Lumbar spinal stenosis



Spinal stenosis is a narrowing of the spinal canal that puts pressure on the spinal cord, the nerve roots branching from it, or both. 

It is estimated that approximately 103 million individuals have symptomatic lumbar spinal stenosis worldwide.

Lumbar spinal stenosis is becoming more common as the population ages.

Annually 90 of 100,000 patients over the age of 60 years undergo lumbar spinal fusion surgery.

Fastest growing type of lumbar surgery 1980-2000 in the U.S.

Lumbar spinal stenosis is  the main reason for spinal surgery in people over age 65.

Narrowing of the spinal canal that produces compression of the neural elements before their exit from the neural foramen.

LSS is characterized by narrowing of the lumbar spinal canal and/or the neural foramina, with compression of the spinal nerve roots.

The nerve roots exit the central canal through neural foramina to innervate the lower extremities.

Spondylolisthesis, or the forward displacement of one vertebrae with respect to an adjacent vertebra, introduces an additional source of compression.

Lumbar spinal stenosis usually develops after age 50 but can occur earlier in people who have had a spine injury or were born with a narrow spinal canal. 


As many as 35% of those seeking help for chronic low back pain may have the disorder. 

Occurs when the vertebral canal is narrowed by surrounding bone and soft tissues, leading to compression of neural structures including spinal nerve roots

Not a single disease process but results from a combination of anatomical changes including inter vertebral disc protrusion or herniation, facet joint hypertrophy, spondylolisthesis, congenital narrowing of the vertebral canal, or hypertrophy of the ligamentum flavum, metabolic syndromes in which overgrowth of bone is present such as paget’s disease, and epidural lipomatosis.

Its main cause is age-related changes in bone and other spinal tissues.

Acquired degenerative lumbar spinal stenosis arises from degenerative changes, including combinations of disc protrusion, facet joint hypertrophy, ligamentum flavum hypertrophy, and spondylolisthesis.

These factors result in disk height loss and weight is transferred to the facet and intervertebral joints, which form osteophytes.

The posterior longitudinal ligament folds and hypertrophies.

The combination of disc protrusion, facet joint osteophytes, ligamentum flavum buckling and hypertrophy, and spondylolisthesis contribute to nerve root displacement in the central canal and or in the neural foramina and lateral recesses, as the nerves exit to the lower extremities.

Most lumbar spinal stenosis is caused by degeneration in the disks, the ligaments, or the facet joints between the vertebrae.

Refers to narrowing of the lumbar spinal canal, lateral recess, or foramen resulting in neurovascular compression that may lead to pain.

The mechanism that compression of nerve root gives rise to back pain, lower extremity pain, paresthesias, and weakness may be related to compression of small arterioles causing ischemia of the nerve or may be related to the prevention of normal venous drainage leading to increased venous pressure, accumulation of toxic metabolites and nerve root damage.

May be classified by etiology, that is, congenital or acquired, or by symptomatology such as radiculopathy, neurogenic claudication, or mechanical back pain.

Further, it can also be classified radiographically, by the location of the stenosis such as central canal, lateral recess, or intervertebral foramen or by the presence of deformity such as spondylolisthesis or scoliosis.

Central stenosis with thecal sac compression usually leads to neurogenic claudication.

Lateral recess compression is associated with compression of an individual nerve root, resulting in radiculopathy.

The radicular pain due to spinal stenosis is probably related to the inhibition of normal nerve root vascular flow with resultant nerve root nutrition, nerve root edema, and nerve root dysfunction.

Symptoms of symptomatic lumbar spinal stenosis is characterized by low back pain and leg pain in the setting of compression of the central canal and/or exiting nerve roots by disc, osteophyte, ligamentum  flavum or other structures.

Not all patients with narrowing develop symptoms.

Spinal stenosis effects may extend to the buttocks, thighs, and lower legs causing pain, numbness or tingling, and weakness. 


In severe spinal stenosis bowel and bladder control may be affected. 

