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Spinal Stenosis/Neurogenic Claudication

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Presentation on theme: "Spinal Stenosis/Neurogenic Claudication"— Presentation transcript:

1 Spinal Stenosis/Neurogenic Claudication
Chris Dowding Half Day Feb

2 Low Back Pain About ¾ of all individuals will experience low back pain at some time in their lives; usually, it resolves in a matter of weeks. Low back pain is the leading cause of disability in people younger than 50 years of age. LBP - M=F Peak incidence between 35 and 50 years of age Primary causes of low back pain Muscle strain or ligament sprain Facet joint arthropathy Discogenic pain or Annular tears Spondylolisthesis Spinal stenosis

3 Anatomy

4 What is Spinal Stenosis?
First described by Verbiest 1954 7 patients with syndrome of the following: Lumbar canal narrowing Neurogenic spinal claudication Radicular pain Motor weakness in lower limb

5 Definition Spinal Stenosis Primary subtypes
Narrowing of the spinal canal, resulting in a clinical syndrome of leg dominant pain Primary subtypes Central canal stenosis Subarticular stenosis (area under facet joints) Neural foramina stenosis Symptoms are caused by compression of the nerve roots Results in neurogenic claudication

6 Definition Neurogenic claudication
Discomfort or pain that radiates from the spinal area into the buttocks and frequently into thigh and lower leg

7 Pattern 4 Leg dominant pain
Pain is brought on by activity and relieved by rest in flexion. Pain is always intermittent. Neurological symptoms usually absent at rest. Vascular – worse with walking, relief with rest, poor or absent pulses Neurogenic – worse with walking or standing, relief with sitting or flexion, physical exam normal, pulses present

8 Claudication Pattern 1 Pattern 2 Pattern 3 Pattern 4 Region Back Leg
Worse with: Flexion Extension Movement Relief with: Fast:Extension Slow: Nil Usually flexion Fast: Posturing Timing: Constant or Intermittent Intermittent Constant Neuro: Normal Present Generator: Degenerative disc; soft tissues Facet arthritis; soft tissues Disc herniation Spinal stenosis Region – location where pain is at its worst. Doesn’t mean that pain is not present elsewhere as well. Again, reminder that this classification system is based on pattern recognition and not necessarily anatomic site or pathologic process. The overwhelming majority of patients with Pattern 1 and Pattern 2 back pain are not surgical candidates. If physical rehab can improve or get rid of pain, the specific anatomic pain generator does not matter. With pattern 3 and pattern 4, surgical management becomes more likely and identification of an anatomic pain generator becomes very important.

9 Claudication Symptoms/Findings Neurogenic Claudication
Vascular Claudication Pain Dermatomal Muscle grip Sensory Loss Stocking Worse with: Variable exercise, standing Fixed amount of exercise Relief with rest: Slow, positional Immediate Foot pallor (elevation) None Marked Pulses Normal Decreased/absent

10 Claudication

11 Etiology Spinal Stenosis Narrowing of spinal canal due to:
Degenerative (most common) Developmental Congenital disorders Post traumatic Steroids Post-surgical Certain disorders

12 Degenerative Stenosis
Narrowing is secondary to arthritis Typically following order Disc degeneration Facet osteoarthritis Flavum hypertrophy Symptoms develop around 60 yo

13 Intervertebral Joints
Two Components: 1. Outer rim of fibrocartilage called the annulus fibrosus (attaches to cartilaginous end plate) Connects vertebral bodies in a fibrocartilaginous joint (no capsule, little motion) 2. Facet (Zygapophyseal) joints

14 Intervertebral Disks Collagen, water, Proteoglycans Fibrocartilaginous
Annulus Fibrosus Obliquely oriented collagen Type I collagen Outer rim contains free nerve endings Central Nucleus Pulposus 88+% water, high polysaccharide content No blood vessels or nerves Type II collagen Structure deforms when pressure is put on vertebral column as in weight bearing Acts as a shock absorber Annulus totally encloses the nucleus and keeps it under constant pressure As you get older, the H2O content decreases and the nucleus becomes more fibrocartilaginous, therefore less easily deformable and more easily damaged Nucleus, when under extreme pressure, can herniate or extrude from the disc in a posterior or posterior-lateral direction Usually occurs in cervical or lumbar region Nucleus can put pressure on spinal nerve causing refereed symptoms (motor and sensory) Can cause pressure on cord itself if true posterior

15 Intervertebral Disks Function Disk is avascular. As Disks ages
spinal motion and stability. Disk is avascular. Nutrients fluid via diffusion through pores in the hyaline cartilage end plates As Disks ages Decreased water content, increased collagen.

