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Faren H Williams, MD, MS Edward Calkins, M.D. Marci Jones, M.D. Anthony Howley, OTR/L, CHT

Peripheral Nerve Trauma: Electrodiagnostic Workup and Indications for Surgical Referral to Limit Pain and Disability. Faren H Williams, MD, MS Edward Calkins, M.D. Marci Jones, M.D. Anthony Howley, OTR/L, CHT U of Massachusetts Medical School.

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Faren H Williams, MD, MS Edward Calkins, M.D. Marci Jones, M.D. Anthony Howley, OTR/L, CHT

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  1. Peripheral Nerve Trauma: Electrodiagnostic Workup and Indications for Surgical Referral to Limit Pain and Disability Faren H Williams, MD, MS Edward Calkins, M.D. Marci Jones, M.D. Anthony Howley, OTR/L, CHT U of Massachusetts Medical School

  2. Peripheral nerve injuries:Electrodiagnostic Considerations Faren H. Williams, M.D., M.S. Chief and Clinical Professor Physical Medicine and Rehabilitation Dept of Orthopedics and Physical Rehabilitation University of Massachusetts

  3. Peripheral nerve injuries • 1167 peripheral nerve injuries – • 5.7% sports – 10% traumatic • Trauma – Falls, MVA’s, GSW’s • UPPER extremities – more mobile • 88% upper extremity

  4. Normal Nerve Faren H. Williams, M.D., M.S.

  5. Nerve Structure Faren H. Williams, M.D., M.S.

  6. Nerve Physiology Faren H. Williams, M.D., M.S.

  7. Peripheral Nerve Injury Faren H. Williams, M.D., M.S.

  8. Electrodiagnostic Testing • Information about Integrity of Anterior Horn Cell Dorsal (Sensory) Ganglion • NERVE • NEUROMUSCULAR JUNCTION • MUSCLE Faren H. Williams, M.D., M.S.

  9. Faren H. Williams, M.D., M.S.

  10. Nerve AnatomyAxon swelling/ Node of Ranvier Faren H. Williams, M.D., M.S.

  11. Overview NCS/ EMG • Sensory distal latency • Time required for nerve impulses to travel between • The stimulation and recording electrodes • Motor distal latency • Time required neuromuscular transmission • Initiation of Action Potential Faren H. Williams, M.D., M.S.

  12. Latency Changes over time

  13. Myelinopathies • Affects the myelin sheath • Intussusception of myelin –occludes • Nodal Gap • Latency slowing • Profound loss of myelin – • Associated Axonal loss

  14. Neural Intussesception

  15. Nerve AnatomySingle nerve fiber Faren H. Williams, M.D., M.S.

  16. Overview NCS/ EMG • Amplitude Measures of the number of nerve fibers conducting impulses from the stimulating to the recording points Relative conduction rates along those fibers Distance between muscle/nerve fibers and recording electrodes Faren H. Williams, M.D., M.S.

  17. Overview NCS/ EMG • Duration • Relative rates in conduction of fibers between • Stimulating & recording points • Prolonged vs. dispersed • Motor – duration of negative response Faren H. Williams, M.D., M.S.

  18. Early NCS’s • First week s/p injury • Allows for precise localization of the injury • Distal stump continues to conduct • Impaired conduction across site of major injury • Ability to localize lost after 1st week as • Distal stump ceases to conduct Faren H. Williams, M.D., M.S.

  19. Overview NCS/ EMG • Conduction block • Amplitude distal to the focal lesion is higher • % loss in amplitude – related to % of fibers/ axons lost • After 7-10 days – can’t localize • Day 1-2 – can’t differentiate axonal loss from demyelination • Latency is usually slowed across the lesion- • Secondary to demyelination Faren H. Williams, M.D., M.S.

  20. Amplitude changes over time

  21. Early NCSs • Lesion – electrophysiologically • Incomplete (Neuropraxia) or Complete • Incomplete lesions – MUAPs voluntarily controlled • Number of MUAPs less with more severe injury • Single MUAP indicates lesion is incomplete • Nerve trunk not disrupted • Better Prognosis Faren H. Williams, M.D., M.S.

  22. Ulnar Motor Inching Study

  23. Contralateral side • NCS’s imperative to determine degree of • AXONAL loss – If distal amplitude is same side: side Then lesion is neuropraxic If distal amplitude on affected side is 50% less then 50% axonal loss 50% conduction block – across lesion Faren H. Williams, M.D., M.S.

