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Lumbar Spinal Stenosis
CHAPTER 56
LUMBAR SPINAL STENOSIS J.M. Whitman, PT, DScPT, OCS, FAAOMPT, and J.M. Fritz, PT, PhD, ATC
1. What is lumbar spinal stenosis (LSS)? LSS can be defined as any narrowing of the lumbar spinal canal, nerve root canals, and/or intervertebral foramina that may encroach on the nerve roots of the lumbar spine. LSS can become a painful and potentially disabling condition in affected individuals. 2. How is LSS classified? There are two means of classification commonly used to describe patients with LSS; one is based on the anatomic location of the narrowing, the other on the etiology of the narrowing. ANATOMIC CLASSIFICATION • Lateral stenosis—narrowing that occurs within the lumbar intervertebral foramina and/or the nerve root canal, causing encroachment around the spinal nerve as it exits • Central stenosis—narrowing that occurs within the spinal canal, causing encroachment around the nerve roots of the cauda equina housed within the dural sac ETIOLOGIC CLASSIFICATION • Primary stenosis—narrowing caused by a congenital malformation or defect in postnatal development. Only about 10% of cases of lumbar stenosis can be considered to be primary stenosis. • Secondary stenosis—narrowing resulting from acquired conditions such as degenerative changes, spondylolisthesis, fractures, and postsurgical scarring. The most common cause of secondary stenosis is degenerative changes. Secondary stenosis may occur in individuals who already have a degree of primary stenosis. 3. What are the most common structural changes associated with LSS? The majority of cases of LSS occur secondary to degenerative changes. Facet joint arthrosis and hypertrophy, bulging and thickening of the ligamentum flavum, loss of disc height and posterior/lateral bulging of the intervertebral disc, and degenerative spondylolisthesis are the most common changes contributing to LSS. Other, less common causes of secondary stenosis include fractures, postoperative fibrosis, tumors, and systemic diseases of the bone, such as Paget’s disease. 4. Is lumbar stenosis a common problem? Yes; LSS is a common cause of low back pain, particularly in older adults. It is the most common reason for undergoing spinal surgery in individuals over the age of 65. Because of increases in life expectancy and improved diagnostic technology, rates of diagnosis of LSS and rates of surgery have increased substantially in the past several decades. 5. How will the typical patient with lumbar stenosis present clinically? In general, because degenerative changes are the predominant cause leading to LSS, affected individuals are typically older than age 50 with a long history of low back pain. Most patients will have symptoms of pain and/or numbness in one or both legs. Chronic nerve compression may lead to diminished lower extremity reflexes and strength or sensation deficits. Lumbar range of motion, particularly in extension, will be limited and painful, often reproducing leg symptoms. Symptoms tend to be posture-dependent, worsening with spinal extension and improving with flexion. Because of this, patients will generally feel better in a sitting position and worse when standing or walking. Several authors have provided information that helps quantify the impact of these various clinical indicators on the ultimate diagnosis of LSS. Katz et al. and Fritz et al. identified several clinical findings with associated sensitivity (Sn) and/or specificity (Sp) values for establishing the diagnosis of LSS. These findings are as follows: age over 65 Sn ¼ 0.77; pain below buttocks Sn ¼ 0.88; no pain
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when seated Sp ¼ 0.93; pain with flexion Sn ¼ 0.88; sitting is the best position Sn ¼ 0.89; standing/walking are worst positions Sn ¼ 0.89. Sugioka et al. sought to develop a score-based prediction rule to assist with diagnosis of LSS from self-report items only. The final predictors of LSS and associated risk scores are shown in Table 56.1. Scores of 7 or more yielded positive likelihood ratios of 1.90 to 3.91. Predictive Variable Age: 60–70 >70 Onset of symptoms >6 months Symptoms: Improve with bending forward Improve with bending backward Exacerbate while standing up Intermittent claudication present Urinary incontinence present
Assigned Risk Score 2 3 1 2 2 2 1 1
Last, Konno et al. also developed a score-based prediction rule for diagnosing LSS. In this analysis, the researchers also included items from the physical examination. Their final predictors for LSS and associated risk scores are shown in Table 56.2. For this prediction rule, total risk scores of 7 or higher yield the following diagnostic indices: sensitivity ¼ 0.93, specificity ¼ 0.72, positive likelihood ratio ¼ 3.31. Predictive Variable Age: 60–70 >70 Absence of diabetes Symptoms: Improve with bending forward Exacerbate while standing up Intermittent claudication present Examination: Symptoms induced by having patients bend forward Symptoms induced by having patients bend backward Good peripheral artery circulation Abnormal Achilles tendon reflex SLR test positive
Assigned Risk Score 1 2 1 3 2 3 1 1 3 1 2
6. Why do patients with LSS feel worse when standing than when sitting? Standing places the lumbar spine in a position close to full extension. Extension of the spine causes further narrowing of the spinal canal. In individuals without stenosis, this narrowing is tolerated without difficulty; however, patients with stenotic narrowing tend to have worse symptoms when standing or when standing and walking. Sitting causes flexion in the spine and therefore will generally reduce the symptoms of individuals with LSS. 7. Are there other factors that exacerbate symptoms for patients with LSS? Axial compression, as is experienced during weight-bearing, also creates increased narrowing of the spinal canal and may exacerbate the symptoms of LSS. Research has demonstrated that the narrowing effects of axial compression are similar in magnitude to those of spinal extension. This helps explain why walking can be difficult for patients with lumbar stenosis. Walking involves extension of the spine and creates increased compressive forces.
456 THE SPINE 8. What is neurogenic claudication? Neurogenic claudication is defined as poorly localized pain, paresthesias, and cramping of one or both lower extremities of a neurologic origin; symptoms are worsened by walking and relieved by sitting. There can be many causes of claudication; therefore the key distinguishing feature of neurogenic claudication is its neurologic origin—mechanical irritation of the cauda equina. The symptoms of neurogenic claudication are often the reason that an individual with LSS is prompted to seek medical treatment. 9. Are there other conditions that might be confused with lumbar stenosis? Other conditions that have been confused with LSS include osteoarthritis of the hip, vascular claudication (with peripheral arterial disease), unstable spondylolisthesis, and lumbar intervertebral disc herniation. Other frequent concomitant problems that may mandate additional differential diagnosis for those with lumbar stenosis may include diabetic neuropathy, other peripheral neuropathies, other lower extremity (LE) disorders, iliacus arterial involvement, and spinal tumors. 10. How can LSS be differentiated from other conditions with a similar presentation in the clinic? The postural-dependency of symptoms (ie, better with flexion or sitting; worse with extension, standing, and walking) is a unique characteristic of patients with LSS. A thorough history, including exacerbating and relieving positions or activities, will often reveal this posture-dependent nature of symptoms (see question 5 for more details). Clinical tests have also attempted to capitalize on the posture-dependency of stenosis symptoms to differentiate spinal stenosis from other conditions with similar symptoms. A “bicycle test” has been described in which the patient first pedals in an upright, seated position with the lumbar spine in extension and then with the spine in a flexed position. If the individual pedals farther in the spine-flexed position, the test is considered positive for LSS. Walking tests have also been described for use in differential diagnosis. The patient walks on a level surface in an upright posture and also in a slumped or flexed posture. If the patient can walk farther with the spine flexed, the test is considered positive for LSS. A variation on this test, called the Two Stage Treadmill Test (TSTT), compares walking on a level treadmill versus an inclined treadmill (15% incline). The incline of the treadmill causes the patient to flex the spine while walking and usually will improve walking capacity in patients with LSS. Earlier onset of symptoms and prolonged recovery with level treadmill walking yields a specificity (Sp) of 0.95 and a positive likelihood ratio (+LR) of 14.5. A longer total walking time on the inclined treadmill versus the level treadmill yields an Sp of 0.92 and a + LR of 6.5. Additionally, a thorough lower extremity neurovascular assessment should be performed, often including assessment of lower extremity muscle strength, reflexes, sensation, and pulses. The clinician should also look for trophic changes of the skin and nails and may opt to perform an ankle-brachial index test. This neurovascular assessment will help with differentiation from other neuropathic or vascular conditions. 11. Are diagnostic imaging studies or electrodiagnostic studies helpful in confirming a diagnosis of LSS? Diagnostic imaging modalities are generally used to confirm the diagnosis of LSS. The most commonly used tests are the following: • Magnetic resonance imaging—MRI is one of the most commonly used imaging studies to confirm a diagnosis of LSS. The anterior-posterior diameter of the spinal canal or the cross-sectional area of the dural sac can be measured to determine the extent of narrowing. • CT scan—The CT scan is also commonly used to assess the diameter or cross-sectional area in the same manner as described for the MRI. It is important to remember that the presence of stenosis with imaging is prevalent in the asymptomatic aging population; therefore correlation of imaging findings with clinical presentation is essential. Examination with electrodiagnostics is occasionally used to assist in the diagnosis of LSS. According to Haig et al., the following factors can help with this diagnosis: • Miniparaspinal mapping with a one side score >4: sensitivity ¼ 0.3; specificity ¼ 1.0 • Fibrillation potential in limb muscles: sensitivity ¼ 0.33; specificity ¼ 0.88 • Absence of tibial H-wave: sensitivity ¼ 0.36; specificity ¼ 0.92 • Composite limb and paraspinal fibrillation score: sensitivity ¼ 0.48; specificity ¼ 0.88
