Spinal Stenosis

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Overview

Spinal stenosis is one of the most common conditions in the elderly. It is defined as a narrowing of the spinal canal. The term stenosis is derived from the Greek word for narrow, which is "stenos." The first description of this condition is attributed to Antoine Portal in 1803. Verbiest is credited with coining the term spinal stenosis and the associated narrowing of the spinal canal as its potential cause. Kirkaldy-Willis subsequently described the degenerative cascade in the lumbar spine as the cause for the altered anatomy and pathophysiology in spinal stenosis.

Narrowing in the spine can occur in the central canal, lateral recess, or foramen, leading to compression of the neural elements in those locations. The symptoms produced vary by the location of the neural compression. Neural compression in the central canal leads to the commonly seen clinical presentation of low back pain radiating into bilateral legs. Patients typically also describe heaviness and weakness in their legs that worsens with ambulation and improves with leaning forward or resting. Degeneration of the spine with aging leads to alteration in the anatomy causing gradually progressive narrowing of the spinal canal.

The term spinal stenosis refers to an anatomic diagnosis that increases with age and can occur in asymptomatic individuals. The exact reason for why some with this condition have debilitating symptoms while others have no symptoms is not well understood. These differences in presentation may be related to the different abilities of individuals to compensate for the anatomic changes that have occurred. When symptoms do present, they usually occur on the basis of the location of neural compression. Patients with central canal stenosis typically present with neurogenic claudication, whereas those with lateral recess and foraminal stenosis present with radicular pain. Patients with significant symptoms that do not respond to conservative treatment often elect surgical treatment. In fact, in adults older than 65, spinal stenosis is the most common reason to undergo lumbar spine surgery.

Anatomy

In order to understand how spinal stenosis causes symptoms, we must first have a good understanding of the normal anatomy of the lumbar spine. The spinal canal's anterior border is formed by the vertebral body, the disc, and the posterior longitudinal ligament. The lateral border is formed by the pedicles, the lateral ligamentum flavum, and the neural foramen. The posterior border is formed by the facet joints, lamina, and ligamentum flavum. The shape of the spinal canal may be circular, oval, or trefoil (Fig. 62-1 ). The circular and oval canal shapes provide the most space for the neural elements centrally and in the lateral recess. The trefoil canal has the smallest cross-sectional area. It is present in 15% of the individuals and predisposes these individuals to lateral recess stenosis.

FIGURE 62-1 The three typical shapes of the spinal canal: Trefoil canals have the smallest cross-sectional area.

Disc

Disc degeneration is believed to be the first step in degeneration of the spine. At birth, the nucleus pulposus and the annulus occupy roughly 50% of the disc area. The nucleus is gelatinous and there is a discrete boundary between the nucleus and the annulus. Over time the collagen content increases and the demarcation between the nucleus and the annulus becomes less distinct. Other structures within the disc also change with aging. The chondroitin sulfate concentration decreases, and the ratio of keratin sulfate to chondroitin sulfate increases. Because keratin sulfate has less hydrophilic potential, the disc dehydrates over time.

Hydration of the disc also changes due to an alteration in the type of collagen within the disc over time. The annulus contains 60% type II and 40% type I collagen, whereas the disc contains mainly type II collagen. Type I collagen is associated with decreased water content compared with type II collagen. Thus as the type I collagen content increases with age, hydration of the disc decreases. The normal nucleus pulposus typically consists of 85% water, whereas the annulus consists of 78% water. With degeneration of the disc, the water content drops to roughly 70%. A desiccated disc has a decreased ability to handle mechanical load.

The Kirkaldy-Willis theory explains how these changes progress over time. This theory is based on viewing the spine as a tripod with the disc and the two facet joints making up the three legs. This analogy makes it easier to understand how alteration in one joint can alter the others. The initial stage in the degenerative cascade is circumferential tearing of the annulus, which progresses to radial tears. This, along with the biochemical changes in the disc described previously, leads to further degeneration of the disc and disc height loss. Altered disc structure and disc height loss lead to bulging of the disc and the posterior longitudinal ligament. This causes narrowing of the spinal canal and potential neural impingement. The lost disc height also leads to buckling of the ligamentum flavum and settling of the facet joints. The facet joints subsequently deteriorate and form osteophytes, which further narrows the spinal canal. The altered structure, motion, and biomechanics then lead to additional disc deterioration, which propagates the cycle of degeneration.

