Lumbar spinal stenosis is a common source of leg and back pain. It refers to a narrowing in the vertebra, in the areas of the central canal, lateral recess, or the neural foramen. When the lateral recess and neural foramen are stenosed, symptoms of lumbar radiculopathy may also present. Despite its prevalence, currently, there is no universally accepted definition of lumbar spinal stenosis, and there is also a lack of generally accepted radiologic diagnostic criteria. Lumbar spinal stenosis is a significant cause of disability in the elderly, and it is the most significant cause of spinal surgery in patients over 65 years of age. Therefore clinicians need to recognize and treat lumbar spinal stenosis effectively.
Degenerative spondylosis is a significant etiology of lumbar spinal stenosis. With aging, wear-and-tear changes, and traumas, amongst other factors, the intervertebral discs can degenerate and protrude posteriorly, causing increased loading of the posterior elements of the vertebrae. These changes can lead to posterior vertebral osteophyte formation (uncinate spurs), facet hypertrophy, synovial facet cysts, and ligamentum flavum hypertrophy, which in turn will cause spinal stenosis.
Degenerative spondylolisthesis is another cause of lumbar spinal stenosis. When degenerative changes of the spine occur, the pars interarticularis can be fractured, and the resulting instability can lead to forward translation of the vertebra. Sufficient anterior slippage of one vertebra on top of the next vertebral segment (most commonly L4-on-L5) can narrow the spinal canal, leading to stenosis.
Other acquired conditions, although rarer than the conditions mentioned above, should also be considered by the clinician. These include space-occupying lesions, post-surgical fibrosis, and rheumatologic conditions as well as other skeletal diseases such as ankylosing spondylitis or diffuse idiopathic skeletal hyperostosis.
Even more rarely, lumbar spinal stenosis may be secondary to congenital causes such as achondroplasia, which can lead to short pedicles with medially placed facets.
Lumbar spinal stenosis can be classified anatomically into central stenosis usually caused by a combination of hypertrophied ligamentaum flavum anteriorly and bulging disc posteriorly with consequent thecal sac compression; Lateral recess stenosis which is due to facet joint arthropathy with overgrowth of the superior articular facet and osteophyte formation. This results in compression of the descending nerve roots. Foraminal stenosis is due to loss of disc height, foraminal disc protrusion, or osteophyte formation with resultant compression of the exiting nerve root. And finally, extraforaminal stenosis which is usually due to far lateral disc herniation again with resultant exiting nerve root compression .
Because of a lack of universally accepted definition for lumbar spinal stenosis, the exact epidemiology is difficult to determine. In an ancillary Framingham study, where test subjects underwent a CT scan to determine the central diameter of lumbar spinal canals, absolute lumbar spinal stenosis was defined as a diameter of less than 10 mm. The prevalence of acquired lumbar spinal stenosis was 19.4% for the population aged between 60 and 69 years. In a Japanese population-based study where subjects completed a symptoms questionnaire to predict lumbar stenosis, the research showed that incidence increased with age, with 1.7 to 2.2% between ages 40 and 49, and 10.3% to 11.2% between ages of 70 to 79. It is also a significant contributor to spinal surgery in the US, 5.9 per 100 patients progressed to lumbar fusion within one year from the time of diagnosis of lumbar degeneration.
The causes of neurologic symptoms of lumbar spinal stenosis have been thought to originate from the compression and ischemia of nerve roots. Nerve root compression can arise from direct mechanical compression or increased intrathecal pressure due to the narrowing of the canal. Inflammation of nerve roots is also a plausible but less likely mechanism of neurologic symptoms in lumbar spinal stenosis.
Classically, lumbar spinal stenosis presents as pain exacerbated by prolonged ambulation, standing, and with lumbar extension, and is relieved by forward flexion and rest. Neurogenic claudication is an important feature of lumbar spinal stenosis. Symptoms are typically bilateral, but usually asymmetric. Low back pain, numbness, and tingling are present in a majority of patients. Numbness and tingling in lumbar spinal stenosis typically involve the entire leg and rarely affect only a single nerve root distribution. Approximately 43 percent of the patients experience weakness. Patients may also report walking upstairs being easier than walking downstairs, as the back is forward flexed with stairs climbing. If patients present with new-onset bowel or bladder dysfunction, saddle anesthesia, bilateral lower extremity weakness, and/or increased lower extremity, the patient may have developed cauda equina or conus medullaris syndromes.
A thorough physical examination is necessary for patients with suspected lumbar spinal stenosis. Unilateral radicular pain from foraminal stenosis can be elicited with passive and active lumbar extension, otherwise known as the Kemp sign . Although patients can have superimposed lumbar radiculopathy, one should keep in mind that neurologic examinations on patients with lumbar spinal stenosis are typically normal. Patients presenting with radicular pain will not have their pain exacerbated by Valsalva as in the case with intervertebral disc prolapse. Only 10 percent of patients would present with a positive straight leg raise test. Pedal pulses should also be checked during the physical exam as vascular claudication can present similarly.
