Spinal stenosis is a narrowing of the spinal canal that occurs as a result of degenerative, developmental, and congenital disorders. Degenerative stenosis, the most common form of spinal stenosis, is a byproduct of arthritic changes in the intervertebral disks, facet joints, and ligaments. Symptoms typically manifest at age 50 to 60 years. In developmental spinal stenosis, narrowing of the spinal canal is caused by a growth disturbance of the posterior elements. Symptoms of congenital stenosis arise earlier in life as a result of anatomic changes and malformations.1
Clinically, spinal stenosis describes a constellation of symptoms that includes leg pain, difficulty with ambulation, and/or neurologic deficit. Stenosis may occur centrally, along the lateral recess and neuroforamina, as a result of degenerative changes involving the disk, hypertrophic facets, and joint capsule; synovial cysts; thickening of the ligamentum flavum; and osteophytic laminae.
Indications and Contraindications
The differential diagnosis of lumbar spinal stenosis is extensive. As such, it is important to rule out other pathologic etiologies with similar clinical presentations. Vascular claudication and neurogenic claudication must be differentiated from each other; both conditions exist in the older population (age 60 to 80 years). Vascular claudication is most commonly associated with cramping or tightness in the calf, associated peripheral vascular changes in the lower extremities (eg, skin ulcers, hair loss), and diminished peripheral pulses. Often, these findings are not present, however, and a careful patient history should be obtained. Vascular claudication is relieved with cessation of activity, whereas neurogenic claudication requires the patient to sit down or forward flex the lumbar spine to increase canal size. The patient with neurogenic claudication typically is capable of engaging in physical activity when he or she is forward-flexed (eg, walking with a shopping cart, bicycling, walking uphill). The vascular patient is unable to participate in such activities.
Hip arthritis may manifest as groin pain and referred pain into the thigh, particularly with increased activity. Physical examination of the hip, with particular attention to internal rotation, often is helpful in elucidating the etiology of the pain. Additionally, anteroposterior lumbar radiographs may demonstrate the hip joint space, thus revealing the severity of degenerative changes.
Diabetes may manifest with symptoms similar to those of spinal stenosis. However, the patient with diabetes typically has sensory changes in a stocking-glove distribution in the foot. Furthermore, diabetic neuropathy does not change with exertional or positional activity.
The elderly patient is commonly affected by lumbar spinal stenosis. As such, particular attention should be given to a thorough cardiac history and examination. The physician should note and carefully evaluate the patient for history of prior cardiac surgery and risk factors for stroke and blood clots as well as medications that may increase surgical complications (eg, clopidogrel bisulfate, aspirin). The patient should be counseled regarding the potential for postoperative myocardial infarction and stroke, which can have a devastating effect on functional outcome following the lumbar procedure.
Rapid symptomatic or functional decline is rare in the patient with lumbar spinal stenosis; initially, a course of nonsurgical management is recommended (eg, activity modification, exercise, nonsteroidal antiinflammatory drugs, epidural injection).2 Surgical indications include progressive neurologic deficit, intractable pain, and persistent impairment and functional limitations. Because low back pain itself is not reliably alleviated with surgery, it alone is not an indication for surgery.
There are no absolute contraindications to surgery. Medical comorbidities significantly influence outcomes. Age in itself is not a contraindication and should be considered as such only in conjunction with the overall health status of the patient.3 The patient without a concordance of history, physical examination, and imaging data should be managed nonsurgically.
The goals of surgery are to increase function, decrease pain, and prevent progression of neurologic deficit. The key to achieving these goals is complete decompression of the neural elements with preservation of stability of the motion segments. The extent of decompression is determined by the pathoanatomy.