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12. Are plain film x-rays helpful in the diagnosis of LSS? Plain film x-rays can show the degenerative changes such as osteophytes and disc degeneration that are often the cause of LSS. Lateral views can demonstrate the diameter of the intervertebral foramina. However, plain film x-rays are limited in their usefulness by their inability to image the central spinal canal and the soft tissue changes that may contribute to LSS. 13. What are the most common impairments and functional limitations found in patients with LSS? The most common impairments found during the examination of the patient are restrictions in spinal range of motion. Side-bending is often limited bilaterally; lumbar extension may be quite limited and reproduce or intensify the patient’s symptoms. Lumbar flexion is also frequently limited in range but will often somewhat relieve the symptoms. Deficits in vibratory or pinprick sensation in one or both lower extremities can occur, along with strength or reflex deficits. Many patients will have a positive straight leg raise test. Another common area of impairment is the hip joint. Restricted range of motion, particularly in extension, and weakness of the hip extensors and abductors are common findings. The most widespread functional limitation in patients with LSS is diminished walking tolerance because of leg symptoms that are relieved by sitting, as well as limitation in prolonged standing postures. 14. Describe the surgical procedure for a patient with LSS. Surgical treatment of LSS is performed to relieve compression on the contents of the central and lateral spinal canals. The most common surgical procedure for patients with LSS is a decompression laminectomy in which portions of the vertebral arch are removed to reduce compression of the lumbar spinal nerves. Sometimes a fusion, with or without instrumentation, will also be performed, although this is usually only done if there is evidence of spondylolisthesis along with the spinal stenosis. 15. Should a patient with LSS have surgery? The decision to pursue surgery should be determined based on careful and shared decision making between providers and patients, with heavy emphasis on patient preferences. Clinical outcomes are generally good for surgical treatment, with high percentages of patients expressing satisfaction and reporting improvement early postoperatively. However, these outcomes tend to deteriorate with time, with only about 60% to 70% of patients satisfied after 4 to 7 years and between-group clinical outcomes for those treated with surgery versus conservative care diminishing within 2 to 8 years after surgery. Sufficient literature describing positive clinical outcomes from various nonsurgical approaches to care is available and often with no reported adverse outcomes. These nonsurgical approaches typically include treatments such as aerobic exercise, stretching, strengthening, mobilization/ manipulation, and patient education. Based on the known risks of surgical complications and the stable nature of spinal stenosis, current recommendations are that patients should be offered a rigorous trial of physical therapy care before pursuing surgery. Patients who do not improve should be well informed of the potential risks and benefits of surgery, including the fact that benefits from surgery will most likely diminish over time. 16. Will the symptoms of lumbar stenosis continue to worsen over time? Research to date shows that LSS is a generally stable condition. Although some patients will deteriorate over time, this is not inevitable, and large percentages of patients can maintain or improve their condition with time. 17. Will epidural steroid injections help patients with lumbar stenosis? Epidural steroid injections have been frequently recommended as a nonsurgical option for patients with LSS. Some patients will receive short-duration benefits from epidural steroid injections. The effectiveness of injections in reducing symptoms beyond a couple of weeks, however, is less likely. 18. What is the best physical therapy treatment for patients with lumbar stenosis? Numerous treatment options have been proposed for use by physical therapists in the treatment of patients with LSS. Flexion-oriented exercises are advocated to capitalize on the postural dependency of symptoms of spinal stenosis. General conditioning activities are useful and may include stationary cycling, aquatic exercise, and walking as tolerated by the patient. Any strength or flexibility deficits identified
458 THE SPINE during the physical examination should be addressed. Manual therapy (including mobilization, manipulation, and stretching) targeting the thoracic and lumbopelvic spine regions and hips may also be helpful. 19. Should traction be used in the treatment of patients with LSS? Pelvic traction has been recommended for the treatment of LSS in an attempt to relieve compression that results from the pathology. Although traction may be helpful for pain reduction in some patients, it should be combined with more active forms of therapy to improve function. 20. Can deweighted treadmill ambulation help patients with LSS? Deweighted treadmill ambulation uses a harness-and-traction device to provide a vertical traction force during ambulation on a treadmill. The traction force reduces the axial compression associated with weight bearing and may permit some individuals with LSS to walk with reduced symptoms of neurogenic claudication. This treatment technique may hold promise for selected patients with stenosis because it provides the benefit of traction while keeping the patient active and exercising. However, in a randomized trial by Pua et al. that compares exercise plus cycling versus exercise plus deweighted treadmill walking, both groups achieved similar pain and disability outcomes at 6 weeks. Therefore the use of deweighting should be considered as a potential rehabilitation tool on a case-by-case basis, based on clinical response, and, in general, should not be viewed as superior to cycling as a part of a comprehensive treatment program. 21. Is it possible to identify patient-centered factors that predict better versus worse outcomes from surgery for lumbar stenosis? Although many researchers have investigated this question, there is some conflicting information in the literature. Some identified predictors of worse surgical outcomes to date include depression, worse emotional health, smoking, Workers’ Compensation, anxiety, life dissatisfaction, higher BMI, longer duration of leg pain/symptoms, cardiovascular comorbidity, scoliosis, other disorders influencing walking ability, predominant back pain (>leg pain), prior lumbar surgery, history of psychiatric disease, female gender, and low baseline disability. In addition to not having these identified predictive factors for worse outcomes, the following factors have been identified as predicting better surgical outcomes: greater central canal stenosis, good or above average self-rated health, younger age, lower duration use of analgesics preoperatively, greater preoperative disability, more ambitious preoperative expectations related to pain and functional improvements, and no lifting required at work. 22. Are there published studies documenting patient outcomes with defined physical therapy treatment approaches? Many studies are now available demonstrating positive clinical outcomes of care for patients treated with interventions often provided by physical therapists, including aerobic exercise, stretching, strengthening, aerobic exercise, and mobilization/manipulation. Some studies also include traction, physical modalities, or lumbopelvic orthoses. Selected studies are described as follows: • Simotas et al. reported on the results of 49 patients treated with a program of physical therapy (flexion-oriented exercises) and epidural steroids. After 3 years, 9 patients (18%) had undergone surgery, 12 patients (24%) reported no change in symptoms, 23 patients (47%) had some amount of improvement, and 5 patients (10%) experienced worsening of symptoms. • Murphy et al. reported clinically meaningful long-term improvements in disability and pain for 57 patients treated with manipulation, neural mobilization, flexion exercises, and lumbar stabilization training in a prospective observational cohort. • Pua et al. conducted a trial that included 68 patients. Both treatment groups received lumbar flexion exercises, lumbar traction, and thermal modalities. One group also performed deweighted treadmill walking, and the other performed stationary cycling. Although there were no between-group differences, both groups improved from baseline to 6 weeks. • Ammendolia and Ngai reported on clinically meaningful improvements in pain and disability for a cohort of 49 patients after a 6-week program, including manual therapy (soft tissue and neural mobilization, manipulation, lumbar flexion-distraction, and muscle stretching), home exercises, and self-management strategies. • Cambron et al. included 60 patients in a pilot RCT that investigated optimal dosages of spinal manipulation. The treatment groups receiving a total of 12 and 18 manipulations over 6 weeks
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demonstrated significant within-group improvements up through 6 months in symptom severity, and the group receiving 18 manipulations had significant within-group improvements in physical function. Whitman et al. conducted an RCT with 58 patients that compared an individualized approach (impairment-based manual therapy interventions to the thoracic spine, lumbopelvic spine, and lower extremities; deweighted treadmill walking; and abdominal retraining exercises) to walking, a standardized flexion exercise, and a subtherapeutic ultrasound program. A greater proportion of patients in the pragmatic, individualized program reported recovery at 6 weeks versus the flexion exercise/walking group. Although both groups demonstrated positive outcomes over the 24-month follow-up, improvements in disability, satisfaction, and treadmill walking tests favored the individualized treatment group at all follow-up points. Delitto et al. conducted a multisite, randomized controlled trial that included 169 surgical candidates with lumbar stenosis. Patients were treated with either surgical decompression or a 6-week, well-defined, twice weekly physical therapy (PT) intervention program, including lumbar flexion exercises, patient education, general conditioning (cycling or treadmill walking), and individualized lower extremity strengthening and flexibility exercises. Those patients undergoing physical therapy intervention had similar outcomes to those treated with surgical decompression at the 2-year follow-up.
