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SPONDYLO is a
Greek word meaning vertebra. Spondylosis generally mean changes in the
vertebral joint characterized by increasing degeneration of the
intervertebral disc with subsequent changes in the bones and soft tissues.
Disc degeneration, spinal canal stenosis, spondylolisthesis are the
resultant pathological changes.
Disc degeneration
is the commonest pathological manifestation of
lumbar spondylosis.
(discussed elsewhere)
Lumbar spinal stenosis
can be defined as ‘narrowing of the lumbar canal in its central part, the
lateral recess or the intervertebral foramen sufficient to impair one or
more roots of the cauda, the impairment resulting in pain, unilateral or
bilateral neurological deficit or neurogenic intermittent claudication’.
Lumbar spinal stenosis appears in different pathological conditions. The
form that is discussed here is mainly due to degenerative disease. The
epidemiology of lumbar spinal stenosis has changed a great deal in the
last few decades, related to the ageing population of industrialized
countries, with a growing impact on national health systems.
Anatomy:
The
spinal canal is formed anteriorly by the intervertebral disc or the
vertebral body, lateral by the pedicles, posterolateral by the facet
joints and posteriorly by the laminae or the yellow ligament. The spinal
canal has paired lateral openings in each segment, the intervertebral
foramina.
The
lateral recess if the lateral part of the spinal canal. It begins at the
tip of the superior articular process of the inferior vertebra, which is
part of the facet joint. It is at this point where the recess is
narrowest. After bending laterally around the pedicle it ends caudal in
the broader lateral opening of the spinal canal, the intervertebral
foramen. The anterior wall of the lateral recess is bounded by the
intervertebral disc superiorly, and the vertebral body inferiorly. The
lateral walls are formed by the vertebral pedicles. The dorsal wall is
bounded by the superior articular process of the lower vertebra, to a
small part by the lamina and also by the yellow ligament. In a narrow
lateral recess, its dorsal walls built only by the articular process, and
it is the degenerative changes of this structure that account for most of
the nerve root compressions in lumbar spinal stenosis.
The nerve roots corresponding
to each segment are separated from the dural sac at the level of the
intervertebral space then they come to lie in the lateral recesses and
exit the spinal canal a level below through the intervertebral foramina.
At each of these points compression is possible.
Pathogenesis and classification:
The term
idiopathic developmental by Verbiest in 1954 as a disease of
unknown origin, with a genetic disturbance in which pathological effects
are revealed in their entirely only when growth is complete and the
vertebrae have attained full size’.
This review will
concentrate on the type of lumbar spinl stenosis that was classified as
idiopathic developmental stenosis by Verbiest or considered to be
degenerative lumbar spinal stenosis by other authors. Most authors accept
the theory that explains lumbar spinal stenosis through degenerative
changes that lead to instability and nerve root compression which causes
problems if the individual anatomy of the spinal canal is unfavorable.
Developmental and congenital factors include some of the anatomical
variations that leave less space for the nerve roots, so even minor
degenerative osseous changes can lead to nerve root compression: a shallow
spinal canal, a trefoil shaped canal, or anomalies of the nerve roots.
Anatomical variations in the orientation, shape, or asymmetry of the facet
joints make degeneration more likely that lead to nerve root compression.
Degeneration is more likely to cause symptomatic nerve root compression in
a narrow spinal canal, than in wide canal in which even pronounced
spondylosis or spondylarthrosis may stay clinically silent.
The
trefoil shape of the spinal canal is anatomical variation of the spinal
canal, caused by the orientation of the laminae and facet joints. Most
often it is found at the levels L3 to L5. This condition is considered to
be a predisposing factor for the development of lateral recess stenosis
through degenerative changes of the facet joints.
Anomalies of the nerve roots, (conjoined roots, redundant roots,
transverse roots) can also contribute to the development of signs. A
disproportion between the size of the lateral recess and the diameter of
an aberrant root is needed to develop symptoms.
Asymmetric facet joints hasten disc degeneration, frontally oriented facet
joints allow a wider range of lateral bending and therefore also have a
negative impact on disc integrity. At the same time they leave less
space in the lateral recess. Sagittally oriented joints allow easier
sagittal displacement of a vertebra-development of degenerative
spondylolisthesis.
Acquired factors
include all degenerative changes that lead to osseous and non-osseous
nerve root compression.
