Key points
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Lumbar spinal stenosis is a complex disease with a plethora of clinical and imaging phenotypes.
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Developmental lumbar spinal stenosis is caused by mal-development of pedicles and posterior elements leading to narrowed bony spinal canals, and these patients are prone to developing symptoms at any spinal level and are at risk of reoperations.
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Degenerative lumbar spinal stenosis is an end result of the degenerative cascade with compression of neural tissues anteriorly by intervertebral disc displacement and posteriorly by hypertrophy of the facet joints and ligamentum flavum.
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Possible pain generators in spinal stenosis include inflammation of the posterior ramus and sinuvertebral nerves, dorsal root ganglion, impaired vascular and nutritional supply to the nerve root, venous stasis, and altered flow of spinal fluid.
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The natural history of spinal stenosis is unpredictable but nonoperative treatment is useful in some patients to halt disease progression.
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Surgical treatment of spinal stenosis involves removing the offending agents that compress the thecal sac and nerve roots and these include discectomy for disc herniation, removal of hypertrophied ligamentum flavum and osteophytes, medial facetectomy of facet joint hypertrophy, stabilization of unstable spinal segments, and correct any deformity that may cause foraminal stenosis.
Acknowledgments
Special thanks to Professor Keith Dip-Kei Luk, Dr. Wai-Yuen Cheung, and Ms Sandra Yu for their assistance in preparing the figures.
Introduction
Stenosis or narrowing of the spinal canal leads to compromise of the dural sac and the nerve roots (see Chapter 1 ). This condition known as lumbar spinal stenosis if involving the lumbar spine is usually secondary to degenerative processes including disc dehydration, collapse of disc space with prolapsed intervertebral discs. Without the normal load absorption of the intervertebral disc, loads to a spinal segment are transferred to the facet joints [ , ]. Increased facet joint stress leads to facet joint degeneration, osteophyte formation, and facet joint hypertrophy. Ligamentum flavum changes occur as a result and with the anterior compression caused by the bulging disc, a circumferential narrowing of the spinal canal occurs. The presence of radiculopathy, neurogenic claudication, or lower limb neurological deficit is key to diagnosing spinal stenosis. An extreme presentation of lumbar stenosis is cauda equina syndrome that demands early surgical intervention. Lumbar spinal stenosis can originate from developmental or degenerative causes. Degenerative stenosis is typically seen in patients in their 50 and 60s while developmental stenosis may occur in the younger population. According to the Framingham study, the prevalence of lumbar spondylosis ranges from 20% to 25% in the general population and increases with persons older than 50 [ ]. Lumbar spinal stenosis is the most common spine pathology that requires surgery in patients over the age of 65 [ ]. This trend will only rise in the coming decades as an estimated 23%–25% of the population will be older than 65 [ , ]. Many known phenotypes exist for lumbar spinal stenosis ( Table 13.1 ). The following chapter discusses lumbar spinal stenosis etiology, diagnosis, and management with specific reference to its clinical and imaging phenotypes ( Table 13.2 ).
| Phenotype | Tool used | Author/reference |
|---|---|---|
| Symptomatology: Neurogenic claudication Pain Numbness Weakness Sphincter disturbance | Clinical | Hall [ ] |
| Foraminal stenosis | Radiographs | Jenis [ ] |
| Spondylolisthesis (grading and dynamic instability) Disc space narrowing Endplate sclerosis Osteophyte formation Facet hypertrophy | Radiographs | Truumees [ ] |
| Central stenosis Lateral recess stenosis Foraminal stenosis | MRI | Daffner [ ] |
| Spinal canal diameter | Cadaveric | Verbiest [ ] |
| Intraoperative measurement | Verbiest [ ] | |
| Dural sac area | CT | Schonstrom [ ] |
| Developmental spinal stenosis: Anteroposterior spinal canal diameter Interpedicular distance | MRI | Cheung [ , ] |
| Annular tear, fissure, facet joint fluid | MRI | Schinnerer [ ] |
| Nerve root sedimentation sign | MRI | Barz [ ] Macedo [ ] |
| Classifier | Subclassifier | Phenotype |
|---|---|---|
| Diagnostic | Developmental | Pedicle length |
| Anteroposterior canal diameter | ||
| Interpedicular distance | ||
| Degenerative | Disc degeneration | |
| Decreased facet joint space | ||
| Subarticular sclerosis | ||
