Stenosis development

LSS can be monosegmental or multisegmental, and unilateral or bilateral. Anatomically, the stenosis can be classified as central, lateral or foraminal. Depending on the extent of the degeneration, central, lateral and foraminal stenosis can occur alone or in combination. The L4–5 spinal discs are most frequently affected by LSS, followed by L3–4, L5–S1, and L1–2.

Multiple factors can contribute to the development of spinal stenosis, and these can act synergistically to exacerbate the condition. Degeneration of the vertebral disc often causes a protrusion, which leads to ventral narrowing of the spinal canal (central stenosis; Figure 1a). As a consequence of disc degeneration, the height of the intervertebral space is further reduced, which causes the recess and the intervertebral foramina to narrow (foraminal stenosis), exerting strain on the facet joints (Figure 1). Such an increase in load can lead to facet joint arthrosis, hypertrophy of the joint capsules and the development of expanding joint cysts (lateral stenosis), which in combination propagate spinal instability.¹¹ The reduced height of the segment leads the ligamenta flava to form creases, which exert pressure on the spinal dura from the dorsal side (central stenosis). Concomitant instability due to loosened tendons (for example, the ligamenta flava) further propagates pre-existing hypertrophic changes in the soft tissue and osteophytes, creating the characteristic trefoil-shaped narrowing of the central canal.^{8, 9, 11, 12, 13, 14, 15, 16}

Figure 1 | Pathoanatomical illustration of LSS.

Osteolisthesis and disc prolapse are distinct entities from LSS, although these conditions will frequently exacerbate the pre-existing lumbar stenosis. a | Coronal, b | dorsal and c | lateral views of LSS. In a | distinct stenosis areas are depicted in red. Ventral compression can be caused by medially bulging or protrusion of intervertebral discs. Lateral stenosis can be caused by lateral prolapse, stenosis of the neuroforamen or hypertrophy of the facet joints. b | Dorsal view of lateral stenosis (red dots) caused by hypertrophic facet joints and narrowing of the neuroforamen. c | Corresponding lateral perspective of narrowed neuroforamen causing a lateral stenosis. Abbreviation: LSS, lumbar spinal stenosis.

• High resolution image and legend (114 KB)
• Figures and tables index
• Download Power Point slide (164 KB)

LSS can also be subdivided into relative and absolute LSS—a classification that has not yet been clinically validated—according to the anterior–posterior diameter of the spinal canal (Figure 1a). Relative LSS (spinal canal 10–12 mm in diameter; physiological value is 22–25 mm) is usually asymptomatic, whereas absolute LSS (spinal canal <10 mm in diameter) is often symptomatic and is associated with absence of free subarachnoid space (as observed on lateral plain X-ray films). The lateral recess can be considered stenotic if it has a diameter of <2 mm (physiological diameter is 3–5 mm).

From stenosis to claudication

Each of the various degenerative processes that participate in the development of LSS can independently cause clinical symptoms that frequently make diagnosis and the choice of therapy difficult. The most common symptom associated with LSS is neurogenic claudication, which comprises limping or cramping lumbar pain that radiates into the legs primarily during walking. Degenerative LSS can ultimately lead to the compression of individual nerve roots, the meninges, the intraspinal vessels, and, in exceptional cases, the cauda equina (Figure 2).¹⁷ Nerve root compression triggers localized inflammation, which affects the nerve root's excitatory state.¹⁸ In addition, at least two interdependent vascular mechanisms are hypothesized to contribute to the development of neurogenic claudication in LSS: reduced arterial blood flow resulting in ischemia, and venous congestion with compression of the nerves and secondary perfusion deficiency.^{19, 20} Conversely, compressive radiculopathy can cause autonomic dysregulation and impaired circulation in the legs.²¹ The extent of compression is increased by hyperextension or hyperlordosis of the lumbar spine, because these postures cause additional narrowing of the spinal canal. By contrast, hyperflexion abrogates lordosis, resulting in a widening of the spinal canal. A functional LSS can be diagnosed only if a clinically relevant LSS develops in certain spinal postures (for example, when standing as opposed to sitting). Such stenoses are frequently exacerbated further by vertical load.²² Indeed, epidural pressure is elevated while standing or walking, and lowered when sitting and in flexion.^{23, 24}

Figure 2 | Processes involved in neurogenic claudication development in lumbar spinal stenosis.

