This article includes discussion of ulnar neuropathies, Guyon canal neuropathy, ulnar neuropathy at the wrist, and flexor carpi ulnaris exit compression.
Jun. 07, 2021
At vero eos et accusamus et iusto odio dignissimos ducimus qui blanditiis praesentium voluptatum deleniti atque corrupti quos dolores et quas.
This article includes discussion of lumbar spinal stenosis, neurogenic claudication, pseudoclaudication, and spinal stenosis. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
Lumbar spinal stenosis is a clinical syndrome with a hallmark of radiating leg pain with standing and walking relieved with bending forward or sitting. MRI findings lack specificity in identifying patients with symptomatic lumbar stenosis and do not correlate well with pain. Lumbar paraspinal needle electromyography lacks sensitivity but is highly specific in mild to moderate symptomatic lumbar stenosis, and is highly sensitive and specific in severe symptomatic lumbar stenosis. There is no radiologic or electrophysiologic gold standard at this time. Symptoms are caused by mechanical compression on the neural elements or their blood supply. Neurogenic claudication is classically described as a poorly localized sense of discomfort and aching pain in the lower back, buttocks, and legs that is precipitated by walking and relieved by sitting or leaning forward. The most common operative treatment is decompressive laminectomy with or without fusion or bilateral laminotomy. Minimally invasive lumbar decompression has demonstrated similar results with less cost, complication, and reoperation rates than open decompression. Interspinous process devices add cost and reoperation risk without additional functional or pain benefit. Of patients successfully treated nonsurgically, 15% to 43% will continue to enjoy improvement over a 1- to 5-year follow-up. The occurrence of concurrent asymptomatic lesions in the cervical or thoracic regions is well-known in elderly patients with surgical decompression for lumbar stenosis. This may have significant bearing on otherwise unexplained findings on physical examination, the position of the patient during surgery, and management in general. Lipoprostaglandin E1 and EP4 agonist at high concentrations might be potential therapeutic agents because they are expected to increase blood flow in nerve roots in patients with spinal canal stenosis, although their value has not been demonstrated as better than or additive to pregabalin in a controlled trial.
• Lumbar spinal stenosis is a very common condition. It is the most common cause of spinal surgery in individuals over 65 years of age.
• Degenerative lumbar spinal stenosis often results in disc space collapse, facet joint hypertrophy, soft-tissue infolding, and osteophyte formation, thus, narrowing the space available for the thecal sac and exiting nerve roots.
• Standard treatment options for patients with lumbar spinal stenosis include nonoperative therapies as well as decompression and fusion surgical procedures.
• Epidural steroid therapy during the acute phase does have the potential to offer significant time limited relief from pain.
• In patients with lumbar stenosis without concomitant degenerative spondylolisthesis, symptoms of predominant back pain over leg pain is associated with inferior outcome following spinal fusion in conjunction with decompression for lumbar spinal stenosis. Additional spinal fusion does not offer added clinically significant benefit.
Stenosis of the lumbar spinal canal is most commonly associated with multilevel degenerative spine disease, although commonly worst at the L4-5 level. Such narrowing of the spinal canal may be asymptomatic, associated with low back pain, cause symptoms and signs of focal nerve root injury, or give rise to neurogenic claudication. The reason why some patients develop symptomatic stenosis and others do not is still unknown. When symptomatic, it is caused by mechanical compression on the neural elements or their blood supply. Neurogenic claudication refers to pain and discomfort in the low back, buttocks, and legs that occurs after walking and is relieved by sitting or leaning forward.
In 1803, Portal first made note of lumbar spinal stenosis from autopsies of patients with rickets. Many of these patients had not been symptomatic during life. In 1911, Dejerine distinguished neurogenic from vascular claudication. In 1950, Verbiest suggested that lumbar spinal stenosis might result in compromise of the cauda equina and produce pain in the lower limbs (83). Kirkaldy-Willis further clarified the pathoanatomic basis of spinal stenosis (40).
Lumbar spinal stenosis is a clinical syndrome with associated typical radiographic findings. Several series have established the prevalence of asymptomatic lumbar spinal stenosis in the older population. Boden and colleagues found that 21% of asymptomatic patients older than 60 years had lumbar spinal stenosis on MRI (08). Other control groups have reported incidence of radiological stenosis by MRI as high as 65% (29; 27).
The clinical manifestations of lumbar spinal stenosis range from disabling to asymptomatic. The characteristic features of neurogenic claudication may be preceded by years of nonspecific low back pain. Commonly, patients present when symptoms interfere with their mobility and associated activities of daily living. Lumbar spinal stenosis generally manifests in older persons and is more common in men.
