Neuroimaging of Spinal Canal Stenosis
Neuroimaging of Spinal Canal Stenosis
Neuroimaging of Spinal Canal Stenosis
C a n a l St e n o s i s
Peter Cowley, MBBS (Lon), BA Oxon, MRCP, FRCR
KEYWORDS
Spinal stenosis Central canal stenosis Lateral stenosis Foraminal stenosis
Neurogenic intermittent claudication Cauda equina compression
Cervical spondylotic myelopathy
KEY POINTS
Spinal stenosis is a broad term encompassing central, lateral, and foraminal narrowing and implies
compromise of the neural structures passing through that space.
Imaging of spinal stenosis is primarily with MR imaging; however, CT and CT myelography (CTM)
are acceptable alternatives.
There is often a mismatch between imaging and clinical findings; accurate and rigorous interpreta-
tion of the imaging is necessary for correct management decisions.
Cross-sectional imaging is usually acquired in a supine neutral position that under-recognizes the
dynamic and load-bearing functions of the spinal column.
LUMBAR SPINAL STENOSIS Given the wide variation in accepted criteria for
defining lumbar spinal stenosis, it is unsurprising
The North American Spine Society 2011 revised
that there is considerable variation in the reported
guidelines1 provide the following definition:
incidence and prevalence of the condition.
Degenerative lumbar spinal stenosis describes
a condition in which there is diminished space
available for the neural and vascular elements in NATURAL HISTORY
the lumbar spine secondary to degenerative There is a conspicuous absence of good-quality
changes in the spinal canal. When symptomatic, longitudinal studies documenting the natural his-
this causes a variable clinical syndrome of gluteal tory of patients with symptomatic lumbar canal
and/or lower extremity pain and/or fatigue, which stenosis. The North American Spine Society is-
may occur with or without back pain. Symptomatic sued a statement that in the absence of reliable ev-
lumbar spinal stenosis has certain characteristic idence, it is likely that the natural history of patients
provocative and palliative features. Provocative with mild to moderate symptomatic degenerative
features include upright exercise, such as walking stenosis is favorable in one-third to one-half of pa-
or positionally induced neurogenic claudication. tients. In patients with mild to moderate symptom-
Palliative features commonly include symptomatic atic stenosis, rapid or catastrophic neurologic
relief with forward flexion, sitting, and/or decline is a rare phenomenon. There is no reliable
recumbency. evidence to define the natural history of clinically
or radiologically severe stenosis.1
Epidemiology/Prevalence
Congenital/Developmental Stenosis
The initial description of mechanical compression
of the cauda equine is attributed to Verbiest6 Primary stenosis is uncommon, occurring in only
from 1954; 60 years later, the incidence and natu- 9% of cases. Congenital malformations include
ral history of the condition remain poorly docu- the following:
mented. The Framingham Study data have been Incomplete vertebral arch closure (spinal
used by Kalichman and colleagues2 to establish dysraphism)
the prevalence of lumbar central canal stenosis Segmentation failure
in a community population. They used anterior- Achondroplasia
posterior dimensions less than 12 mm for relative Osteopetrosis
stenosis and less than 10 mm for absolute steno-
sis on CT imaging (Table 1). Developmental flaws include the following:
The frequency of acquired absolute stenosis of
Early vertebral arch ossification
less than 10 mm increased from 4% in patients un-
Shortened pedicles
der age 40 to 14.3% in those over 60 years of age.
Thoracolumbar kyphosis
In this study the presence of absolute stenosis
Apical vertebral wedging
was significantly associated with low back pain
Anterior vertebral beaking (Morquio syndrome)
but not leg pain. There review of the literature
Osseous exostosis
found a prevalence ranging from 1.7% to 13.1%.
