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Degenerative Lumbar Spinal Stenosis: Evaluation and Management

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Degenerative Lumbar Spinal Stenosis: Evaluation and Management Review Article Degenerative Lumbar Spinal Stenosis: Evaluation and Management Abstract Paul S. Issack, MD, PhD Degenerative lumbar spinal stenosis is caused by mechanical Matthew E. Cunningham, MD, factors and/or biochemical alterations within the intervertebral disk PhD that lead to disk space collapse, facet joint hypertrophy, soft-tissue Matthias Pumberger, MD infolding, and osteophyte formation, which narrows the space available for the thecal sac and exiting nerve roots. The clinical Alexander P. Hughes, MD consequence of this compression is neurogenic claudication and Frank P. Cammisa, Jr, MD varying degrees of leg and back pain. Degenerative lumbar spinal stenosis is a major cause of pain and impaired quality of life in the elderly. The natural history of this condition varies; however, it has not been shown to worsen progressively. Nonsurgical management consists of nonsteroidal anti-inflammatory drugs, physical therapy, and epidural steroid injections. If nonsurgical management is unsuccessful and neurologic decline persists or progresses, surgical treatment, most commonly laminectomy, is indicated. Recent prospective randomized studies have demonstrated that surgery is superior to nonsurgical management in terms of controlling pain and improving function in patients with lumbar spinal stenosis. egenerative lumbar spinal als, particularly the Spine Patient Dstenosis is a major cause of Outcomes Research Trial (SPORT) pain and dysfunction in the elderly. study, have provided compelling evi- Most patients report leg and/or back dence that decompressive surgery is pain and have progressive symptoms an effective treatment that provides after walking or standing for even pain relief and functional improve- short periods of time.1 Diagnosis is ment in patients with degenerative typically made based on clinical his- lumbar spinal stenosis.2,3 tory and physical examination and is confirmed on imaging studies. In most cases, treatment should begin Etiology with nonsurgical management. In the From the Hospital for Special Surgery, New York, NY. rare case of a progressive neurologic Lumbar spinal stenosis is a reduction deficit or cauda equina syndrome, in the volume of the central spinal J Am Acad Orthop Surg 2012;20: urgent surgical decompression is in- 527-535 canal, the lateral recesses, and/or dicated. In most cases, the natural neuroforamina that decreases the http://dx.doi.org/10.5435/ history of degenerative lumbar steno- JAAOS-20-08-527 space available for the thecal sac sis is variable and does not follow a and/or exiting nerve roots.4,5 Ap- Copyright 2012 by the American progressively deteriorating course. Academy of Orthopaedic Surgeons. proximately 20% of the time, this Recent prospective randomized tri- condition is caused or exacerbated August 2012, Vol 20, No 8 527 Degenerative Lumbar Spinal Stenosis: Evaluation and Management by congenital causes, such as failure mains unclear given the lack of pro- weakness (43%) reported.1 These of the posterior elements to develop, spective studies with observational symptoms may be localized to the resulting in short pedicles and cohorts. Johnsson et al9 followed 32 buttocks and can radiate to the laminae.4-6 More commonly, lumbar untreated patients with spinal steno- lower extremities in a proximal to stenosis is the result of degenerative sis over 49 months. Symptoms of distal fashion. Patients with lumbar changes. The degenerative process is neurogenic claudication remained spondylotic stenosis have diminished thought to be initiated by disk dehy- unchanged in 22 patients (70%), standing and walking tolerance; dration, disk bulging, and collapse of symptoms improved in 5 patients however their ability to walk dis- the disk space, which sets in motion (15%), and symptoms worsened in 5 tances can be increased by ambulat- the sequence of events that result in patients (15%). None of the patients ing with the spine in a flexed- narrowing of the spinal canal. Disk had severe deterioration. forward posture such as that used space narrowing and loss of the nor- Cauda equina syndrome is a rare when pushing a shopping cart.4 Typi- mal shock absorptive capacity of the condition caused by compression of cally, spinal extension narrows the spinal segment results in an increased the lumbosacral nerve roots within spinal canal and worsens neurogenic transfer of stress to the facet joints, the spinal canal that produces vary- symptoms, whereas spinal flexion which accelerates facet joint cartilage ing degrees of motor weakness; sad- and sitting increases the diameter of degeneration and osteophyte forma- dle anesthesia; and bowel, bladder, the