Lower extremity pain may be unilateral or bilateral and may be accompanied by numbness in paresthesias of the feet and lower legs.

Late in the course patient may experience worsening of balance and wide base gait reflecting compression of the posterior column fibers that provide awareness of position.

In a study with a mean follow-up of 11.1 years it was found similar proportion of patients with lumbar spinal stenosis treated conservatively experienced improvement, no change, or worsening of symptoms (Minamide A et al).

Most patients with conservative management report stable or improved symptoms at least three years after presentation.

Lumbar spinal stenosis does not refer to the anatomical findings of spinal canal narrowing, but rather it is a syndrome of lower extremity pain caused by mechanical compression on neural elements or their vascular supply.

Unlike acute herniated disc that may resolve overtime, the chronic degenerative changes with lumbar spinal stenosis do not generally regress.

Caused by progressive degenerative changes in intervertebral joints and ligamentous structures leading to spinal canal and neural foraminal narrowing.

Characterized by narrowing of the lumbar spinal canal and/or the neural foramina, with compression of the spinal nerve roots.

Adult degenerative lumbar spinal stenosis is almost always associated with osteophytic enlargement in the region of the degenerating synovial facet joints.

Lumbar spinal stenosis may also be due to hypertrophy of the ligamentum flavum, and protrusion or bulging of intervertebral discs.

Symptoms may be due to direct compression of nerve roots or by compressing nutrient arterioles that supply nerve roots.

As age is the greatest risk factor for spinal degenerative changes, most patients with LSS are over 60 years of age.

Risk factors for LSS include:




Degenerative changes of the spine




Family history of spinal stenosis


Tobacco use


Occupation involving repetitive mechanical stress on the spine

Syndrome of buttock or lower extremity pain, which may occur with or without back pain.

Pain may originate in the low back, but extends below the buttocks into the thigh in nearly 90% of patients.

In approximately 50% of patients with LSS pain because bands below the knee.

Pain is often described as achiness lore and numbness, which is accentuated with walking.

Prolonged standing can precipitate pain.

LSS discomfort is typically exacerbated by standing and walking and relieved by sitting and bending forward.

Pain in the buttocks or lower extremity exacerbated by lumbar extension, that is walking, is referred to as neurogenic claudication.

Absence of low back pain while sitting is approximately 52 to 70% sensitive and approximately 55 to 83% specific for lumbar spinal stenosis.

some patients with spinal stenosis are more comfortable when leaning on a shopping cart, when the spine is flexed.

Increasing of spinal stenosis symptoms occurs when the back is extended and improvement occurs when the lower back is flexed occurs because spinal extension reduces the cross-sectional area of the central spinal canal and neural foramina.

Many patients with LSS report poor balance associated with their back pain and it is 70% sensitive and 53% specific for the diagnosis.

Spinal stenosis can compress the posterior column fibers and reduce proprioception and impaired balance.

LSS pain may be bilateral.

LSS pain may lead to impaired balance and gait, or weakness of the lower extremities which increases with walking.

Neuroclaudication refers to progressive weakness of the legs and balance with walking.

In some patients walking uphill increases lumbar spinal canal volume with flexion of the back and relieves pain.

Clinical findings may be minimum with less than 10% having a positive straight leg raise sign, 25% have decreased lower extremity reflexes, and 60% have proximal weakness.

Diminished space is present for neural and vascular elements in the lumbar spine.

Radiologic imaging is the key for diagnosis, but radiological criteria for the diagnosis is not clear-cut.

Approximately 20% of individuals older than 60 years of age have imaging evidence of lumbar spinal stenosis, and more than 80% of whom or asymptomatic.

Radiologic interpretation has significant variability among readers so that it is difficult to establish the clinical impression of lumbar stenosis.

Anatomical measurements relating to the anterior-posterior spinal canal diameter or the thecal sac diameter measurements are not well tied to clinical evidence or statistical norms.

In a study of 32 asymptomatic individuals radiologic diagnosis of lumbar stenosis was made in 65% of the studies (Haig AJ).