Neurogenic claudication is classically described as a poorly localized sense of discomfort and aching pain in the lower back, buttocks, and legs, precipitated by walking and relieved by sitting. Patients may experience numbness or deadness of the limbs, paresthesias, or subjective weakness that is usually bilateral and asymmetric. The initial symptoms begin in the back and buttocks, and later tend to spread to the thighs and lower legs. Unlike radicular symptoms, the distribution of both motor and sensory symptoms is typically not dermatomal. Hall and colleagues described symptoms involving the whole limb in 78% of cases, with 15% of cases above the knee, and 6% of cases below the knee (31). Up to 11% of patients may present with bladder and sexual dysfunction. Although occasionally present when the patient is standing erect, claudication pain typically supervenes after a symptom-free period of walking. Continued walking is often accomplished with a progressively stooped posture. A point is reached where it is impossible to continue because of the pain. As a result, patients then stop walking, sit down (flexing the spine reduces the stenosis), and rest. Sitting will usually relieve symptoms sufficiently to allow further walking. Relief of symptoms with flexion of the spine explains why it is often easier to walk up an incline than on a level surface, and forms the basis of the bicycle test. A patient with neurogenic claudication will be able to cycle (spine flexed), but will not be able to walk erect (spine extended) for an equivalent time. A patient with vascular claudication is expected to have the same intolerance for both activities. Neurogenic claudication patients often complain that activities resulting in extension of the lumbar spine (standing, reaching repetitively overhead, and carrying heavy objects) precipitate symptoms. Shopping without leaning on a cart is frequently impossible. Furman and colleagues claim that some maneuvers, including lumbar hyperextension, walking, and walking with an exaggerated lumbar lordosis, are provocative for patients suffering from lumbar stenosis to bring on symptoms of neurogenic claudication; they can then lean forward to obtain symptomatic relief (Furman et al 2006). A multicenter Delphi process and patient assessment process identified a series of clinical criteria, when taken together as the N-CLASS, having a sensitivity of 80% and specificity of 92%. This weighted clinical scoring model is based on the following criteria: age greater than 60 years, positive 30-second extension test, pain in both legs, leg pain relieved by sitting, leg pain relieved by leaning forward, and SLR positive at greater than 60 degrees (25).
Other consequences of lumbar spinal stenosis, including nerve root compromise, frequently coexist with neurogenic claudication. Stenosis of the lateral recess of the spinal canal or the intervertebral foramen may lead to focal nerve root injury decades before narrowing of the central spinal canal induces neurogenic claudication. The gradual nature of the nerve root compromises results in less pronounced radicular symptoms. Neural stretch signs are often absent.
Usually, neurogenic claudication is of gradual onset, and once established, results in symptoms that may become disabling (progressively lower symptom threshold or diminished exercise tolerance). Neurogenic claudication is not customarily associated with progressive neurologic deficit.
The few natural history studies of lumbar spinal stenosis are characterized by small sample sizes and are difficult to interpret because of methodological bias in the stratification of surgically and nonsurgically managed patients. In general, these studies suggest that established neurogenic claudication is often nonprogressive. Saal and colleagues documented the outcome of 52 patients treated conservatively: the majority were unchanged clinically at follow-up, and were able to function within their symptomatic limits without surgery. Only four patients eventually had surgery (59). Johnsson and colleagues followed the clinical course of 19 conservatively treated (mean follow-up time of 31 months) and 44 surgically treated patients with lumbar spinal stenosis (mean follow-up time of 53 months). There was no substantial outcome difference between the two groups (36).
Neurologic examination at rest is usually normal. Restricted mobility, local lumbar spine tenderness, and evidence of root compression related to coincidental lumbar spinal degenerative disease are commonly associated with the diagnosis. Patients examined immediately after symptom-provoking treadmill stress tests may have minor motor, sensory, or reflex deficits that rapidly normalize with rest.
Patients with neurogenic claudication often become remarkably well-adapted to their symptoms, and simply stay within the limits of pain-free mobility (ie, they may walk in a stooped fashion with the aid of a cane or walker, and sit when necessary).
Although the symptoms of neurogenic claudication may eventually become intolerable, lumbar spinal stenosis typically does not progress to fixed neurologic deficit. Many patients with lumbar spinal stenosis find that they can remain mobile within the specific constraints of their symptoms.
A 65-year-old man with coronary artery disease and chronic, mild, low back pain complained about three months of disabling leg pain when walking. The pain was located in the buttocks and upper legs in a symmetric distribution, and began after some 10 minutes of walking on the level. The pain would ease after sitting and resting for several minutes, and he was usually able to continue walking. He could ascend the two flights of stairs to his apartment, and he could continue to ride a bicycle. Initial referral was for suspected vascular claudication, but no clinical evidence of vascular insufficiency was found. Ultrasound examination of blood flow in the legs was normal.
