Radiculopathy and Degenerative Spine Disease

Describe the difference between the dorsal and ventral rami of the spinal cord.

Nerve roots are attached to each segment of the spinal cord. Those that exit from the posterior lateral sulcus are called the dorsal roots, whereas the ventral roots emerge anterior over a wider area. Short mixed spinal nerves are formed when a pair of dorsal roots and ventral roots unites beyond the dorsal root ganglion. This mixed spinal root then divides into the thin dorsal root ramus and the thicker ventral root ramus. The dorsal root rami are the central processes of the unipolar cells located in the dorsal root ganglion. These fibers innervate the paraspinal muscles and overlying skin and also carry sensory information. The ventral root rami are essentially extensions of the anterior horn motor neurons, and innervate the muscles of the cervical, brachial, or lumbosacral plexus. In addition to motor fibers, the ventral ramus also contains axons originating from sensory and sympathetic ganglia ( Fig. 7-1 ).

How many spinal nerve pairs exit the spinal cord?

There are 31 pairs of spinal nerves (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal). Because there are only seven cervical vertebrae, the first seven cervical nerves exit above the same numbered cervical vertebrae. The eighth cervical nerve exits above the T1 vertebrae, and the rest of the spinal nerves (T2 to L5) exit below their same numbered vertebrae. Think of it as “the heavenly seven cervical nerves arise above the vertebral body” ( Fig. 7-2 ).

Where do the lumbar nerve roots exit, and which root is most likely to be injured in a disc herniation?

The lumbar nerve roots exit beneath the corresponding vertebral pedicle through the respective foramen. For example, the L5 nerve root exits beneath the L5 vertebral pedicle through the L5/S1 foramen. Since most disc herniations occur posterolaterally, the root that is compressed is actually the root that exits the foramen below the herniated disc. So, a disc protrusion at L4/L5 will compress the L5 root, and a protrusion at L5/S1 will compress the S1 root. Ninety-five percent of disc herniations occur at the L4/5 or L5/S1 disc spaces. Herniations at higher levels are uncommon.

Which anatomic structures are potential pain generators?

Back pain may originate from many spinal structures. These structures include the following: (1) the vertebral body periosteum, (2) intervertebral discs, (3) paravertebral musculature and fascia, (4) ligaments, (5) facet joints, (6) the annulus fibrosus, (7) spinal nerve roots, (8) dorsal root ganglia, and (9) paravertebral blood vessels. The most common causes for pain result from musculoligamentous injuries and age-related degenerative processes of the intervertebral discs and facet joints. Disc herniations and spinal stenosis are other common causes.

What is the distinction between spondylosis, spondylolisthesis, and spondylolysis?

Spondylosis is a nonspecific degenerative process of the spine, often due to osteoarthritis with osteophyte formation. Spondylolisthesis refers to anterior subluxation of one vertebral body on another. Spondylolysis is a defect in the pars interarticularis that allows the vertebra to slip upward. All three of these conditions may cause pain when symptomatic and can be confirmed radiographically.

What is the difference between a disc bulge, protrusion, and herniation?

A bulging disc occurs when dehydration leads to gradual flattening of the disc and an increase in the circumference of the intact annular ring, which then extends beyond the margins of the vertebral body. Disc protrusion occurs when the gelatinous disc material protrudes focally into tears or fissures within the intact annular shell, causing a focal outpouching of the still intact annular fibers. Disc herniation refers to extrusion of nuclear material through the disrupted annular shell.

What are the most common causes of spinal stenosis?

A variety of conditions can cause spinal stenosis. It may result from minor developmental anatomic changes in the diameter of the spinal canal (e.g., shorter than normal pedicles, thickened lamina). These conditions are rarely symptomatic but may predispose to degenerative changes that do become symptomatic. Such changes include degeneration of facets posteriorly and the disc anteriorly. Osteophyte formation may occur, thus narrowing both the nerve root and central canals. Degeneration of the intravertebral disc may also cause narrowing of the nerve root and central canals. Other causes of spinal stenosis include degenerative spondylolisthesis and postoperative spinal stenosis.

What are the differences between radicular and referred pain?

The key feature of radicular pain is hot, electric sensations that radiate in the territory of the affected nerve root. The pain will be sharp, shooting, and burning. The pain radiates down the limb but never up. Sensory loss is rarely complete due to overlapping of other roots.

Referred pain is a phenomenon that occurs when irritated or injured tissues (e.g., muscle, facet joint, or periosteum) cause pain that is perceived in a dermatomal distribution. This pain may be shooting but is typically not hot or electrical as in radicular pain.