MRI studies have no discriminant value to separate clinical stenosis from asymptomatic volunteers (Haig AJ).

Abnormal MRI findings may be present in two-thirds of asymptomatic individuals, and imaging findings of spinal stenosis do not correlate well with symptom severity. 

Among individuals older than 60 years the Framingham study revealed 47% of patients met CT criteria for moderate or severe (Kalichman L).

EMG paraspinal mapping can discriminate between mechanical back pain and asymptomatic individuals.

Treatment is not indicated for asymptomatic stenosis.

Lumbar spinal stenosis non-surgical treatment include activity modification, NSAIDs, physical therapy as well as epidural steroid injections as initial the first treatments of choice for patients suffering from neurogenic intermittent claudication.

Patients benefit from an explanation of the relationship between posture and symptoms: avoiding exacerbating symptoms, and suggesting exercises such as biking or swimming that are typically carried out in a lumbar flexion position.

Weight-loss and exercise programs aimed at decreasing lumbar lordosis can decrease symptoms.

Gabapentin may be effective for pain relief due to LSS.

Overall opioid therapy is associated with small improvements in pain and function with no meaning  difference between nSAIDs and opioids.

Epidural corticosteroid injections provide relief in about 50% of patients, and 25% receive sustained relief.

Overall epidural steroid injections me off a modest short term pain relief but do not appear to last more than three weeks.

In severely affected patients surgery can reduce pain and improve function in approximately 75% of patients at 1 to 2 years, while conservatively treated such patients only 25% will receive similar improvements.

Most commonly affects the middle-aged and elderly population.

Entrapment of the cauda equina roots by hypertrophy of the osseous and soft tissue structures surrounding the lumbar spinal canal is often associated with incapacitating pain in the back and lower extremities, difficulty ambulating, leg paresthesias and weakness and, in severe cases, bowel or bladder disturbances.

The syndrome associated with lumbar stenosis is termed neurogenic intermittent claudication, which must be differentiated from true claudication, which is caused by atherosclerosis of the pelvofemoral vessels.

Most cases are idiopathic.

Computed tomography or magnetic resonance imaging often demonstrates narrowing of the lumbar canal with compression of the cauda equina nerve roots by thickened posterior vertebral elements, facet joints, marginal osteophytes or soft tissue structures such as the ligamentum flavum or herniated discs.

Diagnosis can generally be made with history and physical examination, and imaging can confirm structural diagnosis and clarify anatomy if therapeutic injections or surgery are contemplated.

No historical or physical examination findings that are both highly sensitive or specific for LSS.

A wide based gait and positive Romberg sign are associated with a specificity of more than 90%, but a sensitivity of only 40% for LSS.

In LSS the spine is generally non-tender.

Lumbar extension often elicits pain in the lumbosacral junction, buttocks and thighs: thigh pain on extension is associated with sensitivity in more than 50% of patients and the specificity of 69% for the diagnosis of LSS.

Flexion of the spine typically relieves these symptoms.

When imaging is indicated MRI or CT can confirm the diagnosis.

Treatment for symptomatic lumbar stenosis is usually surgical decompression.

Medical treatment alternatives, such as bed rest, pain management and physical therapy, should be reserved for use in debilitated patients or patients whose surgical risk is prohibitive as a result of concomitant medical conditions.

Due to slow progression of the disease, the diagnosis may be significantly delayed.

The lumbar vertebral canal is roughly triangular in shape and is narrowest in its anteroposterior diameter in the axial plane.

The average anteroposterior diameter of the lumbar canal in adults, ranges from 15 to 23 mm.

The canal is bounded anteriorly by the posterior edge of the vertebral body including the posterior longitudinal ligament, which is closely apposed to the posterior vertebral body surface, laterally by the pedicles, posterolaterally by the facet joints and articular capsules, and posteriorly by the lamina and ligamenta flava.

Entrapment of the cauda equina roots, which pass within the dural sac, can occur as a result of progressive hypertrophy of any of the osseocartilaginous and ligamentous elements surrounding the spinal canal.

