Percutaneous Image-guided Lumbar Decompression for Lumbar Spinal Stenosis

The Centers for Medicare & Medicaid Services (CMS) proposes that PILD for LSS is not reasonable and necessary under section 1862(a)(1)(A) of the Social Security Act. Therefore, CMS proposes that PILD for LSS is non-covered by Medicare.

CMS is seeking comments on our proposed decision. We will respond to public comments in a final decision memorandum, as required by §1862(l)(3) of the Social Security Act.

To:		Administrative File: CAG-00433N  
  
From:	Louis Jacques, MD  
		Director, Coverage and Analysis Group  
  
		Tamara Syrek Jensen, JD  
		Deputy Director, Coverage and Analysis Group  
  
		Jyme Schafer, MD, MPH  
		Director, Division of Medical and Surgical Services  
		Lead Medical Officer  
  
		Deirdre O’Connor  
		Lead Health Policy Analyst  
  
Subject:		Proposed Decision Memorandum for CAG #00433N  
		Percutaneous Image-guided Lumbar Decompression (PILD) for Lumbar Spinal Stenosis (LSS)  
  
Date:		October 17, 2013

I. Proposed Decision

The Centers for Medicare & Medicaid Services (CMS) proposes that PILD for LSS is not reasonable and necessary under section 1862(a)(1)(A) of the Social Security Act. Therefore, CMS proposes that PILD for LSS is non-covered by Medicare.

CMS is seeking comments on our proposed decision. We will respond to public comments in a final decision memorandum, as required by §1862(l)(3) of the Social Security Act.

II. Background

The following acronyms are used throughout this document. For the readers convenience they are listed here in alphabetical order.

AAOS - American Association of Orthopaedic Surgeons
ANOVA - analysis of variance
CT - computed tomography
DVT - deep vein thrombosis
ESI - epidural steroid injection
LF - ligamentum flavum
LOCF - last observation carried forward
LSS- lumbar spinal stenosis
MIC - minimal important change
MILD - minimally invasive lumbar decompression
MRI - magnetic resonance imaging
NASS - North American Spine Society
NC - neurogenic claudication
NCD - national coverage determination
ODI - Oswestry Disability Index
PDI - Pain Disability Index
PE - pulmonary embolism
PILD - percutaneous image-guided lumbar decompression
PRLL - percutaneous remodeling of ligamentum flavum and lamina
RCT - randomized controlled trial
RMQ - Roland-Morris Disability Questionnaire
VAS - visual analog scale
ZCQ - Zurich Claudication Questionnaire

The scope of this national coverage analysis (NCA) includes a review of the evidence on whether percutaneous image-guided lumbar decompression for LSS provides improved health outcomes in Medicare beneficiaries. This also includes the proprietary procedure mild®.

Most people will experience low back pain at some point in their lives. Pain complaints are the leading reason for medical visits. The most common pain complaints are musculoskeletal, and back pain is the most common of these, and the prevalence and impact of back pain have led to an expanding array of tests and treatments, including injections, surgical procedures, implantable devices, and medications. (Deyo et al. 2009)

Spinal stenosis is the most common reason for lumbar spine surgery in adults over the age of 65 years. (Weinstein et al. 2008) Spinal stenosis often results from the normal aging process. Surgery for spinal stenosis was reported to be the fastest-growing type of lumbar surgery in the United States from 1980 to 2000. Rates of surgery for lumbar stenosis declined slightly from 2002-2007, but use of more complex procedures has increased substantially. (Deyo et al. 2010)

A 1995 population study in Sweden reported spinal stenosis incidence of 50 per 100,000; an incidence of 25 per 100,000 inhabitants for spinal stenosis associated claudication; and, an incidence of 1 per 100,000 for cauda equina syndrome. (ECRI Health Technology Assessment Group. Treatment of Degenerative Lumbar Spinal Stenosis. Rockville (MD): Agency for Healthcare Research and Quality (US); 2001 Jun. (Evidence Reports/Technology Assessments, No. 32.) Available from: http://www.ncbi.nlm.nih.gov/books/NBK33617/)

Lumbar spinal stenosis is defined as the reduction of the cross sectional area, i.e. narrowing, of the lumbar spinal canal. It is usually caused by spinal degenerative conditions and is commonly found to be asymptomatic. (Kovacs et al. 2011) Lumbar spinal stenosis is sub-classified into three broad categories, specifically central stenosis, lateral stenosis, and spondylolisthesis. Central stenosis refers to a narrowing of the spinal canal across the anterioposterior diameter, the transverse diameter, or both.” (ECRI Health Technology Assessment Group. Treatment of Degenerative Lumbar Spinal Stenosis. Rockville (MD): Agency for Healthcare Research and Quality (US); 2001 Jun. (Evidence Reports/Technology Assessments, No. 32.) Available from: http://www.ncbi.nlm.nih.gov/books/NBK33617/)

Symptomatic patients typically present with symptoms of radicular leg pain or with neurogenic claudication (pain in the buttocks or legs on walking or standing that resolves with sitting down or lumbar flexion). Indications for surgery appear to vary widely, and rates of procedures vary five-fold or more across geographic areas. (Weinstein et al. 2008)

The geographic variation in treatment of LSS, the lack of a definitive diagnostic tool, and the absence of reliable evidence about the natural history of the condition bring up issues on how to best approach LSS. The North American Spine Society (NASS) evidence-based clinical guideline identified an absence of reliable evidence about the natural history of degenerative lumbar stenosis. (NASS 2011) The ECRI technology assessment reported, “…the presence of apparent stenosis in the asymptomatic population raises a question about whether stenosis per se causes symptoms, those with more severe symptoms are more likely to have stenosis. …The presence of stenosis and slippage in spinal images of asymptomatic people indicates that treatment must be based on the convergence of symptoms and image evidence rather than on either type of evidence alone.” (ECRI Health Technology Assessment Group. Treatment of Degenerative Lumbar Spinal Stenosis. Rockville (MD): Agency for Healthcare Research and Quality (US); 2001 Jun. (Evidence Reports/Technology Assessments, No. 32.) Available from: http://www.ncbi.nlm.nih.gov/books/NBK33617/)

Haig reported, “Some clinicians use the term stenosis to describe statistical deviation from average size of the spinal canal or neural foramen regardless of the symptoms, while others use it to describe a clinical syndrome that presents classically with neurogenic claudication-pain in the back or legs with ambulation.” (Haig et al. 2006) There are no standard criteria for the clinical diagnosis of stenosis. Anatomic measures can be obtained via imaging tests such as magnetic resonance imaging (MRI), which have become a standard for diagnosis. However no clear relation between the severity of symptoms and the extent of stenosis on imaging exists; and surgical outcomes do not clearly relate to the results of imaging measures. In addition, no cutoff for canal size measurement to diagnose the clinical syndrome has been widely accepted. (Haig et al. 2006)

Little is known about the diagnostic accuracy of the different tests available in detecting lumbar spinal stenosis. (de Graaf et al. 2006) de Graaf talked about an ideal situation with a “clear diagnostic entity with an agreed gold standard to prove its existence as well as knowledge about the natural course and effectiveness of treatments.” (de Graaf et al. 2006) However, there is no consensus about the gold standard. (de Graaf et al. 2006) After a systematic review of the accuracy of diagnostic tests for the diagnosis of LSS, de Graaf could not “draw any firm conclusions about the diagnostic accuracy of imaging, clinical, and other tests in diagnosing lumbar spinal stenosis.” (de Graaf et al. 2006)

It appears consensus as to the definition of spinal stenosis has not been reached among experts. There is no “gold standard” for diagnosis and treatment of stenosis because of variable signs and symptoms, physicians’ history-taking and physical methods and diagnostic tests. (Sandella et al. 2013)

Lumbar spinal stenosis is a pathological condition causing a compression of the contents of the canal, particularly the neural structures. In 2003, Gunzburg and Szpalski opined that if compression does not occur, the canal should be described as narrow but not stenotic. Degenerative disc disease is the most common cause of lumbar spinal stenosis. A bulging degenerated intervertebral disc anteriorly, combined with thickened infolding of ligamenta flava and hypertrophy of the facet joints posteriorly result in narrowing of the spinal canal. The site of compression may be central, lateral or a combination, of the two. “When a canal size is too narrow for the dural sac size that it contains, stenosis occurs. An identical canal size can therefore be stenotic for one person while not being stenotic for another who happens to have a smaller dural sac size. Lumbar spinal stenosis is therefore a clinical condition and not a radiological finding or diagnosis.” (Gunzburg and Szpalski 2003)

The utility of diagnostic imaging studies should be to confirm the information gathered from a thorough history and physical exam. (Boden 1996) Boden warned, “Excessive reliance on diagnostic studies without precise clinical correlation can lead to erroneous or unindicated treatment of degenerative disorders of the lumbar spine.” (Boden 1996)

The clinical syndrome for stenosis does not always present with classic complaints on examination, and similar symptoms occur in a wide variety of disorders ranging from vascular disease to polyneuropathy to mechanical back pain. Further confusion can come into play when a radiologist report of stenosis influences the clinician’s impression. (Haig et al. 2006) “Because other causes of back pain are both common and difficult to prove, it is possible that mechanical backache, perhaps in conjunction with coincident neuropathy or other unrelated leg complaint, might lead to inappropriate treatment including surgery. Thus accurate diagnosis of the clinical syndrome of spinal stenosis is of critical importance .” (Haig et al. 2006)

“When a patient presents with LSS symptoms and confirmatory imaging, unless they have an absolute indication for surgery (rapidly progressive neurologic decline, clinically relevant motor deficits, or cauda equina syndrome), the treatment algorithm begins with nonoperative management.” (Kurd et al. 2012) Unfortunately, there remains a lack of consensus among clinicians about the indications for surgical intervention for LSS. (Kurd et al. 2012) Non-surgical or conservative care for LSS may include physical therapy, epidural injections, chiropractic manipulation, acupuncture, lumbar corset, the use of anti-inflammatory drugs, and the use of opioid analgesics.

Treatment options for LSS, historically, have varied from conservative management on the one hand and the invasive surgical decompression on the other hand. There is a gap for patients failing the former but not severe enough or not ready for the latter. (Mekhail et al. 2012) “While conservative measures, such as physical therapy with/without epidural steroid injections, may be adequate for mild cases, they fail to provide long-term relief to the moderate-to-severe LSS patient and, thus the progression to the next treatment option of surgery. The goal of surgical treatment for symptomatic lumbar canal stenosis is to achieve relief of symptoms by adequate neural decompression while preserving as much of the anatomy and not disrupting the biomechanics of the lumbar spine as possible.” (Mekhail et al. 2012)

The AAOS website provided the following information about surgical options for LSS.

“Surgery for lumbar spinal stenosis is generally reserved for patients who have poor quality of life due to pain and weakness.” In the past there have been two main surgical options to treat LSS – laminectomy and spinal fusion when there is spinal instability. The laminectomy procedure involves removing the bone and ligaments that are compressing the nerves. The traditional laminectomy procedure has been performed as an open procedure however a laminectomy can also be done using a minimally invasive method. These newer, minimally invasive decompression procedures are performed using smaller incisions and surgeons rely more on microscopes to see the area of surgery. Another minimally invasive procedure is the placement of an interspinous process device which involves placing a spacer between the spinous process in the back of the spine to keep the space for the nerves open by spreading the vertebrae apart.” (AAOS website http://orthoinfo.aaos.org/topic.cfm?topic=a00329)

The focus of this national coverage analysis is on a newer technique - percutaneous image-guided lumbar decompression (PILD) which is a posterior decompression of the lumbar spine performed under indirect image guidance without any direct visualization of the surgical area. The use of a cannula and trocar provides a portal that allows access to the anatomic area for instruments used for resection. This is a procedure proposed as a treatment for symptomatic LSS unresponsive to conservative therapy. This procedure is generally described as a relatively non-invasive (compared to open surgery) procedure using specially designed instruments to percutaneously remove a portion of the lamina and debulk the ligamentum flavum. (The terms non-invasive, minimally invasive and percutaneous are used interchangeably in the literature.) The procedure is performed under x-ray guidance (e.g., fluoroscopic, CT) with the assistance of contrast media to identify and monitor the compressed area via epiduragram. The procedure that most closely falls under this description is commercially known as the mild® procedure. (Vertos Medical) “The mild procedure offers a minimally invasive alternative to a standard laminotomy-laminectomy." (Deer et al. 2011)

Endoscopically assisted laminotomy/laminectomy, which requires open and direct visualization, as well as other open lumbar decompression procedures for LSS are not within the scope of this NCA.