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Morphologically the following forms of impingement of nervous
structures occur either alone or in combination can be differentiated
in lumbar spinal stenosis:
·
Central spinal stenosis
· Lateral
recess stenosis
· Narrowing
of the intervertebral foramen
· Non-osseous
nerve root compression
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| spinal
canal stenosis-Axial MRI |
Facetal hypertrophy-MRI sagittal |
Spinal
canal stenosis-Sagittal MRI |
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The
causes of central spinal stenosis are spondylarthrosis, formation of
spondylotic ridges, thickened lamina, or degenerative spondylolisthesis.
Spondylarthrotic facet joints can almost touch, narrowing the posterior
portion of the spinal canal. Spondylosis with posteriorly directed
oesteophytes, combined with spondylarthrosis can cause marked narrowing of
the spinal canal with little space left for the nerve roots and an atrophy
of the epidural fat. Thickening of the lamina occurs in advanced cases of
degenerative changes and plays a minor role in reducing the diameter of
the canal.
Different parameters have been used to measure the extent of central
stenosis of the spinal canal, among them measurement of the sagittal
diameters of the spinal canal and measurement of the dural tube in square
millimeters are commonly employed. The traditional measurement of the
sagittal diameter, under 10 mm being considered pathological.
Lateral
recess stenosis is the most common form of degenerative spinal stenosis
that occurs either alone or in combination with central stenosis. Usually
the compression of the nerve root is caused by a spondylarthrotic facet
joint that narrows the subarticular portion of the spinal canal.
Measurement of the width of the lateral recess with values of 2 mm and
less are considered to be pathological. Another possible point of
compression of the nerve root is a narrowing of the most distal part of
the lateral recess, the intervertebral foramen.
Degenerative spondylolisthesis (pseudospondylolisthesis or
degenerative anterior vertebral translation) affects older patients, but
is increasingly seen in middle aged patients, even at the age of 40, the
L4/5 segment being most frequently involved. Sagittal orientation of the
facet joints, surgical removal of the inferior articular process and
degenerative changes of the superior articular process are the
predisposing factors. Due to the anteriorly oriented facet joints, the
L5/S1 segment is rarely involved. Typically, the degree of slipping in
degenerative spondylolisthsis does not exceed 25%.
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Degenerative changes are primarily due to disc degeneration, which
occurs with ageing, infection or trauma. A degenerated disc leads to
narrowing of the intervertebral space and usually is accompanied by
spondylosis, with formation of spondylotic ridges. Degeneration and
loss of height of the disc occurs first in the posterior part. This
deformation of the disc, combined with the plane of orientation of the
facet joints leads to retrolisthesis of the cranial vertebra, which is
the most common form of degenerative vertebral translation. A change
in the relationship of the facet joints causes subluxation, distension
of the joint capsule and spondylarthrosis. Subluxation of the facet
joint occurs first and leads to symptoms only in a lordotic
posture. Degenerative listhesis may present as lumbar instability,
with or without stenosis. In the advanced stage it is fixed, with a
thickened capsule and joints, giving rise to permanent symptoms.
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Clinical
features:
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Spondylolisthesis |
Although
a number of patients have permanent symptoms, the majority of patients
with lumbar spinal stenosis experience symptoms while standing or
walking. Symptoms or signs that occur while walking lead to neurogenic
claudication. Over some time of walking distance shortens, sometimes so
dramatically as to prevent the patient making more than a few steps.
Paucity of findings at physical examination even in a patient with
advanced symptoms is typical.
Permanent symptoms and signs unrelated to posture are caused by a
permanent compression of the nerve roots. Leg pain, motor deficit sensory
deficit and rarely, urinary dysfunction or impotence can be found in this
order of frequency.
Intermittent symptoms and signs occur while the patient is standing,
including low back pain, referred pain or back weakness. These symptoms
are related to a narrowing of the lateral recess while the spine is
extended. Therefore, symptoms are triggered or worsened in postures that
aggravate lumbar lordosis, including standing, walking, especially
downhill or downstairs, as well as while wearing shoes with high heels.
