Acute low back pain

Acute low back pain

Acute low back pain

Acute low back pain

Jon Ford presents a case in which treatment informed by a hypothesis of a nociplastic-dominant pain type was highly effective.

Low-back-pain (LBP) is a common and costly problem in the western world (Hurwitz et al 2018).

Clinical guidelines recommend the identification of red flags and radiculopathy, and in the absence of such features, management of LBP as a ‘non-specific’ condition (Oliveira et al 2018, Foster et al 2018).

However, guideline-based recommendations are based on clinical trials with small effect sizes (Oliveira et al 2018, Foster et al 2018).

Individualising treatment based on clinical reasoning (Jones & Rivett 2019) and a biopsychosocial approach (Foster et al 2018) is likely to be more effective (O’Sullivan et al 2018).

The International Association for the Study of Pain (IASP) describes three pain types (IASP 2018): nociceptive pain (arising from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors), neuropathic pain (caused by a lesion or disease of the somatosensory nervous system) and nociplastic pain (arising from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors, or evidence for disease or lesion of the somatosensory system causing the pain).

This atypical case of acute LBP (

Case presentation

Initial subjective examination

Mr X, a 57-year-old full-time storeperson, was referred by a physiotherapist (also his son) due to uncertainty regarding the nature of the problem, high severity of the symptoms/disability and minimal improvement.

He reported frustration with the lack of available diagnosis and rapid-acting treatment.

Four weeks prior to assessment, Mr X lifted a box at work and noticed a brief lumbar-pulling sensation.

Over the following two weeks, intermittent right lumbar/buttock pain (0–3/10) slowly ensued.

Two- weeks prior to assessment, and with no precipitating factors, Mr X woke with severe right lumbar/buttock/leg pain, paraesthesia and burning (8/10), and was unable to go to work.

The GP who was consulted that day ordered a lumbar spine MRI/right hip ultrasound and three days later prescribed oxycodone (5mg x four per day) and pregabalin (25mg x two per day), resulting in some sleep improvement.

Mr X attended emergency two days prior to the assessment due to not coping with the pain, and was discharged home with a recommendation of physiotherapy, paracetamol (500mg x six per day) and ibuprofen (200mg x six per day), which he added to his medication regime. 


Competing hypotheses were identified for further testing, including:

  • sudden onset of severe symptoms disproportionate to any likely precipitating event—potential red flag for abdominal aortic aneurysm given the age (>50) and gender

  • red flags for cancer—age >50, severe night pain (controlled by medication) and severe pain at rest (Dagenais et al 2010)

  • nociceptive pain type given recent onset, unloading eases symptoms and possible lifting precipitating event. Possible sources of symptoms—lumbar, sacroiliac, hip joints and/or neuromechanosensitivity (underlying and/or capable of referring into the symptom distribution) (Nijs et al 2015, Smart et al 2012)

  • neuropathic pain (Treede et al 2008) unlikely—non-dermatomal distribution and no nerve lesion on MRI

  • nociplastic pain, given the severe and somewhat diffuse, burning, constant/severe symptoms and disability and absence of a clear mechanical pattern (apart from unloading/left side lying easing) or likely precipitating event (Smart et al 2011). High scores for fear avoidance, anxiety and depression on the Örebro.

Initial physical examination

In the waiting room, Mr X was kneeling on the floor/leaning on a chair due to pain, accompanied by his partner and son.

A subjective assessment was completed in crook-lying where he had no symptoms.

Gait/transfers were slow and guarded. Standing posture/alignment was within normal limits (Kendall et al 2010), with increased activity of the external obliques/erector spinae, apical/shallow breathing and resting lumbar/buttock symptoms of 7/10.

There was no change in resting symptoms or muscle activation following one minute of relaxed, controlled breathing sitting on a high plinth with feedback/ strategies for reducing muscle tone.

Sitting posture/alignment was similar to standing but with increased symptoms (9/10).

Lumbar active-movement testing revealed moderate restriction in all movements limited by lumbar/right buttock symptoms but extension and right lateral flexion more limited (less L3–5 segmental motion compared to left lateral flexion).

