The fibrocartilaginous intervertebral disk acts primarily as a shock absorber in the lumbar spine, serving to transmit compressive loads between the adjacent vertebral bodies. With aging, the human intervertebral disk undergoes dramatic degenerative changes, more so than any other tissue in the body. Normally, the intervertebral disk is composed of three primary structures, including the cartilaginous end plates (at the cranial and caudal margins of the disk), the central nucleus pulposus, and the peripherally located annulus fibrosus (Fig. 20.1).

The cartilaginous end plates are located at the cranial and caudal margins of the disk, and serve as the growth plate for the vertebral bodies. In childhood, the end plates are quite thick and occupy most of the disk. With growth and aging, the hyaline cartilage end plates thin until they are only 1-mm thick in adults. The nucleus pulposus serves as the core of the disk. It is sandwiched between the superior and inferior end plates and consists of a proteoglycan and water matrix, held together by type II collagen and elastin fibers. The glycosaminoglycans attract water molecules due to osmotic pressure, allowing the disk to cushion against compressive loads. The nucleus pulposus is surrounded by the annulus fibrosus, which forms multiple lamellar rings of concentrically organized collagen type I fibers. Each layer includes fibers that run nearly perpendicularly to fibers in the adjacent lamellae and intersect the end plate at an approximately 30-degree angle. Its highly specific histology and anatomy, allow the annulus to contain the nucleus and maintain its pressurization under compressive loads. The annulus allows elastic deformation of the nucleus and causes it to recover its original shape and position when the compressive load is reduced. The collagen fibers resist tensile loading in all directions.

The immature disk has blood vessels that penetrate the end plates allowing for nutrition of the disks and cellular elements within it. As the disk matures, capillaries no longer penetrate the end plates and cellular nutrition becomes dependent on diffusion. The number of cells within the disk decreases such that the nucleus is essentially acellular. As such damage to the adult disk is not readily repaired.

The incidence of intervertebral disk degeneration increases with age. It most commonly occurs in the lumbar spine and multiple risk factors have been proposed in its etiology:

The intervertebral disk is the anterior border of the spinal canal at the level of the facet joint. It is covered by the thin posterior longitudinal ligament, which is thickened centrally, leaving the posterolateral areas of the disk less covered. This anatomy allows for disk herniations to most commonly occur in the posterolateral region of the disk, adjacent to the traversing nerve root. Nerve roots branch from the cauda equina one level above their exiting foramen. For instance, the L5 nerve root leaves the cauda equina approximately at the level of the L4 vertebral body, then descends to pass caudal to the L5 pedicle, where it turns laterally to exit the spinal canal. The location of the disk herniation determines which root is primarily affected. The central zone is delineated by the lateral borders of the cauda equina and overlying dura. Central disk herniations in this zone compress the thecal sac and often do not cause radicular symptoms. However, large central herniations can cause cauda equina syndrome. The lateral recess is between the lateral border of the cauda equina and the medial border of the pedicle. Posterolateral and paracentral herniations in this zone tend to compress the traversing nerve root. Within the lateral recess, fragments that migrate medial and caudal to the traversing root are termed axillary herniations. The foraminal zone is between the medial and lateral borders of the pedicle. Herniations beyond the lateral border of the pedicle are within the far lateral or extraforaminal zone. Herniations in the foraminal or extraforaminal zones affect the exiting nerve. Herniated fragments can displace cranially or caudally and affect nerve roots differently compared to the classic cases described above when the herniation is at the level of the disk space.

As previously described, the intervertebral disk consists of a thick outer layer, termed the annulus. The normal biomechanical relationship between the annulus, the nucleus pulposus, and the cartilaginous end plate, allows for appropriate transmission of compressive loads. This three-component system works to resist both compressive and tensile loads. Compression across the disk space results in increased pressure within the nucleus, which causes the nucleus to deform and flatten. This results in an outward-directed force applied to the annulus, creating tensile hoop stresses within the annular collagen fibers and allowing for dissipation of the compressive load and containment of the nucleus.

