Chris Dowding Half Day Feb 16 2012 Slide 2 About 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 Slide 3 Slide 4 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 Slide 5 Spinal Stenosis 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
Slide 6 Neurogenic claudication Discomfort or pain that radiates
from the spinal area into the buttocks and frequently into thigh
and lower leg Slide 7 Slide 8 Pattern 1Pattern 2Pattern 3Pattern 4
RegionBack Leg Worse with:FlexionExtensionMovementExtension Relief
with: Fast:Extension Slow: Nil Usually flexion Fast: Posturing
Slow: Nil Flexion Timing: Constant or Intermittent
IntermittentConstantIntermittent Neuro:Normal PresentNormal
Generator: Degenerative disc; soft tissues Facet arthritis; soft
tissues Disc herniation Spinal stenosis Slide 9
Symptoms/FindingsNeurogenic Claudication Vascular Claudication
PainDermatomalMuscle grip Sensory LossDermatomalStocking Worse
with:Variable exercise, standing Fixed amount of exercise Relief
with rest:Slow, positionalImmediate Foot pallor
(elevation)NoneMarked PulsesNormalDecreased/absent Slide 10
Claudication Slide 11 Spinal Stenosis Narrowing of spinal canal due
to: Degenerative (most common) Developmental Congenital disorders
Post traumatic Steroids Post-surgical Certain disorders Slide 12
Narrowing is secondary to arthritis Typically following order Disc
degeneration Facet osteoarthritis Flavum hypertrophy Symptoms
develop around 60 yo Slide 13 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 Slide 14 Fibrocartilaginous Collagen, water,
Proteoglycans 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 Slide 15 Function 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. Slide 16 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 Slide 17 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 Slide 18 Loss of disc height
Infolding of flavum Increased stress across facets Facet OA and
hypertrophy Osteophytes and capsule thickening Cysts Slide 19 Slide
20 Spondylolithesis (+/- spondylolysis) Can result in stenosis Back
pain is primary symptom Neurogenic claudication is secondary Slide
21 Narrowing of canal due to growth disturbance of posterior
elements Congenitally short pedicles Often present in 20s Slide 22
Constellation of symptoms Leg pain Difficulty ambulating
Comfortable sitting Pain with prolonged walking Neurologic deficits
Slide 23 Age Pain 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? Slide 24 Night sweats Fever Weight loss Bowel/Bladder History
of cancer Immunosuppression Saddle anaesthesia Sexual dysfunction
Age > 60 History of IVDU Chronic infections Rest/night pain
Slide 25 Vitals Inspect Gait Leg length Trendelenburg test Spinal
alignment Palpate Spinous processes Paraspinal muscles Greater
trochanters Slide 26 ROM 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 Slide 27 Slide 28 Romberg maneuver Patient stands with
eyes closed Look for unsteadiness, wide based stance Indicates
damaged proprioception Slide 29 Lumbar x-rays +/- 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 Slide 30 Centrally Lateral recess & neural
foramina Degeneration of Disk Facets (hypertrophy) Synovial cysts
Joint capsule Thickening of ligamentum flavum Osteophytes Slide 31
Differential is broad Some non-spinal causes to keep in mind
Vascular claudication Hip arthritis Diabetes (peripheral
neuropathy) Slide 32 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 Slide 33
Groin pain Referred pain in thigh increased with activity Internal
rotation diminished XR - OA Slide 34 Glove & stocking
distribution Not affected by activity level Slide 35 Physical
therapy Abdominal strengthening Biking Brace/corset Slight lumbar
flexion Limit hours worn per day Avoid atrophy Pain pyramid Tylenol
NSAIDS Narcotics Slide 36 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 Slide 37
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 Slide 38
Progressive neurologic deficit Intractable pain Persistent
impairment and functional limitation Confirmation by imaging LBP is
not alleviated with surgery! Slide 39 Goals of surgery Decompress
central canal and neural foramina Options Laminectomy ** Partial
facetectomy ** Lumbar arthrodesis +/- Instrumentation Interspinous
distraction MIS Slide 40 Edward N. Hanley Jr., MD, Spinal Stenosis,
Charlotte Slide 41 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. 2000. Slide
42 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 Slide 43 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 Slide 44 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 Slide 45 Randomization:
Central office computer generated blocks variable size for each
hospital Physician phoned central office after baseline exam,
questionnaire completed Slide 46 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 Brochure for nature
of disease, symptoms and activities Slide 47 Walking ability
Reported & measured No significant difference between 2 groups
Slide 48 Conclusion 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 Slide 49 SPORT Trial Surgical versus Nonsurgical
Therapy for Lumbar Spinal Stenosis Inclusion 12 weeks of symptoms
typical to stenosis Exclusion Spondylolithesis Slide 50 2 cohorts
A) randomization 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 Slide 51 Randomized cohort 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 Slide 52 Results As-treated
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 Slide 53 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 Doesnt tell us anything about to fuse or not to
fuse Slide 54 Claudication and Spinal Stenosis Non-op Educate,
Analgesia, Exercise (Core, Aerobic), Physio, Lifestyle, Advise CES
Epidural Posterior Decompression (Laminectomy, Foraminotomy) Leg
DominantSignif. Back Pain No Instabilit y Instability Degen.
Spondylolisthesis, Lat. Listhesis, Scoliosis No Instabilit y Fusion
(All Decompressed Levels + ? Additional Levels) Non-instrumented,
Instrumented (Pedicle Screws, TLIF, PLIF) Pt. Choice Medical
Comorbidity Unsure of Diagnosis Willing to wait Assess Additional
Fusion Levels Bone Scan, MRI, Discogram Relative Indication
Claudication Spinal Stenosis From Spine rounds Civic Last Updated:
Oct 18, 2007 Predictors of Good Surgical Outcome 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 (Surgery as P3 to Within Weeks) (Note: Facet Sparing, If No
Fusion) Cauda Equina Syndrome (Acute: Surgery as a P2, Chronic:
Surgery Within Weeks) Progressive Weakness ? No Surger y Slide 55
1. Atlas SJ, Delitto A. Spinal stenosis: surgical versus
nonsurgical treatment. Clin Orthop Relat Res 2006; 443:198. 2. Katz
JN, Harris MB. Clinical practice. Lumbar spinal stenosis. N Engl J
Med 2008; 358:818. 3. Malmivaara A, Sltis P, Helivaara M, et al.
Surgical or nonoperative treatment for lumbar spinal stenosis? A
randomized controlled trial. Spine 2007;32:1-8. 4. Weinstein JN,
Tosteson TD, Lurie JD, et al. Surgical versus nonsurgical therapy
for lumbar spinal stenosis. N Engl J Med 2008;358:794-810.