The Japanese Wakayama Spine Study,3 a
Acquired Stenosis
population-based study of more than 1000 people,
found a prevalence of symptomatic lumbar spinal The most important structures underlying degen-
stenosis of approximately 10%. erative lumbar stenosis are the intervertebral
Neuroimaging of Spinal Canal Stenosis 525
disks, the facet joints, and the ligamentum flavum. Pathophysiology of Neurogenic Intermittent
The intervertebral disk may present with a hernia- Claudication
tion of the nucleus pulposus, a focal protrusion, or
The first description by Verbiest6 postulated direct
a broad-based bulge. Rarely does a disk bulge or
mechanical compression of the nerve roots in the
protrusion cause a full-blown cauda equine syn-
generation of pain and dysfunction. Many experts
drome in isolation. More often it is coupled with
believe that the positional and temporal presenta-
facet and flaval hypertrophy and/or congenital nar-
tion of the syndrome strongly suggests that dy-
rowing of the lumbar canal. Other features that
namic factors, such as compression loading and
may contribute are facet joint synovial cysts, facet
postural change in the size of the canal, are
and vertebral body osteophytes, and epidural lipo-
crucial. The timescale of the relief on sitting and
matosis. An important contributory pathology is
resting also suggests a vascular mediated pro-
spondylolisthesis, which, in the absence of pars
cess. Jinkins7 has shown that enhancement indi-
defects, is strongly associated with lumbar canal
cating blood-nerve barrier breakdown is often
stenosis.4
present in lumbar canal stenosis. Furthermore, it
Systemic processes that may be involved in
occurs more readily due to outflow obstruction
secondary stenosis include Paget disease, fluo-
and venous engorgement than for inflow obstruc-
rosis, acromegaly, neoplasm, and ankylosing
tion and arterial mediated ischemia.8,9 Olmarker
spondylitis.
and colleagues10 demonstrated that the capillaries
and venules of the nerve root could be occluded
CLINICAL PRESENTATION OF LUMBAR SPINAL
by mild compression of approximately 30 mm Hg
STENOSIS
to 40 mm Hg. Takahashi and colleagues11 found
that the epidural pressure is only 15 mm Hg to
The diagnosis of lumbar spinal stenosis may 18 mm Hg during lumbar flexion in in lumbar canal
be considered in older patients presenting stenosis patients but reaches 80 mm Hg to
with a history of gluteal or lower extremity 100 mm Hg during lumbar extension. Ikawa and
symptoms exacerbated by walking or stand- colleagues12 have demonstrated ectopic firing
ing which improves or resolves with sitting and nerve dysfunction due to venous stasis in rat
or bending forward. Patients whose pain is model. Additional observations by Sato and Kiku-
not made worse with walking have a low likeli- chi include the importance of 2 or more zones of
hood of stenosis.1 stenosis, which significantly increas the chance
of having NIC symptoms compared with a
There may be relative relief of symptoms on
single-level stenosis.13
walking up an incline due to flexion of the lower
Inflammatory exudates, cerebrospinal fluid
spine. Saddle anesthesia and bladder disturbance
pressure changes and flow disturbance, endoneu-
are present in approximately 10% of cases. Fixed
rial edema, and increased endoneurial compart-
radicular symptoms of neuropathic pain and
ment pressure have all been implicated in the
dysfunction may coexist due to lateral recess or
pathogenesis of the nerve dysfunction and the
foraminal stenosis.
clinical syndrome. Work by Morishita and col-
The hallmark of central canal stenosis is the
leagues14 has emphasized the role of the neural
bilateral and ill-defined distribution with claudicant
foramen in generating nerve dysfunction.
variation.
The balance of evidence seems to suggest
Presentation of intermittent leg pain and
that the pathophysiology of NIC involves multi-
discomfort, usually during walking, shows some-
factorial pathways in which venous congestion
times subtle differences between the 2 pathol-
plays an important role and identification of all
ogies of neurogenic claudication and peripheral
levels of stenosis, including lateral recess and
arterial claudication. In both, walking becomes
neural foramina as well as central canal, is
impossible but only in neurogenic claudication is
essential.
stooping or sitting necessary to alleviate the symp-
toms. Likewise, claudication appears in both
Imaging Modality Recommendations for
cases during walking whereas cycling is more
Lumbar Canal Stenosis
associated by arterial disease. With advanced
neurogenic claudication, descending stairs be- The North American Spine Society guidelines1
comes impossible, forcing patients to walk down- state the following:
stairs backwards to adopt a forward flexed In patients with history and physical examination
position; going upstairs is usually ok, in contrast findings consistent with degenerative lumbar spi-
to arterial pathologies in which all stair walking is nal stenosis, MR imaging is suggested as the
difficult.5 most appropriate, noninvasive test to confirm the
526 Cowley
presence of anatomic narrowing of the spinal ca- at levels of interest. Correct alignment is clearly
nal or the presence of nerve root impingement. essential for anterior-posterior and dural sac area
If MR imaging is either contraindicated or incon- quantitative measurements.
