Lumbar Spinal Stenosis

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This article relates to degenerative lumbar spinal stenosis, rather than congenital lumbar spinal stenosis. Degenerative lumbar stenosis first starts with disc height loss, that then results in bulging of the anulus fibrosus and ligamentum flavum into the spinal canal. These changes alter the loading of the facet joints, which leads to facet joint osteophytosis. The anteroposterior diameter of the canal is reduced by the bulging annulus anteriorly, and the hypertrophic facet joints posteriorly. Typically, the L4-L5 level is maximally constricted in the condition.


  • Obesity: odds ratio of >2. There are obesity related metabolic pathways that increase the risk of facet joint degenerative changes, disc degeneration, and ligamentous hypertrophy, all of which can contribute to stenosis. Being underweight is protective.[1]
  • Increasing age
  • Progressive disc degeneration from aging, trauma, or other factors. Disc height loss leads to increasing loading of the facet joints which can lead to hypertrophy.
  • Spondylolisthesis
  • Postoperative fibrosis
  • Skeletal disease
  • Epidural lipomatosis
  • Family history


Pain is thought to arise from mechanical compression and ischaemia. Unlike with lumbar radicular pain, inflammation is not usually thought to play a prominent role.

Pain tends to be exacerbated by the standing extended position. In this position there is a reduction in the lumbar canal space. This is because of the reduction in interlaminar spacing which results in overlap of the laminae and buckling inward of the ligamentum flavum and supero-anterior translation of the superior articular processes. With walking there may be increased metabolic demand on the spinal nerve roots and a resulting mismatch of demand vs supply.

Clinical Features

The cluster of Cook are features on history to determine the probability of lumbar spinal stenosis.[2] The features on history are 1) bilateral symptoms; 2) leg pain more than back pain; 3) pain during walking/standing; 4) pain relief upon sitting; and 5) age>48 years. Having no findings has a sensitivity of 96%, with a negative likelihood ratio of 0.19. Having four of five findings has a sensitivity of 6%, and specificity of 98%, with a positive likelihood ratio of 4.6. Three of five findings had a higher sensitivity, but a lower LR+ of 2.5.

Diagnostic value of the history and physical examination.[3]
Test Name LR+ LR- Sens Spec Kappa
Wide-based gait 14 0.6 43% 97%
Urinary disturbance 7.0 0.9 14% 98%
No pain when seated 6.6 0.6 46% 93%
Improvement when bending forward 6.5 0.5 52% 92%
Numbness of perineal region 5.0 1.0 5% 99%
Abnormal Romberg test 4.3 0.7 39% 91%
Neurogenic claudication 3.7 0.2 82% 78%
Symptoms improve when seated 3.1 0.6 52% 83%
Vibration deficit 1st metatarsal head 2.8 0.6 53% 81%
Pinprick deficit foot or calf 2.5 0.7 47% 81%
Age > 65 yrs 2.5 0.3 77% 69%
Weakness 2.1 0.7 47% 78%
Absent Achilles reflex 2.1 0.7 46% 78%
Bilateral plantar numbness 2.1 0.8 27% 87%
Severe lower-extremity pain 2.0 0.5 65% 67%
Thigh pain w/ 30 sec lumbar extension 1.6 0.7 51% 69%
Pain below knees 1.5 0.7 56% 63%
Numbness 1.5 0.6 63% 59%
Poor balance 1.5 0.6 70% 53%
No pain with flexion 1.4 0.5 79% 44%
Pain below buttocks 1.3 0.4 88% 34%
Worse when walking 1.0 1.0 71% 30%


Injections: epidural corticosteroid injection (interlaminar or transforaminal) with lidocaine is not more effective than lidocaine alone in lumbar spinal stenosis.[4]

Surgery: Decompression without fusion is usually preferred over more complex surgical procedures in the absence of instability. The benefits of surgery decline over time. There is a high rate of repeat operation due to recurrence or adjacent segment disease (15-25%)

Surgery can still be successful in obese patients but it is associated with poorer outcomes.[5] Obese patients also tend to maintain or gain weight following successful lumbar spinal stenosis surgery. In other words obesity is an independent disease not related to reduced exercise capacity from spinal stenosis.[6]



  1. Knutsson, Björn; Sandén, Bengt; Sjödén, Göran; Järvholm, Bengt; Michaëlsson, Karl (2015-09-15). "Body Mass Index and Risk for Clinical Lumbar Spinal Stenosis: A Cohort Study". Spine (in English). 40 (18): 1451–1456. doi:10.1097/BRS.0000000000001038. ISSN 0362-2436.
  2. Cook et al.. The clinical value of a cluster of patient history and observational findings as a diagnostic support tool for lumbar spine stenosis. Physiotherapy research international : the journal for researchers and clinicians in physical therapy 2011. 16:170-8. PMID: 21077266. DOI.
  3. Katz et al.. Degenerative lumbar spinal stenosis. Diagnostic value of the history and physical examination. Arthritis and rheumatism 1995. 38:1236-41. PMID: 7575718. DOI.
  4. Friedly, Janna L.; Comstock, Bryan A.; Turner, Judith A.; Heagerty, Patrick J.; Deyo, Richard A.; Sullivan, Sean D.; Bauer, Zoya; Bresnahan, Brian W.; Avins, Andrew L.; Nedeljkovic, Srdjan S.; Nerenz, David R. (2014-07-03). "A randomized trial of epidural glucocorticoid injections for spinal stenosis". The New England Journal of Medicine. 371 (1): 11–21. doi:10.1056/NEJMoa1313265. ISSN 1533-4406. PMID 24988555.
  5. Knutsson B, Michaëlsson K, Sandén B. Obesity is associated with inferior results after surgery for lumbar spinal stenosis: a study of 2633 patients from the Swedish spine register. Spine (Phila Pa 1976). 2013 Mar 1;38(5):435-41. doi: 10.1097/BRS.0b013e318270b243. Erratum in: Spine (Phila Pa 1976). 2015 Dec;40(24):E1348. PMID: 22941097.
  6. Garcia RM, Messerschmitt PJ, Furey CG, Bohlman HH, Cassinelli EH. Weight loss in overweight and obese patients following successful lumbar decompression. J Bone Joint Surg Am. 2008 Apr;90(4):742-7. doi: 10.2106/JBJS.G.00724. PMID: 18381310.

Literature Review