23. Should patients with lumbar stenosis wear a brace or corset? The use of a rigid corset to limit spinal extension or a soft corset for general support has been recommended. A soft corset may provide a measure of relief for patients. A more rigid brace, although effective in limiting or preventing extension, is often cumbersome and restrictive for the patient and should likely be reserved for those individuals not responding to other forms of nonoperative treatment. 24. How should the outcomes of treatment for patients with lumbar stenosis be measured? Measuring the effectiveness of any treatment for LSS is an important consideration. Patient-reported measures, such as the Oswestry or Roland Morris disability scales, as well as the condition-specific Swiss Spinal Stenosis Questionnaire, are useful for documenting functional limitations and disability. The measurement of walking tolerance, usually conducted on a treadmill or with a 6-minute walking test, is an important assessment and monitoring tool because it measures the most common and troublesome functional limitation in these patients. 25. Does stenosis occur in the cervical spine as well? Yes; stenotic narrowing can and does occur in the cervical spine. Similar to the lumbar spine, the narrowing may occur laterally, in the intervertebral foramen, or centrally, in the spinal canal. The etiology may be primary (ie, congenital), secondary to degenerative conditions, or a combination of these two factors. The presence of congenital stenosis of the central canal in the cervical spine is a particular concern for participants of collision sports, such as football. The normal sagittal plane diameter of the spinal canal in the cervical region is 17 to 18 mm. The diameter of the spinal cord is about 10 mm. If the sagittal plane diameter of the canal is diminished, the safety margin within the canal is compromised, and symptoms of compression of the spinal cord may result. As with lumbar stenosis, the presence of cervical stenosis on imaging may be present in absence of clinical symptoms, therefore mandating corroboration of clinical and imaging findings. 26. What symptoms will a patient with cervical stenosis exhibit? The symptoms of lateral and central cervical stenosis differ substantially. Lateral cervical stenosis typically results in compression of the cervical nerve root and produces symptoms of radiculopathy. Central cervical stenosis may compress the spinal cord, resulting in a condition termed cervical myelopathy. Symptoms of radiculopathy include neck and upper extremity pain and paresthesia in a dermatomal pattern. There may also be complaints of upper extremity muscle weakness in the affected arm. Symptoms of myelopathy are often subtler, particularly in the early stages. Neck pain is not always present. Unsteadiness in gait or clumsiness is often an early symptom. Wasting of the intrinsic hand muscles is common. An extrasegmental distribution of paresthesia in one or both hands and feet may be present, followed by a perception of weakness. Gait disturbances can become severe, significantly interfering with functional activities and safety.
460 THE SPINE 27. What is the typical clinical presentation for patients with central cervical stenosis? The signs of central cervical stenosis (myelopathy) are those of upper motor neuron, or long tract, disorders. Clinical signs may include weakness with spasticity, clonus, present Hoffmann and Babinski signs, hand withdrawal reflex, and an inverted supinator sign. Vibratory sensation is typically diminished in the lower extremities, and both upper and lower extremity reflexes may become hyperactive. Cervical range of motion is typically restricted in all planes. Lhermitte’s sign (spinal pain and/or radiating extremity pain and paresthesias with forced cervical flexion or extension) may be present. Spurling’s sign is expected to be negative, and manual cervical traction will not have any effect on symptoms. According to Cook et al., at least 3 of the following five clinical tests helps rule in cervical myelopathy: 1) gait deviation, 2) present Hoffmann’s test, 3) + inverted supinator sign, 4) present Babinski test, 5) age >45 y (specificity ¼ 0.99; CI ¼ 0.97–0.99); + LR ¼ 30.9; 95% CI ¼ 5.5–181.8). 28. Is treatment by a physical therapist helpful for cervical myelopathy? Nonsurgical care is often recommended for patients with mild myelopathy, although scant evidence exists investigating the impact of treatment by a physical therapist for this disorder. Intermittent cervical traction is often recommended as a potentially helpful intervention. In a small case series, Browder et al. reported improvements in pain and disability for 7 patients with cervical myelopathy who were all treated with intermittent cervical traction and thrust manipulation targeting the thoracic spine. No adverse events or outcomes were reported. 29. Is surgery recommended for patients with cervical myelopathy? The disorder is considered to be progressive in nature and potentially disabling, but those with cervical myelopathy (CM) often experience long periods of stable neurologic status between episodes of exacerbation. Conservative nonsurgical treatment is often recommended for patients with mild cervical myelopathy. In contrast, surgical management is typically considered for those with moderate to severe CM. Although one prospective RCT demonstrated no significant differences between groups (surgery versus no surgery) at 10 years, several other studies conclude that those with moderate to severe CM who undergo surgery experience improved outcomes over those who do not. Performing surgery early in the course of the condition is believed to lead to a better long-term outcome. Laminotomy or laminoplasty is typically performed to increase the dimensions of the central spinal canal and may be accompanied by cervical fusion. BIBLIOGRAPHY Ammendolia, C., & Chow, N. (2015). Clinical outcomes for neurogenic claudication using a multimodal program for lumbar spinal stenosis: A retrospective study. Journal of Manipulative and Physiological Therapeutics, 38(3), 188–194. Atlas, S. J., et al. (1996). The Maine lumbar spine outcome study, part III. 1-year outcomes for surgical and non-surgical management of lumbar spinal stenosis. Spine, 21, 1787–1795. Backstrom, K. M., Whitman, J. M., & Flynn, T. W. (2011). Lumbar spinal stenosis—diagnosis and management of the aging spine. Manual Therapy, 16, 308–317. Bridwell, K. H. (1994). Lumbar spinal stenosis. Diagnosis, management, and treatment. Clinics in Geriatric Medicine, 10, 677–701. Browder, D. A., Erhard, R. E., & Piva, S. R. (2004). Intermittent cervical traction and thoracic manipulation for management of mild cervical compressive myelopathy attributed to cervical herniated disc: A case series. Journal of Orthopaedic and Sports Physical Therapy, 34(11), 701–712. Cambron, J. A., Schneider, M., Dexheimer, J. M., Iannelli, G., Chang, M., Terhorst, L., & Cramer, G. D. (2014). A pilot randomized controlled trial of flexion-distraction dosage for chiropractic treatment of lumbar spinal stenosis. Journal of Manipulative and Physiological Therapeutics, 37(6), 396–406. Chang, Y., et al. (2005). The effect of surgical and nonsurgical treatment on longitudinal outcomes of lumbar spinal stenosis over 10 years. Journal of the American Geriatrics Society, 53, 785–792. Cook, C., et al. (2010). Clustered clinical findings for diagnosis of cervical spine myelopathy. Journal of Manual & Manipulative Therapy, 18(4), 175–180. Delitto, A., Piva, S. R., Moore, C. G., Fritz, J. M., Wisniewski, S. R., Jospeno, D. A., … , Welch, W. C. (2015). Surgery versus nonsurgical treatment of lumbar spinal stenosis: A randomized trial. Annals of Internal Medicine, 162, 465–473. http://dx.doi.org/10.7326/M14-1420. Deyo, R. A., Cherkin, D. C., & Loeser, J. D. (1992). Morbidity and mortality in association with operations on the lumbar spine. The influence of age, diagnosis, and procedure. Journal of Bone and Joint Surgery, 74-A, 536–543. Dvorak, J. (1998). Epidemiology, physical examination and neurodiagnostics. Spine, 23, 2663–2673. Fritz, J., Erhard, R., Delitto, A., Welch, W., & Nowakowski, P. (1997a). Preliminary results of the use of a two-stage treadmill test as a clinical diagnostic tool in the differential diagnosis of lumbar spinal stenosis. Journal of Spinal Disorders, 10(5), 410e6. Fritz, J. M., Erhard, R. E., & Vignovic, M. (1997b). A nonsurgical approach for patients with lumbar spinal stenosis. Physical Therapy, 77, 962–973.