The intervertebral disc is prone to rupture or herniate posteriorly or posterolaterally as a result of degenerative changes or trauma, producing neural element compromise.

The cone-shaped terminus of the spinal cord, conus medullaris, normally ends at about the L1 or L2 level in adults.

Caudal to L1 or L2 levels, the roots of the cauda equina are contained within the subarachnoid space of the dura-enclosed thecal sac.

Canal stenosis at lumbar levels results in nerve root dysfunction rather than spinal cord dysfunction.

Causes of lumbar stenosis divided into two types: conditions that lead to progressive bony encroachment of the lumbar canal or stenosis produced by nonosseous structures such as ligaments, intervertebral discs and other soft tissue masses.

The etiologies of lumbar stenosis can be divided into congenital or acquired forms.

Few causes of lumbar stenosis are truly congenital.

Narrowed or shallow lumbar canals may be a result of congenitally short pedicles, thickened lamina and facets, or excessive scoliotic or lordotic curves.

These anatomic changes may lead to clinically significant stenosis if additional elements such as herniated intervertebral discs or other space-occupying lesions further narrow the canal and contribute to the compression.

Lumbar canal diameters from 10 to 12 mm may be associated with claudication if additional elements encroach on the canal-relative canal stenosis.

In most cases, stenosis of the lumbar canal is due to acquired degenerative or arthritic changes of the intervertebral discs, ligaments and facet joints surrounding the lumbar canal, including cartilaginous hypertrophy of the articulations surrounding the canal, intervertebral disc herniations or bulges, hypertrophy of the ligamentum flavum and osteophyte formation.

Micro-instability refers to minute, abnormal repetitive motion of the joints that link adjacent vertebra may result in progressive loss of strength in the joint capsules and lead to reactive bony and cartilaginous hypertrophy, thickening or calcification of the ligamentum flavum, or spondylolisthesis, all of which may contribute to narrowing of the lumbar canal.

Compression of the microvasculature of the lumbar nerve roots, leading to ischemia, is believed to be a major contributing factor in the development of neurogenic claudication.

Neurogenic claudication is divided into two major types based on pathophysiologic mechanisms postural or ischemic.

Postural neurogenic claudication is induced when the lumbar spine is extended and lordosis is accentuated, whether at rest or during exercise in the erect posture.

With extension of the spine, degenerated intervertebral discs and thickened ligamenta flava protrude posteriorly into the lumbar canal, producing transient compression of the cauda equina.

In the ischemic form, it is theorized that transient ischemia occurs in compressed lumbosacral roots when increased oxygen demand occurs during walking.

Other acquired conditions associated with lumbar canal stenosis as a result of osseous or fibrocartilaginous hypertrophy include: fluorosis, hyperparathyroidism, Paget’s disease, ankylosing spondylitis, Cushing’s disease and acromegaly.

Men are affected with slightly higher frequency than women.

Usually a disease of the middle-aged and the elderly.

Younger patients may also be affected, although less commonly.

The earliest complaint is usually back pain, which is relatively nonspecific and may result in delayed diagnosis.

Patients often experience leg fatigue, pain, numbness and weakness, sometimes several months to years after the back pain was first noticed.

Leg pain is most commonly bilateral, involving the buttocks and thighs and spreading distally toward the feet, typically with the onset and progression of leg exercise.

In some patients, the pain, paresthesias and/or weakness are limited to the lower legs and feet.

The lower extremity symptoms are almost always described as burning, cramping, numbness, tingling or dull fatigue in the thighs and legs.

Disease onset is usually insidious.

Symptom severity does not always correlate with the degree of lumbar canal narrowing.

The symptoms begin or worsen with the onset of ambulation or by standing, and are promptly relieved by sitting or lying down.

Thigh or leg pain typically precedes the onset of numbness and motor weakness.

Patients commonly complain of difficulty walking even short distances.

Patients walk with a characteristic stooped or anthropoid posture in more advanced cases.

