INTRODUCTION — The term "lumbar spinal stenosis" (LSS) can refer to one or more of the following anatomic states:
●Narrowing of the intraspinal (central) canal
●Narrowing of the lateral recess
●Narrowing of the neural foramen
This topic will focus on the pathophysiology, clinical features, and diagnosis in regard to stenosis of the intraspinal (central) lumbar canal. This condition, most commonly caused by degenerative bone disease, is increasingly recognized as a cause of disability in the aging population [1,2].
Lateral recess and neural foraminal stenosis can give rise to lumbar radiculopathy. Lumbosacral radiculopathy and general issues related to degenerative bone disease and back pain are discussed separately. The prognosis and treatment of LSS are also discussed separately.
ANATOMY — Five lumbar vertebral bodies (L1-5) comprise the lumbar spine. The lumbar spine curves slightly, forming the lumbar lordosis. The sacrum is made up of five developmentally fused vertebral levels (S1-5), followed by a terminal bony prominence, the coccyx (figure 1).
The spinal cord terminates at the conus medullaris within the lumbar intraspinal canal between the T12 and L2 vertebral levels. Exceptions include patients with congenital spinal deformities known as spina bifida, in which the fetal conus is tethered to ligamentous or bony structures, causing lengthening of the spinal cord during development. In such patients, the conus medullaris can be displaced downward to the middle or lower lumbar spine.
All lumbar and sacral spinal nerve roots are constituted at the T10-L1 vertebral level, where the spinal cord ends as the conus medullaris. The roots then course down through the intraspinal canal, forming the cauda equina, until they exit at their respective neural foramina.
The cross-sectional anatomy of the lumbar canal is demonstrated in the figure (figure 1). The canal is bounded anteriorly by the vertebral body and/or vertebral disc and the posterior longitudinal ligament, laterally by the pedicles and facet joints, and posteriorly by the lamina and ligamenta flava. Pathology involving these structures is frequently responsible for producing lumbar central canal stenosis (figure 1).
ETIOLOGIES — Causes of LSS can be congenital or acquired .
Spondylosis, or degenerative arthritis affecting the spine, is the most common cause of LSS and typically affects individuals over the age of 60 years . Obesity and family history may also be risk factors [5,6]. Progressive disc degeneration due to aging, trauma, or other factors can lead to disc protrusion and/or loss of disc height with attendant loading of the posterior elements of the spine, including the facet joints. Facet joint arthropathy and osteophyte formation follow, along with hypertrophy of the ligamentum flavum. All of these processes (facet osteophytes, ligamentum flavum hypertrophy, and disc bulging) can encroach on the central canal and the neural foramina (figure 1).
Spondylolisthesis, in which one vertebral body translates anteriorly or posteriorly with respect to an adjacent vertebral body, can also occur, exacerbating the spinal canal narrowing (figure 1). The L4-5 level is most commonly involved, followed by L5-S1 and L3-4. In patients with LSS, degenerative changes can involve the pars interarticularis, leading to fracturing and vertebral body displacement due to instability. (See "Clinical manifestations and diagnosis of osteoarthritis", section on 'Facet joint'.)
Other acquired causes include:
●Space-occupying lesions (lipoma, synovial and neural cysts, neoplasms). (See "Clinical features and diagnosis of neoplastic epidural spinal cord compression".)
●Traumatic and postoperative causes (fibrosis).
●Skeletal disease (Paget, ankylosing spondylitis, rheumatoid arthritis, diffuse idiopathic skeletal hyperostosis). (See "Clinical manifestations and diagnosis of Paget disease of bone" and "Clinical manifestations of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults" and "Clinical manifestations of rheumatoid arthritis" and "Diffuse idiopathic skeletal hyperostosis (DISH)".)
Congenital and developmental causes of LSS include:
●Dwarfism (achondroplasia, Morquio syndrome, other spondyloepiphyseal dysplasias). (See "Achondroplasia" and "Skeletal dysplasias: Specific disorders" and "Mucopolysaccharidoses: Complications", section on 'Dysostosis multiplex'.)
●Spinal dysraphism (spina bifida, spondylolisthesis, myelomeningocele). (See "Myelomeningocele (spina bifida): Management and outcome", section on 'Orthopedic problems'.)