III. History of Medicare Coverage

CMS does not currently have an NCD on PILD.

A. Current Consideration

CMS internally decided to open this national coverage analysis (NCA) to thoroughly review the evidence on whether the PILD procedure provided improved health outcomes in Medicare beneficiaries with symptomatic LSS.

B. Benefit Category

Medicare is a defined benefit program.  An item or service must fall within a benefit category as a prerequisite to Medicare coverage.  An item or service must meet one of the statutorily defined benefit categories in the Social Security Act and not otherwise be excluded. PILD may be considered to be within the benefits described under sections;

• 1861(b) as an inpatient hospital service,
• 1861(s)(2)(B) as a hospital service incident to physicians’ services rendered to outpatients, and
• 1861(s)(1) as a physician service.

Note: This may not be an exhaustive list of all applicable Medicare benefit categories for this item or service.

IV. Timeline of Recent Activities

V.  Food and Drug Administration (FDA) Status

Various devices implanted during spine surgery may fall under the FDA regulatory oversight. The focus of our review is for the PILD procedure and no devices are implanted during this procedure, however there are specialized instruments that are used which are under the oversight of the FDA.

The mild® tool kit (Vertos Medical) initially received 510(k) clearance as the X-Sten MILD Tool KIT (X-Stern Corp.) in 2006. The indications for use are identified as, “The X-Sten MILD Tool Kit is a set of specialized surgical instruments intended to be used to perform percutaneous lumbar decompressive procedures for the treatment of various spinal conditions.” (http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfPMN/pmn.cfm?ID=22165)

VI. General Methodological Principles

When making national coverage decisions under §1862(a)(1)(A), CMS generally evaluates relevant clinical evidence to determine whether or not the evidence is of sufficient quality to support a conclusion that an item or service falling within a benefit category is reasonable and necessary for the diagnosis or treatment of illness or injury or to improve the functioning of a malformed body member.  The critical appraisal of the evidence enables us to determine to what degree we are confident that: 1) the specific assessment questions can be answered conclusively; and 2) the intervention will improve health outcomes for patients.  An improved health outcome is one of several considerations in determining whether an item or service is reasonable and necessary.

A detailed account of the methodological principles of study design that the agency utilizes to assess the relevant literature on a therapeutic or diagnostic item or service for specific conditions can be found in Appendix A. In general, features of clinical studies that improve quality and decrease bias include the selection of a clinically relevant cohort, the consistent use of a single good reference standard, and the blinding of readers of the index test, and reference test results.

Public comments sometimes cite the published clinical evidence and give CMS useful information.  Public comments that give information on unpublished evidence such as the results of individual practitioners or patients are less rigorous and therefore less useful for making a coverage determination.  Public comments that contain personal health information (PHI) will be redacted and the PHI will not be made available to the public.  CMS uses the initial public comments to inform its proposed decision.  CMS responds in detail to the public comments on a proposed decision when issuing the final decision memorandum.

VII. Evidence

A.         Introduction

Assessment of outcomes for symptomatic degenerative lumbar spinal stenosis

Neurogenic claudication and various back and leg pains are symptoms. Sustained improvement in these symptoms of pain perception and a reduction in the pain-related functional restrictions are appropriate outcomes of clinical trials. It is challenging to attribute symptom changes to treatment because the natural history of degenerative lumbar spinal stenosis is unclear. (Issack 2012) Additionally, pain perception is subject to regression to the mean and the placebo effect. Therefore, clinical trials with appropriate controls utilizing independently assessed validated instruments are most heavily weighted.

Patient reported outcomes reflecting symptoms and function are often used to measure the effects of treatment for symptomatic degenerative lumbar spinal stenosis. Standardizing the measures facilitates study comparison. The most commonly used instruments are the Oswestry Disability Index (ODI) and the visual analog scale (VAS). The ODI is used to measure a patient’s functional disability on a scale of 1 to 100. VAS measures pain intensity on a scale of 0 to 10. The Zurich Claudication Questionnaire (ZCQ) is a less commonly used assessment tool for patient function and has several domains. The Pain Disability Index (PDI) and the Roland-Morris Disability Questionnaire (RMQ) are also tools for measuring disability. The SF-36 and shorter version, SF-12, are measures of general health status. CMS attributes more evidentiary weight to those studies reporting reliable, validated outcomes.

With the use of any of these instruments, consideration must be given to the clinical meaning of a change in the reported score. How well, if at all, does a score change of some increment reflect a meaningful change in symptom or function experienced by the patient? Other considerations include the error of measurement of the instrument used and the clinical importance of a statistically significant score change. In a 2003 study by Hagg of 289 patients treated surgically or non-surgically in a randomized controlled trial, the standard error of measurement of the ODI was four units, with a 95% tolerance interval of 10, and the minimum difference that appeared clinically important was 10 units. The minimal clinically important difference of VAS back pain was 18-19 units [on a 100 point scale] with a 95% tolerance interval of 1.5. (Hagg et al. 2003) These recommendations are similar to those by Ostelo who also noted that when baseline was taken into account a 30% improvement, when comparing before and after measures for individual patients, should be the guide for the minimal important change (MIC). (Ostelo et al. 2008) Ostelo, in an aim towards international consensus regarding minimal important change, noted that workshop participants (during the Low Back Pain Forum VIII) stressed that proposed MIC values were for individual rather than group changes. (Ostelo et al. 2008) The clinically important change is based on an individual, but is often misused to compare the difference in mean scores between two groups, but this is not a clinically important difference. (MEDCAC 2006)

Well-designed clinical trials can provide the strongest evidence for treatment effect. Well-constructed randomization protects against bias and inclusion of an appropriate comparator facilitates study interpretation. In pain treatment trials, the natural history of the disease, regression toward the mean and the placebo response are important considerations. For these reasons, an appropriate comparator is necessary for accurate interpretation. Accurate interpretation of pain treatment trials also necessitates reporting of concomitant pain treatments, most importantly analgesic use. In the case of research in the area of pain treatment, more evidentiary weight is accorded to studies that are designed to mitigate the bias of placebo response and that account for the natural history of the disease and regression toward the mean.

B.    Literature Search

CMS performed a literature search on 5/3/2013 utilizing PubMed for randomized controlled trials (RCTs) and nonrandomized controlled trials, cohort or case-control studies, case series studies and systemic reviews for “percutaneous image-guided lumbar decompression for lumbar spinal stenosis.” The literature search was limited to the English language and specific to the human population, but included studies conducted in all countries, including the United States.

Evidence for percutaneous image-guided lumbar decompression for lumbar spinal stenosis comes from the mild® literature and includes one randomized study, seven case series, one meta-analysis and one systematic review. Single site reports of larger reported studies were reviewed but not listed in the evidence section of this PDM so as to not duplicate patient reporting. Studies with ten patients or less were reviewed but not listed in the evidence section. Studies identified as follow-up studies from earlier studies were listed together.

C. Discussion of Evidence Reviewed

1. Question:

The question of interest for this NCA is:

Is the evidence sufficient to conclude that PILD improves health outcomes in Medicare beneficiaries with lumbar spinal stenosis?

Health outcomes of greatest interest include significant pain relief and improved function in day-to-day activities.

2. External technology assessment (TA)

An external TA was not commissioned.

3. Internal technology assessment

Lingreen R, Grider S. Retrospective review of patient self-reported improvement and post-procedure findings for mild® (minimally invasive lumbar decompression). Pain Physician 2010; 13:555-560.

Lingreen and Grider reported on 42 consecutive patients ages 52 – 86 “meeting magnetic resonance imaging (MRI) criteria” who underwent the procedure performed by two pain management physicians at the same clinic. The aim of the study was to “fill important gaps in this emerging body of literature concerning Minimally Invasive Lumbar Decompression or mild.” The inclusion criteria were spinal stenosis and ligamentum flavum hypertrophy on MRI; no details were provided. All patients had undergone previous conservative treatment including lumbar epidural steroid injections, opioid and non-opioid medication and physical therapy. Patient reported VAS, ADLs, opioid use, patient satisfaction and complication data were collected. Patients were contacted on post-procedure days three, seven and 14.

No major adverse events were reported. Five of 42 patients required post-procedure opioids. A survey was done at some point and 36 or 42 (86%) of patients reported that they would recommend the mild procedure to others. The VAS pre- and 30 day post-procedure were reported as 9.6 ± 0.42 and 5.8 ± 2.5, with the difference being p < 0.05. Pre-procedure only one patient reported he could walk greater than 15 minutes, while 25 reported this 30 days post-procedure. For standing greater than 15 minutes, six could do so pre-procedure and 31 post-procedure.

The authors noted, “At present there are no clear-cut standards as to what constitutes radiologic spinal stenosis, much less ligamentum flavum hypertrophy.” While ligamentum hypertrophy is one of two inclusion criteria, the authors noted, “The lack of documented ligamentum flavum thickening for each patient is a drawback to the current study. Future studies could attempt to standardize the selection criteria of patients for this procedure with vigorous determination of ligamentum flavum thickness perhaps better predicting who will benefit from the procedure.”

The authors concluded, “The results of the current study suggest that minor adverse events with mild consist mainly of soreness at the procedure site which is self-limiting, infrequently requiring additional procedures or even post-procedure opioid as an intervention. In keeping with other reports, the procedure appears to offer a safe and effective alternative to patients suffering from LSS. Clearly prospective, randomized trials comparing safety and efficacy of mild to other established treatments for spinal stenosis will be necessary.”

Schomer DF, Solsberg D, Wong W, Chopko BW. mild® Lumbar decompression for the treatment of lumbar spinal stenosis. The Neuroradiology Journal 2011; 24:620-626.

The purpose of this report is “to present a meta-analysis of acute safety and three-month clinical outcomes of over 250 mild patients.” Demographics were available on 163 patients, acute safety on 253 patients, and VAS and ODI on 107 patients. The patients in the study were treated from January, 2008 through July, 2010, and patient information appeared to come from a variety of sources. The study included patients with IRB approval and patient consent as well as retrospective surveys of “case procedural notes where IRB approval was not required or obtained.” Mean age was 68.8 years and with 40.5% male. Patients with both unilateral and bilateral treatments were included. There were no reports of major complications, defined as dural tears, nerve root injury, post-op infection, hemodynamic instability, and post-op spinal structural instability. VAS was 7.4 at baseline with a three-month follow-up of 3.9, p < 0.0001 using a t-test for correlated samples. ODI at baseline was 48.0 with a three month follow-up of 30.9, p < 0.0001 using the t-test for correlated samples. No ranges were given for baseline or follow-up measurements. Comparisons were made to the surgical cohort in the SPORT trial. The authors concluded, “As a less-invasive alternative to decompression surgery, mild Lumbar Decompression has demonstrated comparable patient outcomes to standard decompressive laminectomy, with shorter procedure times, less blood loss, shorter hospital stays, and significantly better safety.”

Chopko BW. A novel method for treatment of lumbar spinal stenosis in high-risk surgical candidates: pilot study experience with percutaneous remodeling of ligamentum flavum and lamina. J Neurosurg Spine 2011; 14;46 - 50.