Two patient positions are recommended for decompressive laminectomy: supine on a four-poster frame (Jackson table) or in a 90°-90° kneechest position (Andrews table) (Figure 1). Both positions allow the abdomen to hang freely, which allows reduction of epidural venous pressure, thereby decreasing blood loss and improving surgical visualization. However, because the kneechest position reduces anatomic lordosis, it should be used only in the patient who does not require a concomitant fusion. When fusion is anticipated, a Jackson table is preferred because it maintains normal sagittal contour.4
Localization and Surgical Visualization
Intraoperative localization may be performed based on evaluation of a lateral radiograph or a fluoroscopic image. Preoperative localization is particularly important for minimally invasive and microscopic procedures. With the aid of a fluoroscope, spinal needles may be placed percutaneously into the desired spinous processes (ie, cephalad, caudad) of the affected levels. The surgeon can accurately localize the level and minimize the size of the surgical incision. We prefer to use a microscope for visualization when decompression alone is performed. A microscope can be angulated in a cephalad or caudad direction, thus improving visualization and decreasing the need to expand the incision for a direct view, as is required with loupe magnification.5
A midline posterior longitudinal incision provides proper exposure of the spinous processes at the level of pathology (Figure 2) (Symbolvideo, Laminectomy). Subperiosteal dissection is meticulously executed with the aid of electrocautery. Care is taken to preserve the facet capsules and the attaching paraspinal musculature, particularly when performing decompression only.
Laminectomy, whether performed microscopically, endoscopically, or via loupe magnification, begins with central decompression. A rongeur is used to remove the inferior one half of the cephalad spinous process and the superior one half of the inferior spinous process, along with all intermediate spinous processes (Figure 3).
An angled curet is used to detach the ligamentum flavum from the ventral surface of the lamina (Figure 4) (Symbolvideo, Laminectomy, 0:55). Next, a Leksell rongeur is used to remove additional bone and soft tissue, thereby thinning the laminae. Central decompression is begun with the aide of a Kerrison rongeur, using the ligamentum flavum as a barrier between the lamina and the dura (Figure 5). After removal of the distal one third of the lamina, the ligamentum flavum ceases to be a protective barrier. A cottonoid patty and a Woodson elevator are used to gently depress the dura while the central decompression is completed with a Kerrison rongeur. For an adjacent-level decompression, we recommend first removing the cephalad inferior lamina, which enables use of the ligamentum flavum as a protective barrier. The ligamentum flavum can then be separated, lifted, and removed in one or two large pieces. Removing the ligamentum flavum piecemeal in a cephalad fashion is more time-consuming and dangerous, as it potentially increases the risk of dural tear.
The lateral recess and the neuroforamen are addressed next (Symbolvideo, Laminaplasty, 1:50). The medial wall of the pedicle delineates the lateral extent of the decompression. A 45° Kerrison rongeur is used to perform a partial medial facetectomy and undercut the foraminal entrance. The best way to achieve adequate facet removal is with resection performed from the contralateral surgical side (Figure 6). To avoid potential spinal instability, the surgeon should be careful not to remove more than 50% of the facet. The facet joint is undercut to preserve the integrity of the dorsal structures. Kerrison rongeurs should be used in parallel with the nerve roots, thereby minimizing the risk to the nerve root. With a severely narrowed lateral recess, insertion of the Kerrison rongeur may compromise nerve root function. We recommend first removing the bone with a burr, osteotome, or Kerrison rongeur, then lifting away the ligamentum flavum from the nerve root. An angled dural separator or ball-tip probe may be used to assess the adequacy of the decompression. A 4-mm probe should pass without difficulty. The root is gently retracted with a Penfield dissector; the root should demonstrate 1 cm of medial displacement at the level of the lateral recess. Lack of thorough foraminal decompression may result in failed back syndrome.6 Foraminal decompression is initially accomplished via removal of the facet joint laterally using an osteotome or power burr. The foramen then is undercut with the Kerrison rongeur, ensuring that the nerve root is free and mobile.
Disk herniation is seen occasionally in conjunction with lumbar spinal stenosis (Symbolvideo, Laminaplasty, 2:25). Lateral or foraminal disk herniation may require removal. Central bulges alone are adequately decompressed with laminectomy. Following careful dural retraction, a pituitary rongeur can be used to excise the disk fragment. When the excursion of the nerve is still limited, further foraminal or extraforaminal decompression should be performed. A more lateral removal of the facet joint may help identify neural entrapment between the superior facet of the vertebra below and the posterolateral aspect of the vertebral body or pedicle of the vertebra above.
Neural decompression may be accomplished by excising the superior tip of the superior facet or by complete facetectomy (Figure 7). Neural entrapment may occur between the herniated disk and the pedicle of the supra-adjacent vertebra. Lateral annulectomy or resection of the inferomedial aspect of the pedicle may allow for full nerve root decompression. The adequacy of nerve root decompression is assessed by two factors: patency of the neuroforamen and nerve root mobility.
