Clinical Electrodiagnostics in the Diagnosis of Radiculopathy January 2021

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Clinical Electrodiagnostics in the Diagnosis of Radiculopathy January 2021 Clinical Electrodiagnostics in the Diagnosis of Radiculopathy January 2021 Jeremy Simon, MD Assistant Professor of Rehabilitation Medicine Sidney Kimmel Medical College of Thomas Jefferson University Division Chief, Department of Physical Medicine and Rehabilitation The Rothman Institute Outline Pathophysiology Nerve conduction studies Late responses Needle Electromyography Cases Rothman Institute of Orthopaedics at Thomas Jefferson University My Clinical Criteria for Diagnosing Radiculopathy Myotomal pain Dermatomal symptoms Physical exam findings Provocative Reflex changes/pathologic Gait/balance testing Rothman Institute of Orthopaedics at Thomas Jefferson University What Do I Use Electrodiagnostics For? Rule out other IN A CLEAR CUT conditions: RADICULOPATHY, I CTS DON’T BELIEVE THAT AIDP/CIDP EDX CONTRIBUTES TO Diabetic amyotrophy MANAGEMENT Peroneal Neuropathy Rothman Institute of Orthopaedics at Thomas Jefferson University Anatomy Rothman Institute of Orthopaedics at Thomas Jefferson University Pathophysiology Compressive Pathophysiology Compressive Pathophysiology (other) Idiopathic (autoimmune/microvascular?) Diabetic/Non‐Diabetic Lumbosacralradiculoplexopathy (Bruns‐Garland Syndrome) Neuralgic amyotrophy (Parsonage‐Turner Syndrome) Electrodiagnostics in Radiculopathies Nerve Conduction Studies Motor NCS Latency Conduction velocity Amplitude Dysmyelination/conduction block vs axonopathy Sensory Nerve Conductions Preganglionic sensory neurons Anterior disc horn cell Post‐ganglionic motor neurons L5-S1 Axial View Late Responses F‐Waves Motor‐motor,5% CMAP Dual innervation of Roots studied? muscle Frequently normal Sensory neurons not studied Slowing may not occur in the fibers tested, F waves in compressive obscured radiculopathy (Wilbourn)? Rothman Institute of Orthopaedics at Thomas Jefferson University H‐Reflex Sensory‐motor Like F‐wave, abnormal if any portion is affected in the pathway Mostly performed in the S1 pathway Can use amplitude ratio and/or latency side to side (<0.4 amplitude ratio symptomatic/non‐ symptomatic) (Jankus and Robinson 1994) Acute? Chronic? Old? Needle Electromyography Oldest/most established method of defining nerve root compromise (Johnson 1965) Assesses motor fibers only, majority of findings in axonal loss (Wilbourn 1988) Fibrillations/sharp waves in specific nerve root distribution with absence in other myotomes if axonal death is recent. Needle Electromyography Fibrillations/sharp waves: MOST sensitive indications of recent motor axon loss Motor unit action potential abnormalities may be minimal and not detectable (Wilbourn 1988, Dumitru 2002) Sensitivity 50‐71% (AANEM practice parameters 1999) Correlation with imaging and surgical findings 65‐85% (ibid) Needle EMG (Lumbosacral) Utility for : Peripheral limb EMG (Class II, Level B rec.) Paraspinal mapping (beyond scope, Class II Level B) H reflex for S1 (Class II and III, Level C) Low sensitivity for : F waves Cho et al Utility of edx testing in evaluating pts with ls radiculopathy: an evidence based review MuscNer 2010 Needle EMG Fibrillations occur in proximal to distal sequence in recent axonopathy Acute lesion: can take up to 5 to 6 weeks to develop fibrillations in the distal lower extremity muscles, usually seen in 3 weeks (Lambert 1971) Needle EMG Total myotomal involvement rare (Wilbourn 1998) Variable root innervation of muscles Root compromise often incomplete/minority of fibers affected Timing Irregular fibrillations and acuity (Wilbourn) Needle EMG • Earliest finding can be REDUCED RECRUITMENT PATTERN • “Chronic” polyphasic –what does it imply? • Old static lesions polys only; not an indicator of an active ongoing lesion (Wilbourn 1998) NORMAL NERVE CRUSH from DISK CRUSH > AXONAL DEATH AXONAL DEATH > SCHWANN CELL PROLIFERATION CALLED BAND of BUNGNER AXONAL REGENERATION after MORE AXONAL REGENERATION 6 MONTHS. SMALLER AXON & after 1 YEAR. FURTHER SHRINKAGE INCREASED INTERNODES DISTAL ENDONEURIAL TUBE DISTAL ENDONEURIAL > FIBROTIC INTRANEURAL NEUROTMESIS: = INTRANEURAL NEUROTMESIS ONLY REINNERVATION from REMAINING INTACT AXONS CRUSH from DISK AXON DEMYELINATED > RAPID REMYELINATION and RECOVERY Needle EMG • C5 and C6 radiculopathy – Difficult to distinguish, often grouped together – Difficult to make a distinction from upper trunk lesion – Rhomboids – C6 more common clinically (Dumitru 2002) • C7 radiculopathy – Most common cervical radiculopathy (Yoss 1957) – Easiest to localize; circumscribe lesion by normal C5/6 and C8/T1 innervatedmuscles and abnormalities in C7 distribution Needle EMG C8/T1 radiculopathy Significant myotomal overlap C8 more common clinically (C7‐T1 disc