Hip active-movement testing/overpressure and lower-limb neurological testing was normal apart from some inconsistent sensory changes in the right antero-medial thigh.

Neurodynamic testing (Shacklock 2005, Butler 2000) showed normal straight-leg raise with right femoral nerve slump reproducing typical lumbar/buttock/leg symptoms at full knee flexion and –5 degrees of hip extension and variable effect of cervical structural differentiation (Coppieters & Butler 2008).

Soft-tissue palpation confirmed moderately increased trunk muscle tone.

Passive accessory intervertebral movements (PAIVMs) revealed P2 at 30 per cent of resistance on L3–5 central and right-sided postero-anterior pressures.

Mini-treatments (Ford et al 2011) provide a small treatment dose sufficient for within but not between-session change and is useful in complex, severe and/or irritable conditions where the provision of multiple treatments in one session can adversely impact on between-session clinical reasoning (Ford et al 2011).

A pain-modulating mini-treatment of GIII-- (Petty et al 2018) right rotation (30 seconds) was applied due to high severity (Maitland et al 2005) and point of P2.

On reassessment, there was improved trunk muscle tone/resting pain, right lateral-flexion segmental motion/range/pain severity but no change in femoral nerve slump test was noted.

Additional tests showed:

  • piriformis muscle length equal bilaterally—soft end feel producing a ‘good’ sensation on the right

  • provocative sacroiliac joint tests (Laslett et al 2005) were normal. Active straight-leg-raise (Mens et al 1998) showed right weakness improved with posterior pelvic compression

  • simulated rotation and light axial compression (Apeldoorn et al 2012) reproduced lumbar pain revealing possible evidence of inconsistency in clinical presentation.


After physical examination, preliminary hypotheses were refined, with the most relevant being:

  • reduced likelihood of nociceptive hip contribution; some positive findings for the sacroiliac joint and piriformis as contributors to the LBP

  • additional evidence of nociceptive pain (Smart et al 2012)—active movements, PAIVMs and positive response to mini-treatment being consistent with right-sided articular impairment. Further evidence included the patient tolerating physical testing well and the presence of an antalgic (crook-lying) posture

  • reduced likelihood of neuropathic pain—minimal evidence of radiculopathy

  • additional evidence of nociplastic pain—degree of inconsistency on simulated rotation, axial compression and sensory testing

  • other physical examination findings (eg, breathing pattern, guarded gait, muscle overactivity) potentially reflective of a variety of pain types and contributing factors

  • no evidence of nerve injury on MRI with relevance of the other changes uncertain, given high false positives in people of similar age to Mr X (Hartvigsen et al 2018)

  • red flags less likely relevant but caution with treatment indicated (particularly with severity) and monitoring of oxycodone required given the associated risks (Foster et al 2018).

Treatment goals/outcomes (sessions 1–3)

Based on clinical guidelines, Mr X had non-specific LBP and poor prognosis (Örebro score) requiring advice to remain active and prognostic reassurance.

However, in order to refine hypotheses relevant to optimising recovery (Jones & Rivett 2019, Ford et al 2019) within a biopsychosocial framework, an individualised treatment approach was taken, consisting of:

  • evaluating the effect of passive movement treatment on the hypothesised articular impairment based on evidence in acute LBP (Slater et al 2012) and recommendations from some clinical guidelines (Oliveira et al 2018)

  • refining hypotheses through within/between-session response to treatment of relevant ‘asterisks’ (Ford et al 2011)

  • providing guideline-based advice to positively influence fear avoidance and mood (descending inhibition) via prognostic reassurance and returning to meaningful/pleasurable activities (Kanter et al 2010), but qualified within the context of the high severity (only small/graded increases in activities and remain off work)

  • using the Oswestry as a validated/reliable outcome measure with a plan to re-measure after 3–6 weeks.

Treatment during sessions 1–3 demonstrated small, short-term improvements in muscle tone/resting pain in standing and lumbar active movement in response to progressively increasing/ more specific L4/5 PPIVMs.