PATHOPHYSIOLOGY — Mechanical compression and ischemia of nerve roots have been proposed as causes of the neurologic symptoms in LSS. Either or both of these mechanisms may operate in individual patients. A role for inflammation of nerve roots is less certain .
Nerve root compression may result from direct mechanical compression or occur indirectly from increased intrathecal pressure, which rises as the canal area is reduced . Increased intrathecal pressure can also cause venous congestion, reduced arterial blood flow, and reduction of impulse conduction along nerve roots [9-15]. Some evidence suggests that multilevel stenosis is necessary for this process to occur [16,17].
The erect, extended position narrows the lumbar canal by reducing the interlaminar space, causing overlap of laminar edges of adjoining vertebral bodies, relaxing and inward buckling of the ligamentum flavum, and rostral-anterior migration of the superior facets [3,18]. This may explain the onset or persistence of symptoms with prolonged standing. It is also possible that increased metabolic demands on spinal nerve roots during walking may exceed the available microvascular blood flow, especially when intrathecal pressures are elevated [11,15].
CLINICAL PRESENTATION — The clinical features of LSS were characterized in a study of 68 patients with radiographic and surgical confirmation of disease .
Symptoms — Neurogenic (or pseudo) claudication is a hallmark of LSS . This is the tendency for symptoms, usually pain, to be exacerbated with walking, standing, and/or maintaining certain postures, and relieved with sitting or lying . Many patients with LSS are symptomatic only when active. In one systematic review of clinical findings in LSS, neurogenic claudication was moderately sensitive and present in 82 percent of patients . Exacerbation by prolonged standing in an erect posture was an even more sensitive but less specific sign. No pain with sitting was the most specific finding. More than half of patients with LSS also reported relief with sitting or flexion at the waist (squatting, leaning forward), findings that were relatively specific for LSS (84 and 92 percent, respectively), but less sensitive.
The primary symptoms of LSS include discomfort, sensory loss, and weakness in the legs, reflecting involvement of spinal nerve roots within the lumbar spinal canal. In the clinical series described above, pain was the most common symptom, occurring in 93 percent of patients, followed by numbness and/or tingling in 63 percent, and weakness in 43 percent . Symptoms were bilateral in most (68 percent), but often asymmetric, and usually involved the entire leg rather than just the upper or lower leg (78 versus 15 and 6 percent, respectively). Pain in a single nerve root distribution occurred in only 6 percent. Low back pain occurred in 65 percent and was described as mechanical and mild. Low back pain in LSS is not necessarily associated with the claudication symptoms.
Examination — The neurologic examination is often normal in patients with LSS. The straight leg raising sign is present only in a minority of patients (10 percent) [19,21]. However, in some patients with LSS, more prolonged or severe nerve root involvement may lead to fixed and/or progressive neurologic deficits.
●Patients may have symptoms or neurologic signs of single or multiple lumbosacral radiculopathies, superimposed on more typical symptoms of LSS. The neurologic examination may demonstrate focal weakness and/or sensory loss in the distribution of one or more spinal nerve roots. In the study described above, deep tendon reflexes were absent at the ankle in 43 percent, and at the knee in 18 percent . Weakness was seen in 37 percent and was usually mild and isolated to the L5 and S1 root distributions . A wide-based gait and/or positive Romberg in the setting of low back pain had a specificity of more than 90 percent for LSS [1,21]. (See "Overview of lower extremity peripheral nerve syndromes", section on 'Lumbosacral radiculopathy'.)
●The cauda equina syndrome is an uncommon complication of LSS, but is associated with marked neurologic disability. The clinical presentation is dominated by bilateral leg weakness in multiple root distributions (L3-S1) and may be associated with bowel, bladder, and erectile dysfunction due to involvement of the S2-4 spinal nerve roots. This is a neurologic emergency and requires immediate surgical consultation.
●When the intraspinal site of compression is between T12 and L1, the conus medullaris may also be damaged, producing a mixed picture of spinal nerve root and spinal cord dysfunction (myelopathy). The clinical manifestations of myelopathy in this setting include bowel, bladder, and erectile dysfunction; diffuse leg weakness; sensory deficit level at T11 or below; saddle-distribution anesthesia; increased tone in the legs; and extensor plantar responses. This is a neurologic emergency and requires immediate surgical consultation.