clusive, CTM is suggested as the most appropriate
test to confirm the presence of anatomic narrow- Additional MR imaging sequences
ing of the spinal canal or the presence of nerve High-resolution 3-D acquisition, for example,
root impingement. SPACE or CISS
If MR imaging and CTM are contraindicated, Postcontrast with or without fat saturation
inconclusive, or inappropriate, CT is the preferred Diffusion tensor imaging and methods for axial
test to confirm the presence of anatomic narrow- loading
ing of the spinal canal or the presence of nerve
root impingement. Quantitative Criteria for Lumbar Spinal
MR imaging or CT with axial loading is sug- Stenosis
gested as a useful adjunct to routine imaging in pa- Table 2 shows a simplified presentation of the
tients who have clinical signs and symptoms of findings from Steurer and colleagues,37 who un-
lumbar spinal stenosis, a dural sac area of less dertook a literature review of the quantitative
than 110 mm2 at 1 or more levels, and suspected radiologic signs used in the diagnosis of lumbar
but not verified central or lateral stenosis on spinal stenosis.
routine unloaded MR imaging or CT. Mamisch and colleagues44 continued from this
Kent and colleagues15 undertook a systematic systematic review to perform a Delphi survey, poll-
meta-analysis assessing the accuracy of CT, MR ing 41 international experts in an attempt to gain a
imaging, and myelography in diagnosing patients broad consensus on the qualitative and quantita-
with lumbar spinal stenosis: they identified 14/ tive radiologic features of lumbar spinal stenosis.
116 relevant studies with a reference standard Results of the survey suggest that there are no
other than another imaging test. The sensitivity of broadly accepted quantitative criteria and only
MR imaging in the diagnosis of adult spinal steno- partially accepted qualitative criteria for a diag-
sis was 81% to 97%, sensitivity of CT was 70% to nosis of lumbar spinal stenosis. The latter include
100%, and sensitivity of myelography was 67% to disk protrusion, lack of perineural intraforaminal
78%. fat, hypertrophic facet joint degeneration, absent
Numerous more recent studies have demon- fluid around the cauda equina, and hypertrophy
strated the approximate equivalence of MR imag- of the ligamentum flavum. Cutoff values for the
ing versus CTM for the diagnosis of lumbar spinal highest rated quantitative parameters given by
stenosis. Modic and colleagues16 found the accu- the experts were 12 mm for the anteroposterior
racy of MR imaging to be 82%, CT/CTM 83%, and diameter of the osseous spinal canal (and midsag-
myelography 71%, with respect to surgical find- ittal diameter of the dural sac), 3 mm for the diam-
ings at 151 examined levels. The concordance be- eter of the foramen, and 3 mm for the lateral recess
tween MR imaging and CT/CTM was 86.8%. height.
Schnebel and colleagues17 retrospectively found The multiplicity of quantitative measures that
96.6% correlation between MR imaging and CTM. have been proposed over the past 3 decades is
The technical advances of MR imaging and CT testament that none of them has proved satisfac-
technology have undoubtedly improved the quality tory and it seems highly likely that a simple dimen-
and resolution of spinal imaging; it is difficult to sion definition of a complex pathology, such as
quantify the relative changes brought about in spinal stenosis, is fundamentally flawed.
both these modalities; however, there seems to
be a general consensus that diagnostically, MR
Degenerative Spondylolisthesis
imaging is first line, with CT/CTM and conventional
myelography satisfactory alternatives if required. First described by McNab45 as “spondylolisthesis
with an intact neural arch,” vertebral displacement
Standard MR imaging protocol most commonly seen at L4/L5 is due to facet hy-
Sagittal T2-weighted (T2W) imaging with or pertrophy. It is common and affects 4% to
without proton density images. 14%46 of the elderly population, more frequently
Turbo spin echo is preferred to gradient echo in women than men. Unlike isthmic spondylolis-
due to the susceptibility artefact causing overesti- thesis, it is self-limiting and rarely reaches grade
mation of stenotic lesions. II; however, it can critically narrow the canal. Clau-
Sagittal T1W imaging as standard. dication, or more often radicular pain, is a symp-
Axial T2W imaging 3-mm to 5-mm slice thick- toms of stenosis secondary to degenerative
ness arranged perpendicular to longitudinal axis spondylolisthesis. Degenerative spondylolisthesis
Neuroimaging of Spinal Canal Stenosis 527
Table 2
Signs used in the diagnosis of lumbar spinal stenosis
Table 2
(continued)
40
Lateral recess angle <30
normally affects a single level and thus is less likely colleagues8 performed studies on dogs that
to cause NIC. Central stenosis is rare in lytic spon- applied circumferential pressure on the cauda
dylolisthesis but in some cases of L5/S1 displace- equina. Histologic examination showed conges-
ment the posterior element can be pulled forward tion and dilation in many of the intraradicular veins
compressing the cauda against the body of S1.47 as well as inflammatory cell infiltration. The intrara-
More frequently, posterior disk bulging caused dicular edema caused by venous congestion and
by the listhesis and loss of disk height can trap wallerian degeneration can also occur at sites
the nerve root in the foramen combined with facet that are not subject to mechanical compression.