This progression was to ensure the primary hypothesis of segmental articular impairment as the source of symptoms was not under-treated and due to positive within-session changes. In parallel, further passive-movement assessment/mini-treatments on the right piriformis and femoral nerve were undertaken.

However, in all passive techniques, progressions were limited by pain severity.

More consistent sensory findings were identified with brush allodynia and pin prick secondary hyperalgesia in the anterior thigh.

Advice/reassurance were progressed to include a graduated walking program, reassurance and discussion around work planning/prognosis, exploration of contingencies regarding prognosis (uncertain but a return to full function likely), reassurance regarding MRI findings and the challenges providing a diagnosis in LBP (Oliveira et al 2018).

Medication remained unchanged.

Treatment goals/outcomes (sessions 4–8)

Between session 3 and 4 the partner of Mr X reported major concerns that he was in bed most of the day and had withdrawn from social/family engagement.

On questioning during session 4, Mr X reported feeling depressed, teary and irritable, acknowledging that his pain symptoms were worse during these periods of distress.

Further valid/reliable questionnaires were completed including the Brief Pain Inventory (Song et al 2016), Depression Anxiety Stress Scale (DASS21) (Nieuwenhuijsen et al 2003), Pain Self Efficacy Questionnaire (Chiarotto et al 2016) and Pain Catastrophising Scale (Osman et al 2000), which, combined with the initial Örebro, confirmed significant pain interference, mood, fear avoidance and self-efficacy issues.

Low DASS21 scores were discussed with Mr X, revealing that he had under-reported his mood issues on questionnaire completion.


Over the initial three sessions, further refinement of hypotheses was enabled with the most relevant being:

  • reduced likelihood of nociceptive pain (Smart et al 2012) with treatment of right-sided articular impairment showing within but no between-treatment change. Treatment was limited by heightened pain response potentially due to central sensitisation 

  • with lack of improvement, a heightened priority of ruling out serious pathology and obtaining a medical opinion regarding pain type as well as harms versus benefits of medication regime

  • significant psychosocial distress, which, in association with the above-described relevant assessment findings including sensory changes, could be reflective of nociplastic pain as the dominant pain type. 

The worsening of Mr X’s pain symptoms when distressed supported a central sensitisation mechanism based on modulation within the central nervous system, including reduced descending inhibition (al’Absi & Flaten 2016).

Based on these hypotheses, a referral was facilitated to a pain physician and psychologist.

A five minute mini-treatment using the Smiling Minds app (‘Exploring the Breath’ meditation) in crook-lying resulted in a 2–3 point reduction in standing resting pain and anxiety supporting the nociplastic pain hypothesis.

It is not possible to make definitive conclusions on pain type from clinical assessment.

However, rather than pursue further nociceptive-based treatment (eg, further exploration of the effect of altering muscle activation and/or movement strategies), a program of pain neurophysiology education and structured, goal-oriented, graded activity/exercise (Moseley & Butler 2017) was conducted.

This approach could potentially improve any non-dominant, nociceptive component (eg, via improved strength/movement, normalisation of muscle activation).

However, the program had the explicit goal of ceasing ‘passive’ treatments that may reduce self-efficacy (Trifiletti 2006) and time rather than pain-contingent increases in exercise/activity to facilitate insight that exercise/activity can be helpful even in the presence of some pain (Ford et al 2012).

The primary hypothesis became acute nociplastic-dominant pain type with significant psychosocial factors and central sensitisation treated based on extrapolation of evidence for mechanisms and effectiveness in chronic nociplastic LBP (Oliveira et al 2018, Foster et al 2018, O’Sullivan et al 2018, Moseley & Butler 2017, Hodges 2019, Wood & Hendrick 2019).

There is limited evidence for most treatments in acute LBP (Oliveira et al 2018) and clinical reasoning suggested the mechanisms common in chronic LBP were relevant in directing the treatment approach with Mr X.

A simple pain neurophysiology explanation on heightened sensitivity of the central nervous system and the potential relevance of mood/thoughts in ‘turning up the amplifier’ was discussed with reference to Mr X’s own observations on the effect of mood and the breathing medication mini-treatment on his LBP. 