| Facet cyst | ||
| Facet and endplate osteophytes | ||
| Traction spur | ||
| Anatomical | Central stenosis | Central disc herniation |
| Ligamentum flavum hypertrophy | ||
| Lateral recess stenosis | Facet joint hypertrophy | |
| Ligamentum flavum hypertrophy | ||
| Posterolateral disc herniation | ||
| Foraminal stenosis | Far lateral disc herniation | |
| Spondylolisthesis | ||
| Clinical | Pain | Neurogenic claudication |
| Back pain | ||
| Neurology | Numbness | |
| Weakness | ||
| Sphincter dysfunction | ||
| Imaging | Disc | Annular tear (MRI) |
| Disc bulge (MRI) | ||
| Disc height loss (XR/MRI) | ||
| Facet joint | Osteophytes (XR/MRI) | |
| Facet joint hypertrophy (XR/MRI) | ||
| Ligamentum flavum | Buckling (MRI) | |
| Hypertrophy (MRI) | ||
| Spondylolisthesis | Severity of slip (XR) | |
| Dynamic instability (XR) | ||
| Slip angle (XR) | ||
| Disc height (XR/MRI) | ||
| Sagittal alignment (XR) | ||
| Severity | Canal area/diameter (MRI) | |
| Others | Ossification of yellow ligament (XR/CT) | |
| Nerve sedimentation sign (MRI) | ||
| Treatment | Nonoperative | Good/poor responder |
| Operative | Good/poor responder |
Pathogenesis
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 [ ].
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.
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.
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 [ ].
Manifestations and natural history
The presentation of lumbar spinal stenosis includes leg and/or back pain, motor or sensory deficit, and reflex alterations of varying degrees due to compression of segmental nerve roots [ ]. The factors that are believed to be responsible for leg pain are nerve dysfunction via direct mechanical compression or secondary to vascular embarrassment of its blood supply. Mechanical compression includes narrowing of the central spinal canal due to medial encroachment from facet hypertrophy, posterior encroachment from ligamentum flavum hypertrophy and buckling, and anterior compression from disc-level osteophytes, disc bulges, and herniations. All these are possible phenotypes visualized on imaging. Inflammatory mediators may also contribute. Mechanically, the nerve roots are fixed to surrounding skeletal and ligamentous structures. A blockage of physiologic movements by bony entrapment or disc herniation leads to diminished root function, radicular pain, and neurologic deficits. This assembly of symptoms constitutes neurogenic claudication, which is a result of cauda equina irritation or from exercise-induced ischemia and following small intraneural arterial occlusion and venous congestion [ ].
Symptoms and signs of lumbar spinal stenosis are clinical phenotypes for diagnosing disease individually but can also be used for severity phenotyping. In cases of extreme lumbar spinal stenosis, subjects may present with cauda equina syndrome. This phenomenon is caused by severe central canal stenosis due to the factors suggested earlier. This is characterized by an acute onset of increased low back pain, sciatica involving both limbs, saddle area paresthesia, lower limb motor weakness, gait dysfunction, and sphincter incontinence in extreme cases. Patients can be categorized as acute with large central disc herniations or chronic with deterioration of existing lumbar spinal stenosis. These cases are emergency conditions requiring surgical decompression to avoid irrecoverable deficits, especially that of bladder function [ ]. Most authors recommend surgical decompression within 48 h of presentation [ ].
Many patients with radiographic evidence of spinal stenosis are clinically asymptomatic. Thus, the distinction between clinical and imaging phenotypes must be classified with care. Patients may present with clinical or imaging independent of each other. Nevertheless, those with pain usually have spinal canal encroachment by an osteophyte, ligamentum flavum, or disc material. Despite these mechanical compressions, stenotic symptoms may not persist or worsen but may regress without surgery. Thus, the natural history of spinal stenosis is not easily predictable. A general trend observed is that over a period of 2–5 years after the initial presentation of symptoms secondary to spinal stenosis, approximately 20% of patients worsen with nonoperative treatment, 40% stay the same, and 40% improve [ ]. Typically, over a period of 2–3 years, patients with moderate stenosis may be treated without surgery, because acute deterioration is uncommon. Minamide et al. showed that over a period of at least 10-year follow-up, spinal stenosis improved in 30% of patients, symptoms unchanged in 50%, and deteriorated in 30% [ ]. Regardless of the decreased walking tolerance and gait disturbances, most patients still lead active lives.
