Lower Back Pain

Types of pain:

  • Somatic pain is evoked by noxious nerve ending stimulation. This pain is broad and poorly localized.
  • Somatic referred pain is a function of interneuronal convergence within the spinal cord.
  • Radicular pain occurs because ectopic impulses generated in the dorsal root ganglion are perceived as pain arising in the territory innervated by the affected axon.
  • Neuropathic pain is evoked by impulses generated in the axons of a peripheral nerve.

Reported prevalence in Australia of low back pain: Point prevalence 15-30%; 1 year prevalence 50%; lifetime prevalence 60-80%.

Non-osseus causes of low back pain

Any of the following structures may cause low back pain: the vertebral venous plexus; dura mater; ligaments of the vertebral arches; muscles and fascia; vertebral bodies; laminae; apophyseal joints and the annulus fibrosis of the disc.

Damage to the intervertebral discs and apophyseal joints are the most common causes of low back pain.

Pathophysiology of disc and facet joint degeneration

Posterior elements of the lumbar spine typically bear less weight than anterior elements in all positions. Anterior elements bear over 90% of forces transmitted through the lumbar spine in sitting and this ↓ to ~80% with standing. As the degenerative process progresses, relative anterior-to-posterior force transmission approaches parity. Persistent, recurrent, non-mechanical, and/or excessive forces to the motion segment beyond minimal thresholds lead to microtrauma of the disc and facet joints, triggering and continuing the degenerative process.

There are said to be 3 phases of degenerative change rather than distinct clearly definable stages.

Phase I:

This is characterized histologically by circumferential tears or fissures in the outer annulus. Tears can be accompanied by endplate separation or failure, interrupting blood supply to the disc and impairing nutritional supply and waste removal. Since the outer ⅓ of the annular wall is innervated, tears or fissures in this area may be painful. Circumferential tears may coalesce to form radial tears. The nucleus pulposus may lose its normal water-imbibing abilities as a result of biochemical changes in aggregating proteoglycans.

Proteoglycan destruction may result from an imbalance between the matrix metalloproteinase-3 (MMP-3) and tissue inhibitor of metalloproteinase-1 (TIMP-1). This imbalance results in diminished capacity for imbibing water, causing loss of nuclear hydrostatic pressure and leading to buckling of the annular lamellae. This leads to increased focal segmental mobility and shear stress to the annular wall. Delamination and fissuring within the annulus can result. Annular delamination has been shown to occur as a separate and distinct event from annular fissures. Low nuclear pressure correlates with disc pain. In 20% of cases nerves and vessels can grow into the nucleus.

MRI at this stage may reveal desiccation, disc bulging without herniation, or a high-intensity zone (HIZ) within the annulus.

Structural alteration of the facet joint following disc degeneration is acknowledged widely, but this expected pathologic alteration does not necessarily follow. Changes associated with zygapophyseal joints during the dysfunctional phase may include synovitis and hypomobility. The facet joint may serve as a pain generator.

Phase II:

Disc-related changes include multiple annular tears (eg, radial, circumferential), internal disc disruption and resorption, or loss of disc-space height. Concurrent changes in the zygapophyseal joints include cartilage degeneration, capsular laxity, and subluxation. The biomechanical result of these alterations leads to segmental instability. Clinical syndromes of segmental instability, internal disc disruption syndrome, and herniated disc seem to fit within this phase.

Phase III:

This is characterized by further disc resorption, disc-space narrowing, endplate destruction, disc fibrosis, and osteophyte formation. Discogenic pain from such discs may be of much lower incidence than pain from discs in phases I and II; however, great variation of phases can be expected within different discs in any given individual, since much variation exists between individuals of similar ages.

Investigations of low back pain

In the absence of red flag symptoms like loss of weight; history of malignancy, trauma, steroids, or IV drug abuse; deformity;  widespread neurology or fever imaging is rarely necessary unless there is no improvement after 6 weeks.

AP and lateral plain films result in total body radiation exposure of around 1 mSV (compared with 2.5 mSV total annual exposure). Oblique films dramatically ↑ this level, and will expose vulnerable tissue such as ovaries.

Conventional investigations (such as radiography and MRI) only reveal the cause of pain in <10% of cases. Degenerative changes and conditions such as spondylolysis and spondylolisthesis are not valid diagnoses of the cause of pain, as they are no more common in patients with pain than in asymptomatic individuals.

MRI: On MRI disc degeneration results in diminished signal intensity on T1 and T2-weighted images. These signal intensity changes are from diminished water and glycosaminoglycan content and ↑ collagen content of the disc.

MRI findings of a high intensity zone within the disc (representing a tear of the annulus fibrosis) ↑ the pretest odds for the patient having discogenic pain. It represents T2 signal in the posterior annulus fibrosis surrounded by areas of low signal intensity on all sides and thus clearly separated from the nucleus. Recent papers show that some HIZ’s will resolve, while others worsen. It is thought that they represent an annular fissure, and their correlation with actual pain is in doubt.

Modic changes:

An important component of the degenerative process of the lumbar disc is degeneration of the cartilaginous endplate. It cannot be identified discretely by MRI because of its thinness and the presence of chemical shift artefacts at the endplate. However, MRI demonstrates reactive changes within the bone marrow secondary to the degenerative process in the discovertebral joint. Disruption and fissuring of the endplate result in changes where adjacent marrow is replaced by vascularized fibrous tissue. Normal adult endplates as well as the outer annulus fibrosis have low signal on both T1 and T2 weighted images.

Type 1 changes are characterized by ↓ signal in T1 and ↑ signal on T2 images.

Type 2 changes may result from endplate disruption with replacement of the hematopoietic elements within the adjacent marrow by fat. The endplate changes show ↑ T1 signal and isointensity or ↑ on T2. Type 1 changes appear to convert to type 2 changes over time.

Type 3 changes demonstrate ↓ signal intensity on both T1 and T2-weighted images where bone sclerosis is extensive.

Joint blocks & medial branch blocks can be used to pinpoint pain from the SIJ or lumbar facet joints. The sensory innervation of each facet joint is derived from the medial branch of the dorsal ramus of the spinal nerve at both the level of the joint and the level immediately above. Therefore facet joints should be injected at both of these levels.

Provocation & CT discography can be used to diagnose discogenic pain and internal disc disruption. Provocation discography involves injection of contrast into a disc- the disc is deemed to be the source of pain if it is reproduced at low pressure of injection. CT discography demonstrates the internal architecture of the disc- radial fissures correlate strongly with painful discs. The Dallas discogram grade is illustrated.

Using these more detailed investigations pain can be identified in the following:

Internal disc disruption (in over 40%)
Zygapophysial joint pain (in 15%–40%)
Sacroiliac joint pain (in about 20%)