Low back
pain is a common complaint for a long time before radicular compression
occurs. Back weakness is a specific complaint described by patients as if
their back is going to give away, probably caused by a proprioceptive
sensation from vertebral joints and muscles. Both complaints, as well as
the referred pain (pseudoradicular pain) are due to segmental instability
of the spine and are relieved by a posture that diminishes lumbar lordosis:
leaning forward while walking, standing, sitting or by lying down. While
walking, permanent symptoms can spread to previously unaffected dermatomes
or to the other leg, indicating involvement of other nerve roots. Leg
pain can even diminish, which is an unexplained phenomenon. Due to
postural widening of the foramina, some patients are able to ride a
bicycle without complaints, at the same time having intermittent symptoms
after only a short walking distance.
Neurogenic intermittent claudication is experienced by up to 80% of
patients, depending on the severity of narrowing of the spinal canal.
Symptoms and signs leading to it are motor deficit, sensory deficit, leg
pain, in that order of frequency and rarely urinary incontinence. Resting
with the lumbar spine flexed lessens the symptoms, but not resting in
erect posture, in contrast t vascular intermittent claudication.
Neurogenic
intermittent claudication is caused by the insufficiency of vascular
supply in one or more nerve roots of the cauda equine occurring during
motor activity and the increased oxygen demand related to it. A focal
area of deprived circulation occurs at the point of mechanical
compression, with neuronal hyperexcitability that leads to pain or
paresthesia. Demyelination or loss of large neuronal fibres leads to
weakness and numbness. Another effect of mechanical compression is the
archnoidal adhesions that fix the nerve root and impair CSF circulation
around it with a negative impact on its metabolism.
Imaging:
Plain
X-rays in anteroposterior, lateral and oblique views are useful in
showing lumbarisation or sacralisation, in determining the shape of the
intervertebral formina and the facet joints, showing spondylosis,
spondlarthrosis, retrolisthesis, spondylolysis and spondylolisthesis.
Central spinal stenosis or lateral recess stenosis cannot be quantified by
this method.
Myelography
(out dated now) was helpful in determining the degree and longitudinal
extent of stenosis because more than one point of compression may be
insufficient.
CT
is the best method to evaluate osseous compression and at the same
time other structures are visualized. With 3 mm thick slices the size and
shape of the spinal canal, lateral recess, facet joints, laminae, as well
as the morphology of the intervertebral disc, epidural fat and ligamentum
flavum are shown.
MRI
is clearly superior to CT in the visualization of non-osseous
structures and currently the best method for evaluating the contents of
the spinal canal. Despite this, apart of showing disc degeneration in
T2-weighted images, it usually does not add substantial information
necessary in the diagnosis of lumbar spinal stenosis. However, considering
the rapidly growing experience with MRI, which is a non-invasive method
the role of MRI in the diagnosis of this disease, will increase.
Especially a possibility of performing functional sequences of the lumbar
spine would be very valuable.
It
is very important that all radiological findings are correlated with the
symptoms, since asymptomatic narrowing seen on MRI or CT is often found,
either as stenosis of an asymptomatic segment, or in completely
asymptomatic patients and should be ignored.
Treatment:
The treatment has to be adapted to the patient, his age and aims. In the
majority of patients a significant improvement or a relief of symptoms can
be achieved. Radicular symptoms and neurogenic intermittent claudication
are more likely to resolve with treatment than back pain, which persists
in up to one third of patients.
Conservative treatment consists of analgesia and wearing a lumbar
corset which by alleviating lumbar lordosis can lessen symptoms and
increase the walking distance. For a group of patients the relief they
experience is satisfactory and the walking distance suffices for their
daily needs.
A trial
of three months’ duration is recommended as the initial form of
treatment, unless motor deficit or progressive neurological deficit is
present. Conservative therapy of lumbar spinal stenosis with permanent
symptoms is rarely successful on a long term basis, in contrast to
conservative therapy of a herniated disc.
Surgical treatment is indicated if conservative therapy fails, and
in the presence of incapacitating permanent symptoms, especially a motor
deficit. Depending on the clinical symptoms and signs, and partly due to
a different approach to lumbar spinal stenosis three groups of operative
procedures are performed:
·
decompression operations
·
combined decompression and stabilization of unstable motion
segments
·
operative stabilization of unstable motion segments alone.
The
decompression procedures are: decompression of the spinal canal,
decompression of the spinal canal with decompression of the lateral recess
and the intervertebral foramen, selective decompression of the nerve
roots.