Chopko reported initial experience in the application of the PRLL technique to a patient population in which medical comorbidities placed the patients into a high-risk stratification with regard to open surgical decompression. PRLL stands for percutaneous remodeling of ligamentum flavum and lamina. Age ranged from 44 to 84, with unilateral and bilateral treatments in the lumbar spine, some with multiple levels. Dates of treatment ranged from April, 2008 to May, 2009. BMI ranged from 19.9 to 44.3. Comorbidites included diabetes, hypertension, muscular dystrophy, and cancer with metastasis.

During the procedure, patients received both local anesthesia (18.5 ml of 1% lidocaine and 11.8 ml of 0.5% bupivacaine) and minimal intravenous sedation and analgesia. The author stated, “In a typical case, the instruments are used to resect between 20 and 50 fragments of bone and ligamentous tissue per single hemilaminar segment, with each tissue fragment measuring between 0.5 and 3.0 mm in greater dimension. A relative flattening of the epidural contrast layer, combined with less restricted flow of contrast, are used as factors to determine when to conclude the decompression.”

Twelve of 14 patients reported a statistically significant improvement in VAS score (preoperative average score of 7.61 ± 2, postoperative average score of 3.61 ± 2.9). ODI change was not statistically significant. Patient follow-up ranged from 4 to 72 weeks. Two patients had postoperative complications, one with a deep vein thrombosis (DVT) and pulmonary embolism (PE), another with an incarcerated small bowel herniation where the patient underwent urgent bowel resection and colostomy followed by an eight-week hospitalization. Another patient had a laminectomy due to continued decline. An additional three patients died during the postoperative observation period from unrelated conditions. Of 11 patients receiving narcotics preoperatively, six had either reduced or eliminated narcotic usage by the time of final postoperative evaluation.

The author stated, “The weaknesses of the present study are many, including the lack of a control group and the variability of follow-up periods.” In addition, the author stated, “although the precise mechanism of action is not addressed in this clinical study, potential mechanisms may include a reduction in the dorsal-to-ventral directed tension within a pathologically “buckled” ligament, as well as an overall increase in the cross-sectional diameter of the spinal canal. In essence, the PRLL strategy is an investigation into the minimum amount of ligamentous resection that is sufficient to achieve a positive clinical effect. Neuroimaging studies and measurements of intraligament pressures before and after a PRLL procedure may shed some light on the basic mechanism of the pain reduction.” The author concluded, “The PRLL procedure, although clearly not equivalent to an open decompressive procedure, nevertheless had a moderate effect on pain reduction, as evidenced by this small pilot study.”

The author acknowledged, “A future study to include a substantial expansion in patient population as well as uniform long-term follow-up will be critical to a better understanding of the ultimate role of the PRLL strategy.”

Deer TR, Kim C K, Bowman II RG, Ranson MT, Yee BS. Study of percutaneous lumbar decompression and treatment algorithm for patients suffering from neurogenic claudication. Pain Physician 2012; 15:451-460.

The authors stated, “The goal of this study was to evaluate the safety and outcome of symptomatic LSS patients treated with mild percutaneous lumbar decompression (Vertos Medical, Aliso Viejo, CA).” Forty-six patients were enrolled from a single center between March 2010 and January 2011, with a mean age of 66.1 (range 46 to 80). Thirty-four patients (74%) had been under medical management for over 6 months; three patients (7%) for three to six months; and nine patients (20%) under medical management for less than three months. The author stated, “…43 patients (93%) suffered from facet hypertrophy, and 41 patients (89%) suffered from a bulging disc.” Inclusion criteria were, “adult LSS patients suffering from NC [neurogenic claudication] primarily caused by ligamentum flavum (LF) hypertrophy, although the presence of other less predominant contributing factors was not exclusionary. Preoperative magnetic resonance (MRI) or computed tomography (CT) provided radiologic evidence of hypertrophic LF > 2.5 mm, as well as a clearly reduced central canal cross-sectional area.” Patients had to walk at least 10 feet unaided before being limited by pain and must have failed conservative therapy, which was not defined. Patients were also excluded if they “suffered from severe back or leg pain from causes other than LSS,” recent spinal fracture or prior surgery at treatment level, if “disc protrusion or facet hypertrophy were deemed severe enough to potentially confound study outcomes,” used non-steroidal anti-inflammatory drugs within 5 days, or had an epidural steroid injection within three weeks prior to the study.

The VAS, ODI, and ZCQ were assessed at baseline, 12 weeks, 6 months, and one-year. Safety was monitored. Serious adverse events were defined as blood loss requiring transfusion, nerve injury, epidural bleeding or hematoma, dural puncture or tear, or “any other device or procedure-related significant complications.” For data, missing value imputations were performed using the last-observation-carried-forward (LOCF) method. No data tables were provided. Patients underwent the procedure at various levels. Fluoroscopy time ranged from 38 to 279 seconds. The authors stated there were no major device or procedure-related complications. The authors reported that data were available for 35 of 46 patients for all follow-up periods.

For this group of 35 patients the VAS difference from baseline was statistically significant from a mean of 6.9 (95% CI ± 0.6) at baseline to a mean of 4.2 (95% CI ±1.0) at 12 weeks, a mean of 4.4(95% CI ±1.0) at six months, and a mean of 4.0 (95% CI ± 1.0) at one year. For this group of patients the ODI difference from baseline was statistically significant from a mean of 49.4 (95% CI ± 2.5) at baseline to a mean of 35.1 (95% CI ± 5.6) at 12 weeks, a mean of 35.0 (95% CI ± 5.5) at 6 months, and a mean of 32.0 (95% CI ± 5.8) at one year. ZCQ was analyzed for 34 patients and the authors reported a statistically significant improvement in all ZCQ domains. Of 11 patients missing data and not included in the reported outcomes, one had a fusion and one had a laminectomy and were not included in the 35 patients that were reported. Pre and post-procedure medications were not reported. It was not mentioned if there were any additional procedures other than the two back surgeries. Any additional therapies such as physical therapy were not reported. Patient comorbidities were not reported. The authors concluded, “In this study, the mild procedure was shown to be safe, with properly diagnosed patents experiencing significant improvement in mobility and significant reduction of pain at one year after the procedure.”

Wong W. mild interlaminar decompression for the treatment of lumbar spinal stenosis, procedure description and case series with 1-year follow-up. Clin J Pain 2012; 28:534-538.

The author reported on 17 patients treated between April, 2008 and August, 2009 at five different sites. The mean age was 73.1 years (range 63 to 86). The author stated all patients had previously failed conservative therapy. No details were provided. The author noted, “In our practice, the mild procedure is complete when we are no longer able to readily remove further ligamentum flavum, and a repeat epidurogram shows considerable improvement in flow of contrast across the stenotic segment.” He further added, “Volumetric measurements of removed tissues are not collected, primarily because of the fact that only a very small amount is removed during the procedure and quantification is problematic.” Baseline VAS was 7.6 and was 2.3 at one-year follow-up. Average baseline ODI decreased from 48.4 to 21.7 at 1-year. No details were provided on any other pre or post procedure treatments or comorbidities. The author concluded, “This clinical outcome assessment demonstrates that, for this patient series, the mild procedure provided significant pain relief at 1-year posttreatment and increased mobility for patients with symptomatic LSS.”

Brown LL. A double-blind, randomized, prospective study of epidural steroid injection vs. the mild® procedure in patients with symptomatic lumbar spinal stenosis. Pain Practice 2012, 12:333-341.

Brown reported on 38 patients in a double-blind, randomized study of the mild procedure and epidural steroid injections (ESI) at a single site, 21 in the mild group and 17 in the ESI group. Fifty patients were screened and 38 patients were enrolled. Inclusion criteria were 18 years old at minimum, previously failed conservative therapy, ODI > 20, radiologic evidence of L3-L5 LSS, ligamentum flavum > 2.5 by MRI or CT, central canal cross sectional area ≤ 100mm², anterior listhesis confirmed to be ≤ 5.0 mm, and ability to walk at least 10 feet unaided. Exclusion criteria included prior surgery at the intended treatment level or had previously been treated with epidural steroids, recent spinal fractures, disabling back or leg pain from causes other than LSS, fixed spondylolisthesis > Grade 1, disk protrusion or osteophyte formation, excessive facet hypertrophy, bleeding disorders, current use of anticoagulants, would healing pathologies deemed to compromise outcomes such as diabetes, cancer, severe COPD, ASA or NSAID within five days of treatment, pregnancy, inability to lie prone for any reason, inability to give informed consent, on Workman’s compensation, and considering litigation associated with the back pain.

Patients were randomized in blocks of four. Patients randomized to ESI received 80mg of triamcinolone acetate (40 mg in diabetic patients). All patients were followed postoperatively by an independent third party. Patients were unblinded at six weeks and cross-over was offered. The primary endpoint was VAS. Other measures included ODI and ZCQ. Mean age in the mild group was 74.2 (range 51 to 89), with a mean age of 78.7 (range 64 to 89) in the ESI group. Sixty-two percent of the mild patients were male and 47% of the ESI patients were male. The pre-procedure duration of medical management ranged from less than one month (four in the mild group and two in the ESI group) to greater than six months (13 in each group). Patients in the mild group underwent 68 procedures, 33 levels bilaterally and two levels unilaterally, whereas patients in the ESI group had only one injection, even though “…there is no consensus among interventional pain management specialists regarding type, dosage, frequency, approach, and total number of injections in ESI therapy, generally multiple injections are administered at various intervals.” Patients in both groups were discharged on the same day on their procedures.

The author reported that 16 of 21 mild patients experienced a two point or greater improvement in VAS at six weeks, versus only six of 17 ESI patients. Patients in the mild group improved from an average VAS baseline of 6.3 (95% CI ± 0.7) to a mean of 3.8 (95% CI ± 1.3) at six week follow up. Patients in the ESI group had a mean of 6.4 (95% CI ± 1.0) at baseline compared with 6.3 (95% CI ± 1.4) at six-week follow-up. For ODI, patients in the mild group had a decrease from a baseline mean ODI from 38.8 (95% CI ± 4.2) to 27.4 (95% CI ± 7.0) at six week follow-up, and in the ESI group the baseline ODI was 40.5 (95% CI ± 5.9) and six week follow-up ODI of 34.8 (95% CI of ± 8.2). The change in VAS and ODI in the mild group from week six to 12 was not significant. The ESI group was not measured at week 12. The ZCQ difference between groups was not significant at week six. Many patients in the ESI group crossed-over before 12 weeks. Eventually, all ESI patients had the mild procedure performed. For 14 of these 17 patients in the cross-over ESI group, their baseline VAS was 7.4 (95% CI ± 0.98) with improvement to a mean of 4.5 (95% CI ± 1.46) after mild. Comorbidities, pain medications, and other relevant therapies were not reported. Adequacy of blinding was not reported.

The author concluded, “The findings from this double-blind, randomized, prospective study of ESI vs. the mild procedure in the treatment of LSS patients suffering from symptomatic neurogenic claudication indicate that mild provides statistically significantly better pain reduction and improved functional mobility vs. treatment with ESI.”

Deer TR and Kapural L. New Image-guided ultra-minimally invasive lumbar decompression method: the mild® procedure. Pain Physician 2010; 13:35-41.

A chart review was conducted by 14 physicians on 90 patients from 12 medical centers January 2008 through July 2009. The authors stated, “This technical survey was conducted to assess any significant issues with the procedure’s safety profile.” Factors evaluated were incidence of dural puncture or tear, blood transfusion, nerve injury, and epidural bleeding or hematoma. “To be included in the study, the procedural record was reviewed for content including age, gender, etiology of spinal stenosis (specifically hypertrophic ligamentum flavum), and complete notes stating any procedural difficulties, pre-procedural neurological status, and baseline co-morbidities.” None of the procedures resulted in what the authors defined as adverse events occurring during or immediately following the procedure prior to discharge. The authors concluded, “This review demonstrates the acute safety of the mild procedure with no report of significant or unusual patient complications.”