Which spinal disorders cause both axial pain (back or neck) and disturbances in neurologic function of the limb (leg or arm)?

Three syndromes are recognized in which spinal disorders cause both back or neck pain and neurologic dysfunction. The following examples are from the lumbar spine:

• Herniated disc causing a single nerve root compression (leg pain > back pain). Clinical features include positive straight leg-raising test and radicular pain in the limb disproportionate to pain in the spine. Loss of strength, reflex, and sensation occurs in the territory of the compressed root.

• Lateral recess syndrome (leg pain ≥ back pain). Single or multiple nerve roots on one or both sides become compressed. Pain in the limb is usually equal to or greater than that in the spine. Symptoms are brought on by either walking or standing and are relieved with sitting. Testing by straight leg raise may be negative.

• Spinal stenosis (leg pain < back pain). Multiple nerve roots are involved, and the pain in the spine is significantly greater than that in the limb. Symptoms develop with standing or walking. Impairment in bowel and bladder dysfunction as well as sexual dysfunction may occur.

What are the clinical features of lumbar disc disease?

Acute lumbosacral disc herniation may cause a continuum of pain ranging from an isolated dull ache to severe radicular pain due to neurocompression in the foramen or lateral recess. A rare complication is cauda equina syndrome due to a massive central herniation. Pain is often sudden in onset and exacerbated with the Valsalva maneuver. Concomitant paraspinal spasm is often present. Ninety-five percent of disc herniations occur at the L4/5 or L5/S1 disc spaces. Herniations at higher levels are uncommon.

What are the signs of an L4 radiculopathy?

Compression of the L4 root produces pain and paresthesias radiating to the hip, anterior thigh, and medial aspects of the knee and calf. Sensation is impaired over the medial calf. Weakness occurs in the quadriceps and hip adductors. The knee jerk is diminished.

What are signs of an L5 radiculopathy?

L5 root compression produces pain radiating to the posterolateral buttock, lateral posterior thigh, and lateral leg. Sensory loss is most likely in a triangular wedge involving the great toe, second toe, and adjacent skin on the dorsum of the foot. Weakness occurs in the muscles innervated by the L5 root (gluteus medius, tibialis anterior and posterior, peronei, and extensor hallucis longus). This results in difficulty in ankle dorsiflexion, eversion, inversion, and hip abduction. It is most easily identified by weakness in the extensor hallucis longus (extension of the big toe). The ankle reflex is usually normal.

What are the signs of an S1 radiculopathy?

S1 root compression causes pain to radiate to the posterior buttock, posterior calf, and lateral foot (classic sciatica). Sensory loss occurs along the lateral aspect of the foot, especially in the third, fourth, and fifth toes. Weakness may occur in the gluteus maximus (hip flexor) and plantar flexors. The ankle jerk is usually diminished ( Fig. 7-3 ).

What are the clinical features of lumbar stenosis?

Most patients are age 50 years and older and have had symptoms referable to lumbar spinal stenosis for more than 1 year. Neurogenic intermittent claudication or pseudoclaudication is the most common presenting and constant symptom in lumbar spinal stenosis. Symptoms are usually bilateral, with one leg more involved than the other, but they may be unilateral. The whole lower extremity is generally affected. Pain is provoked by walking and, in many patients, merely by standing. It is typically dull in character and is quickly relieved by sitting or leaning forward. In some patients, the pain is accompanied by numbness of the affected leg and the feeling that it “may give out” on them.

What is the mechanism for neurogenic claudication in lumbar spinal stenosis?

Symptoms are related to the increase in lordotic posture provoked by standing or walking. Myelographic studies have shown that in lordosis, the cross-sectional area of the spinal canal narrows because of anterior encroachment by bulging discs, posterior encroachment by shortening and thickening of the ligamentum flavum, and lateral approximation of the articular facets. In flexion (as in sitting), all of these encroachments reverse, with a resultant increase in the cross-sectional area of the spinal canal. This may explain why some patients with neurogenic claudication may be able to ride a stationary bike (in the sitting position), while patients with vascular claudication may still have pain.

What is the differential diagnosis of low back pain?

The most common alternate diagnoses include focal hip pathology, vertebral compression fractures, metastasis from malignancy, ankylosing spondylitis, and vertebral osteomyelitis. Rare causes of low back pain include abdominal aortic aneurysm, pelvic disorders, abdominal visceral pathology, and other neuropathic disorders (e.g., inflammatory polyneuropathies or mononeuropathies).