DISCOGENIC LUMBAR PAIN

Author(s): Alexios Carayannopoulos, DO

Originally published:11/10/2011
Last updated:04/13/2016

1. DISEASE/DISORDER:

Definition

Discogenic lumbar pain (DLP) is low back pain from degenerative disk disease (DDD), occurring without
spinal deformity, radicular pain, neurologic symptoms, or spinal stenosis.

Etiology

 Strong familial predisposition to DLP

 DDD is associated with advanced age, male sex, and smoking
 Associated with particular occupations:
 Sitting positions and vibratory forces may expose disks to stresses, favoring DLP (truck drivers, manual
laborers).
 Intradiscal pressures increase during sitting.1
 Physically strenuous activities and repetitive motion may contribute to disk degeneration and facilitate
annular injury.

Epidemiology including risk factors and primary prevention

Primarily adults between the ages of 20 and 50 years.

Patho-anatomy/physiology

Disruption of the posterior annulus fibrosus can cause an inflammatory, biochemical response, irritating
nociceptive nerve terminals from vertebral endplate compression. Pain occurs from chemical irritation of nerve
endings in the outer annulus, or from excessive strains in the course of normal activities of daily living.2 The
nerve supply to the annulus is derived from the sinuvertebral nerve and a branch from the lumbar sympathetic
chain. Higher proportions of inflammatory markers such as lactate, growth factors, macrophages, and
granulation tissue occur. These variations occur primarily or secondary to injury.
 Disease progression including natural history, disease phases or stages, disease trajectory
(clinical features and presentation over time)

New onset/acute:

Pain lasting less than 6 weeks.

Subacute:

Pain lasting between 6 and 12 weeks.

Chronic/stable:

Pain persisting beyond 12 weeks.

Preterminal:

(N/A)

Specific secondary or associated conditions and complications

 Spondylolysis
 Spondylolisthesis
 Facet arthropathy/facet syndrome
 Myofascial pain syndrome

2. ESSENTIALS OF ASSESSMENT

History

Pain may refer to the buttocks, but generally does not extend below the gluteal folds. Pain is frequently
exacerbated by standing or sitting and relieved by lying down. The typical mechanism of many low back
injuries is the result of cumulative trauma, and not the result of a single exposure to a high-force load. Such
trauma places sub-failure magnitude loads on the spine. These include repeated small loads, such as bending or
sustained loads, such as sitting. In particular, injury to the disc has been shown to result from repetitive motion
at the end range, which can reduce failure tolerance over time.3
 Physical examination

Neurological examination is normal. Structural exam reveals limited range of motion and/or antalgic gait.
There is often para-midline tenderness.

Functional assessment

Oswestry Disability Index (ODI), Medical Outcomes Study Short-Form 36, and Pain Interference (PI) are used
to assess function.

Generally, laboratory studies are non-diagnostic, but may be required for work-up of systemic inflammatory
disease, infection, or malignancy including complete blood count (CBC) with differential, C-reactive protein
(CRP), erythrocyte sedimentation rate (ESR), and blood cultures.

Biopsy may be indicated if drug abuse is suspected, to rule out organisms other than Staphylococcus aureus.

Imaging

Magnetic resonance imaging (MRI) is the optimal investigation.

 Imaging is not indicated unless more than 6 weeks have passed or a red flag is present in the history.
 In general, findings may not correlate well with symptom severity or surgical outcome; however, findings
of a high intensity zone could potentially be specific and predictive of a symptomatic disk with severe
annular tear.
 Vertebral body endplate signal intensity changes can be seen on MRI in the setting of degenerative disc
disease of the lumbar spine. These signal intensity changes were first described and classified by Modic et
al in 1988 and have been since referred to as Modic changes.4 Currently, three types of Modic changes are
identified. Type I changes represent bone marrow edema and inflammation and appear hypointense on T1-
weighted imaging (T1WI) and hyperintense on T2-weighted imaging (T2WI). Type II changes are
associated with fatty replacement of normal hematopoietic bone marrow and appear hyperintense on T1WI
and isointense or slightly hyperintense on T2WI. Modic type III changes represent subchondral bone
sclerosis and appear hypointense on both T1WI and T2WI. Additionally, the absence of Modic changes,
indicating normal anatomical appearance, is designated as Modic type 0 by some clinical investigators
 The Pfirrmann grading system assesses degenerated intervertebral discs by MRI for the asymmetry in disc
structure, distinction of the nucleus and the annulus, signal intensity of intervertebral discs and height of
intervertebral discs and assigns grade I to V for disc degeneration. This system can provide a morphologic
 and semi-quantitative evaluation of intervertebral disc degeneration in vivo; however, it is a subjective
rating system and is inadequate for evaluating severe disc degeneration6.
 Functional imaging techniques such as MR spectroscopy, T1p calculation, T2 relaxation time measurement,
diffusion quantitative imaging, and radio nucleotide imaging provide measurement of some of the
degenerative features.7

Other investigations include plain radiographs, computed tomography scanning, or radionuclide bone scans.

