The Metro Pain Clinic Group

Disc prolapse

Displacement of disc material is common, and occurs across a spectrum of severity. Least severe is a disc bulge, in which displacement affects more than 50% of the disc circumference, and usually extends less than 3 mm beyond the bony margin.10 A disc bulge is a normal finding, and its identification on imaging does not allow any inference to be drawn as to the source of pain.

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A disc prolapse is any displacement more severe than a disc bulge. Prolapse thus defines a broad category of changes to the disc, which are further sub-classified according to severity and morphology. In disc prolapse, the nucleus pulposus, anulus fibrosus, end-plate cartilage and fragmented vertebral bone may all be displaced. A disc may compress and/or contribute to inflammation of the spinal nerve roots, spinal dura, cauda equina; however, it not invariably prolapses without consequence.  

Prolapse compressing the nerve root is a very common finding, observed in 70% of the asymptomatic population.25 The factors that cause pain in a minority of such prolapses are not well understood, though inflammation is thought to play a key role. Disc prolapse accounts for 5% of low back disorders, and is one of the commonest reasons that patients undergo surgery.12

Classification

Disc prolapse can be sub-classified by morphology and severity, as revealed in radiological findings. The key distinction is that between a protrusion and an extrusion.

Disc protrusion occurs when “the greatest distance, in any plane, between the edges of the disc material beyond the disc space is less than the distance between the edges of the base in the same plane.”10 Protrusions affecting less than 25% of the disc circumference are said to be “focal,” while those involving 25-50% of the circumference are termed “broad based” protrusions.10

Disc extrusion is diagnosed when “in at least one plane, any one distance between the edges of the disc material beyond the disc space is greater than the distance between the edges of the base measured in the same plane, or when no continuity exists between the disc material beyond the disc space and that within the disc space.”10 If the extruded material has no connection with the disc it may be considered to be “sequestrated.”

Pathophysiology

Prolapse occurs when intra-discal pressure exceeds the capacity of the external disc to contain it. The healthy disc is exceedingly strong (compressive loads are more likely to cause vertebral fracture than disc prolapse)22 but degenerates much earlier than other musculoskeletal structures.25 The earliest unequivocal findings of disc degeneration have been found in children and adolescents aged between 11 and 16, while 10% of 50 year olds have severely degenerated discs, a figure rising to 60% by the age of 70.25 Except when loading forces are enormous, the process leading to disc prolapse seems related to the abnormal mechanics associated with biochemical changes in the disc and disc degeneration.4

The process leading to prolapse is thought to begin with an injury, which may or may not be painful. Injuries involving the nucleus/end-plate interface are particularly implicated.1 This injury causes the release of chemical factors, which alter the internal structure of the disc. This in turn causes a change in load bearing characteristics, and exposes the anulus fibrosus to greater stress. The anulus is particularly vulnerable to injury from micro-trauma during bending and lifting tasks, although is is somewhat protected by the facet joints during torsional stresses (such as sudden twisting).2 These factors contribute to progressive deterioration of both the nucleus pulposus and the anulus fibrosis. The final prolapse, when it occurs, may be triggered by quite trivial stress. In other cases, the cause may not be identifiable.

Prolapse is more likely to occur in individuals in whom the nucleus occupies a more posterior position within the disc. Such a prolapse is more likely to produce clinical features in those with narrower spinal canals. Lifting can cause disc injury and prolapse. Asymmetrical lifting (lifting to the side) is implicated experimentally.20

The pain of disc prolapse is due to compression of the nerve root. One study has demonstrated, however, that such compression is observed in 70% of the asymptomatic population.25 Further, it has been shown that mechanical stimulation alone does not cause sustained radicular pain: sustained pain may only arise when the nerve root is damaged, or when inflammation is present.6 The factors mediating a transition from asymptomatic compression to a painful, symptomatic case are not well understood. Two factors thought to be important, however, are the site of prolapse and the propensity of an individual nerve to become painful when exposed to chemical insult.

