L4/5 Disc Protrusion Case Study



This case report will outline the relevant subjective history and discuss the relevance of the objective examination. Then the analysis behind the rationale for the clinical diagnosis is reviewed. This is followed by an outline of the treatment plan and the discussion and evaluation that led to its formation. Why the objective markers were chosen is discussed, followed by how the treatment progressed and an explanation of why modifications were made. Lastly a reflection on the effectiveness of the treatment is given including the impact of the orthopaedic medicine course on the treatment approach and improvements for the future are presented.


History (Subjective Examination)


The patient was a twenty seven year old female academic. She had a five-month history of back pain, which had developed insidiously. Initially it was attributed to a reduced lumbar curve and she was treated with an epidural steroid injection to L4/5. This resolved the pain. One week ago the pain returned at much more severe level at 10/10 on numerical rating scale (NRS). She underwent lumbar spine magnetic resonance imaging that showed a disc protrusion at the L4/5 level. As a result she received another epidural corticosteroid injection at L4/5 level, which helped to reduce the pain to a 6/10 on NRS. The pain also radiated laterally to the mid point of iliotibial band. Prolonged sitting aggravates and lying down or walking help reduce the symptoms. Her symptoms were worse as the day progressed. 400mg three times a day of Ibuprofen was controlling her pain.  Her pain disability questionnaire (PDQ) score was 42/100.

She spends the majority of the day seated in a fully flexed position usually but at initial assessment she stated she could only sit pain free for five minutes before the pain came on. She goes to the gym three times a week doing mainly cardiovascular exercise on the x-trainer and plays tennis once a week.
Examination (Objective Examination)


On observation there were no changes in facial expression or gait. She had a visually obvious layered syndrome posture with a flat lumbar spine, increased thoracic kyphosis, and a forward head posture.

On inspection, postural assessment showed a lumbar lordosis of 17˚, where 30-35˚ is considered normal. There were no obvious deviations in the coronal or transverse planes, colour changes, wasting or obvious swelling. At rest she had 6/10 pain on NRS. She pointed to the region of L4/5.

On examination by selective tension in standing she had 35 degrees of active extension and no pain. On right side flexion her pain was reproduced at 7/10, left side flexion was pain free. Side flexion range was full bilaterally. However, active flexion was limited by pain of 8/10 at 40°. She described this as her pain. All neurological tests were negative.

Posterior sacroiliac shear testing produced a minor pain on all three positions bilaterally. She did not feel this was her pain, but she had experienced this before when sitting crosslegged and bent over from extended periods. She scored the active straight leg raise (ASLR) test as a 2/5 on the right and 1/5 on the left. This was not affected by compression at the anterior superior iliac spine level or level of the greater trochanter. However, difficulty in lifting the leg was reduced to 0/5 with a supero-medial compression to the ilia at the level of the posterior superior iliac spine. This suggested multifidus weakness.

On palpation her supraspinous ligaments at L4/5 and L5/S1 were tender as were her long dorsal sacroiliac ligaments bilaterally. The iliolumbar, sacrospinous, sacrotuberous and Champenois’ band were negative. In addition there was a lack of muscle bulk in the multifidus from the L4 level down. Multifidus activation was decreased on the right compared to the left.

Analysis of her seated posture showed that she was sitting in an excessively flexed position, with a decreased lumbar lordosis and an excessive thoracic kyphosis coupled with a significant forward head posture.


Clinical Diagnosis


There are no red flags and this appears an acute episode back pain. The assessment and history suggest mechanical low back pain brought on through sitting for extended periods leading to creep in passive structures (Panjabi 2006) and cumulative trauma to the passive structures of the spine (Tozzi 2012). The assessment findings suggest her presentation fits with clinical model 1 as there was a gradual onset, pain is not below the knee, the pain appeared to be precipitated by prolonged flexion, there were no neurological signs, there was pain on side flexion to the painful side and a non capsular pattern (Kesson and Atkins 2005).

