Spinal Stenosis Treatment & Management

Management of spinal stenosis is aimed toward symptomatic relief and prevention of neurologic sequelae. Conservative measures such as pharmacologic therapy and physical therapy provide temporary relief but remain an important adjunct in the overall treatment algorithm preceding surgical decompression. Nonsurgical measures are aimed at symptomatic relief; analgesics, anti-inflammatory agents (including judicious use of steroids), and antispasmodics can provide relief during acute exacerbations. ^[10] However, conservative and surgical treatments have not been subjected to rigorous, well-designed studies, and there is very little data comparing conservative and surgical treatment for lumbar spinal stenosis (LSS). ^[40]

Surgery is indicated when the signs and symptoms correlate with the radiologic evidence of spinal stenosis. Generally, surgery is recommended when significant radiculopathy, myelopathy (cervicothoracic), neurogenic claudication (lumbar), or incapacitating pain is present. The choice of surgical procedure and the decision to fuse the spine should be individualized to optimize the outcome.

Patient characteristics associated with greater treatment effects of surgery include baseline Oswestry Disability Index ≤56, not smoking, neuroforaminal stenosis, predominant leg pain, not lifting at work, and the presence of a neurologic deficit. In general, with the exception of smokers, patients who meet strict inclusion criteria improve more with surgery than with other treatments. Patients with spinal stenosis should consider smoking cessation before surgery. ^[41]

Unlike acute lumbar disc herniation, spinal stenosis is not typically treated using interventional radiologic techniques. Pain management, including facet injections, may provide temporary relief in patients; however, biopsy of metastatic spinal disease is performed easily using CT guidance. Spinal stenosis associated with compression fractures has been successfully treated using percutaneous vertebroplasty. ^{[42, 43, 44]}

Cervical stenosis progresses to myelopathy in as many as one third of affected individuals. Unfortunately, late treatment of myelopathy by decompression does not always reverse the neurologic deficit, and thus, individuals with severe cervical stenosis should undergo close neurologic follow-up. ^[11]

Treatment outcome predictors do not exist; specifically, severe spinal degenerative changes do not necessarily correlate with an unfavorable prognosis or mandate surgery.

Simotas and colleagues noted that 12 of 49 patients treated conservatively with incorporation of analgesics, physical therapy, and epidural steroid injection reported sustained improvement. ^[45]

Physical therapy with traction and strengthening exercises helps to relieve associated symptoms or muscular spasms and mechanical back pain. Unfortunately, most of these approaches provide only temporary relief. Decompression and inversion tables have also been used, with great initial success and varying amounts of lasting benefit. ^[46]

Acupuncture has shown significant short-term benefits in LSS with regard to pain and quality of life. ^[47]

With all these different modalities, it is not uncommon for patients, and even practitioners, to debate whether surgical treatment or conservative management is most appropriate. A recent study of comparative effectiveness evidence for intervertebral disk herniation, spinal stenosis, and degenerative spondylolisthesis from the Spine Patient Outcomes Research Trial (SPORT) shows good value for surgery compared with nonoperative care over 4 years. ^[48]

A study by Pochon et al indicated that although women with disk herniation, degenerative spondylolisthesis, or spinal stenosis tend to have worse preoperative symptoms than men do, postoperative outcomes for these conditions do not significantly differ by sex. In the study, which included 1518 patients (812 men and 706 women), the investigators found that women scored worse preoperatively on the Core Outcome Measures Index (COMI) for all three disorders; 12 months postoperatively, however, COMI scores showed no significant variation between males and females, with the minimal clinically important change score having been reached by 71.3% of men and 72.9% of women. ^[49]

Evidence-based guidelines from the North American Spine Society (NASS) for the diagnosis and treatment of degenerative LSS state that medical/interventional treatment may be considered for patients with moderate symptoms of LSS. These treatments include all nonoperative options, including physical therapy, medications, exercise, and spinal interventions such as epidural steroid injections (ESIs). ^{[50, 51]}

First-line pharmacotherapy for lumbar spinal stenosis (LSS) includes NSAIDs, which provide analgesia at low doses and quell inflammation at high doses. An appropriate therapeutic NSAID plasma level is required to achieve anti-inflammatory benefit.