Chemical factors are important both as a cause of insult which may make a nerve painful, and in mediating anatomical change which may be further associated with pain. A chemical soup occupies the area surrounding the nerve and contributes to the maintenance of radicular pain.15;27;30.4 The presence or interaction of these factors may play an important role in determing which cases in which nerve root compression are asymptomatic, and which are associated with clinical features.

Changes in disc structure and function after disc prolapse can also affect structures such as the facet joints, tendons, muscles, and neural foramina. Morphological changes in the intervertebral disc are the most common cause of canal stenosis and radicular pain in the aged population.25 

Although small, there are some established significant risk factors for lumbar disc herniation leading to discectomy. These are in males daily smoking, and in females, frequent sport and being overweight.19

Clinical Presentation

The pre-eminent consideration for any clinician is that disc prolapse identified by any imaging technique can occur in the asymptomatic population.5;23;23 Thus, considerable care and clinical acumen is required before any presentation of pain and/or neurological impairment can be ascribed to be due to a disc prolapse.

The typical presentation is of radicular pain and/or neurological deficit due to spinal nerve root damage. Radicular pain is well defined in the lumbar spine: it is typically long and thin lancinating pain, and it may be either or both superficial and deep.11;13 However, if a central disc protrusion causes pain, the pain is in the low back, with or without pain and/or neurological deficit in either one or both legs.3 While radicular pain does not follow dermatomal patterns, accompanying sensory symptoms or signs typically do.

Postero-lateral disc prolapse commonly produces radicular pain and/or neurological symptoms in a typical nerve root distribution. For example, L5 nerve root irritation can cause pain into the foot, often associated with lateral leg pain and pins and needles, classically extending into the greater toe. L5 nerve root irritation generally comes from a more medial L4/5 prolapse or a more lateral L5/S1 prolapse.

It is also possible for radicular pain to occur in the absence of disc prolapse or spinal stenosis. Such cases are thought to occur when inflammatory exudates exit the disc via an anular tear and contact the nerve root.

Diagnosis

The diagnosis is usually made after careful consideration of the history of the presenting complaints and the examination. The history of the complaint is variable. A typical scenario includes a long standing duration of chronic or recurrent acute back pain, but it is possible for the radicular pain of a disc prolapse to occur without any antecedent pain. It is also common for chronic low back pain to disappear when the disc prolapses. In these cases it is thought that pain prior to the prolapse is intra-discal somatic (discogenic) pain, which the prolapse relieves.

The clinician will perform a physical examination.  Findings on physical examination are dependent on the position and level of the prolapse. At L5/S1, postero-lateral disc prolapse can produce radicular leg pain, and neurological loss attributable to the L5 or S1 nerve root. Substantial straight leg raise (SLR) restriction is common, and neurological signs may also be present. SLR is the only sign that is consistently shown to be sensitive for sciatica, though specificity is low. One systematic review has reported a sensitivity of 0.85 and a specificity of 0.52.26 The diagnostic accuracy of other neurological signs has not been established.26 At L4/5, the L4 or L5 nerve roots may be affected. Again, SLR is typically restricted. The SLR test may especially help identify patients who have disc prolapses with root compression requiring surgery.18  At L3/4, the L3 nerve root is generally affected. As the sciatic nerve contains nerves from L4 and below, SLR restriction does not occur when the L3 root is injured. The L3 nerve root stretch test, however, is generally positive.

When MRI is available it is the best test. One systematic review has shown that the sensitivity and specificity of MRI are higher than that of other imaging modalities.26 MRI provides clear views of the entire course of the nerves, as well as showing the extent of disc protrusion and the degree of nerve root distortion. Any narrowing of the bony canal is also clearly visible. 