hypertrophy to cause lateral recess stenosis. The Enhanced MR imaging showed enhancement of
osteofibrous callus present at the isthmic fracture the cauda equina at the stenosed region, demon-
level can occasionally hypertrophy to form Gill strating the presence of edema. This breakdown
nodules48 and compress the spinal canal. 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
Redundant Nerve Root and Sedimentation
pathologies.
Signs
Redundant nerve roots of the cauda equina is a
DYNAMIC IMAGING
phrase first coined by Cressman and Pawl,49,50
although the first descriptions are attributed to Imaging of the spine is routinely performed with
Verbiest. The entity characterized by elongated, the patient supine and in as relaxed a state as
enlarged, and tortuous nerve roots in the sub- possible. The symptoms of spinal stenosis are
arachnoid space adjacent to a level of lumbar spi- commonly exacerbated by standing, walking,
nal stenosis. The abnormality is seen above the and extension. Imaging in extension versus neutral
level of the stenosis in 85%.51 The presence of versus flexion and in an upright position or with
nerve thickening as well as elongation suggests a axial loading applied have all been investigated
chronic reactive pathologic process repetitive to assess the relative effects on the spinal canal.
traction and/or venous congestion. In the early Multiple studies have demonstrated a reduction
stages, it seems likely that flexion/extension of in both dural sac area and midsagittal diameter
the spine causes traction that pulls the roots on extension. Wei and colleagues54 have attemp-
through the stenosis, which then cannot slide ted to quantify the dural sac area change versus
back into position on returning the spine to a angular rotation. Hansson and colleagues55
neutral position. The redundant nerve root sign is showed that external load decreased the size of
best appreciated in the sagittal plane on T2W se- the spinal canal. Bulging of the ligamentum flavum
quences. It occurs in 34% to 42% of surgical can- contributed to between 50% and 85% of the spi-
didates with NIC.52 There was a tendency to nal canal narrowing. It was concluded that the lig-
increased age, worse clinical symptoms, and amentum flavum, not the disk, had the dominant
poorer postsurgical outcomes in the study by role for load-induced narrowing of the lumbar spi-
Min and colleagues.52 Attempts to quantify the nal canal. Also, in the standing position, extension
observational findings through measurement of of the lumbar spine has the greater effect on canal
the lengths of the redundant roots has not yet narrowing compared with axial loading.
achieved a practical application. It remains a qual- Greater changes in dural sac area with axial
itative finding with interpretational subjectivity but loading have been noted in older and in more
is an important observation that should be looked symptomatic patients. There is reported correla-
for in all cases of central lumbar canal stenosis. tion between stenosis present only on axially
More recently Barz and colleagues53 have loaded patients and improved surgical outcomes.
described a nerve root sedimentation sign; it is
considered positive if the roots of the cauda
Advanced Techniques
equina fail to sediment into the posterior half of
the dural sac on either side of a stenotic lesion Eguchi and colleagues56 performed a pilot study
(on T2W axial images). This sign has been shown that elegantly demonstrated the ability of 3T
highly associated with high-grade lesions with systems to visualize lumbar nerve roots and struc-
dural sac area less than 80 mm2; however, it is tural abnormality, such as thinning, deviation, and
yet to be shown to add specificity (or sensitivity) interruption. Also the fractional anisotropy is
in a general population. decreased in the affected nerves in all their cases.
It has long been noticed that the nerve roots The patients were highly selected for pure single-
at and either side of a stenosis demonstrate level degenerative radiculopathy with central canal
postgadolinium enhancement.7 Kobayashi and stenosis and myelopathy excluded. Double-crush
530 Cowley
lesions have also been visualized with this tech- next most commonly affected levels are C7
nique (Figs. 1–6).57 and C5.