Neurologic examination showed limited mobility of the lumbar spine, but no local tenderness or deformity. The right straight leg raising sign elicited pain in the back and right buttock at 50° elevation of the right leg above the horizontal. Muscle bulk, tone, and power in the lower limbs were normal. Tendon reflexes were symmetric at the knees and depressed at the right ankle. Proprioception and vibration sensation were slightly diminished at the toes, consistent with the patient's age.
MRI of the lumbosacral spine showed widespread degenerative spine disease, central disc bulges at L3-L4 and L4-L5, and a focal, right-sided, posterolateral disc protrusion at L5-S1. Deformation of the thecal sac at the lower lumbar levels, and multilevel neuroforaminal narrowing were present. Needle EMG revealed mild chronic partial denervation with reinnervation in the medial head of the right gastrocnemius muscle. A diagnosis of neurogenic claudication secondary to lumbar spinal stenosis associated with a mild right-sided S1 radiculopathy was made. The patient underwent a trial of conservative treatment (physical therapy and anti-inflammatory medication), but felt that no symptomatic improvements had been made after six months. His quality of life was significantly diminished by his reduced mobility. L3-S1 decompressive laminectomies with posterior fusion were performed. Nine months after surgery, he was able to walk continuously for 30 minutes on a level platform without pain or needing to rest.
Dagi and colleagues were the first to use the term "tandem spinal stenosis" to describe combined stenosis (16). The occurrence of concurrent asymptomatic lesions in the cervical or thoracic regions is well-known in elderly patients with surgical decompression for lumbar stenosis. Kim and colleagues reported a prevalence of 76.2% for cervical lesions, 29.7% for thoracic lesions, and 25.7% for concurrent cervical and thoracic asymptomatic lesions with lumbar spinal stenosis, investigated postoperatively (38). This may have significant bearing on unexplained findings on physical examination, the position of the patient during surgery, and management in general.
Lumbar spinal stenosis may result from congenital or acquired causes. Subjects of normal stature with short vertebral pedicles that narrow the anteroposterior diameter of the spinal canal may become symptomatic in their third decade and fourth decade of life. Achondroplastic dwarfism, hereditary exostosis, and other infrequently encountered conditions may also result in a narrowed spinal canal. Congenital stenosis is frequently exacerbated by secondary degenerative disease.
Most commonly, acquired lumbar spinal stenosis is found in an older age group. Typically, multiple levels of the lumbosacral spine are involved by degenerative discogenic, ligamentous, or spondylotic change. Spondylolisthesis (the anteroposterior slippage of a vertebra on the one adjacent to it), most often at L4-L5, is frequently coexistent. Central canal stenosis, lateral recess stenosis (13) and foraminal stenosis may coexist and contribute to neurogenic claudication. Other causes of acquired lumbar spinal stenosis include Paget disease (88), diffuse idiopathic spinal hyperostosis, fluorosis (seen in parts of India with excessive fluoride supplementation of drinking water), postsurgical change, trauma, acromegaly (18), and ankylosing spondylitis.
The pathogenesis of intermittent neurogenic claudication resulting from lumbar spinal stenosis is not completely understood. Symptoms are thought to be caused by direct mechanical compression or indirect vascular compression of the nerve roots or the cauda equine (19). A small, but provocative amount of research literature makes use of animal models of cauda equina compression. Any proposed model of etiology must account for several highly characteristic clinical features of the syndrome:
(1) Neurogenic claudication is precipitated by walking and relieved by rest.
(2) Sitting, even with sustained exercise (biking), improves symptoms.
(3) Lumbar spinal canal stenosis is present.
(4) The spinal canal stenosis is almost always multilevel.
The most common scenario is that of progressive, chronic, degenerative lumbar spine disease on a background of a congenitally narrow lumbar spinal canal. Cross-sectional narrowing of the central canal occurs at adjacent segmental levels, or central narrowing at a single segment together with contiguous multilevel neuroforaminal narrowing. The acute or subacute focal stenosis seen with epidural compression by tumor or herniated disc does not precipitate neurogenic claudication.
Reduction in the cross-sectional dimensions of the lumbar spinal canal and an increase in epidural pressure are the result of an erect posture. Extension of the lumbar spine, axial loading with standing, and the exertion of walking are all factors that contribute to symptoms. Takahashi and colleagues have demonstrated increased epidural pressure in human subjects with walking and venous congestion of the cauda equina by myeloscopy (77).