Further discussions were had around the absence of a rapid acting treatment and prognosis.

Collaborative identification of meaningful goals (relationships, home, recreational, work) (Moseley & Butler 2017) led to the development of low intensity/duration exercises/activities to minimise perceived threat (Moseley & Butler 2017) with graded progressions over time.

The exercise/activity focus was on walking, sitting, driving and return to work, which required employer liaison.

Graded social activity was also commenced with family/friends as well as desensitisation training to light touch in the anterior thigh (Moseley & Butler 2017).

Mr X engaged well with the program with slow but consistent progressions in activity/exercise as expected in severe nociplastic-dominant LBP.

However, at session 6, he described difficulty/distress in accepting an absence of a rapidly acting treatment.

Extended collaborative discussion on the nociplastic-dominant nature of his pain problem (with psychosocial factors and central sensitisation) led to marked improvement in symptoms and disability in session 7.

Mr X believed this change was due to acceptance of the nature of his LBP leading to a reduced perceived threat/anxiety/depression and a resultant ‘winding down’ of his nociplastic pain (Moseley & Butler 2017).

Treatment goals/outcomes (sessions 9–11)

Ten sessions were completed over an eight-week period with marked improvement. After a graded return-to-work program (including physiotherapist certification of capacity and employer liaison), Mr X was comfortably completing normal hours and modified duties (forklift).

He had worked up to a daily high-level exercise program by session 9, comprising:

  • barbell deadlift and squats (25kg)

  • Arabesque (5kg)

  • single leg squat (progressing from ¼ bilateral squat initially)

  • dumbbell lunge, bicep curls, forward raise and shoulder press 4.5kg (progressing from 1kg initially)

  • running for 10 minutes (progressing from two-minute walks initially).

All exercises were progressed from initial low intensities/repetitions with an increase in weight, and reduction in repetitions to minimise the risk of exacerbations, occurring when 3 x 15 repetitions had been achieved (Ford et al 2012).

The pain physician confirmed the nociplastic pain type and replaced oxycodone with tapentadol (50mg x 2) and lignocaine patches. By session 11, all medication had ceased.

Three sessions of psychology focused on supporting the graded activity/exercise program and re-engagement with social/family activities. Mr X found both these interventions helpful.

Between session 10 and 11, Mr X returned to normal storeperson duties. In a final session, 12 weeks after initial assessment, a graded return to surfing and soccer was collaboratively planned over the following three months with advice to make contact for guidance as required.

Outcome measures were essentially normal. 

Discussion and conclusion

Nociplastic pain is a pain type likely to be underpinned by a range of mechanisms including central sensitisation as well as psychosocial, immune and/or genetic factors (O’Sullivan et al 2018).

This case study describes a patient with acute LBP that, through sequential testing of hypotheses, was deemed likely to have nociplastic- dominant LBP.

There have been few studies evaluating the most effective treatment for such patients, particularly in acute LBP; however, by applying the best available evidence for chronic pain within a biopsychosocial model, excellent outcomes were achieved.

It is possible that Mr X would have recovered at the same trajectory with different treatment; however, based on measures such as the Örebro, high level of severity, and strongly entrenched beliefs about his pain, it is more probable that recovery would have been slower without the program.

In order to positively impact upon this complex acute LBP case, a larger number of sessions than would be normally expected was required; analogous to the intensive treatment required for complex chronic LBP.

This case study illustrates an evidence-based approach applied in a manner that allowed individualising treatment to the presenting clinical features in a complex case of acute LBP.

>> Written patient consent for use of the information in this case study was obtained.

Dr Jon Ford (PhD), MACP, is a registrar undertaking Fellowship of the Australian College of Physiotherapists by Clinical Specialisation in the pain discipline. He is Associate Professor of Physiotherapy at La Trobe University; and Clinical and Managing Director of Advance Healthcare, a network of practices providing multidisciplinary pain management services to the community.


1.         Hurwitz EL, Randhawa K, Yu H, Cote P, Haldeman S. The Global Spine Care Initiative: a summary of the global burden of low back and neck pain studies. Eur Spine J. 2018.

