What is the pathophysiology of low back pain (LBP) and sciatica?

Updated: Aug 22, 2018
  • Author: Jasvinder Chawla, MD, MBA; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
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The lumbar spine forms the caudal flexible portion of an axial structure that supports the head, upper extremities, and internal organs over a bipedal stance. The sacrum forms the foundation of the spine through which it articulates with the sacroiliac joints to the pelvis. The lumbar spine can support heavy loads in relationship to its cross-sectional area. It resists anterior gravitational movement by maintaining lordosis in a neutral posture.

Unlike the thoracic spine, the lumbar spine is unsupported laterally and has considerable mobility in both the sagittal and coronal planes. The bony vertebrae act as specialized structures to transmit loads through the spine. Parallel lamellae of highly vascularized cancellous bone form trabeculae, which are oriented along lines of biomechanical stress and encapsulated in a cortical shell. Vertebral bodies progressively enlarge going down because gravitational loads increase from the cephalic to the caudal segments. Bony projections from the lumbar vertebrae, including the transverse processes and spinous processes, maintain ligamentous and muscular connections to the segments above and below them.

The intervertebral disk is composed of the outer annulus fibrosis and the inner nucleus pulposus. The outer portion of the annulus inserts into the vertebral body and accommodates nociceptors and proprioceptive nerve endings. The inner portion of the annulus encapsulates the nucleus, providing the disk with extra strength during compression. The nucleus pulposus of a healthy intervertebral disk constitutes two thirds of the surface area of the disk and supports more than 70% of the compressive load.

The nucleus is composed of proteoglycan megamolecules that can imbibe water to a capacity approximately 250% of their weight. Until the third decade of life, the gel of the inner nucleus pulposus is composed of approximately 90% water; however, the water content gradually diminishes over the next 4 decades to approximately 65%. Nutrition to the inner annulus fibrosis and nucleus pulposus depends on the diffusion of water and small molecular substances across the vertebral endplates because only the outer third of the annulus receives blood supply from the epidural space.

Repeated eccentric and torsional loading and recurrent microtrauma result in circumferential and radial tears in the annular fibers. Some annular tears may cause endplate separation, which results in additional loss of nuclear nutrition and hydration. The coalescence of circumferential tears into radial tears may allow nuclear material to migrate out of the annular containment into the epidural space and cause nerve root compression or irritation.

Throughout the first 2 decades, 80-90% of the weight of the lumbar spine's trijoint complex is transmitted across the posterior third of the disk; however, as disk height decreases and the biomechanical axis of loading shifts posteriorly, the posterior articulations (ie, facet joints) bear a greater proportion of the weight distribution. Bone growth (in the form of new osteophytes) compensates for this increased biomechanical stress to stabilize the trijoint complex.

Over time, hypertrophy of the facets and bony overgrowth of the vertebral endplates contribute to progressive foraminal and central canal narrowing. In addition to relative thickening of the ligament flavum and disk herniation, these changes contribute to a reduction of the anteroposterior canal diameter and foraminal patency with neural compression. Spinal stenosis reaches a peak later in life and may produce radicular, myelopathic, or vascular syndromes such as pseudoclaudication and spinal cord ischemia.

LBP is most common in the early stages of disk degeneration, in what Kirkaldy-Willis called the stabilization phase. Impaired healing of the intervertebral disk due to its poor peripheral blood supply has been proposed as a possible explanation for the divergent behavior of this structure, which can produce chronic nociception. Also, the discovery of the biochemical factors that are responsible for causing increased sensitization of the disk and other pain-sensitive structures within the trijoint construct will eventually explain the mechanism of this discrepancy.

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