Epidemiology/Prevalence

The initial description of mechanical compression of the cauda equine is attributed to Verbiest from 1954; 60 years later, the incidence and natural history of the condition remain poorly documented. The Framingham Study data have been used by Kalichman and colleagues to establish the prevalence of lumbar central canal stenosis in a community population. They used anterior-posterior dimensions less than 12 mm for relative stenosis and less than 10 mm for absolute stenosis on CT imaging ( Table 1 ).

The frequency of acquired absolute stenosis of less than 10 mm increased from 4% in patients under age 40 to 14.3% in those over 60 years of age.

In this study the presence of absolute stenosis was significantly associated with low back pain but not leg pain. There review of the literature found a prevalence ranging from 1.7% to 13.1%.

The Japanese Wakayama Spine Study, a population-based study of more than 1000 people, found a prevalence of symptomatic lumbar spinal stenosis of approximately 10%.

Given the wide variation in accepted criteria for defining lumbar spinal stenosis, it is unsurprising that there is considerable variation in the reported incidence and prevalence of the condition.

Congenital/Developmental Stenosis

Primary stenosis is uncommon, occurring in only 9% of cases. Congenital malformations include the following:

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  Incomplete vertebral arch closure (spinal dysraphism)

  
  
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  Segmentation failure

  
  
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  Achondroplasia

  
  
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  Osteopetrosis

Developmental flaws include the following:

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  Early vertebral arch ossification

  
  
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  Shortened pedicles

  
  
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  Thoracolumbar kyphosis

  
  
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  Apical vertebral wedging

  
  
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  Anterior vertebral beaking (Morquio syndrome)

  
  
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  Osseous exostosis

Acquired Stenosis

The most important structures underlying degenerative lumbar stenosis are the intervertebral disks, the facet joints, and the ligamentum flavum. The intervertebral disk may present with a herniation of the nucleus pulposus, a focal protrusion, or a broad-based bulge. Rarely does a disk bulge or protrusion cause a full-blown cauda equine syndrome in isolation. More often it is coupled with facet and flaval hypertrophy and/or congenital narrowing of the lumbar canal. Other features that may contribute are facet joint synovial cysts, facet and vertebral body osteophytes, and epidural lipomatosis. An important contributory pathology is spondylolisthesis, which, in the absence of pars defects, is strongly associated with lumbar canal stenosis.

Systemic processes that may be involved in secondary stenosis include Paget disease, fluorosis, acromegaly, neoplasm, and ankylosing spondylitis.

Pathophysiology of Neurogenic Intermittent Claudication

The first description by Verbiest postulated direct mechanical compression of the nerve roots in the generation of pain and dysfunction. Many experts believe that the positional and temporal presentation of the syndrome strongly suggests that dynamic factors, such as compression loading and postural change in the size of the canal, are crucial. The timescale of the relief on sitting and resting also suggests a vascular mediated process. Jinkins has shown that enhancement indicating blood-nerve barrier breakdown is often present in lumbar canal stenosis. Furthermore, it occurs more readily due to outflow obstruction and venous engorgement than for inflow obstruction and arterial mediated ischemia. Olmarker and colleagues demonstrated that the capillaries and venules of the nerve root could be occluded by mild compression of approximately 30 mm Hg to 40 mm Hg. Takahashi and colleagues found that the epidural pressure is only 15 mm Hg to 18 mm Hg during lumbar flexion in in lumbar canal stenosis patients but reaches 80 mm Hg to 100 mm Hg during lumbar extension. Ikawa and colleagues have demonstrated ectopic firing and nerve dysfunction due to venous stasis in rat model. Additional observations by Sato and Kikuchi include the importance of 2 or more zones of stenosis, which significantly increas the chance of having NIC symptoms compared with a single-level stenosis.

Inflammatory exudates, cerebrospinal fluid pressure changes and flow disturbance, endoneurial edema, and increased endoneurial compartment pressure have all been implicated in the pathogenesis of the nerve dysfunction and the clinical syndrome. Work by Morishita and colleagues has emphasized the role of the neural foramen in generating nerve dysfunction.

The balance of evidence seems to suggest that the pathophysiology of NIC involves multifactorial pathways in which venous congestion plays an important role and identification of all levels of stenosis, including lateral recess and neural foramina as well as central canal, is essential.

Imaging Modality Recommendations for Lumbar Canal Stenosis

The North American Spine Society guidelines state the following:

In patients with history and physical examination findings consistent with degenerative lumbar spinal stenosis, MR imaging is suggested as the most appropriate, noninvasive test to confirm the presence of anatomic narrowing of the spinal canal or the presence of nerve root impingement.

If MR imaging is either contraindicated or inconclusive, CTM is suggested as the most appropriate test to confirm the presence of anatomic narrowing of the spinal canal or the presence of nerve root impingement.

If MR imaging and CTM are contraindicated, inconclusive, or inappropriate, CT is the preferred test to confirm the presence of anatomic narrowing of the spinal canal or the presence of nerve root impingement.

MR imaging or CT with axial loading is suggested as a useful adjunct to routine imaging in patients who have clinical signs and symptoms of lumbar spinal stenosis, a dural sac area of less than 110 mm ² at 1 or more levels, and suspected but not verified central or lateral stenosis on routine unloaded MR imaging or CT.

