Lumbar Discogenic Pain

Original Editors - Jon Ford as part of the STOPS Project.

Top Contributors - Evan Thomas, Jon Ford, Anne-Laure Vanherwegen, Rachael Lowe and Wanda van Niekerk


Of all the patients who are dealing with low back pain, it appears that in approximately 28 to 40% of these cases, pain is caused by a discogenic affliction.[1] 

Detailed structure of the intervertebral disc (adapted from Bogduk 2005)

Pain can be related to different types of pain which come from muscles, bones, vertebral joints other than the intervertebral disc or other structures in the spine. A degenerated intervertebral disk can release nociceptive molecules and growth factors which result in nerve ingrowth into the disc.[2] (level:3A)

Discogenic pain is pain arising from stimulation of pain sensitive afferents within the annulus fibrosus and is a separate condition from disc herniation with associated radiculopathy.[3] (level: 5)

Detailed structure of the intervertebral disc
(adapted from Bogduk 2005)

Clinically relevant anatomy

The intervertebral disc (IVD) is the principal joint between two vertebrae in the vertebral column.
Each IVD is composed of three structures:
1. The nucleus pulposus (NP), a gelatinous inner part;
2. The annulus fibrosus (AF), an outer ring of fibrous tissue that encloses the nucleus pulposus;
3. Two endplates of hyaline cartilage.[2] (level: 3A)

The endplates serve as an interface between the disc and the vertebrae, they cover the upper and lower level of the annulus fibrosus and the nucleus pulposus.
The cells in the outer region of the annulus fibrosus are fibroblast-like cells which are disposed parallel to the collagen fibers, while those in the inner annulus fibrosus are chondrocyte-like cells.
The nucleus pulposus is made from randomly arranged collagen fibers and radially organized elastin fibers surrounded in a highly hydrated aggrecan-containing gel. There are a few chondrocyte-like cells in the nucleus pulposus.[2](level: 3A)

The intervertebral disc is mechanically similar to a thick-walled fiber-reinforced pressure vessel absorbing strain energy and transferring loads down the spine. The outer annulus fibrosus provides structural stability as the vessel wall with collagen fibril families layered in concentric lamellae of diversified orientation (between 45° and 65° off spinal axis), it is primarily a tensile member.
The nucleus pulposus mainly consists of hydrophilic proteoglycans; which absorb water and pressurize the disc, it also distributes weight to the annulus fibrosus and vertebral endplates and conserves disc height.
The graded properties of the disc change with degeneration and this can be visualized morphologically, biochemically and mechanically.[4](level: 3A)

Discogenic pain is attributed to degenerative changes in the intervertebral disc due to aging or a trauma. The healthy disc of an adult has scattered nerves which are mainly restricted to the outer lamellae. Degenerated discs have nerves that go through deeper intradiscal structures till the inner third of the annulus and the nucleus. These nerves contain nociceptive neurotransmitters and initiate production of cytokines, provoking nociceptive information from within the disc.[1](level: 3A)

Epidemiology/ Etiology

Discogenic pain is a form of low back pain, caused by chemically or mechanically damaged intervertebral discs.[2](level: 3A)

This damage can find its origin in traumatic events, as well as in deterioration due to aging.

In patients dealing with discogenic low back pain, there were findings of high levels of proinflammatory mediators (cytokines). The production of these proinflammatory mediators occurs in the nucleus pulposus of the disc and is in general viewed as a major cause of the discogenic low back pain.[1](level: 3A)

Characteristics/clinical presentation

There is a lot of literature to support that the underlying mechanisms of these features are indicators for discogenic pain. Although this wasn’t validated, it makes clinical sense that combining these features with radiological criteria will increase diagnostic certainty.
The symptoms of lumbar discogenic afflictions are not experienced in the exact same way by every patient. Most patients that experience chronic low back pain, often report this pain radiating into the buttock and the leg. This pain can be experienced uni- or bilaterally, but without radicular pain. These patients can also experience a sitting intolerance.[5](level 2A)
An important mechanism behind the diagnosis of discogenic pain is nuclear pulposus migration, resulting in a directional preference. Mechanical loading strategies (MLS), like repeated movements and sustained positioning, can cause proximal movement