Aspirin, which binds irreversibly to cyclo-oxygenase and requires larger doses to control inflammation, may cause gastritis; consequently, it is not recommended. Additionally, it may induce multiorgan toxicity, including renal insufficiency, peptic ulcer disease, and hepatic dysfunction. Cyclo-oxygenase isomer type 2 (COX-2) NSAID inhibitors reduce such toxicity. NSAIDs retain a dose-related analgesic ceiling point, above which larger doses do not confer further pain control. Tramadol and acetaminophen confer analgesia but do not affect inflammation.

Muscle relaxants may be used to potentiate NSAID analgesia. Sedation results from muscle relaxation, promoting further patient relaxation. Such sedative side effects encourage evening dosing for patients who need to get sufficient sleep but may limit safe performance of some functional activities.

Tricyclic antidepressants (TCAs) are often given for neuropathic pain, but their adverse effects limit their use in elderly persons. These include somnolence, dry mouth, dry eyes, and constipation. More concerning are the possible arrhythmias that may occur when TCAs are used in combination with other medications.

Oral opioids may be prescribed on a scheduled short-term basis. Consequently, cotreatment with a psychologist or other addiction specialist is recommended for patients with a history of substance abuse. All patients on long-term opiates may be expected to sign a medication agreement restricting them to 1 practitioner, 1 pharmacy, scheduled medication use, scheduled refills, and no medication sharing, selling, or other transfers. They are also typically expected to partake in random urine screening.

Membrane-stabilizing anticonvulsants, such as gabapentin and carbamazepine, may reduce neuropathic radicular pain from lateral recess stenosis. ^[52] These agents have central and peripheral anticholinergic effects, as well as sedative effects, and block the active reuptake of norepinephrine and serotonin. The multifactorial mechanism of analgesia could include improved sleep, altered perception of pain, and increase in pain threshold. Rarely should these drugs be used in treatment of acute pain, since a few weeks may be required for them to become effective.

Matsudaira et al tested the effectiveness of limaprost, an oral prostaglandin E1 derivative, against that of etodolac, an NSAID, in improving the health-related quality of life in patients with symptomatic LSS. ^[53] In a randomized, controlled trial, 66 patients suffering from central stenosis with acquired, degenerative LSS, along with neurogenic intermittent claudication and bilateral leg numbness related to the cauda equina, were administered a daily dose of limaprost (15 μg) or etodolac (400 mg) for 8 weeks. The results indicated that limaprost was more effective than etodolac in improving patients' physical functioning, vitality, and mental health and in reducing pain and leg numbness.

Citing insufficient evidence, the North American Spinal Society (NASS), in a set of evidence-based guidelines on the diagnosis and treatment of degenerative LSS, states that a recommendation cannot be made for or against the pharmacologic treatment of LSS. ^{[50, 51]}

Epidural steroid injection (ESI) provides aggressive-conservative treatment for patients with lumbar spinal stenosis (LSS) who demonstrate limited response to oral medication, physical therapy, and other noninvasive measures.

The North American Spine Society (NASS), in its evidence-based guidelines for the diagnosis and treatment of degenerative LSS, suggests that, in patients with radiculopathy or neurogenic intermittent claudication from LSS, medium-term pain relief (ie, 3-36 months) can be achieved with a multiple-injection regimen of radiographically guided transforaminal ESIs or caudal injections. In this regimen, the patient is injected either on demand or when his or her pain exceeds a preset level. ^{[50, 51]}  (In contrast, according to a literature review by Ammendolia et al, moderate-quality evidence suggests that in comparison with epidural lidocaine injections, clinically important improvements, either short- or long-term, are not derived from the use of ESIs in LSS with neurogenic claudication. ^[54] )