Porter, among others, has suggested that with low-pressure compression of two adjacent spinal segments, exercise may induce congestion in the venous plexus draining the cauda equina and secondary arterial insufficiency to these neural structures (57). In Olmarker's pig model, 2-level compression diminished blood flow to the cauda equina and reduced nerve conduction velocity when the nerve roots were stimulated directly (56). Similar mechanisms may precipitate neurogenic claudication: walking in the presence of lumbar spinal stenosis results in ischemic neurapraxia of the cauda equina and produces pain in the buttocks or legs. Pain subsides when the stenosis is relieved by sitting and flexing the spine, and the muscular activity of walking ceases. Ikawa and colleagues performed an electrophysiologic analysis on a chronic lumbar spinal stenosis model of rats (33). They demonstrated that ectopic firing was elicited by venous stasis only in the lumbar spinal canal stenosis animals, thereby suggesting that the venous stasis may be a major factor of neurogenic intermittent claudication.
Low back pain secondary to degenerative spine disease is a major cause of morbidity and lost work place productivity in the general population. Lumbar spinal stenosis is particularly prevalent in older people and is the most frequent cause of spinal surgery in this population (76). Large prospective studies of the natural history of lumbar spinal stenosis or neurogenic claudication are lacking. Only a few studies have examined the prevalence of lumbar spinal stenosis in the general population. Yabuki and colleagues estimate the prevalence of lumbar spinal stenosis to be 5.7% in Japanese subjects aged 40 to 79 years, affecting about 3,650,000 Japanese (91). Correlated factors with lumbar spinal stenosis included an advanced age (60 years or older), diabetes mellitus, depressive symptoms, urological disorders, and osteoarthritis/fracture. A strictly sampled representative population was used for this study. Recent studies show a dose relationship between smoking and lumbar spinal stenosis requiring surgical treatment in a cohort of construction workers (42).
Anecdotal experience suggests that practical public health advice (posture, correct lifting technique, avoidance of trauma) may reduce the likelihood of developing spinal degenerative disease and lumbar spinal stenosis.
The diagnosis of neurogenic claudication as a manifestation of lumbar spinal stenosis requires the recognition of the highly characteristic history together with radiologic evidence of lumbar spinal stenosis. An International Delphi study noted that the questions most likely to be asked by clinical experts in ascertaining the diagnosis of symptomatic lumbar spinal stenosis are leg pain with walking, leaning forward to relieve pain, use of a shopping cart or bicycle for relief, and presence of motor and/or sensory symptoms. Additional queries include presence of foot pulses, presence of weakness, presence of low back pain, walking with a limp, and lacking a history of diabetes (78).
Degenerative lumbar spine disease in the absence of lumbar spinal stenosis can cause intrinsic low back and leg pain that may be exacerbated by activity; however, it does not demonstrate a stereotyped relationship to walking, and does not improve with sitting. Usually, the pain from lumbar spinal stenosis is less intense and more diffuse. Radiculopathies frequently result in focal neurologic findings, whereas the neurologic examination in lumbar spinal stenosis is most often normal. More often than not, straight leg raising signs are absent in lumbar spinal stenosis and often present with L5 or S1 nerve root injury. Facet joint-associated ganglions, spondylodiscitis, paravertebral abscesses, neoplasms, and intraspinal hematoma (spontaneous or posttraumatic) are less common reasons of radiculopathies. Hematomas in the lumbar ligamentum flavum are rare and might mimic neurogenic claudication (73).
Vascular claudication may be confused with neurogenic claudication. Typically, vascular claudication causes burning pain in the calves when walking up an incline. Proximal arterial stenosis (bifurcation of the aortic, common iliac, hypogastric, or hip arteries) can be easily confused with neurogenic claudication. Hip or buttock pain is often the leading symptom, involving the area of the trochanter, groin, or thigh. Characteristically, symptoms appear with walking, are relieved by rest, and recur when walking resumes again. Arteriography is the examination of choice, performed during treatment, to guide angioplasty (46). Neurogenic claudication is less symptomatic when walking uphill due to the flexed position of the spine. The bicycle test facilitates differentiation of these two distinct entities: the leg pain of vascular claudication occurs with any muscular activity of the legs that increases demand for increased regional blood flow to muscle (vascular claudication is triggered by the exertion of pedaling a bicycle). In contrast, neurogenic claudication is not caused by cycling as the increased demand for regional blood flow to nerve roots is mitigated by the increased cross-sectional area of the spinal canal with the spine in flexion.
The symptoms of vascular claudication are evident after a relatively constant walking distance. Pain tends to begin in the calves, spread proximally, and resolve rapidly with rest. Evidence of peripheral vascular disease (diminished distal pulses, poor capillary filling, reduced skin temperature, shiny skin, or hair loss) is apparent on examination of the feet. Low back pain is usually absent. Dabasia and colleagues reported a case of neurogenic claudication from lumbar epidural varices secondary to obstruction of the inferior vena cava due to follicular lymphoma (15). Successful chemotherapy resulted in resolution of the varices and the symptoms of neurogenic claudication, suggesting that epidural venous engorgement can result in neurogenic claudication in the absence of spinal stenosis.
