Internal disc disruption


Original Editors - Alexander Chan

Top Contributors - Alexander Chan, Dorien De Strijcker   

Contents

Definition/Description

Internal disc disruption, first proposed by Crock (1970), has been defined as lumbar spinal pain, with or without referred pain, stemming from an intervertebral disc, caused by internal disruption of the normal structural and biochemical integrity of the symptomatic disk.[1][2]

Crock (1970) postulated that traumatic damage to the vertebral end plate could cause an irritant substance to drain into the spinal canal and/or vertebral body. This could initiate an autoimmune response, causing an internal process of disc degradation, which would lead to annular tearing and irritation of the free nerve endings in the outer third of the annulus fibrosis.

Clinically Relevant Anatomy

Click on the link for more specific details about intervertebral disc.

Epidemiology /Etiology

Internal disc disruption is a subgroup of discogenic pain. The epidemiology/etiology of discogenic pain can be found here andhere.

The prevalence of IDD has been estimated to be 39% (95% CI: 29% to 49%) in ninety-two patients with chronic LBP.[3] In a more recent study, it has been estimated at 42% (95% confidence interval [CI] = 35% to 49%).[4] 


Characteristics/Clinical Presentation

Crock’s (1986) description of IDD included the following features:

  • Intractable back pain with aggravation of pain and low of spinal motion with any physical exercises


  • Leg pain


  • Loss of energy


  • Marked weight loss
  • Profound depression[5]

In the IASP’s Classification of Chronic Pain, IDD has the features of:

  • lumbar spinal pain, with or without referred pain in the lower limb girdle or lower limb;
  • aggravated by movements that stress the symptomatic disk[1]

According to Sehgal (2000), most of the patient’s experience:

  • diffuse, dull ache
  • a deep-seated, burning, lancinating pain in the back
  • a sensation of a weak, unstable back
  • referral of pain into the hips and lower limbs is not uncommon.
  • a varying degree of sitting intolerance
  • lumbar spine movements are slow, guarded and restricted
  • a history of lifting trauma precedes the back pain in acute cases
  • pain and muscle spasm are less dramatic and more nondescript in persistent cases[6]

Differential Diagnosis

- Disc herniation:
In which the herniated nucleus pulposus is capable of generating back/leg pain when it causes a mechanical compression of the nerve-root.


- Ruptured disc:
Fernston observed that a simple, ruptured disc without herniation can have a clinical presentation similar to herniated nucleus pulposus[7].


Degenerative disc disease:
The intervertebral disc transitions from being asymptomatic to pain generating as a result of degenerative changes. Although altered disc morphology may be asymptomatic, various mechanisms that may give rise to a symptomatic degenerate disc exist.[8][9]

Diagnostic Procedures

Physical examination alone is insufficient to establish a diagnosis of IDD. Diagnostic imaging, however, has contributed to the understanding of IDD.

Plain Xrays and Computerized Tomograms (CT) are generally normal.[6]

Magnetic Resonance Imaging (MRI) of the lumbosacral spine can identify areas where there are changes to signal intensity, with a loss of signal intensity correlating with abnormal disc morphology on discography.[10][11]

Provocative discography is physiologic test that explicitly determines whether a disc is painful. The disc suspected of causing pain is injected with radiolucent dye. The aim is to provoke clinical symptoms and reveal morphological abnormalities in the annulus fibrosis.[12]The test is considered positive if the individual’s concordant pain is reproduced upon stimulating the suspected painful disc, and injection of adjacent discs does not reproduce the typical symptoms.[3][13] In asymptomatic individuals, discography is not painful, but is frequently painful in those with low back pain. A post-discography CT scan can be used to evaluate the extent of internal disruption within the disc.

Despite the clinical use of discography, its utility has been questioned due to high false positive rates.[12][14][15] It is also associated with procedural risks, is expensive, and can be difficult to access.[16] Discography has also been shown to result in accelerated disc degeneration compared to match-controls.[17]

The criteria for diagnosing IDD from the International Association for the Study of Pain’s Taxonomy Working Group is:

1. Lumbar spinal pain, with or without referred pain in the lower limb girdle or lower limb

2. Aggravated by movements that stress the symptomatic disc
3. Diagnostic criteria for lumbar discogenic pain must be satisfied including either:
    a) Selective anesthetization of the putatively symptomatic intervertebral disc completely relieves accustomed pain, or save that whatever pain persists can be ascribed to some other coexisting source or cause
    b) Provocative discography of the putatively symptomatic disc reproduces the patient’s accustomed pain, but not at least two adjacent discs, and the pain cannot be ascribed to some other source innervated by the same segments as the symptomatic disc

4. CT-discography must demonstrate a grade 3 or greater grade of annular disruption
 

Outcome Measures

add links to outcome measures here (also see Outcome Measures Database)

Examination

It is very difficult to establish a clinical diagnosis only based on history and physical examination when there are no objective clinical findings. There is no clinical test that can make a distinction between IDD patients and patients with other conditions.[3] The only convincing means to establish IDD is provocative discography as described above.

