1. Nerve Injuries: PNS reaction & EMG findings §William McKinley MD §Associate Professor PM&R §Virginia Commonwealth University

2. Normal Nerve Anatomy §Axon §Myelin sheath with schwann cell l Nodes of Ranvier (more Na+ channels) l Internodal region §Connective tissue coverings l Endoneurium (surrounds nerve axon fibers) l Perineurium (surrounds fiber groups to form a fascicle) l Epineural (binds fascicles into nerves)

4. Pathophysiology of Nerve Injury §Ischemia & pressure will decrease intraneural flow §Ischemia: l 15-45 min causes neuropraxia (reversible) l > 8 hrs is NOT reversible §Stretch 5-10% leads to nerve elongation

5. Pathophysiology (cont) §Mechanical pressure leads to structural changes l largest fibers (motor, vib, proprioception) l peripheral fibers §Pressure: l pressure 30mmHg blocks venous bl flow l pressure 30-60mmHg blocks axonal transport l pressure 60-120mmHg blocks intraneural blood flow §Chronic pressure leads to perinodal demyelination

6. Demyelination §It is not uncommon for a disease process to preferentially injure the nerve’s myelin l Chronic ETOH, DM, lead, diptheria, porphyria §Damaged myelin is removed / replaced (Demyelination / re-myelination) §In profound demyelinating diseases, it is not uncommon to see secondary axonal injury

7. Axonal Injury §Wallarian degeneration - Secondary axon degeneration distal to site of injury §Also see some axonal degeneration proximally along with nerve cell body alterations due to edema and blocked axonal flow/transport

8. Nerve Regeneration §Distal portion of surviving axon begins to swell & sprouts “growth cone” (4-8 weeks) §Re-growth rates.5-5 mm/d (1 inch/mo) l small diameter, initially unmyelinated §Remyelination (proximal-distal, matures at 1 year) l slower cond velocity (more nodes of Ranvier)

9. Nerve Re-innervation §Endoneurial tube (ET) - re-innervation occurs thru ET to distal target site §Recovery plateaus 18-24 months §Physical separation of ET leads to poor prognosis l misdirection of nerve sprouting l less common with compression injuries §Muscle atrophy seen if not re-innervated by 1-1.5 yrs

11. Categories of Nerve Injury §1. Minimal - rapidly reversible conduction block, slowing of nerve conduction (primarily affects FF fibers) §2. Intermediate - focal demyelination w/o axonal damage, prolonged conduction block §3. Severe - Axonal damage with wallerian degeneration

12. Classification of Nerve Injury §Seddon’s Classification - based on amount of nerve injury l Neuropraxia (mild conduction block) l Axonotmesis (axon disruption with intact endoneurium) l Neurotmesis (axon disruption with loss of endoneurium)

13. Neuropraxia §“Conduction block” §no axonal degeneration §large myelinated fibers more susceptible to compression, ischemia (motor) l Nerve conduction is normal distally, but altered across “injury” site l Needle EMG shows decreased recruitment, but no abnormal spontaneous potentials l Normal Conduction returns in days/weeks (due to re-myelination of damaged segment)

14. Axonotmesis §Axon damage w/ preservation of endoneurium, perineurium & epineurium l Etiology - compression, traction §Wallerian Degeneration of axon l Motor NCS lost day 4-7 (NMJ fragmentation) l Sensory NCS lost day 8-10 §Preservation of endoneurium allows for regeneration with re-innervation l Recovery time dependent on distance for re- innervation

15. Neurotmesis §Disruption of axon, endoneurium & connective tissue (perineurium & epineurium) §Poor prognosis for re-innervation

16. Sunderland’s Classification of Nerve Injury §1.Conduction block (Seddon’s 1) §2.Axonotmesis (Seddon’s 2) §3. Loss of endoneurium §4.Loss of perineurium §5.Loss of epineurium

18. Electrodiagnostic Findings in Nerve injury (summary) §Neuropraxia (Np) l Decreased evoked potential (EP) with proximal stimulus l Normal EP distal l Decreased recruitment l No EMG abnormalities §Axonotmesis l Day 0-3: same as Np l Day 4-7: decreased motor amplitude l Day 8-10: decreased sensory amplitude l Day 10-14: abnormal spontaneous potentials on EMG (PSW, Fibs) l Month 6-12: “nascent pot’s (S>M) & “jitter”

19. Edx findings (cont) §Performing Edx too early may lead to misleading information (wait 2-4 weeks) §An early sign of axonotmesis is decreased CMAP amplitude l > 30-40% lower than contralateral side §Repeat in 2 weeks

20. Conduction Block §Focal site of demyelination §Decreased amplitude on proximal stimulation (normal distally) §On proximal stimulation: l decreased amplitude & decreased “area” (less fibers conducting, but speed preserved) l (consider axonal loss if amplitude decreased proximally AND distally)

21. “Mixed” Demyelinative/Axonal Injuries §“Common” to present in this way as opposed to “purely” one or the other §Criteria for predominant etiology: l Demyelination present if...: NCV 80% NCV < 70% (LLN) if Amplitude < 80% distal latency >125% if Amplitude > 80% distal latency >150% if Amplitude < 80% –(LLN = lower limits of normal)

23. Clinical Case §Axonotmesis l amplitude decreased l area decreased l duration decreased §Demyelination l amplitude decreased l area similar l duration increased