16 Disk Degeneration Begins roughly third decade of life.
Characterized by a decline in proteoglycan concentration with resultant loss of hydration and a decreased number of viable cells L4-5 and L5-S1 are the disks that typically degenerate first

17 Degenerative Disks Disk height decreases, resulting in alteration of the segmental spinal biomechanics Increasing wear on facet joints The precise cause(s) of disk degeneration are unclear, and there are several potential contributors Comorbidities like diabetes, vascular insufficiency, and smoking are potentially associated with disk degeneration There appears to be a genetic component to disk degeneration

18 Degenerative Stenosis
Loss of disc height  Infolding of flavum  Increased stress across facets  Facet OA and hypertrophy  Osteophytes and capsule thickening  Cysts


20 Degenerative Stenosis
Spondylolithesis (+/- spondylolysis) Can result in stenosis Back pain is primary symptom Neurogenic claudication is secondary

21 Developmental Stenosis
Narrowing of canal due to growth disturbance of posterior elements Congenitally short pedicles Often present in 20’s

22 Presentation Constellation of symptoms Leg pain Difficulty ambulating
Comfortable sitting Pain with prolonged walking Neurologic deficits

23 History Age Pain Aggravating or relieving factors? Previous therapy?
Location Timing Characteristics Aggravating or relieving factors? Previous therapy? PMHx Social History/Occupation Meds/Allergies Functional Inquiry How far can you walk? Can they bike? The two most important questions on history are: Back dominant vs Leg dominant; Constant vs intermittent Characteristics of pain – dull, sharp, electric, shooting. Numbness, tingling. Relief with certain posturing

24 Red Flags Night sweats Saddle anaesthesia Fever Sexual dysfunction
Weight loss Age > 60 Bowel/Bladder History of IVDU History of cancer Chronic infections Immunosuppression Rest/night pain Pain not relieved when patient lies down.

25 Physical Exam Vitals Palpate Inspect Spinous processes Gait
Paraspinal muscles Leg length Greater trochanters Trendelenburg test Spinal alignment

26 Physical Exam ROM Neuro
Spine flexion, extension, rotation, lateral bend Hip flexion, extension, rotation Pain with etxension, relieved by flexion Neuro Strength Sensation Reflexes Half of patients with symptomatic stenosis have motor or sensory deficits Usually mild

27 Neurologic Examination

28 Special Tests Romberg maneuver Patient stands with eyes closed
Look for unsteadiness, wide based stance Indicates damaged proprioception

29 Imaging Lumbar x-rays CT/MRI +/- spondylolithesis
Extent of disc narrowing Foramina osteophytes CT/MRI Can illustrate reductions in cross sectional diameter of central canal or foramina Useful for pre-op planning or assessing candidacy for epidural injections Large number of people may have radiologic findings but are asymptomatic SLR defined as the reproduction of sciatica symptoms when the hip is flexed passively with a straight leg between 30 and 70 degrees. The diagnostic odds ratio remains low because surgical patients WITHOUT a disc herniation are likely to have a positive SLR. Straight leg raising, by itself, can produce pain from a variety of sources, including myogenic pain, ischialburisitis, annular tear, and hamstring tightness, as well as herniated disc.

30 Location of stenosis Centrally Lateral recess & neural foramina
Degeneration of Disk Facets (hypertrophy) Synovial cysts Joint capsule Thickening of ligamentum flavum Osteophytes

31 Identifying the cause Differential is broad
Some non-spinal causes to keep in mind Vascular claudication Hip arthritis Diabetes (peripheral neuropathy)

32 Vascular Claudication
Cramping/tightness in calf PVD (skin ulcers, trophic changes) Diminished pulses Relieved by cessation of activity Versus neurogenic (flexion or sitting down) Capable of activity while flexed shopping cart Cycling walking uphill

33 Hip Arthritis Groin pain Referred pain in thigh
increased with activity Internal rotation diminished XR - OA

34 Diabetes Glove & stocking distribution Not affected by activity level

35 Conservative Management
Physical therapy Abdominal strengthening Biking Brace/corset Slight lumbar flexion Limit hours worn per day Avoid atrophy Pain pyramid Tylenol NSAIDS Narcotics

36 Conservative Management
Epidural injections Theory is that compression of nerve roots causes inflammation and thus symptoms Cortocosteroids to reduce inflammation Evidence is not convincing one way or another Although this practice is increasing

37 Natural History? Natural course of disease
Pain / function of patients with lumbar stenosis remains unchanged in majority patients After one year of non-op management the majority of patients will be neither worse nor better Rapid decline uncommon Therefore prophylactic treatment non indicated Improvement is also uncommon If patient is miserable at baseline, non-op management may not be appropriate

38 Surgical indications Progressive neurologic deficit Intractable pain
Persistent impairment and functional limitation Confirmation by imaging LBP is not alleviated with surgery!

39 Lumbar Stenosis: So when should we operate?
Goals of surgery Decompress central canal and neural foramina Options Laminectomy ** Partial facetectomy ** Lumbar arthrodesis +/- Instrumentation Interspinous distraction MIS

40 Algorithm? Edward N. Hanley Jr., MD, Spinal Stenosis, Charlotte

41 Treatment – Spinal Stenosis
Maine lumbar spine study 119 patients 67 treated surgically 52 treated nonsurgically After 4 years 70% of surgically treated and 52% of nonsurgically treated reported that their predominant pain was better. Satisfaction 63% of surgically treated and 42% of nonsurgically treated. Atlas et al. Spine Over time, relative benefits of surgery declined but still remained superior to nonsurgical management Better, same or worse rating scale.