First described by Stookey and Fleming in
1928,58 compressive cervical spondylomyelop-
CERVICAL STENOSIS athy (CSM) has a more complex constellation of
Cervical spondylosis is a common finding that in- symptoms and signs. Patients with chronic mild
creases with age. Degeneration of nucleus pulpo- CSM may be unaware of subtle changes in bal-
sus of the intervertebral disk leads to narrowing of ance and fine motor dexterity.
the disk space, bulging of the annulus fibrosis, Although culturally slightly specific, the
buckling of the ligamentum flavum, disk- Japanese Orthopaedic Association scale for spon-
osteophyte bar formation, and hypertrophic osteo- dylotic myelopathy59 provides an excellent over-
arthritic changes of the facet and uncovertebral view of the less subtle manifestations of cervical
joints. This cascade of degenerative processes myelopathy (Table 3).
may or may not result in cervical stenosis. As in Detailed neurologic examination, including deep
the lumbar canal, cervical stenosis may refer to tendon reflexes and Hoffman, Romberg, and
central, lateral, or foraminal narrowing. In contrast Babinski signs, are all important given the lack of
to the lumbar region, the clinically manifest lesions diagnostic and prognostic accuracy that imaging
are dominated by foraminal stenosis, causing has displayed.
radicular symptoms, and central canal stenosis,
causing myelopathy.
Pathology of Cervical Spondylomyelopathy
It is widely acknowledged that both static and dy-
Clinical Presentations
namic factors are implicated in the pathophysi-
Cervical pain may manifest locally or radiate to ology of CSM. Direct compression of the neural
occiput, shoulder, scapular, and arm. There is vari- tissue is compounded by repetitive injury to cause
ability with position may be associated with head- secondary ischemia, inflammation, and apoptosis.
ache and interfere with sleep. The specific nerve The histologic hallmarks of the compressive mye-
roots involved demonstrate sensory and/or motor lomalacia are cystic cavitation and gliosis of the
dysfunction. Pain, tingling, and dysesthesia are central grey matter and demyelination of the white
the most common presentations, with loss of fine matter long tracts. Wallerian degeneration extends
motor skill, weakness, and muscle wasting also caudally in the anterior horn cells and corticospinal
frequently present. The most commonly affected tracts and rostral in the posterior columns and
level is C5/C6 resulting in C6 radiculopathy; the posterolateral tracts.
Fig. 2. Grade II spondylolisthesis with high-grade lumbar canal stenosis and bilateral L4 foraminal stenosis. The
patient was unable to mobilize unaided and was complaining of sphincter disturbance.
Static and Dynamic Factors they assessed the segmental angular motion in
60 flexion and extension and found that those with
The work of Morishita and colleagues has shown
developmentally narrow canals had significantly
that the constitutionally or developmentally narrow
greater angular motion at C4/C5 to C6/C7
canal is an important factor in the etiology of CSM.
(although less at C3/C4), and this was associated
Based on the midsagittal diameter of the canal at
with greater degenerative disk changes.
each segmental level, patients were classified as
Several investigators have demonstrated
developmentally narrow less than 13 mm, normal
decreased cross-sectional area of the cervical ca-
13 mm to 15 mm, and wide greater than 15 mm.
nal on both flexion and extension compared to the
They showed that developmentally narrow canals
neutral position.61–63 The greater decrease is seen
had a significantly increased frequency of cervical
in extension where buckling of the ligamentum fla-
cord compression at all levels except C2/C3. Also
vum plays a major role.
Fig. 3. Multilevel degenerative changes with central canal and foraminal narrowing causing thickened and
serpiginous roots of the cauda equine: the redundant root sign.
532 Cowley
Fig. 4. Two-level lumbar canal stenosis is more likely associated with NIC.
Table 3
Japanese Orthopaedic Association scale for spondylotic myelopathy
been found to correlate well with degree of canal Reductions in fractional anisotropy have consis-
narrowing. tently been shown in canal stenosis and cervical
Signal change within the cord remains a crucial cord compression. The clinical severity of CSM
observation with subtle ill-defined T2W hyperin- (inversely) correlates well with fractional anisot-
tensity likely representing reversible edema ropy and postsurgical prognosis (Figs. 7–14).
whereas bright well-defined T2W hyperintensity
more likely is fixed gliosis/cystic necrosis/demye- THORACIC SPINAL STENOSIS
lination. T1W hypointensity almost certainly repre-
sents irreversible myelomalacia. Degenerative thoracic stenosis occurs much less
High-field systems now have the capability of commonly than cervical or lumbar stenosis; this
acquiring diffusion tensor imaging, which allows is likely due to the structural support of the rib
mapping of the fractional anisotropy in the cord. cage and the relative reduced movement. When
Fig. 8. Flexion extension sagittal T2W acquisitions reveal the exacerbation of the cervical stenosis in extension.
