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Lumbar Spinal Stenosis

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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):

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