Spinal Stenosis
Niall Craig Consultant Orthopaedic
Spinal Surgeon Aberdeen
25th February 2011
Plan
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Anatomy
History
Clinical Findings
Pathophysiology
Pain Sources
Investigation
Treatment
Spinal Stenosis
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Coined 1855-60
Greek derivation
Pathology – noun
Narrowing or stricture of a passage or canal
Commonest in the cervical and lumbar spine
Also occurs in the thoracic region
History
Henk Verbiest
First coined expression
lateral stenosis in
1940s
Dutch surgeon
Now we think of this
as lateral recess or
foraminal stenosis
Spinal Canal Development
185 skeletons from the Spitalfield Collection at
the Natural History Museum - French Huguenots
(1646 and 1852)
date of birth and death known
41 infants between 15 months and 5 years of age
L1 to L4 the cross sectional area and the mid
sagittal diameters - fully mature by 1 year
canal size reached maturity at L5 by 5 years of
age gradual trend from a circular towards a trefoil
shape at L5 – trefoil shape not present prior to
adulthood.
Anatomy
C – central zone
F – foramen
E – extraforaminal zone
Normal relationships
Remember most people with
symptoms will not have
normal anatomy
Anatomy
Normal canal showing space
available space for thecal sac and
exiting roots
Specimen courtesy of Prof
Rauschning Uppsala
Lateral Recess Stenosis
• Lateral region is compartmentalized into
entrance zone, mid zone, exit zone, and farout stenosis
Classification
• Keim et al mention the following simplistic LSS
anatomical classification scheme:2
• Lateral, secondary to SAP hypertrophy
• Medial, secondary to IAP hypertrophy
• Central, due to hypertrophic spurring, bony
projection, or ligamentum flavum/laminar
thickening
• Fleur de lis (clover leaf), from laminar thickening
with subsequent posterolateral bulging
Lateral Recess Stenosis
• Lateral recess stenosis (ie, lateral gutter
stenosis, subarticular stenosis, subpedicular
stenosis, foraminal canal stenosis,
intervertebral foramen stenosis) - narrowing
(less than 3-4 mm) between the facet superior
articulating process (SAP) and posterior
vertebral margin - impinge the nerve root and
subsequently elicit radicular pain.
Entrance Zone
• The entrance zone - medial to the pedicle and
SAP – stenosis from facet joint SAP hypertrophy.
• Other causes - developmentally short pedicle and
facet joint morphology, as well as osteophytosis
• Disc prolapse anterior to the nerve root
• The lumbar nerve root compressed below SAP
retains the same segmental number as the
involved vertebral level (eg, L5 nerve root is
impinged by L5 SAP).
Mid Zone
• Mid zone extends from the medial to the
lateral pedicle edge. Mid-zone stenosis arises
from osteophytosis under the pars
interarticularis and bursal or fibrocartilaginous
hypertrophy at a spondylolytic defect
Exit Zone
• Exit-zone stenosis involves an area
surrounding the foramen and arises from facet
joint hypertrophy and subluxation, as well as
superior disc margin osteophytosis. Such
stenosis may impinge the exiting spinal nerve
Extra-canalicular Stenosis
• Far-out (extracanalicular) stenosis entails
compression lateral to the exit zone
• Occurs with far lateral vertebral body endplate
osteophytosis and when the sacral ala and L5
transverse process impinge on the L5 spinal
nerve
History
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Patient will describe buttock pain or leg pain
Heaviness weakness
Tiredness in legs on walking
Neurogenic claudication
History
• Lumbar spinal stenosis classically presents as
bilateral neurogenic claudication
• Unilateral radicular symptoms may result from
severe foraminal or lateral recess stenosis
• Patients, typically aged more than 50 years
• insidious-onset NC - intermittent, crampy, diffuse
radiating thigh or leg pain with associated
paresthesias
• Leg pain affects 90% of patients with LSS
History
• Retrospective review of 75 patients with
radiographically confirmed LSS, reports of weakness,
numbness or tingling, radicular pain, and NC were in
almost equal proportions. The most common symptom
was numbness or tingling of the legs
• NC pain exacerbated by standing erect and downhill
ambulation, alleviated with lying supine more than
prone, sitting, squatting, and lumbar flexion
• Getty et al documented 80% pain diminution with
sitting and 75% with forward bending.9
History
• Lumbar spinal canal and lateral recess cross-sectional
area increases with spinal flexion and decreases with
extension
• cross-sectional area is reduced 9% with extension in
the normal spine and 67% with severe stenosis
• Penning rule of progressive narrowing implies that the
more narrowed the canal by stenosis, the more it
narrows with spinal extension
• Schonstrom et al have shown that spinal compressive
loading from weight bearing reduces spinal canal
dimensions
History
• NC not exacerbated with biking, uphill
ambulation, and lumbar flexion and is not
alleviated with standing
• compensate for symptoms by flexing forward,
slowing their gait, leaning onto objects (eg, over a
shopping trolley) and limiting distance of
ambulation. Unfortunately this promotes disease
progression and vertebral fracture. Pain radiates
downward in NC and up in vascular claudication
• Hall et al note the presence of radiculopathy in
6% and NC in 94% of LSS patients
History
• Distinguishing between neurogenic and vascular
claudication is important
• Treatments and implications quite different
• Vascular claudication is a manifestation of
peripheral vascular disease and arteriosclerosis.