 

• High resolution image and legend (29 KB)
• Figures and tables index
• Download Power Point slide (79 KB)

Experimental animal models have been developed to investigate the underlying pathophysiology of LSS in more detail²⁵ and to test pharmacological interventional strategies,²⁶ but the validity of these models for the multifaceted, etiologically diverse human condition remains limited. In one such experimental model for spinal canal stenosis, a piece of silicon is placed under the lamina at lumbar level 4 in young adult rats. This model might only deliver incomplete information, since acute narrowing of the spinal canal per se does not fully recapitulate the features of chronic degenerative LSS in humans, and the young adult animals used in those experiments lack comorbidities. In addition, the spine biomechanics of quadripedal rats differ substantially from those of bipedal patients.

Differential diagnoses

In contrast to the situation in LSS, hyposensibility resulting from peripheral neuropathies usually exhibits a bilateral distal stocking-shaped pattern, irrespective of posture, rest or physical stress. Iliosacral joint disorder occasionally mimics LSS, with low back pain radiating to the buttocks and the thighs when standing and walking. Unlike LSS, however, iliosacral joint pain is characterized by tenderness of the joint. The development of cauda equina syndrome, which comprises sacral hypesthesia, loss of tendon reflexes in the lower limbs and incontinence, as a result of LSS is only found in exceptional cases. Sphincter involvement is very rare in LSS, as the sacral nerves are relatively protected from compression owing to their central position within the cauda equina.³¹ In patients exhibiting vesicorectal voiding and upper motor neuron signs (for example, Babinski's reflex and hyperreflexia), cervical or thoracic myelopathy needs to be ruled out.

Neuroradiological assessment

When performing radiological assessment of LSS, some inherent problems with imaging of the lumbar spinal canal need to be considered. First, imaging of symptomatic patients is confounded by the fact that degenerative changes in the lumbar spine are highly prevalent in the asymptomatic population: among patients over 60 years of age, 20% will reveal signs of LSS.³² Second, imaging tends to exaggerate pronounced degenerative changes and effects on the spinal canal.³³ Thus, radiologically diagnosed LSS usually identifies involvement of more segments than is suspected clinically. In the majority of cases, a presumptive diagnosis of LSS can be made on the basis of the clinical appearance of the condition and the patient's medical history. Imaging tends, therefore, to be selectively employed when any type of interventional or surgical therapy is contemplated. Notably, imaging tends to be used most frequently in patients with medium to severe symptoms of LSS.³⁴

In presurgical patients with symptoms of LSS, the purpose of imaging is to confirm the presence or absence of LSS, to exclude differential diagnoses, to relate congesting symptoms to osseous and discoligamentous structures, and to identify the exact location of LSS for accurate presurgical planning.³⁵ As described previously, LSS mostly results—at least initially—from degenerative disc disease. Morphological alterations, such as loss of disc height, disc signal, bulging discs, disc herniations, reactive end-plate and bone marrow changes, and spondylophytes, can be visualized to differing degrees by the various imaging techniques applied. Increased stress on the facet joints leads to hypertrophic facet degeneration, as well as inwardly buckled and hypertrophied ligamenta flava. These changes can lead to central, lateral or foraminal stenoses (Figure 1).

MRI

MRI is the preferred imaging modality for the radiological assessment of LSS.³⁶ This technique provides superior soft-tissue contrast compared with other imaging modalities, has multiplanar imaging capabilities and does not produce ionizing radiation. In patients with pacemakers, certain other types of metal implants or claustrophobia, however, MRI is contraindicated or impossible to perform.

MRI of patients with LSS usually comprises orthogonal T1-weighted and T2-weighted images (sagittal and axial). A fat-suppressed T2-weighted sequence can be added, as such images seem to allow more accurate detection of associated degenerative bone marrow changes. With T2-weighted images and the inherent signal intensity of cerebrospinal fluid, 'myelography-like' images that illustrate the thecal sac, the intrathecal and intraforaminal nerve roots, and the spinal cord can be obtained noninvasively. LSS can be monosegmental (Figure 3) or occur on multiple levels (Figures 4 and 5). Like CT imaging, MRI can define the contribution of osseous and discoligamentous structures to LSS.

