Anatomy of Nerve Root Compression, Nerve Root Tethering, and Spinal Instability

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Chapter 11 Anatomy of Nerve Root Compression, Nerve Root Tethering, and Spinal Instability

The majority of the population will experience spine-related pain at some time in their lives. The greatest component of this pain is low back pain, typically occurring in patients 35 to 55 years of age. Fortunately, the majority of acute back pain is self-limited, with over 90% of patients recovering within 6 weeks. Unfortunately, back pain has a high recurrence rate, with symptoms returning within the year in two thirds of patients. Sciatica-type pain is also common. The majority of sciatic pain is also self-limiting. Certain aspects of lifestyle, such as a lack of physical activity, obesity, and smoking, predispose patients to recurrent episodes of back pain and sciatica.1 Determining the precise causes of these types of pain presents a challenge to spine care physicians. Understanding the pathology of normal spinal degeneration will aid in the diagnosis and treatment of spine-related pain.

Causes of Back Pain

Subaxial spine pain is often caused by either muscular spasm or a failure of the joints and discs that comprise the complex anatomy of the spine. When examining the causes of isolated back pain in patients who present to a primary care physician, one study found that 4% had a compression fracture, 3% spondylolisthesis, 0.7% a tumor or metastasis of another tumor, 0.3% ankylosing spondylitis, and 0.01% an infection. Therefore, most patients who present with the complaint of low back pain will leave their primary care physician’s office without a definitive diagnosis.2,3 For most of these patients, some form of spinal degenerative change is the likely cause.

Spinal Degeneration

In spinal degeneration, also termed spondylosis, disc degeneration seems to occur first. Changes to the biologic structure of the disc lead to the mechanical failure of that disc. Normally, anulus cells synthesize mostly collagen type I in response to deformation, whereas nucleus cells respond to hydrostatic pressure by synthesizing proteoglycans and fine collagen type II fibrils. Cell density declines during growth and is extremely low in the adult, especially in the nucleus. In adult discs, blood vessels are normally restricted to the outermost layers of the anulus. Metabolite transport is by diffusion, which is important for small molecules, and by bulk fluid flow, which is important for large molecules. Low oxygen tension in the center of a disc leads to anaerobic metabolism, resulting in a high concentration of lactic acid and low pH.4 Chronic lack of oxygen causes nucleus cells to become quiescent, whereas a chronic lack of glucose can kill them. Deficiencies in metabolite transport appear to limit both the density and metabolic activity of disc cells. As a result, discs have only a limited ability to recover from any metabolic or mechanical injury.5 Disc cells synthesize their matrix and break down existing matrix by producing and activating degradative enzymes, including matrix metalloproteinases and “a disintegrin and metalloproteinase” (ADAMs). The proteoglycan content of the disc is primarily responsible for the disc’s ability to act as a compressive buffer. It is maximal in the young adult and declines later in life,6 presumably because of proteolysis. Disc cells appear to adapt the properties of their matrix to suit their environment. With increasing age, the overall proteoglycan and water content of the disc decreases, especially in the nucleus.6 There is a corresponding increase in collagen content, a tendency for fine type II collagen fibrils in the inner anulus to be replaced by type I fibers as the anulus encroaches on the nucleus, and a tendency for type I fibers throughout the disc to become coarser. Loss of proteoglycan fragments from the disc is a slow process owing to the entrapment of the nucleus by the fibrous anulus and the cartilage end plates of the vertebrae.7 Reduced matrix turnover in older discs enables collagen molecules and fibrils to become increasingly cross-linked with each other, and existing cross-links become more stable.5 In addition, reactions between collagen and glucose lead to so-called nonenzymatic glycation, causing even more cross-linking and imparting a yellow color to the aging disc. With increasing age, the hydrostatic nucleus becomes smaller and the proteoglycan content of the nucleus decreases. As such, its ability to hold water and withstand compressive loads declines. The anulus becomes stiffer and ultimately weaker.