Mekhail N, Costandi S, Abraham B, Samuel SW. Functional and patient-reported outcomes in symptomatic lumbar spinal stenosis following percutaneous decompression. Pain Practice 2012; 12: 417-425.

The authors stated, “The goal of this study was to report changes in the functional abilities and pain relief for the first 40 consecutive LSS study patients treated with mild percutaneous lumbar decompression at the Pain Management Department of the Cleveland Clinic.” Study inclusion criteria included neurogenic claudication, radiographic T2-weighted MRI-confirmed LF hypertrophy ≤ 4.0 mm, failure of conservative treatment, ability to walk at least 10 feet unaided before being limited by pain. Patients were excluded if they had prior surgery at the treatment level and/or significant radicular leg pain not attributed to LSS, use of anticoagulants, NSAIDs within 7 days, ESIs within 4weeks prior to the procedure, and mobile or greater than Grade 1 spondylolisthesis. Patients were treated September 2010 through August 2011.

Age ranged from 53 to 86, with a mean of 72.2 years, with 62.5% female. “On average, patients had endured painful neurogenic claudication for 5 years prior to study enrollments, and 8 patients had symptoms for over 10 years.” Co-morbidities that were mentioned include radicular pain and osteoarthritis of the knee (five patients), sacroiliac (four patients), and hip (three patients), and cardiac disease (three patients). The authors stated that the mean pretreatment LF thickness was 7.1 mm, no post treatment measurement was reported. Patients underwent procedures at one and two levels, unilaterally and bilaterally. Outcomes include the Pain Disability Index (PDI), the Roland-Morris Disability Questionnaire (RMQ), standing time and walking distance prior to experiencing symptoms, and VAS for pain. These measures were evaluated at baseline and again at four postoperative visits that ranged from three months post-op to one year. The last reported visit was recorded as the one year visit. Safety data were collected at the time of treatment and at follow-up visits. Statistical tests included analysis of variance (ANOVA) with repeated measures and the post-hoc Tukey HSD test.

The authors reported that there were no reports of device or procedure related serious adverse events at the time of the procedure and at any point during the follow-up. “Six patients have not yet been seen for the 1-year visit, but are included in posttreatment analyses prior to 1 year. Two of these 6 patients underwent subsequent spine surgery during the 1-year follow-up period and were discontinued from the study. Both patients, although improved after the mild procedure, chose to undergo additional back surgery (1with fusion and the other with discectomy) to address ongoing radicular pain. The remaining 34 patients were available for all follow-up periods and comprise the cohort population.” For the 34 patients, the reported measures showed improvement. The intention to treat population (ITT) included all 40 patients. The PDI cohort had a statistically significant improvement from a mean of 41.4 (95% CI ± 4.6) at baseline to an average of 18.8 (95% CI ± 4.9) at one-year, with each interim follow-up also statistically significant. The RMQ study cohort baseline average of 14.3 (95% CI ± 2.1) improved at one year to a mean of 6.6 (95% CI ± 2.0), with each interim measure statistically significant from baseline. Standing time improved from a baseline of eight minutes to 56 minutes at 12 month follow-up, with walking distance improving from a baseline mean of 246 feet to 3,956 feet at month 12. VAS for the cohort improved from 7.1 (95% CI ± 0.8) to 3.6 (95% CI ± 0.9) at 12 months for the 34 patients. The authors stated that the 1-year ITT analysis of PDI, RMQ, standing time, walking distance, and VAS were statistically significant (ANOVA, p < 0.0001). Additional therapies or change in therapies both pre and post procedure were not reported.

The authors concluded, “This study demonstrated significant functional improvement as well as decreased disability secondary to neurogenic claudication at 1 year following percutaneous lumbar decompression.”

Chopko B and Caraway DL. MIDAS 1 (mild® decompression alternative to open surgery): a preliminary report of a prospective, multi-center clinical study. Pain Physician 2010; 13:369-378.

Mekhail N, Vallejo R, Coleman MH. Benyamin Ramsin M.; Long-term results of percutaneous lumbar decompression mild® for spinal stenosis. Pain Practice 2012; 12(6):184-193.

Chopko B. Long-term results of percutaneous lumbar decompression for LSS, two-year outcomes. Clin J Pain 2013;

The above three articles report six week (Chopko et al. 2010), one year (Mekhail et al. 2012), and two year (Chopko 2013) follow-up for the observational trial listed as NCT00956631 in clinical trials.gov. Chopko (2010) stated, “The study was conducted by 14 US spine specialists from July 2008 through January 2010.” Seventy-eight patients entered the study. Inclusion criteria were symptomatic LSS primarily caused by dorsal element hypertrophy, prior failure of conservative therapy, radiologic evidence of LSS, hypertrophic LF > 2.5 mm, central canal sectional area ≤ 100 square mm, anterior listhesis ≤ 5mm, and ability to walk at least 10 feet unaided before being limited by pain.

Additional criteria included availability to complete follow-up and ability to provide informed consent. Conservative therapy was not defined. Exclusion criteria included prior surgery at the treatment level, history of recent spinal fractures with pain symptoms, disabling back or leg pain from causes other than LSS, significant/symptomatic disc protrusion or osteophyte formation, excessive/symptomatic facet hypertrophy, bleeding disorders or current use of anticoagulants, use of ASA or NSAID within five days of treatment, epidural steroids within prior 3 weeks, potential wound healing pathologies, dementia, pregnancy, Worker’s Compensation, and considering litigation associated with the pain. The authors also stated, “Although patients who also had foraminal stenosis and lateral recess stenosis were not excluded, the target patient population was those with lumbar central canal stenosis with hypertrophic LF as a contributing factor.” Outcomes were assessed with VAS, ODI, ZCQ, and the SF-12V2®. Reported patient demographics on 75 patients included an age range from 37 years old to 88 years with an average of 70.0 years and 61.3% female. Other demographics and baseline information such as comorbidities and duration of back pain or previous treatments was not reported.

Fifty-one percent of patients were treated at two levels, one patient was treated at three levels, and of the 115 total treated levels, 11 were treated unilaterally. At six weeks, the authors reported no major device or procedure-related complications, with major complications defined as dural tears, nerve root injury, post-op infection, hemodynamic instability, and post-op spinal structural instability. The authors stated that minor complications were not tracked. For 75 patients, the average baseline VAS was 7.3 (range three to 10), and the six-week follow-up average was 3.7 (range 0 to 10) with a statistically significant difference using t-test for correlated samples. For 75 patients, the average baseline ODI was 47.4 (range 16 to 84), and the six-week follow-up was 29.5 (range 0 to 72) with a statistically significant difference using t-test for correlated samples. For the ZCQ components, between 61 and 67 patients had reported outcomes. Sixty two patients had reported scores for ZCQ overall symptom severity, with a pre-treatment mean score of 3.69 (range 1.57 to 5) and post-treatment mean score of 2.35 (range one to 4.57). For ZCQ physical function domain, 61 patients had a pre-treatment mean of 2.67 (range of one to four), with a post-treatment score of 1.96 (range of one to 3.20). Sixty-seven patients reported the SF-12V2. The results are shown in a bar graph and the authors reported, “The patients’ health status was improved for the two summary surveys (PCS and MCS) and all 8 survey scales as compared to baseline.” They further said, “This improvement is statistically significant (95%CI) for all but the General Health (GH) survey scale.” The use of any additional therapies such as pain medication or physical therapy was not reported.

The authors concluded, “In this 75-patient MiDAS I trial, and in keeping with a previously published 90-patient safety cohort, the mild procedure proved to be safe. Further, based on near-term follow-up, the mild procedure demonstrated efficacy in improving mobility and reduced pain associated with lumbar spinal canal stenosis.”

The one year follow-up (Mekhail et al. 2011) was reported from 11 US sites with a cohort of 58 patients who had undergone 170 procedures. At one year, there was no major device or procedure-related complications. Of the 58 patients reported, 44 had conservative medical management for symptomatic LSS for more than six months before the procedure, while 12 had conservative medical management for six months or less. For two patients this was not reported. The authors added: “Sairyo et al. reported average thickness of ligamentum flavum in non LSS patients to be 2.44 mm. This was based on 308 measurements in 77 patients at various ligamentum flavum levels via magnetic resonance imaging (MRI). This finding was used to determine 2.5mm as the minimum starting point for patient entry into the study.” It was acknowledged that patients may have a number of other structural factors such as foraminal stenosis and lateral recess stenosis, so the study was not designed to exclude these factors. The treating physician was ultimately responsible for determining which patients would be best suited for percutaneous laminotomy with ligamentum flavum resection.

The authors explained one of the inclusion/exclusion criteria, “To accomplish true baseline recordings for this patient population, it was determined that patients should be free of steroid injections within the prior 3 weeks of baseline.” Patient success at one year was determined if the patient experienced a two-point improvement in VAS, with secondary outcomes being: the procedure was completed as planned; the patient had a decrease in ODI; the patient did not have a significant device or procedure related adverse effect; and, no re-operation. For analytic purposes, mean change from baseline was assessed for VAS, ODI, ZCQ, and SF-12V2 using the paired t-test. It was noted that half of the 58 patients had an overnight hospital stay associated with the initial procedure.

For these 58 patients, VAS at one year follow-up was an average of 4.5 (95% CI ± 0.8), a statistically significant difference from baseline. ODI average at one year was 36.7 (95% CI ± 5.8), a statistically significant difference from baseline. ZCQ overall symptom severity score at one-year was 2.88 (95% CI ± 0.34) for 51 patients. ZCQ physical function domain score for 49 patients was 2.19 (95% CI ± 5.8), a statistically significant difference from baseline. For the SF-12V2, 58 patients were included in the analysis that was done by component. The physical component summary mean improvement at one-year was statistically significant, and the mental component summary mean improvement was not. Any additional therapies such as pain medication, injections, or physical therapy were not reported. The authors stated, “The authors plan continued follow-up of ongoing RCTs comparing mild with a series of epidural steroid injections.” The authors concluded, “In this 58-patient 1-year cohort, the mild procedure proved to be safe. In addition, at 1-year follow-up mild demonstrated efficacy by significantly improving mobility and reducing pain associated with lumbar spinal stenosis.”

Chopko 2013 reported on the two-year follow-up for 45 patients at 11 US sites. Outcome measures reported included VAS, ODI, and ZCQ. Thirteen of the 58 patients from the one year follow-up were not reported. Of these 13, three had lumbar spine surgery after the one-year follow-up and one patient died. Nine patients could not be contacted. There was no major device or intraprocedural adverse event during the two-year follow-up. Mean VAS for this 45 patient cohort at 2-year follow-up was 4.8 (95% CI ± 0.8), a statistically significant change from baseline. Mean ODI value at two year follow-up for this cohort was 39.8 (95% CI ± 7.38), a statistically significant from baseline. For 37 patients, ZCQ overall symptom severity score at two-years was 2.7 (95% CI ± 0.2). For 38 patients, ZCQ physical function domain score was 2.6 (95% CI ± 0.4), a statistically significant difference from baseline. They do not report any additional therapies such as pain medications, injections, or physical therapy. The author concluded, “In this report of 2-year follow-up on 45 patients treated with mild percutaneous lumbar decompression, patients experienced statistically significant improvement in pain levels and functional mobility.”

Levy RM and Deer TR. Systematic safety review and meta-analysis of procedural experience using percutaneous access to treat symptomatic lumbar spinal stenosis. Pain Medicine 2012; 13:1554-1561.

