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Lumbar spinal stenosis

Lumbar spinal stenosis (LSS) is a medical condition


Lumbar spinal stenosis
in which the spinal canal narrows and compresses the
nerves and blood vessels at the level of the lumbar
vertebrae. Spinal stenosis may also affect the cervical
or thoracic region, in which case it is known as
cervical spinal stenosis or thoracic spinal stenosis.
Lumbar spinal stenosis can cause pain in the low back
or buttocks, abnormal sensations, and the absence of
sensation (numbness) in the legs, thighs, feet, or
buttocks, or loss of bladder and bowel control.

The precise cause of LSS is unclear. Narrowing of


spinal structures in the spinal cord such as the central
canal, the lateral recesses, or the intervertebral
foramen (the opening where a spinal nerve root Lumbar vertebra showing central stenosis and
passes) must be present, but are not sufficient to cause lateral recess stenosis.
LSS alone.[1] Many people who undergo MRI
Specialty Orthopedics
imaging are found to have such changes but have no
symptoms.[1] These changes are commonly seen in Symptoms Pain, numbness, or weakness in
people who suffer from spinal degeneration that the low back, buttocks, or legs
occurs with aging (e.g., spinal disc herniation). LSS typically worsened with prolonged
may also be caused by osteophytes, osteoporosis, a walking or standing and relieved
tumor, trauma, or various skeletal dysplasias, such as with sitting or lying down
with pseudoachondroplasia and achondroplasia. Usual Gradual (months to years)
onset
Medical professionals may clinically diagnose lumbar
Types Congenital, acquired
spinal stenosis using a combination of a thorough
medical history, physical examination, and imaging Causes Narrowed spinal cord due to spinal
(CT or MRI).[1] EMG may be helpful if the diagnosis degeneration or abnormal
is unclear.[1] Useful clues that support a diagnosis of anatomy
LSS are age; radiating leg pain that worsens with Diagnostic Clinical (a combination of history,
prolonged standing or walking (neurogenic method physical examination, and
claudication) and is relieved by sitting, lying down, or imaging)
bending forward at the waist; and a wide stance when Differential Claudication from peripheral artery
walking.[1] Other helpful clues may include objective diagnosis disease
weakness or decreased sensation in the legs, decreased
Treatment Medication, physiotherapy,
reflexes in the legs, and balance difficulties, all of
injections, surgery
which are strongly associated with LSS.[1] Most
people with LSS qualify for initial conservative non-operative treatment. Nonsurgical treatments include
medications, physiotherapy, and injection procedures.[1] Decompressive spinal surgery may modestly
improve outcomes but carries greater risk than conservative treatment.[1] Overall, there is limited
supporting evidence to determine the most effective surgical or nonsurgical treatment for people with
symptomatic LSS.[1] Evidence to support the use of acupuncture is also limited.[1]
Lumbar spinal stenosis is a common condition and causes substantial morbidity and disability. It is the
most common reason people over the age of 65 pursue spinal surgery.[1] The condition affects over
200,000 people in the United States.[1]

Contents
Signs and symptoms
Causes
Degenerative spondylolisthesis
Ankylosing spondylitis
Diagnosis
Bicycle test of van Gelderen
MRI
Establishing the diagnosis
Management
Medication
Surgery
Prognosis
Epidemiology
History
Society and culture
United States
References
External links

Signs and symptoms


Understanding the meaning of signs and symptoms of lumbar stenosis requires an understanding of what
the syndrome is, and the prevalence of the condition. A recent review of lumbar stenosis in the Journal of
the American Medical Association's "Rational Clinical Examination Series"[2] emphasized that the
syndrome can be considered when lower extremity pain occurs in combination with back pain. The
syndrome occurs in 12% of older community-dwelling men[3] and up to 21% of those in retirement
communities.[4]

Because the leg symptoms in lumbar spinal stenosis (LSS) are similar to those found with vascular
claudication, the term pseudoclaudication is often used for symptoms of LSS.[5] These symptoms include
pain, weakness, and tingling of the legs,[5] which may radiate down the legs to the feet.[6] Additional
symptoms in the legs may be fatigue, heaviness, weakness, a sensation of tingling, pricking, or
numbness, and leg cramps, as well as bladder symptoms.[6] Symptoms are most commonly bilateral and
symmetrical, but they may be unilateral; leg pain is usually more troubling than back pain.[6]

Pseudoclaudication, now generally referred to as neurogenic claudication, typically worsens with


standing or walking, and improves with sitting, and is often related to posture and lumbar extension.
Lying on the side is often more comfortable than lying flat, since it permits greater lumbar flexion.
Vascular claudication can resemble spinal stenosis, and some individuals experience unilateral or
bilateral symptoms radiating down the legs rather than true claudication.[7]

The first symptoms of stenosis include bouts of low back pain. After a few months or years, this may
progress to claudication. The pain may be radicular, following the classic neurologic pathways. This
occurs as the spinal nerves or spinal cord become increasingly trapped in a smaller space within the
canal. Determining whether pain in the elderly is caused by lack of blood supply or stenosis is difficult;
testing can usually differentiate between them, but patients can have both vascular disease in the legs and
spinal stenosis.