The use of epidural injection may get a patient through the more severe phases of pain and thus obviate the need for surgery. Newer medications, such as TNF blockers, injected around the nerve root to block the inflammatory process are currently being studied at international pain management sites such as at the Metro Spinal Clinic in Caulfield. However, traditional MRI does miss anything up to 30% of disc prolapses discerned from clinical examination.31 CT scan provides an alternative if MRI is unavailable or contraindicated, though clarity does not approach that achieved with MRI. Plain x-rays provide little information.

Although there is not enough definitive literature to allow for conclusive statements about the use oftransforaminal epidural injections particularly as a diagnostic tool, they seem to have a useful role in assessment as they have a high negative predictive value.8 Thus, in a clinical situation where pain appears to be radicular, yet imaging is inconclusive, a negative selective nerve root injection has a good chance of excluding pain from that particular nerve root and thus obviating further consideration of exploratory surgery.

Treatment

Explanation

Most patients with radicular pain due to disc prolapse recover spontaneously without the need for surgery. The first aim of the treating practitioner should be to deliver this information, and to use appropriate management strategies to minimize pain while the healing process occurs. However, the radicular pain associated with disc prolapse is often severe, and can continue for weeks or months. Early, severe pain is due to a combination of nerve compression and inflammation. This pain typically settles. Ongoing pain is likely to be associated either with continuing compression or nerve root damage such as neuroma.

Patients need to understand that the long term prognosis for this condition is generally good, though considerable support is often required during recovery. Practitioners can help by providing information, hope and optimal pain management.

Analgesia

The first line of treatment is analgesia, both for pain relief and to prevent long term spinal changes associated with ongoing pain. Required doses are commonly high, however, meaning that side effects are a prominent consideration. Oral medication includes steroidal and non-steroidal anti-inflammatories, with oral prednisolone commonly prescribed despite limited evidence. Strong analgesics including narcotics are often required. Neuropathic pain can be managed with low dose tricyclic antidepressants or anti-epileptics. Such treatments are indicated especially when night pain is severe. A number of studies have shown that conservative treatment is no more effective than the natural history of the condition.

Epidural injection

Epidural injection may be delivered by transforaminal, inter-laminar or caudal approach. Traditional epidural injection is not curative but provides short and medium term pain relief while recovery occurs. The use of epidural injection may get a patient through the more severe phases of pain and thus obviate the need for surgery. Newer medications, such as TNF blockers, injected around the nerve root to block the inflammatory process are currently being studied at international pain management sites such as at the Metro Spinal Clinic in Caulfield.

Physical therapy and exercise

Bed rest should not be prolonged. Gentle progressive exercise can be commenced soon after an attack. Physiotherapists can prescribe exercise. Sometimes a treatment regime of exercises called McKenzie exercises are used. 

Surgery

The fundamental question for the treating practitioner is whether or not surgery is required. In most cases, the intensity of pain and the ability to control it are the prime factors in this decision.

There is a spectrum of opinion about the requirements for surgery in the presence of radiculopathy. If the deficit is extreme and implicates bladder and bowel function (called a cauda equine syndrome), surgery is generally considered necessary and urgent. It is recommended that surgery in such a rare instance be performed within 48 hours of onset, though symptoms can still be improved if treatment is delayed.24 For lesser neurological deficits, the indication for surgery is less clear. Most power deficits recover within 12-18 months, while sensory deficits tend to persist, at some level, for longer. There is no way to predict which deficits will or will not recover. In the cervical spine, radiculopathy usually recovers without surgery.14

For patients deciding between surgical and non-surgical treatment, expectations of benefit are the primary determinant of preferences.17 Expectations of the benefit associated with surgery are generally high, and sometimes unrealistic.17 It is likely that these expectations create a preference for surgical treatment in a disproportionate number of patients.17

In severe cases, surgical decompression may be appropriate. In the lumbar spine, micro-discectomy is favoured, while cervical discectomy and fusion or disc replacement are favoured at cervical levels. While surgery provides prompt relief of severe radicular pain, it does not necessarily improve prognosis beyond a period of 2–4 years.6