Standing and walking exacerbate the extreme discomfort.

Bicycle riding can often be performed without much difficulty because of the theoretic widening of the lumbar canal that occurs with flexion of the back.

Some patients obtain transient relief of pain by assuming a squatting position, as it flexes the trunk.

Lying prone or in any position that extends the lumbar spine exacerbates the symptoms, presumably because of ventral in-folding of the ligamentum flavum in a canal already significantly narrowed by degenerative osseus changes.

Other common symptoms include: stiffness of the thighs and legs, back pain and, in severe cases, visceral disturbances such as urinary incontinence that may be a result of impingement of sacral roots.

Back pain, a symptom in nearly all patients with lumbar stenosis.

Back pain may be present with or without claudication, particularly in the earlier stages of the disorder.

Lasègue’s sign, the straight leg raising test is performed by raising the straight lower extremity and dorsiflexing the foot, is classically associated with reproduction of ipsilateral radicular pain secondary to nerve root compression by a herniated lumbar disc, presumably by stretching the compressed ipsilateral nerve root.

Lasègue’s sign, the straight leg raising test sign is usually absent in patients with lumbar stenosis.

Most patients with a true positive straight leg raising sign complain of excruciating sciatica-like pain in the elevated leg at 30 to 40 degrees of elevation.

Herniation of disc material and subsequent reparative processes may contribute to the overall picture of stenosis, but acute disc herniations generally produce a clinical picture that differs from the more chronic symptoms of canal stenosis.

Patrick’s sign, reproduces leg pain with lateral rotation of the flexed knee, implies ipsilateral degenerative hip joint disease, and is important in the differential diagnosis in patients with stenosis.

The neurologic examination with degenerative lumbar stenosis may not reveal significant sensorimotor deficits at rest or in a neutral position, but deep tendon reflexes may be decreased, absent or normal, depending on the chronicity of the caudal root compression.

Upper motor neuron signs, such as hyperactive deep tendon reflexes or the presence of pathologic reflexes, such as the Babinski’s sign or Hoffmann’s sign, are typically absent.

With the onset of walking, sensory deficits may appear, and motor weakness or reflex changes may be elicited.

A neurologic examination should be done before and immediately after symptoms appear following a short period of ambulation, and neurologic changes with variations in posture should be noted.

Neurological claudication, In contrast to claudication that is due to cauda equina compression, vaso-occlusive leg claudication usually does not occur with changes in posture, and patients typically obtain relief from the leg pain by simply resting the legs even while in the upright position.

Diagnosis of lumbar stenosis depends largely on the clinical history and physical examination.

Radiographic confirmation of the diagnosis can be accomplished using various imaging modalities.

Plain films of the spine may demonstrate degenerative changes in the vertebrae or disc spaces, or disclose occult spina bifida, spondylolisthesis or scoliosis in some patients.

The most commonly involved levels are L3 through L5.

Neuroimaging techniques such as computed tomographic (CT) scanning and magnetic resonance imaging (MRI) facilitate the diagnosis.

CT scans with or without intrathecal contrast injection are able to demonstrate the lumbar subarachnoid space well, may demonstrate encroachment of the canal by hypertrophied lamina, osteophytes, facets or pedicles, and can provide excellent visualization of the vertebral canal so that measurements of the canal diameter can be made.

Hypertrophy of the lamina, pedicles and apophyseal joints, along with a thickened ligamentum flavum, impinge on the posterolateral aspects of the lumbar canal, giving it the classic appearance on axial CT scans.

CT scans with intrathecal contrast injection are able to demonstrate the lumbar subarachnoid space and nerve roots with enhanced sensitivity, but this is an invasive test with potential morbidity.

MRI scanning is currently the preferred modality for establishing a diagnosis and excluding other conditions.

MRI depicts soft tissues, including the cauda equina, spinal cord, ligaments, epidural fat, subarachnoid space and intervertebral discs.