Chronic myelopathic signal change already established.
Neuroimaging of Spinal Canal Stenosis 535
Fig. 14. OPLL is a multifactorial condition, which has a strong association with CSM. It is more frequently seen in
Asian and elderly patients, and it is independently associated with diffuse idiopathic skeletal hyperostosis, ossi-
fication of the ligamentum flavum, and inflammatory spondyloarthropathies. CT and MR imaging are both
required for assessment and management.
Neuroimaging of Spinal Canal Stenosis 537
claudication in patients with lumbar canal stenosis. 23. Lee B, Kazam E, Newman A. Computed tomogra-
World J Orthop 2014;5(2):134–45. phy of the spine and spinal cord. Radiology 1978;
10. Olmarker K, Rydevik B, Holm S. Edema formation in 128(1):95–102.
spinal nerve roots induced by experimental, graded 24. Ullrich C, Binet E, Sanecki M, et al. Quantitative
compression. An experimental study on the pig assessment of the lumbar spinal canal by computed
cauda equina with special reference to differences tomography. Radiology 1980;134(1):137–43.
in effects between rapid and slow onset of compres- 25. Verbiest H. The significance and principles of
sion. Spine (Phila Pa 1976) 1989;14:569–73. computerized axial tomography in idiopathic devel-
11. Takahashi K, Kagechika K, Takino T, et al. Changes opmental stenosis of the bony lumbar vertebral ca-
in epidural pressure during walking in patients with nal. Spine (Phila Pa 1976) 1979;4(4):369–78.
lumbar spinal stenosis. Spine (Phila Pa 1976) 26. Airaksinen O, Herno A, Turunen V, et al. Surgical
1995;20:2746–9. outcome of 438 patients treated surgically for lum-
12. Ikawa M, Atsuta Y, Tsunekawa H. Ectopic firing due bar spinal stenosis. Spine (Phila Pa 1976) 1997;
to artificial venous stasis in rat lumbar spinal canal 22(19):2278–82.
stenosis model: a possible pathogenesis of neuro- 27. Herno A, Airaksinen O, Saari T. Computed tomogra-
genic intermittent claudication. Spine (Phila Pa phy after laminectomy for lumbar spinal stenosis.
1976) 2005;30(21):2393–7. Patients’ pain patterns, walking capacity, and sub-
13. Sato K, Kikuchi S. Clinical analysis of two-level jective disability had no correlation with computed
compression of the cauda equina and the nerve tomography findings. Spine (Phila Pa 1976) 1994;
roots in lumbar spinal canal stenosis. Spine (Phila 19(17):1975–8.
Pa 1976) 1997;22(16):1898–903. 28. Jönsson B, Annertz M, Sjöberg C, et al.
14. Morishita Y, Hida S, Naito M, et al. Measurement of A prospective and consecutive study of surgically
the local pressure of the intervertebral foramen treated lumbar spinal stenosis. Part I: clinical fea-
and the electrophysiological values of the epidural tures related to radiographic findings. Spine (Phila
nerve roots in the vertebral foramen. Spine (Phila Pa 1976) 1997;22(24):2932–7.
Pa 1976) 2006;31(26):3076–80. 29. Sortland O, Magnaes B, Hauge T. Functional mye-
15. Kent DL, Haynor DR, Larson EB, et al. Diagnosis of lography with metrizamide in the diagnosis of lum-
lumbar spinal stenosis in adults: a metaanalysis of bar spinal stenosis. Acta Radiol Suppl 1977;355:
the accuracy of CT, MR, and myelography. AJR 42–54.
Am J Roentgenol 1992;158(5):1135–44. 30. Verbiest H. Neurogenic intermittent claudication in
16. Modic MT, Masaryk T, Boumphrey F, et al. Lumbar cases with absolute and relative stenosis of the
herniated disk disease and canal stenosis: pro- lumbar vertebral canal (ASLC and RSLC), in cases
spective evaluation by surface coil MR, CT, and with narrow lumbar intervertebral foramina, and in
myelography. AJR Am J Roentgenol 1986;147(4): cases with both entities. Clin Neurosurg 1973;20:
757–65. 204–14.
