september 5 th – 8 th 2013 nottingham conference centre, united kingdom nspine.co.uk

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September 5 th – 8 th 2013 Nottingham Conference Centre, United Kingdom www.nspine.co.uk

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September 5 th – 8 th 2013 Nottingham Conference Centre, United Kingdom www.nspine.co.uk. LUMBAR SPINAL STENOSIS. Evidence Based Masterclass Eleanor Dunstan Spinal Physiotherapy ESP. LUMBAR SPINAL STENOSIS (LSS). - PowerPoint PPT Presentation

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Page 1: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

September 5th – 8th 2013Nottingham Conference Centre, United Kingdom

www.nspine.co.uk

Page 2: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

LUMBAR SPINAL STENOSIS

Evidence Based Masterclass

Eleanor DunstanSpinal Physiotherapy ESP

Page 3: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

LUMBAR SPINAL STENOSIS (LSS)

‘A clinical syndrome of buttock or lower extremity pain, which may occur with or

without back pain, associated with diminished space available for the neural and vascular

elements in the lumbar spine’

Watters 2008

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AGE CHANGES IN THE SPINE

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ETIOLOGY

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PATIENT PRESENTATION• Back pain, usually prolonged Hx

• Leg pain, (approx 90% of cases, Fritz 1998) unilateral or bilateral but of more recent onset.

• Neurogenic claudication (NC) - progressive weakness, tiredness or heaviness of the legs when walking. Evident in 62% of LSS, (Turner et al)

• Stooped posture

• Wide based gait

• Symptoms exacerbated with extension and relieved with flexion. Extension usually limited.

• Motor or sensory disturbance, 50% (Fritz et al) show objective signs.

Page 7: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

PATHOPHYSIOLOGY

• Lumbar extension reduces cross sectional area of central canal, and foramina reported as 20-67% in stenotic spine.

• Pressure is exerted on venules surrounding nerve fibers, leading to engorgement and ischemic nerve impairment, (Katz, 2008)

• Neurogenic claudication is thought to result from intermittent hypoxia resulting in ischemic nerve conduction failure and transient chemical and electrophysiological changes, (Adamova, 2003)

• The proposal of transient ischemia may account for symptom reversibility in spinal flexion when sitting or leaning forwards.

Page 8: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

IMAGING• MRI is the study of choice in

diagnosis of LSS - can visualise disc, soft tissue,bony change and intrathecal content.

• No image can diagnose stenosis without a corresponding clinical history.

• Imaging can appear worse than the symptoms suggest and doesn’t necessarily correlate with clinical findings.

• Boden et al, reported 21% prevelance of stenosis on MRI in asymptomatic individuals over 65.

Page 9: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

CASE HISTORY

Subjective Examination• 64 year old male.• R TKR, HTN• 20yr Hx LBP• 12mth Hx bilat L/L numbness,

knees-feet.• 6/12 Hx right leg pain.• Worse with walking/lifting• Min Sx when pushing trolley• Denies leg weakness / falls• Co-codamol 30/500, helps.

Objective Examination• Stooped posture, flat Lsp.• Full Lsp flexion, painful restricted

extension.• Alt LT sens right outer shin.• Normal power• +ve SLR right 60 degrees• AJ/KJ, P&E

Page 10: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

MRI RESULTS

a) L4/5 stenosis

b) Narrowed L4/5 neuroforamen, L4 NR comp.

c) Hypertrophic Facets, with intra-articular effusions and hypertrophy of lig flavum.

Page 11: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

DIAGNOSTIC UTILITY

• De Graaf et al, 2006, systematic review of diagnostic accuracy for LSS, (24 articles).

• Revealed considerable variation in clinical tests. Some showed high sensitivity others high specificity, but not both.

• Poor quality and incomparability of studies mean conclusions regarding diagnostic accuracy and utility could not be drawn.

Page 12: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

ANYONE NEED A REMINDER?

Sensitivity : True +ve rate• Proportion of patients with LSS who test positive.Specificity : True –ve rate• Proportion of patients without LSS who test

negative.

Likelihood Ratios: Expression of diagnostic usefulness+VE LR >5 Rules in diagnosis-VE LR <.30 Rules out diagnosis

Page 13: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

DIAGNOSTIC VALUESAx Sens Spec +ve LR -VE LR

MRI 77-87% 94-100% 8 .03

Ease sit 52% 83% 3.1 .58

Agg walk 71% 30% 1.0 .96

Trolley +ve 63% 67% 1.9 .55

Pain free flexion

79% 44% 1.4 .48

Leg pain extension

51% 69% 1.6 .71

Treadmill incline (Sx)

68% 83% 4.1 .93

Treadmill incline (recovery)

82% 68% 2.6 .26

Page 14: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

IN SUMMARY• Acquired degenerative stenosis is the most

common reason for spinal surgery in >65. (Deyo,2010)

• Pathophysiology surrounding phenomenon of NC is still unclear.

• Index of suspicion for LSS raised from multiple sources. No one gold standard test.

• MRI will rule in the diagnosis of LSS, but needs

careful clinical correlation to action appropriate management.

