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Electrodiagnostic Testing MAJ Min Ho Chang MD. Outline What is EDX? Anatomy & Physiology Nerve Injury Nerve Conduction Studies/Needle Exam Clinical Utility.

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Presentation on theme: "Electrodiagnostic Testing MAJ Min Ho Chang MD. Outline What is EDX? Anatomy & Physiology Nerve Injury Nerve Conduction Studies/Needle Exam Clinical Utility."— Presentation transcript:

1 Electrodiagnostic Testing MAJ Min Ho Chang MD

2 Outline What is EDX? Anatomy & Physiology Nerve Injury Nerve Conduction Studies/Needle Exam Clinical Utility

3 EMG and Nerve Conduction Studies An extension of the Physical Examination Assess physiology of nerve and muscle Quantitates nerve and/or muscle injury Real time data Provides Useful Data Regarding Nerve Injury – Diagnosis- Duration – Prognosis- Site – Treatment- Type – Further Testing- Severity

4 Anatomy & Physiology Motor Unit – Anterior Horn Cell – Axon – Terminal Branches – Neuromuscular Junction – Muscle Fibers

5 Epineurium Perineurium Endoneurium Myelin Axons


7 Action Potential

8 Nerve Fiber Classificaton Fiber Type FunctionDiameterConduction Velocity AαAα Proprioception, somatomotor, touch AβAβ Touch, pressure, extrafusal AγAγ Motor to muscle spindle AδAδ Pain (esp cold) B Preganglionic autonomic C Pain/temp/postganglionic autonomic/mechanoreceptor <1<2

9 NMJ Anatomy Synaptic cleft Acetylcholine Motor end plate

10 Electrochemical Conduction Acetylcholine – In presynaptic vesicles (Quanta=10000) – Exocytosis via Ca++ mediated pathway

11 Muscle Fibers

12 MUSCLE CONTRACTION Troponin-Tropomyosin complex Calcium Binding Excitation-Contraction Coupling

13 MUSCLE FIBER TYPES Type 1 – Slow Twitch – Small Cell Body – Thinner axon Type 2 – Fast Twitch – Larger Cell Body – Thicker Axon


15 NERVE INJURY Seddons Classification – Neurapraxia (Conduction Block) – Axonotmesis – Neurotmesis

16 Neurapraxia – Demyelination – Axon Intact – No Wallerian Degeneration – Action Potential slowed – Prognosis Good

17 Wallerian Degeneration

18 Axonotmesis – Axon disrupted – Connective Tissue (endoneurial/perineural) may or may not be intact. – Wallerian Degeneration DOES occur – Denervation – Prognosis depends

19 Neurotmesis – Axon and connective tissue disrupted – Complete severance of nerve – Surgical Repair – Poor prognosis

20 Mechanisms of Recovery – Remyelination – Collateral Sprouting – Regeneration

21 NERVE INJURY Collateral Sprouting


23 For Practical Purposes Demyelinating Injury – Neurapraxia (Conduction Block) – Diffuse Demyelination – Good prognosis Axonal Injury – Axonotmesis – Neurotmesis – Prognosis depends on length/severity


25 INSTRUMENTATION Electrodes – Active (Recording) G1, E1 Action Potential Electrical Noise – Reference G2, E2 No Action Potential Electrical Noise – Ground Excess Charge G2 G1 GROUND


27 3 Main AP measured Compound Motor Action Potential (CMAP) Sensory Nerve Action Potential (SNAP) Compound Nerve Action Potential (CNAP)

28 NCS Parameters Latency – determined by conduction velocity of the nerve, neuromuscular junction & muscle Amplitude – determined by number of muscle fibers activated Conduction velocity – determined by conduction velocity of the fastest fibers

29 Important Patterns Axonal Loss – Decreased amplitude – Maintain latency Demyelination – Prolonged latency Conduction Block – 50% drop in amplitude (variable)

