Degenerative cascade

Knowledge of the degenerative cascade in the lumbar spine is important for proper phenotyping of spinal stenosis (see Chapter 6 ). Encroachment of the neural elements in the lumbar spine can be contributed by disc herniation, facet joint, and ligamentum hypertrophy as well as osteophyte formation (see Chapter 7, Chapter 8 , 12, and 14). As such, many of these pathological processes involved in the degenerative cascade may overlap. Hence, stenosis severity can be gauged by the number of contributing phenotypes.

The intervertebral disc supports the spinal segments anteriorly while the facet joints form the posterior column support. In the healthy spine, the discs, vertebral bodies, facets, and ligaments all work in synchrony to maintain normal motion and spine biomechanics (see Chapter 2 ). Any alteration in one can contribute to abnormal stress and force in the others, resulting in degeneration, abnormal bone formation, altered spinal column stability, and risk of injury to neural tissues. This is a process that occurs with aging. The intervertebral disc, a structure important for load transmission, loses its ability to absorb loads [ ]. The disc desiccates as a result, leading to cleft formation in the dehydrated nucleus pulposus (NP) that gradually reaches the peripheral annulus fibrosus and the endplate. Further loads lead to annular tears and subsequently disc bulging and extrusions that may compromise the spinal canal [ , ].

As the disc height decreases, the two ends of the vertebral bodies come into contact with the narrowing of the neuroforamen. This causes a redistribution of the stress and loads to the facet joints that may bear up to 25% of the axial loads [ , ]. Increased stress leads to capsular synovitis, cartilage thinning, and eburnation. As a result of these altered biomechanics, facet degeneration, increased segmental motions, and osteophytes become apparent ( Fig. 13.1 ). Osteophytes, a manifestation of facet hypertrophy, proliferate secondary to the microinstability to stabilize the degenerated spinal segment. These facet joints collapse in sequence with interspace narrowing following enhanced disc degeneration [ ]. Collapse leads to overriding of the articular surfaces and predisposes the spinal column to potential subluxation or spondylolisthesis. These manifestations can compress the neural elements in the foramen, the lateral recess, or the central zone. The exiting nerve root normally occupies 30% of the neuroforamen. As the disc loses height, there is reduced space available for the nerve root to exit the neuroforamen that may lead to radiculopathy [ ].

Axial T2-weighted MRI showing facet joint degeneration with joint fluid ( red arrow ).

In addition to osteophyte formation, ligamentum flavum buckling and hypertrophy can also contribute to lumbar spinal stenosis. With decreasing intervertebral height, the ligamentum flavum buckles and thickens ( Fig. 13.2 ) leading to narrowing of the central canal. Microscopically, hypertrophy entails the proliferation of type II collagen, ossification and proliferation of chondrocytes, hyalinization of collagen fibers, and calcium crystal deposition. With canal encroachment caused by bulging discs, overriding osteophytes, and hypertrophy of the ligamentum flavum, circumferential reduction in the canal’s cross-sectional area is observed. Normally, extension and axial loading further decreases the size of the neuroforamen and the spinal canal by 15%–20% and 9%–12%, respectively [ ]. This volume decrease can be up to 67% in both the foramen and canal in a severely stenotic spine.

Sagittal T2-weighted MRI showing buckling of the ligamentum flavum at L2-L3 and L4-L5 ( white arrows ).

Pathology in the canal

In addition to pathology, phenotyping can be classified anatomically by the location of canal narrowing in spinal stenosis. Increased spinal contents or relative vertebral movements within the lumbar spine lead to compression of the thecal sac and the traversing or exiting nerve roots [ , ]. These phenomena most commonly occur at the L3-L4 and L4-L5 disc levels, followed by L2-L3 and L5-S1 [ ]. The location of the stenosis within the spinal canal is important for full comprehension of the patient’s symptomatology. Spinal stenosis is commonly classified into central, lateral recess, or foraminal stenosis, which can be used as anatomical phenotypes [ ]. Central stenosis ( Fig. 13.3 ) is narrowing of the central zone of the spinal canal and the usual culprit includes disc herniation anteriorly or hypertrophy of the inferior articular facet and ligamentum flavum posteriorly. Lateral recess stenosis is narrowing of the subarticular recess causing nerve root compression as it exits the dural sac at the inferior-medial border of the pedicle. Causes include superior articular facet or flavum hypertrophy. Thus, removal of the lateral insertion of the ligamentum flavum as it merges with the articular facet capsule is important to achieve good decompression of the nerve root. Posterolateral disc protrusions ( Fig. 13.4 ) are also common contributors to lateral recess stenosis. Foraminal spinal stenosis is a compression in the neuroforamen that is anteriorly bounded by the disc and endplate, posteriorly by the pars interarticularis, and superiorly and inferiorly by the pedicles. The effects of disc degeneration lead to foraminal compression via posterolateral disc protrusions and collapse of the neuroforamen by the pedicles with vertebral collapse. Single or combination of these compression events can exist.

Axial T2-weighted MRI showing significant central and lateral recess stenosis ( white arrow ).

Axial T2-weighted MRI showing lateral recess stenosis caused by left posterolateral disc herniation ( white arrow ).