Corticosteroids may inhibit edema formation from microvascular injury sustained by mechanically compressed nerve roots. Furthermore, corticosteroids inhibit inflammation by impairing leukocyte function, stabilizing lysosomal membranes, and reducing phospholipase A2 activity. Lastly, corticosteroids may block nociceptive transmission in C fibers. When using oral steroids (in rapid tapering fashion), remember that possible side effects may include fluid retention, skin flushing, and shakiness. Local anesthetic may be combined with corticosteroids to provide immediate pain relief and diagnostic feedback on the proximity of the injectate to the putative pain generator. A study by Elsheikh and Amr showed improved outcomes when calcitonin is added to an ESI. ^[55]

Caudal ESI entails needle placement through the sacral hiatus into the sacral epidural space. Advantages include ease of performance and low risk of dural puncture. Disadvantages include large injectate volumes (6-10 mL) necessary to ensure adequate medication spread to more cephalad pathology (ie, above L4-L5); such large volumes may dilute the effect of the corticosteroid. Alternatively, a catheter may be used through the caudal ESI needle for more directed medication placement requiring smaller volumes.

Interlaminar ESI entails needle passage through the interlaminar space, with subsequent injection directly into the posterior epidural space. Consequently, delivery of medication occurs closer to the affected spinal segmental level than in caudal ESI. Disadvantages include greater potential for dural puncture and, as with caudal ESI, limited spread of medication to the target site if a midline raphe or epidural scarring exists. Interlaminar ESIs should not be attempted at levels where posterior surgery has been performed, since a scarred or absent ligamentum flava typically results in a dural puncture. Furthermore, interlaminar injection delivers medication to the posterior epidural space, with possible limited ventral diffusion to nerve root impingement sites.

Transforaminal ESI facilitates precise deposit of higher steroid concentrations closer to the involved spinal segment and, consequently, may prove more efficacious in reducing pain. Transforaminal ESI may be used for unilateral radicular pain provoked by lateral recess or foraminal stenosis. Unilateral transforaminal ESI will typically not result in bilateral flow.

Bilateral transforaminal ESI may be used to treat bilateral foraminal pathology or central stenosis-induced neurogenic claudication (NC) pain. It is also preferred when imaging studies demonstrate limited posterior epidural space or at levels with previous posterior surgery, when safe interlaminar ESI is precluded. Otherwise, interlaminar ESI may be used to treat bilateral or multilevel NC or radicular pain.

Anticoagulation and ESI

Relative contraindications to ESI include bleeding diathesis and anticoagulation (AC) therapy, because of the increased risk of epidural hematoma. However, the actual incidence of this complication is unknown; estimates in the literature suggest that it occurs in less than 1 in 150,000 outpatient epidural injections. It is worth noting that most studies evaluating the epidural hematoma risk are based on thoracic epidurals or procedures involving catheters on fully anticoagulated patients (ie, heparin, warfarin). Even these studies do not show a significantly increased incidence of hematoma formation in patients who undergo anticoagulation. ^[56] Several practice audits and case reports have demonstrated minimal risk of adverse events with neuroaxial procedures. ^{[57, 58]}

In some patients, it is riskier to stop their AC, since this can potentially lead to a life-threatening event, such as myocardial infarction. Current cardiac guidelines typically recommend AC therapy 12 months after stent placement. ^[59] Patients are anticoagulated for many reasons, including, but not limited to, a history of deep venous thrombosis (DVT), pulmonary embolus (PE) or cerebral vascular accident (CVA). Some have mechanical cardiac valves or cardiac stents or have atrial fibrillation, and the AC is preventing embolic and/or ischemic events. ^[60]

For those patients with recent stent placement or who have mechanical heart valves, their acute risk from stopping the ACs is extremely high. For other patients, such as those with atrial fibrillation, the short-term risk from AC cessation is much lower. The stroke literature suggests that holding AC leads to an increased risk of thrombotic events. ^[61] Therefore, International Spine Intervention Society (ISIS) guidelines recommend that the risk/benefit ratios be contemplated on an individualized basis in conjunction with the prescribing physician. ^[57]

When stopping AC therapy (eg, warfarin, heparin), it should be done a few days prior to injection, based on medication half-life and hematologic profile. (Alternative methods of DVT prophylaxis, such as serial compression hose, should be instituted in the interim). In the case of patients taking warfarin, prothrombin time/international normalized ratio (PT/INR) should be drawn the day of the procedure. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) should be discontinued before the procedure, in accordance with their half-life and hematologic profile. ^[58]

Other contraindications

Absolute contraindications to ESIs include systemic infection and pregnancy (because of the teratogenicity of fluoroscopy). Relative contraindications include diabetes mellitus (DM) and congestive heart failure, given the hyperglycemic and fluid retention properties of corticosteroids, respectively. Other relative contraindications include adrenal dysfunction and hypothalamic-pituitary axis suppression.