Figure 3 | Spinal alterations in a patient with monosegmental LSS at L4–5.

Sagittal and axial images were obtained using T2-weighted turbo spin-echo MRI. a | A sagittal image reveals reductions in the disc signal and the disc space height, which are attributable to dehydration. Disc bulging and slight ventral listhesis of L4 (arrow) can also be observed. b | Narrowing of the neuroforamen (arrow), which affects the right L4 radix, is caused by c | consecutive hypertrophic facet joint degeneration with intra-articular effusions (arrowheads) and hypertrophy of the ligamentum flavum (arrow), as observed on an axial image.

• High resolution image and legend (57 KB)
• Figures and tables index
• Download Power Point slide (106 KB)

Figure 4 | Spinal alterations in a patient with multisegmental LSS.

Sagittal and axial images were obtained using T2-weighted turbo spin-echo MRI. a | A sagittal image reveals multisegmental LSS with signs of spondylosteochondrosis, such as disc height and signal reduction, disc herniation, irregularity of end plates and bone marrow degeneration (arrows), and spondylarthrosis (hypertrophy and sclerosis of the facet joints; arrowheads). The axial images depict b | a moderate (arrow) and c | a severe (arrow) central LSS with different degrees of disc pathology, hypertrophy of ligamenta flava and facet joints. Abbreviation: LSS, lumbar spinal stenosis.

• High resolution image and legend (30 KB)
• Figures and tables index
• Download Power Point slide (80 KB)

Figure 5 | Multisegmental disc degeneration revealed by CT myelography.

a | A sagittal reformatted CT myelograph reveals a multisegmental severe disc degeneration, with disc space height reduction, vacuum phenomenon and end-plate sclerosis of the lower lumbar spine, as well as thecal sac compressions at the L3–4 and L4–5 levels (arrows). b–d | Axial reformatted images show a circumscribed severe LSS of L3–4, with a typical hourglass constriction of the thecal sac (arrow) adjacent to relatively normal areas. Abbreviation: LSS, lumbar spinal stenosis.

• High resolution image and legend (47 KB)
• Figures and tables index
• Download Power Point slide (96 KB)

Despite detailed depiction of the spinal anatomy, studies have produced conflicting results concerning the clinical usefulness of the information gained by MRI.^{37, 38} Results from a study conducted by Modic and colleagues, in patients with radiculopathy, low back pain and sciatica, implied that changes observed by means of MRI add little or no clinically useful information to clinical assessment alone in relation to prognosis and predicting the outcome of surgery.^{37, 39}

Gadolinium-based contrast media are not routinely required for imaging of LSS unless previous surgery was performed and fibroid scar tissue might have to be identified by its contrast enhancement.^{40, 41} Some studies, however, indicate a possible superior role for contrast-enhanced MRI in LSS patients with neurogenic claudication, as enhancement of compressed nerve roots can be visualized in a subset of these patients.^{42, 43, 44} This enhancement is thought to reflect either obstructed periradicular veins, indicating venous stasis, or breakdown of the blood–nerve barrier, a sign of chronic compressive radiculitis (Figure 2).

Through the use of heavily T2-weighted fat-suppressed sequences, magnetic resonance (MR) myelography can be performed noninvasively and without contrast administration. Despite the capacity of this technique to accurately depict the thecal sac, however, studies have yielded contradictory results regarding the usefulness of this sequence.^{45, 46} The use of MR myelography is, therefore, only advocated as an additional sequence to conventional MRI. Currently, open MRI is the only technique that enables a functional investigation of spinal flexion and extension during the application of axial loading, or even in the supine position.⁴⁷