Clinical phenotypes
The most common presentation of spinal stenosis is neurogenic claudication (94%), followed by pain (93%), numbness (63%), and weakness (43%) [ ]. The classical complaint is buttock pain that radiates to the lower extremities. The area of pain involvement can help distinguish the nerve root involved. Typically an L4 nerve root compression involves the anterior shin, L5 involves the posterolateral calf and foot dorsum, and S1 involves the posterior calf and sole. L4-L5 posterolateral disc protrusions compress the exiting L5 nerve root. With far lateral L4-L5 disc protrusions, the L4 exited nerve root may be compressed outside of its foramina ( Fig. 13.5 ). In patients with concomitant lumbar spondylosis, mechanical back pain is also present along with diminished tolerance to prolonged standing. In spondylolisthesis, patients usually experience central canal stenosis but present often also bilateral radicular pain.
Typical neurological complaints are consistent with neurogenic claudication, radiculopathy, or both. Patients develop burning or aching pain in the lumbar region, buttocks, or lower extremities in an upright posture. This is often associated with numbness, paresthesia, or subjective weakness. Neurogenic claudication commonly presents with insidious onset of buttock, thigh, and calf pain. The pain is often poorly localized in comparison to radicular pain at symptomatic onset but eventually develops into a classic neurogenic pattern. Extension of the spine narrows the canal size and thus worsens symptoms while lumbar flexion increases the canal size and alleviates symptoms [ , , ]. Standing, walking and climbing stairs will cause symptoms to develop and symptoms are partially relieved by flexion posture with sitting, squatting, or leaning forward. Yet, the usual disability reported by patients is diminished walking tolerance due to neurogenic claudication. Patients with spinal stenosis are known to have worse walking ability than even patients with knee or hip osteoarthritis [ ]. As symptoms progress, weakness or giving way may also be seen. Severe cases present with rest pain, neurogenic bladder, and in extreme cases, cauda equina syndrome.
When taking the medical history from a patient with back and leg symptoms, it is important to differentiate neurogenic claudication from vascular claudication. The latter may also present with diminished walking tolerance but the cause is calf cramping on exertion or a sensation of tightness that proceeds from distal to proximal. This is in contrast to neurogenic claudication where discomfort with numbness proceeds from proximal to distal. Other differentiating evidence includes lack of improvement in the symptoms with postural changes and improvement when stationary [ ]. Bicycle versus treadmill tests offer a way to differentiate these etiologies. Patients with vasculogenic pain develop symptoms with both bicycle and treadmill testing. Vasculogenic patients are more comfortable early on with the treadmill in comparison to neurogenic patients. Furthermore, neurogenic patients tend to do well on the bicycle. Uphill versus downhill walking also provides some insight into the diagnosis. Uphill walking forces patients to lean forward, which places the spine in flexion. This leads to an increase in the spinal canal space, thus relief for stenotic patients. The same concept applies to leaning forward on a grocery cart. Walking downhill leads to lumbar spine extension and is less tolerable for patients with spinal stenosis. Patients with vascular claudication often feel better walking uphill.
A thorough physical examination is important for diagnosis and gauging the severity of the disease. Patients should be observed while walking to detect any unusual limping. Documentation of strength, sensation, and reflexes should be performed. Lumbar extension on physical examination can elicit back or leg pain but the extension position should be held for at least 30s to provoke stenotic symptoms. Objective sensory examination should pinpoint the specific dermatome or the suggested nerve root compressed. Motor weakness usually suggests a more long-standing nerve compression. Vascular examination should be performed including observation for trophic changes in the skin and nails of the lower limbs ( Fig. 13.6 ) and diminished distal pulses that would suggest a vasculogenic cause for the pain. Other pain sources should be investigated such as cervical spine pathologies with an examination of the neck and the upper limb neurological status and reflexes. The hip should also be examined to rule out osteoarthritis.
Imaging phenotypes
Proper radiographic evaluation includes AP, lateral and flexion-extension views (see Chapter 5 ). Plain standing radiographs can demonstrate spondylolisthesis, disc space narrowing, endplate sclerosis, osteophytes, and facet hypertrophy [ ]. Lateral dynamic flexion and extension radiographs can determine whether spondylolisthesis is demonstrating instability ( Fig. 13.7 ). Other views include oblique radiographs and Ferguson view (view of the lumbosacral junction taken in 25 degrees caudo-cephalic AP) to look for nerve compression between the sacral ala and L5 transverse processes. Prone traction films are also useful to assess vertical instability in the discs [ ]. The ability to regain disc height with surgery can be predicted with these films. Whole spine standing radiographs are also used to assess the sagittal alignment.
