Transcript Nerve Injuries: PNS reaction & EMG findings

Nerve Injuries: PNS reaction &
EMG findings
 William McKinley MD
 Associate Professor PM&R
 Virginia Commonwealth University
Normal Nerve Anatomy
 Axon
 Myelin sheath with schwann cell
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Nodes of Ranvier (more Na+ channels)
Internodal region
 Connective tissue coverings
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Endoneurium (surrounds nerve axon fibers)
Perineurium (surrounds fiber groups to form a
fascicle)
Epineural (binds fascicles into nerves)
Pathophysiology of Nerve Injury
 Ischemia & pressure will decrease
intraneural flow
 Ischemia:
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15-45 min causes neuropraxia (reversible)
> 8 hrs is NOT reversible
 Stretch 5-10% leads to nerve elongation
Pathophysiology (cont)
 Mechanical pressure leads to structural
changes
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largest fibers (motor, vib, proprioception)
peripheral fibers
 Pressure:
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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
Demyelination
 It is not uncommon for a disease process to
preferentially injure the nerve’s myelin
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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
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
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)
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small diameter, initially unmyelinated
 Remyelination (proximal-distal, matures at
1 year)
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slower cond velocity (more nodes of Ranvier)
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
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misdirection of nerve sprouting
less common with compression injuries
 Muscle atrophy seen if not re-innervated by
1-1.5 yrs
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
Classification of Nerve Injury
 Seddon’s Classification - based on amount
of nerve injury
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Neuropraxia (mild conduction block)
Axonotmesis (axon disruption with intact
endoneurium)
Neurotmesis (axon disruption with loss of
endoneurium)
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)
Axonotmesis
 Axon damage w/ preservation of
endoneurium, perineurium & epineurium
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Etiology - compression, traction
 Wallerian Degeneration of axon
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Motor NCS lost day 4-7 (NMJ fragmentation)
Sensory NCS lost day 8-10
 Preservation of endoneurium allows for
regeneration with re-innervation
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Recovery time dependent on distance for reinnervation
Neurotmesis
 Disruption of axon, endoneurium &
connective tissue (perineurium &
epineurium)
 Poor prognosis for re-innervation
Sunderland’s Classification
of Nerve Injury
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1.
2.
3.
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5.
Conduction block (Seddon’s 1)
Axonotmesis (Seddon’s 2)
Loss of endoneurium
Loss of perineurium
Loss of epineurium
Electrodiagnostic Findings in
Nerve injury (summary)
 Neuropraxia (Np)
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Decreased evoked
potential (EP) with
proximal stimulus
Normal EP distal
Decreased recruitment
No EMG abnormalities
 Axonotmesis
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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”
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
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> 30-40% lower than contralateral side
 Repeat in 2 weeks
Conduction Block
 Focal site of demyelination
 Decreased amplitude on proximal
stimulation (normal distally)
 On proximal stimulation:
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decreased amplitude & decreased “area” (less
fibers conducting, but speed preserved)
(consider axonal loss if amplitude decreased
proximally AND distally)
“Mixed” Demyelinative/Axonal
Injuries
 “Common” to present in this way as
opposed to “purely” one or the other
 Criteria for predominant etiology:
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Demyelination present if...:
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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)
Clinical Case
 Axonotmesis
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amplitude decreased
area decreased
duration decreased
 Demyelination
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amplitude decreased
area similar
duration increased