Distal polyneuropathy often presents with distal symmetric pain in the feet or legs that is worse when walking, but also present at rest. In contrast to both neurogenic claudication and vascular claudication, the pain of polyneuropathy has a distinct distribution (typically the feet) and quality (burning or painful paresthesias), and is often associated with distal symmetric sensory or motor deficit.
MRI imaging is the study of choice, although CT myelography is still utilized, especially in patients with adjacent spine fusion surgery and in patients for whom MRI is contraindicated (those with some pacemakers, spinal cord stimulators, and other implanted neuromodulation and stimulation devices). Flexion extension radiographs are used to evaluate segmental instability.
Measures of spinal canal and thecal sac anteroposterior diameter or cross-sectional area are used to make the radiologic diagnosis. CT is superior for visualizing the bony elements of the spine, lateral recess, and intervertebral foramen, but exposes patients to ionizing radiation.
MRI provides soft tissue detail (including neural structures) without exposure to ionizing radiation.
The literature documents a variety of measurements used to establish the diagnosis of lumbar spinal stenosis. Schonstrom and colleagues considered the following dimensions of the cross-sectional area of the thecal sac at its narrowest point significant: greater than 100 mm² (normal), 76 mm² to 100 mm² (moderate stenosis), and less than 76 mm² (severe stenosis) (65). Anteroposterior diameters of the lumbar spinal canal ranging from 10 mm to 15 mm have been used as a cut-off between stenosis and a normal canal (37). Imaging of lumbar spinal stenosis is surveyed in reviews by Saifuddin (60) and Schonstrom (64). However, when evaluating for symptomatic lumbar stenosis pain, neuroradiologists diagnosed lumbar stenosis in 65% of asymptomatic volunteers, and the central canal diameter was no different in symptomatic and asymptomatic patients (29; 27). In adults over 65 with no red flags, another study showed that the severity of disc and facet degeneration was not correlated with neurogenic claudication and pain (32). Studies indicate a poor relationship between pain and a variety of anatomic measures of stenosis accounting for facet hypertrophy, ligamentum flavum hypertrophy, and stenosis centrally at the foramen and at the lateral recess (10; 85).
In practice, radiologic spinal stenosis is commonly found in asymptomatic patients. MRI sensitivity and specificity in mild to moderate lumbar stenosis is 59% and 42%, respectively (29; 27), although severe stenosis approaches 95% and 90% (92). No substantial relationship exists between the degree of stenosis and the severity of symptoms. Clinical judgment is required in each case to decide on the probable contribution of the stenosis to patient symptoms. A more recent study on CT evaluation of L5-S1 foraminal stenosis indicated that completing this evaluation in the sagittal plane (compared to coronal and axial) had the best inter-observer agreement as well as the best predictor of symptoms and operability defined as no clinical improvement with three months’ conservative treatment (68).
Typically, standard nerve conduction studies and needle EMG are normal. This observation complements animal models that suggest the neural basis of neurogenic claudication is ischemic neurapraxia of sensory more than motor roots of the cauda equina. This proposed mechanism is congruent with the observed time course of recovery of neurogenic claudication symptoms after rest with the spine flexed. This time course is too rapid for demyelination and remyelination or axonal loss with regeneration. As a result, electrophysiologic investigation has a role limited to investigation of focal symptoms and signs of nerve or nerve root injury and to evaluate mimics of lumbar stenosis. Nerve conduction studies performed after exercise may reveal slowing in proximal motor and sensory segments (07). London found a reduced H-wave recruitment curve after exercise (49). Similarly, dynamic F-waves showed prolonged latencies and chronodispersion. Stolov found that somatosensory evoked responses were abnormal in several patients with normal nerve conduction studies. F wave studies after walking stress tests provide more information for the diagnosis of neurogenic claudication (06). Electromyography continues to be the single most useful test to diagnose nerve root compromise in lumbar spinal stenosis. Typically, multiple root involvement is seen at the paraspinal level as opposed to single root in radiculopathy. In particular, this is useful when lumbar stenosis and radiculopathy coexist. Abnormal electrophysiologic findings at the paraspinal levels seen in spinal stenosis can be mimicked by the combination of diabetic polyneuropathy and polyradiculopathy (89) and may require thoracic paraspinal examination to distinguish these mimics.
Electromyography in a study group with mild and moderate lumbar stenosis distinguished these patients from asymptomatic control and back pain controls with 79% sensitivity and 50% specificity. Paraspinal mapping score showed 100% specificity (30). Paraspinal mapping also shows the ability to distinguish clinical and radiologic spinal stenosis from asymptomatic patients with radiological stenosis in a group of patients with more severe spinal stenosis (92). Common bilateral paraspinal mapping abnormalities may be indicative of relative spinal instability rather than due to anatomical stenosis (28).