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Fritz, J. M., et al. (1998). Lumbar spinal stenosis: A review of current concepts in evaluation, management, and outcome measurements. Archives of Physical Medicine and Rehabilitation, 79, 700–708. Haig, A. J., Tong, H. C., Yamakawa, K. S. J., et al. (2005). The sensitivity and specificity of electrodiagnostic testing for the clinical syndrome of lumbar spinal stenosis. Spine, 30, 2667–2676. Hurri, H., et al. (1998). Lumbar spinal stenosis: Assessment of long-term outcome 12 years after operative and conservative care. J Spinal Disease, 11, 110–115. Johnsson, K. E., Rosen, I., & Uden, A. (1992). The natural course of lumbar spinal stenosis. Clinical Orthopaedics, 279, 82–86. Katz, J., Dalgas, M., Stucki, G., Katz, N., Bayley, J., & Fossel, A. (1995). Degenerative lumbar spinal stenosis. Arthritis and Rheumatism, 38, 1236e41. Katz, J. N., et al. (1995). Degenerative lumbar spinal stenosis: Diagnostic value of the history and physical examination. Arthritis and Rheumatism, 38, 1236–1241. Katz, J. N., et al. (1996). Seven- to 10-year outcome of decompressive surgery for degenerative lumbar spinal stenosis. Spine, 21, 92–98. Konno, S., Hayashino, Y., Kukuhara, S., Kikuchi, S., Kaneda, K., & Seichi, A. (2007). Development of a clinical diagnosis support tool to identify patients with lumbar spinal stenosis. European Spine Journal, 16, 1951e7. Murphy, D. R., Hurwitz, E. L., Gregory, A. A., & Clary, R. (2006 Feb 23). A non-surgical approach to the management of lumbar spinal stenosis: A prospective observational cohort study. BMC Musculoskeletal Disorders, 7, 16. Penning, L. (1992). Functional pathology of lumbar spinal stenosis. Clinical Biomechanics, 7, 3–17. Porter, R. W. (1996). Spinal stenosis and neurogenic claudication. Spine, 21, 2046–2052. Pua, Y. H., Cai, C. C., & Lim, K. C. (2007). Treadmill walking with body weight support is no more effective than cycling when added to an exercise program for lumbar spinal stenosis: A randomised controlled trial. Australian Journal of Physiotherapy, 53(2), 83–89. Schonstrom, N., et al. (1989). Dynamic changes in the dimensions of the lumbar spinal canal: An experimental study in vitro. Journal of Orthopaedic Research, 7, 115–121. Simotas, A. C., et al. (2000). Nonoperative treatment for lumbar spinal stenosis: Clinical outcome results and a 3-year survivorship analysis. Spine, 25, 197–203. Sugioka, T., Hayashino, Y., Konno, S., Kikuchi, S., & Fukuhara, S. (2008). Predictive value of self-reported patient information for the identification of lumbar spinal stenosis. Family Practice, 25(4), 237e44. Whitman, J. M., Flynn, T. W., Childs, J. D., Wainner, R. S., Gill, H. E., Ryder, M. G., et al. (2006). A comparison between two physical therapy treatment programs for patients with lumbar spinal stenosis: A randomized clinical trial. Spine, 31(22), 2541–2549. Willen, J., et al. (1997). Dynamic effects on the lumbar spinal canal: Axially loaded CT-myelography and MRI in patients with sciatica and/or neurogenic claudication. Spine, 22, 2968–2976. Zdeblick, T. A. (1995). The treatment of degenerative lumbar disorders: A critical review of the literature. Spine, 20(Suppl), 126s–137s.
CHAPTER 56 QUESTIONS 1.
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Current best evidence leads us to include the following in our physical therapy–related care for patients with lumbar spinal stenosis: a. Double and single knee to chest exercises, quadruped “cat and camel” (flexion and extension) exercises, hot packs, and electrical stimulation. b. Repeated flexion exercises, double and single knee to chest exercises, and abdominal (“core”) retraining c. Aerobic exercise (cycling and/or walking), manual therapy to the lower quarter, lower quarter and abdominal muscle stretching and strengthening, and lumbo-pelvic flexion exercises d. Traction, electrical stimulation, cycling, and thermal modalities e. None of the above Which findings are most helpful in making a clinical diagnosis of lumbar spinal stenosis? a. Standing and walking aggravate symptoms, and sitting eases symptoms; younger age; low back pain only (none in the lower extremities) b. Standing and walking aggravate symptoms, and sitting eases symptoms; older age; presence of pain, paresthesia, and/or cramping into one or both lower extremities below the buttocks c. Sitting aggravates symptoms and standing and walking ease symptoms; older age; low back pain only (none in the lower extremities) d. Sitting aggravates symptoms and standing and walking ease symptoms; younger age; presence of pain, paresthesia, and/or cramping into one or both lower extremities below the buttocks Which answer below includes disorders that may present similarly to lumbar spinal stenosis in the clinical exam? Pick the best answer. a. Deep vein thrombosis, spondylitis of the lumbar spine, post-polio syndrome b. Femoral neck fracture, mechanical low back pain, hip and knee osteoarthritis
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c. Iliacus arterial disorder, fibular nerve adverse neural dynamics, mechanical low back pain d. Hip osteoarthritis, peripheral arterial disease, lumbar radiculopathy, peripheral neuropathy, spinal tumors What are common symptoms for a patient with cervical stenosis? a. Neck pain and headache, referral of symptoms into the thoracic region, absence of symptoms below the acromioclavicular joint b. Unsteadiness and clumsiness in gait, lower motor neuron changes in the upper and lower extremities, and an absence of neck pain c. Neck and upper extremity pain and paresthesia, intrinsic muscle wasting of the hands, upper extremity weakness, absence of symptoms beyond the upper quarter d. Neck and upper extremity pain and paresthesia, upper extremity muscle weakness, unsteadiness in gait, wasting of the intrinsic muscles of the hands Which answer below includes a list of clinical signs that are most helpful in identifying the presence of central cervical stenosis? a. Gait deviation, present Hoffmann’s test, positive inverted supinator sign, present Babinski test, age > 45 yrs, hand withdrawl reflex b. Age range of 20–40, present Hoffman’s test, absent Babinski test, positive inverted pronator sign, hand withdrawl reflex, relief with manual cervical traction c. Gait deviation, present Babinski test, absent Hoffman’s test, abnormal lower extremity neural dynamics tests, positive inverted pronator sign d. Age > 45 yrs, neck pain and headache, referred symptoms to the medial scapular border, lower motor neuron findings in both the upper and lower extremities
LUMBAR SPINAL STENOSIS J.M. Whitman, PT, DScPT, OCS, FAAOMPT, and J.M. Fritz, PT, PhD, ATC
1. What is lumbar spinal stenosis (LSS)? LSS can be defined as any narrowing of the lumbar spinal canal, nerve root canals, and/or intervertebral foramina that may encroach on the nerve roots of the lumbar spine. LSS can become a painful and potentially disabling condition in affected individuals. 2. How is LSS classified? There are two means of classification commonly used to describe patients with LSS; one is based on the anatomic location of the narrowing, the other on the etiology of the narrowing. ANATOMIC CLASSIFICATION • Lateral stenosis—narrowing that occurs within the lumbar intervertebral foramina and/or the nerve root canal, causing encroachment around the spinal nerve as it exits • Central stenosis—narrowing that occurs within the spinal canal, causing encroachment around the nerve roots of the cauda equina housed within the dural sac ETIOLOGIC CLASSIFICATION • Primary stenosis—narrowing caused by a congenital malformation or defect in postnatal development. Only about 10% of cases of lumbar stenosis can be considered to be primary stenosis. • Secondary stenosis—narrowing resulting from acquired conditions such as degenerative changes, spondylolisthesis, fractures, and postsurgical scarring. The most common cause of secondary stenosis is degenerative changes. Secondary stenosis may occur in individuals who already have a degree of primary stenosis. 3. What are the most common structural changes associated with LSS? The majority of cases of LSS occur secondary to degenerative changes. Facet joint arthrosis and hypertrophy, bulging and thickening of the ligamentum flavum, loss of disc height and posterior/lateral bulging of the intervertebral disc, and degenerative spondylolisthesis are the most common changes contributing to LSS. Other, less common causes of secondary stenosis include fractures, postoperative fibrosis, tumors, and systemic diseases of the bone, such as Paget’s disease. 4. Is lumbar stenosis a common problem? Yes; LSS is a common cause of low back pain, particularly in older adults. It is the most common reason for undergoing spinal surgery in individuals over the age of 65. Because of increases in life expectancy and improved diagnostic technology, rates of diagnosis of LSS and rates of surgery have increased substantially in the past several decades. 5. How will the typical patient with lumbar stenosis present clinically? In general, because degenerative changes are the predominant cause leading to LSS, affected individuals are typically older than age 50 with a long history of low back pain. Most patients will have symptoms of pain and/or numbness in one or both legs. Chronic nerve compression may lead to diminished lower extremity reflexes and strength or sensation deficits. Lumbar range of motion, particularly in extension, will be limited and painful, often reproducing leg symptoms. Symptoms tend to be posture-dependent, worsening with spinal extension and improving with flexion. Because of this, patients will generally feel better in a sitting position and worse when standing or walking. Several authors have provided information that helps quantify the impact of these various clinical indicators on the ultimate diagnosis of LSS. Katz et al. and Fritz et al. identified several clinical findings with associated sensitivity (Sn) and/or specificity (Sp) values for establishing the diagnosis of LSS. These findings are as follows: age over 65 Sn ¼ 0.77; pain below buttocks Sn ¼ 0.88; no pain