The pain on posterior sacroiliac sheer and on palpation of the long dorsal sacroiliac ligament suggest strain to the long dorsal sacroiliac ligaments. Similarly, the pain at the L4/5 level on flexion fits with the MRI finding of L4/5 level disc protrusion. These tissue lesions are most likely chronic. Hashemirad et al (2010) found that as little as 7 minutes was sufficient to delay the flexor-relaxation phenomenon, which Panjabi (2006) discuss can lead to a chronic response over time. The optimal response is a switch from active system support to passive system support at 90% of full flexion or 45˚ of trunk flexion. Passive support involves contraction of abdominal inner unit, transversus abdominis and internal oblique among others to place tension through the thoracolumbar fascia. The thoracolumbar fascia applies an extension moment on the lumbar spine and the whole posterior ligamentous system through its direct connections (Willard et al 2012). Once this response is delayed greater erector spinae contraction remains for longer, the lumbar spine goes in to increased flexion and there is greater load on the posterior of the annulus fibrosis of the intervertebral disc and posterior ligamentous system may be under an increased load (Wallden 2010).

The weakness on ASLR that was alleviated with supero-medial compression of the ilia at the level of the PSIS suggests weakness of the multifidus. From manual assessment and palpation, the right side appeared to swell less than the left side, suggesting the right side was either atrophied or receiving less neural stimulation.


Treatment Plan


The aim of treatment for the patient to be able sit for up to six hours pain free within six weeks and reduce the likelihood of future episodes. To achieve this the goals were to eliminate pain on flexion. The longer-term goal was to increase the patient’s lumbar lordosis to 30-35 degrees, for the patient to have pain free ligament provocation tests and 0/5 both sides for the ASLR.

To achieve this orthopaedic medicine treatment (Kesson and Atkins 2005) was used in the context of the integrated model of joint function (Lee 2004). The integrated model of joint function builds on the seminal hypothesis of Panjabi (1992). The model outlines the importance of four elements in joint stability, active, passive, neural and cognitive. In this patient the aim was to optimise the passive structures through grade C manipulation firstly. This was done with the hypothesis that successful manipulation does not alter joint position but does reset mechanoreceptors. Optimising mechanoreceptor feedback may help normalise the flexor-relaxation mechanism.

The technique used was the distraction technique described by Kesson and Atkins (2005). The couch was lowered to near the bottom of its range to suit the 192cm tall therapist. The patient was positioned in left side lying with the painful right side, facing up. The upper hip and knee were flexed with the knee resting just off the bed and the lower leg extended. The underneath shoulder was then gently pulled forward so that the uppermost shoulder was positioned backwards and the pelvis was positioned forwards. One hand was placed on the greater trochanter, skin exposed to ensure grip, with the fingers facing down the femur. The cranial hand was placed on the ipsilateral shoulder with the fingers facing away from the lower hand, From this position the weight was applied evenly between both hands until all the slack was taken up and then a high velocity low amplitude thrust was applied with therapist using the trigger of nodding his head. An audible cavitation was heard and the treatment was considered successful.

On re-examination the NRS was reduced to 2/10. In addition right side flexion was no longer painful and flexion only produced a 4/10 pain. There were no changes in her ligament provocation tests or ASLR.

Following this the neural system was targeted with work in prone to facilitate the contraction of the multifidus muscles. This approach was based on the work of improving motor cortex reorganisation as described by Tsao et al (2010b). The intervention used was similar to that described by Tsao et al (2010a) in improving multifidus recruitment in their skilled exercise group. After five minutes of intermittent work on consciously contracting these muscles the patient had an improved ability to swell the multifidus and ASLR difficulty was 0/5 bilaterally. The patient was then shown extension in prone with patient overpressure as described in McKenzie and May (2003). This can be viewed as a specific form of grade B mobilisation. After repeating two sets of 10 repetitions she had no pain. She was asked to return the following day to be taken through her exercise programme.

I then wrote to the patient’s general practitioner (GP) and the referring pain management specialist and discussed the strategy with the senior physiotherapist at my clinic. He agreed with my plan to use further manipulation as appropriate and a corrective stretching and exercise programme. He suggested that if she returned with no pain at rest then there is probably no indication for manual treatment at that time. If her pain had returned to a two or more on a NRS then he recommended the potential use of posterior-anterior mobilisation to the lumbar spine starting at the L4 level.  I agreed this was an option, but that as the patient had responded favourably to manipulation on the initial visit at least one further treatment with manipulation would be indicated if symptoms returned.

