Introduction
Low back pain is a common cause of disability among the general population with a well-documented cost burden placed on the U.S. healthcare system. There are multiple sources of chronic low back pain, often divided into whether the pain is facet-mediated, secondary to fracture, or discogenic in nature. This article will focus on the pathophysiology, evaluation, and treatment of lumbosacral discogenic syndrome and pain arising from pathology involving the intervertebral disc.
Intervertebral discs are pads of fibrocartilage that sit between the spinal vertebrae, occupying roughly one-third of the height of the spinal column.[1] Their major role lies in the transmission of mechanical loading from body weight and muscle activity, allowing bending, flexion, and torsion of the bony spine.
Each disc consists of two main components: a central, gel-like substance called the nucleus pulposus, and an outer, firmer annulus fibrosis. The consistency of the nucleus is a result of its water and proteoglycan content and is held together by a network of type II collagen and elastin fibers. The high anionic glycosaminoglycan content of this network gives the nucleus pulposus its osmotic properties, which allow it to resist compression. The annulus fibrosis is composed of bundles of type I collagen arranged in multiple oblique layers called lamellae. Characteristics of a normal, healthy disc demonstrate high water content in the nucleus and inner annulus. The most outer annulus provides tensile strength. Specifically, in the lumbar region, a healthy disc is typically 7-10 mm thick and 4 cm in AP diameter with approximately 20 layers of lamellae.[1]
The interverbal discs are supplied by the sinuvertebral nerve (SVN), which innervates the posterior annulus and posterior longitudinal ligament. In healthy subjects, the neural penetration of the annulus is about 3 mm, which corresponds to the outer three lamellae. It is a mixed nerve, containing a somatic root from the ventral ramus, as well as an autonomic root from the grey ramus. Once the nerve takes a recurrent course through the intervertebral foramen and enters the spinal canal, it divides into superficial and deep networks. The superficial network branches to multiple vertebral levels and contains mostly sympathetic fibers, while the deep network contains primarily somatic fibers and innervates the corresponding segment.[2]
The intervertebral discs are relatively avascular with the nucleus and inner annulus being supplied by capillaries that arise in the vertebral bodies and terminate at the bone-disc junction. Nutrients and small molecules such as glucose and oxygen reach the disc cells by diffusion.[3] Additionally, only the outermost portion of the annulus is vascularized. As a result, intervertebral discs are very limited in their ability to heal from injury, and, as a result, the healing process is overtaken by degenerative changes. This is not just due to avascularity, however, but also due to decreased cell population, which diminishes the structure’s ability to break down and turn over large collagen bundles.
Axial back pain may be of discogenic origin; however, not all damaged or degenerated discs cause pain. Disc abnormalities are commonly seen on MRI in asymptomatic individuals. Considered in the setting of other possible etiologies of axial low back pain with similar clinical presentation, this presents a challenge to the treatment provider.