Facet Joints

The lumbar facet joints are encapsulated structures that have a uniform cartilaginous surface to produce a smooth gliding motion. The superior articular process is concave and its articular surface faces medially and dorsally. The inferior articular process is convex and its articular surface faces laterally and ventrally. Lumbar facet joints are oriented 90 degrees in the sagittal plane and 45 degrees anterior in the coronal plane. Studies show that more sagittally oriented facet joints are associated with a degenerative spondylolisthesis. The two facet joints are usually symmetric with respect to their joint angles at each level. Facet tropism refers to an asymmetry between the facet joints and has been theorized to lead to degeneration.

As the disc degenerates and narrows, the facet joints settle and increased stress is placed across the facet joint. This leads to facet joint degeneration, hypertrophy, and osteophyte formation. These osteophytes can cause impingement of the thecal sac within the spinal canal or the nerve root in the neural foramen.

Intervertebral Foramen

The anterior boundary of the intervertebral foramen is made up of the posterior wall of the vertebral body and the disc. The posterior boundary is made up of the lateral aspect of the facet joint and the ligamentum flavum. Superior and inferior boundaries are formed by the pedicles of the vertebral bodies corresponding to that segment. The foramen is typically larger than the ganglion and the nerve that it contains. The additional space is occupied by fat and loose areolar tissue that can accommodate for motion. With degeneration, hypertrophy of the facets can cause posterior compression of the neural elements (Fig. 62-2) . Anterior compression of the neural elements usually arises from endplate osteophytes or foraminal disc herniations. Decrease in disc height with degeneration can cause a decrease in the foraminal height and neural compression. This type of vertical or up-down foraminal stenosis is important to recognize because a posterior decompression alone may not significantly improve the vertical compression and may result in persistent symptoms after surgery.

FIGURE 62-2 Sagittal cross section demonstrating disc desiccation (D), endplate sclerosis (S), osteophyte formation (0), hypertro.

Cauda Equina

The thecal sac lies in the spinal canal and gives rise to nerve roots at each segment. The nerve root initially courses along the medial aspect of the pedicle and then progresses laterally, inferior to the pedicle in the neural foramen. The nerve roots within the cauda equina are arranged in a predictable pattern within the thecal sac (Fig. 62-3). Cross section of the thecal sac demonstrates the most caudal roots to be present in a central and posterior position. The more cephalad roots are located sequentially more lateral and anterior. At each level, the motor fibers of a root are anterior and medial to the larger sensory component. Dorsal root ganglia exist at every level and can be intraspinal or intraforaminal. A variety of clinical presentations arise on the basis of the anatomic location of neural compression.

Classification

Stenosis can be anatomically classified as central, lateral recess, and foraminal on the basis of the location of neural compression. With aging, central canal stenosis occurs as degenerative changes progress. As the axial height of the disc and facet joints decreases, the disc bulges into the spinal canal. The central canal is further narrowed by posterior impingement from enlarged facets and the hypertrophied ligamentum flavum (Fig. 62-4 ) . Hypertrophy of the soft tissues is responsible for 40% of spinal stenosis. With extension, the hypertrophied ligamentum buckles centrally into the canal and worsens the central stenosis. This explains why patients with stenosis typically report worsening of their symptoms in extension.

FIGURE 62-4 Axial view cross section at the L4-5 disc level showing advanced degenerative changes. Cauda equina (CE) compress...

Lateral recess stenosis typically results from posterior disc protrusion in combination with some superior articular facet hypertrophy. Lateral recess stenosis can present with lumbar radiculopathy, and incidence of lateral recess stenosis ranges from 8% to 11%. These patients present with pain or neurologic symptoms in a dermatomal distribution on the basis of the nerve that is compressed in the lateral recess.

Foraminal stenosis causes compression of the exiting nerve root and ganglion and also leads to lumbar radiculopathy. Foraminal stenosis occurs most commonly in the lower lumbar spine with the fifth lumbar nerve root being the most commonly involved. Foraminal stenosis can occur from loss of disc height, vertebral endplate osteophytes, facet osteophytes, spondylolisthesis, and disc herniations. Like central canal stenosis, foraminal stenosis is worse in extension and thus exacerbating and alleviating factors for symptoms from foraminal compression are similar to those from central canal stenosis.