CT scanning

CT can be performed rapidly and allows precise evaluation of the spinal canal and differentiation between spinal canal compression caused by discs, ligaments and bony structures. In the latter respect, this approach is superior to MRI. At present, CT is usually performed using a spiral multislice technique, acquiring isotropic data that enables multiplanar reformatting in any desired plane and three-dimensional reconstructions. Even in pronounced torsion scoliosis, therefore, multisegmental imaging in one plane can be achieved, which is not possible with MRI. A limitation of CT is that intrathecal nerve roots and the spinal cord cannot be visualized, because these structures have similar densities to the cerebrospinal fluid. This problem might be circumvented by using CT myelography (Figure 5). CT myelography entails spiral CT imaging acquired after inthecal administration of iodine, which is commonly performed under fluoroscopic guidance. In some cases of extensive degenerative or postsurgical changes, lumbar puncture can also be performed under CT guidance. Such CT-guided puncture of the thecal sac is a robust technique, even in patients who cannot be assessed by other means. CT and CT myelography might be indicated in patients where MRI is contraindicated, the MRI results are inconclusive or where clinical symptoms correlate poorly with MRI findings.⁴⁷ Furthermore, CT techniques might be used for presurgical planning in cases where bony anatomy needs to be accurately depicted.

Conventional X-rays and myelography

The usefulness of routinely acquired plain radiographs in the initial evaluation of patients with LSS has been questioned.^{48, 49} Indeed, the acquisition of such radiographs is no longer part of the Agency for Health Care Policy and Research guidelines.³⁴ Many patients, however, undergo conventional radiography as part of their initial evaluation, as this procedure is inexpensive and uncomplicated to perform. Conventional radiographs might be of use, albeit in a limited fashion, in assessing the contribution of bony degeneration to LSS and the alignment of the vertebral bodies in lateral and coronal planes. This technique can also potentially be used to rule out traumatic changes or other unanticipated findings (for example, Paget disease, spondylodiscitis or scoliosis) as possible differential diagnoses.⁵⁰ After surgery, plain radiographs are useful in determining the integrity and the correct position of fusion material, and to visualize signs of loosening of implanted fixating plates and/or screws. The sensitivity and specificity of plain radiographs concerning the contribution of bony changes to central spinal stenosis were reported to amount to 66% and 98% respectively of those of CT. The acquisition of additional lateral radiographs in flexion and extension positions (so-called functional radiographs) to rule out segmental instability is not routinely required, as signs of segmental instability can be detected on conventional lateral radiographs in a sufficiently accurate manner.⁵¹ Furthermore, no additional benefits were gained from these additional views in a recently conducted study.⁵⁰ Even in patients for whom segmental instability was expected, the diagnostic value of lateral radiographs in flexion and extension could not be definitively determined.⁵²

Conventional functional myelography has long been the method of choice for diagnosing LSS and is still an important method for investigating the influence of hyperextension and hyperflexion on the extent of the stenosis. This technique might still be the only routine method that is suitable for detecting the morphological correlates of a functional, posture-dependent, symptomatic LSS (Figure 6).³⁵ Furthermore, it is the only accurate imaging technique for patients with spinal metallic implants, which can cause artifacts on MRI and CT. Moreover, conventional functional myelography allows the lumber spine to be examined in a standing position, and, hence, under the normal stress of the body weight. Conventional myelography is an invasive procedure that requires intrathecal administration of iodinated contrast agent, and is consequently associated with adverse effects such as postpunctional headaches, and rare life-threatening complications such as anaphylactic reactions and spinal infections. Like other imaging techniques, conventional myelography frequently reveals abnormalities that were not suspected clinically.³³ One of the few reliable prognostic signs is the block of contrast flow, which is a good predictor of the successful outcome of decompression surgery.⁵³ Conventional myelography is limited by its inability to determine the cause of block or compression and to visualize extrathecal nerve root compression. This technique is usually combined, therefore, with a CT scan performed after myelography (postmyelographic CT), which compensates for these limitations (Figure 5). Myelography combined with postmyelographic CT might be indicated for preoperative surgical planning, so as to assess the thecal sac and the bony status of the surgical area.

Figure 6 | Conventional myelography in a patient with a posterior lumbal intervertebral fusion and positional back pain.

A reactive hypermobility adjacent to the fused segment is viewed in a | a reclined position and b | an inclined position. A moderate ventral slipping is evident in the inclined position. No substantial positional effect on the sagittal diameter of the thecal sac can be observed.