The authors stated, “The purpose of this systematic safety review is to report multicenter procedural safety results of patients treated with percutaneous lumbar decompression.” The patient information appeared to come from a variety of sources including retrospective data and publications. The exact methods were not reported. The review included 373 reported patients in 31 centers in the United States and one in Canada from January 2008 to November 2011. The authors reported there were no major device or procedure-related adverse events, but do not give a time frame of follow-up. Major adverse events were defined as any device or procedure related finding that required intervention.

4. MEDCAC

The MEDCAC was not convened for this review.

5. Evidence-based guidelines

No guidelines that referenced evidence were found.

6.  Public Comments

Initial 30 day comment period - (04/05/2013 – 05/05/2013)

During the initial 30 day comment period, CMS received 114 comments. Of the 114 comments, 99 advocated coverage for PILD, four advocated non-coverage and eleven were either unclear as to what position they took or outside the scope of the NCA.

CMS identified comments from five national physician organizations – three for coverage, one for non-coverage and one was unclear in its position. A number of state physician organizations provided comments for coverage. One comment was submitted from America’s Health Insurance Plans for non-coverage and three comments were submitted by instrument manufacturers - two for coverage and one off topic comment.

The comments that were outside the scope of this NCA were related to endoscopic or microsurgical procedures. This NCA is limited to percutaneous image-guided decompression procedures. Procedures performed under direct visualization through an endoscope or microscope are not within the scope of this NCA.

Numerous commenters provided references with their comments. All references were reviewed for relevance to the scope of the NCA and a list of these references is provided in Appendix B. The references that were determined to relevant to the scope of this NCA are incorporated into the bibliography.

The comments can be viewed in their entirety on our website at http://www.cms.gov/medicare-coverage-database/details/nca-view-public-comments.aspx?NCAId=269&ExpandComments=n&NcaName=Percutaneous+Image-guided+Lumbar+Decompression+for+Lumbar+Spinal+Stenosis&bc=ACAAAAAACAAAAA%3d%3d&.

VIII. CMS Analysis

National coverage determinations (NCDs) are determinations by the Secretary with respect to whether or not a particular item or service is covered nationally by Medicare (§1862(l) of the Social Security Act).

In order to be covered by Medicare, an item or service must fall within one or more benefit categories contained within Part A or Part B, and must not be otherwise excluded from coverage. Moreover, section 1862(a)(1) of the Social Security Act in part states, with limited exceptions, no payment may be made under part A or part B for any expenses incurred for items or services:

• which are not reasonable and necessary for the diagnosis or treatment of illness or injury or to improve the functioning of a malformed body member (§1862(a)(1)(A)).

As noted earlier, our review sought the answer to the question below.  We have repeated it here for the convenience of the reader.

Is the evidence sufficient to conclude that PILD improves health outcomes in Medicare beneficiaries with lumbar spinal stenosis?

There are several fundamental limitations of the evidence that cause us to reach conclusions that disagree with the conclusions of the studies that have been used to support claims of clinical benefit. The absence of diagnostic consensus leads us to question whether the enrolled study subjects indeed have LSS, and if so to what degree. The absence of diagnostic consensus constrains any significant consensus on treatment. The general reliance on case series rather than robust randomized sham controlled clinical trials with explicit protocol driven criteria further limits the persuasiveness of the evidence. These limitations are particularly challenging with back pain in light of subjective nature of patients’ symptoms and the failure to adequately account for the biases and confounding that arise from placebo effects and spontaneous symptom improvement in the natural history of the condition. We describe these concerns in greater detail below.

Lack of consensus on diagnostic criteria

Based on our review, we are concerned that the lack of consensus on the definition of spinal stenosis poses a significant challenge to the persuasiveness of the available evidence that might be used to support PILD coverage. Given the many conditions that lead to complaints of back pain, the consistent application of explicit and reproducible diagnostic criteria are needed to assure that patients in clinical trials are comparable to patients in community settings who may be labeled with the same diagnosis but who may have other causes of back pain.

Unfortunately, the available clinical studies generally did not include explicit descriptions of their diagnostic criteria when they reported other descriptive information. This makes it difficult for the reader to understand whether the reported results are generalizable to individual patients (i.e., do these enrolled subjects have the same characteristics as my patient) or to the broad Medicare beneficiary population. This lack of consensus has been cited by others.

• Presumed diagnosis can be postulated with clinical symptoms and radiographic studies, but, “There is no criterion standard for the clinical diagnosis.” (Haig 2006)
• For radiographic studies, “No consensus exists regarding the definition of spinal stenosis in terms of the diameter of the spinal canal or area measurements.” (Issack et al 2012)
• Complicating the exact cause and effect, the relationship between objective measurements and subjective symptoms and the degree of narrowing of the spinal canal is unclear. In fact, many patients with radiographic changes consistent with stenosis do not have symptoms. Thus, the “gold standard” for diagnosis as well as treatment of stenosis does not exist. (Sandella et al. 2013)

Other diagnoses can mimic LSS. (Siebert et al. 2009) A number of structural issues, mostly degenerative, can lead to lumbar spinal stenosis. Based on the totality of the evidence reviewed a few common attributes are agreed upon. When we think of LSS we think of some type of connective tissue structural impingement. Accepted qualitative criteria for the diagnosis of lumbar spinal stenosis are the presence of disk protrusion, lack of perineural intraforaminal fat, presence of hypertrophic facet joint degeneration, absence of fluid around the cauda equina, and hypertrophy of the ligamentum flavum. (Mamisch et al. 2012)

Lack of consensus on the treatment of LSS

Non-surgical or conservative care of LSS may include the following either separately or in various combinations: patient education, physical therapy, epidural injections, manual therapy, behavioral therapy, acupuncture, lumbar corset, and pharmacologic intervention. For patients with more severe symptoms surgery is an option. In addition to open techniques, there are minimally invasive techniques for laminectomy.

Because there is no consensus diagnostic definition for LSS, there is a corresponding lack of consensus on treatment. “Given the considerable pathological and clinical heterogeneity of LSS, the lack of therapeutic recommendations and the large number of distinct therapies, the selection of an appropriate procedure is difficult.” (Siebert et al. 2009) “Class I evidence-based recommendations cannot be made for any conservative or surgical therapy in relation to mid-term and long-term patient outcomes.” (Siebert et al. 2009) In LSS patients without objective neurologic findings such as cauda equina syndrome, it is important to understand which patients will benefit from true structural decompression.

PILD as a treatment

The recognition of a plausible mechanism of action is necessary if a treatment is to be deemed efficacious. Uncertainty leads to reasonable doubt that a witnessed event is causally related to any specific intervention. For invasive treatments there is generally a well-defined structural target. One does not operate on pain per se, but on the pain generator.

The stated goal of PILD is to reduce the thickness of the ligamentum flavum and thereby reduce the connective tissue impingement that is believed to cause the pain. The procedure relies upon removing various types and amounts of connective tissue to conform to a radiographic picture of intraoperative fluoroscopy (with epidural contrast) to reduce the functional stenosis. One article describes this as removing 20 to 50 fragments of bone and ligamentous tissue per single hemilaminar segment, with each fragment measuring between 0.5 to 3 mm in maximal dimension. We cannot be certain that removing a few tiny segments of connective tissue with the PILD tool makes any real structural difference despite the fluoroscopy image of the patient bent forward during the procedure. As with any invasive procedure where tissue is altered, changes from the preoperative radiographic evaluation should correlate with outcomes after decompression. (Mattei 2013) The only post-procedure study to date, which is small, suggests this does not happen. (Wilkinson and Fourney 2012)

Analysis of evidence for PILD as a treatment

Case Series

Case series design is commonly used in reports of therapies. Carey and Boden (2003) in Spine suggest that case series can provide some important information in the area of case definition, trend analyses regarding outcomes, and hints as to causation; however, high quality case series study design and reporting is required to be able to obtain useful information for patient management. While there are conveniences in reviewing case series their methodologic limitations reduce their evidentiary persuasiveness. Case series cannot adequately control for bias and confounding and thus do not provide conclusive evidence in the true benefit or harm of an intervention. This is particularly troublesome for interventions addressing pain, such as the PILD procedure, where the placebo effect introduces a significant risk of bias.

We cannot determine from the published reports what prior therapies we attempted without success. The PILD reports do not furnish enough detail about their protocols to allow other investigators to replicate the studies. For example, does the fluoroscopic endpoint which is reported as procedural success vary depending on how the patient is positioned or on other variables, or is it somehow standardized?

Does the contrast media contain anesthetic or steroid? What co-interventions were used, as patients generally receive multiple co-interventions?

The case series for PILD did not report patient follow-up data. Thus we cannot determine whether even any transient effect is present for long enough to signify durable benefit or harm. Given the chronicity of back pain symptoms, we do not believe that patients can make truly informed choices if there is no persuasive evidence on the ultimate outcomes of the PILD procedure. Less evidentiary weight is given to studies that do not report information that is important in understanding the ultimate impact of the intervention on the patient.

The PILD case series lacked reporting of co-interventions. Typically, patients with LSS receive a variety of co-interventions. If additional treatments are furnished, such as analgesic medications or physical therapy, and there is no controlling for these confounders, it is difficult if not impossible to ascertain PILD treatment success or failure. Without reporting relevant co-interventions results may not be replicated. It could give the appearance that the reported treatment is causal to a successful result, when in fact it is the unreported active treatment, such as narcotic analgesics, that is the causal factor.

The PILD case series did not define key patient indications well. Therefore, we do not know who, if anyone, will benefit from the procedure. In some of the PILD studies, the inclusion criteria require a ligamentum flavum of > 2.5mm, others > 4.0 mm, and still other studies the thickness is not mentioned. In the Lindren and Grider study the authors stated, “The lack of documented ligamentum flavum thickening for each patient is a drawback to the current study. Future studies could attempt to standardize the selection criteria of patients for this procedure with vigorous determination of ligamentum flavum thickness perhaps better predicting who will benefit from the procedure.” The important point may be that ligamentum flavum thickness, despite being the treatment target, does not appear to matter to the reported results.

Many of the PILD studies had short or variable follow-up. While some patients over their followed time appeared to have reduction in pain, pain did not appear to be alleviated completely as witnessed by VAS scores > 0. We do not know if this pain worsened or in the case of those that were pain free at the time of measurement recurred, necessitating narcotics or surgery. Many of the studies had significant missing data. It is important to understand why data was missing, as it could be that these patients had worsening problems and sought care elsewhere. There were no clear definitions of success or failure. This matters when we try to interpret outcome data. For instance, Chopko 2011 reported a statistically significant VAS change, but no change in ODI, this does not support a positive VAS outcome. Clinically significant change on an individual basis is meaningful, group means comparison is not. Data can be imputed when it is missing. While last observation carried forward is a popular method, a sensitivity analysis should be done with best and worst case scenarios to give a more complete picture which is lacking in the studies we reviewed.

PILD RCT

There was a single randomized trial (Brown 2012) reported. Like the PILD case series we had many concerns with the trial. The trial had a short-term outcome of six weeks, with only the experimental group reported at 12 weeks. It was designed to have 20 subjects per group but ended up having 21 in the experimental group and 17 in the control group without explanation as to why it was different than the trial design. The trial did not clearly define for the reader what definition of conservative care was used. For example, some patients were reported to have a month or less of medical management. Similar to the case series described above, the clinical trial report lacked details of co-interventions. Again, without reporting relevant co-interventions results may not be replicated. It could give the appearance that the reported treatment is causal to a successful result, when in fact it is the unreported active treatment, such as narcotic analgesics, that is the causal factor.