30 Important Patterns Proximal Lesions (Radiculopathy) – Sensory Nerve Root Proximal to DRG Peripheral Axon Intact – Motor Nerve Root Distal to Anterior Horn Cell Axonal Degeneration Occurs



33 Needle EMG Parameter Spontaneous Muscle Membrane Electrical Activity Motor Unit Configuration Motor Unit Recruitment

34 Spontaneous Activity: – Electrical Waveforms not under voluntary control – Healthy muscle is normally electrically silent at rest

35 Abnormal Spontaneous Activity Fibrillation Potential (Fib) – Membrane Instability Denervation Myopathy Trauma Positive Sharp Wave (PSW) – Same significance as Fib

36 NEEDLE EMG: Spontaneous Activity

37 Motor Unit Analysis Morphology – Duration – Amplitude – Phases Stability Recruitment

38 Common Patterns Axonal Loss – PSWs and Fibs present – Decreased Recruitment – MUAP changes Increased Duration Polyphasia Increased Amplitude Demyelinating Lesion – NO PSWs and Fibs – No MUAP changes – Decreased Recruitment Myopathy

39 Common Patterns EMG and NCS changes evolve over time….. – Wallerian Degeneration 3-5 days for motor fibers 6-10 days for sensory fibers – Reinnervation

40 Evolution of NCS/EMG Changes Axonal Loss – <3 days old No Wallerian Degeneration DISTAL NCS normal!! No PSWs/Fibs Normal MUAPs Decreased Recruitment

41 Evolution of NCS/EMG Changes Axonal Loss: 1-6 weeks old – NCS: Decreased Amplitude Normal CV* Normal Latency* – EMG: Fibs/PSWs present Decreased Recruitment Normal MUAP

42 Evolution of NCS/EMG Changes Axonal Loss: Months- Years Later – NCS: Decreased Amplitude Normal CV* Normal Latency* – EMG: No Fibs/PSWs Decreased Recruitment MUAP – Long Duration – High Amplitude – Polyphasic

43 Evolution of NCS/EMG Changes Demyelination – NCS Decreased Conduction Velocity Prolonged Latency Variable changes in Amplitude – Normal EMG!! Conduction Block – NCS Decreased Amplitude Prolonged Latency – EMG Decreased Recruitment Normal MUAPs No PSWs/Fibs

44 Clinical Use Common Entrapment Syndrome Median at the Wrist (CTS) Ulnar at the Elbow Peroneal Palsy at the Fibular Head

45 Carpal Tunnel EDX Grading Simple Grading Scheme for median neuropathies at the wrist - Mild --> sensory latencies prolonged - Moderate --> motor latencies prolonged - Severe --> motor amplitude reduced and/or evidence of EMG abnormalities on EMG.

46 CTS Clinical Pearl By 6 months post-surgery, the maximum improvement in latencies will have occurred 1/2 of patients post surgery do not return to normal latencies Must compare to post-operative latencies to pre-op latenciec to determine an unsuccessful surgery If no preoperative latencies, wait another 3-6 months and assess the interval change

47 Tarsal Tunnel EMG: Footwear and trauma cause low level of spontaneous activity in foot muscles Controversial

48 Radiculopathy Can confirm the presence of a radiculopathy with or without findings on imaging studies EMG is not needed in all radic patients Most useful w/ multi-level pathology on MRI but inconclusive PE – Can help determine location of radiculopathy Multi-level radics present in 12-30% Excludes other possible diagnoses Can determine time course or severity of radiculopathy

49 NCS usually WNL in radics; abnormalities are found on needle EMG – SNAP is normal in lesions prox to DRG, and nearly all radics damage nv root proximal to DRG The NCS is done to r/o other conditions, specifically entrapment neuropathy and plexopathy

50 False positive rates on MRI are 10% (cervical) Radics can be seen without structural abnormalities on MRI Sensitivity ranges from 55-84% – Slightly lower compared to MRI – Sensitivity increases w/ neurologic abnormalities Specificity ranges upto 90-95% – Slightly higher than MRI

