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Nerve Injuries: PNS reaction & EMG findings
William McKinley MDAssociate Professor PM&R
Virginia Commonwealth University
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Normal Nerve Anatomy
AxonMyelin sheath with schwann cell
Nodes of Ranvier (more Na+ channels) Internodal region
Connective tissue coverings Endoneurium (surrounds nerve axon fibers) Perineurium (surrounds fiber groups to form a
fascicle) Epineural (binds fascicles into nerves)
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Pathophysiology of Nerve Injury
Ischemia & pressure will decrease intraneural flow
Ischemia: 15-45 min causes neuropraxia (reversible) > 8 hrs is NOT reversible
Stretch 5-10% leads to nerve elongation
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Pathophysiology (cont)Mechanical pressure leads to structural changes
largest fibers (motor, vib, proprioception) peripheral fibers
Pressure: pressure 30mmHg blocks venous bl flow pressure 30-60mmHg blocks axonal transport pressure 60-120mmHg blocks intraneural blood
flow
Chronic pressure leads to perinodal demyelination
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Demyelination
It is not uncommon for a disease process to preferentially injure the nerve’s myelin 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
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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
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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) small diameter, initially unmyelinated
Remyelination (proximal-distal, matures at 1 year) slower cond velocity (more nodes of Ranvier)
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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
misdirection of nerve sprouting less common with compression injuries
Muscle atrophy seen if not re-innervated by 1-1.5 yrs
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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
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Classification of Nerve Injury
Seddon’s Classification - based on amount of nerve injury Neuropraxia (mild conduction block) Axonotmesis (axon disruption with intact
endoneurium) Neurotmesis (axon disruption with loss of
endoneurium)
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Neuropraxia“Conduction block”no axonal degeneration large myelinated fibers more susceptible to
compression, ischemia (motor) Nerve conduction is normal distally, but altered
across “injury” site Needle EMG shows decreased recruitment, but
no abnormal spontaneous potentials Normal Conduction returns in days/weeks (due
to re-myelination of damaged segment)
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Axonotmesis
Axon damage w/ preservation of endoneurium, perineurium & epineurium Etiology - compression, traction
Wallerian Degeneration of axon Motor NCS lost day 4-7 (NMJ fragmentation) Sensory NCS lost day 8-10
Preservation of endoneurium allows for regeneration with re-innervation Recovery time dependent on distance for re-
innervation
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Neurotmesis
Disruption of axon, endoneurium & connective tissue (perineurium & epineurium)
Poor prognosis for re-innervation
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Sunderland’s Classificationof Nerve Injury
1. Conduction block (Seddon’s 1)2. Axonotmesis (Seddon’s 2)3. Loss of endoneurium4. Loss of perineurium5. Loss of epineurium
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Electrodiagnostic Findings in Nerve injury (summary)
Neuropraxia (Np) Decreased evoked
potential (EP) with proximal stimulus
Normal EP distal Decreased recruitment No EMG abnormalities
Axonotmesis Day 0-3: same as Np Day 4-7: decreased motor
amplitude Day 8-10: decreased
sensory amplitude Day 10-14: abnormal
spontaneous potentials on EMG (PSW, Fibs)
Month 6-12: “nascent pot’s (S>M) & “jitter”
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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 > 30-40% lower than contralateral side
Repeat in 2 weeks
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Conduction Block
Focal site of demyelinationDecreased amplitude on proximal stimulation
(normal distally)On proximal stimulation:
decreased amplitude & decreased “area” (less fibers conducting, but speed preserved)
(consider axonal loss if amplitude decreased proximally AND distally)
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“Mixed” Demyelinative/Axonal Injuries
“Common” to present in this way as opposed to “purely” one or the other
Criteria for predominant etiology: Demyelination present if...:
• NCV < 80% (LLN) if Amplitude > 80% • NCV < 70% (LLN) if Amplitude < 80%• distal latency >125% if Amplitude > 80%• distal latency >150% if Amplitude < 80%
– (LLN = lower limits of normal)
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Clinical Case
Axonotmesis amplitude decreased area decreased duration decreased
Demyelination amplitude decreased area similar duration increased
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