For patients with injectate allergies, such as to contrast agents or anesthetics, ESI may be performed with premedication protocols or without using the offending medication.

ESI-associated limitations

Serious complications, although rare, include infection (eg, epidural or subdural abscess) and epidural hematoma. Epidural hematoma has been associated with traumatic needle insertions, but this is neither sensitive nor specific for predicting development. Vandermeulen and colleagues reported 61 case reports in the literature between 1904 and 1994 after central nervous blocks. ^[62] Dural puncture (in 5% of lumbar interlaminar ESIs and 0.6% of caudal injections) with possible subsequent subarachnoid anesthetic/corticosteroid deposition may provoke neurotoxicity, sympathetic blockade with hypotension, and/or spinal headache; however, contrast-enhanced fluoroscopic guidance minimizes the possibility of dural puncture and intravascular injection.

Therapeutic ESI techniques are performed ideally using fluoroscopic guidance and radiologic contrast dye enhancement to ensure delivery of injectate to the target site. Studies document misplacement of 40% of caudal and 30% of interlaminar injections performed without fluoroscopy, even by experienced injectionists.

Transient corticosteroid dose-related side effects include facial flushing, low-grade fever, insomnia, anxiety, agitation, hyperglycemia, and fluid retention. Steroids may suppress the hypothalamic-pituitary axis for 3 months following the injection. Lastly, vasovagal reaction, nerve root injury, injectate allergy, and temporary pain exacerbation can occur as well.

Results of ESI for spinal stenosis

Recent studies assessing efficacy of fluoroscopically guided, contrast-enhanced ESI, even for herniated nucleus pulposus (HNP)-induced radicular pain, appear promising, suggesting that a significant inflammatory component amenable to corticosteroid treatment may accompany HNP-nerve root pathology.

Studies of ESI for LSS treatment demonstrate mixed results due to varying injection and guidance techniques, patient populations, follow-up periods and protocols, ancillary treatments (eg, physical therapy, oral medication), and outcome measures. This lack of consistency limits the ability to assess ESI efficacy for LSS.

Some studies, nevertheless, suggest that, unlike HNP-provoked radicular pain, NC may be more mechanical or ischemic than inflammatory in nature. Consequently, corticosteroid anti-inflammatory properties may fail to provide designed long-term symptom relief. Studies report that 50% of patients with LSS or HNP-provoked radicular pain received temporary relief and that such results were close to those associated with the placebo effect.

Because of concomitant lateral recess stenosis from facet hypertrophy or lateral HNP, patients may fail transforaminal ESI therapy for HNP-induced radicular pain. ESI may do little to relieve chronic lateral recess stenosis-related radicular pain. Additionally, studies show patients with a preinjection duration of symptoms greater than 24 weeks may respond to ESI as favorably as those with symptoms of less than 24 weeks' duration. This finding, may suggest that chronic nerve compression could induce irreversible neurophysiologic change that ultimately renders the nerve root refractory to ESI.

A meta-analysis by Manchikanti et al suggested that epidural injection with lidocaine alone or in combination with a corticosteroid is significantly effective on pain and function in spinal stenosis (as well as lumbar radiculopathy), with the impact of lidocaine by itself being comparable to that of the combination. However, bupivacaine and sodium chloride solution were each found to be ineffective. ^[63]

Future studies require controlled design, contrast-enhanced fluoroscopic guidance, and objective validated outcome measures before definitive conclusions can be drawn regarding efficacy of ESI treatment of LSS.