Ultimately, aged discs fail to function properly and place additional strains on the facet joints and adjacent spinal motion segments. In the disc itself, the accumulated products of degeneration affect the metabolism of the remaining viable cells. This further hastens disc failure, resulting in changes that may be seen on MRI. These MRI changes include decreased water content, which is visible on T2-weighted images and is termed dark disc disease (Fig. 11-1). The end result of this cascade of failure is disc collapse.5


FIGURE 11-1 Sagittal MRI showing dark disc disease.

(From Lavelle WF, Carl AL, Lavelle ED, et al: Back pain. In Smith H, editor: Current therapy in pain, Philadelphia, 2009, Saunders Elsevier, pp 167–181.)

Isolated back pain may be due to a variety of forms of disc dysfunction. Pain may occur at any point of degeneration. Crock studied pain related to disc failure and coined the term internal disc derangement in 1970.8 The term was used to describe a large group of patients whose disabling back and leg pain worsened after an operation for suspected disc prolapse. Internal disc derangement was intended to describe a condition marked by alterations in the internal structure and metabolic functions of the disc thought to be attributable to injury or a series of injuries that may even have been subclinical.8 Despite Crock’s attempts to categorize disc failure, no direct and reliable relationship between measurable disc failure and pain has been developed.

As the disc fails, additional degenerative changes to the surrounding spinal structures may also occur. Disc failure is often the first of a series of failures in the spine. It has been hypothesized that disc failure causes the spinal ligaments to buckle and hypertrophy because of exposure to excessive forces, including new torsion forces.1,4 These abnormal forces may cause instability. Facet joint degenerative changes are believed to follow. When pain arises from the facet joints, patients often complain of greater discomfort with spine extension or hyperextension. Once muscles weaken, as is often seen with any form of spinal degeneration, any position can cause discomfort. As the degeneration progresses, further instability and joint hypertrophy may result. Similar to the degenerative changes seen in large appendicular joints such as the knee, significant radiographic degeneration may be seen in patients who have little or no back pain. These degenerative changes may, however, impinge on or stretch the neural elements, causing neuropathic pain.

In the most common scenario, more than one type of degenerative change is responsible for nerve compression. As the nerve roots traverse the spinal canal, they pass through regions adjacent to the facet joints termed the lateral recesses. In this region they may be encroached on by any combination of hypertrophic facet joints, infolded ligamentum flavum, and perhaps bulging disc material. All of these changes result in nerve compression within the spinal canal.

Degenerative changes can also cause nerve root impingement in the neural foramen. The anteroposterior diameter of the foramen may be reduced by bulging disc material anteriorly and hypertrophic facets posteriorly. Foraminal height is reduced merely by the loss of intervertebral disc height. Facet subluxation can further decrease foraminal volume, making the exiting nerve roots in these patients even more susceptible to the compression caused be small amounts of disc bulging or facet hypertrophy.9

The areas of the degenerating spine may fail at different rates, leading to different clinical pictures of back pain, leg pain, or instability. If the anterior disc and ligaments fail at the same rate as the posterior structures, such as the facet joints, anterior subluxation of one vertebra is a possible result. This is termed spondylolisthesis. If failure occurs asymmetrically and there is a rotational or lateral translation, the deformity is termed olisthesis. Degenerative spondylolisthesis is most common at the L4-5 level5 and occurs 6 to 10 times more often here than at any other level. It is more common in women than men and in African Americans than whites.10 The increased motion caused by disc degeneration, combined with decreased shear resistance, allows for the anterior slip. Degenerative spondylolisthesis at the L4-5 level may result in a combination of central stenosis with lateral recess stenosis that compresses the traversing L5 nerve roots. Degenerative spondylolisthesis rarely exceeds 35% translation of the vertebrae.11