51 EMG Caveats Time Course in Radiculopathy – Acute phase: decreased MUAP recruitment but NML morphology – Day 10-14: + waves/fibs in paraspinals – Day 14-21: + waves/fibs in prox peripheral muscles – Day 21-28: + waves/fibs in distal peripheral muscles (up to 5-6 wks total time) – MUAP morphology is the same as denervation occurs, but polyphasia (also paraspinal prox distal muscles) heralds reinnervation (over the course of months, i.e. chronic radic)

52 Caveats Limitations of Needle EMG – May have NML EMG in acute phase – If only demyelination is present, EMG can be NML (only sig CB w/ weakness will give decreased MUAP recruitment (rare in radic)) – If sensory root is predominantly affected, EMG will be NML – Different fascicles may be more or less involved (i.e. some muscles of a particular myotome may be involved while others spared)

53 Caveats The double crush – Cervical radic (C6-C7) plus median neuropathy at the wrist – C8-T1 radic plus ulnar neuropathy at the elbow – Does not infer that radic predisposes to median neuropathy at the wrist

54 Peripheral Neuropathy

55 Plexopathy Compression (CABG) Inflammatory(Parsonage-Turner Syndrome) Radiation Injury (Radiotherapy) Traumatic Injury (Traction, laceration, missile) Ischemia(Diabetic amyotrophy)

56 Neurogenic Thoracic Outlet Syndrome Incidence 1:1,000,000 A partial lower trunk plexopathy or C8/T1 root injury Secondary to prominent C7 transverse process or prominent cervical rib Normal study focused on brachial plexus trunk essentially rules out

57 Other Pearls Electrodiagnostic studies are a supplement to, and not a replacement, for the history and physical examination Electrodiagnostic results are often time- dependent Electrodiagnostic studies are not standardized investigations and may be modified by the practitioner to answer the diagnostic question

58 EDX Testing

59 When to order EDX testing Neck/arm pain, back/leg pain, suspected CTS, peripheral neuropathy, weakness, wasting, cramps. Sort out these problems, establish etiology, assess severity, provide objective/prognostic information. Accurate diagnosis leads to effective treatment.

60 Typical diagnosis for consideration on EDX consultation Mononeuropathy Mononeuropathy Multiplex Radiculopathy Plexopathy (Brachial or Lumbosacral) Anterior Horn Cell Disorders Diffuse neuropathies Cranial neuropathies Neuromuscular Junction Disorders Myopathy Traumatic nerve injury – Intervention vs wait – Assess improvement – 18 month time frame

61 When Not to order EDX Central Nervous System Disorders (Stroke, TIA, Encephalopathy, spinal cord injury) Multiple Sclerosis Total body fatigue, fibromyalgia Joint pain EDX consult is not a substitute for PM&R/Neurology/Orthopedic etc…

62 Counseling Patients Inform the patient about the test and the reasons behind it. Give them heads up about what to expect. – Small gauge solid needle test portion – Electrical stimulation portion – Duration of test depends on findings but typically about 60minutes. – Not the most comfortable but tolerable for just about anyone. – Risks very small. Verbal consent only.

63 Reading EMG Reports Tailored to referring provider – Specific questions from ie Hand surgeon, spine surgeon – Fuzzier question, ie generalized weakness Two broad styles – Tabular or narrative – Most read final impression only Clinical Management usually deferred to referring provider Clinical vs Electro diagnostic impression An outline of the localization, severity, and acuity of the process Notation of other diagnoses that are detected/excluded Explanation of any technical problems

64 Summary: Utility of EMG/NCS Highly sensitive indicator of early nerve injury Detects dynamic and functional injury missed by MRI Provides information regarding chronicity of nerve injury Provides prognostic data Highly localizing Clarifies clinical scenarios when one disorder mimics another Identifies combined multi-site injury, avoiding missed diagnoses Identifies more global neuromuscular injury with focal onset Provides longitudinal data for charting course, response to therapy


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