Additionally, it is relevant to know that the recurrence rate of lumbar disc herniation in young adults has been shown to be in the order of 7% at a mean follow-up of 8.55 years, and to be significantly higher for protruded discs compared with other types.16 However, recurrent radicular pain when treated surgically does not result in altered activity of daily living outcome, and the extent of epidural fibrosis also did not alter outcome.7

Decompression by discectomy is usually approached in one of two ways. The first (“aggressive”) approach (first reported in 1951) involves a large incision, aggressive removal of disc fragments and curettage of the disc.28 The second (“conservative”) approach (first described in 1982 and made possible by advances in surgical lighting and microscopy) involves a smaller incision and removal of disc fragments with minimal invasion of the disc.28 A systematic review has compared the aggressive and conservative approaches, concluding that in conservative discectomy, operative times are generally shorter, return to work is quicker, and the incidence of long term recurrence of low back pain is reduced.28 Conservative discectomy is also associated, however, with an increased incidence of recurrent herniation.28

A large multicenter study (the SPORT trial) compared the outcomes of surgical and non-surgical treatment.29 In this study1244 patients were enrolled, 501 in the randomized group and 743 in the observational group. Of the randomized cohort, 245 were allocated to surgery, and 256 to non-surgical treatment. Surgery was standard open discectomy with examination of the affected nerve root. Non-surgical care was individually tailored, but minimally included active physical therapy, education/counseling, home exercise instruction, and NSAIDs where appropriate.

Outcomes were followed up at four years. Significant crossover occurred, meaning that by the time of the four year follow up, 59% of all patients had received surgery. Primary outcomes measured were SF-36 bodily pain and physical function indices, and Oswestry disability index. Secondary outcomes measured were sciatica bothersomeness index, leg pain, low back pain bothersomeness, work status, self rated progress, and satisfaction with symptoms and care. Mean changes (at four years) for primary measures in the randomized group are presented below.29

 

Mean changes

Outcome measures

Surgical group

Non-surgical group

SF-36 bodily pain index (0 – 100 points)

43

31.6

SF-36 physical function index (0 – 100 points)

43.6

30.2

Oswestry disability index (0 – 100 points)

37.2

24.6

At the four year follow up, surgical patients experienced greater improvements in primary outcomes when compared with non-surgical patients. The authors concluded that, for patients with disc herniation confirmed by imaging and leg symptoms, which had persisted for at least six weeks, surgery produced better symptom relief and greater improvement in function.29 The study design and interpretation of this trial have been criticized, especially in terms of the very high cross over rate, which makes it impossible to validly compare surgical and non-surgical treatment on an intent-to-treat basis.29 Data was instead analysed on an ‘as treated’ basis.

Four other RCTs have sought to compare discectomy with non-surgical treatment, but, according to a Cochrane review, results have been inconclusive.12 Other RCTs, however, have shown that discectomy is more effective than chemonucleolysis, which in turn is more effective than placebo.12 It has been demonstrated that the results of discectomy and microdiscectomy are comparable.12

Despite the lack of clarity on long term outcomes, it is clear that surgical treatment for disc prolapse provides more rapid symptom relief than non-surgical treatment.12 Prognosis following minimally invasive discectomy is excellent: patients are commonly able to walk the day after surgery, and discharge may be as early as day two.

The larger the disc prolapse the greater the chances of good success with operative treatment. This stands to reason as a larger fragment is unlikely to spontaneously regress and is easier to access than a small contained fragment. One recommendation is that patients with contained disc prolapses, a predominance of back pain, on restricted duty and smoking should be counselled before surgery of the potential for less satisfaction, poorer outcomes scores, and decreased return to duty rates.9

Longer term follow up of patients undergoing surgery for disc prolapse reveals that although a majority recover well, a reasonable number (about 25%) have moderate LBP requiring conservative treatment only, and about 10% have severe LBP that might require further surgery such as fusion.21

Summary

Disc prolapse causing radicular pain can be a significant problem. It is encouraging that the general prognosis for this condition is good. Surgery is required for severe cases where pain control is poor with other measures, including trial of transforaminal or other epidural injection. The larger the prolapse, the better the long term outlook.