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DIFFERENTIAL DIAGNOSIS

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CASE STUDIES

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CASE STUDY 1

Subjective Examination• 67 year old lady.• Coeliac, T2 DM

(Metformin), HTN.• 18mth Hx painful

parasthesias both legs.• Limited walking distance

1/2mile- Pain in calf and feet- Fatigue

Objective Examination• Limited, painful Lsp ROM.• Normal power and sens.• Reflexes P&E, AJ/KJ• -VE SLR bilat• Wide BOS, slight ataxic gait

pattern.• UMN exam - NAD

Page 18: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

CASE STUDY 2

Subjective Examination• 75 year old lady.• T2 DM, HTN,AF, Hypothyroid

(Rx),CKD.• Bilateral Foot Pain 5yrs- Shooting / tingling- Worsening numbness- Pain / cramps at night- Neck pain, no LBP- Diclofenac /Co-codamol,

unable to tolerate pregabalin.

Objective Examination• Normal Csp ROM, no pain.• Alt sens LT/PP, buttocks,

thighs, calf and feet bilat.• No weakness• Absent AJ’s bilaterally• Normal Csp XR• Normal routine bloods.

Page 19: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

CASE STUDY 3

Subjective Examination• 70 year old male.• IHD, HTN, Prostate CA,

Smoker, Obesity.• 6/12 Hx bilat thigh and calf

pain.- Cramping pain with walking.- Intermittent calf numbness.- Tired, heavy legs.- Cold feet.• No help with analgesia.

Objective Examination• Limited and painful Lsp mvt.• Normal Sens and power.• -VE SLR• P&E, AJ/KJ• Discolouration right foot,

slow capillary refill.• Normal / equal dorsalis

pedis pulses.

Page 20: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

PERIPHERAL ARTERY DISEASE (PAD)

• Atherosclerosis leads to arterial insufficiencies and intermittent ischemia, vascular claudication.

• Symptoms: cramping/ache in posterior leg muscles. Occurs with exercise, subsides with rest.

• Blockages may be in the abdomen, pelvis, groin, thigh and/or calf.

• Associated CVS risk factors.

Page 21: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

EXAMINATIONCapillary Return

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AORTIC PALPATION

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PERIPHERAL PULSE CHECK

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DIAGNOSIS

• Pulses• Ankle–brachial index (ABI)• Doppler Ultra Sound• CT angiography• MR angiography• Angiogram

Page 25: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

VASCULAR V NEUROGENIC CLAUDICATION

• Leg pain with walking – NOT alleviated with sitting / stooping.

• Leg pain with cycling – NOT with LSS

• Stairs elicit pain – Only coming downstairs with LSS

• Symptoms in posterior leg muscles.

• CV History

Page 26: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

CASE STUDY 3

Subjective Examination• 70 year old male.• IHD, HTN, Prostate CA,

Smoker, Obesity.• 6/12 Hx bilat thigh and calf

pain.- Cramping pain with walking.- Intermittent calf numbness.- Tired, heavy legs.- Cold feet.• No help with analgesia.

Objective Examination• Limited and painful Lsp mvt.• Normal Sens and power.• -VE SLR• P&E, AJ/KJ• Discolouration right foot,

slow capillary refill.• Normal / equal dorsalis

pedis pulses.

Page 27: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

DIABETIC POLYNEUROPATHY (DPN)• Prevalence: 66% Type I, 59% Type II

• Pathogenisis: metabolic and vascular- Poor glucose control +/or duration- Associated with modifiable CVS risk factors

• Clinical manifestations mostly sensory. Length related distribution, toes and feet most affected.

• Significant distal weakness is uncommon.

• AJ reflexes absent.

Page 28: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

Diabetes damages the nervous system in 2 main ways:

1. High glucose levels causes biological change, resulting in nerve break down

2. High glucose levels damage the blood vessels that supply nerves with oxygen and nutrition, accelerating the neural break down.

Page 29: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

LSS V DPN

• Clinical history and note of other sensory sx

• Presence of retinopathy / nephropathy.

• Use of vibration/monofilament sensory examination.

• Nerve conduction studies: Electophysiological examination contributes to the differential diagnostics between LSS and DPN (Adamova, 2003)

Page 30: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

CASE STUDY 2

Subjective Examination• 75 year old lady.• T2 DM, HTN,AF, Hypothyroid

(Rx),CKD.• Bilateral Foot Pain 5yrs- Shooting / tingling- Worsening numbness- Pain / cramps at night- Neck pain, no LBP- Diclofenac /Co-codamol,

unable to tolerate pregabalin.

Objective Examination• Normal Csp ROM, no pain.• Alt sens LT/PP, buttocks,

thighs, calf and feet bilat.• No weakness• Absent AJ’s bilaterally• Normal Csp XR• Normal routine bloods.

Page 31: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

VITAMIN B12 DEFICIENCY

• B12 works with folate in the synthesis of DNA and RBC

• Involved in production of myelin sheath and conduction of nerve impulses.