Microdecompressive laminoplasty has been advocated in the patient with predominantly unilateral lower extremity symptoms who has only mild to moderate central stenosis7,8(Symbolvideo, Laminoplasty). Hemilaminectomy is performed on the symptomatic side, and the spinous process and the contralateral lamina are undercut to decompress the central canal (Figure 8). Advantages of laminoplasty include preservation of the posterior spinal elements (eg, supraspinous ligament, facet joints) that potentially preserve spinal stability.
Use of a surgical microscope is recommended. Subperiosteal paraspinal dissection is done unilaterally. Hemilaminectomy is completed in a routine fashion; this procedure simultaneously accomplishes lateral recess decompression. The operating table is then tilted away from the surgeon, and the microscope is adjusted to allow visualization of the undersurface of the spinous process (Symbolvideo, Laminoplasty, 1:45). A Kerrison rongeur is used to undercut the undersurface of the spinous process and the contralateral lamina indirectly decompressing the central canal (Figure 9). When decompression is difficult to perform or when complications (eg, dural tear) occur, a laminoplasty may be easily converted to a laminectomy at any point during the procedure.
Limited Laminotomy (Fenestration)
Laminotomy is another common method of decompression. Unilateral laminotomy has been advocated in the patient with localized lateral recess stenosis and isolated radiculopathy. More often, however, bilateral laminotomy is recommended as a spinous process- and ligamentsparing alternative to complete laminectomy. This procedure is contraindicated in the patient with global narrowing caused by congenital stenosis. Posterior element preservation may minimize the risk of progression. The role of limited laminotomy in the patient with scoliosis and spondylolisthesis remains to be defined. Limited laminotomy techniques should not be used for the patient with significant neuroforaminal compression.
The patient is mobilized to a chair the evening of surgery, and ambulation is begun the next morning. Postoperative bracing is done only when a concomitant fusion has been performed (in a patient with osteoporosis) or when fixation has been compromised. Drains are removed on the first or second postoperative day. Antibiotics are given preoperatively and continued for 24 hours, regardless of the presence of indwelling drains or catheters. Most patients are discharged home after 2 to 4 days, depending on the extent of the surgical procedure. The elderly patient with multiple medical comorbidities may require inpatient rehabilitation. The patient is instructed to refrain from bending, lifting, and twisting for 6 to 12 weeks. The time and extent of rehabilitation is related to the underlying surgical procedure. The patient is seen at 6 weeks postoperatively and undergoes physical therapy for an additional 6 weeks to regain strength and mobility. The patient is discharged to unrestricted activity at 3 months postoperatively.
There is a paucity of information on the natural course of the disease compared with surgical decompression and nonsurgical treatment. Malmivaara et al9 recently conducted a randomized controlled trial evaluating surgical versus nonsurgical management of lumbar spinal stenosis. The authors noted that although patients improved over the 2-year follow-up regardless of initial treatment, those who underwent decompressive surgery reported greater improvement of leg pain, back pain, and overall disability. The relative benefit of the initial surgical treatment diminished over time, but outcomes of surgery remained favorable at 2 years.
Complications can be divided into four groups: infectious, vascular, cardiopulmonary, and neurologic. Mortality rates are related to age and the presence of comorbidities. In patients younger than age 75 years, the mortality rate is <1%. In patients older than age 80 years, the mortality rate rises to 2% to 3%.3,10
In lumbar spine surgery, the prevalence of dural tears ranges from 1% to 17%; this rate varies according to the series reviewed as well as the type of surgical procedure performed.11 Deyo et al11 evaluated postoperative complications, including dural tears, in a large series of spinal procedures. Morbidity was lower for younger patients (aged 25 to 40 years) and for patients who underwent herniated disk surgery. The complication rate increased with age, with procedures for spinal stenosis, and with revision procedures. Various consequences of dural tears have been reported. A persistent dural tear may lead to meningeal pseudocyst formation or potential nerve root entrapment, with resultant neurologic symptoms (eg, sciatica). Rates of neurologic deficit after lumbar decompression alone are unknown but appear to be correlated with the rate of incidental durotomy.12 Recommendations for the treatment of dural tears have included primary repair with sutures; closed subarachnoid drainage; laser tissuewelding; muscle, fat, and fascia grafts; blood patches; fibrin-adhesive or cyanocrylate polymer sealant; Gelfoam (Pfizer, New York, NY); bed rest; and avoidance of wound drains. Subarachnoid drains are effective when a persistent dural leak cannot be repaired surgically. Routine use of these drains is not recommended, however, because most dural tears do not lead to persistent leaks.
