4 Anatomic Origin of Spinal Pain and Clinical Presentations

4.1 Introduction

4.2 Pain from Spine Muscles and Ligaments

4.2.1 Muscles and Back Pain

The spine is covered by multiple layers of muscles ( Fig. 4.1). In the lumbar area, there are thoracolumbar fascia, erector spine, spinalis muscles, longissimus muscles, iliocostalis muscles, and quadratus lumborum.

• Twisting, improperly lifting of objects, or overstretching of the back muscles can cause muscle strains or tears in the back. Patient may experience severe pain in the lower back. Physical examination can reveal tenderness and spasm of the back muscles.

• Conditions such as myofascial pain syndrome and fibromyalgia may also cause pain, tenderness, and spasm in the spine muscles.

• Patients with other pathology in spine, such as disk herniation, radiculopathy, annular tear, facet joint syndrome, vertebral fracture, tumor, or failed back surgery syndrome (FBSS), could present with pain, tenderness, and spasm of back muscles.

• Clinicians should try to look for possible underlying pathology while treating patients with pain in the back muscles.

4.2.2 Ligaments and Back Pain

• Damage of anterior longitudinal ligament in whiplash injury may lead to instability and pain.1 Kinetic functional magnetic resonance imaging (MRI) study may help to define such ligament damage, abnormal movement, and spine instability.

• Ossification of the ligamentum flavum is mainly seen in the Japanese population, but rare cases have been reported in Caucasian and black populations. Patients may have back pain, decreased range of motion in the involved spine segment, or even paralysis.

• Loosening of anterior and posterior longitudinal ligament, ligamentum flavum, and supraspinous ligament can all contribute to the formation of spondylolisthesis.

• Hypertrophy of posterior longitudinal ligament and ligamentum flavum can cause spinal stenosis.

• Clinically, it is very seldom that ligament abnormality alone presents as a pure source of pain. More studies are needed to further define the role of the spine ligaments in pathogenesis of back pain.

4.3 Pain from Intervertebral Disks

4.3.1 Anatomy of the Intervertebral Disk

A lumbar intervertebral disk is composed of the annulus fibrosus and nucleus pulposus ( Fig. 4.2). Annulus fibrosus, composed of a three-dimensional network of collagen fibers, surrounds the internal gelatinous nucleus pulposus. This arrangement provides very strong bands between adjacent vertebrae while allowing some degree of movement of the vertebrae. A normal nucleus pulposus made of proteoglycans and collagens serves as a shock absorber for axial forces and as a semifluid ball during flexion, extension, rotation, and lateral flexion of the vertebral column. As the intervertebral disk ages, the number of viable cells in the inner regions of the disk decreases. Collagen cross-links formed by enzymatically mediated glycosylation diminish with age. Loss of large aggrecan and proteoglycans molecules reduces the amount of hydration in the disk, changing its shape and volume. This likely affects the ability to absorb and distribute loads effectively and makes the tissues more susceptible to mechanical failure. Common types of intervertebral disk disease include acute disk herniation, annular tears, and chronic degenerative changes such as disk dehydration, loss of height, and diffuse disk bulging.

4.3.2 Acute Disk Herniation and Lumbar Radiculopathy

Acute lumbar disk herniation ( Fig. 4.3) is usually a result of heavy lifting, injury, or an accident. A herniated disk may exert mechanic pressure on the nerve root(s), causing ischemia of the nerve root(s) or chemical irritation to the nerve root. Chemical substance such as phospholipase A2 leaking from the herniated disk can initiate a process of nerve root inflammation by increasing the concentration of inflammatory mediators such as prostaglandin E2 (PGE2), tumor necrosis factor (TNF)-alpha, cytokines, for example, interleukin-(IL)-1 and IL-15, and nitric oxide around the nerve root.²

Fig. 4.1 Muscles of the back. (a) Superficial layer muscles: trapezius, rhomboids, levator scapulae, and latissimus dorsi muscles; cadaver dissection of superficial layer muscles. (b) Deep-layer muscles: erector spinae and transversospinalis muscles; cadaver dissection of deep-layer muscles.

Fig. 4.2 Intervertebral disk. (a) The nucleus pulposus is central; annulus fibers are concentric and peripheral. (b) The disk lies between adjacent vertebral bodies. Each layer of annulus fibers is oriented in the same fashion, but the orientation of the fibers in adjacent layers differs by 30 degrees.