1)Decompression of the Spinal Canal
Laminectomy is the standard method of decompression of the central
part of the spinal canal. The advantages are that it is usually easily
performed and has a high initial success rate. The failure rate with
recurrence of symptoms was one fourth of patients after 5 years in one
study. There is a relatively low rate of non-specific postoperative
complications and epidural scarring.
Traditionally, laminectomy alone was thought not to impair the stability
of the lumbar spine, as long as the other structures of the spine were
intact, particularly in older patients. In a degenerative spine other
important elements such as the intervertebral disc and facet joints are
often impaired. This might explain the occurrence of postoperative
spondylolisthsis after laminectomy, which leads to a poor result.
If
laminectomy is performed in the presence of degenerative spondylolisthsis
or if it is combined with operative impairment of the disc or the facet
joints there is a high incidence of postoperative instability.
Preservation of the disc, even of a degenerated one, seems to help
segmental stability (Goel, 1986). It is for this reason that discectomy
is not recommended in lumbar spinal stenosis in which the symptoms are
precipitated through a disc protrusion or herniation, unless the herniated
disc compresses the nerve root even after decompression of the lateral
recesses.
Epidural
scarring occurs after laminectomy and is sometimes located in the next,
non-operated segment. If scarring is very pronounced, it is termed
‘postlaminectomy membrane’. Fat auto transplants are applied epidurally
by some surgeons in an attempt to reduce fibrosis. While some results
seem to support this, postoperative swelling of fat can result in nerve
root compression.
If
decompression has to be performed in a patient with osteoporosis, it
should be very limited, since eventual postoperative instability is
difficult to treat.
Laminectomy with partial facetectomy is the standard procedure in
the treatment of spinal canal stenosis associated with lateral recess
stenosis. It is seldom that a pure laminectomy is sufficient in spinal
canal stenosis, so it usually has to be combined with some form of partial
facetectmy. “unroofing” of the vertebral foramen in the strict sense of
the word can be performed only from a lateral approach, as for an
extraforaminal herniation of the disc.
Another
infrequently used possibility is the wedge procedures (laminoplasty),
with removal and reinsertion of the laminar arches and spinous process.
2)Selective Nerve root decompression:
Unless a
pronounced narrowing of the sagittal diameter of the spinal canal exists,
a selective nerve root decompression can suffice, especially if the
patient has strictly unilateral symptoms. A medial facetectomy through a
laminotomy can be performed. Usually the medial portion of the facet joint
that overlies the nerve root is removed. Specific complications of the
procedure include insufficient decompression, instability caused by a
removal of 30%-50% of the facet joint, or a fatigue fracture of the
thinned pars articularis.
3)Decompression and stabilization:
Laminectomy can be combined with various methods of stabilization. Newer
systems using pedicular screws, as well as older systems like the Knodt
rods, Harrington rods, and the Luque frame with sublaminl wiring are used.
In
degenerative spondylolisthesis laminectomy and intertransverse process
fusion with or without internal fixation is thestandard procedure,
posterior lumbar interbody fusion and anterior interbody fusion are
alternatives. Laminectomy with spinal fusion, some claim, is superior to
laminectomy alone, since laminectomy alone was associated with a high
incidence of progressive spondylolisthsis.
Complications of stabilization procedures include breakage of
osteosynthetic material, neurovascular trauma, fractures of the spinous
process, the laminae or the pedicles, pseudoarthrosis, paralytic ileus,
and pain at the iliac graft donor site. Degeneration and postfusion
stenosis at the next motion segment to a fusion caused by hypermobility
may occur. Although experimental results support this theory, the
clinical effects of this complication are unknown.
Apart
from degenerative spondylolisthesis where decompression and stabilization
is the recommended procedure, there is no consensus as to the most
effective treatment. Lumbar spinal stenosis is treated operatively
in a large number of series, with favorable short term results. However,
after more than 40 years of research and experience in treatment the
etiology is not fully understood. In addition, definition and
classification are difficult because the degree of stenosis does not
always correlate with symptoms.
A
recommended surgical protocol is
·
in patients who have permanent symptoms that increase on standing
or cause neurogenic intermittent claudication decompression and
stabilization,
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in patients who have no permanent symptoms but clearly posture
related intermittent symptoms a stabilization procedure, especially if
there is relief with a lumbar brace.
Weight reduction, and
exercises to improve posture and strengthen abdominal and spinal muscles
must accompany any form of
treatment, surgical or conservative. |