- Flexion-extension lateral radiographs are necessary to detect dynamic instability and evaluate sagittal alignment.
- In the setting of severe spinal stenosis, a round-tip burr can be used to thin the overlying lamina. An angled curet is used to break off the remaining laminar shell. Next, the ligamentum flavum is teased off the dura, thereby limiting the passing of instruments into the canal.
- Even in the patient who presents with unilateral symptoms, unilateral surgery should be avoided when there is radiographic evidence of bilateral symptoms.
- Inadequate foraminal decompression may result in persistent radiculopathy.
- Identify preoperative instability to include a possible fusion.
- Undercut the facet to prevent iatrogenic instability.
Another potential source of clinical failure is recurrent stenosis as a result of regrowth of the lamina. Long-term failure includes recurrent stenosis at levels adjacent to those previously treated. In the patient undergoing spinal fusion, changes in segmental stiffness may increase forces applied to adjacent segments, thereby accelerating degeneration.
Spinal stenosis is a manifestation of several distinct etiologies that result in narrowing of the spinal canal. Degenerative changes involving the facet joints, intervertebral disks, and ligaments all may contribute to stenosis or exacerbate symptoms in the patient with congenitally narrowed canals. For most patients, spinal stenosis is successfully managed with activity modification, exercise, nonsteroidal anti-inflammatory drugs, and epidural injection. Correlating patient symptoms with radiographic evidence of neurologic compression helps ensure a more predictable outcome. Surgical intervention may be necessary in the patient with intractable pain, neurologic compromise, or mechanical instability. Various interventions exist, including microscopic laminectomy, lumbar laminoplasty, and lumbar laminotomy. Surgery should be individualized to address the specific spinal pathology and to allow for complete neurologic decompression. Using the principles of spinal surgery reviewed herein, one can expect improved patient outcomes.
Evidence-based Medicine: Level I/II prospective, randomized studies include references 1, 2, and 9. Level III/IV case-control and cohort studies include references 3, 6-8, and 10-12. Citation numbers printed in bold type indicate references published within the past 5 years.
. Singh K, Samartzis D, Vaccaro AR, et al: Congenital lumbar spinal stenosis: A prospective, control-matched, cohort radiographic analysis. Spine J
. Murphy DR, Hurwitz EL, Gregory AA, Clary R: A non-surgical approach to the management of lumbar spinal stenosis: A prospective observational cohort study. BMC Musculoskelet Disord
. Galiano K, Obwegeser AA, Gabl MV, Bauer R, Twerdy K: Long-term outcome of laminectomy for spinal stenosis in octogenarians. Spine
. Knaub MA, Won DS, McGuire R, Herkowitz HN: Lumbar spinal stenosis: Indications for arthrodesis and spinal instrumentation. Instr Course Lect
5. Riew KD, Rhee J: Microsurgical techniques in lumbar spinal stenosis. Instr Course Lect
6. Jenis LG, An HS, Gordin R: Foraminal stenosis of the lumbar spine: A review of 65 surgical cases. Am J Orthop
. Adachi K, Futami T, Ebihara A, et al: Spinal canal enlargement procedure by restorative laminoplasty for the treatment of lumbar canal stenosis. Spine J
. Kawaguchi Y, Kanamori M, Ishihara H, et al: Clinical and radiographic results of expansive lumbar laminoplasty in patients with spinal stenosis. J Bone Joint Surg Am
2005;87(suppl 1 pt 2):292-299.
. Malmivaara A, Slätis P, Heliövaara M, et al: Surgical or nonoperative treatment for lumbar spinal stenosis? A randomized controlled trial. Spine
. Atlas SJ, Keller RB, Wu YA, Deyo RA, Singer DE: Long-term outcomes of surgical and nonsurgical management of lumbar spinal stenosis: 8 to 10 year results from the Maine Lumbar Spine Study. Spine
11. Deyo RA, Cherkin DC, Loeser JD, Bigos SJ, Ciol MA: Morbidity and mortality in association with operations on the lumbar spine: The influence of age, diagnosis, and procedure. J Bone Joint Surg Am
. Saxler G, Krämer J, Barden B, Kurt A, Pförtner J, Bernsmann K: The longterm clinical sequelae of incidental durotomy in lumbar disc surgery. Spine