4.3.3 Annular Tear and Diskogenic Pain

The lumbar intervertebral disk is composed of the nucleus pulposus and annulus fibrosus ( Fig. 4.2). Extreme external pressure or shear force can cause rupture of the annulus fibrosus or annular tear to the disk, regardless of whether the disk has existing degenerative changes or not. There are different kinds of annular tears, including radial tear and circumferential tears. Pathogenesis of diskogenic low back pain may be different from the lumbar radicular pain caused by lumbar disk herniation. There is no direct nerve root compression or ischemia in the nerve roots in patients with back pain due to annular tear ( Fig. 4.4).

The mechanism of diskogenic pain due to annular tear is still unclear. However, increased expression of nerve endings sensitive to pain in the ruptured disk, epidural inflammation due to leakage of substance such as phospholipase A2, and increased concentration of the inflammatory mediators such as IL-1beta, IL-6, IL-8, PGE2, nitric oxide, monocyte chemoattractant protein-1 (MCP-1), basic fibroblast growth factor, and transforming growth factor-beta all have been involved in the pathogenesis of diskogenic pain.³

Fig. 4.3 Disk herniation. Superior view at the level of the L4–L5 intervertebral disk. A noncontained herniated nucleus pulposus is seen compressing the exiting L4 nerve root as well as the traversing L5 nerve.

Fig. 4.4 Annular tear pain mechanism generation. Superior view at the level of the L4–L5 intervertebral disk. A posterolateral annular tear generates pain signal through the sinuvertebral nerve and gray ramus communicans. The pain signal is transmitted to the dorsal root ganglion.

Fig. 4.5 High-intensity zone in the posterior part of the L5–S1 disk on a T2-weighted MR image.

• MRI may find a high-intensity zone in the posterior part of the disk ( Fig. 4.5) with approximately 50% of sensitivity and specificity.

• Definitive diagnosis of diskogenic pain with annular tear has to be made with a diskography ( Fig. 4.6), confirming a positive annular tear with concordant pain when the contrast is injected.

4.3.4 Chronic Degenerative Changes of the Lumbar Disks

Degenerative changes of lumbar disks such as loss of disk height, disk dehydration, and diffuse disk bulging are commonly seen in senior population. Almost 100% of normal population who are 70 years old or older have some degree of degenerative changes. Fig. 4.7 shows a typical lumbar spine MRI with diffuse degenerative changes including dehydration, bulging, and loss of heights of the lumbar intervertebral disks in a senior citizen. However, less than 30% of senior population have lower back pain, meaning that there is a 70% or more chance that these degenerative changes are not directly causing pain. In patients with low back pain, disk dehydration, loss of disk heights, and diffuse annular bulging, there are often other changes in the spine as well that may cause pain. It is still unclear whether these degenerative anatomic changes alone cause pain. When a patient with such a diffuse degenerative change starts to have pain, sometimes it is very difficult to anatomically localize the source of pain.

Fig. 4.6 Lumbar diskogram shows an X-ray picture of lumber diskography. There is a leakage of contrast at both L4–L5 and L5–S1 disks, indicating an annular tear.

4.4 Pain from Lumbar Facet Joints

Facet joints or zygapophyseal joints are a set of synovial joints between the articular processes of two adjacent vertebrae ( Fig. 4.8). The biomechanical function of each pair of facet joints is to guide and limit the movement of the spinal motion segment. In the lumbar spine, the function of facet joint is to protect the motion segment from anterior shear forces, excessive rotation, and flexion. Degenerative changes, osteoarthritis, dislocation, fracture, injury, and instability from trauma and surgery can disrupt the function of lumbar facet joints and cause chronic low back pain or pain due to lumbar facet joint syndrome. It has been reported that lumbar facet joint syndrome accounts for more than 30% of cases of chronic low back pain.

Fig. 4.7 Lumbar degenerative changes. T2-weighted MRI of the lumbar spine of a 74-year-old patient. It shows diffuse degenerative changes in the lumbar and thoracic spine. There are multiple chronic compression fractures at T12 and L1 vertebrae with retropulsion (T12). All the lumbar intervertebral disks are dark and dehydrated. There are multilevel disk bulging and osteophytes at T12–L1, L1–L2, L2–L3, L3–L4, and L4–L5. There is moderate to severe spinal stenosis at L2–L3, L3–L4, and L4–L5, and mild spinal stenosis at T12–L1 and L1–L2.

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