Among people with lower-extremity pain in combination with back pain, lumbar stenosis as the cause is
two times more likely in those older than 70 years of age while in those younger than 60 years it is less
than half as likely. The character of the pain is also useful for diagnosis. When the discomfort does not
occur while seated, the likelihood of lumbar spinal stenosis increases considerably, around 7.4 times.
Other features increasing the likelihood of lumbar stenosis are improvement in symptoms on bending
forward (6.4 times), pain that occurs in both buttocks or legs (6.3 times), and the presence of neurogenic
claudication (3.7 times).[2] On the other hand, the absence of neurogenic claudication makes lumbar
stenosis much less likely as the explanation for the pain.[8]

Causes
Spinal stenosis may be congenital (rarely) or acquired (degenerative), overlapping changes normally seen
in the aging spine.[6][7] Stenosis can occur as either central stenosis (the narrowing of the entire canal) or
foraminal stenosis (the narrowing of the foramen through which the nerve root exits the spinal canal).
Severe narrowing of the lateral portion of the canal is called lateral recess stenosis. The ligamentum
flavum (yellow ligament), an important structural component intimately adjacent to the posterior portion
of the dural sac (nerve sac) can become thickened and cause stenosis. The articular facets, also in the
posterior portion of the bony spine can become thickened and enlarged, causing stenosis. These changes
are often called “trophic changes” or “facet trophism” in radiology reports. As the canal becomes smaller,
resembling a triangular shape, it is called a "trefoil" canal.

Degenerative spondylolisthesis
Forward displacement of a proximal vertebra in relation to its adjacent vertebra in association with an
intact neural arch, and in the presence of degenerative changes, is known as degenerative
spondylolisthesis,[9][10] which narrows the spinal canal, and symptoms of spinal stenosis are common. Of
these, neural claudication is most common. Any forward slipping of one vertebra on another can cause
spinal stenosis by narrowing the canal. If this forward slipping narrows the canal sufficiently, and
impinges on the contents of the spinal column, it is spinal stenosis by definition. If associated symptoms
of narrowing exist, the diagnosis of spinal stenosis is confirmed. With increasing age, the occurrence of
degenerative spondylolisthesis becomes more common. The most common spondylolisthesis occurs with
slipping of L4 on L5. Frymoyer showed that spondylolisthesis with canal stenosis is more common in
diabetic women who have undergone oophorectomy (removal of ovaries). The cause of symptoms in the
legs can be difficult to determine. A peripheral neuropathy secondary to diabetes can have the same
symptoms as spinal stenosis.[11]

Ankylosing spondylitis
L5 S1 Lumbar spine
Spondylolisthesis showing advanced
Grade II with ankylosing
forward slipping of spondylitis which
L5 on S1 <50% can lead to spinal
stenosis

Diagnosis
The diagnosis is based on clinical findings.[7] Some patients can
have a narrowed canal without symptoms, and do not require
therapy.

The normal lumbar central canal has a midsagittal diameter (front


to back) greater than 13 mm, with an area of 1.45 cm2. Relative
stenosis is said to exist when the anterior-posterior canal diameter
measures between 10 and 13 mm. Absolute stenosis of the
lumbar canal exists anatomically when the anterior-posterior
measurement is 10 mm or less.[12][13][14]
Normal lumbar vertebra showing
Plain X-rays of the lumbar or cervical spine may or may not large, round spinal canal
show spinal stenosis. The definitive diagnosis is established by
either computerized tomography or magnetic resonance imaging
(MRI) scanning. Identifying the presence of a narrowed canal makes the diagnosis of spinal
stenosis.[15][16][17]