 Plain films often show disk space narrowing, consistent with degenerative disk changes, and can rule out
instability from spondylolysis and/or spondylolisthesis.7
 Both conventional bone SPECT and bone SPECT scans co-registered with CT are reliable for the
identification of disk pathology; however, bone SPECT-CT scans showed greater agreement for localized
facet joint pathology. These studies should be considered to assist in surgical planning and identification of
levels that may benefit from intervention.
 CT scan can be useful because it’s easier to see the bony elements, such as when a bone spur is pressing on
a nerve. 7
 Bone scan can be ordered to detect spinal problems such as osteoarthritis, fractures, or infections, which can
all be related to DDD.7

Supplemental assessment tools

 Provocative discography (PD) is a diagnostic procedure used to confirm a discogenic pain source. It should
be considered in patients for whom surgical intervention is a consideration.
 PD assesses for pain concordant with DLP after injection of radiographically corroborated levels with saline
or contrast.
 PD has high sensitivity but low specificity for discogenic pain.
 Common criteria for diagnosis of a painful, internally disrupted disk include a pain level of 7 or higher,
concordant pain reproduction at a pressure less than 50 mmHg above opening pressure, annular tear grade
III or higher, injected contrast volume of 3.5 mL or less, and a pain-free control disk at an adjacent level.8,9
 Careful psychological screening is invaluable in selecting appropriate patients.9

Early predictions of outcomes

Poor prognostic factors:10,11,12,13,14

 Emotional distress, complex social circumstances

 Litigation or compensation vendettas
 Abnormal psychometric testing including chronic pain and somatization
 Chronic tobacco abuse

Good prognostic factors:10,11,12,13,14

 Good social support system

 Few confounding factors
 Symptoms consistent with MRI findings

Environmental

Machine drivers had a higher incidence of DLP than carpenters, who had a higher ratio than office workers.

Social role and social support system

Although genetic and demographic characteristics are primary risk factors for DLP, socioeconomic factors are
important risk factors for pain and disability.15

Low Back Pain (LBP) and disability are associated with job dissatisfaction, physically strenuous work,
psychologically stressful work, low education level, and worker’s compensation insurance.

Good social support is associated with less pain and disability.15

Professional Issues

Familial predisposition to DLP may be relevant in prevention and screening.

 Families with 2 or more subjects with DLP at risk.

 In pre-employment screenings, subjects from predisposed families could be redirected to work activities
with lower abnormal functional stresses and protective ergonomic measures.16

DLP is associated with increased medical liability when acute cauda equina syndrome, conus medullaris
syndrome, discitis, malignancy, and spinal hematoma are not recognized.

3. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND

PRACTICE
 Artificial disk surgery

 Approved in 2004 for lumbar spine; indicated for DDD at 1 or 2 levels of the spine.
 Efficacy of disk replacement has not been demonstrated in prospective, randomized studies.

Biologic therapy

 Recently, a research group from Denmark and the United Kingdom proposed an association between
infections of herniated discs caused by Propionibacterium acnes(PA), chronic low back pain (CLBP) and
bone marrow edema in the adjacent vertebral endplates 26. In a parallel publication, they reported on the
successful treatment of this condition with antibiotics as compared to placebo 26,27.
 IL-10 and TGF-B have potential bio-therapeutic use for treatment of DDD. 28

Stem cell therapy for intervertebral disc regeneration

 Current in vitro and in vivo studies show that stem cells have the capacity to repair degenerative disks.
 Repair occurs by differentiation toward chondrocyte-like cells, which are capable of producing
proteoglycans and type II collagen.
 Mesenchymal stem cells derived from bone marrow or adipose tissue have the advantage for stem cell
therapy on source, safety, and tolerance.
 Stem cell-based treatments of DDD are promising, but further clinical studies are warranted. 29
 Recently, a study shows that percutaneous injection of autologous bone marrow concentrate cells
significantly reduced DLP through 12 months. 28

Nonsurgical spinal decompression (NSSD)

 Procedure decompresses the spine similar to traction units.

 Outcomes:
 In presence of overt, symptomatic disk disease, preliminary results of NSSD suggest a stronger
therapeutic effect than conventional traction.
 No trials have looked at the effectiveness of this therapy.

4. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

 Non-operative treatments
 There is a need for more high quality studies
 Provocative discography
 Based on 2007 American Pain Society (APS) guidelines, patients with chronic nonspecific LBP should
not undergo provocative discography for diagnosing discogenic LBP.
 Use of provocative discography is controversial and presents a large gap in evidence-based knowledge.
 Specificity of producing concordant pain by stimulating an anatomic site has not been proven in PD.
 In presence of chronic pain, there is increased responsiveness to normative innocuous stimuli.
Furthermore, hyperalgesia of uninjured tissue occurs around an area of injury.
 Stimulation of structures proximal to a lesion may mimic patient’s usual pain.
 Psychogenic pain may also be simulated by anatomical stimulation. Therefore, it cannot be assumed
that reported reproduction of pain by stimulation of an anatomic structure implicates the disk as the
primary pain generator.30
 Spinal fusion
 Based on 2007 APS guidelines for patients with non-radicular LBP, common degenerative spinal
changes, and persistent/disabling symptoms, clinicians should discuss risks and benefits of surgery as an
option.
 Small- to moderate-average benefits from surgery versus nonsurgical therapies seen in highly selected
patients, and the majority of such patients undergoing surgery do not experience an optimal outcome.
 In comparing nonsurgical treatment for non-radicular LBP with degenerative disk disease, lumbar inter-
body fusion is probably not very effective. Fusion appears to have a superior outcome when compared to
standard nonsurgical therapy, but not better than intensive interdisciplinary rehabilitation.

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Source: https://now.aapmr.org/discogenic-lumbar-pain/