17. Schnebel B, Kingston S, Watkins R, et al. Compari- 31. Hamanishi C, Matukura N, Fujita M, et al. Cross-
son of MRI to contrast CT in the diagnosis of spinal sectional area of the stenotic lumbar dural tube
stenosis. Spine 1989;14(3):332–7. measured from the transverse views of magnetic
18. Fukusaki M, Kobayashi I, Hara T, et al. Symptoms of resonance imaging. J Spinal Disord 1994;7(5):
spinal stenosis do not improve after epidural steroid 388–93.
injection. Clin J Pain 1998;14(2):148–51. 32. Mariconda M, Fava R, Gatto A, et al. Unilateral lam-
19. Koc Z, Ozcakir S, Sivrioglu K, et al. Effectiveness of inectomy for bilateral decompression of lumbar spi-
physical therapy and epidural steroid injections in nal stenosis: a prospective comparative study with
lumbar spinal stenosis. Spine (Phila Pa 1976) conservatively treated patients. J Spinal Disord
2009;34(10):985–9. Tech 2002;15(1):39–46.
20. Herzog RJ, Kaiser JA, Saal JA, et al. The importance 33. Laurencin C, Lipson S, Senatus P, et al. The steno-
of posterior epidural fat pad in lumbar central canal sis ratio: a new tool for the diagnosis of degener-
stenosis. Spine (Phila Pa 1976) 1991;16(6 Suppl): ative spinal stenosis. Int J Surg Investig 1999;1(2):
S227–33. 127–31.
21. Bolender N, Schönström N, Spengler D. Role of 34. Schonstrom N, Bolender N, Spengler D. The patho-
computed tomography and myelography in the morphology of spinal stenosis as seen on CT scans
diagnosis of central spinal stenosis. J Bone Joint of the lumbar spine. Spine (Phila Pa 1976) 1985;
Surg Am 1985;67(2):240–6. 10(9):806–11.
22. Haig AJ, Geisser ME, Tong HC, et al. Electromyo- 35. Schonstrom N, Willen J. Imaging lumbar spinal ste-
graphic and magnetic resonance imaging to predict nosis. Radiol Clin North Am 2001;39(1):31–53.
lumbar stenosis, low-back pain, and no back symp- 36. Wilmink J, Korte J, Penning L. Dimensions of the
toms. J Bone Joint Surg Am 2007;89(2):358–66. spinal canal in individuals symptomatic and
Neuroimaging of Spinal Canal Stenosis 539
non-symptomatic for sciatica: a CT study. Neuroradi- spinal stenosis. Clin Neurol Neurosurg 2008;110(1):
ology 1988;30(6):547–50. 14–8.
37. Steurer J, Roner S, Gnannt R, et al. Quantitative 53. Barz T, Melloh M, Staub LP, et al. Nerve root sedi-
radiologic criteria for the diagnosis of lumbar spinal mentation sign: evaluation of a new radiological
stenosis: a systematic literature review. BMC Muscu- sign in lumbar spinal stenosis. Spine (Phila Pa
loskelet Disord 2011;12:175. 1976) 2010;35(8):892–7.
38. Ciric I, Mikhael MA, Tarkington JA, et al. The lateral 54. Wei F, Wang J, Zou J, et al. Effect of lumbar angular
recess syndrome. A variant of spinal stenosis. motion on central canal diameter: positional MRI
J Neurosurg 1980;53(4):433–43. study in 491 cases. Chin Med J 2010;123(11):1422–5.
39. Dincer F, Erzen C, Basgöze O, et al. Lateral recess 55. Hansson T, Suzuki N, Hebelka H, et al. The narrow-
syndrome and computed tomography. Turkish Neu- ing of the lumbar spinal canal during loaded MRI:
rosurg 1991;2:30–5. the effects of the disc and ligamentum flavum. Eur
40. Mikhael M, Ciric I, Tarkington J, et al. Neuroradiolog- Spine J 2009;18(5):679–86.
ical evaluation of lateral recess syndrome. Radi- 56. Eguchi Y, Ohtori S, Orita S, et al. Quantitative evalu-
ology 1981;140(1):97–107. ation and visualization of lumbar foraminal nerve root
41. Strojnik T. Measurement of the lateral recess angle entrapment by using diffusion tensor imaging: pre-
as a possible alternative for evaluation of the lateral liminary results. AJNR Am J Neuroradiol 2011;32:
recess stenosis on a CT scan. Wien Klin Wo- 1824–9.