Bicycle test of van Gelderen


In 1977, Dyck and Doyle reported on the bicycle test, a simple procedure in which the patient is asked to
pedal on a stationary bicycle. If the symptoms are caused by peripheral artery disease, the patient will
experience claudication, a sensation of not getting enough blood to the legs; if the symptoms are caused
by lumbar stenosis, symptoms will be relieved when the patient is leaning forward while bicycling.
Although diagnostic progress has been made with newer technical advances, the bicycle test remains an
inexpensive and easy way to distinguish between claudication caused by vascular disease and spinal
stenosis.[18]

MRI
MRI is the preferred method of diagnosing and evaluating spinal stenosis of all areas of the spine,
including cervical, thoracic, and lumbar.[19][20] MRI is useful to diagnose cervical spondylotic
myelopathy (degenerative arthritis of the cervical spine with associated damage to the spinal cord).[21]
The finding of degeneration of the cervical spinal cord on MRI can be ominous; the condition is called
myelomalacia or cord degeneration. It is seen as an increased signal on the MRI. In myelopathy
(pathology of the spinal cord) from degenerative changes, the findings are usually permanent and
decompressive laminectomy will not reverse the pathology. Surgery can stop the progression of the
condition. In cases where the MRI changes are due to vitamin B12 deficiency, a brighter prospect for
recovery can be expected.[22][23][24]

Establishing the diagnosis


The detection of spinal stenosis in the cervical, thoracic, or lumbar spine confirms only the anatomic
presence of a stenotic condition. This may or may not correlate with the diagnosis of spinal stenosis
which is based on clinical findings of radiculopathy, neurogenic claudication, weakness, bowel and
bladder dysfunction, spasticity, motor weakness, hyperreflexia and muscular atrophy. These findings,
taken from the history and physical examination of the patient (along with the anatomic demonstration of
stenosis with an MRI or CT scan), establish the diagnosis.[25]

Management
Nonoperative therapies and laminectomy are the standard treatment for LSS.[26] A trial of conservative
treatment is typically recommended.[7] Individuals are generally advised to avoid stressing the lower
back, particularly with the spine extended. A physical-therapy program to provide core strengthening and
aerobic conditioning may be recommended.[7] Overall scientific evidence is inconclusive on whether
conservative approach or a surgical treatment is better for lumbar spinal stenosis.[27]

Medication
The evidence for the use of medical interventions for LSS is poor.[28] Injectable but not nasal calcitonin
may be useful for short-term pain relief.[28] Epidural blocks may also transiently decrease pain, but no
evidence of long-term effect has been found.[28] Adding corticosteroids to these injections does not
improve the result;[28][29] the use of epidural steroid injections is controversial and evidence of their
efficacy is contradictory.[7]

Nonsteroidal anti-inflammatory drugs, muscle relaxants, and opioid analgesics are often used to treat low
back pain, but evidence of their efficacy is lacking.[7]

Surgery
Surgery appears to lead to better outcomes if symptoms continue after 3–6 months of conservative
treatment.[30] Laminectomy is the most effective of the surgical treatments.[26] In those who worsen
despite conservative treatments surgery leads to improvement in 60–70% of cases.[7] Another procedure
using an interspinous distraction device known as X-STOP was less effective and more expensive when
more than one spinal levels are repaired.[26] Both surgical procedures are more expensive than medical
management.[26]
Prognosis
Most people with mild to moderate symptoms do not get worse.[7] While many improve in the short term
after surgery, this improvement decreases somewhat with time.[7] A number of factors present before
surgery are able to predict the outcome after surgery, with people with depression, cardiovascular disease,
and scoliosis doing in general worse, while those with more severe stenosis beforehand and better overall
health doing better.[6]

The natural evolution of disc disease and degeneration leads to stiffening of the intervertebral joint. This
leads to osteophyte formation—a bony overgrowth about the joint. This process is called spondylosis,
and is part of the normal aging of the spine. This has been seen in studies of normal and diseased spines.
Degenerative changes begin to occur without symptoms as early as age 25–30 years. Not uncommonly,
people experience at least one severe case of low back pain by the age of 35. This can be expected to
improve and become less prevalent as the individual develops osteophyte formation around the discs.[31]

In the US workers' compensation system, once the threshold of two major spinal surgeries is reached, the
vast majority of workers never return to any form of gainful employment. Beyond two spinal surgeries,
any more are likely to make the patient worse, not better.[32]

Epidemiology
There are many causes for spinal stenosis but degenerative changes are a precursor to spinal stenosis
becoming symptomatic.[33] While the exact prevalence of degenerative LSS is unknown, it is estimated
that it ranges from 1.7% - 13.1%.[34] However, the results from these statistics have been put into
question. This is mainly due to unclear diagnostic criteria. For example, magnetic resonance imaging
(MRI) and computed tomography (CT) are the most common ways to diagnosis LSS, but clinically
significant definitions of canal, foraminal, or subarticular narrowing do not exist.