2.         Oliveira CB, Maher CG, Pinto RZ, Traeger AC, Lin CC, Chenot JF, et al. Clinical practice guidelines for the management of non-specific low back pain in primary care: an updated overview. Eur Spine J. 2018.

3.         Foster NE, Anema JR, Cherkin D, Chou R, Cohen SP, Gross DP, et al. Prevention and treatment of low back pain: evidence, challenges, and promising directions. The Lancet. 2018;391(10137):2368-83.

4.         Jones M, Rivett D. Clinical reasoning in musculoskeletal practice. 2nd ed. Edinburgh: Elsevier; 2019.

5.         O'Sullivan PB, Caneiro JP, O'Keeffe M, Smith A, Dankaerts W, Fersum K, et al. Cognitive Functional Therapy: An Integrated Behavioral Approach for the Targeted Management of Disabling Low Back Pain. Phys Ther. 2018;98(5):408-23.

6.         IASP. IASP Taxonomy 2018 [Available from:

7.         Nicholas M, Vlaeyen JWS, Rief W, Barke A, Aziz Q, Benoliel R, et al. The IASP classification of chronic pain for ICD-11: chronic primary pain. Pain. 2019;160(1):28-37.

8.         Gabel CP, Burkett B, Melloh M. The shortened Orebro Musculoskeletal Screening Questionnaire: evaluation in a work-injured population. Man Ther. 2013;18(5):378-85.

9.         Fritz JM, Irrgang J. A comparison of a modified Oswestry Low Back Pain Disability Questionnaire and the Quebec Back Pain Disability Scale. Phys Ther. 2001;81(2):776-88.

10.       Dagenais S, Tricco AC, Haldeman S. Synthesis of recommendations for the assessment and management of low back pain from recent clinical practice guidelines. The Spine Journal. 2010;10(6):514-29.

11.       Nijs J, Apeldoorn A, Hallegraeff H, Clark J, Smeets R, Malfliet A, et al. Low back pain: guidelines for the clinical classification of predominant neuropathic, nociceptive, or central sensitization pain. Pain Physician. 2015;18(3):E333-46.

12.       Smart KM, Blake C, Staines A, Thacker M, Doody C. Mechanisms-based classifications of musculoskeletal pain: part 3 of 3: symptoms and signs of nociceptive pain in patients with low back (+/- leg) pain. Man Ther. 2012;17(4):352-7.

13.       Treede R, Jensen T, Campbell J, Cruccu G, Dostrovsky J, Griffin J, et al. Neuropathic pain.  Redefinition and a grading system for clinical and research purposes. Neurology. 2008;70:1630–5.

14.       Smart KM, Blake C, Staines A, Doody C. The Discriminative validity of "nociceptive," "peripheral neuropathic," and "central sensitization" as mechanisms-based classifications of musculoskeletal pain. Clin J Pain. 2011;27(8):655-63.

15.       Kendall FP, McCreary E, Provance P, Rodgers M, Romani W. Muscles: Testing and Function, with Posture and Pain. 5th ed. Baltimore: Lippincott, WIliams and Wilkins; 2010.

16.       Shacklock M. Clinical Neurodynamics: A New System of Neuromusculoskeletal Treatment. Oxford: Butterworth Heinemann; 2005.

17.       Butler D. The sensitive nervous system. Adelaide: Noigroup Publications; 2000.

18.       Coppieters MW, Butler DS. Do 'sliders' slide and 'tensioners' tension? An analysis of neurodynamic techniques and considerations regarding their application. Man Ther. 2008;13(3):213-21.

19.       Ford JJ, Thompson SL, Hahne AJ. A classification and treatment protocol for low back disorders. Part 1: specific manual therapy. Physical Therapy Reviews. 2011;16(3):168-77.

20.       Petty NJ, Barnard K, Lewis J. Principles of Musculoskeletal Treatment and Management. 3rd ed. Edinbugh: Elsevier; 2018.