Other vessels, including the coronary, vertebral,
and carotid, are also often affected
• Remember neurogenic and vascular claudication
may occur together
Pathophysiology
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Congenital
Narrow canal
Short pedicles
Arrested growth
Achondroplasia
Congenital or Primary
• Congenital malformations and developmental
flaws
• incomplete vertebral arch closure (spinal
dysraphism), segmentation failure,
achondroplasia, and osteopetrosis
• developmental early vertebral arch ossification,
shortened pedicles, thoracolumbar kyphosis,
apical vertebral wedging, anterior vertebral
beaking (Morquio syndrome), and osseous
exostosis
• uncommon, occurring in only 9% of cases.
Pathophysiology
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Acquired
By far the commonest
Aging spine
Osteopetrosis
Paget’s disease
Acquired or Secondary
• Secondary (acquired) from degenerative changes,
iatrogenic causes, systemic processes, and trauma.
• Degenerative changes - central canal and lateral recess
stenosis from posterior disc protrusion, zygapophyseal
joint and ligamentum flavum hypertrophy, and
spondylolisthesis
• Iatrogenic - surgical procedures such as laminectomy,
fusion, and discectomy. Systemic processes that may
be involved in secondary stenosis include Paget
disease, fluorosis, acromegaly, neoplasm, and
ankylosing spondylitis
Lumbar Stenosis
disc degeneration and facet arthropathy investigated
extensively
nature and etiology of pain generation - still debated
degeneration of the annulus fibrosis - radial tears through
which a posteriorly migrated nucleus pulposus can herniate
disc herniation in the typical posterolateral region
nerve root impingement (usually of the root passing to the
next lower foramen).
lateral recess stenosis is the result of such herniations,
leading to radiculopathy. The most common site for this is
L5-S1 followed by L4-L5. Central disk bulges or herniations
contribute to central canal stenosis
Pathophysiology
Disc degeneration
Facet arthrosis
Hypertrophy of the
ligamentum flavum
Pathophysiology
Canal narrowing
Venous stricture
Cervical Stenosis
• Congenital cervical stenosis predisposes to myelopathy
• age-related degenerative changes of the cervical spine
• These changes can narrow the cervical spinal canal.
Cervical spondylotic myelopathy (CSM) - clinical
presentation resulting from these degenerative
processes
• most common cause of spinal cord dysfunction in
adults older than 55 years
• degenerative changes of the cervical spine 95% of
asymptomatic individuals older than 65 years.
Myelopathy is believed to develop in up to 20% of
individuals with evidence of spondylosis
Cervical Stenosis
Lumbar Stenosis
• Narrowing of canal increasingly common
• 1 per 1000 persons older than 65 years
• degeneration of vertebral motion segment
(intervertebral disk and facet joints
• pathophysiologic mechanism involved with
the development of stenosis
Cause of Symptoms
• Cauda equina microvascular ischemia, venous
congestion, axonal injury, and intraneural fibrosis.
• Ooi at al myeloscopically observed ambulationprovoked cauda equina blood vessel dilation with
subsequent circulatory stagnation
• Ambulation dilates the epidural venous plexus,
which, amidst narrow spinal canal diameter,
increases epidural and intrathecal pressure
• This ultimately compresses the cauda equina,
compromises its microcirculation, and causes
pain.
