Neurosurg Focus 14 (1):Article 6, 2003, Click here to return to Table of Contents Pathogenesis, presentation, and treatment of lumbar spinal stenosis associated with coronal or sagittal spinal deformities JUSTIN F. FRASER, B.A., RUSSEL C. HUANG, M.D., FEDERICO P. GIRARDI, M.D., AND FRANK P. CAMMISA, JR., M.D. Hospital for Special Surgery; Bronx Veterans Affairs Hospital; and the Weill Medical College of Cornell University, New York, New York Sagittal- or coronal-plane deformity considerably complicates the diagnosis and treatment of lumbar spinal steno- sis. Although decompressive laminectomy remains the standard operative treatment for uncomplicated lumbar spinal stenosis, the management of stenosis with concurrent deformity may require osteotomy, laminectomy, and spinal fusion with or without instrumentation. Broadly stated, the surgery-related goals in complex stenosis are neural decom- pression and a well-balanced sagittal and coronal fusion. Deformities that may present with concurrent stenosis are scoliosis, spondylolisthesis, and flatback deformity. The presentation and management of lumbar spinal stenosis asso- ciated with concurrent coronal or sagittal deformities depends on the type and extent of deformity as well as its impact on neural compression. Generally, clinical outcomes in complex stenosis are optimized by decompression combined with spinal fusion. The need for instrumentation is clear in cases of significant scoliosis or flatback deformity but is controversial in spondylolisthesis. With appropriate selection of technique for deformity correction, a surgeon may profoundly improve pain, quality of life, and functional capacity. The decision to undertake surgery entails weighing risk factors such as age, comorbidities, and preoperative functional status against potential benefits of improved neu- rological function, decreased pain, and reduced risk of disease progression. The purpose of this paper is to review the pathogenesis, presentation, and treatment of lumbar spinal stenosis complicated by scoliosis, spondylolisthesis, or flat- back deformity. Specific attention is paid to surgery-related goals, decision making, techniques, and outcomes. KEY WORDS • spinal stenosis • spinal deformity • spondylolisthesis • scoliosis • spinal fusion • lumbar spine Lumbar stenosis exists when there is compression of sis, or lumbar kyphosis (flatback deformity). These le- neural elements and their nutrient supply in the central sions may be idiopathic, degenerative, or surgery induced canal, lateral recess, or neural foramen. Stenosis may exist and can complicate presentation and surgical treatment in any or all of these zones concurrently. The prevalence of lumbar spinal stenosis. Additionally, independent rigid of lumbar spinal stenosis, which should increase as popu- sagittal-plane deformities can also complicate spinal ste- lation demographics shift, is reported to be between 1.7 nosis and must be effectively addressed in therapeutic and 8% in the general population. Lumbar stenosis occur- plans. Evaluation and treatment of complex lumbar steno- ring in a congenitally small canal is termed constitutional sis requires an understanding of stenosis in the context stenosis and may present as early as the third decade of of these complicated deformities. The pathophysiological life. Most commonly stenosis develops from degenerative features, clinical history and examination, and radiograph- changes in the setting of a previously normal spinal canal. ic findings distinguish the presentation of stenosis that Classically, degenerative stenosis presents in the fifth and is complicated by spondylolisthesis, scoliosis, or flatback sixth decades. The current gold-standard treatment for deformity. A thorough understanding of these principles is essential to the appropriate treatment of complex lumbar uncomplicated lumbar spinal stenosis is neural element stenosis. decompressive laminectomy with or without lateral recess and foraminal decompression. Complex lumbar stenosis presents concurrently with LUMBAR STENOSIS AND ASSOCIATED other spinal deformities such as spondylolisthesis, scolio- DEFORMITIES Pathogenesis of Disease Abbreviations used in this paper: AP = anteroposterior; CT = computerized tomography; MR = magnetic resonance; VB = verte- Degenerative lumbar spinal stenosis results from patho- bral body. logical degeneration of the facet joints, disc herniation, Neurosurg. Focus / Volume 14 / January, 2003 1 Unauthenticated | Downloaded 09/28/21 11:14 AM UTC J. F. Fraser, et al. hypertrophy and buckling of the ligamentum flavum, and more levels, relatively short curves, and moderate ampli- spondylolisthesis. Degenerative changes in the three-joint tudes of scoliotic curvature.38 Asymmetrical vertebral col- complex (the intervertebral disc and two facet joints) lapse and listhesis contribute to the compromise of nerve explain the fluctuation in symptoms with alterations in roots, and may cause back pain and coronal decompen- posture, load, and duration of load.42 Lumbar interverte- sation. Thus, scoliosis complicates both the presenting bral disc degeneration represents a cascade of events in- symptoms as well as the treatment of lumbar stenosis. volving disc herniation, bulging of the disc and ligamen- Idiopathic and postsurgical flatback syndrome represent tum flavum into the canal, and resulting chronic facet another spinal deformity that may complicate presentation arthrosis, sclerosis, and osteophytic growth. Hypertrophy and treatment of lumbar spinal stenosis. For the purposes of the ligamentum flavum is also an important element of this review, we consider the more common postsurgical in the development of spinal stenosis. Lumbar spinal type. Flatback deformity is a relative reduction of normal encroachment induces ligamentum flavum hypertrophy, lumbar lordosis that may produce fixed sagittal imbal- which further aggravates stenosis. Disease of the nerve ance. Because flatback usually develops in the setting of roots and cord, however, does not typically result directly posterior spinal fusions in which distraction instrument- from compression of the nerves. Rather, the resulting ation has been placed, it is commonly accompanied by stenosis causes decreased flow of cerebrospinal fluid, junctional degeneration, instability, and stenosis. Other which represents approximately 60% of the nutritional causes include prior spinal trauma and systemic rheuma- supply to the cauda equina, and increased venous pres- tological illnesses such as ankylosing spondylitis.8 The sure. In such a scenario, any concurrent spinal deformities resulting sagittal deformity produces increased biome- may critically compromise the nerve roots and cord, as chanical demands on surrounding muscles, ligaments, and well as exacerbate neurological symptoms of lumbar ste- intervertebral discs, which may cause back pain and pro- nosis. gressive degeneration. Therefore, the treatment of lumbar Spondylolisthesis can be caused by congenital, devel- stenosis in the setting of flatback deformity must address opmental, traumatic, neoplastic, or degenerative condi- not only the decompression of neural elements but also tions. In degenerative spondylolisthesis, the most com- sagittal alignment and back pain. mon type observed with lumbar stenosis, anterior/ A fixed sagittal spinal deformity may result in added posterior displacement of a VB results from facet joint back pain, decreased ability to ambulate, and an inability erosion and attenuation of the muscular, capsular, and lig- to stand with both the hips and knees extended. Phys- amentous structures. Fourfold more common in females iological sagittal alignment of the spine includes a tho- than in males, degenerative spondylolisthesis occurs most racic kyphosis of 25 to 55° with apex at the T6–7 level and frequently at the L4–5 and L5–S1 levels.9 Disc degenera- a lumbar lordosis of 40–70° with apex at the L3–4 in- tion causes spondylolisthesis with resulting segmental terspace. Fixed deviation from such a sagittal alignment hypermobility, compounded by arthritis in sagittal facet represents a deformity, and this can occur throughout joints.4 These facet joints, which support up to one third of the spine. In addition, fixed deformities may present con- the spinal static compression load and axial loads, lose comitantly with spinal stenosis. The pathogenesis of such resistance to shear forces in the sagittal plain.17,46 The deformities may include nonstructural and structural caus- resulting degenerative anterior vertebral subluxation, es. Nonstructural causes include psychopathological fac- which is usually no greater than 30% of the VB width, and tors such as depression, neuromuscular disease, improper vertebral instability can contribute to the neurogenic clau- posture, and irritative lesions such as those in metastatic dication of spinal stenosis. Isthmic spondylolisthesis re- disease. Structural causes can be degenerative, congenital, sults from bilateral defects in the pars interarticularis; a compensatory in response to other spinal lesions, sec- widening of the central canal occurs as the posterior arch ondary to inflammatory diseases, iatrogenic, or idiopathic. of the cephalad vertebrae remains in place while the VB Degenerative causes include lumbar stenosis, facet joint displaces anteriorly. Although this represents a direct arthritis, and degenerative disc disease. Sagittal deformity widening of the spinal canal, callus formation around the may represent compensation for thoracolumbar kyphosis