Kent and colleagues undertook a systematic meta-analysis assessing the accuracy of CT, MR imaging, and myelography in diagnosing patients with lumbar spinal stenosis: they identified 14/116 relevant studies with a reference standard other than another imaging test. The sensitivity of MR imaging in the diagnosis of adult spinal stenosis was 81% to 97%, sensitivity of CT was 70% to 100%, and sensitivity of myelography was 67% to 78%.

Numerous more recent studies have demonstrated the approximate equivalence of MR imaging versus CTM for the diagnosis of lumbar spinal stenosis. Modic and colleagues found the accuracy of MR imaging to be 82%, CT/CTM 83%, and myelography 71%, with respect to surgical findings at 151 examined levels. The concordance between MR imaging and CT/CTM was 86.8%. Schnebel and colleagues retrospectively found 96.6% correlation between MR imaging and CTM.

The technical advances of MR imaging and CT technology have undoubtedly improved the quality and resolution of spinal imaging; it is difficult to quantify the relative changes brought about in both these modalities; however, there seems to be a general consensus that diagnostically, MR imaging is first line, with CT/CTM and conventional myelography satisfactory alternatives if required.

Quantitative Criteria for Lumbar Spinal Stenosis

Table 2 shows a simplified presentation of the findings from Steurer and colleagues, who undertook a literature review of the quantitative radiologic signs used in the diagnosis of lumbar spinal stenosis.

Mamisch and colleagues continued from this systematic review to perform a Delphi survey, polling 41 international experts in an attempt to gain a broad consensus on the qualitative and quantitative radiologic features of lumbar spinal stenosis. Results of the survey suggest that there are no broadly accepted quantitative criteria and only partially accepted qualitative criteria for a diagnosis of lumbar spinal stenosis. The latter include disk protrusion, lack of perineural intraforaminal fat, hypertrophic facet joint degeneration, absent fluid around the cauda equina, and hypertrophy of the ligamentum flavum. Cutoff values for the highest rated quantitative parameters given by the experts were 12 mm for the anteroposterior diameter of the osseous spinal canal (and midsagittal diameter of the dural sac), 3 mm for the diameter of the foramen, and 3 mm for the lateral recess height.

The multiplicity of quantitative measures that have been proposed over the past 3 decades is testament that none of them has proved satisfactory and it seems highly likely that a simple dimension definition of a complex pathology, such as spinal stenosis, is fundamentally flawed.

Degenerative Spondylolisthesis

First described by McNab as “spondylolisthesis with an intact neural arch,” vertebral displacement most commonly seen at L4/L5 is due to facet hypertrophy. It is common and affects 4% to 14% of the elderly population, more frequently in women than men. Unlike isthmic spondylolisthesis, it is self-limiting and rarely reaches grade II; however, it can critically narrow the canal. Claudication, or more often radicular pain, is a symptoms of stenosis secondary to degenerative spondylolisthesis. Degenerative spondylolisthesis normally affects a single level and thus is less likely to cause NIC. Central stenosis is rare in lytic spondylolisthesis but in some cases of L5/S1 displacement the posterior element can be pulled forward compressing the cauda against the body of S1. More frequently, posterior disk bulging caused by the listhesis and loss of disk height can trap the nerve root in the foramen combined with facet hypertrophy to cause lateral recess stenosis. The osteofibrous callus present at the isthmic fracture level can occasionally hypertrophy to form Gill nodules and compress the spinal canal.

Redundant Nerve Root and Sedimentation Signs

Redundant nerve roots of the cauda equina is a phrase first coined by Cressman and Pawl, although the first descriptions are attributed to Verbiest. The entity characterized by elongated, enlarged, and tortuous nerve roots in the subarachnoid space adjacent to a level of lumbar spinal stenosis. The abnormality is seen above the level of the stenosis in 85%. The presence of nerve thickening as well as elongation suggests a chronic reactive pathologic process repetitive traction and/or venous congestion. In the early stages, it seems likely that flexion/extension of the spine causes traction that pulls the roots through the stenosis, which then cannot slide back into position on returning the spine to a neutral position. The redundant nerve root sign is best appreciated in the sagittal plane on T2W sequences. It occurs in 34% to 42% of surgical candidates with NIC. There was a tendency to increased age, worse clinical symptoms, and poorer postsurgical outcomes in the study by Min and colleagues. Attempts to quantify the observational findings through measurement of the lengths of the redundant roots has not yet achieved a practical application. It remains a qualitative finding with interpretational subjectivity but is an important observation that should be looked for in all cases of central lumbar canal stenosis.

More recently Barz and colleagues have described a nerve root sedimentation sign; it is considered positive if the roots of the cauda equina fail to sediment into the posterior half of the dural sac on either side of a stenotic lesion (on T2W axial images). This sign has been shown highly associated with high-grade lesions with dural sac area less than 80 mm ² ; however, it is yet to be shown to add specificity (or sensitivity) in a general population.

It has long been noticed that the nerve roots at and either side of a stenosis demonstrate postgadolinium enhancement. Kobayashi and colleagues performed studies on dogs that applied circumferential pressure on the cauda equina. Histologic examination showed congestion and dilation in many of the intraradicular veins as well as inflammatory cell infiltration. The intraradicular edema caused by venous congestion and wallerian degeneration can also occur at sites that are not subject to mechanical compression. Enhanced MR imaging showed enhancement of the cauda equina at the stenosed region, demonstrating the presence of edema. This breakdown of the blood-nerve barrier not only is an important observation that has a role in improved specificity but also should not be mistaken for other pathologies.