Causes of Symptoms
• Another pain generator may be the DRG, which
contains pain-mediating neuropeptides, such as
substance P - possibly increase with mechanical
compression
• DRG varies spatially within the lumbosacral spine
• L4 and L5 DRG in an intraforaminal position
• S1 DRG located intraspinally
• This may lead to stenotic compression with
subsequent radicular symptomology
Causes of Pain
Severe radiologic stenosis in otherwise
asymptomatic individuals suggests
inflammation, not just mechanical nerve root
compression
Specific inflammation generators may include
disc prolapses, ligamentum flavum, and facet
joint capsule
Causes of Pain
• Katz et al report that the historical findings
associated with LSS include advanced age, severe
lower extremity pain, and absence of pain when
the patient is in a flexed position
• Fritz et al - most important elements involve the
postural nature of the patient's pain
• absence of pain or improvement of symptoms
when seated assists in ruling in LSS
• Stenosis cannot be ruled out when sitting is the
most comfortable position for the patient and
standing/walking is the least comfortable
Clinical Findings
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Physical examination findings frequently normal
diminished lumbar extension appears most consistent
loss of lumbar lordosis and forward-flexed gait
Radiculopathy may be noted with motor, sensory,
and/or reflex abnormalities
• Asymmetric muscle stretch reflexes and focal
myotomal weakness with atrophy occur with lateral
recess
• Some report objective neurologic deficits in
approximately 50% of LSS cases
• Pain on walking
Clinical Findings
• may also have a positive stoop test
• Dyck in 1979 - patient walks with an exaggerated
lumbar lordosis until symptoms appear or are
worsened.
• Then leans forward. Reduction of symptoms
positive
• Negative findings in the physical examination
include skin color, turgor, and temperature;
normal distal lower extremity pulses; and an
absence of arterial bruits
• Always check the pulses
Studies
• Katz et al - examination findings most strongly
associated with LSS include wide-based gait, abnormal
Romberg test, thigh pain following 30 seconds of
lumbar extension, and neuromuscular abnormalities
• Fritz et al - examination findings do not seem helpful
• Johnsson et al - single study of the natural course unchanged symptoms in 70% , improvement in 15%,
and worsening in 15% after a 49-month observation
period. Walking capacity improved in 37% of patients,
remained unchanged in 33%, and worsened in 30%
Studies
• Amundsen et al - concomitant lateral recess
stenosis all cases of central canal stenosis
• In his study, pure central stenosis without
lateral stenosis failed to exist
Investigations
• Plain radiographs - narrow anteroposterior
diameter in both congenital and acquired
spinal stenosis
• degenerative changes and spondylolisthesis
• CT - info. on canal diameter, spur formation,
and foraminal stenosis
• with myelography - demonstrates central or
lateral canal stenosis (sagittal and axial planes)
Investigations
• MRI - most useful for soft tissues and neural
structures
• disc degeneration, ligamentous and facet
hypertrophy, malalignment, central or lateral
canal stenosis, and intrinsic cord or root
abnormalities (syrinx or contusion)
• MRI is not optimal for visualization of bony
details (ie, spurs).
Investigations
• Myelography can be diagnostic
• revealing a narrow dye column or a complete
blockage in advanced forms
• Lumbar puncture may be difficult in severe
stenosis
• Combined CT and myelography provide most
information in sagittal and axial planes
• good visualization of bony anatomy.
CT
Myelogram
MRI
MRI
MRI
MRI
MRI Lateral Recess Stenosis
Treatment
• Cervical stenosis progresses in as many as one
third of affected individuals
• propensity for initial deterioration, followed by a
period of stability (may require years), and
subsequent progressive myelopathy
• Late treatment of myelopathy by decompression
does not always reverse the neurologic deficit,
and thus, individuals with severe cervical stenosis
should undergo close neurologic follow-up
Treatment
• Natural history lumbar stenosis not well
understood
• Slow progression in all
• Even if very6 narrow - very unlikely to develop
an acute cauda equina syndrome
• Slow progression leads to a feeling of heaviness
in the legs relieved by rest.
• Infrequently, a facet cyst will lead to severe canal
stenosis and subacute radiculopathy
• Pain and mild weakness
Treatment
• Nonsurgical measures aimed at symptomatic
relief: analgesics, anti-inflammatory agents
(including judicious use of steroids), and
antispasmodics can provide relief during acute
exacerbations
Treatment
• Epidural steroids have been used
• success rate low.
• Physical therapy with traction and
strengthening exercises helps relieve
associated symptoms or muscular spasms and
mechanical back pain
• Only provide temporary relief
• Inversion tables - great initial success and
varying benefit
Surgical Treatment
• Surgery - indicated for significant myelopathy,
radiculopathy, and/or neurogenic claudication
• Choice of - approach depends on the spinal
region, the spinal alignment, and the
anatomic nature of the compressive elements
(ie, spurs vs ligamentum flavum)
• Controversy about need for concomitant
stabilization - reserved for gross instability
(eg, unstable spondylolisthesis).
Surgical Treatment
• Cervical spine - anterior versus posterior approaches.
