Electrodiagnosis of Peripheral Nerve Injury

Electrodiagnosis of Peripheral Nerve Injury There are two possible electrophysiological consequences of a peripheral nerve injury:  1) Conduction Block and 2) Axonal Loss with secondary Wallerian Degeneration)

  • Conduction Block – Normally, the AP is generated by sufficient temporal and spatial summation of excitatory inputs to motor or sensory axons. Blocking of transmission of the generated AP is the basis of conduction block, which usually is the result of segmental demyelination but may also occur with axonal loss before wallerian degeneration has occurred.
  • Wallerian Degeneration  –  is the process of degeneration of the axon distal to a site of trauma. Macrophages enter the area and begin to remove axonal and myelin debris. Denervation atrophy of muscles occurs.

Wallerian Degeneration

  1. Normal nerve innervating skeletal muscle. The blue lines indicate the basement membrane.
  2. The nerve has been transected and Wallerian degeneration has begun. There is corresponding atrophy in the muscle
  3. Proximal nerve terminals send sprouts toward the Schwann cell tubes.
  4. Some of the sprouts make it into tubes and reinnervate the muscle, which has undergone neurogenic rearrangement

Role of EDX in PNS injuries

  • Localize injury
  • Determine pathophysiology (axonal/demyelinating)
  • Estimate severity
  • Assess progress of reinnervation for axonal injuries

  Electrodiagnosis of Conduction Block

  • Conduction block refers to the failure of an action potential to propagate along a structurally intact axon. This is usually due to dissipation of the AP in a region of demyelination.
    • Typically diagnosed if stimulation at or proximal to the site of injury results in > 20-50 % decrease in CMAP amplitude and CMAP area with ≤ 15% prolongation of CMAP duration as compared to stimulation distal to the injury
    • If proximal stimulation results in no CMAP while distal stimulation triggers a normal CMAP then the block is complete at the site of injury. If some APs pass then CB is partial, which can be quantified as a % of the distal CMAP amplitude
    • Another manifestation of CB is the loss of F waves with then distal CMAP remains normal.
    • Potential for false-positives
      • Submaximal stimulation is applied proximally (i.e., risk in obese patients)
      • Anatomical variants that allow for the possibility that distal stimulation activates additional fibers not present at the proximal stimulation site. (i.e., Martin-Gruber anastomosis)
  • Temporal Dispersion
    • Refers to the prolongation of the CMAP duration with proximal stimulation due to variance in conduction times between fast and slow conducting motor axons. In the normal state, the increase in CMAP duration with proximal stimulation is between 15-30 miliseconds.
      • With demyelinating injury, the difference in conduction times between fast and slow conducting motor axons may be accentuated due to pathological slowing of NCV in demyelinated fibers. As a result, the duration of the CMAP may increase beyond normal limits. Also the morphology of the CMAP elicited with stimulation proximal to the demyelinative injury can change in appearance and show an irregular contour that is not typically seen with axonal nerve injury.

Electrodiagnosis of Axonal Loss

  • CMAP declines to its nadir within 5 days
  • SNAP declines to its nadir within 10 days
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