It may also be useful to examine the patient after physical activity, as this might elicit neurologic deficits. (See 'Other diagnostic tools' below.)
DIFFERENTIAL DIAGNOSIS — Peripheral vascular disease may be mistaken for LSS because both are associated with exertional exacerbation. However, symptoms of neurogenic claudication can usually be distinguished from vascular claudication (table 1). Neurogenic, but not vascular, claudication often persists with rest when standing still in an erect posture, and can be ameliorated somewhat by assumption of stooped, flexed posture, even without rest. Similarly, bicycling is frequently better tolerated by patients with LSS compared with similar intensity walking, while this is not true for patients with vascular claudication. (See "Clinical features and diagnosis of lower extremity peripheral artery disease".)
Other diagnoses should also be considered in the differential diagnosis of LSS:
●Nonspecific back pain from spondylosis without LSS and referred pain from the retroperitoneum due to infection or malignancy may resemble some of the features of LSS; however, classic neurogenic claudication is unusual.
●Distal polyneuropathy may produce bilateral asymmetric pain, paresthesias, and numbness, as does LSS. It is unusual, however, for symptoms of polyneuropathy to be strongly influenced by activity or posture.
●The pain of osteoarthritis of the hips or knees may be exacerbated by walking. Pain in these conditions usually localizes to the involved joints, but may also radiate to the groin or buttocks. (See "Clinical manifestations and diagnosis of osteoarthritis", section on 'Knee' and "Clinical manifestations and diagnosis of osteoarthritis", section on 'Hip'.)
●Spinal cord vascular malformations are rare, but can produce symptomatic deficits of the lumbosacral nerve roots and symptoms of neurogenic claudication . Symptoms often fluctuate in this condition, but usually in a less predictable fashion as compared with LSS. Patients with spinal cord vascular malformations also often have long tract signs, although these may be subtle.
●A number of inflammatory conditions involving the lumbosacral nerve roots or cauda equina can produce neurologic deficits that overlap with those seen in LSS. Neurogenic claudication, however, would not be expected. These conditions include spinal arachnoiditis, chronic inflammatory demyelinating polyneuropathy [23,24], sarcoidosis, carcinomatous meningitis, and a variety of infections (eg, cytomegalovirus, herpes simplex virus, herpes zoster virus, Epstein-Barr virus, Lyme disease, mycoplasma, tuberculosis).
●Congenital tethered cord syndrome usually presents in childhood, but occasionally individuals with occult spinal dysraphism first come to medical attention as adults [25-27]. Such patients present with complaints that may be similar to LSS with a mixture of leg and back pain, motor and sensory symptoms, and bowel or bladder dysfunction. Neuroimaging will reveal this condition, which is often amenable to surgical untethering.
DIAGNOSIS — The diagnosis of LSS requires the presence of typical symptoms combined with a neuroimaging study showing structural narrowing of the intraspinal canal. The imaging study usually also identifies the underlying etiology.
Neuroimaging — In general, new-onset symptoms and signs of multilevel lumbosacral radiculopathy and/or spinal stenosis provide an indication for neuroimaging. (See "Evaluation of low back pain in adults".)
While findings on plain radiographs of the lumbar spine can lend support for the diagnosis of LSS and may suggest the underlying pathology, magnetic resonance imaging (MRI) is the modality of choice for the diagnosis of LSS (image 1 and image 2). MRI defines the bony anatomy and visualizes soft tissues and neural structures, such as the conus medullaris and spinal nerve roots within the canal and neural foramina. Computed tomography (CT) may be preferable to MRI for bony anatomy and, when combined with myelography, provides imaging of neural elements. Studies indicate a good correlation between MRI and CT myelography for LSS diagnosis [28,29]. Because myelography is an invasive procedure with an attendant risk of complications, MRI is generally preferred. However, CT myelography is a good alternative in patients in whom MRI is contraindicated. Contrast administration provides little additional information to the MRI and is unnecessary unless either new spinal symptoms arise postoperatively or there is a question of intraspinal infection or metastasis. (See "Principles of magnetic resonance imaging", section on 'Precautions'.)