Posterior decompressive laminectomy in multilevel disease
and congenital stenosis
• can lead to instability and kyphotic (swan neck) deformity
• laminoplasty (typically used in younger patients) to
preserve the integrity of the posterior elements and motion
• arthrodesis and fixation (ie, lateral mass fixation) reduces
the risk of postoperative instability and deformity
• limits flexibility
• posterior approach is not recommended as the sole
approach for the kyphotic cervical spine
Cervical Disc Replacement
Surgical Treatment
• The anterior approach addresses the pathology
from disc herniation and spur formation
• can be used with almost any spinal alignment,
but associated risks of morbidity exist. Singlelevel discectomies can be performed with or
without concomitant fusion with good results
• most surgeons believe the risk of collapse is
present without the placement of an interbody
graft, spacer, cage, or disc replacement device
Surgical Treatment
• Plate is not always needed in single-level disease
• multilevel discectomies or corpectomies anterior
fixation should be strongly considered
• risk of complications is higher when corpectomies
are performed on 3 or more levels
• some augment their multilevel anterior
decompression and fusion with posterior
stabilization
• decision-making - alignment of the spine, the
nature of the compressive element, and the
surgeon's preference
Surgical Treatment
• Lumbar spine - single or multilevel laminotomy for
canal decompression and foraminotomy
• Partial or complete facetectomies and discectomy may
be needed
• microdecompression in the lateral recess with the use
of hemilaminotomies instead of complete
laminectomies preserve the biomechanical integrity of
the posterior tension band and avoid potential
instability or postlaminectomy flat-back syndrome
• bilateral total facetectomies consider concomitant
fusion and/or stabilisation
Surgical Treatmant
• Stabilisation in stable spinal stenosis is
controversial
• Some report the use of ipsilateral nerve root
decompression and fusion; others have reported
their preference of contralateral autologous bone
fusion to preserve segmental stability
• posterolateral intertransverse fusion bilaterally
through a midline approach with an autologous
hip graft, local autograft or allogaraft
• interbody space best biomechanically
Surgical Treatment
• Interbody fusion with transpedicular fixation
most stable
• Need for fusion controversial instability
• Anterior lumbar interbody fusion indirect root
decompression (restoration of disk space
height) used for severe back pain with limited
disc bulging
Lumbar Fusion
Wallis Ligament
Surgical Treatment
• Dynamic stabilization and mobile devices
• popular -protect adjacent segments from
more rapid degeneration
• Dynamic devices stiffen the spinal motion
segment but do not eliminate motion
completely
Surgical Treatment
• Minimally invasive techniques
• decrease trauma and indirectly decompress
neural elements
Surgical Treatment
• Internal fixation is controversial
• Better fusion results but outcome may not
improve significantly
• Pedicle screw fixation widely accepted device
• but associated with morbidity, increased
operative time
• Some use translaminar facet screws instead
Studies
• Chou et al
• randomized, controlled studies of surgery for symptomatic
spinal stenosis, nonradicular back pain with common
degenerative changes, and radiculopathy with herniated
lumbar disc
• surgery for symptomatic spinal stenosis and for
radiculopathy with herniated lumbar disc is associated with
short-term benefits (1-2 years) - benefits decreased over
time
• nonradicular back pain - fusion no more effective than
intensive rehabilitation, but small to moderate benefits
when compared to standard (nonintensive) nonsurgical
therapy
Studies
• Weinstein et al
• degenerative spondylolisthesis associated with
spinal stenosis to compare surgical versus
nonsurgical
• standard decompressive laminectomy (with or
without fusion) or nonoperative care
• degenerative spondylolisthesis and associated
spinal stenosis treated surgically maintained
substantially greater pain relief and improvement
in function for 4 years versus nonoperative
therapy.
Studies
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Voulgaris et al
prospective study of 23 patients who underwent decompressive
laminectomy for lumbar spinal stenosis
efficacy of transcranial motor evoked potentials (TcMEP) and
continuous electromyography (EMG) - prevent irreversible
pyramidal tract damage during laminectomy.
17 patients - an increase in TcMEP amplitudes of more than 50% slightly increased or remained unchanged in 6
increased TcMEP amplitudes - greatest improvement 3 and 12
months postoperatively, according to neurologic examination and
visual analog scale pain ratings
concluded that monitoring may allow rapid identification of
potential damage of the neural structures
Conclusion
• Management of spinal stenosis aimed at
symptomatic relief and prevention of neurologic
sequelae. Conservative measures - temporary
relief
• important preceding surgical decompression
• Surgery is recommended when significant
radiculopathy, myelopathy (cervicothoracic),
neurogenic claudication (lumbar), or
incapacitating pain is present
• Choice of procedure and the decision to fuse
individualised