• High resolution image and legend (15 KB)
• Figures and tables index
• Download Power Point slide (64 KB)

In summary, recent studies have shown that the diagnostic and predictive values of conventional myelography, CT myelography and MRI are not markedly different.⁵⁴ One important point to consider when assessing imaging methods is that the radiological degree of LSS, both before and after surgery, does not necessarily correlate with the degree of the clinical signs and symptoms.^{32, 54, 55, 56, 57, 58}

Additional diagnostics

Selective diagnostic injections can be useful in some patients to estimate the contribution of different pain components to the patient's overall health, especially against the background of pain psychology in chronic pain. If vascular genesis of the symptoms is suspected, noninvasive diagnostic techniques include determination of the ratio of the systolic blood pressure of the ankles to that of the arms (ankle–brachial index), which can be considered to be pathological when the value is <0.5. In addition, routine duplex Doppler angiography, contrast-enhanced MR angiography and—in rare cases before intervention—digital subtraction angiography can also be employed to determine the involvement of vascular genesis in causing pain. Given the low practical importance of classical electromyograghy and nerve conduction studies in diagnosing LSS, an electrophysiological examination is only recommended to exclude other disorders, especially if the distribution of pain and numbness is unusual (for example, suspicion of peripheral polyneuropathy or myopathy, which might both occur concomitantly with LSS).^{55, 56} Walking on a treadmill is an appropriate provocation test for such examinations, although this technique is not yet common in daily practice.^{55, 56} Routine laboratory tests can be used to detect comorbidities, such as diabetes or diabetic polyneuropathy (by detection of glucose and HbA1c), and infections such as spondylodiscitis (by measurement of C-reactive protein).

Natural disease course

LSS is a degenerative condition that develops slowly over time, and for much of the clinical course of the disease the neurological deficits are only subtle. For these reasons, LSS is usually diagnosed in patients over the age of 50 years. There are, however, no prospective long-term studies that document the natural symptomatic changes over time.^{31, 58} This makes the initiation and choice of a specific therapy difficult, as such decisions ideally require an estimate of the natural course of the condition.⁶ Limited information is available from the subgroups of untreated patients in some intervention trials. The Spine Patient Outcomes Research Trial (SPORT) reported that there was no worsening of symptoms over 2 years in most patients in the conservatively treated (see below) control group.⁵⁷ Another study reported an increase in the severity of symptoms in 20% of the untreated cases,³¹ whereas a further trial focusing on pain development over almost 5 years found that the clinical symptoms of 70% patients reached a plateau, 15% experienced pain exacerbation and 15% spontaneously improved.^{11, 59} Given that long-term clinical stability is common in LSS, the acute exacerbations of symptoms should not be confused with a change in the patient's trajectory.

Conservative therapy

The conservative treatment of LSS comprises a wide variety of methods, such as physical therapy, ergotherapy, behavioral therapy, delordosing orthopedic devices, girdles, acupuncture, manual therapy and pharmacological intervention. Few studies have been conducted to demonstrate the effectiveness of conservative therapy in treating LSS, although those that reported the use of such an approach had success rates of up to 70%.^{61, 62, 63} None of the available studies, however, provide sufficient data to support the superiority, or even the effectiveness, of any one of the wide range of conservative treatments.^{6, 64} In the absence of evidence-based clinical guidelines, an intensified, multidisciplinary approach should be given preference over a singular therapy.^{64, 65} The objectives of applicable physiotherapy and manual therapy approaches are flexion, distraction, neural mobilization and relief of the affected segments, as well as improvements in paravertebral muscle tone through the use of stabilizing exercises.^{61, 66} There is wide agreement between clinicians that bed rest is not recommended in the therapy of chronic and acute pain.⁶⁴ Advice tailored to individual patients is of central importance in LSS, particularly in cases with mild symptoms, because the simple modification of an individual's behavior can be sufficient to stabilize or improve the condition.

The pharmacological component of conservative therapy aims to relieve painful nerve-root pathologies and is identical to the medication given for a disc prolapse (herniation). Agents used to treat LSS include NSAIDs, other peripheral analgesics, steroids, muscle relaxants, opioids, antidepressants and, in very severe cases where quality of life is impaired, neuroleptics. Besides oral medication, weekly therapeutic injections can offer short-term to medium-term alleviation. Frequently, steroids are used in combination with local anesthetics in epidural, deep paravertebral, pararadicular and facet joint injections. Such invasive procedures are, however, associated with a risk of developing infections.