Treadmill exercise testing with recording of the mean time to the development of claudication pain is helpful in quantifying the functional impact of spinal stenosis, as well as predicting response to surgery (71). In addition to history and physical examination, uniform well-defined, unambiguous radiologic criteria are still needed for accurate diagnosis of spinal stenosis. The importance of this cannot be overemphasized as the study of many modes of treatment and treatment outcomes is heavily dependent on the same. Li and Yen observe that there is often a poor correlation between clinical and radiologic diagnoses of spinal stenosis (48). In their study, the final number of surgical candidates remained unchanged in spite of an increase in the number of MRI and CT scans.
Selective nerve root block had a high sensitivity, specificity, and positive predictive value in identifying patients with foraminal stenosis who go on to have successful clinical outcome with endoscopic decompression surgery (47).
Additional techniques that have been considered include measuring distal motor latency with root level stimulation in foraminal versus central lumbar stenosis (34). Cauda equina motor conduction time has also shown promise in distinguishing patients with lumbar spinal stenosis (66). Neither of these techniques have been used enough to know their added utility in patient evaluation.
Operative treatment for lumbar spinal stenosis is the most common spine surgery performed in adults over 45 years of age in the United States. A study of 65 patients with symptomatic lumbar stenosis and stable grade 1 spondylolisthesis randomized to complete laminectomy and medial facetectomy or decompression with pedicle screw fixation showed an improved SF-36 out to four years in the fusion group and a reoperation rate in the decompression only group of 34% (26). Reoperation in the fusion group began at year 3. However, in a study of 247 randomly assigned patients to decompression versus fusion with 1 to 2 level disease and stratified for spondylolisthesis indicated no difference in pain or function (measured by the Oswestry Disability Index) out to six and a half years with similar reoperation rates (20). A recent PRISMA-compliant meta-analysis did not show superiority of decompression with fusion over decompression alone with regard to pain, Oswestry Disability Index, and patient satisfaction, although follow up rates ranged from 12 to 120 months in the studies included (90). In 1992, Turner and colleagues showed the following complication rates for lumbar decompressive surgery for spinal stenosis: perioperative mortality -0.3%, dural tears -5.9%, deep infection -1.1%, superficial infection -2.3%, and deep vein thrombosis -2.7%, for an overall complication rate of 12.6% (81).
Studies that look at long term surgical outcomes need to account for the observation that surgery for adjacent segment disease escalates after the tenth year postfusion to 25.6% and to 37.5% at year 15 (52). European registry data of 4768 patients indicates that outcome is not impacted by age at the time of surgery and that quality of life outcomes were most related to the ASA status of the patient (72). Pain and functional outcome are not negatively impacted by increased time for conservative therapy compared to proceeding immediately to surgery (95). Amundsen and colleagues concluded that for lumbar spinal stenosis, the outcome was most favorable for surgical treatment (03). But they still recommended conservative management for many symptomatic patients from lumbar spinal stenosis, with the hope that those with unrelieved symptoms can be treated surgically later with a good outcome as demonstrated by Zweig and colleagues (95). Weinstein and colleagues, though their study was somewhat limited, note that in patients with symptomatic spondylolisthesis, nonrandomized comparisons of surgical intervention versus nonsurgical interventions revealed substantially better outcomes in pain and function, as well as satisfaction, three months after surgery (86). In a study published a year later it was found that patients with degenerative spondylolisthesis and spinal stenosis treated surgically showed substantially greater improvement in pain and function during a period of two years than patients treated nonsurgically. Prior to the subjective opinion to proceed to surgery, 68% received physical therapy, 54% had spine injection therapy, 55% were treated with NSIADs, and 27% received opioids. In the conservative treatment group, only 39% received spine injection therapy (87), indicating that conservative therapy was not a standard or robust intervention prior to surgical treatment in this study. Clinical cauda equina syndrome with appropriate symptoms and signs is an absolute indication for surgery. A long-term outcome study of results after laminectomy for lumbar spinal stenosis in an elderly group of patients found that the Oswestry Disability Index is more sensitive than the Pain Visual Analog Scale score in assessing prognostic value and that patient satisfaction is difficult to prognosticate, underscoring the particularities that this population presents regarding functionality assessment (09). Prognostic value of preoperative factors, when considered, report a negative influence of low-back pain and female sex. One study concludes that lumbar laminectomy appears to be the most cost-effective treatment strategy for patients with symptomatic lumbar spinal stenosis (11). In efforts to analyze the role and outcome of spinal fusion in conjunction with decompression for lumbar spinal stenosis without concomitant degenerative spondylolisthesis, Sigmundsson and colleagues concluded that predominance of back pain over leg pain is associated with inferior outcome (70). Although additional spinal fusion improves unadjusted outcome, the benefit is small and not clinically significant, and generally disappears in the adjusted analysis.