  24. Ulnar Inching

  25. NEEDLE EMG • RESTING MUSCLE is ELECTRICALLY SILENT • with Needle EMG Faren H. Williams, M.D., M.S.

  26. Overview NCS/ EMG • Needle EMG • Insertional activity • Injury potentials mechanically evoked by needle movement • Decreased when muscle atrophied, fatty, or fibrotic • Increased (muscle membrane activity >300ms) • Non-specific • Can be seen associated with denervation • No diagnosis made based on this finding alone Faren H. Williams, M.D., M.S.

  27. Abnormal potentials • Proximal muscles after 10-14 days • Distal muscles after 3-4 weeks Faren H. Williams, M.D., M.S.

  28. Abnormal Potentials Faren H. Williams, M.D., M.S.

  29. Needle EMG • Assists in localization • Allow sufficient time for Wallerian degeneration • Prognosis • Follow changes over time More sensitive for detecting motor loss than NCSs Complete lesion – no MUAPs Incomplete lesion – reduced recruitment (rapid firing)

  30. Faren H. Williams, M.D., M.S.

  31. NCS/ EMG Overview Faren H. Williams, M.D., M.S.

  32. Normal AVI Faren H. Williams, M.D., M.S.

  33. Needle EMG and NCSs • BOTH NEEDED for INTERPRETATION • NCSs -50% axonal loss, 50% conduction block • Need data from contralateral (normal) limb • 4+ fibs/ positive waves and no MUAPs Doesn’t correlate with percent of axonal loss • Represents neuropraxia and axonotmesis • Not complete axonal lesion Faren H. Williams, M.D., M.S.

  34. Neurotmesis • No motor or sensory potentials – over time • Axons and epineurium disrupted • MRI neurography – localization • Intraoperative electrodiagnosis • Surgical repair tenuous

  35. Nerve Regeneration • Depends on distance from nerve lesion to muscle • Type of Nerve Injury • Age of Patient • General Health of Patient/ Co-morbities Faren H. Williams, M.D., M.S.

  36. Overview NCS/ EMG • Motor Unit Analysis • Early reinnervation • MUAP’s – Increased polyphasicity and duration • Temporal dispersion • Poor synchronization of muscle fiber discharges • Later • Axonal sprouts mature – polyphasicity reduced • Late • High amplitude, long duration, occ polyphasic Faren H. Williams, M.D., M.S.

  37. Distal Wallerian DegenerationProximal Sprouting Faren H. Williams, M.D., M.S.

  38. Faren H. Williams, M.D., M.S.

  39. Regenerating Sprouts MatureRe-myelination Faren H. Williams, M.D., M.S.

  40. Polyphasic MUAPs Faren H. Williams, M.D., M.S.

  41. Overview EMG/ NCS • Polyphasicity – suggests reinnervation • MUAPs with >5 phases • Isolated finding – non-specific • Overreported, Overinterpreted • 20-30% polyphasic MUAPs - normal Faren H. Williams, M.D., M.S.

  42. Overview NCS/ EMG • Recruitment – helpful for prognosis • Reduction in lower motor neuron pool • Increased firing rate (fewer vs. more MUAPs) • Poor central effort • Effort, Pain inhibition, CNS problem • Non-diagnostic Faren H. Williams, M.D., M.S.

  43. Intrepretation/ Recommendations • Diagnosis – type of nerve injury/ Localization • Demyelination, Axonopathy, or both (mixed) Prognosis Recommendations- therapeutic regimen, medications Repeat study to follow/ monitor progress Surgical referral/ intervention Faren H. Williams, M.D., M.S.

  44. Patient Informatiion • History • Dominant arm • Motor, sensory, reflexes • Mechanism of injury • Timing s/p Injury Faren H. Williams, M.D., M.S.

  45. Peripheral nerve injury • Physical Examination • Strength • Sensation – dermatomal, peripheral • Reflexes – UMN, LMN • Contralateral limb • Muscle atrophy • Deformities, i.e. Claw hand

  46. Sensation – Ventral Arm

  47. Sensation – Dorsal Arm

  48. Case #1 • 25 y/o R HD male, with R humerusfx, s/p MVA 2 months prior to EDX study – brachial a. repair PE – triceps 3/5, B-R 2-/5, ECRL 2-/5, FDP to middle, ring and little fingers 2/5, FDP –index 0/5 FPL 0/5, APB ?tr, impaired sensation median n Faren H. Williams, M.D., M.S.

  49. R Median motor response, s/p MVA Faren H. Williams, M.D., M.S.

  50. Left median motor Faren H. Williams, M.D., M.S.

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