As mentioned previously, there is no consensus on the definition of lumbar spinal stenosis diagnostic criteria. However, in evaluating low back pain, neuroimaging is indicated when there are new-onset symptoms and suspicion of lumbosacral radiculopathy or spinal stenosis. In patients without suspicion of infection, metastasis, or postoperative spine symptoms, non-contrast MRI of the lumbosacral spine is the modality of choice for lumbar spinal stenosis, and CT myelography is an option when MRI is contraindicated. Many authors use an intraspinal canal area of less than 76 mm^2and 100 mm^2 for severe and moderate stenosis, respectively. Anteroposterior spinal canal diameters of less than 10 mm are also frequently used for the diagnosis of lumbar spinal stenosis. One must note that lumbar spinal stenosis is a common incidental radiological finding, especially in patients over 60 years old, and there is also a lack of correlation between the severity of the imaging studies versus the symptom severity reported by patients. MRI or CT myelography with axial loading may be a useful adjunct to routine imaging.
Electromyography and nerve conduction studies (EMG) are also used to aid the diagnosis of diagnosis, as this distinguishes polyneuropathy, radiculopathy, or other peripheral nerve disorders from lumbar spinal stenosis. EMG exams are often normal in patients with lumbar spinal stenosis.
Management for lumbar spinal stenosis aims at reducing symptoms and improving functional status. Conservative treatment is the first-line treatment for this condition. Conservative treatment options include physical therapy, oral anti-inflammatory medications, and epidural steroid injections. Although there is no standardized physical therapy regimen, many therapists focus on stretching and strengthening the core muscles, which can lead to correction of posture and improved symptoms. Although there are short-term benefits, lumbar epidural steroid injections have not shown to have long-term improvement of pain and disability in lumbar spinal stenosis patients, and there is no statistical difference between epidural injections with anesthetics alone versus a mixture of anesthetics with corticosteroids. Lumbar corsets may also be trialed for temporary relief of pain.
Barring emergencies such as cauda equina syndrome, surgical management for lumbar spinal stenosis is usually elective, as the goal of treatment is to improve function, rather than preventing neurologic impairment. The most frequently performed surgical procedure is a laminectomy (Wide pedicle-to-pedicle decompression). This is usually indicated in cases of ongoing pain despite conservative measures for 3 to 6 months and where there is progressive neurologic deterioration e.g motor weakness, bowel and/or bladder dysfunction. A randomized trial has shown that there is a greater improvement of symptoms in patients undergoing laminectomy compared to the non-surgical group; however, the symptom improvement between the surgical and non-surgical groups diminishes over time. Laminectomy with fusion (wide pedicle-to-pedicle decompression with instrumented fusion) is indicated when further stability is required. Which is typically reserved for patients with concurrent segmental instability e.g spondylolisthesis (degenerative or isthmic) or degenerative scoliosis. Also, indicated in cases of surgical instability as in cases of complete laminectomy or excision of more than half of the facet joints. A less invasive approach is interspinous spacer implantation; this procedure is appropriate for patients with intermittent claudication symptoms without spondylolisthesis.
Differential diagnoses for lumbar spinal stenosis include, but not limited to:
Lumbar spinal stenosis is a significant cause of pain and disability, and approximately half the patients have involvement of other spinal segments over time; however, it typically follows a benign course. In one cohort study, 30% of patients electing to manage lumbar spinal stenosis with non-surgical procedures eventually requested for surgical management, and approximately 19% of patients who had an initial surgery eventually underwent a repeat surgery.
Complications are usually due to surgical intervention and incidence increases with advancing age, increased blood loss, and increased extent of the levels fused. This includes but not limited to: wound infection, deep infection necessitating surgical debridement, and irrigation, neurologic deficits, dural tear, epidural hematoma, instability and failed surgery which is most commonly due to recurrence of the disease proximal or distal to the decompressed level. Other general complications include anemia necessitating blood transfusion, urinary tract infection, pneumonia, renal failure.
Lumbar spinal stenosis is a common disease process in the outpatient setting. These patients have symptoms such as leg pain and low back pain. The cause of this condition is most likely secondary to chronic wear-and-tear damages to the vertebral column. Despite the fact that imaging studies can show there is indeed lumbar spinal stenosis, the patient's may or may not have corresponding symptoms. Because there is no evidence to demonstrate the superiority of surgical versus non-surgical treatments of lumbar spinal stenosis, it is essential to take an interprofessional approach. [Level 1]
Primary physicians must recognize the patient's presentation; the care of the patient must include coordinated effort with physical medicine and rehabilitation, pain management, orthopedist, and/or neurosurgeons (if there is a neurosurgical emergency). Physical therapists must also have involvement as physical therapy is the mainstay in the conservative treatment of this condition. In patients who need to undergo surgical treatment, the nursing staff (including orthopedic specialty nurses) must be aware of the patient's medical status. In short, the care of patients suffering from lumbar spinal stenosis requires an interprofessional team-based cooperative model.