Repeated extension in lying: a common mechanical loading strategy

 and can put an end to distal symptoms. It has been stated by researchers that the mechanism that underlies this response, is caused by a reduction or a migration of a painful and abnormally displaced nucleus pulposus to a position in the lumbar disc that is more central, causing less pain.[1][4][2] (level: 5, 2B en 1A)

Associated with centralisation is directional preference, the direction of MLS that result in centralization. [6][2] (level: 5 en 3A) 
Patients with a directional preference due to discogenic pain can be diagnosed as having reducible discogenic pain (RDP).[7] (level: 5)

By evaluating responsiveness to a MLS, CT/MRI/discography results and other clinical features, a confident diagnosis can be uptained. Based on this diagnosis, a treatment plan can be made.
Experienced practitioners have hypothesised that more than one type of discogenic pain may exist including non-reducible discogenic pain, discitis, unstable disc and adolescent disc.[7](level: 5) 
From a pathoanatomical perspective, different morphological and pathophysiological changes may also represent subgroups of clinical relevance such as end plate changes, variations in annular tears and inflammatory/immune responses. Practitioners attempting to diagnose discogenic pain should be aware of these possible subgroups and potential impact on patient presentation.

Differential diagnosis

• Lumbosacral Disc Injuries
The causative factor of the intervertebral discs of the lumbosacral spine injuries are low back pain (LBP). It is a more frequent source than muscular strain or ligamentous sprain. There is no single injury to the intervertebral disc that has been unequivocally identified as a pain generator.[8](level: 2A)

Lumbosacral Facet Syndrome
Zygapophyseal -joints are not the single or primary cause of LBP and are often mistaken for discogenic pain. The Z-joint is one of the most common sources of low back pain (LBP).[9] (level: 2A)

Lumbosacral Radiculopathy
However radiculopathy is not the cause of back pain, some of the major causes of acute and chronic low back pain (LBP) are associated with it. The cause of lumbosacral radiculopathy is nerve root impingement and/ or inflammation with neurologic symptoms in the areas that are supplied by the affected nerve root or rots.[7](level : 2A)

Lumbosacral Spondylolisthesis
Spondylolisthesis is most common in the lower lumbar spine region. Causes are minor overuse trauma, particularly repetitive hyperextension of the lumbar spine. If the pars defect is bilateral, it may allow slippage of the vertebra, typically L5 on S1, resulting in spondylolisthesis.[6](level: 2A)

Lumbosacral Spondylolysis
Causes of Lumboscaral spondylolyse are mostly mechanical factors, they could trigger or develop lubar spondylolysis. There is also a heredity factor. The most common place is at L5 (85%) and may be observed as high as L2. Lumbosacral spondylolysis (lumbar spondylolysis) is the cause of the most common type of spondylolisthesis.[3] (level:2A)

Diagnostic procedures

Diagnostic procedures can reveal 90% of all sources of Chronic low back pain. There are two types of internal disc disruption (IDD)- induced low back pain (IAD) and internal endplate disruption-induced low back pain (IED). Clinically and pathologically seen, the term IAD is more correct than the term IDD. The lumbar intervertebral discs without disc herniation are 26%-42% of the cause of chronic low back pain. It results in a nociceptive pain syndrome. The source of the pain is in the innervated outer third of the annulus.[10] (level: 2A)

Diagnosis and treatment of lumbar discogenic pain due to internal disc disruption (IDD) Internal disc disruption remains a challenge. Magnetic resonance imaging (MRI) can find high-intensity zone as an indirect indication of IDD.

However, relative low sensitivity (26.7% to 59%) and high false-positive (24%) and false-negative (38%) rates reduce the value of MRI in screening for the existence of painful IDD.

There is a positive predictive value of up to 89%. Provocative discography can provide unique information about the source of pain and the morphology of the disc. It may also provide information for selecting appropriate treatment for the painful annular tear.[5] (level: 2A)

A subsequent CT scan with stimulation of a disc is of exclusive diagnostic value. The clinical picture of discogenic pain does not correlate with degenerative changes. There is no difference from any other back pain. It has a prevalence of 39%, thus it is one of the most important causes for patients with a specified source of back pain.[5](level: 3A)

