming, Pilates or yoga. This is a very ‘easy sell’ to patients, as the typical patient with ankylosing spondylitis has always felt better for exercising, without knowing that they have been treating their chronic inflammatory condition with exercise therapy.

I direct patients towards websites such as (UK National Ankylosing Spondylitis Society with an exercise app for download), (US patient-run site) as a starting point. Group exercise sessions are to be encouraged.

Non-steroidals have a significant role in treatment, unlike in rheumatoid arthritis, with the majority of axSpA patients showing a very good (>50 per cent) improvement on these drugs. There is some evidence also that their long-term use (as always balanced against their side-effect profile) may slow disease progression, including new spinal bone formation.

The biologics revolution has had most impact on this disease group. Whereas traditional DMARDs such as methotrexate and sulfasalazine have proven value in inflammatory arthritis, including peripheral SpA, they have no useful effect on spinal disease. All anti-TNF drugs are licensed for AS and psoriatic spinal disease and are increasingly being used and studied in nraxSpA (ie, MRI-positive, plain-film negative disease) with excellent results.

Using the validated disease activity measure ASAS 5/6, where five of six clinical markers (pain; patient global assessment; function; inflammation; spinal mobility; and C-reactive protein) have significantly improved, sustained response to anti-TNF therapy is seen across the biologics. These drugs now have over 12-to-15 years of use in clinical practice, with gratifying results for all involved.

Importantly, they are well tolerated, with an even smaller risk profile in axSpA than in rheumatoid arthritis. Improvements in quality of life, anaemia, sleep quality and fatigue have been found in AS (Davis JC et al, Deodhar et al). [Figure 2]


Figure 2: long-term clinical efficacy of tnF
-blocker in aS results 
over seven years. anti-tnF therapy has shown significant clinical 
effects in aS sustained to over 10 years of treatment


 This disease group is prevalent, heterogenous and often insidious in onset. But once one has suspicion — and looks for inflammatory back pain and associated skin, bowel or other inflammatory disease and considers further assessment (radiological and rheumatological) — it is imminently treatable. An oft-quoted statistic is that it takes an average of seven years of symptoms until a diagnosis is made. If undiagnosed over a prolonged period of time, this painful condition also represents a substantial psychological burden for young patients and early recognition of axSpA might affect vocational training and quality-of-life aspects.

However, earlier diagnosis is now a possibility, with effective strategies in place to improve daily functioning and prevent the spinal deformities of times gone by.

Full references on request

Leave a Comment

You must be logged in to post a comment.

Scroll To Top