Besides the position of the stenosis, measurements of canal narrowing can also be a useful phenotype for grading the severity of stenosis. As Verbiest suggests, the midsagittal diameter of a lumbar spinal canal should be greater than 13 mm [ ]. Relative stenosis is defined as an anteroposterior (AP) canal diameter between 10 and 13 mm, and absolute stenosis is present when the AP canal diameter is less than 10 mm [ ]. The normal thecal sac usually measures 16–18 mm, and the area of the normal sac should be more than 100 mm [ ]. When the sac is compressed to an area measuring between 76 and 100 mm ² , the compression is described as moderate stenosis. An area less than 76 mm [ ] suggests severe spinal stenosis. Based on cadaveric studies, Schonstrom et al. demonstrated that a minimal cross-sectional area of 77 ± 13 mm [ ] at L3 is necessary to accommodate the neural elements in the dural sac [ ]. Delamarter et al. proposed that constriction of 50% or more of the spinal canal’s cross-sectional area may contribute to motor and sensory deficits [ ]. The dural sac diameter or cross-sectional area has thus been shown to be predictive for the type of spinal stenosis that fails conservative treatment and requires surgery [ ].

Developmental spinal stenosis

Lumbar spinal stenosis can also be related to congenital malformations such as mal-development of the dorsal elements of the spine that manifests as short pedicles and laminae [ , , ]. This relationship is independent of patient size [ ]. This condition known as developmental spinal stenosis in which preexisting narrowed bony spinal canals makes the neural elements prone to compression and hence stenosis symptoms [ ]. It is a likely autosomal dominant in inheritance with a defect in the Wnt signaling pathway [ , ]. Phenotyping developmental spinal stenosis will be based purely on imaging as the clinical presentation is similar to the degenerative type. Patients may experience claudication and radicular symptoms at multiple levels similar with patients suffering from achondroplasia. This group of patients is also more susceptible to restenosis after surgical treatment due to multiple level narrowing. The pedicle is a unique structure as it has variable increasing widths progressing from cranially to caudally. This may be the reason why the majority of stenotic manifestations occur at the lower lumbar region. The L4-L5 segment is also especially prone to stenosis in comparison to the L5-S1 segment because motion is limited due to the stabilization effects exerted upon the L5 vertebra by the iliolumbar ligament [ ]. The imaging phenotype of developmental spinal stenosis has been defined by studies comparing asymptomatic and symptomatic subjects requiring surgery [ , ]. Findings suggest that developmental stenosis plays an important role in lumbar spinal stenosis. Critical stenosis has been defined as <14 mm at L4, <14 mm at L5, and <12 mm at S1 [ ]. It often has a multilevel involvement and can be characterized as cut-off anteroposterior vertebral canal diameters of 19 mm at L1, 19 mm at L2, 18 mm at L3, 18 mm at L4, 18 mm at L5, and 16 mm at S1 with 81%–96% sensitivity and 72%–91% specificity [ ]. A simple radiological assessment may prove useful when screening. A ratio between the vertebral body width to pedicle width >3 on a lateral plain radiograph is suggestive of developmental spinal stenosis [ ].

Developmental spinal stenosis has some important clinical implications. Individuals are more likely to have radicular leg pain in a population-based cohort [ ]. It is also related to surgical outcomes. Developmental spinal stenosis is a major risk factor for reoperation at the adjacent level following lumbar decompression surgery. After exclusion of instability and deformity causes and controlled for the degree of disc degeneration and ligamentum flavum thickness, developmental narrowing of the bony spinal canal has an odds ratio of 3.93 for reoperation at the adjacent segment after decompression-only surgery [ ]. The amount of dura expansion is also relevant. In narrower spinal canals, the dura sac size is also smaller [ ]. This has bearing on the degree of cerebrospinal fluid to rootlet ratio expected in compression and after decompression surgery. This ratio may be disproportionate to the severity of spinal stenosis and should be taken into consideration when risk profiling for complications after surgery.

Pain generators

The pain generators in lumbar spinal stenosis have been extensively investigated. Inflammation of the posterior ramus and the sinuvertebral nerves have been implicated as possible pain generators [ ]. Other reports have suggested that the dorsal root ganglion is an important factor but its position is not constant and may be present in the canal, foramen, or beyond the foramen [ , ]. The size of the dorsal root ganglion also varies from level to level with the largest being at L5 and S1 where it is typically 5–6 mm wide and 11–13 mm long. Compression of the neural elements impairs the vascular and nutritional supply to the nerve root and contributes to edema, fibrosis, inflammation, ischemia, and altered metabolic processes. These resultant mechanisms have been associated with pain and neurological dysfunction seen in lumbar spinal stenosis. Venous stasis has also been targeted as a pain generator [ ]. However, its role may not be significant. Stasis, in theory, cannot be severe as the lumbar spine houses a large anastomotic plexus and postural changes can relieve pain rapidly. This rapid alleviation of pain is uncharacteristic of venous stasis. Altered spinal fluid flow has also been proposed as a mechanism to provoke pain and neurologic dysfunction. Rydevik et al. [ , ] found that the spinal fluid is responsible for up to 58% of the spinal nerve nutrition and impedance of spinal fluid can obstruct nutrition to the neural elements [ ].