454
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when seated Sp ¼ 0.93; pain with flexion Sn ¼ 0.88; sitting is the best position Sn ¼ 0.89; standing/walking are worst positions Sn ¼ 0.89. Sugioka et al. sought to develop a score-based prediction rule to assist with diagnosis of LSS from self-report items only. The final predictors of LSS and associated risk scores are shown in Table 56.1. Scores of 7 or more yielded positive likelihood ratios of 1.90 to 3.91. Predictive Variable Age: 60–70 >70 Onset of symptoms >6 months Symptoms: Improve with bending forward Improve with bending backward Exacerbate while standing up Intermittent claudication present Urinary incontinence present
Assigned Risk Score 2 3 1 2 2 2 1 1
Last, Konno et al. also developed a score-based prediction rule for diagnosing LSS. In this analysis, the researchers also included items from the physical examination. Their final predictors for LSS and associated risk scores are shown in Table 56.2. For this prediction rule, total risk scores of 7 or higher yield the following diagnostic indices: sensitivity ¼ 0.93, specificity ¼ 0.72, positive likelihood ratio ¼ 3.31. Predictive Variable Age: 60–70 >70 Absence of diabetes Symptoms: Improve with bending forward Exacerbate while standing up Intermittent claudication present Examination: Symptoms induced by having patients bend forward Symptoms induced by having patients bend backward Good peripheral artery circulation Abnormal Achilles tendon reflex SLR test positive
Assigned Risk Score 1 2 1 3 2 3 1 1 3 1 2
6. Why do patients with LSS feel worse when standing than when sitting? Standing places the lumbar spine in a position close to full extension. Extension of the spine causes further narrowing of the spinal canal. In individuals without stenosis, this narrowing is tolerated without difficulty; however, patients with stenotic narrowing tend to have worse symptoms when standing or when standing and walking. Sitting causes flexion in the spine and therefore will generally reduce the symptoms of individuals with LSS. 7. Are there other factors that exacerbate symptoms for patients with LSS? Axial compression, as is experienced during weight-bearing, also creates increased narrowing of the spinal canal and may exacerbate the symptoms of LSS. Research has demonstrated that the narrowing effects of axial compression are similar in magnitude to those of spinal extension. This helps explain why walking can be difficult for patients with lumbar stenosis. Walking involves extension of the spine and creates increased compressive forces.
456 THE SPINE 8. What is neurogenic claudication? Neurogenic claudication is defined as poorly localized pain, paresthesias, and cramping of one or both lower extremities of a neurologic origin; symptoms are worsened by walking and relieved by sitting. There can be many causes of claudication; therefore the key distinguishing feature of neurogenic claudication is its neurologic origin—mechanical irritation of the cauda equina. The symptoms of neurogenic claudication are often the reason that an individual with LSS is prompted to seek medical treatment. 9. Are there other conditions that might be confused with lumbar stenosis? Other conditions that have been confused with LSS include osteoarthritis of the hip, vascular claudication (with peripheral arterial disease), unstable spondylolisthesis, and lumbar intervertebral disc herniation. Other frequent concomitant problems that may mandate additional differential diagnosis for those with lumbar stenosis may include diabetic neuropathy, other peripheral neuropathies, other lower extremity (LE) disorders, iliacus arterial involvement, and spinal tumors. 10. How can LSS be differentiated from other conditions with a similar presentation in the clinic? The postural-dependency of symptoms (ie, better with flexion or sitting; worse with extension, standing, and walking) is a unique characteristic of patients with LSS. A thorough history, including exacerbating and relieving positions or activities, will often reveal this posture-dependent nature of symptoms (see question 5 for more details). Clinical tests have also attempted to capitalize on the posture-dependency of stenosis symptoms to differentiate spinal stenosis from other conditions with similar symptoms. A “bicycle test” has been described in which the patient first pedals in an upright, seated position with the lumbar spine in extension and then with the spine in a flexed position. If the individual pedals farther in the spine-flexed position, the test is considered positive for LSS. Walking tests have also been described for use in differential diagnosis. The patient walks on a level surface in an upright posture and also in a slumped or flexed posture. If the patient can walk farther with the spine flexed, the test is considered positive for LSS. A variation on this test, called the Two Stage Treadmill Test (TSTT), compares walking on a level treadmill versus an inclined treadmill (15% incline). The incline of the treadmill causes the patient to flex the spine while walking and usually will improve walking capacity in patients with LSS. Earlier onset of symptoms and prolonged recovery with level treadmill walking yields a specificity (Sp) of 0.95 and a positive likelihood ratio (+LR) of 14.5. A longer total walking time on the inclined treadmill versus the level treadmill yields an Sp of 0.92 and a + LR of 6.5. Additionally, a thorough lower extremity neurovascular assessment should be performed, often including assessment of lower extremity muscle strength, reflexes, sensation, and pulses. The clinician should also look for trophic changes of the skin and nails and may opt to perform an ankle-brachial index test. This neurovascular assessment will help with differentiation from other neuropathic or vascular conditions. 11. Are diagnostic imaging studies or electrodiagnostic studies helpful in confirming a diagnosis of LSS? Diagnostic imaging modalities are generally used to confirm the diagnosis of LSS. The most commonly used tests are the following: • Magnetic resonance imaging—MRI is one of the most commonly used imaging studies to confirm a diagnosis of LSS. The anterior-posterior diameter of the spinal canal or the cross-sectional area of the dural sac can be measured to determine the extent of narrowing. • CT scan—The CT scan is also commonly used to assess the diameter or cross-sectional area in the same manner as described for the MRI. It is important to remember that the presence of stenosis with imaging is prevalent in the asymptomatic aging population; therefore correlation of imaging findings with clinical presentation is essential. Examination with electrodiagnostics is occasionally used to assist in the diagnosis of LSS. According to Haig et al., the following factors can help with this diagnosis: • Miniparaspinal mapping with a one side score >4: sensitivity ¼ 0.3; specificity ¼ 1.0 • Fibrillation potential in limb muscles: sensitivity ¼ 0.33; specificity ¼ 0.88 • Absence of tibial H-wave: sensitivity ¼ 0.36; specificity ¼ 0.92 • Composite limb and paraspinal fibrillation score: sensitivity ¼ 0.48; specificity ¼ 0.88
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12. Are plain film x-rays helpful in the diagnosis of LSS? Plain film x-rays can show the degenerative changes such as osteophytes and disc degeneration that are often the cause of LSS. Lateral views can demonstrate the diameter of the intervertebral foramina. However, plain film x-rays are limited in their usefulness by their inability to image the central spinal canal and the soft tissue changes that may contribute to LSS. 13. What are the most common impairments and functional limitations found in patients with LSS? The most common impairments found during the examination of the patient are restrictions in spinal range of motion. Side-bending is often limited bilaterally; lumbar extension may be quite limited and reproduce or intensify the patient’s symptoms. Lumbar flexion is also frequently limited in range but will often somewhat relieve the symptoms. Deficits in vibratory or pinprick sensation in one or both lower extremities can occur, along with strength or reflex deficits. Many patients will have a positive straight leg raise test. Another common area of impairment is the hip joint. Restricted range of motion, particularly in extension, and weakness of the hip extensors and abductors are common findings. The most widespread functional limitation in patients with LSS is diminished walking tolerance because of leg symptoms that are relieved by sitting, as well as limitation in prolonged standing postures. 