The annulus is normally able to withstand the compressive loads transferred to it from the nucleus pulposus. When the annulus becomes disrupted, either due to trauma or degeneration, compressive loads can cause herniation of disk material through the disrupted annulus. In order for this to occur, the nuclear material must be appropriately hydrated to be of a consistency to allow for herniation. Thus, disk herniations are more likely to occur in younger patients with well-hydrated disks. Older patients, with more dessicated disks, are less likely to sustain disk herniations through this mechanism. Approximately 2/3 of herniations include end plate material in addition to nucleus, with the remainder being comprised of nucleus alone.

Disk herniation results in altered disk mechanics. Frie et al. have demonstrated that nucleotomy alters the loading pattern across the disk space, resulting in the annulus sustaining higher compression forces than normal. These increased pressures are transmitted to the vertebral end plates at the insertion of the annulus, resulting in chondrosseous metaplastic changes including sclerosis and osteophytosis.

Despite our understanding of the pathophysiology of disk herniation, the exact inciting event that causes the herniation itself is still unknown. Some theories propose that an acute traumatic event imparted to an already degenerated disk with focal annular weakness results in displacement of disk material and subsequent herniation. In support of this idea, acute sciatica from disk herniation often is preceded by a prodrome of low back pain. Many biomechanical studies, including one conducted by Wilder et al. which studied the influence of postural variations on intradiscal pressures, have demonstrated that a combination of lateral bending, flexion, and axial rotation with vibration exposure results in tears extending from the nucleus through the annulus. In this same study, the highest disk pressures have been recorded in patients carrying a weight in hand while forward flexed.

The relationship between disk herniation and radiculopathy is not completely understood. In animals and humans, pure compression of a noninflamed nerve produces sensory and motor changes without pain, whereas pain can be elicited with manipulation of inflamed nerves. These findings suggest that herniated disks large enough to cause mechanical compression of a nerve root may produce neurologic deficits, but radicular pain is produced only if the nerve root is inflamed. The cause of this inflammation has been attributed to both ischemia caused by compression of the perineural vessels and the presence of inflammatory mediators that can accompany a herniation. The latter cause may explain the presence of severe radicular pain in patients with small disk protrusions in the absence of significant neural compression.

Specific inflammatory mediators such as IgG, IgM, and tumor necrosis factor-α (TNF-α) have been
implicated as having a role in producing sciatic pain. Spiliopoulou et al. examined IgG and IgM levels in disks excised from patients with sciatica and controls and found elevated IgM levels in disks from sciatica patients, but not in controls, suggesting that an inflammatory reaction may play a role in sciatica. Additionally, studies conducted in porcine models with herniated disks in which TNF-α was selectively inhibited revealed decreased evidence of nerve root injury in treated animals when compared with controls. This and multiple other studies have implicated the role of additional cytokines including matrix metalloproteinases (MMPs), nitric oxide, prostaglandin E₂ (PGE₂), and interleukin-6 (IL-6) in sciatica associated with disk herniations.

Disk herniations have been classified based on their morphology, location, and duration of symptoms. The advent and regular use of advanced imaging modalities like magnetic resonance imaging (MRI) have led to the development of a morphologic classification for disk herniations. The morphologic classification system was first classified by Spengler et al., who divided disk herniations into three morphologic types:

These morphologic types have been illustrated in Figure 20.2.

Additionally, other authors have further morphologically categorized herniations into two major categories:

A topographical classification system, categorizing herniations based on anatomic location, has also been described:

These morphologic locations are shown in Figure 20.3.

Finally, herniations can also be classified based on timing from initial symptom onset, which includes two, somewhat arbitrarily defined categories:

Based on a survey of the literature, it appears that the results of disk excision are compromised if delayed more than 2 to 16 months from symptom onset.