For less invasiveness, the technique of unilateral laminotomy for bilateral decompression was developed. This also offers better preservation of spinal stability. Oertel and associates, in their 10-year experience with unilateral laminotomy for bilateral decompression in symptomatic lumbar spinal stenosis, confirm that unilateral laminotomy for bilateral decompression allows good and long-lasting operative results in patients; furthermore, postoperative deterioration, recurrences, and spinal instability are infrequent in their experience (55). By preserving the posterior ligament complex integrity, spinoplasty is a good alternative to long-segment fusion to enable desired decompression and, at the same time, avoid iatrogenic instability (12; 80). Two systematic reviews of minimally invasive lumbar decompression shows no difference in outcome compared to open decompression with fusion, with complication rates of 3.3% versus 12.8%, and reoperation rates of 5.8% versus 16.3%, respectively (54; 63).
X-STOP is the first interspinous process decompression device that was shown to be superior to nonoperative therapy in patients with neurogenic intermittent claudication secondary to spinal stenosis in the multicenter randomized study at one and two years. Postoperative complications may include infection, iatrogenic instability, pseudarthrosis, hardware failure, and the need for future surgery because of the development of new diseases at the same or adjacent levels (43).
Coe and colleagues recommended posterior pedicle-based dynamic stabilization using the NFlex Dynamic Stabilization System as an effective alternative to rigid fusion to treat pain and functional loss (14). A randomized controlled trial comparing interspinous spacer surgery to decompression alone in 159 patients showed no difference in quality of life outcomes with higher costs for the device and higher reoperation rates (21% vs. 6%) in the spacer group (82), confirmed by systematic review and meta-analysis (94). Cochrane reviews indicated that surgical techniques were comparable, yet techniques that required hardware were more expensive, had higher complication rates, and required longer operating room and hospitalization time (50). A more recent controlled trial confirmed the lack of difference in patient-reported outcomes but noted that patients with interlaminar stabilization had much more improvement in walking distance and were much less likely to require postsurgical injection therapy than patients treated with decompression alone (61).
The most recent modification of methods used to achieve lumbar interbody fusion includes the use of minimally invasive surgical (MIS) techniques. The clinical outcomes are comparable with equivalent open procedure, but the advantages include less soft tissue injury, minimized blood loss, reduced postoperative pain, and shortened length of stay. Jhala and colleagues in their study of MIS-transforaminal lumbar interbody fusion (TLIF), report good clinic-radiological outcome in addition to finding it superior in terms of postoperative back pain, blood loss, hospital stay, and recovery time as well as medication use (35). On the contrary, minimally invasive TLIF requires more radiation time during surgery and takes longer operative time than a conventional open lumbar fusion, and it is difficult to treat bilateral symptoms using a unilateral approach (44; 84). Like any other surgical procedure, it has its own learning curve.
Epidural steroids were not better than lidocaine alone in a study of 400 patients treated with epidural injection with central stenosis with leg pain scores greater than 4. Transforaminal approach was directed based on patient symptoms and intralaminar injection at the level below greatest stenosis. No sham treatment was used as comparison (22). Nonoperative treatment for patients with various lumbar spinal stenosis conditions is a reasonable alternative to spinal surgery. Several studies involving patients with nonsurgical therapy suggest that 15% to 43% will continue to enjoy improvement over a 1- to 5-year follow-up period (04; 75). This includes observational studies of epidural injection, which show a 32% operation rate in the first 24 months and 44% satisfaction with a single injection protocol with no further treatment needed over two years (17). Manchikanti and colleagues reported significant improvement with caudal and interlaminar epidural approaches with local anesthetic only or with steroids in a long-term follow-up of up to two years in patients suffering with chronic lumbar spinal stenosis (51). They also reported significantly better results with the interlaminar approach. Symptomatic medical treatment of lumbar spinal stenosis may include limited bedrest, antiinflammatory and analgesic medication, and physical therapy. Fluoroscopically guided caudal epidural steroid injection was effective for the management of degenerative lumbar spinal stenosis, especially central canal stenosis, with excellent short-term and good long-term pain relief, without significant outcome predictors (45). Epidural steroids can lead to sustained cortisol suppression at least through the three-week measurement window of a study in patients with lumbar spinal stenosis. This effect is more pronounced when using particulate steroids (21).