herniation) Lower trunk lesions may mimic Paraspinals helpful Medial antebrachial cutaneous response Needle EMG L2,3,4 radiculopathies Significant overlap Tibialis anterior Mostly proximal lower limb muscles therefore reinnervate sooner Diabetic amyotrophy? No reliable sensory NCS for evaluating L2‐4 Difficult to distinguish from plexopathy. Saphenous technically difficult Needle EMG • L5 radiculopathy – EMG findings – Normal superficial peroneal response…except if not (Levin K 1998) – CMAPs • S1/2 radiculopathy – Often lumped together, but S2 radiculopathy clinically rare – H-reflex – CMAP amplitude – Can be bilateral (Hasegawa 1996) – Location of DRG may be vulnerable (more medial in canal) Guidelines (NOT standards) EMG/NCS‐ What to test? • American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) guidelines, for radiculopathy screen, a “reasonable examination consists of”: • Cervical radiculopathy – A sensory and motor NCS (low threshold for examining ulnar and median) – An F wave to exclude polyneuropathy (optional) – A needle EMG screen: 6 upper limb muscles, including the paraspinals (marginal increase in sensitivity if 7) (Lauder TD 1996, Dillingham 1999, 2001, 2002) – Contralateral 1 or more muscles if abnormalites (optional) – At least 1 muscle innervated by C5, C6, C7, C8, T1 in symptomatic limb. What to study (guidelines)? Lumbar radiculopathy: One motor and sensory NCS F wave or H‐reflex to exclude polyneuropathy (optional) Needle EMG screen: 5 lower limb muscles including the paraspinals (adding one muscle marginally increases sensitivity). If s/p posterior lumbar surgery, can exclude paraspinals and 8 distal muscles optimal (Dillingham 2000, 2002) Pitfalls DRG location (Levin 1998) L5 up to 40% DRG in spinal canal Abnormalities in foot muscles Dysmyelation vs predominance of axonal pathology Timing/reinervation Overlap of innervation Prior spinal surgery/paraspinals Cases (names have been changed) 50 year old with pain radiating right posterior limb Lifting twisting injury 3 months ago pain worse w/sitting and flexion activities, can’t sit >20 mins “Can I return to work today?” Positive SLR and slump test on right 4/5 FHL, gastroc, TFL strength on right Decreased sensation to light touch in S1 dermatome right Absent right ankle jerk Why do it? Electrodiagnostic study Normal sensory and motor NCS Reduced right H‐reflex amplitude, normal left H‐reflex (ratio 0.2) Needle EMG: +1 fibs/sharp waves in the medial gastroc, TFL and lower lumbar paraspinals remainder normal. Clinical and Electrodiagnostic Impression There is clinical and electrodiagnostic evidence of SUBACUTE RIGHT S1 RADICULOPATHY as demonstrated by the fibrillations in the S1 innervated muscles. ‐‐‐does the H reflex abnormality say it’s a new problem? ‐‐‐what if sural response had reduced amplitude? REASONS FOR PROGNOSIS Seddon & Sunderland’s classification systems can be broadened to include the potential for an axonotmesis to evolve into an intraneural neurotmesis. PRE-CRUSH – 4 NORMAL INTERNODES (NEURAPRAXIA0 • pain radiating right posterior limb for 1 month • 3 previous work comp claims for back pain over 12 years, months of PT, anti- inflammatory meds, muscle relaxers, membrane stabilizers, oxycodone • MRI disc bulges at L4-5, L5- S1 • “I can’t go back to work! They don’t follow the restrictions you gave!” Rothman Institute of Orthopaedics at Thomas Jefferson University • Positive supine SLR right, negative slump and seated SLR • Decreased sensation to pin prick but not light touch in a non-dermatomal distribution – Why is that important? • Normal reflexes except +1 right ankle jerk • 5/5 strength left, poor effort right/give-way weakness • Why do the study? Electrodiagnostic study Normal sensory and motor NCS Prolonged right H‐reflex, normal left H‐reflex Needle EMG: polyphasic motor units of increased duration in the medial gastroc, TFL, remainder normal PRE-CRUSH – 4 NORMAL INTERNODES Clinical and Electrodiagnostic Impression There is electrodiagnostic evidence for an OLD (static) RIGHT S1 RADICULOPATHY. Clinically, this does not support the patient’s sensory symptoms involving the entire right lower extremity as well as the imaging findings. Bigg Hits‐ History • Professional football safety • Head-first tackle 4 weeks ago, immediate pain in neck and right arm • 4/5 strength in right deltoid, biceps, and triceps • Altered sensation in the 1st digit of left hand, reduced bicep reflex • MRI right C5-6 HNP Rothman Institute of Orthopaedics at Thomas Jefferson University Electrodiagnostic Study Normal median/ulnar CMAPs Normal median, ulnar, radial and lateral antebrachial cutaneous SNAPs Needle EMG: +2 fibrillations in the right deltoid, biceps and cervical paraspinals without polyphasia, remainder of study normal Clinical and Electrodiagnostic
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