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

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

2. LUMBAR SPINAL STENOSIS Evidence Based Masterclass Eleanor Dunstan Spinal Physiotherapy ESP

3. 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

4. AGE CHANGES IN THE SPINE

5. ETIOLOGY

6. 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.

7. 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.

8. 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.

9. CASE HISTORY Subjective Examination 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 • 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.

10. 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.

11. 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.

12. 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

13. DIAGNOSTIC VALUES

14. 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.

15. DIFFERENTIAL DIAGNOSIS

16. Case Studies

17. CASE STUDY 1 Subjective Examination 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 • 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

18. CASE STUDY 2 Subjective Examination 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. • 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.

19. CASE STUDY 3 Subjective Examination 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. • 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.

20. 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.

21. EXAMINATIONCapillary Return

22. AORTIC PALPATION

23. PERIPHERAL PULSE CHECK

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

25. 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

26. 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. CASE STUDY 3

27. 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.

28. Diabetes damages the nervous system in 2 main ways: • High glucose levels causes biological change, resulting in nerve break down • High glucose levels damage the blood vessels that supply nerves with oxygen and nutrition, accelerating the neural break down.

29. 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)

30. CASE STUDY 2 Subjective Examination Objective 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. 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.

31. 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.

32. Symptoms Include: Tiredness Lethargy Paraesthesia's of extremities Ataxia Neurological Disturbance

33. CASE STUDY 1 Subjective Examination Objective 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 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

34. 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.

35. 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.

36. 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.

37. 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.