Importantly, the comparator does not appear to be adequate to lead to a conclusion of superiority to an inferior treatment. Patients in the mild group underwent procedures bilaterally and at different levels, whereas patients in the ESI group had only one injection, even though “…there is no consensus among interventional pain management specialists regarding type, dosage, frequency, approach, and total number of injections in ESI therapy, generally multiple injections are administered at various intervals.” (Brown et al. 2012) Blinding was not confirmed. Well-designed and reported RCTs carry the most weight. However, despite the author’s reported positive results the weaknesses in the study design and the lack of reporting on important elements calls into question the value of the study and the confidence of the results.

Some authors such as Schomer et al. have claimed comparable results to other therapies, particularly decompressive laminectomy, touting a better safety profile. Without a head to head trial or at the minimum adequate demonstration of comparable patients this claim is not valid. An alternative to open decompression is minimally invasive decompression that is done under direct observation and has not generally been mentioned in the PILD studies. This technique may be a more appropriate comparison for PILD.

Several articles reported a good safety profile, however there have also been serious adverse events reported. Chopko (2011) reported two very serious post-op complications. Tumialan reported on 10 patients with persistent symptoms after the mild procedure, including eight with refractory neurogenic claudication, two patients with cerebrospinal fluid leak, and one with a dural tear and transected nerve roots identified during revision surgery. (Tumialan et al. 2012) He added that all of these patients required additional surgery with exploration. Although Levy and Deer reported on 373 patients, the data sources were unclear and we cannot be assured of consistent and reliable reporting when data collection methods are not reported in detail. We cannot exclude the duplication of subjects as well as lack of systematic adverse event collection, including failure to report serious complications arising post-op such as the ones in Chopko 2011. It is unclear why only a few studies reported adverse events of significance. With any invasive procedure, particularly in the complex area of the spinal cord with direct CSF and nerve connection to the brain, risk is not insignificant and should be realistically accessed and communicated to the patient.

Much of the mild evidence appears to have authorship or other relationships to the manufacturer. A number of the authors of these studies have had a financial relationship with Vertos Medical and the manufacturer provided funding for some of the studies.

It is important that well-designed, high-quality clinical trials must address both the complexities and biases, real and/or perceived, that exist. This includes the potential biases from funding sources. Shah’s retrospective review of articles published in the journal Spine identified, “industry supported studies had a greater frequency of positive results than studies with any other funding sources.” (Shah, Albert et al. 2005)

Conflict of interest can be defined as, “A conflict of interest is a set of circumstances that creates a risk that professional judgment or actions regarding a primary interest will be unduly influenced by a secondary interest.” (IOM 2009) Disclosure is a necessary, but not sufficient, element to assess this risk. (IOM 2009) Unfortunately, policies for publications are not uniform, and are sometimes insufficient to deal with the complex nature of relationships.

Summary

CMS identified a number of studies related to the PILD procedure for LSS. The majority of studies were case series which have inherent limitations in providing a level of reliable evidence of benefit for a procedure, especially a procedure addressing pain. The case series for the PILD procedure suffered from additional limitations in failing to report information important for anyone to assess the clinical utility of this procedure for a particular patient. The one RCT had a small enrollment and major design flaws that called into question the results of the trial.

In reviewing the evidence on PILD we are confronted with weak studies, questions about missing information, questions about adverse events and conflicts of interest. After thoroughly reviewing the evidence for PILD for LSS, we have determined the evidence does not support a conclusion of improved health outcomes for our Medicare beneficiaries.

B.    Disparities

The current PILD literature does not address disparities, with the exception that gender is reported in some studies.

IX. Conclusion

The CMS proposes that PILD for LSS is not reasonable and necessary under section 1862(a)(1)(A) of the Social Security Act. Therefore, CMS proposes that PILD for LSS is non-covered by Medicare.

When making national coverage determinations, CMS evaluates relevant clinical evidence to determine whether or not the evidence is of sufficient quality to support a finding that an item or service falling within a benefit category is reasonable and necessary for the diagnosis or treatment of illness or injury or to improve the functioning of a malformed body member. The critical appraisal of the evidence enables us to determine whether: 1) the specific assessment questions can be answered conclusively; and 2) the intervention will improve health outcomes for patients. An improved health outcome is one of several considerations in determining whether an item or service is reasonable and necessary.

CMS divides the assessment of clinical evidence into three stages: 1) the quality of the individual studies; 2) the relevance of findings from individual studies to the Medicare population; and 3) overarching conclusions that can be drawn from the body of the evidence on the direction and magnitude of the intervention’s risks and benefits.

The issues presented here represent a broad discussion of the issues we consider when reviewing clinical evidence. However, it should be noted that each coverage determination has unique methodological aspects.

1. Assessing Individual Studies

Methodologists have developed criteria to determine weaknesses and strengths of clinical research. Strength of evidence generally refers to: 1) the scientific validity underlying study findings regarding causal relationships between health care interventions and health outcomes; and 2) the reduction of bias. In general, some of the methodological attributes associated with stronger evidence include those listed below:

• Use of randomization (allocation of patients to either intervention or control group) in order to minimize bias.
• Use of contemporaneous control groups (rather than historical controls) in order to ensure comparability between the intervention and control groups.
• Prospective (rather than retrospective) studies to ensure a more thorough and systematical assessment of factors related to outcomes.
• Larger sample sizes in studies to help ensure adequate numbers of patients are enrolled to demonstrate both statistically significant as well as clinically significant outcomes that can be extrapolated to the Medicare population. Sample size should be large enough to make chance an unlikely explanation for what was found.
• Masking (blinding) to ensure patients and investigators do not know to which group patients were assigned (intervention or control). This is important especially in subjective outcomes, such as pain or quality of life, where enthusiasm and psychological factors may lead to an improved perceived outcome by either the patient or assessor.

Regardless of whether the design of a study is a randomized controlled trial, a non-randomized controlled trial, a cohort study or a case-control study, the primary criterion for methodological strength or quality is the extent to which differences between intervention and control groups can be attributed to the intervention studied. This is known as internal validity. Various types of bias can undermine internal validity. These include:

• Different characteristics between patients participating and those theoretically eligible for study but not participating (selection bias)
• Co-interventions or provision of care apart from the intervention under evaluation (confounding)
• Differential assessment of outcome (detection bias)
• Occurrence and reporting of patients who do notcomplete the study (attrition bias)

In principle, rankings of research design have been based on the ability of each study design category to minimize these biases. A randomized controlled trial minimizes systematic bias (in theory) by selecting a sample of participants from a particular population and allocating them randomly to the intervention and control groups. Thus, randomized controlled studies have been typically assigned the greatest strength, followed by non-randomized clinical trials and controlled observational studies. The following is a representative list of study designs (some of which have alternative names) ranked from most to least methodologically rigorous in their potential ability to minimize systematic bias:

• Randomized controlled trials
• Non-randomized controlled trials
• Prospective cohort studies
• Retrospective case control studies
• Cross-sectional studies
• Surveillance studies (e.g., using registries or surveys)
• Consecutive case series
• Single case reports

When there are merely associations but not causal relationships between a study’s variables and outcomes, it is important not to draw causal inferences. Confounding refers to independent variables that systematically vary with the causal variable. This distorts measurement of the outcome of interest because its effect size is mixed with the effects of other extraneous factors. For observational, and in some cases randomized controlled trials, the method in which confounding factors are handled (either through stratification or appropriate statistical modeling) are of particular concern. For example, in order to interpret and generalize conclusions to our population of Medicare patients, it may be necessary for studies to match or stratify their intervention and control groups by patient age or co-morbidities.

Methodological strength is, therefore, a multidimensional concept that relates to the design, implementation and analysis of a clinical study. In addition, thorough documentation of the conduct of the research, particularly study’s selection criteria, rate of attrition and process for data collection, is essential for CMS to adequately assess the evidence.

2. Generalizability of Clinical Evidence to the Medicare Population

The applicability of the results of a study to other populations, settings, treatment regimens, and outcomes assessed is known as external validity. Even well-designed and well-conducted trials may not supply the evidence needed if the results of a study are not applicable to the Medicare population. Evidence that provides accurate information about a population or setting not well represented in the Medicare program would be considered but would suffer from limited generalizability.

The extent to which the results of a trial are applicable to other circumstances is often a matter of judgment that depends on specific study characteristics, primarily the patient population studied (age, sex, severity of disease, and presence of co-morbidities) and the care setting (primary to tertiary level of care, as well as the experience and specialization of the care provider). Additional relevant variables are treatment regimens (dosage, timing, and route of administration), co-interventions or concomitant therapies, and type of outcome and length of follow-up.

The level of care and the experience of the providers in the study are other crucial elements in assessing a study’s external validity. Trial participants in an academic medical center may receive more or different attention than is typically available in non-tertiary settings. For example, an investigator’s lengthy and detailed explanations of the potential benefits of the intervention and/or the use of new equipment provided to the academic center by the study sponsor may raise doubts about the applicability of study findings to community practice.

Given the evidence available in the research literature, some degree of generalization about an intervention’s potential benefits and harms is invariably required in making coverage decisions for the Medicare population. Conditions that assist us in making reasonable generalizations are biologic plausibility, similarities between the populations studied and Medicare patients (age, sex, ethnicity and clinical presentation), and similarities of the intervention studied to those that would be routinely available in community practice.

A study’s selected outcomes are an important consideration in generalizing available clinical evidence to Medicare coverage determinations because one of the goals of our determination process is to assess health outcomes. We are interested in the results of changed patient management not just altered management. These outcomes include resultant risks and benefits such as increased or decreased morbidity and mortality. In order to make this determination, it is often necessary to evaluate whether the strength of the evidence is adequate to draw conclusions about the direction and magnitude of each individual outcome relevant to the intervention under study. In addition, it is important that an intervention’s benefits are clinically significant and durable, rather than marginal or short-lived.

If key health outcomes have not been studied or the direction of clinical effect is inconclusive, we may also evaluate the strength and adequacy of indirect evidence linking intermediate or surrogate outcomes to our outcomes of interest.

3. Assessing the Relative Magnitude of Risks and Benefits

Generally, an intervention is not reasonable and necessary if its risks outweigh its benefits. Health outcomes are one of several considerations in determining whether an item or service is reasonable and necessary. For most determinations, CMS evaluates whether reported benefits translate into improved health outcomes. CMS places greater emphasis on health outcomes actually experienced by patients, such as quality of life, functional status, duration of disability, morbidity and mortality, and less emphasis on outcomes that patients do not directly experience, such as intermediate outcomes, surrogate outcomes, and laboratory or radiographic responses. The direction, magnitude, and consistency of the risks and benefits across studies are also important considerations. Based on the analysis of the strength of the evidence, CMS assesses the relative magnitude of an intervention or technology’s benefits and risk of harm to Medicare beneficiaries.

CMS does from time to time include requirements for facility and/or physician standards, or certain certification requirements in our NCDs; however, we exercise this option after considered counsel and cognizant of the responsibility such requirements establish. Some of the considerations that may inform our decision to include facility and/or physician standards, or certification requirements are: intended patients who are medically fragile undergoing high risk procedures; procedures that are new or not generally disseminated in the medical community at large; technically complex procedures; procedures experiencing a rapid growth in the medical community before the opportunity for the establishment of generally accepted standards; procedures that impose what we believe to be a significantly higher risk for our Medicare beneficiaries. While this is not intended to be an all-inclusive list of what may inform CMS’s decision to include facility and/or physician standards, or certification requirements, it is provided to give some insight into our decision making process. Ultimately, it is the convincing nature of the circumstances and/or the evidence surrounding the item or service under review that guides CMS to conclude that such standards and/or certification requirements will benefit our Medicare beneficiaries.

References submitted in first public comment period. References are listed as submitted by the commenter.

References

1. Deer TR, Kapural L. New image-guided ultra-minimally invasive lumbar decompression method: The mild® procedure. Pain Physician 2010;13:35-41.

2. Chopko B, Caraway DL. MiDAS I (mild® Decompression Alternative to Open Surgery): A preliminary report of a prospective, multi-center clinical study. Pain Physician 2010;13:369-378.