Spinal stenosis can also be classified on the basis of the etiology, which can be congenital, acquired, or both. Congenital stenosis is present as a normal variant in the population and is part of certain conditions such as dwarfism. In these conditions, patients have short pedicles that are closer together than the normal lumbar spine. In congenital stenosis, few degenerative changes are sufficient to cause neural compression and symptoms. As one would expect, congenital stenosis becomes symptomatic much earlier in life and patients usually become symptomatic in the fourth decade. Acquired stenosis can be caused by trauma, neoplasms, and infection, along with other causes listed in Box 62-1.

BOX 62-1 Classification of spinal stenosis

  1. Congenital/developmental
    1. Idiopathic
    2. Achondroplastic
    3. Osteopetrosis
  2. Acquired
    1. Degenerative
      1. Central
      2. Lateral recess
      3. Foraminal
    2. latrogenic
      1. Postlaminectomy
      2. Adjacent to fusion
      3. Malposition of hardware in the canal
      4. Post-procedure epidural hematoma
    3. Miscellaneous disorders
      1. Acromegaly
      2. Paget's
      3. Fluorosis
      4. Ankylosingspondylitis
    4. Traumatic
  3. Combined

Any combination of congenital/developmental or acquired stenosis

Deformity and Instability

The static changes that we discussed thus far can be worsened by dynamic factors such as segmental instability. Instability typically arises from degenerative changes and can be in the form of translational or rotational abnormality. Translational abnormality is found most commonly in women as a degenerative anterolisthesis of L4 on L5. The attachment of the iliolumbar ligaments to the L5 level may act as a restraining force and cause more relative motion at L4-5. The more sagittally oriented facet joints between the fourth and fifth lumbar vertebrae can be an additional predisposing factor for instability at this level. Because the lamina and the spinous process typically project inferior to the vertebral body, the amount of room available between the inferior aspect of the L4 lamina and the posterior superior aspect of L5 is substantially decreased. This anterior translation of the L4 posterior elements, along with hypertrophy of the facets and the ligamentum flavum, leads to central and lateral recess stenosis. Foraminal stenosis can also occur in this setting with collapse of the disc space, disc herniation, endplate osteophytes, or facet hypertrophy. With scoliosis, lateral subluxation and rotational instability can cause altered biomechanics that leads to degeneration. The altered anatomy can also be a cause of narrowing of the central canal, lateral recess, and foraminal regions. Degenerative changes superimposed on abnormal anatomy lead to stenosis in these patients.

Pathophysiology

The term spinal stenosis describes the anatomic narrowing of the spinal canal. How does spinal stenosis result in pain and altered neurologic function? A number of cadaver and animal studies have attempted to elucidate the mechanism of these symptoms. Schonstorm evaluated the changes in nerve pressure that occur as the spinal canal narrows. In his human cadaver study, the thecal sac constriction of 45% or more led to an increased pressure in the nerve roots. As the degree of compression increased, the pressure in the nerve roots increased. Delamarter and colleagues also demonstrated the importance of the magnitude of thecal sac compression in alteration of neural function. They noted no alteration in neurologic function when the animal's cauda equina was constricted by 25%, whereas more than 50% compression led to motor or sensory deficits. Pedowitz and colleagues demonstrated that the duration of compression was also an important factor in neural dysfunction.

Rydevik and colleagues demonstrated another effect of compression of the thecal sac. They noted that once pressure of more than 50 mm Hg was achieved, capillary restriction and electrophysiologic alteration occurred in the nerve roots. Even at pressures as low as 5 to 10 mm Hg, venous congestion of the intraneural microcirculation occurred. Solute transport decreased 45% across nerve root segments with the low pressure of 10 mm Hg. This suggests that low-grade sustained compression of the nerve roots could lead to vascular impairment and potential detrimental changes in the function of the nerve roots. In addition to neural compression and altered nutrition, inflammatory chemical mediators have also been shown to be a cause of pain.

The presence of stenosis increases with aging; however, it often does not produce any symptoms. What causes pain in some individual with mild spinal stenosis and no symptoms in others with severe stenosis? The experimental evidence reviewed earlier suggests that each individual may have an innate ability to compensate for the accumulating pathologic changes. Because the magnitude an individual can compensate for is different for different people, two individuals with the same amount of stenosis may not exhibit the same symptoms. The rate at which these changes are occurring also appears to be important. Individuals may become symptomatic with a lower magnitude of compression if it occurs rapidly. This explains how a patient with stenosis can become symptomatic with an acute mild disc herniation.