The following day the patient returned to be taken through their corrective stretching and exercise programme which combined grade A and B mobilisations. This took the form of a structured rehabilitation programme shown in Appendix A. The patient was instructed in how to do each stretch and exercise, and repeated them herself for a full set each with prompting on correct technique where appropriate. Facilitation of the right multifidus was repeated and incorporated in to the alternating superman exercise. The patient was asked to complete the programme on alternate days for 1 week and then return for reassessment.

Information, therapeutic patient education and functional restoration were provided as suggested by Rozenberg et al (2012). In addition, the pathophysiology of intervertebral discs injuries was explained so as to confer that it was a minor injury that can heal over time and is often asymptomatic. This was done to avoid the patient catastrophising their condition. The patient was also given therapeutic education on sitting posture, standing posture, turning, sit to stand and using stairs. Functional restoration was encouraged through the guidance on pacing and a graded return to more demanding daily activities.




The patient emailed the therapist one week after she was due to return for follow up. She reported she had not returned as she had been too busy but she was still pain free at rest and could now sit for two hours without pain. She felt her pain was coming on because was slouching at that point and after doing the McKenzie prone extension exercise she could return to sitting pain free.

She returned for assessment two later, four weeks after initial assessment. On assessment her lumbar lordosis was 25˚. This of course is no guarantee that the resting lordosis in standing had increased this much. The patient may well have been very aware of what was being measured and consciously or subconsciously increased her lordosis. ASLR difficulty was 0/5 bilaterally and ligament provocation tests were negative.

The patient was taught the multi-directional lunge exercise as preparatory exercise for returning to tennis and advised to continue with the rehabilitation programme.

The patient confirmed via email that at six weeks she was able to sit for six hours as long she got up and walked around throughout the day. She has returned to tennis and considers herself fully rehabilitated with a PDQ of 0/150.


Discussion and Evaluation


The programme overall produced a positive result. The patient’s aim of being able to sit for six hour periods was achieved. In addition she has retuned to  tennis. Further the patient made good progress in reaching the postural objectives set and although not assessed the indication from the early progress was that she was progressing towards having a normal lumbar lordosis. Whilst the programme produced the desired result in the short term it is possible the result could have been achieved faster.

The European guidelines (van Tulder et al 2009) for treatment of acute non-specific low back pain advise adequate information and reassuring the patient, not to prescribe bed rest as a treatment, advise patients to stay active and continue normal daily activities including work if possible, prescribe medication if necessary for pain relief. All of these were implemented with this patient. They further state that spinal manipulation should be considered for patients who are failing to return to normal activities. In contrast, Edzard Ernst has conducted systematic review of systematic reviews on spinal manipulation (Ernst and Canter 2006).  Ernst is a vocal anti-alternative writer and it is not surprising he concludes that there is no support for manipulative treatment. However, there is some bias in his analysis and other groups producing guidelines have disagreed with his findings as discussed above. This patient was struggling to return to normal activities, thus the application followed the European guidelines.

The evidence for exercise based approaches remains controversial. Hayden et al (2005) found that in acute low back pain exercise therapy was no more effective than no exercise or other conservative treatments.  In contrast, Machado et al (2006) found some support for the use of the McKenzie approach in acute low back in their meta-analysis. Therefore whilst a general exercise approach may not be indicated, an approach based on a directional preference may have value.

In this instance I only communicated with the patient’s GP and the senior physiotherapist at my clinic. I was right to inform the patient’s GP and should ensure I continue to do this in future. Potentially I could have gained more insight by consulting with additional professionals at the clinic I work in.