Siebert and colleagues emphasized the need for multimodal conservative management including patient education, pain medication, de-lordosing physiotherapy, and epidural injections for symptomatic patients with mild to moderate lumbar spinal stenosis (69). They feel surgery is indicated only in patients where conservative management proves ineffective after three to six months, or in patients with severe symptoms. Epidural injections, group exercise and manual therapy resulted in improvement in walking distance to a similar degree. Manual therapy resulted in statistically greater improvement in Spinal Stenosis Score than the other treatments but the change was not to a degree that would be considered clinically meaningful (62). A comprehensive conservative treatment program of manual therapy, education, and exercise was better than self-directed exercise with improved walking distance and statistically but not clinically significant pain score improvement over the one-year follow-up (02). In one study, patients who successfully completed conservative treatment for lumbar stenosis were more likely than not to have sustained these benefits for five years or more posttreatment (79). In military healthcare beneficiaries with low back pain applying lumbar manipulation techniques, both lumbopelvic and lumbar neutral gap groups experienced statistically significant reductions in pain and disability at 48 hours posttreatment (74). The authors claim the outcomes are predictable if the patients satisfy the clinical prediction rule. Babb stresses that finding the imbalance, treating to correct the imbalance, and instruction on proper movement patterns in a safe, proactive way are vital for success of physical therapy in patients with low back pain (05). Ahmed and colleagues report that patients with chronic low back pain treated with shortwave diathermy, in addition to nonsteroidal anti-inflammatory drugs, exercises, and activities of daily living instructions, improved significantly compared to similar patients not treated with shortwave diathermy (01).
Lipoprostaglandin E1 and EP4 agonist at high concentrations might be potential therapeutic agents because they are expected to increase blood flow in nerve roots in patients with spinal canal stenosis, although their value has not been demonstrated as better than or additive to pregabalin in a controlled trial (39). Calcitonin appears to relieve claudication pain in patients with Paget disease and has anecdotally been found to relieve symptoms associated with degenerative lumbar spinal stenosis (58). The basis for this effect is not clear. Murakami found that lipo prostaglandin E1 increased cauda equina blood flow and relieved symptoms of neurogenic claudication in a small series of patients with lumbar spinal stenosis (53). EP4 agonist at high concentrations might be a potential therapeutic agent as it is expected to increase blood flow in nerve roots in patients with spinal canal stenosis (67).
Undoubtedly, surgery benefits many patients. No controlled, prospective trials of surgical versus conservative management have taken place. Knutsson and colleagues reported that although obese patients achieved significant pain reduction and improved ambulation and QoL after surgical treatment for lumbar spinal stenosis, obesity was associated with a higher degree of dissatisfaction and poorer outcomes after surgery (41).
After analyzing randomized controlled trials comparing surgical versus nonoperative treatments in participants with lumbar spinal stenosis confirmed by clinical and imaging findings, Zaina and colleagues concluded that they have very little confidence to conclude whether surgical treatment or a conservative approach is better for lumbar spinal stenosis, and provided no new recommendations to guide clinical practice (93). However, they drew attention to the fact that the rate of side effects ranged from 10% to 24% in surgical cases, and no side effects were reported for any conservative treatment. They emphasized that clinicians should be very careful in informing patients about possible treatment options, especially given that conservative treatment options have resulted in no reported side effects.
Gauthé and associates reported a case of symptomatic postoperative pneumocephalus, an uncommon complication after lumbar decompression (24). After one day, computed tomography was performed to explore intense lumbar pain and revealed a voluminous pneumorachis. This was followed by a generalized tonic-clonic seizure. Imaging revealed a voluminous pneumocephalus responsible for a significant space-occupying effect on the frontal lobe. A conservative treatment was initiated, including bed rest, oxygen therapy, neurologic monitoring, and antiepileptic therapy, followed by progressive improvement and a total radiological regression occurring in 21 days. This case highlights the fact that prevention of postoperative pneumocephalus should include a systematic repair of iatrogenic dural tear, and even in the presence of severe symptomatic manifestations, a conservative treatment is associated with total recovery.
The existence of spinal stenosis may affect a decision to use epidural anesthesia.
Anthony E Chiodo MD
Dr. Chiodo of the University of Michigan Medical School has no relevant financial relationships to disclose.See Profile
Matthew Lorincz MD PhD
Dr. Lorincz of the University of Michigan received honorariums from Alexion and Xenith for advisory board service.See Profile
Nearly 3,000 illustrations, including video clips of neurologic disorders.
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
Full spectrum of neurology in 1,200 comprehensive articles.
This article includes discussion of ulnar neuropathies, Guyon canal neuropathy, ulnar neuropathy at the wrist, and flexor carpi ulnaris exit compression.
Jun. 07, 2021
May. 26, 2021
May. 04, 2021
Epilepsy & Seizures
Apr. 09, 2021
Apr. 03, 2021
Apr. 03, 2021
Apr. 01, 2021
Acute traumatic spinal cord injury (TSCI) is a global epidemic in modern society. Yearly, there are over 12,000 new cases of acute spinal cord injury
Mar. 31, 2021