|||Ciol MA,Deyo RA,Howell E,Kreif S, An assessment of surgery for spinal stenosis: time trends, geographic variations, complications, and reoperations. Journal of the American Geriatrics Society. 1996 Mar [PubMed PMID: 8600197]|
|||Kalichman L,Cole R,Kim DH,Li L,Suri P,Guermazi A,Hunter DJ, Spinal stenosis prevalence and association with symptoms: the Framingham Study. The spine journal : official journal of the North American Spine Society. 2009 Jul [PubMed PMID: 19398386]|
|||Zaina F,Tomkins-Lane C,Carragee E,Negrini S, Surgical Versus Nonsurgical Treatment for Lumbar Spinal Stenosis. Spine. 2016 Jul 15 [PubMed PMID: 27128388]|
|||Binder DK,Schmidt MH,Weinstein PR, Lumbar spinal stenosis. Seminars in neurology. 2002 Jun [PubMed PMID: 12524561]|
|||Jenis LG,An HS, Spine update. Lumbar foraminal stenosis. Spine. 2000 Feb 1; [PubMed PMID: 10703115]|
|||Yabuki S,Fukumori N,Takegami M,Onishi Y,Otani K,Sekiguchi M,Wakita T,Kikuchi S,Fukuhara S,Konno S, Prevalence of lumbar spinal stenosis, using the diagnostic support tool, and correlated factors in Japan: a population-based study. Journal of orthopaedic science : official journal of the Japanese Orthopaedic Association. 2013 Nov [PubMed PMID: 23963588]|
|||Buser Z,Ortega B,D'Oro A,Pannell W,Cohen JR,Wang J,Golish R,Reed M,Wang JC, Spine Degenerative Conditions and Their Treatments: National Trends in the United States of America. Global spine journal. 2018 Feb [PubMed PMID: 29456916]|
|||Jinkins JR, Gd-DTPA enhanced MR of the lumbar spinal canal in patients with claudication. Journal of computer assisted tomography. 1993 Jul-Aug [PubMed PMID: 8331225]|
|||Hall S,Bartleson JD,Onofrio BM,Baker HL Jr,Okazaki H,O'Duffy JD, Lumbar spinal stenosis. Clinical features, diagnostic procedures, and results of surgical treatment in 68 patients. Annals of internal medicine. 1985 Aug [PubMed PMID: 3160275]|
|||Katz JN,Dalgas M,Stucki G,Katz NP,Bayley J,Fossel AH,Chang LC,Lipson SJ, Degenerative lumbar spinal stenosis. Diagnostic value of the history and physical examination. Arthritis and rheumatism. 1995 Sep [PubMed PMID: 7575718]|
|||Saifuddin A, The imaging of lumbar spinal stenosis. Clinical radiology. 2000 Aug [PubMed PMID: 10964728]|
|||Haig AJ,Tong HC,Yamakawa KS,Quint DJ,Hoff JT,Chiodo A,Miner JA,Choksi VR,Geisser ME, The sensitivity and specificity of electrodiagnostic testing for the clinical syndrome of lumbar spinal stenosis. Spine. 2005 Dec 1 [PubMed PMID: 16319753]|
|||Mazanec DJ,Podichetty VK,Hsia A, Lumbar canal stenosis: start with nonsurgical therapy. Cleveland Clinic journal of medicine. 2002 Nov [PubMed PMID: 12430977]|
|||Fukusaki M,Kobayashi I,Hara T,Sumikawa K, Symptoms of spinal stenosis do not improve after epidural steroid injection. The Clinical journal of pain. 1998 Jun [PubMed PMID: 9647457]|
|||Prateepavanich P,Thanapipatsiri S,Santisatisakul P,Somshevita P,Charoensak T, The effectiveness of lumbosacral corset in symptomatic degenerative lumbar spinal stenosis. Journal of the Medical Association of Thailand = Chotmaihet thangphaet. 2001 Apr [PubMed PMID: 11460971]|
|||Malmivaara A,Slätis P,Heliövaara M,Sainio P,Kinnunen H,Kankare J,Dalin-Hirvonen N,Seitsalo S,Herno A,Kortekangas P,Niinimäki T,Rönty H,Tallroth K,Turunen V,Knekt P,Härkänen T,Hurri H, Surgical or nonoperative treatment for lumbar spinal stenosis? A randomized controlled trial. Spine. 2007 Jan 1 [PubMed PMID: 17202885]|
|||Machado GC,Ferreira PH,Yoo RI,Harris IA,Pinheiro MB,Koes BW,van Tulder MW,Rzewuska M,Maher CG,Ferreira ML, Surgical options for lumbar spinal stenosis. The Cochrane database of systematic reviews. 2016 Nov 1; [PubMed PMID: 27801521]|
|||Chang Y,Singer DE,Wu YA,Keller RB,Atlas SJ, The effect of surgical and nonsurgical treatment on longitudinal outcomes of lumbar spinal stenosis over 10 years. Journal of the American Geriatrics Society. 2005 May [PubMed PMID: 15877553]|