Completing the orthopaedic medicine module B has greatly improved my theoretical knowledge. Coming from a corrective exercise background prior to studying physiotherapy I have always worked mainly from a functional holistic model of rehabilitation. Now I integrate the two approaches and I have found frequently I can conduct shorter assessments and treatments and achieve more immediate results in acute patients. I am also able to gain patient confidence with treatments and assessments that are highly specific. Furthermore in chronic patients I am more able to identify the specific structure that is giving rise to symptoms. I still view this specific tissue within a functional holistic model but with a more specific diagnosis I can target the functional approach more directly. For example, a specific postural rehabilitation protocol based on specific measurement may be prescribed for conditions known to be associated with poor posture such as low back pain. Although this concept remains controversial, despite being widely accepted (Lederman 2011).




This case history describes a patient referred for acute low back pain, and MRI findings consistent with a posterior disc protrusion at the L4/5 level following prolonged periods of flexed sitting. On assessment there was a 6/10 pain on NRS at rest, reduction in lumbar lordosis and pain at 8/10 on NRS produced on lumbar flexion. The patient’s presentation fitted with clinical model ….. After treatment with grade C spinal manipulation there was an immediate reduction the NRS to 2/10. This was further reduced with repeated prone extension and successfully managed using a corrective stretching and exercise programme. The patient’s care was discussed with the senior physiotherapist at the clinic and the referring consultant and the patient’s GP were informed. The patient failed to return for follow up when advised but did respond favourably.   On reviewing the evidence the treatment provided fits with current guidelines although elements of the philosophy on which the treatment was based remain controversial. My work with this patient and many others has been improved for studying the orthopaedic medicine programme. The programme has added specificity to my existing functional rehabilitation paradigm.

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Hayden, J.A., van Tulder, M.W., Malmivaara, A.V. and Koes, B.W. 2005. Meta-Analysis: Exercise Therapy for Nonspecific Low Back Pain. Available from; http://www.annals.org/content/142/9/765.abstract [Accessed 11th April 2012].


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Lederman, E. 2011. The fall of the postural-structural-biomechanical model in manual and physical therapies: exemplified by lower back pain. Journal of Bodywork and Movement Therapies15(2), 131-138.


Machado, L. A. C., De Souza, M. V. S., Ferreira, P. H., & Ferreira, M. L. 2006. The McKenzie method for low back pain: a systematic review of the literature with a meta-analysis approach. Spine31(9), E254-E262.


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Panjabi, M. M. 2006. A hypothesis of chronic back pain: ligament subfailure injuries lead to muscle control dysfunction. European Spine Journal15(5), 668-676.


Rozenberg, S., Foltz, V., & Fautrel, B. 2012. Treatment strategy for chronic low back pain. Joint Bone Spine.


Tozzi, P., 2012. Selected aspects of fasci in osteopathic medicine. Journal of osteopathic medicine, Epub ahead of print. Available from; http://www.sciencedirect.com/science/article/pii/S1360859212000629 [Accessed 30th August 2012].


Tsao, H., Druitt, T. R., Schollum, T. M., & Hodges, P. W. 2010a. Motor training of the lumbar paraspinal muscles induces immediate changes in motor coordination in patients with recurrent low back pain. The Journal of Pain,11(11), 1120-1128.


Tsao, H., Galea, M. P., & Hodges, P. W. 2010b. Driving plasticity in the motor cortex in recurrent low back pain. European Journal of Pain14(8), 832-839.


van Tulder, M., Becker, A., Bekkering, T., Breen, A., del Real, M.T.G., Hutchinson, A. Koes, B. Laerum, E. and Malmivaara, A., 2009. On Behalf Of The Cost B13 Working Group On Guidelines For The Management Of Acute Low Back Pain In Primary Care: European Guidelines For The Management Of Acute Nonspecific Low Back Pain In Primary Care . Available from; http://www.backpaineurope.org/web/files/WG1_Guidelines.pdf [Accessed 11th April 2012].


Wallden, M. 2010. Chains, trains and contractile fields. Journal of bodywork and movement therapies14(4), 403.


Willard, F. H., Vleeming, A., Schuenke, M. D., Danneels, L., & Schleip, R. 2012. The thoracolumbar fascia: anatomy, function and clinical considerations. Journal of Anatomy.

case study, disc protrusion, L4/5 posterior disc protrusion

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