1. Lumbar Spinal Stenosis
Diagnosis and Management:
A 30 year legend
Philip R. Weinstein, MD
UCSF Dept. of Neurosurgery
San Francisco, California

2. My Legends
Brain WR, Wilkinson M, eds. Cervical Spondylosis and other Disorders of the Cervical Spine, Phila. Saunders, 1967
Wilson, CB: Significance of the small Lumbar Spinal Canal: Cauda Equina Compression Syndromes due to Spondylosis. III. Intermittent Claudication J Neurosurg 31 :499, 1969
Lord Russell Brain and Marcia Wilkinson

3. Classic case: 74 yo male; postural + ambulation claudication, bilat
Classic case: 74 yo male; postural + ambulation claudication, bilat. footdrop, calf/thigh atrophy, incontinence

4. Why so mysterious?
Lumbar spondylostenosis, one of the most common neuro-spinal disorders, was not regularly recognized and treated until The diagnosis was not considered as an alternative to disc, infection or tumor because:
Stenosis not described/identified
Spondylosis not appreciated/visualized
Postural radiculopathy not understood
Atypical leg pain not interpreted
Neurogenic claudication not defined/explained
Cauda equina syndrome not diagnosed
Role of associated LBP/deformity not appreciated

5. Why has treatment been unsuccessful (20-40%)?
Clinical history/diagnosis not appreciated
Anatomy/imaging misinterpreted
Surgical plan incomplete or excessive
Surgical decompression inadequate
Fusion/fixation omitted/incomplete
Post-operative instability; ASD
Neuropathic radiculopathy
Progressive disc/facet DJD, spondy, scolio
Recurrent/progressive stenosis
Co-morbidities

6. Books on Lumbar Stenosis
Neurogenic Intermittent Claudication, Verbiest H, 1976, Elsevier
Lumbar Spondylosis, Weinstein P, et al,
1977, Year Book Medical
Cheirolumbar Dysostosis,
Wachenheim A, et al, 1980, Springer
Lumbar Spinal Stenosis,
Postacchini F, et al, 1989, Springer
Lumbar Spinal Stenosis, Andersson GBJ,
et al, 1992, Mosby-Year Book
Lumbar Spinal Stenosis, Gunzberg R, et al,
2000, Lippincott-Williams&Wilkins

7. Evolution of a Concept: 1911-’25-’60 Spondylotic Caudal Radiculopathy (SCR)
Bailey P, Casamajor L, Osteoarthritis of the Spine as a Cause of Compression of the Spinal cord and its roots: With report of five cases, J. Nerv. and Mental Dis. 38:588, 1911
Parker JL, Adson AW, Compression of the Spinal Cord and its roots and hypertrophic Osteoarthritis, Surg. Gynec. Obstet. 41:1, 1925

8. Pioneering Intra-operative Measurements: Define the Syndrome Confirm the Diagnosis
Verbiest H, Further experiences on the Pathological influence of a Developmental narrowness of the bony Lumbar Vertebral canal, J. Bone Joint Surg. 37B:576, 1955
Classification of Pure, Relative and Mixed types
Unable to publish in NS journals in English or from 1940’s until 1955
Van Gelderen (collaborator) published 3 cases with postural claudication in 1948 in a Scandinavian J. (not Dutch)

9. Developmental Variations/Stenosis Documented in Normal Sized Cadavers
Epstein BS, Epstein JA, Lavine L, The Effect of Anatomic variations of the Lumbar vertebra and Spinal canal on Cauda equina nerve root syndromes, Am. J. Roentgenol. Radium Ther. Nucl. Med. 91:105, 1964

10. Vertebral Embryology
Unique paired growth centers for neural arch; vertebral body centers unite at 9 weeks
Premature arrest only dorsally in LS;
both arch and body in dwarfism
Conus reaches L2; 22 weeks gestation
Most rapid canal growth; weeks
L3-4 canal 80% at birth; 100%-1year; stops
L5 canal 50% at birth; 100%-5years
Canal deficiency: birth age/weight, mater. age
L5 trefoil canal: 15-25%
Papp T, et al, JBJS 1995, 77B:
Angevine JB, Clin. NS 1973, 20:95-113