14. Describe the surgical procedure for a patient with LSS. Surgical treatment of LSS is performed to relieve compression on the contents of the central and lateral spinal canals. The most common surgical procedure for patients with LSS is a decompression laminectomy in which portions of the vertebral arch are removed to reduce compression of the lumbar spinal nerves. Sometimes a fusion, with or without instrumentation, will also be performed, although this is usually only done if there is evidence of spondylolisthesis along with the spinal stenosis. 15. Should a patient with LSS have surgery? The decision to pursue surgery should be determined based on careful and shared decision making between providers and patients, with heavy emphasis on patient preferences. Clinical outcomes are generally good for surgical treatment, with high percentages of patients expressing satisfaction and reporting improvement early postoperatively. However, these outcomes tend to deteriorate with time, with only about 60% to 70% of patients satisfied after 4 to 7 years and between-group clinical outcomes for those treated with surgery versus conservative care diminishing within 2 to 8 years after surgery. Sufficient literature describing positive clinical outcomes from various nonsurgical approaches to care is available and often with no reported adverse outcomes. These nonsurgical approaches typically include treatments such as aerobic exercise, stretching, strengthening, mobilization/ manipulation, and patient education. Based on the known risks of surgical complications and the stable nature of spinal stenosis, current recommendations are that patients should be offered a rigorous trial of physical therapy care before pursuing surgery. Patients who do not improve should be well informed of the potential risks and benefits of surgery, including the fact that benefits from surgery will most likely diminish over time. 16. Will the symptoms of lumbar stenosis continue to worsen over time? Research to date shows that LSS is a generally stable condition. Although some patients will deteriorate over time, this is not inevitable, and large percentages of patients can maintain or improve their condition with time. 17. Will epidural steroid injections help patients with lumbar stenosis? Epidural steroid injections have been frequently recommended as a nonsurgical option for patients with LSS. Some patients will receive short-duration benefits from epidural steroid injections. The effectiveness of injections in reducing symptoms beyond a couple of weeks, however, is less likely. 18. What is the best physical therapy treatment for patients with lumbar stenosis? Numerous treatment options have been proposed for use by physical therapists in the treatment of patients with LSS. Flexion-oriented exercises are advocated to capitalize on the postural dependency of symptoms of spinal stenosis. General conditioning activities are useful and may include stationary cycling, aquatic exercise, and walking as tolerated by the patient. Any strength or flexibility deficits identified
458 THE SPINE during the physical examination should be addressed. Manual therapy (including mobilization, manipulation, and stretching) targeting the thoracic and lumbopelvic spine regions and hips may also be helpful. 19. Should traction be used in the treatment of patients with LSS? Pelvic traction has been recommended for the treatment of LSS in an attempt to relieve compression that results from the pathology. Although traction may be helpful for pain reduction in some patients, it should be combined with more active forms of therapy to improve function. 20. Can deweighted treadmill ambulation help patients with LSS? Deweighted treadmill ambulation uses a harness-and-traction device to provide a vertical traction force during ambulation on a treadmill. The traction force reduces the axial compression associated with weight bearing and may permit some individuals with LSS to walk with reduced symptoms of neurogenic claudication. This treatment technique may hold promise for selected patients with stenosis because it provides the benefit of traction while keeping the patient active and exercising. However, in a randomized trial by Pua et al. that compares exercise plus cycling versus exercise plus deweighted treadmill walking, both groups achieved similar pain and disability outcomes at 6 weeks. Therefore the use of deweighting should be considered as a potential rehabilitation tool on a case-by-case basis, based on clinical response, and, in general, should not be viewed as superior to cycling as a part of a comprehensive treatment program. 21. Is it possible to identify patient-centered factors that predict better versus worse outcomes from surgery for lumbar stenosis? Although many researchers have investigated this question, there is some conflicting information in the literature. Some identified predictors of worse surgical outcomes to date include depression, worse emotional health, smoking, Workers’ Compensation, anxiety, life dissatisfaction, higher BMI, longer duration of leg pain/symptoms, cardiovascular comorbidity, scoliosis, other disorders influencing walking ability, predominant back pain (>leg pain), prior lumbar surgery, history of psychiatric disease, female gender, and low baseline disability. In addition to not having these identified predictive factors for worse outcomes, the following factors have been identified as predicting better surgical outcomes: greater central canal stenosis, good or above average self-rated health, younger age, lower duration use of analgesics preoperatively, greater preoperative disability, more ambitious preoperative expectations related to pain and functional improvements, and no lifting required at work. 22. Are there published studies documenting patient outcomes with defined physical therapy treatment approaches? Many studies are now available demonstrating positive clinical outcomes of care for patients treated with interventions often provided by physical therapists, including aerobic exercise, stretching, strengthening, aerobic exercise, and mobilization/manipulation. Some studies also include traction, physical modalities, or lumbopelvic orthoses. Selected studies are described as follows: • Simotas et al. reported on the results of 49 patients treated with a program of physical therapy (flexion-oriented exercises) and epidural steroids. After 3 years, 9 patients (18%) had undergone surgery, 12 patients (24%) reported no change in symptoms, 23 patients (47%) had some amount of improvement, and 5 patients (10%) experienced worsening of symptoms. • Murphy et al. reported clinically meaningful long-term improvements in disability and pain for 57 patients treated with manipulation, neural mobilization, flexion exercises, and lumbar stabilization training in a prospective observational cohort. • Pua et al. conducted a trial that included 68 patients. Both treatment groups received lumbar flexion exercises, lumbar traction, and thermal modalities. One group also performed deweighted treadmill walking, and the other performed stationary cycling. Although there were no between-group differences, both groups improved from baseline to 6 weeks. • Ammendolia and Ngai reported on clinically meaningful improvements in pain and disability for a cohort of 49 patients after a 6-week program, including manual therapy (soft tissue and neural mobilization, manipulation, lumbar flexion-distraction, and muscle stretching), home exercises, and self-management strategies. • Cambron et al. included 60 patients in a pilot RCT that investigated optimal dosages of spinal manipulation. The treatment groups receiving a total of 12 and 18 manipulations over 6 weeks
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•
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demonstrated significant within-group improvements up through 6 months in symptom severity, and the group receiving 18 manipulations had significant within-group improvements in physical function. Whitman et al. conducted an RCT with 58 patients that compared an individualized approach (impairment-based manual therapy interventions to the thoracic spine, lumbopelvic spine, and lower extremities; deweighted treadmill walking; and abdominal retraining exercises) to walking, a standardized flexion exercise, and a subtherapeutic ultrasound program. A greater proportion of patients in the pragmatic, individualized program reported recovery at 6 weeks versus the flexion exercise/walking group. Although both groups demonstrated positive outcomes over the 24-month follow-up, improvements in disability, satisfaction, and treadmill walking tests favored the individualized treatment group at all follow-up points. Delitto et al. conducted a multisite, randomized controlled trial that included 169 surgical candidates with lumbar stenosis. Patients were treated with either surgical decompression or a 6-week, well-defined, twice weekly physical therapy (PT) intervention program, including lumbar flexion exercises, patient education, general conditioning (cycling or treadmill walking), and individualized lower extremity strengthening and flexibility exercises. Those patients undergoing physical therapy intervention had similar outcomes to those treated with surgical decompression at the 2-year follow-up.