Loss of epidural fat on T1-weighted images, loss of cerebrospinal fluid signal around the dural sac on T2-weighted images and degenerative disc disease are common features of lumbar stenosis on MRI.

The combination of ligament and facet joint hypertrophy concentrically reduces the diameter of the lumbar canal.

Electromyelograms with nerve conduction velocity studies may help confirm the multiradicular involvement of cauda equina compression, diagnosing demyelinating or inflammatory neuropathies, and distinguishing vascular from neurogenic claudication in situations where the clinical and radiographic pictures are equivocal.

Imaging studies are essential in the diagnosis of lumbar stenosis and, in most cases, electromyelography and nerve conduction velocity studies will not be required.

Few conditions produce the typical clinical picture of neurogenic claudication that occurs in lumbar stenosis.

Differential diagnosis: Conus medullaris and cauda equina neoplasms, and benign cystic lesions such as neurofibromas, ependymomas, hemangioblastomas, dermoids, epidermoids, and lipomas, neural compression from metastatic disease to bone, centrally herniated discs, degenerative spondylolisthesis, trauma/fractures, epidural abscess and Inflammatory arachnoiditis.

Cauda equina syndromes usually occur as a result of compression of the nerve roots in the lumbosacral spine distal to the conus medullaris.

Lumbar canal stenosis can manifest by dysfunction in multiple root distributions, and cause pain and other sensory deficits in several lumbar and/or sacral dermatomal territories, as well as weakness in the various muscle groups supplied by these nerve roots.

Cauda equina syndromes also may occur secondary to neoplasms, trauma, and inflammatory or infectious processes.

In individuals with neurogenic claudication an MRI aids in the exclusion of more serious conditions, such as tumors of the conus medullaris or cauda equina, or infectious processes.

Pain associated with a lumbosacral spinal tumor typically worsens with recumbency, awakens the patient at night and is relieved with walking.

Lumbar epidural abscesses usually are manifested by rapidly evolving neurologic abnormalities with , severe back pain. possibly fever and marked tenderness to palpation localized to the levels of suppuration.

Pathologic, traumatic or osteoporotic compression fractures of lumbar vertebrae may present with symptoms of cauda equina syndrome.

Healing silent fractures may produce exuberant growth of bone, which may lead to canal stenosis and root impingement.

Degenerative subluxation of lumbar vertebrae can cause of acquired stenosis of the lumbar spinal canal, particularly at the L4 and L5 levels, manifesting as neurogenic intermittent claudication.

L4-5 is the most frequently involved space in LSS.

Study show greater than 90% of stenosis at L4-5, 66% at L3-4, , 28% at L2-3 and 26% in L5 – S1.

MRI spinal canal cross sectional area of less than 191 m² has a sensitivity of 93% and a specificityof 45% for the diagnosis of lumbar spinal stenosis.

A spinal cross-sectional area less than 147 mm² has a sensitivity of 75% is specificity of 79% for diagnosis of lumbar spine stenosis.

Sensory deficits to pin prick with vibration, weakness of ankle or great toe flexion or extension, and loss of ankle reflexes have sensitivities of approximately 50% and specificities of approximately 80% for LSS.

Neurogenic claudication from LSS has thigh and occasional lower leg pain worsen with standing and relieved by sitting.

Lumbar stenosis can occur following posterior lumbar fusions, due to reactive bony hypertrophy at the fused segments.

Surgical treatment includes decompressive lumbar laminectomy.

The risks of laminectomy include the number of levels to be decompressed, comorbid medical problems, difficult anatomy as a result of scarring from previous operations or a markedly stenotic canal that may require extensive bone removal and dissection, as well as the overall risks imposed by general anesthesia.

Complications of the standard decompressive laminectomy include wound infection, hematoma formation, dural tears with subsequent cerebrospinal fluid leaks and risk of meningitis, nerve root damage and the potential for creating postoperative spinal instability, with an overall surgical mortality associated with decompressive laminectomy is approximately 1 percent.

The standard decompressive lumbar laminectomy involves a midline incision over the involved levels, dissection down to the spinous processes.