Medical Management 

1) Pharmacological management
Pharmacological management if for analgesic purposes and may include the use of Acetaminophen (Paracetamol), non-steroidal anti-inflammatories, muscle relaxants, or opioids.[18]


2) Minimally invasive interventional procedures:
- Intradiscal steroid injection
- Radiofrequency denervation
- Intradiscal Electrothermal (IDET) Therapy

3) Surgical treatment:
Internal disc disruption can be managed surgically by fusing the vertebrae at the level of disc disruption.
Disadvantages of surgical fusion include:
- failure to maintain the height of the intervertebral disc
- less segmental motion at the fused levels, which may contribute cephalocaudal neuroforaminal stenosis and overloading of adjacent disc levels [6]


Physical Therapy Management

The main goals of treatment are improving function and quality of life, treat pain and in long term, prevent future back injury and disability.


1) Dynamic lumbar stabilisation (core stability):
Traditionally core stability has referred to the active component to the stabilizing system. This includes local muscles that provide segmental stability (eg transversus abdominis, lumbar multifidus) and/or the global muscles (eg rectus abdominis, erector spinae) that enable trunk movement/torque generation and assistance in stability in more physically demanding tasks.[19] This is discussed in more detail here.

2) Mechanical Diagnosis and Therapy (McKenzie Method) [20]:
The McKenzie method utilizes the patient’s response to repeated lumbar movements to assess which movements reduce the individual’s most peripheral symptoms. These movements are then combined into an individualized exercise regimen. This is discussed in more detail here

Key Research

Resources


Clinical Bottom Line


Recent Related Research (from Pubmed)

Intradiscal Electrothermal Therapy (IDET) for the Treatment of Discogenic Low Back Pain: Patient Selection and Indications for Use

References

  1. 1.0 1.1 IASP Taxonomy Working Group, Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms, 2011.
  2. Crock, H.V., A reappraisal of intervertebral disc lesions. Med J Aust, 1970. 1(20): p. 983-9.
  3. 3.0 3.1 3.2 Schwarzer, A.C., et al., The prevalence and clinical features of internal disc disruption in patients with chronic low back pain. Spine (Phila Pa 1976), 1995. 20(17): p. 1878-83.
  4. DePalma, M.J., J.M. Ketchum, and T. Saullo, What is the source of chronic low back pain and does age play a role? Pain Med, 2011. 12(2): p. 224-33.
  5. Crock, H., Internal disc disruption: A challange to disc prolapse fifty years on. Spine (Phila Pa 1976), 1986. 11(6): p. 650-3.
  6. 6.0 6.1 6.2 Sehgal, N. and J.D. Fortin, Internal disc disruption and low back pain. Pain Physician, 2000. 3(2): p. 143-157
  7. Fernstrom, U., A discographical study of ruptured lumbar intervertebral discs. Acta Chir Scand Suppl, 1960. Suppl 258: p. 1-60.
  8. Roberts, S., et al., Histology and pathology of the human intervertebral disc. J Bone Joint Surg Am, 2006. 88 Suppl 2(Supplement 2): p. 10-4.
  9. Bogduk, N., Clinical anatomy of the lumbar spine and sacrum. 4th ed. 2005, New York: Churchill Livingstone.
  10. Milette, P., et al., Differentiating lumbar disc protrusions, disc bulges, and disc with normal contour but abnormal signal intensity. Magnetic resonance imaging with discographic correlations. Spine, 1999. 24(1): p. 44-53.
  11. Schneiderman, G., et al., Magnetic resonance imaging in the diagnosis of disc degeneration: correlation with discography. Spine, 1987. 12: p. 276-281.
  12. 12.0 12.1 Carragee, E.J., et al., A gold standard evaluation of the "discogenic pain" diagnosis as determined by provocative discography. Spine (Phila Pa 1976), 2006. 31(18): p. 2115-23.
  13. Merskey, H. and N. Bogduk, Classification of chronic pain: Descriptions of chronic pain syndromes and definitions of pain terms. 1994: IASP Press (Seattle).
  14. Carragee, E.J., T.F. Alamin, and J.M. Carragee, Low-pressure positive Discography in subjects asymptomatic of significant low back pain illness. Spine (Phila Pa 1976), 2006. 31(5): p. 505-9.
  15. Carragee, E., et al., The rates of false-positive lumbar discography in select patients without low back symptoms. Spine (Phila Pa 1976), 2000. 25(11): p. 1373-1380.
  16. Hancock, M.J., et al., Systematic review of tests to identify the disc, SIJ or facet joint as the source of low back pain. Eur Spine J, 2007. 16(10): p. 1539-50.
  17. Carragee, E., et al., 2009 ISSLS Prize Winner: Does discography cause accelerated progression of degeneration changes in the lumbar disc: a ten-year matched cohort study. Spine (Phila Pa 1976), 2009. 34(21): p. 2338-2345.
  18. Simon, J., et al., Discogenic low back pain. Phys Med Rehabil Clin N Am, 2014. 25(2): p. 305-17.
  19. McNeill, W., Core stability is a subset of motor control. J Bodyw Mov Ther, 2010. 14(1): p. 80-3.
  20. McKenzie, R. and S. May, The lumbar spine: Mechanical diagnosis and therapy. 2nd ed. 2003, Waikanae, New Zealand: Orthopedic Physical Therapy Products.