11. Dwarfism

12. Familial Cases Developmental non-dwarf (2 brothers and a sister)
Postacchini F, et al, JBJS 67A:321, 1985

13. Incidence of Lumbar Stenosis in radiculopathy cases
Primary stenosis 2%
Primary disc
31%
Primary degenerative
28%
Combined
39%
N=227
Paine K, Haung P, Lumbar Disc Syndrome JNS 37:75, 1972

14. Imaging Pearls for the Diagnostic Necklace
Thin section axials; no skipped levels
Compare disc vs mid-body sections
View images; beware report omissions/LRS
Sagittals for foraminal height/lat. osteophytes
Sagittals for disc height, spondylolisthesis
Coronals for scoliosis/foramen stenosis
Add CT to MRI for bone detail/facet tropism
CT myelo for postop cases/instrumented fusions
3D CT to rule out pseudarthrosis
IV contrast CT for foraminal root constriction Radiculogram for foraminal fibrosis (TFESI)
Flexion-extension MRI for borderline cases
Intraop fluoro-CT useful for complex stenosis/deformity

15. Quantification of stenosis correlates with symptoms
Mean L4-5 canal area by CTM in extension in normals = 145mm2 (range )
Myelographic block occurs = 40mm2
Transverse canal diameter below 11mm is symptomatic
Lateral recess height 2-4mm is symptomatic
Jonsson B et al, Spine, 1997, 22(24)
AP canal diam. L1-2 to L5-S1 N=105. Measured # of sites <10mm. And width at narrowest level.
No correlation with sx and signs, duration, severity
Wilmink JT et al, Neuroradiology,
1988,3:
Wilmink JT, AJNR,
1989,26:

16. Radiographic-Clinical Correlation: Limitations of Measurements
Asymptomatic abnormalities seen
Magnification is variable
Imaging window, slice thickness, scan angle, alter bone/soft tissue measurements
Flex-ext. changes relationships
Ca on MR; CSF on CT not well visualized

17. Mechanisms of neurogenic claudication: compression, ischemia or both
83yo male with L4-5 spondy II and stenosis 5yr. hx of leg pain during 1block walk relieved by standing
At autopsy: radicular arteries straightened veins compressed, neuronal loss, empty axons, demyelinization, arachnoid fibrosis, adjacent AV coiling-anastomosis
Ischemic, compressed, large fiber depleted roots fibrotic roots are more sensitive to metabolic deprivation induced by increased activity and axonal firing and aggravated by CSF depletion which normally supplies 58% of nutrition (Rydevik,1984 in pigs).
Hyper-sensitive roots have reduced function during rest and are activated by discharge causing pain and paresthesias when AV shunts and coils proximal and distal to compression sites dilate. Ectopic discharges generated causing pain, paresthesias and cramps with increased blood flow that subside when activity decreases.
Watanabe R, Parke W, JNS 64:64-70, 1986

18. Problems in Patient Selection and Surgical Planning
Patient age/co-morbidities
Previous surgery
Unilateral or bilateral decompression
“Asymptomatic” levels
MIS vs open
Disc “herniation”
Disc collapse/foramen stenosis
Spondylolisthesis/scoliosis/kyphosis
“Back pain” without instability (arthrogenic vs radicular)
Fusion: instrumented/PSF vs interbody fusion

19. What do Evidence-based Guidelines Tell Us?
Surgery resulted in better improvement in pain and function than non-operative rx for stenosis/deg. 2yrs. 17% crossover to surg.
Weinstein JN, (SPORT STUDY) NEJM, 2007;356(22):
Surgery better for leg pain and back related function but equal to non-op rx for pt. satisfaction, back pain and primary sx 39% non-ops had surg.
23% reops.
Atlas SJ, (MAINE STUDY) Spine, 2005;30(8):936-43
N= SF36, ODI. Lam +/- fusion. 17% crossover to surgery; 3% to non-op. No adverse effects of either group.
Rx decision shared by pt. and MD. Most had lam. 23% 10yrs in surg. pts. 39% of non-ops had surgery.
BP better in 53 vs 50%. Primary sx better in 54 vs 42%: surg vs non-op. 105/148 alive.

20. Clinical Trial Results
Unilat Laminotomy for Bilateral Microdecompr: 520 levels/374pts
88% improved VAS/Prolo scale 5yr f/u
0.8% instability: none reoperated
Costa F etal.
JNS-Spine 2007;7(6):