Patients with lumbar spinal stenosis (LSS) often benefit from conservative treatment and participation in a physical therapy (PT) program. However, the NASS guideline states that there is insufficient evidence to support the effectiveness of physical therapy. ^[50]  Nonetheless, the aforementioned literature review by Ammendolia et al indicated that moderate-quality evidence exists for the effectiveness of a 6-week multimodal program of manual therapy and exercise (either with or without education) in the treatment of neurogenic claudication in LSS. ^[54]

Lumbar extension exercises should be avoided in patients with LSS, as spinal extension and increased lumbar lordosis are known to worsen the condition. Flexion exercises for the lumbar spine should be emphasized, as they reduce lumbar lordosis and decrease stress on the spine. Spinal flexion exercises increase the spinal canal dimension, thus reducing neurogenic claudication (NC). Williams' flexion-biased exercises target increased lumbar lordosis, paraspinal and hamstring inflexibility, and abdominal muscle weakness. These exercises incorporate knee-to-chest maneuvers, pelvic tilts, wall-standing lumbar flexion, and avoidance of lumbar extension.

Two-stage treadmill testing has demonstrated longer walking times on an inclined treadmill, presumably due to promotion of spinal flexion. Conversely, level treadmill testing is thought to promote more spinal extension-induced NC and elicit earlier symptom onset and longer recovery time. Ancillary exercises to target weak gluteals, as well as shortened hip flexors and hamstrings, are indicated. Physical examination should be performed to assess for concurrent degenerative hip disease, which may mimic LSS. Traction harness-supported treadmill and aquatic ambulation to reduce compressive spine loading has been shown to improve lumbar range of motion (ROM), straight leg raising, gluteal and quadriceps femoris muscle force production, and maximal (up to 15 min) walking time. ^[64]

Others advocate stationary cycling and abdominal muscle strengthening. Passive modalities such as heat, cold, transcutaneous electrical nerve stimulation (TENS), and ultrasound may provide transient analgesia and increased soft tissue flexibility in LSS patients.

The addition of a rolling walker is necessary in many cases. The rolling walker provides some stability and promotes a flexed posture, which allows the afflicted patient to ambulate greater distances.

The North American Spine Society (NASS), in its aforementioned guidelines on the diagnosis and treatment of degenerative LSS, states that there is insufficient evidence to either support the use of physical therapy or exercise as a stand-alone treatment for LSS or to recommend against it. However, the guidelines' physical therapy/exercise work group suggests that despite an absence of reliable evidence regarding its efficacy, a limited course of active physical therapy should nonetheless be a treatment option in LSS. ^{[50, 51]}

Surgery for spinal stenosis is indicated for significant myelopathy, radiculopathy, and/or neurogenic claudication. Which decompressive approach is chosen depends on the spinal region, the spinal alignment, and the anatomic nature of the compressive elements. Whether concomitant stabilization is needed remains controversial. More often than not, fusion is not necessary after decompressive lumbar laminectomy.

A study by Försth et al indicated that in patients with lumbar spinal stenosis (LSS), with or without spondylolisthesis, treatment with decompressive surgery by itself was no less effective than treatment with decompressive surgery plus fusion surgery. The study, which included 247 patients, found that the mean Oswestry Disability Index score did not significantly differ between the two groups at 2-year follow-up. Clinical outcomes also did not significantly differ between members of the two groups who were followed up at 5 years. ^[65]

In recent years, the availability of interspinous process devices, such as X-stop and Coflex, has provided a less-invasive surgical approach for LSS. The success of this type of surgery relies on careful patient selection. ^{[66, 67, 68, 69]}

Outcomes for LSS surgery vary and are difficult to assess because of vaguely defined outcome measures, study designs, observer bias, and inadequate outcome data categorization.