23. Should patients with lumbar stenosis wear a brace or corset? The use of a rigid corset to limit spinal extension or a soft corset for general support has been recommended. A soft corset may provide a measure of relief for patients. A more rigid brace, although effective in limiting or preventing extension, is often cumbersome and restrictive for the patient and should likely be reserved for those individuals not responding to other forms of nonoperative treatment. 24. How should the outcomes of treatment for patients with lumbar stenosis be measured? Measuring the effectiveness of any treatment for LSS is an important consideration. Patient-reported measures, such as the Oswestry or Roland Morris disability scales, as well as the condition-specific Swiss Spinal Stenosis Questionnaire, are useful for documenting functional limitations and disability. The measurement of walking tolerance, usually conducted on a treadmill or with a 6-minute walking test, is an important assessment and monitoring tool because it measures the most common and troublesome functional limitation in these patients. 25. Does stenosis occur in the cervical spine as well? Yes; stenotic narrowing can and does occur in the cervical spine. Similar to the lumbar spine, the narrowing may occur laterally, in the intervertebral foramen, or centrally, in the spinal canal. The etiology may be primary (ie, congenital), secondary to degenerative conditions, or a combination of these two factors. The presence of congenital stenosis of the central canal in the cervical spine is a particular concern for participants of collision sports, such as football. The normal sagittal plane diameter of the spinal canal in the cervical region is 17 to 18 mm. The diameter of the spinal cord is about 10 mm. If the sagittal plane diameter of the canal is diminished, the safety margin within the canal is compromised, and symptoms of compression of the spinal cord may result. As with lumbar stenosis, the presence of cervical stenosis on imaging may be present in absence of clinical symptoms, therefore mandating corroboration of clinical and imaging findings. 26. What symptoms will a patient with cervical stenosis exhibit? The symptoms of lateral and central cervical stenosis differ substantially. Lateral cervical stenosis typically results in compression of the cervical nerve root and produces symptoms of radiculopathy. Central cervical stenosis may compress the spinal cord, resulting in a condition termed cervical myelopathy. Symptoms of radiculopathy include neck and upper extremity pain and paresthesia in a dermatomal pattern. There may also be complaints of upper extremity muscle weakness in the affected arm. Symptoms of myelopathy are often subtler, particularly in the early stages. Neck pain is not always present. Unsteadiness in gait or clumsiness is often an early symptom. Wasting of the intrinsic hand muscles is common. An extrasegmental distribution of paresthesia in one or both hands and feet may be present, followed by a perception of weakness. Gait disturbances can become severe, significantly interfering with functional activities and safety.
460 THE SPINE 27. What is the typical clinical presentation for patients with central cervical stenosis? The signs of central cervical stenosis (myelopathy) are those of upper motor neuron, or long tract, disorders. Clinical signs may include weakness with spasticity, clonus, present Hoffmann and Babinski signs, hand withdrawal reflex, and an inverted supinator sign. Vibratory sensation is typically diminished in the lower extremities, and both upper and lower extremity reflexes may become hyperactive. Cervical range of motion is typically restricted in all planes. Lhermitte’s sign (spinal pain and/or radiating extremity pain and paresthesias with forced cervical flexion or extension) may be present. Spurling’s sign is expected to be negative, and manual cervical traction will not have any effect on symptoms. According to Cook et al., at least 3 of the following five clinical tests helps rule in cervical myelopathy: 1) gait deviation, 2) present Hoffmann’s test, 3) + inverted supinator sign, 4) present Babinski test, 5) age >45 y (specificity ¼ 0.99; CI ¼ 0.97–0.99); + LR ¼ 30.9; 95% CI ¼ 5.5–181.8). 28. Is treatment by a physical therapist helpful for cervical myelopathy? Nonsurgical care is often recommended for patients with mild myelopathy, although scant evidence exists investigating the impact of treatment by a physical therapist for this disorder. Intermittent cervical traction is often recommended as a potentially helpful intervention. In a small case series, Browder et al. reported improvements in pain and disability for 7 patients with cervical myelopathy who were all treated with intermittent cervical traction and thrust manipulation targeting the thoracic spine. No adverse events or outcomes were reported. 29. Is surgery recommended for patients with cervical myelopathy? The disorder is considered to be progressive in nature and potentially disabling, but those with cervical myelopathy (CM) often experience long periods of stable neurologic status between episodes of exacerbation. Conservative nonsurgical treatment is often recommended for patients with mild cervical myelopathy. In contrast, surgical management is typically considered for those with moderate to severe CM. Although one prospective RCT demonstrated no significant differences between groups (surgery versus no surgery) at 10 years, several other studies conclude that those with moderate to severe CM who undergo surgery experience improved outcomes over those who do not. Performing surgery early in the course of the condition is believed to lead to a better long-term outcome. Laminotomy or laminoplasty is typically performed to increase the dimensions of the central spinal canal and may be accompanied by cervical fusion. BIBLIOGRAPHY Ammendolia, C., & Chow, N. (2015). Clinical outcomes for neurogenic claudication using a multimodal program for lumbar spinal stenosis: A retrospective study. Journal of Manipulative and Physiological Therapeutics, 38(3), 188–194. Atlas, S. J., et al. (1996). The Maine lumbar spine outcome study, part III. 1-year outcomes for surgical and non-surgical management of lumbar spinal stenosis. Spine, 21, 1787–1795. Backstrom, K. M., Whitman, J. M., & Flynn, T. W. (2011). Lumbar spinal stenosis—diagnosis and management of the aging spine. Manual Therapy, 16, 308–317. Bridwell, K. H. (1994). Lumbar spinal stenosis. Diagnosis, management, and treatment. Clinics in Geriatric Medicine, 10, 677–701. Browder, D. A., Erhard, R. E., & Piva, S. R. (2004). Intermittent cervical traction and thoracic manipulation for management of mild cervical compressive myelopathy attributed to cervical herniated disc: A case series. Journal of Orthopaedic and Sports Physical Therapy, 34(11), 701–712. Cambron, J. A., Schneider, M., Dexheimer, J. M., Iannelli, G., Chang, M., Terhorst, L., & Cramer, G. D. (2014). A pilot randomized controlled trial of flexion-distraction dosage for chiropractic treatment of lumbar spinal stenosis. Journal of Manipulative and Physiological Therapeutics, 37(6), 396–406. Chang, Y., et al. (2005). The effect of surgical and nonsurgical treatment on longitudinal outcomes of lumbar spinal stenosis over 10 years. Journal of the American Geriatrics Society, 53, 785–792. Cook, C., et al. (2010). Clustered clinical findings for diagnosis of cervical spine myelopathy. Journal of Manual & Manipulative Therapy, 18(4), 175–180. Delitto, A., Piva, S. R., Moore, C. G., Fritz, J. M., Wisniewski, S. R., Jospeno, D. A., … , Welch, W. C. (2015). Surgery versus nonsurgical treatment of lumbar spinal stenosis: A randomized trial. Annals of Internal Medicine, 162, 465–473. http://dx.doi.org/10.7326/M14-1420. Deyo, R. A., Cherkin, D. C., & Loeser, J. D. (1992). Morbidity and mortality in association with operations on the lumbar spine. The influence of age, diagnosis, and procedure. Journal of Bone and Joint Surgery, 74-A, 536–543. Dvorak, J. (1998). Epidemiology, physical examination and neurodiagnostics. Spine, 23, 2663–2673. Fritz, J., Erhard, R., Delitto, A., Welch, W., & Nowakowski, P. (1997a). Preliminary results of the use of a two-stage treadmill test as a clinical diagnostic tool in the differential diagnosis of lumbar spinal stenosis. Journal of Spinal Disorders, 10(5), 410e6. Fritz, J. M., Erhard, R. E., & Vignovic, M. (1997b). A nonsurgical approach for patients with lumbar spinal stenosis. Physical Therapy, 77, 962–973.