21.       Maitland G, Hengeveld E, Banks K, English K, editors. Maitland's vertebral manipulation. 7th ed. Philadelphia: Elsevier; 2005.

22.       Laslett M, Aprill CN, McDonald B, Young SB. Diagnosis of sacroiliac joint pain: validity of individual provocation tests and composites of tests. Man Ther. 2005;10(3):207-18.

23.       Mens J, Vleeming, A, Snijders, CJ & Stam, HJ, editor Active straight leg raising. A clinical approach to the load transfer function of the pelvic girdle. 1998 Fifth International APA Congress; 1998 May 11-15 1998; Hobart, Tasmania: Australian Physiotherapy Association (Tasmanian Branch).

24.       Apeldoorn AT, Bosselaar H, Ostelo RW, Blom-Luberti T, van der Ploeg T, Fritz JM, et al. Identification of patients with chronic low back pain who might benefit from additional psychological assessment. Clin J Pain. 2012;28(1):23-31.

25.       Hartvigsen J, Hancock MJ, Kongsted A, Louw Q, Ferreira ML, Genevay S, et al. What low back pain is and why we need to pay attention. The Lancet. 2018;391(10137):2356-67.

26.       Ford J, Hahne A, Surkitt L, Chan A, Richards M. The Evolving Case Supporting Individualised Physiotherapy for Low Back Pain. Journal of Clinical Medicine. 2019;8(9).

27.       Slater SL, Ford JJ, Richards MC, Taylor NF, Surkitt LD, Hahne AJ. The effectiveness of sub-group specific manual therapy for low back pain: a systematic review. Man Ther. 2012;17(3):201-12.

28.       Kanter JW, Manos RC, Bowe WM, Baruch DE, Busch AM, Rusch LC. What is behavioral activation?A review of the empirical literature. Clin Psychol Rev. 2010;30(6):608-20.

29.       Song C-Y, Lin S-F, Huang C-Y, Wu H-C, Chen C-H, Hsieh C-L. Validation of the Brief Pain Inventory in Patients With Low Back Pain. Spine. 2016;41(15):E937-E42.

30.       Nieuwenhuijsen K, de Boer A, Verbeek J, Blonk R, van Dijk FJH. The Depression Anxiety Stress Scales (DASS): detecting anxiety disorder and depression in employees absent from work because of mental health problems. J Occup Environ Med. 2003;60(Suppl 1):i77-82.

31.       Chiarotto A, Vanti C, Cedraschi C, Ferrari S, De Lima E Sà Resende F, Ostelo RW, et al. Responsiveness and Minimal Important Change of the Pain Self-Efficacy Questionnaire and Short Forms in Patients With Chronic Low Back Pain. The Journal of Pain. 2016;17(6):707-18.

32.       Osman A, Barrios FX, Gutierrez PM, Kopper BA, Merrifield T, Grittmann L. The Pain Catastrophizing Scale: Further Psychometric Evaluation with Adult Samples. J Behav Med. 2000;23(4):351-65.

33.       al’Absi M, Flaten M. The Neuroscience of Pain, Stress, and Emotion. London: Elsevier; 2016.

34.       Moseley G, Butler D. Explain Pain Supercharged. Adelaide City West: NOI Group Publishers; 2017.

35.       Trifiletti B. Getting the at risk patient back to work:  a strategy. Aust Fam Physician. 2006;35(12):952-6.

36.       Ford JJ, Richards MJ, Hahne AJ. A classification and treatment protocol for low back disorders. Part 4: functional restoration for low back disorders associated with multifactorial persistent pain. Physical Therapy Reviews. 2012;17(5):322-34.

37.       Hodges PW. Hybrid Approach to Treatment Tailoring for Low Back Pain: A Proposed Model of Care. J Orthop Sports Phys Ther. 2019;49(6):453-63.

38.       Wood L, Hendrick PA. A systematic review and meta-analysis of pain neuroscience education for chronic low back pain: Short-and long-term outcomes of pain and disability. Eur J Pain. 2019;23(2):234-49.





© Copyright 2024 by Australian Physiotherapy Association. All rights reserved.