It is clear that patients with severe LSS with significant symptoms can benefit from lumbar decompressive surgery. However, whether patients with moderate LSS with less severe symptoms should also have surgery is unclear. A randomized, controlled study of 94 patients with moderate LSS who underwent either surgical or nonsurgical treatment suggested that decompressive surgery of moderate lumbar spinal stenosis can provide slight, but consistent, functional ability improvement, especially compared with nonoperative measures. The results were based on a 6-year follow-up. ^[70]

North American Spine Society (NASS) guidelines suggest the use of decompressive surgery as a means of improving outcomes not only in patients with severe symptoms of LSS but in those with moderate symptoms as well. ^{[50, 51]}

A study by Sobottke et al indicated that open decompression is effective in the treatment of LSS for patients in all age groups. Using data from 4768 patients, as drawn internationally from the Spine Tango registry, the investigators found after dividing the patients into three age groups (20-64 years, 65-74 years, 75 years and older) that age had no significant impact on the outcomes of decompression with regard to improvement in quality of life and relief from back and leg pain. ^[71]

A study by Hermansen et al found clinical outcomes for three different lumbar decompressive procedures to be comparable in patients with LSS. Patients underwent spinous process osteotomy (103 patients), bilateral laminotomy (966 patients), or unilateral laminotomy with crossover (462 patients), with mean improvements in the Oswestry Disability Index score at 12 months being 15.2, 16.9, and 16.7, respectively. Length of hospital stay was shortest for the bilateral laminotomy patients (2.1 days) and longest for patients who underwent spinous process osteotomy (6.9 days). ^[72]

A study by Zotti et al indicated that in patients undergoing lumbar spinal decompression for symptomatic spinal stenosis, preoperative MRI demonstrating a lumbar multifidus muscle (LMM) cross-sectional area of under 8.5 cm², as well as LMM atrophy, predicts worse outcomes from the procedure. ^[73]

A retrospective study by Hwang et al indicated that in patients who have undergone microdecompression for LSS, moderate disk degeneration (Pfirrmann grade IV) in the lower lumbar segments predicts disk herniation or foraminal stenosis necessitating subsequent surgery. ^[74]

A study by Ilyas et al indicated that in patients suffering from lumbar spinal stenosis with claudication who undergo posterior lumbar decompression (with or without fusion), risk factors for 90-day readmission include the postoperative development of surgical site infection (SSI), acute kidney injury (AKI), and urinary tract infection (UTI). A history of congestive heart failure (CHF) was determined to be a risk factor as well. Risk factors for 90-day reoperation were found to include SSI, sepsis, and UTI, along with increased length of stay. ^[75]

Complications that may develop in patients with lumbar spinal stenosis (LSS) include the following:

• Cauda equina syndrome (in rare cases)

• Lower extremity weakness and numbness

• Intractable axial, radicular, or NC pain

• Disability and loss of productivity

Complications that may develop in patients after surgery include the following:

• Sustained axial and radicular pain

• Progressive spinal deformity

• Cerebrospinal fluid leak

• Epidural hematoma

• Pulmonary embolism (PE)

Some authors report spondylolisthesis as a complication of lumbar decompression without arthrodesis, especially after total facetectomy. Preoperative risk factors for postoperative development or progression of L4 or L5 spondylolisthesis include the following:

• Absence of degenerative osteophytosis

• Small and sagittally oriented facets

• Well-maintained disk height

Ciol and colleagues report a substantial reoperation rate following LSS surgery in the Medicare population, for reasons that remain unclear. ^[76] Possible explanations may include the following:

• Failure of implanted devices

• Changed patient expectations

• Aggressive surgical philosophy

Inpatient care is necessary for patients with lumbar spinal stenosis (LSS) who elect to undergo surgery. The length of stay in the hospital is dependent on the type of procedure performed, but, on average, the patient is released 2-5 days following surgery. Following the operation, it is important that these patients resume basic mobility, activities of daily living (ADL), and ambulation as soon as possible and become educated on proper body mechanics and back safety techniques before discharge. A short course of active physical therapy may be recommended after surgery to strengthen the lower back and abdominal muscles to speed recovery time. Ideally, an appropriate exercise program can be initiated before surgery and continued thereafter.

Many patients with lumbar spinal stenosis choose to receive conservative treatment for back and leg pain. An active physical therapy program often is beneficial for these patients to improve flexibility and strength to maintain or improve their current activity levels. Other forms of treatment (eg, ESI) may be administered on an outpatient basis and used in conjunction with other medications and physical therapy. Please see Physical Therapy for further discussion of these treatments.