The posterior elements of the vertebra may also be disrupted by a stress fracture of an area of the spine called the pars interarticularis. The pars interarticularis is the lateral part of the posterior element that connects the superior and inferior facets (the term literally means “part between the articulations”). Repetitive flexion-extension and rotation lead to microtrauma at this junction and thereby fracture. Studies show that most patients with a spondylolysis or isthmic spondylolisthesis are unlikely to be at risk for increased back pain symptoms.12

Neuropathic Pain in Spinal Degeneration

There are primarily two types of pain that result from degenerative spinal disease: radicular pain and claudicant pain. Radicular pain, or radiculitis, is pain that radiates along a dermatome of a nerve. This may be due to inflammation, pressure, or stretch of the nerve root. Claudicant pain is more difficult for patients to describe. When forced to describe this type of pain, patients may describe it as leg cramping, “aching,” or heaviness that reliably occurs with walking. Claudication is often associated with spinal stenosis. Spinal stenosis is the narrowing of the spinal canal due to any of the causes described previously, including hypertrophy of the ligaments, facets, or discs. This topic is reviewed in detail in a later chapter.

The exact pathophysiology of the mechanisms of radicular and claudicant pain remains elusive. The sequences of neuropathologic changes that result from neurologic compression in the lumbar spinal canal have been investigated in animal studies. Delamarter et al.13 used a dog model in which they created varying degrees of stenosis and demonstrated deleterious effects on the neural elements by increasing the degree of the stenosis. They found that cortical evoked potentials were highly sensitive to this compression and were affected long before any clinical signs occurred. These authors also demonstrated venous congestion and arterial constriction around compressed nerve roots and dorsal root ganglia. The result was blockage of axoplasmic flow, with resulting edema, demyelination, and wallerian degeneration of motor and sensory fibers. Other authors have shown that sensory fibers are more susceptible to pressure and slower to recover than motor fibers,14 which may explain the presence of subjective sensory changes in the absence of objective physical findings. Arnoldi et al.15 suggested that increased venous pressure may explain the symptoms of neurogenic claudication. Others have suggested that narrowing of the spinal canal may lead to a reduction in blood supply to the cauda equina, resulting in ischemic changes from the diffusion of metabolites.16 These changes may stimulate the sinuvertebral nerve or lead to secretion of pain mediators, such as substance P, from the dorsal root ganglion. Perineural inflammation of unknown origin may also result in pain generation.

Most of the literature examining the causes of neurologic pain resulting from spinal pathology attributes compression as the principal cause.1727 There are, however, instances where patients have persistent neuropathic pain, particularly radicular symptoms, in the absence of imaging studies displaying compressive pathology.

Motion of Neural Elements in the Spine: How Nerve Roots Can Be Stretched

Breig and Marions28 and Breig and Troup29 initially described movements of the nerve root sleeve in relation to a change in posture. They hypothesized that these patterns of movement might be related to changes in the length of the spinal canal during postural changes and motion.

To understand fully the impact of motion on neural elements, a basic understanding of the anatomic relationships of the nerve roots within the functional spinal unit (FSU) or motion segment is required. In the FSU, nerve roots are enclosed in a mobile osteoligamentous space and are exposed to dynamic stretch and compressive strains. This is most often observed in the situation in which nerve roots traverse a particularly long course through the central and lateral recess. Although compression is the mechanism most commonly associated with pain, inflammation as well as nerve root tethering are also possible causes.17,30 Tethering of the nerve root has been shown to be deleterious to nerves in clinical scenarios other than pathologic spinal degeneration, such as scoliosis, spina bifida occulta, and intrathecal spinal tumors.31 Stretch-induced nerve injury is also a well-known complication of lumbosacral spondylolisthesis reduction.32

As described earlier, lumbar nerve roots are enclosed in the lateral recess, a hollow, hemicylindrical recess that traverses mobile FSUs. The lateral recess is bordered laterally by the pedicle, posteriorly by the superior articular facet, and anteriorly by the dorsolateral surface of the vertebral body and the adjacent intervertebral disc (Fig. 11-2).