3. Lingreen R, Grider JS. Retrospective review of patient self-reported improvement and post-procedure findings for mild® (minimally invasive lumbar decompression). Pain Physician 2010;13:555-60.

4. Chopko B. A novel method for treatment of lumbar spinal stenosis in high-risk surgical candidates: pilot study experience with percutaneous remodeling of ligamentum flavum and lamina. J Neurosurg Spine 2011;14:46–50.

5. Mekhail N, Vallejo R, Coleman MH, Benyamin RM. Long-term results of percutaneous lumbar decompression mild® for spinal stenosis. Pain Pract 2012;12(3):184-193.

6. Deer TR, Mekhail N, Lopez G, Amirdelfan K. Minimally invasive lumbar decompression for spinal stenosis. JNR 2011;1(S1):29-32.

7. Schomer DF, Solsberg D, Wong W, Chopko BW. mild® lumbar decompression for the treatment of lumbar spinal stenosis. The Neuroradiology Journal 2011;24:620-626.

8. Wong WH. mild interlaminar decompression for the treatment of lumbar spinal stenosis: procedure description and case series with 1-year follow-up. Clin J Pain 2012;28(6):534–538.

9. Brown LL. A double-blind, randomized, prospective study of epidural steroid injection vs. the mild® procedure in patients with symptomatic lumbar spinal stenosis. Pain Pract 2012;12(5):333-341.

10. Basu S. mild® procedure: single-site prospective IRB study. Clin J Pain 2012;28(3):254-258.

11. Mekhail N, Costandi S, Abraham B, Samuel S. Functional and patient-reported outcomes in symptomatic lumbar spinal stenosis following percutaneous decompression. Pain Pract 2012;12(6):417-425.

12. Chen H, Kelling J. mild procedure for lumbar decompression: A review. Pain Pract 2013;13(2):146-153. 13. Deer T. Minimally invasive lumbar decompression for the treatment of spinal stenosis of the lumbar spine. Pain Management 2012;2(5):457-465.

14. Levy RM, Deer TR. Systematic safety review and meta-analysis of procedural experience using percutaneous access to treat symptomatic lumbar spinal stenosis. Pain Med 2012;13:1554-1561.

15. Deer TR, Kim CK, Bowman RG, Ranson MT, Yee BS. Study of percutaneous lumbar decompression and treatment algorithm for patients suffering from neurogenic claudication. Pain Physician 2012;15:451-460.

16. Chopko B. Long-term results of percutaneous lumbar decompression for LSS. Clin J Pain: Feb 26, 2013 [Epub ahead of print]

17. Wilkinson JS, Fourney DR. Failure of percutaneous remodeling of the ligamentum flavum and lamina for neurogenic claudication. Neurosurgery 2012;71(1):86-92.

18. Sigmundsson FR, Kang XP, Jönsson B, Strömqvist B. Correlation between disability and MRI findings in lumbar spinal stenosis. A prospective study of 109 patients operated on by decompression. Acta Orthopaedica 2011;82:204-210.

[i] Chopko BW. Long-term results of percutaneous lumbar decompression for LSS: Two-year outcomes. The Clinical Journal of Pain. February 26, 2013. PMID: 23446067

[ii] Chopko, BW. A novel method for treatment of lumbar spinal stenosis in high-risk surgical candidates: pilot study experience with percutaneous remodeling of ligamentum flavum and lamina. J Neurosurg Spine. 2011 Jan;14(1):46-50. PMID: 21142460

[iii] American Association of Neurological Surgeons. Technical Assessment of M.I.L.D Vertos Medical http://www.aans.org/Education%20and%20Meetings/Emerging%20Technology/Tech%20Assessment%20of%20MILD.aspx

1. Brown LL. A double-blind, randomized, prospective study of epidural steroid injection vs. the mild® procedure in patients with symptomatic lumbar spinal stenosis. Pain Pract 2012; 12(5):333-341.

2. Chopko, B. Long-term Results of Percutaneous Lumbar Decompression for LSS Two-Year Outcomes. Clin J Pain 2013; DOI. 10.1097/AJP.0b013e31827fb803 [Epub ahead of print].

3. Mekhail, Nagy, et al. Functional and Patient-Reported Outcomes in Symptomatic Lumbar Spinal Stenosis Following Percutaneous Decompression. Pain Pract 2012; 12(6):417–425.

4. Mekhail N, Vallejo R, Coleman MH, Benyamin RM. Long-term results of percutaneous lumbar decompression mild® for spinal stenosis. Pain Pract 2012; 12(3):184-193.

5. Chopko B, Caraway DL. MiDAS I (mild® Decompression Alternative to Open Surgery): A preliminary report of a prospective, multi-center clinical study. Pain Physician 2010; 13:369-378.

6. Wong WH. mild interlaminar decompression for the treatment of lumbar spinal stenosis: procedure description and case series with 1-year follow-up. Clin J Pain 2012; 28(6):534–538.

7. Basu S. mild® procedure: single-site prospective IRB study. Clin J Pain 2012; 28(3):254-258.

8. Levy, R, et al. Systematic Safety Review and Meta-Analysis of Procedural Experience Using Percutaneous Access to Treat Symptomatic Lumbar Spinal Stenosis. Pain Medicine 2012; 13:1554-1561.

9. Deer TR, Kapural L. New image-guided ultra-minimally invasive lumbar decompression method: The mild® procedure. Pain Physician 2010; 13:35-41.

10. Lingreen R, Grider JS. Retrospective review of patient self-reported improvement and post-procedure findings for mild® (minimally invasive lumbar decompression). Pain Physician 2010; 13:555-60.

11. Chopko B. A novel method for treatment of lumbar spinal stenosis in high-risk surgical candidates: pilot study experience with percutaneous remodeling of ligamentum flavum and lamina. J Neurosurg Spine 2011; 14:46–50.

12. Schomer, Donald, et al. Minimally Invasive Lumbar Decompression for the Treatment of Lumbar Spinal Stenosis. The Neuroradiology Journal 2011; 24:620-626.

13. Deer, Timothy, et al. Minimally Invasive Lumbar Decompression for Lumbar Spinal Stenosis. Journal of Neurosurgical Review 2011; 1(S1):29-32.

14. Deer, Timothy, et al. Minimally Invasive Lumbar Decompression for the Treatment of Spinal Stenosis of the Lumbar Spine. Pain Management 2012; 2(5):457–465.

15. Deer, Timothy, et al. Study of Percutaneous Lumbar Decompression and Treatment Algorithm for Patients Suffering from Neurogenic Claudication. Pain Physician 2012; 15:451-460.

16. Wang JJ, Bowden K, Pang G, Cipta A. Decrease in health care resource utilization with MILD. Pain Med: April 2013 [Epub ahead of print].

17. Durkin B, Romeiser J, Shroyer AL, Schiller R, Bae J, Davis RP, Peyster R, Benveniste H. Report from a quality assurance program on patients undergoing the MILD procedure. Pain Med: Mar 14, 2013 [Epub ahead of print] 18. Chen H, Kelling J. mild® Procedure for Lumbar Decompression: A Review. Pain Pract: 2013;13(2):146-153.

1. Deer TR, Kapural L. New image-guided ultra-minimally invasive lumbar decompression method: The mild® procedure. Pain Physician 2010;13:35-41.

2. Deer TR, Mekhail N, Lopez G, Amirdelfan K. Minimally invasive lumbar decompression for spinal stenosis. JNR 2011;1(S1):29-32.

3. Deer, T. Minimally Invasive Lumbar Decompression for the Treatment of Spinal Stenosis of the Lumbar Spine. Pain Management 2012; 2(5):457–465.

4. Deer TR, Kim CK, Bowman RG, Ranson MT, Yee BS. Study of percutaneous lumbar decompression and treatment algorithm for patients suffering from neurogenic claudication. Pain Physician 2012;15:451-460.

5. Levy RM, Deer TR. Systematic safety review and meta-analysis of procedural experience using percutaneous access to treat symptomatic lumbar spinal stenosis. Pain Med 2012;13:1554-1561.

1. Deer TR, Kapural L. New image-guided ultra-minimally invasive lumbar decompression method: The mild® procedure. Pain Physician 2010;13:35-41.

2. Chopko B, Caraway DL. MiDAS I (mild® Decompression Alternative to Open Surgery): A preliminary report of a prospective, multi-center clinical study. Pain Physician 2010;13:369-378.

3. Lingreen R, Grider JS. Retrospective review of patient self-reported improvement and post-procedure findings for mild® (minimally invasive lumbar decompression). Pain Physician 2010;13:555-60.

4. Deer TR, Kim CK, Bowman RG, Ranson MT, Yee BS. Study of percutaneous lumbar decompression and treatment algorithm for patients suffering from neurogenic claudication. Pain Physician 2012;15:451-460.

5. Chopko B. A novel method for treatment of lumbar spinal stenosis in high-risk surgical candidates: pilot study experience with percutaneous remodeling of ligamentum flavum and lamina. J Neurosurg Spine 2011;14:46–50.

6. Mekhail N, Vallejo R, Coleman MH, Benyamin RM. Long-term results of percutaneous lumbar decompression mild® for spinal stenosis. Pain Pract 2012;12(3):184-193.

7. Schomer DF, Solsberg D, Wong W, Chopko BW. mild® lumbar decompression for the treatment of lumbar spinal stenosis. The Neuroradiology Journal 2011;24:620-626.

8. Wong WH. mild interlaminar decompression for the treatment of lumbar spinal stenosis: procedure description and case series with 1-year follow-up. Clin J Pain 2012;28(6):534–538.

9. Brown LL. A double-blind, randomized, prospective study of epidural steroid injection vs. the mild® procedure in patients with symptomatic lumbar spinal stenosis. Pain Pract2012;12(5):333-341.

10. Basu S. mild® procedure: single-site prospective IRB study. Clin J Pain 2012;28(3):254-258.

11. Wilkinson JS, Fourney DR. Failure of percutaneous remodeling of the ligamentum flavum and lamina for neurogenic claudication. Neurosurgery 2012;71(1):86-92.

1.Brown LL. A Double-blind, Randomized, Prospective Study of Epidural Steroid Injection vs. The mild® Procedure in Patients with Symptomatic Lumbar Spinal Stenosis. Pain Pract. 2012, Volume 12, Issue 5:333–341.

2.Basu S. Mild procedure: single-site prospective IRB study. Clin J Pain. 2012, Mar-Apr;28(3):254-8.

3.D.F. Schomer, mild ® Lumbar Decompression for the Treatment of Lumbar Spinal Stenosis, NJR, Volume 24 - No. 4 - August 2011 - 620-626.

4.Lingreen R, Grider JS. Retrospective review of patient self-reported improvement and post-procedure findings for mild (minimally invasive lumbar decompression). Pain Physician. 2010 Nov-Dec;13(6):555-60.

5.Mekhail N, Vallejo R, Coleman MH, Benyamin RM. Long-term results of percutaneous lumbar decompression mild® for spinal stenosis. Pain Pract. 2012 Mar;12(3):184-93.

6.Wilkinson JS, Fourney DR. Failure of Percutaneous Remodeling of the Ligamentum Flavum and Lamina for Neurogenic Claudication. Neurosurgery. 2012 Mar 8.

12. Mekhail N, Costandi S, Abraham B, Samuel S. Functional and patient-reported outcomes in symptomatic lumbar spinal stenosis following percutaneous decompression. Pain Pract 2012;12(6):417-425.

13. Levy RM, Deer TR. Systematic safety review and meta-analysis of procedural experience using percutaneous access to treat symptomatic lumbar spinal stenosis. Pain Med2012;13:1554-1561.