In addition to this, the lumbar and cervical types are more common than the rarer thoracic stenosis.[35]
Although stenosis can be found isolated in one region of the spine, developmental spinal stenosis will
most likely involve both the cervical and lumbar sections.[36]

The age that people develop spinal stenosis is correlated with change in the joint’s biomechanics.[33]
Because of this, there has been a recent increasing trend seen by physicians, of lumbar spinal stenosis
being more commonly diagnosed in older patients. Low back pain accounts for 17% of all physician
visits of people aged 65 and older.[37] From this population, a large portion of radicular pain stems not
from disk pathology, but from lumbar spinal stenosis.[37] According to Kalff et al., 21% of people over
the age of 60 have lumbar spinal stenosis, as confirmed by radiological screening.[38] Degenerative
lumbar spinal stenosis has been predominantly seen in the 50 to 60-year-old population. A recent study in
Japan found that the incidence of LSS increases with age. The study supports that LSS incidence
increases incrementally in the following age groups, 1.7–2.2% in 40–49 years old population, and
10.3%–11.2% in 70–79 years old population.[39] It is estimated that around 200,000 adults are afflicted
with LSS in the United States and that by the year 2025, this number will rise to 64 million elderly.[34]
The syndrome occurs in 12% of older community-dwelling men[40] and up to 21% of those in retirement
communities.[37]

Spinal stenosis generally affects more men than women. A study in Geneva found that the ratio between
men and women is 1.28.[41] It went on to state that while the disease is strongly related to aging, men are
affected earlier in life than women. This is likely due to heavy workload and a higher body mass index
(BMI).[41] Although spinal stenosis tends to affect men more than women, degenerative
spondylolisthesis in association with spinal stenosis is more prevalent in women.[33] Occupation, race,
and smaller canal diameter also do not appear to have a correlation with the development of spinal
stenosis.[33]

Furthermore, there is now a disproportionate rise in spinal surgery being performed. The incidence in the
1980s in Sweden was 5 per 100,000 people and increased 300% between 1987 and 1999.[42] Again in
2013, Sweden reported an incidence of 40 per 100,000 people.[42] The large increase in surgical
treatment for this disease is well known and studied. The United States has also followed similar trends.

History
A description of LSS was published by Sachs and Frankel in 1900,[43] but the first clinical description of
LSS is usually attributed to the Dutch neurosurgeon Henk Verbiest, whose report appeared in
1954.[6][7][44]

Spinal stenosis began to be recognized as an impairing condition in the 1950s and 1970s. Individuals
who experience back pain and other symptoms are likely to have bigger spinal canals than those who are
asymptomatic.[45] A normal-sized lumbar canal is rarely encountered in persons with either disc disease
or those requiring a laminectomy.[31]

During the 1970s and 1980s, many case reports showed successful surgical treatment rates, but these
were based on subjective assessment by surgeons.[7] In 1992, Johnsson, Rosén and Udén described the
natural history of LSS, with different conclusions about prognosis and treatment: "70% of patients
reported no significant change in symptoms, 15% showed significant improvement, whereas 15%
showed some deterioration.[46] The investigators concluded that observation is a reasonable treatment
option for lumbar stenosis and that significant neurologic deterioration is rare."[7]

Society and culture

United States
Under rules promulgated by Titles II and XVI of the United States Social Security Act, spinal stenosis is
recognized as a disabling condition under Listing 1.04 C. The listing states: "Lumbar spinal stenosis
resulting in pseudoclaudication, established by findings on appropriate medically acceptable imaging,
manifested by chronic nonradicular pain and weakness, and resulting in inability to ambulate effectively,
as defined in 1.00B2b."[47] The regulation is written specifically for lumbar stenosis.[48]

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External links
Classification ICD-10: M48.0 (htt D
p://apps.who.int/cla
ssifications/icd10/br
owse/2016/en#/M4
8.0) · ICD-9-CM:
723.0 (http://www.ic
d9data.com/getICD
9Code.ashx?icd9=7
23.0)-724.0 (http://w
ww.icd9data.com/g
etICD9Code.ashx?i
cd9=724.0) · MeSH:
D013130 (https://w
ww.nlm.nih.gov/cgi/
mesh/2015/MB_cg
i?field=uid&term=D
013130) ·
DiseasesDB:
31116 (http://www.d
iseasesdatabase.co
m/ddb31116.htm)

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