The standard decompressive lumbar laminectomy involves the removal of the posterior elements of the lumbar canal- the spinous processes, laminae and pedicles, as well as removal of thickened ligamenta flava.

Typically, decompressive laminectomies over multiple levels are performed since canal stenosis commonly occurs over several vertebra.

Rarely is excision of herniated intervertebral discs required.

A relative small proportion of patients who have persistent symptoms and functional limitations, despite non-operative treatment to referred for spinal decompressive surgery.

Direct surgical decompression, in which bone and/or disk are removed away from the effective nerve roots can be performed through an open or minimally invasive approach for lumbar spinal stenosis.

Randomized trials, comparing non-operative regimens with the compressive surgery show mixed results, but suggest the benefit of the compressive surgery compared with non-operative care.

Removal of the medial portions of the articular facets is often performed, particularly if there is evidence of osteophyte formation.

Decompression surgery has the potential of creating instability at the levels undergoing surgery.

With decompression surgery bone resection extends too far laterally, particularly if bilateral facetectomies are performed, instability occurs.

Lateral recess stenosis syndrome can cause back pain and claudication, when the lateral recess is the space within the spinal canal adjacent to the exit zone of the nerve roots is involved.

Most patients benefit from wide decompression of the lumbar canal, with the percentage of patients benefiting from surgery at 95 percent, with greater than 90 percent of patients returning to their previous activity levels.

Others claim long-term neurologic improvement in approximately 65 percent of patients.

In most patients with radiographic and clinical evidence of stenosis, decompressive surgery provides significant relief.

Patients with comorbid illnesses reported less relief of pain and less functional recovery than expected following decompression.

With chronic, severe symptoms, decompression of the neural elements may not result in immediate pain resolution.

In longstanding preoperative motor deficits immediate resolution is not likely.

With cauda equina decompression, progression of neurologic dysfunction may be slowed or halted.

Conservative management: lumbar bracing, bed rest, physical therapy and pain management, has few proven benefits in the long term.

Physical therapy can be effective for patients with lumbar spinal stenosis.

Medical or nonsurgical management of lumbar stenosis is not practical if symptoms are incapacitating.

Nonsurgical management may be attempted initially in patients with mild symptoms of short duration.

Morbidly obese patients with symptoms of neurogenic claudication may improve following weight loss.

Back strengthening exercises, physical therapy regimens and symptomatic management with nonsteroidal analgesics also may benefit some patients, but, often show no improvement on long-term follow-up.

Randomized clinical trials typically demonstrate benefits of structured, supervised exercise programs and manual therapy for improving pain and functional status in persons with lumbar stenosis.

Exercise treatments include cycling, treadmill walking, aquatic therapy, ambulation stretching, and deep water exercising.

Clinical trials have shown that manual therapy for spinal stenosis including: lumbar distraction mobilization, hip and sacroiliac joint mobilization, manual stretching, and monthly muscle strengthening resulted in a 79% improvement rate following a six week program.

Studies have shown that manual therapy combined with individual exercise compared with medications and the epidural injections and similar improvement rates.

Early surgery is the best way to return them to full activity and independent living.

In patients with concomitant degenerative, spondylolisthesis, and or scoliosis, decompression for lumbar spinal stenosis, is often performed in combination with lumbar fusion, in which adjacent vertebrae refuse to prevent motion.

Rationale for a fusion is that pain may arise from spinal instability, which may worsen following decompression, unless there is fusion.

Indications for a fusion in the setting of concomitant, spondylolisthesis, are debated, given the greater risk of complications and higher cost of fusion, balance, with the potential for improved outcomes with fusion.

Overall studies indicate the decompression alone is non-inferior to decompression plus fusion with concomitant spondylolithesis.

Fusion is generally accomplished, with autologous bone graft from the iliac crest, and often supplemented with instrumentation, in which screws, rods, interbody cages are inserted through anterior, anterior lateral, lateral, posterior lateral, or posterior approaches.

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