As for all conservative treatment strategies, the effectiveness of drug regimens has only been investigated in a few studies. Evidence-based recommendations cannot, therefore, be made for long-term administration of NSAIDs and muscle relaxants, or for the use of steroids, antidepressants and long-acting opioids.^{6, 65} Likewise, the evidence for the efficacy of therapeutic injections for LSS has not been confirmed.^{67, 68, 69}

Surgery

If a diagnosis of LSS has been established with consistent results from clinical history taking, physical examination and radiological assessment, conservative treatment should be applied for 3–6 months, with the aim of achieving satisfactory improvement of the symptoms. In patients in whom severe symptoms persist and functional impairment develops, surgery is the recommended option, unless this approach is contraindicated for other reasons. Clinicians should also consider that some patients simply do not want to have surgery, despite meeting these criteria, whereas many others have unrealistic expectations of what can be achieved with surgical procedures.⁷⁰

All surgical procedures used in LSS aim to decompress the entrapped neural elements, without disrupting the stability of the segment. Such decompression surgery usually leads to spontaneous relief of pain in the legs, and, to a lesser degree, of low back pain.⁷¹ The speed and extent of recovery is, however, unpredictable, even if pressure on nerve roots, dura and blood vessels is sufficiently eliminated. Decompressive surgical procedures include laminectomy and hemilaminectomy, hemilaminotomy, fenestration, foraminotomy and the implantation of interspinous distraction devices.^{11, 69, 72, 73} The complication rates for decompression surgery (during and after the surgical procedure) range from 14%⁵⁷ to 35% or more.^{74, 75, 76} Fusion surgery, which is a more invasive procedure than decompression surgery and is used in cases of instability, is associated with higher complication rates. Typical complications of both decompression and fusion surgery include dura vessel lacerations, epidural hematomas, inadequate decompression with significant residual stenosis, instability, and reossification. All of these complications result in renewed nerve compression.^{58, 59, 75, 76, 77, 78} The 10-year reoperation rates after decompressive surgical procedures are reported to range from 10–23%.^{71, 79} Additional fusion surgery lowered the rate of reoperation in one study.⁷⁹ Additive fusion surgery might be needed in cases of instability (rotational or vertical mobility of the vertebral body >3 mm), spondylolisthesis (>5 mm forward movement of a lumbar vertebra relative to one below)⁸⁰ or scoliosis (lateral curvature of the spine) >20°,⁸¹ because instability can foster spinal root congestion. Success rates for decompression surgery in cases of LSS range from 40–90% in the literature and depend on a wide variety of factors such as type of decompression, duration of follow-up, age of patients and comorbidities.^{77, 82, 83, 84, 85, 86, 87, 88}

Results from one study showed that patients who underwent laminotomy were more likely to show a marked improvement in lumbago than patients who underwent laminectomy.⁸⁷ A randomized trial revealed that bilateral laminotomy conferred greater clinical benefit than unilateral laminotomy or laminectomy in patients with LSS at 1 year post-surgery.⁷⁶ Another study compared the 1-year results after tissue sparing—so-called undercutting decompression—with those after the more-invasive laminectomy procedure and found no statistically significant difference between the two procedures.⁸⁹ Of patients who underwent unilateral foraminotomy for degenerative foraminal stenosis, 91% reported an improvement of leg pain, although there was a concomitant increase in lumbago in one-third of patients.⁹⁰ Resection of the pars interarticularis does not seem to result in segment instability, but might cause an increase in the frequency of lumbalgias.⁹¹ Laminoplasty is recommended for central LSS as two-thirds of patients show improvement after 6 years.⁹² Even in cases of mild degenerative spondylolistheses (complex stenosis), laminoplasty can produce good results, which are similar to those obtained with additive fusion.⁸⁶ To date, there is no agreement as to whether only the symptomatic level and side should be decompressed, or whether additional nonsymptomatic—but evidently confirmed—neighbouring stenoses should also be decompressed.^{58, 59, 93, 94, 95, 96} In general, as for the preoperative diagnosis, the paraclinical assessment of a successful surgical intervention is hampered by the fact that the imaging data do not correlate well with the clinical presentation.