chenschr 2001;113(Suppl 3):53–8. 57. Kanamoto H, Eguchi Y, Suzuki M, et al. The diag-
42. Wildermuth S, Zanetti M, Duewell S, et al. Lumbar nosis of double-crush lesion in the L5 lumbar nerve
spine: quantitative and qualitative assessment of using diffusion tensor imaging. Spine J 2015;16(3):
positional (upright flexion and extension) MR imag- 315–21.
ing and myelography. Radiology 1998;207:391–8. 58. Stookey B, Fleming GWTH. Compression of the Spi-
43. Lee S, Lee JW, Yeom JS, et al. A practical MRI nal Cord due to Ventral Extradural Cervical Chondro-
grading system for lumbar foraminal stenosis. AJR mas. (Arch. of Neur. and Psychiat., August, 1928.).
Am J Roentgenol 2010;194(4):1095–8. Br J Psychiatry 1929;75(309):333.
44. Mamisch N, Brumann M, Hodler J, et al, Lumbar Spi- 59. Hukuda SMT, Ogata M, Schichikawa K, et al. Oper-
nal Stenosis Outcome Study Working Group Zurich. ations for cervical spondylotic myelopathy: a com-
Radiologic criteria for the diagnosis of spinal steno- parison of the results of anterior and posterior
sis: results of a Delphi survey. Radiology 2012; procedures. J Bone Joint Surg Br 1985;67B:609–15.
264(1):174–9. 60. Morishita Y, Naito M, Hymanson H, et al. The rela-
45. McNab I. Spondylolisthesis with an intact neural tionship between the cervical spinal canal diameter
arch; the so-called pseudo-spondylolisthesis. and the pathological changes in the cervical spine.
J Bone Joint Surg Br 1950;32-B(3):325–33. Eur Spine J 2009;18(6):877–83.
46. Kauppila LI, Eustace S, Kiel DP, et al. Degenerative 61. Chen IH, Vasavada A, Panjabi MM. Kinematics of
displacement of lumbar vertebrae. A 25-year follow- the cervical spine canal: changes with sagittal plane
up study in Framingham. Spine (Phila Pa 1976) loads. J Spinal Disord 1994;7(2):93–101.
1998;23(17):1868–73 [discussion: 1873–4]. 62. Zhang L, Zeitoun D, Rangel A, et al. Preoperative
47. Wiltse LL, Rothman SLG. Lumbar and lumbosacral evaluation of the cervical spondylotic myelopathy
spondylolisthesis. In: Wiesel SW, Weinstein JN, with flexion-extension magnetic resonance imaging:
Herkowitz H, et al, editors. The lumbar spin. Phila- about a prospective study of fifty patients. Spine
delphia: Saunders; 1996. p. 621–54. (Phila Pa 1976) 2011;36(17):E1134–9.
48. Gill GG, Manning JG, White HL. Surgical treatment 63. Muhle C, Weinert D, Falliner A, et al. Dynamic
of spondylolisthesis without spine fusion; excision changes of the spinal canal in patients with cervical
of the loose lamina with decompression of the nerve spondylosis at flexion and extension using magnetic
roots. J Bone Joint Surg Am 1955;37-A(3):493–520. resonance imaging. Invest Radiol 1998;33(8):444–9.
49. Cressman MR, Pawl RP. Serpentine myelographic 64. Saetia K, Cho D, Lee S, et al. Ossification of the pos-
defect caused by a redundant nerve root. Case terior longitudinal ligament: a review. Neurosurg
report. J Neurosurg 1968;28(4):391–3. Focus 2011;30(3):E1.
50. Schizas C, Rienmuller A, Pierzchala K, et al. Redun- 65. Naganawa T, Miyamoto K, Ogura H, et al. Compari-
dant nerve root sign. EuroSpine Liverpool, UK; 2013. son of magnetic resonance imaging and computed
51. Poureisa M, Daghighi MH, Eftekhari P, et al. Redun- tomogram-myelography for evaluation of cross sec-
dant nerve roots of the cauda equina in lumbar spi- tions of cervical spinal morphology. Spine (Phila Pa
nal canal stenosis, an MR study on 500 cases. Eur 1976) 2011;36(1):50–6.
Spine J 2015;24(10):2315–20. 66. Matsumoto M, Fujimura Y, Suzuki N, et al. MRI of cer-
52. Min JH, Jang JS, Lee SH. Clinical significance of vical intervertebral discs in asymptomatic subjects.
redundant nerve roots of the cauda equina in lumbar J Bone Joint Surg Br 1998;80(1):19–24.