• Dietry source is from animal products.

• Pernicious Anaemia – autoimmune condition affecting 1:10,000.

• Can mimic symptoms of stenosis and occur as a dual pathology.

Page 32: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

Symptoms Include:

•Tiredness•Lethargy•Paraesthesia's of extremities•Ataxia•Neurological Disturbance

Page 33: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

CASE STUDY 1

Subjective Examination• 67 year old lady.• Coeliac, T2 DM

(Metformin), HTN.• 18mth Hx painful

parasthesias both legs.• Limited walking distance

1/2mile- Pain in calf and feet- Fatigue

Objective Examination• Limited, painful Lsp ROM.• Normal power and sens.• Reflexes P&E, AJ/KJ• -VE SLR bilat• Wide BOS, slight ataxic gait

pattern.• UMN exam - NAD

Page 34: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

CONSIDER

• Retrospective study of 457 spinal out-patients, 8.5% were B12 deficient.(Patel, Rasul & Sell, 2011)

• Literature suggest as common as 1:10 >75yrs

• Detection of deficiency with consequent treatment results in better outcomes.

• Conclude that in older, stenotic population, with sensory symptoms B12 deficiency should be considered.

Page 35: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

IN SUMMARY

• Even if LSS has been confirmed via MRI, other conditions may co-exist.

• Careful questioning and examination should aim rule out other possible pathologies.

• Further diagnostics may be required to confirm suspicions.

• Successful treatment outcome depends on correct differential diagnosis.

Page 36: September 5 th  – 8 th  2013 Nottingham Conference Centre, United Kingdom nspine.co.uk

REFERENCES

• Adamova B, Vohanka S, Dusek L. Differential diagnostics in patients with mild lumbar spinal stenosis: the contributions and limits of various tests. Eur Spine J, 2003 12:190-196.

• Anekstein Y, Smorgick Y, Lotan R et al. Diabetes Mellitus as a risk factor for the development of lumbar spinal stenosis. IMAJ 2010;12:16-20.

• Agency for Healthcare Research and Quality. Treatment of Degenerative Lumbar Spinal Stenosis. Summary, Evidence report/technology assesment:number 32. AHRQ Publication No. 01-E047, March 2001.

• Barz T, Melloh M, Staub L et al. The diagnostic value of a treadmill test in predicting lumbar spinal stenosis. Eur Spine J 2008;17:686-690.

• Boden S, Davies DO, Dina TS et al. Abnormal magnetic resonance scans of the lumbar spine in asymptomatic subjects. A positive investigation. J Bone J Surg Am 1990;72:403-408.

• Deyo RA, Mirza SK, Martin BL et al. Trends, major medical complications, and charges associated with surgery for lumbar spinal stenosis in older adults. JAMA 2010;303(13):1259-65.

• Fritz JM, Delitto A, Welch WC et al. Lumbar spinal stenosis: a review of current concepts in evaluation, management and outcome measurements. Arch Phys Med Rehabil 1998: 79;700-708.

• Goldman SM. Diabetis peripheral neuropathy and spinal stenosis: prevalence of overlap and misdiagnosis. An introductory report. Diabetic Medicine 2004;21:393-399.

• Graaf I, Prak A, Zeinstra S et al. Diagnosis of lumbar spinal stenosis. Spine 2006;31(10):1168-1176.• Jeon CH, Han SH, Chung NS et al. The validity of ankle-brachial index for the differential diagnosis of peripheral arterial

disease and lumbar spinal stenosis in patients with atypical claudication. Eur Spine J 2011;22:PMID: 22105308.• Kazt JN, Dalgas M, Stucki G et al. Diagnosis of lumbar spinal stenosis. Rheum Disease clinics of North Amer 1994;20(2):309-

529.• Katz JN, Harris MB. Lumbar Spinal Stenosis. N Engl J Med 2008;358:818-25.• Lotan R, Oron A, Anekstein Y et al. Lumbar stenosis and systemic diseases: is there any relevance? J Spinal Disord Tech

2008;21(4):247-251.

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REFERENCES

• Patel MS, Rasul Z, Sell P. Dual pathology as a result of spinal stenosis and vitamin B12 deficiency. Eur Spine J 2011;20:2247-2251.

• Richmond BJ, Ghodadra T. Imaging of spinal stenosis. Phys Med Rehabil Clin N Am 2003;14:41-56.• Sugioka T, Hayashino Y, Konno S et al. Predictive value of self-reported patient information for the identification of lumbar

spinal stenosis. Family Practice 2008;237-244.• Szpalski M, Gunzburg R. Lumbar spinal stenosis in the elderly:an overview. Eur Spine J 2003;12:88-93.• Turner JA, Ersek M, Herron L et al. Surgery for lumbar spinal stenosis: An attempted meta-analysis of the literature. Spine

1992;17:1-8.• Watters WC, Baisden J, Gilbert TJ et al. Degenerative lumbar spinal stenosis:an evidence-based clinical guideline for the

diagnosis and treatment of degenerative lumbar spinal stenosis. Spine J 2008;8(2):305-10.