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Fritz, J. M., et al. (1998). Lumbar spinal stenosis: A review of current concepts in evaluation, management, and outcome measurements. Archives of Physical Medicine and Rehabilitation, 79, 700–708. Haig, A. J., Tong, H. C., Yamakawa, K. S. J., et al. (2005). The sensitivity and specificity of electrodiagnostic testing for the clinical syndrome of lumbar spinal stenosis. Spine, 30, 2667–2676. Hurri, H., et al. (1998). Lumbar spinal stenosis: Assessment of long-term outcome 12 years after operative and conservative care. J Spinal Disease, 11, 110–115. Johnsson, K. E., Rosen, I., & Uden, A. (1992). The natural course of lumbar spinal stenosis. Clinical Orthopaedics, 279, 82–86. Katz, J., Dalgas, M., Stucki, G., Katz, N., Bayley, J., & Fossel, A. (1995). Degenerative lumbar spinal stenosis. Arthritis and Rheumatism, 38, 1236e41. Katz, J. N., et al. (1995). Degenerative lumbar spinal stenosis: Diagnostic value of the history and physical examination. Arthritis and Rheumatism, 38, 1236–1241. Katz, J. N., et al. (1996). Seven- to 10-year outcome of decompressive surgery for degenerative lumbar spinal stenosis. Spine, 21, 92–98. Konno, S., Hayashino, Y., Kukuhara, S., Kikuchi, S., Kaneda, K., & Seichi, A. (2007). Development of a clinical diagnosis support tool to identify patients with lumbar spinal stenosis. European Spine Journal, 16, 1951e7. Murphy, D. R., Hurwitz, E. L., Gregory, A. A., & Clary, R. (2006 Feb 23). A non-surgical approach to the management of lumbar spinal stenosis: A prospective observational cohort study. BMC Musculoskeletal Disorders, 7, 16. Penning, L. (1992). Functional pathology of lumbar spinal stenosis. Clinical Biomechanics, 7, 3–17. Porter, R. W. (1996). Spinal stenosis and neurogenic claudication. Spine, 21, 2046–2052. Pua, Y. H., Cai, C. C., & Lim, K. C. (2007). Treadmill walking with body weight support is no more effective than cycling when added to an exercise program for lumbar spinal stenosis: A randomised controlled trial. Australian Journal of Physiotherapy, 53(2), 83–89. Schonstrom, N., et al. (1989). Dynamic changes in the dimensions of the lumbar spinal canal: An experimental study in vitro. Journal of Orthopaedic Research, 7, 115–121. Simotas, A. C., et al. (2000). Nonoperative treatment for lumbar spinal stenosis: Clinical outcome results and a 3-year survivorship analysis. Spine, 25, 197–203. Sugioka, T., Hayashino, Y., Konno, S., Kikuchi, S., & Fukuhara, S. (2008). Predictive value of self-reported patient information for the identification of lumbar spinal stenosis. Family Practice, 25(4), 237e44. Whitman, J. M., Flynn, T. W., Childs, J. D., Wainner, R. S., Gill, H. E., Ryder, M. G., et al. (2006). A comparison between two physical therapy treatment programs for patients with lumbar spinal stenosis: A randomized clinical trial. Spine, 31(22), 2541–2549. Willen, J., et al. (1997). Dynamic effects on the lumbar spinal canal: Axially loaded CT-myelography and MRI in patients with sciatica and/or neurogenic claudication. Spine, 22, 2968–2976. Zdeblick, T. A. (1995). The treatment of degenerative lumbar disorders: A critical review of the literature. Spine, 20(Suppl), 126s–137s.
CHAPTER 56 QUESTIONS 1.
2.
3.
Current best evidence leads us to include the following in our physical therapy–related care for patients with lumbar spinal stenosis: a. Double and single knee to chest exercises, quadruped “cat and camel” (flexion and extension) exercises, hot packs, and electrical stimulation. b. Repeated flexion exercises, double and single knee to chest exercises, and abdominal (“core”) retraining c. Aerobic exercise (cycling and/or walking), manual therapy to the lower quarter, lower quarter and abdominal muscle stretching and strengthening, and lumbo-pelvic flexion exercises d. Traction, electrical stimulation, cycling, and thermal modalities e. None of the above Which findings are most helpful in making a clinical diagnosis of lumbar spinal stenosis? a. Standing and walking aggravate symptoms, and sitting eases symptoms; younger age; low back pain only (none in the lower extremities) b. Standing and walking aggravate symptoms, and sitting eases symptoms; older age; presence of pain, paresthesia, and/or cramping into one or both lower extremities below the buttocks c. Sitting aggravates symptoms and standing and walking ease symptoms; older age; low back pain only (none in the lower extremities) d. Sitting aggravates symptoms and standing and walking ease symptoms; younger age; presence of pain, paresthesia, and/or cramping into one or both lower extremities below the buttocks Which answer below includes disorders that may present similarly to lumbar spinal stenosis in the clinical exam? Pick the best answer. a. Deep vein thrombosis, spondylitis of the lumbar spine, post-polio syndrome b. Femoral neck fracture, mechanical low back pain, hip and knee osteoarthritis
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5.
c. Iliacus arterial disorder, fibular nerve adverse neural dynamics, mechanical low back pain d. Hip osteoarthritis, peripheral arterial disease, lumbar radiculopathy, peripheral neuropathy, spinal tumors What are common symptoms for a patient with cervical stenosis? a. Neck pain and headache, referral of symptoms into the thoracic region, absence of symptoms below the acromioclavicular joint b. Unsteadiness and clumsiness in gait, lower motor neuron changes in the upper and lower extremities, and an absence of neck pain c. Neck and upper extremity pain and paresthesia, intrinsic muscle wasting of the hands, upper extremity weakness, absence of symptoms beyond the upper quarter d. Neck and upper extremity pain and paresthesia, upper extremity muscle weakness, unsteadiness in gait, wasting of the intrinsic muscles of the hands Which answer below includes a list of clinical signs that are most helpful in identifying the presence of central cervical stenosis? a. Gait deviation, present Hoffmann’s test, positive inverted supinator sign, present Babinski test, age > 45 yrs, hand withdrawl reflex b. Age range of 20–40, present Hoffman’s test, absent Babinski test, positive inverted pronator sign, hand withdrawl reflex, relief with manual cervical traction c. Gait deviation, present Babinski test, absent Hoffman’s test, abnormal lower extremity neural dynamics tests, positive inverted pronator sign d. Age > 45 yrs, neck pain and headache, referred symptoms to the medial scapular border, lower motor neuron findings in both the upper and lower extremities