42 Malmivaara 2007 Design RCT 4-university hospitals 94 patients Surgical
Laminectomy 10 patients also had transpedicular fusion Outcome Oswestry Disability Index (0-100) Intensity of pain (0-10) Walking ability – self-reported 6,12&24 months

43 Malmivaara 2007 Inclusion Criteria
Back pain radiation to lower limb/buttock Fatigue loss sensation aggravated by walking Persistent pain without progressive neurologic dysfunction SAC (sagital) < 10 mm Duration of symptoms > 6 months Signs & symptoms correspond to segmental radiographs Severity of disease to justify surgical/non- surgical rx

44 Malmivaara 2007 Exclusion Severe LSS intractible pain
Progressive neurologic dysfunction Mild LSS with clinical signs feeble enough to exclude surgical treatment Spondylolysis and spondylolytic disease Earlier back operation due to stenosis Herniated disc during last 12 months Another spinal disorder Intermittent claudication due to PVD Severe OA of L/E Neurologic disease with impaired function of L/E Psych Alcoholic

45 Malmivaara 2007 Randomization:
Central office computer generated blocks variable size for each hospital Physician phoned central office after baseline exam, questionnaire completed

46 Malmivaara 2007 Intervention Surgical group Segmental decompression
Facetectomy Instability treated at surgeon discretion Fusion of lumbar spine +/- instrumentation Degenerative listhesis warranting procedure Brochure for nature of disease, symptoms and activities Non-operative group Physiatrist followed throughout Physiotherapist followed Exercises

47 Malmivaara 2007 Walking ability Reported & measured
No significant difference between 2 groups

48 Malmivaara 2007 Conclusion Issues
Those undergoing surgery reported greater improvement over non-operative treatment Benefit diminished over time Issues Longer f/u needed Surgical treatment differed Selected bias from exclusion criteria Screened for those who may benefit from surgery

49 Weinstein 2008 SPORT Trial “Surgical versus Nonsurgical Therapy for Lumbar Spinal Stenosis” Inclusion 12 weeks of symptoms typical to stenosis Exclusion Spondylolithesis

50 Weinstein 2008 2 cohorts Outcomes A) randomization B) observational
Op vs non-op B) observational Elective op vs. elective non-op Outcomes Bodily pain and physical function SF-36 Modified Oswestry disability index 6 weeks, 3 months, 6 months, 1 year, 2 years

51 Weinstein 2008 Randomized cohort Interventions
En bloc at 13 institutions 289 patients Interventions Op: “Standard posterior decompressive laminectomy: Non Op: At least physical therapy, education or counseling NSAIDs if tolerated

52 Weinstein 2008 Results As-treated ITT
Significant advantage of operative management at 6 weeks, peaked at 6 months and lasted for 2 years Significant across all outcomes ITT Significant difference in pain scale favouring operative management No difference in physical function rating or Oswestry disability scale

53 Weinstein 2008 Issues: Significant cross-over:
“At 2 years, 67% of patients who were randomly assigned to surgery had undergone surgery, whereas 43% of those who were randomly assigned to receive nonsurgical care had also undergone surgery.” Excludes spondylolithesis Doesn’t tell us anything about to fuse or not to fuse

54 Claudication Spinal Stenosis Claudication and Spinal Stenosis Non-op
Educate, Analgesia, Exercise (Core, Aerobic), Physio, Lifestyle, Advise CES Cauda Equina Syndrome (Acute: Surgery as a P2, Chronic: Surgery Within Weeks) Leg Dominant Signif. Back Pain ? No Surgery Pt. Choice Medical Comorbidity Unsure of Diagnosis Willing to wait Progressive Weakness No Instability Instability No Instability (Surgery as P3 to Within Weeks) Degen. Spondylolisthesis, Lat. Listhesis, Scoliosis Posterior Decompression (Laminectomy, Foraminotomy) Epidural (Note: Facet Sparing, If No Fusion) Predictors of Good Surgical Outcome Relative Indication Assess Additional Fusion Levels Leg Dominant Pain Not Foraminal ? Degree of Stenosis ? # of Levels ? No scoliosis No WSIB / Disability No Blame No Hysteria No Comorbidity < 6 months pain Baseline fitness ? Surgery for pain as opposed to for neuro deficit Bone Scan, MRI, Discogram Fusion (All Decompressed Levels + ? Additional Levels) Non-instrumented, Instrumented (Pedicle Screws, TLIF, PLIF) From Spine rounds Civic Last Updated: Oct 18, 2007

55 Refs Atlas SJ, Delitto A. Spinal stenosis: surgical versus nonsurgical treatment. Clin Orthop Relat Res 2006; 443:198. Katz JN, Harris MB. Clinical practice. Lumbar spinal stenosis. N Engl J Med 2008; 358:818. Malmivaara A, Slätis P, Heliövaara M, et al. Surgical or nonoperative treatment for lumbar spinal stenosis? A randomized controlled trial. Spine 2007;32:1-8. Weinstein JN, Tosteson TD, Lurie JD, et al. Surgical versus nonsurgical therapy for lumbar spinal stenosis. N Engl J Med 2008;358:

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