spinal canal, partially alleviating tion.5,7 Facet joint hypertrophy, in- and gait dysfunction. Acute presenta- symptoms.4,5,11 folding of the ligamentum flavum, tion frequently occurs in patients On physical examination, back and development of bulging disk os- with large central disk herniation, pain or lower extremity symptoms teophyte complexes all contribute to whereas delayed presentation often can be elicited with lumbar exten- circumferential narrowing of the cen- occurs in patients with chronic spinal sion. Objective sensory findings such tral spinal canal and lateral recesses, stenosis. Surgical decompression as diminished sensation along a spe- that is, the area of the spine bordered should be performed as soon as pos- cific dermatome or motor weakness by the superior articular facet poste- sible to avoid progression of neuro- suggest long-standing neural com- riorly, the disk and vertebral body logic deficits.10 pression. Radicular symptoms are anteriorly, the thecal sac medially, most commonly seen in patients with and the pedicle laterally. These lateral recess or foraminal stenosis. stenotic changes cause neural com- Diagnosis Patients with spondylotic stenosis pression that presents clinically as may also present with neurogenic or variable degrees of leg and back Clinical Presentation vascular claudication. The orthopae- pain, as well as gait deterioration Patients with lumbar spondylotic dic surgeon must distinguish neuro- and other neurologic deficits (eg, stenosis most commonly present genic claudication from vascular numbness and weakness). with neurogenic claudication and re- claudication; patients with vascular port discomfort while standing as claudication may present with di- Natural History well as diminished walking capacity. minished walking capacity due to In a series of 68 patients with lumbar cramping of lower extremity muscles Prevalence of degenerative lumbar spinal stenosis confirmed with mye- on exertion. Unlike patients with spondylosis in the general popula- lography and surgery, neurogenic neurogenic claudication, patients tion ranges from 20% to 25% and claudication was observed in 94% of with vascular claudication cannot increases with age >50 years.8 The patients, with primary symptoms of improve walking tolerance with pos- natural history of this disease re- pain (93%), numbness (63%), or tural changes. Patients with neuro- Dr. Hughes or an immediate family member is a member of a speakers’ bureau or has made paid presentations on behalf of NuVasive; serves as a paid consultant to BOSS Medical, Bovie Medical Corporation, Orthovita, and SpineView; and has received research or institutional support from NuVasive. Dr. Cammisa or an immediate family member has received royalties from NuVasive; serves as a paid consultant to Alphatec Spine, Centinel Spine, Disc Motion Technologies, HealthpointCapital Partners, IVY Healthcare Partners, Mazor Surgical Technologies, NuVasive, Orthogem, Orthovita, Paradigm Spine, Spinal Kinetics, Spinal Partners III, and Viscogliosi Brothers; and has stock or stock options held in Alphatec Spine, BI Members, Centinel Spine, Disc Motion Technologies, HealthpointCapital Partners, IVY Healthcare Partners, Mazor Surgical Technologies, NuVasive, Orthovita, Orthopaedic Investment Partners, Paradigm Spine, Small Bone Innovations, Spinal Kinetics, and Viscogliosi Brothers. None of the following authors or any immediate family member has received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Issack, Dr. Cunningham, and Dr. Pumberger. 528 Journal of the American Academy of Orthopaedic Surgeons Paul S. Issack, MD, PhD, et al Figure 1 A, Parasagittal T2-weighted magnetic resonance image of the lumbar spine demonstrating multilevel lumbar spondylosis, with disk dehydration (arrowhead), disk protrusion (arrow), and central canal narrowing at L2-S1. Hypertrophic changes in the ligamentum flavum and facet joint are most prominent at L4-S1. B, Axial T2-weighted magnetic resonance image of the L4-5 interspace showing hypertrophy of the facet joint (arrowhead) and ligamentum flavum (arrow), causing severe central canal and lateral recess stenosis. C, Parasagittal T1-weighted magnetic resonance image of the lumbar spine demonstrating loss of epidural fat (arrow) about the lower lumbar exiting nerve roots (L3, L4, and L5) and neuroforaminal stenosis. genic claudication typically cannot involved as well as any associated stenosis with compression of travers- alleviate symptoms simply by ceasing pathology. Plain standing AP and lat- ing nerve roots. The degree of spinal to walk; these patients must sit or eral radiographs may demonstrate stenosis is best evaluated on MRI be- adopt a flexed-foward posture to al- spondylolisthesis, disk space narrow- cause it can demonstrate disk degen- leviate symptoms.
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