Outcome measures

Sereveral tests can be used to determine the bottom line for patients with lumbar discogenic pain. The questionnaire from The North American spine society is a frequently used instrument. This has a high test-retest reliability and internal reliability. This questionnaire is recommended to be used for monitoring of individual patient’s progress during treatment.[1](level: 2B)
The Roland Morris questionnaire is also a good instrument to evaluate the progress during treatment but the questions on the list only asks about the situation on the date of examination, they do not consider the whole situation.[4](level: 2A)

The pain visual numeric is the last frequently used instrument for patients. The patients score their selves themselves by the amount of pain they are feeling. It is a modified version of the visual analogue scale.[2](level: 2A)


Neurological tests showed that the problem was not caused by neurological deficits. These findings were confirmed by the results of the Straight Leg Raise test, which also showed no signs of possible neurological deficits.[1](level: 3A)

Much of the controversy around discogenic pain comes from confusion and misinformation on diagnosis. “Disc degeneration” is a poorly defined term perhaps best described as “an aberrant, cell-mediated response to progressive structural failure. The degenerate disc is one with structural failure combined with accelerated or advanced signs of ageing”.[1](level: 1A)

The outcome of degeneration can include annular fissures, disc herniation, endplate damage, collapse of the annulus, and disc narrowing which in some cases will produce lumbar related symptoms. Radiological tests such as CT scan and MRI are able to image the external and internal morphology of the intervertebral disc in identifying such structural failure. However these changes in isolation do not predict the presence or absence of lumbar related symptoms[4] (level: 2B) and radiology alone is not recommended for the diagnosis of LBD.[2](level: 3A). Lumbar discography is an where the nucleus of the IVD suspected of causing low back pain is injected with radiolucent dye, with the aim of provoking clinical symptoms and revealing morphological abnormalities in the annulus fibrosus. The test is considered positive if the patient’s concordant pain is reproduced upon stimulating the suspected painful disc, and stimulation of adjacent discs does not reproduce the patient’s typical symptoms. Carefully controlled discography is likely to be the best diagnostic tool available for discogenic pain although it has significant risks[10](level: 2B) and has a relatively high false positive rate.[5](level: 2B)

It is clear from the literature that a single test for diagnosing discogenic pain is not possible and therefore the methodology of “diagnostic accuracy” to evaluate the validity of clinical tests is somewhat flawed.[8](level: 5)

From a clinical perspective however a number of features have long been associated with discogenic pain based on hypothetical and proven causal mechanisms.[9](level: 5)
These features have been identified in a recent Delphi study of international experts[7] (level: 5) and are summarised in the following table:

i. Directional preference
ii. Symptoms being aggravated by prolonged sitting (>60 minutes)
iii. Symptoms being aggravated by lifting
iv. Symptoms being aggravated by forward bending
v. Symptoms being aggravated by sit to stand
vi. Symptoms being aggravated by cough/sneeze
vii. History of working in a job with heavy manual handling
viii. The mechanism of injury being associated with flexion/rotation and/or compression loading
ix. Symptoms much worse the next morning or day after onset of injury

Medical management

Minimally invasive treatments bring alternatives for discogenic pain in order to cost-effectiveness and less long-term side effects (if possible). Effectiveness of most of these therapies is yet to be established.
More clinical studies are needed to improve the clinical efficacy of minimally invasive treatments for lumbar discogenic pain.[5] (level: 2A)
Additional therapies, including nonsteroidal anti-inflammatory drugs (NSAID’s), physical therapy, rehabilitation, antidepressants, antiepileptic’s and acupuncture have been used for low back pain.
The effectiveness of these treatments for discogenic pain is yet to be established.[5](level: 2A)

Thermal annular procedures (TAPs) have been developed in an effort to provide a minimally invasive treatment for this complaint. Multiple techniques such as intradiscal electrothermal therapy (IDET), radiofrequency annuloplasty and intradiscal biacuplasty (IDB) were used.
However, these treatments continue to be controversial associated with a lack of evidence.[7] (level: 2A)

Intradiscal electrothermal therapy (IDET)
This is a minimally invasive treatment option between conservative nonoperative management and spinal surgery. Remaining clinical improvements can be realized in patients with mild disc degeneration.[8] (level: 1B)
It may offer some pain relief for a small group of patients.[5] (level: 2A)
This procedure appears to offer sufficiently symptom progress without additional complications.[9] (level: 2A)
It also offers functionally significant relief in 50% of chronic discogenic low back pain patients.[7] (level: 2A)