Patients often describe a prodrome of mild to moderate low back pain prior to the development of radiculopathy. Some patients will also describe a specific event (i.e., a fall, twist, heavy lifting) that triggered their symptoms. Pain is typically the most common complaint and can be present as axial back pain, radicular pain, or most frequently, a combination of both. The radicular pain is typically predominant and responds more predictably to treatment than axial back pain. Lower lumbar or
lumbosacral disk herniations typically present with pain radiating below the knee in a dermatomal distribution. S1 radicular pain classically radiates to the posterior leg or the lateral aspect or sole of the foot. L5 radicular pain can lead to symptoms affecting the lateral leg and dorsum of the foot. The L4 dermatome includes the anterior knee and medial leg. L2 and L3 radiculopathy can produce anterior or medial thigh (Fig. 20.4). Groin pain is typically a result of hip pathology, though it can also be present with L1 and L2 radiculopathy. While these pain distributions represent classic dermatomal patterns, radicular pain may present more diffusely across the buttock, thigh, and leg. The character of the pain can be described as sharp, dull, burning, or dysesthetic. Activities that increase intradiscal pressure including sitting, bending, twisting, lifting, forward flexion, and Valsalva maneuver can exacerbate radicular pain, whereas standing or lying prone can provide some relief. Radiculopathy patients frequently describe the pain as constant, and it tends to be less related to position than spinal stenosis patients with classic claudication.

In addition to pain, radiculopathy can include sensory and motor deficits related to the affected nerve. Sensory deficits are common and frequently occur in the dermatomal distributions described above for each nerve root. Classic motor deficits can be attributed to each lumbar nerve root, though there is substantial overlap across roots as most muscles are innervated by multiple roots. L2 radiculopathy classically causes hip flexor weakness, L3 quadriceps weakness, L4 ankle dorsiflexion weakness (foot drop), L5 extensor hallucis longus weakness, and S1 gastrocnemius weakness. L5 radiculopathy can also cause hip abductor weakness and a Trendelenburg gait. This has been summarized in Table 20.1.

As always, the physical examination first begins with inspection. Gait can be assessed as the patient initially walks into the examination room. Gait observation may on occasion reveal a sciatic list where the patient leans away from the side of leg pain, and is typically seen in paracentral and posterolateral herniations. The list is thought to be a mechanism to relieve tension by drawing the nerve root away from the herniated fragments. High-steppage and foot-slapping gaits are indicative of
a foot drop and classically present with L4 radiculopathy. Trendelenburg gait due to hip abductor weakness can be observed in L5 radiculopathy or patients with hip pathology. During inspection of the spine, alignment in the coronal and sagittal planes should be assessed. A sciatic scoliosis or loss of the normal lumbar lordosis can be present due to underlying muscle spasm.

The next step in the examination should involve systematic palpation of the back. The spinous processes are palpated individually, in a step-wise fashion. Tenderness to palpation of one or two levels is more consistent with bone or disk pathology than tenderness at multiple levels. Additionally, the lumbosacral junction, the sacral prominences, sacroiliac joints, and the greater sciatic notches should be palpated. Inflammation in these regions can often mimic symptoms of sciatic back pain and can be confused with symptoms of a disk herniation. However, identifying the pain generator based on palpation and patient description of the location of low back pain is difficult due to significant overlap among disk, facet, and sacroiliac joint pathology.

A thorough neurologic examination is required in all patients with a suspected disk herniation. Sensory function can be assessed by light-touch and pinprick (sharp/dull discrimination) modalities. Although standard dermatomal charts are helpful, there is often significant variability in sensory distributions across individuals. The most discrete levels of testing are for the L4, L5, and S1 nerve roots. The best locations to test each of these nerve roots are included below:

Unlike motor strength, quantifying sensation is somewhat difficult. As a result, it is often best to characterize sensation as either normal, diminished, or absent. Often, comparing sensory status with the contralateral side can be helpful in detecting differences.

Similarly, the motor examination should also proceed in a systematic fashion. Each nerve root level can be assessed by a specific muscle group.