Reference List

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11.   Freynhagen R, Rolke R, Baron R et al. Pseudoradicular and radicular low-back pain--a disease continuum rather than different entities? Answers from quantitative sensory testing. Pain 2008;135:65-74.

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14.   Heckmann JG, Lang CJ, Zobelein I et al. Herniated cervical intervertebral discs with radiculopathy: an outcome study of conservatively or surgically treated patients. J Spinal Disord. 1999;12:396-401.

15.   Kawakami M, Tamaki T, Matsumoto T et al. Role of leukocytes in radicular pain secondary to herniated nucleus pulposus. Clin.Orthop.Relat Res. 2000;268-77.

16.   Kim MS, Park KW, Hwang C et al. Recurrence rate of lumbar disc herniation after open discectomy in active young men. Spine 2009;34:24-9.

17.   Lurie JD, Berven SH, Gibson-Chambers J et al. Patient preferences and expectations for care: determinants in patients with lumbar intervertebral disc herniation. Spine 2008;33:2663-8.

18.   Majlesi J, Togay H, Unalan H et al. The sensitivity and specificity of the Slump and the Straight Leg Raising tests in patients with lumbar disc herniation. J Clin.Rheumatol. 2008;14:87-91.

19.   Mattila VM, Saarni L, Parkkari J et al. Early risk factors for lumbar discectomy: an 11-year follow-up of 57,408 adolescents. Eur.Spine J 2008;17:1317-23.

20.   Natarajan RN, Williams JR, Lavender SA et al. Relationship between disc injury and manual lifting: a poroelastic finite element model study. Proc.Inst.Mech.Eng [H.] 2008;222:195-207.

21.   Parker SL, Xu R, McGirt MJ et al. Long-term back pain after a single-level discectomy for radiculopathy: incidence and health care cost analysis. J Neurosurg Spine 2010;12:178-82.

22.   Porter RW, Adams MA, Hutton WC. Physical activity and the strength of the lumbar spine. Spine 1989;14:201-3.

23.   Quiroz-Moreno R, Lezama-Suarez G, Gomez-Jimenez C. [Disc alterations of lumbar spine on magnetic resonance images in asymptomatic workers]. Rev.Med Inst.Mex.Seguro.Soc. 2008;46:185-90.

24.   Raj D, Coleman N. Cauda equina syndrome secondary to lumbar disc herniation. Acta Orthop.Belg. 2008;74:522-7.

25.   Raj PP. Intervertebral disc: anatomy-physiology-pathophysiology-treatment. Pain Pract. 2008;8:18-44.

26.   Rubinstein SM, van TM. A best-evidence review of diagnostic procedures for neck and low-back pain. Best.Pract.Res.Clin.Rheumatol. 2008;22:471-82.

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28.   Watters WC, III, McGirt MJ. An evidence-based review of the literature on the consequences of conservative versus aggressive discectomy for the treatment of primary disc herniation with radiculopathy. Spine J 2008.

29.   Weinstein JN, Lurie JD, Tosteson TD et al. Surgical versus nonoperative treatment for lumbar disc herniation: four-year results for the Spine Patient Outcomes Research Trial (SPORT). Spine 2008;33:2789-800.

30.   Yamashita M, Ohtori S, Koshi T et al. Tumor necrosis factor-alpha in the nucleus pulposus mediates radicular pain, but not increase of inflammatory peptide, associated with nerve damage in mice. Spine (Phila Pa 1976.) 2008;33:1836-42.

31.   Zou J, Yang H, Miyazaki M et al. Missed lumbar disc herniations diagnosed with kinetic magnetic resonance imaging. Spine 2008;33:E140-E144.


Last Updated ( Friday, 15 April 2011 00:40 )  

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