Radiofrequency annuloplasty
There is minimal evidence supporting the use of radiofrequency annuloplasty.[7] (level: 2A)

Intradiscal biacuplasty (IDB)
The clinical benefits observed in the study of Kapural et al. are the result of non-placebo treatment effects given by IDB,[6] (level: 1B) but there is minimal evidence supporting the use of IDB in other studies.[7] (level: 2A)
This should be recommended as a selection method for patients with chronic discogenic low back pain.[6] (level: 1B)

Other treatments are :

Bi-annular pulsed radiofrequency disc method
The bi-annular pulsed radiofrequency disc method with consecutive P-RF 5/5/60 V, 12-min (with Diskit needle), appears to be a safe, minimally invasive treatment option for patients with chronic discogenic low back pain.[3] (level: 2B)

Intradiscal steroid injections
This method has not been proved to determine long-term benefits.[5] (level: 2A)

Intradiscal radiofrequency thermocoagulation
No benefits have been found for the intradiscal radiofrequency thermocoagulation.[5] (level: 2A)

Spinal fusion
If a spinal fusion surgery is performed, its aim is to stop the motion at a painful vertebral segment. There are many different approaches but they all involve the following process: firstly they add bone graft to a segment of the spine , secondly they set up a biological response that causes the bone graft to grow between two vertebral elements. This creates a bone fusion which leads to one fixed bone replacing a mobile joint, so it will stop the motion at that segment.[10] (level: 5)

Ramus communicans block
A block in the ramus communicans is able to interrupt the passage of painful information from the discs to the central nervous system.[5](level: 2A)

Disc cell transplantation
Disc cell transplantation is in the experimental stage, it has the potential to become useful for the prevention and treatment of discogenic pain.[5](level: 2A) More research is needed.

Physical treatment management

In a case study, the therapist chose to introduce left lumbar side bending to the treatment. The patient was placed in a left lateral recumbent position and was asked to bend side wards over a pillow. He used a non-weight bearing position because the patient has reported an increase of her symptoms after eight repetitions when it is was performed as a weight bearing side glide.
Another thing that was introduced was transverse plane motion via repeated right rotation from the left side bent position. This combined motion abolished the patient’s pain completely and restored considerable range of motion in the sagittal plane after been tested again in standing. This treatment is equivalent to the flexion-rotation mobilization with the notable difference being that the motion is coming from below in the latter method. The patient also got some homework exercises to do during the treatment. She was sent home with instructions in posture considerations and also replicating the repeated right rotation in left side lying 6-8 times a day.[5] (level: 4)

The treatment of all possible types of discogenic pain is complex and beyond the bounds of this article. There are many different treatments, not all of them are proven to be effective yet. Some examples of possible treatments for low back pain are acupuncture, anti-inflammatory drugs, physical therapy, rehabilitation, antidepressants, anti-epileptics and adjunctive therapies. Some of the treatments have shown to be effective, but only for a certain group of patients and they do not always show long-term benefits. Intradiscal steroid injection and intradiscal electrothermal therapy are well-known examples of this issue. Further on, there were no clear benefits found for the intradiscal radiofrequency thermocoagulation.[5](level 2A) 

In carefully identified cases of RDP a regime can be applied of regular participant application of helpful MLSs, education, postural advice, lumbar taping techniques and in some cases therapist applied forces.

To evaluate the response to a MLS, you need to be careful. A recent randomized control trial on the treatment of reducible discogenic pain used the following criteria. A positive response to at least 10 repeated movements or a period of sustained positioning by:
• An increase in possible range of motion of the MLS during application by at least 50% or
• An increase in lumbar active range of motion in any movement by at least 50% after application or
• An increase in observed segmental intervertebral motion during lumbar active range of motion testing after application or
• An improvement in resting pain[10] (level : 1B) (by at least 1 point on a numerical rating scale or by centralisation of symptoms) that lasted for at least 1 minute after application or
• A reduction in an observed lateral shift postural abnormality that lasted for at least 1 minute after application[7] (level: 5)

A summary of the key components of an effective treatment program for RDP is provided in the table below:

Treatment protocol component Rationale
Determine whether clinical evidence exists of inflammation (At least 2 of: constant symptoms, getting out of bed at night due to the pain, early morning symptoms > 60 minutes) The McKenzie method is predominantly for mechanical problems and inflammation, if present, requires specific management
In the absence of inflammation, assess for relevant MLS and identify key asterisks. Confirmation of the most effective MLS to be used for treatment
Explanation regarding RDP, treatment options, treatment timeframes and recovery expectations. Engaging the participant with the treatment process is critical to effective specific treatment
Management of inflammation if applicable including provision of information sheet, lumbar taping, recommend pharmacy consultation regarding non-prescription NSAIDs and walking program short of pain onset Relative rest from aggravating postures/activities, NSAIDs and sub-clinical activity in neutral spine position may prevent an excessive and counter-productive inflammatory response
In the absence of inflammation provide an appropriate dosage of the relevant MLS and reassess asterisks. Additional hypothesis testing
Provide homework for regular application of the relevant MLS as an exercise. Self management of the RDP through home application of MLSs is an essential component of the McKenzie approach
Provide a lumbar roll, postural education, a walking program, and lumbar taping in neutral lumbar spine position. These strategies were described on the information sheet Education of the participant regarding postural control is an essential component of the McKenzie approach

The application of MLSs need to be carefully performed according to the following criteria:
• Ensuring correct starting position
• Clear and specific participant instructions
• Careful observation by the physiotherapist of participant performance of the MLS
• Provision of verbal and tactile feedback to the participant during and after the MLS
• In most cases instructing the participant to perform the MLS to the point of pain onset. In the event of pain onset progressing further into the MLS range during application, the trial physiotherapist encouraged the participant to progress the movement to the new point of pain onset aiming for end of range when possible
• Close monitoring of symptom response including centralization during and after the MLS

MLS are generally recommended as a home exercise every 1-2 hours for 6-10 repetitions (with careful patient monitoring of symptom response). Patients with true RDP tend to respond quite quickly over a period of days. If this does not occur then the accuracy of the diagnosis should be considered.

DPM should rarely be used in isolation to treat discogenic pain, rather combined with other therapeutic methods including manual therapy, motor control training and functional restoration. In the presence of significant psychosocial and neurophysiological factors the administration of DPM should be carefully weighed up against other treatment approaches (e.g. cognitive behavioral approach, graded activity, neurophysiological education).[6][3][1][4][2][10] (level : 2A)

Key Research

Adams, M. and P. Roughley (2006)."What is intervertebral disc degeneration, and what causes it?" Spine 31(18): 2151-2161

Maurer P, Block JE, Squillante D.Intradiscal electrothermal therapy (IDET) provides effective symptom relief in patients with discogenic low back pain. J Spinal Disord Tech. 2008

Recent Related Research (from pubmed)

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  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 José García-Cosamalón et al. Intervertebral disc, sensory nerves and neurotrophins: who is who in discogenic pain? J Anat. 2010 July; 217(1): 1–15. Level : 3A
  3. 3.0 3.1 3.2 3.3 Bogduk, N. (2012). Clinical and radiological anatomy of the lumbar spine. New York, Churchill Livingstone. Level : 5
  4. 4.0 4.1 4.2 4.3 4.4 Schultz et al. Mechanical profiling of intervertebral discs. J Biomech. 2009 May.Level : 3A
  5. 5.00 5.01 5.02 5.03 5.04 5.05 5.06 5.07 5.08 5.09 5.10 5.11 5.12 Zhou Y, Abdi S. Diagnosis and minimally invasive treatment of lumbar discogenic pain--a review of the literature. Clin J Pain. 2006 Jun;22(5):468-81. Level : 2A
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  7. 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 Chan, A. Y., J. J. Ford, et al. (2013). Preliminary evidence for the features of non-reducible discogenic low back pain: survey of an international physiotherapy expert panel with the Delphi technique. Physiotherapy. Level : 5
  8. 8.0 8.1 8.2 Robert E Windsor. Lumbosacral Disc Injuries. Medscape. 2013 june 3. Level : 2A
  9. 9.0 9.1 9.2 Gerard A Malanga, Lumbosacral Facet Syndrome.Medscape. 2013 april 5. Level : 2A
  10. 10.0 10.1 10.2 10.3 10.4 Bao-Gan Peng. Pathophysiology, diagnosis, and treatment of discogenic low back pain. World J Orthop. 2013 April 18; 4(2): 42–52. Level : 2A