Uncertainty regarding the diagnosis of LSS even after MRI results from variety in the criteria used to define spinal stenosis . There is no consensus on the best criteria to diagnose LSS or to define its severity . Examples of criteria include an intraspinal canal area of less than 76 mm2 and 100 mm2 to identify severe and moderate stenosis, respectively . Anteroposterior diameters of less than 10 mm are also often used as a cutoff, but provide a less complete measure of anatomic disease. Area measurements, however, are more complicated to perform and have a less certain interrater reliability [28,32]. Other qualitative assessments to grade disease and predict prognosis and treatment response as well as dynamic MRI techniques have been proposed but require independent validation [33-35]. Some clinicians require that more than one spinal level be affected to diagnose LSS.
Another important caveat is that radiologic spinal stenosis is a common incidental finding, occurring in 6 to 7 percent of asymptomatic adults in two series [1,30,36,37]. In adults over 60 years old, the prevalence may be as high as 20 to 30 percent [37,38]. There is no substantive relationship between the severity of radiologic findings and the severity of clinical symptoms or prognosis. Findings on neuroimaging must be carefully interpreted in the context of the clinical history and examination.
Other diagnostic tools — Electromyography and nerve conduction studies (EMG/NCS) are not required for the diagnosis of LSS, and are generally ordered when alternative diagnoses (eg, neuropathy) are considered . However, they can provide information about nerve root damage in this setting. The most common EMG/NCS abnormality in patients with LSS is an absent H reflex, a subtle manifestation of S1 nerve root involvement (see "Overview of lower extremity peripheral nerve syndromes", section on 'Lumbosacral radiculopathy'). Many patients with LSS have a normal EMG/NCS evaluation . Patients with fixed clinical symptoms and signs of nerve root injury are more likely to have abnormal EMG/NCS; however, EMG/NCS is more sensitive than the clinical examination.
When there is a superimposed radiculopathy, EMG/NCS can help localize the nerve root injury and provide some prognostic information as well [40,41]. (See "Overview of lower extremity peripheral nerve syndromes", section on 'Lumbosacral radiculopathy'.)
Exercise testing may be helpful but does not have a defined role in the clinical evaluation of patients with LSS [39,42]. Some clinicians report that exercise can elicit neurologic signs and/or EMG/NCS abnormalities that are not apparent at rest. A treadmill exercise test can also quantify the time to onset of symptoms and total ambulation endurance with good test-retest reproducibility . This has been used to define baseline functional status and evaluate postoperative symptom relief .
When other entities in the differential diagnosis are considered as an alternative to LSS, other specific testing may be indicated. Examples include Doppler ultrasound studies of the lower extremities for peripheral vascular disease and plain films of the hips or knees for osteoarthritis. LSS, peripheral vascular disease, and osteoarthritis are each prevalent in the older adult population and can be comorbid. (See "Clinical features and diagnosis of lower extremity peripheral artery disease" and "Clinical manifestations and diagnosis of osteoarthritis".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Spinal stenosis (The Basics)")
SUMMARY AND RECOMMENDATIONS — Lumbar spinal stenosis (LSS) can be caused by a variety of congenital or acquired conditions. The most common cause is degenerative spondylosis, which typically affects individuals over the age of 60 years. (See 'Etiologies' above.)
●LSS is clinically manifested by neurogenic claudication, a syndrome of bilateral, often asymmetric pain, sensory loss, and/or weakness affecting the legs, which is produced or exacerbated by walking or prolonged standing in an erect posture. (See 'Clinical presentation' above.)
●These symptoms represent intermittent mechanical and/or ischemic disruption of lumbosacral nerve root function. (See 'Pathophysiology' above.)
●In a few patients, more fixed nerve root injury may occur, causing lumbosacral radiculopathy, cauda equina syndrome, or conus medullaris syndrome. (See 'Clinical presentation' above.)
●The diagnosis of LSS requires a neuroimaging study. Magnetic resonance imaging (MRI) of the lumbosacral spine is the test of choice for most patients. In some patients, electrophysiologic tests, vascular ultrasound, and other tests may be required to rule out other disorders in the differential diagnosis. (See 'Diagnosis' above.)
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