14. Chopko B. Long-term results of percutaneous lumbar decompression for LSS. Clin J Pain: Feb 26, 2013 [Epub ahead of print].

15. Durkin B, Romeiser J, Shroyer AL, Schiller R, Bae J, Davis RP, Peyster R, Benveniste H. Report from a quality assurance program on patients undergoing the MILD procedure. Pain Med: Mar 14, 2013 [Epub ahead of print].

16. Wang JJ, Bowden K, Pang G, Cipta A. Decrease in health care resource utilization with MILD. Pain Med: April 2013 [Epub ahead of print].

Weinstein JN. Surgical versus non-surgical treatment of lumbar spinal stenosis. New Engl J Med 2008(8): 794-810. Brown LL. A double-blind, randomized, prospective study of epidural steroid injection vs. the mild® procedure in patients with symptomatic lumbar spinal stenosis. Pain Pract 2012;12(5):333-341.

Mekhail N, Vallejo R, Coleman MH, Benyamin RM. Long-term results of percutaneous lumbar decompression mild® for spinal stenosis. Pain Pract 2012;12(3):184-193.

Wong WH. mild interlaminar decompression for the treatment of lumbar spinal stenosis: procedure description and case series with 1-year follow-up. Clin J Pain 2012;28(6):534–538.

Schomer DF, Solsberg D, Wong W, Chopko BW. mild® lumbar decompression for the treatment of lumbar spinal stenosis. The Neuroradiology Journal 2011;24:620-626.

Basu S. mild® procedure: single-site prospective IRB study. Clin J Pain 2012;28(3):254-258.

Chopko B, Caraway DL. MiDAS I (mild® Decompression Alternative to Open Surgery): A preliminary report of a prospective, multi-center clinical study. Pain Physician 2010;13:369-378.

Deer TR, Mekhail N, Lopez G, Amirdelfan K. Minimally invasive lumbar decompression for spinal stenosis. JNR 2011;1(S1):29-32.

Chopko B. A novel method for treatment of lumbar spinal stenosis in high-risk surgical candidates: pilot study experience with percutaneous remodeling of ligamentum flavum and lamina. J Neurosurg Spine 2011;14:46–50.

Deer TR, Kapural L. New image-guided ultra-minimally invasive lumbar decompression method: The mild® procedure. Pain Physician 2010;13:35-41.

Deer, Timothy, et al. Minimally Invasive Lumbar Decompression for the Treatment of Spinal Stenosis of the Lumbar Spine. Pain Management 2012; 2(5):457–465.

Levy, R, et al. Systematic Safety Review and Meta-Analysis of Procedural Experience Using Percutaneous Access to Treat Symptomatic Lumbar Spinal Stenosis. Pain Medicine 2012; 13:1554-1561.

Mekhail, Nagy, et al. Functional and Patient-Reported Outcomes in Symptomatic Lumbar Spinal Stenosis Following Percutaneous Decompression. Pain Pract 2012; 12(6):417–425.

Deer, Timothy, et al. Study of Percutaneous Lumbar Decompression and Treatment Algorithm for Patients Suffering from Neurogenic Claudication. Pain Physician 2012; 15:451-460.

Lingreen R, Grider JS. Retrospective review of patient self-reported improvement and post-procedure findings for mild® (minimally invasive lumbar decompression). Pain Physician 2010;13:555-60.

Chen H, Kelling J. mild® Procedure for Lumbar Decompression: A Review. Pain Pract: 2013;13(2):146-153.

Chopko, B. Long-term Results of Percutaneous Lumbar Decompression for LSS Two-Year Outcomes. Clin J Pain 2013; DOI. 10.1097/AJP.0b013e31827fb803 [Epub ahead of print].

Wang JJ, Bowden K, Pang G, Cipta A. Decrease in health care resource utilization with MILD. Pain Med: April 2013 [Epub ahead of print].

(Deer, Timothy, et al. (2011), Minimally Invasive Lumbar Decompression for Spinal Stenosis. Journal of Neurosurgical Review, 1(S1): 29-32.)

(Deer, Timothy, et al. (2010), New Image-Guided Ultra-Minimally Invasive Lumbar Decompression Method: The mild® Procedure. Pain Physician, 13(1): 35-41, ISSN 1533-3159.)

(Schomer, Donald, et al. (2011), mild® Lumbar Decompression for the Treatment of Lumbar Spinal Stenosis. Neuroradiology Journal, 24(4): 620-626.)

1. "Functional and Patient-Reported Outcomes in Symptomatic Lumbar Spinal Stenosis Following Percutaneous Decompression” Nagy Mekhail, Shrif Costandi, Benjamin Abraham, Samuel Samuel 2012; 12(6): 417-425.

2. "A Double-blind, Randomized, Prospective Study of Epidural Steroid Injection vs. The mild® Procedure in Patients with Symptomatic Lumbar Spinal Stenosis" Lora Brown 2012; 12(5): 333-341.

1. Chopko B, Caraway DL. MiDAS I (milt!> Decompression Alternative to Open Surgery): A preliminary report of a prospective, multi-center clinical study. Pain Physician 20IO; I3:369-378.

2. Deer TR, Kapural L. New image-guided ultra-minimally invasive lumbar decompression method: The mild® procedure. Pain Physician 20IO; 13:35-41.

3. Chopko B. A novel method for treatment of lumbar spinal stenosis in high-risk surgical candidates: pilot study experience with percutaneous remodeling of ligamentum flavum and lamina. J Neurosurg Spine 20 II; I4:46 50.

4. Lin green R, Grider JS. Retrospective review of patient self-reported improvement and post-procedure findings for mild® (minimally invasive lumbar decompression). Pain Physician 20IO; I3:555-60.

5. Basu S. milt!> procedure: single-site prospective IRB study. Clin J Pain 20I2; 28(3):254-258.

6. Mekhail N, Vallejo R, Coleman MH, Benyamin RM. Long-term results of percutaneous lumbar decompression miltP for spinal stenosis. Pain Pract 2012; 12(3): 184-193.

7. Wong WH. mild interlaminar decompression for the treatment of lumbar spinal stenosis: procedure description and case series with 1-year follow-up. Clin J Pain 2012; 28(6):534 538.

8. Mekhail, Nagy, et al. Functional and Patient-Reported Outcomes in Symptomatic Lumbar Spinal Stenosis Following Percutaneous Decompression. Pain Pract 20 12; 12( 6):417-425.

9. Brown LL. A double-blind, randomized, prospective study of epidural steroid injection vs. the mil~ procedure in patients with symptomatic lumbar spinal stenosis. Pain Pract 2012; 12(5):333-341.

10. Schomer, Donald, et al. Minimally Invasive Lumbar Decompression for the Treatment of Lumbar Spinal Stenosis. The Neuroradiology Journal20 II; 24:620-626.

11. Deer, Timothy, et al. Minimally Invasive Lumbar Decompression for Lumbar Spinal Stenosis. Journal of Neurosurgical Review 20 1I; 1 (S 1 ):29-32.

12. Chen H, Kelling J. mild® Procedure for Lumbar Decompression: A Review. Pain Pract: 2013; I3(2): I46-I53.

13. Deer, Timothy, et al. Minimally Invasive Lumbar Decompression for the Treatment of Spinal Stenosis of the Lumbar Spine. Pain Management 2012; 2(5):457-465.

14. Levy, R, et al. Systematic Safety Review and Meta-Analysis of Procedural Experience Using Percutaneous Access to Treat Symptomatic Lumbar Spinal Stenosis. Pain Medicine 2012; 13:1554-1561.

15. Deer, Timothy, et al. Study of Percutaneous Lumbar Decompression and Treatment Algorithm for Patients Suffering from Neurogenic Claudication. Pain Physician 2012; 15:451-460.

16. Chopko, B. Long-term Results of Percutaneous Lumbar Decompression for LSS Two-Year Outcomes. Clin J Pain 2013; DOL 10.1097/AJP.Ob013e31827tb803 [Epub ahead of print].

17. Wang JJ, Bowden K, Pang G, Cipta A. Decrease in health care resource utilization with MILD. Pain Med: April20I3 [Epub ahead of print].

18. Deyo, Richard A, et al. Trends, Major Medical Complications, and Charges Associated with Surgery for Lumbar Spinal Stenosis in Older Adults. JAMA 20IO; 303(13):I259-1265.

I9. Wilkinson, J, et al. Failure of Percutaneous Remodeling of the Ligamentum Flavum and Lamina for Neurogenic Claudication. Neurosurgery20 I2; 7I :86-92.

1.Weinstein JN et al. Surgical versus Nonsurgical Therapy for Lumbar Spinal Stenosis. N Engl J Med 2008;358:794810

2. Mekhail N et al. Functional and Patient-Reported Outcomes in Symptomatic Lumbar Spinal Stenosis Following Percutaneous Decompression. Pain Practice 2012;12(6): 417-425

3. Brown LL. A Double-blind, Randomized, Prospective Study of Epidural Steroid Injection vs. The Mild Procedure in Patients with Symptomatic Lumbar Spinal Stenosis. Pain Practice 2012;12(5): 333-341

Chopko B, Caraway DL. MiDAS I (mild® Decompression Alternative to Open Surgery): A preliminary report of a prospective, multi-center clinical study. Pain Physician 2010; 13:369-378.

2. Deer TR, Kapural L. New image-guided ultra-minimally invasive lumbar decompression method: The mild® procedure. Pain Physician 2010; 13:35-41.

3. Chopko B. A novel method for treatment of lumbar spinal stenosis in high-risk surgical candidates: pilot study experience with percutaneous remodeling of ligamentum flavum and lamina. J Neurosurg Spine 2011; 14:46–50.

4. Lingreen R, Grider JS. Retrospective review of patient self-reported improvement and postprocedure findings for mild® (minimally invasive lumbar decompression). Pain Physician 2010; 13:555-60.

5. Basu S. mild® procedure: single-site prospective IRB study. Clin J Pain 2012; 28(3):254-258.

6. Mekhail N, Vallejo R, Coleman MH, Benyamin RM. Long-term results of percutaneous lumbar decompression mild® for spinal stenosis. Pain Pract 2012; 12(3):184-193.

7. Wong WH. mild interlaminar decompression for the treatment of lumbar spinal stenosis: procedure description and case series with 1-year follow-up. Clin J Pain 2012; 28(6):534–538.

8. Mekhail, Nagy, et al. Functional and Patient-Reported Outcomes in Symptomatic Lumbar Spinal Stenosis Following Percutaneous Decompression. Pain Pract 2012; 12(6):417–425.

9. Brown LL. A double-blind, randomized, prospective study of epidural steroid injection vs. the mild® procedure in patients with symptomatic lumbar spinal stenosis. Pain Pract 2012; 12(5):333-341.

10. Schomer, Donald, et al. Minimally Invasive Lumbar Decompression for the Treatment of Lumbar Spinal Stenosis. The NeuroradiologyJournal 2011; 24:620-626.

11. Deer, Timothy, et al. Minimally Invasive Lumbar Decompression for Lumbar Spinal Stenosis. Journal of Neurosurgical Review 2011; 1(S1):29-32.

12. Chen H, Kelling J. mild® Procedure for Lumbar Decompression: A Review. Pain Pract: 2013;13(2):146-153.

13. Deer, Timothy, et al. Minimally Invasive Lumbar Decompression for the Treatment of Spinal Stenosis of the Lumbar Spine. Pain Management 2012; 2(5):457–465.

14. Levy, R, et al. Systematic Safety Review and Meta-Analysis of Procedural Experience Using Percutaneous Access to Treat Symptomatic Lumbar Spinal Stenosis. Pain Medicine 2012; 13:1554- 1561.

15. Deer, Timothy, et al. Study of Percutaneous Lumbar Decompression and Treatment Algorithm for Patients Suffering from Neurogenic Claudication. Pain Physician 2012; 15:451-460.

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