What are the patterns of peripheral nerve damage?
The nerve can be damaged by injury to the myelin, axon, cell body, or vasa nervorum.
Four basic pathologic mechanisms underlie nerve injury
1. Wallerian degeneration
This degeneration develops after injury to the axon and myelin, as in transection of the nerve.
Distal to the transection, the axon and then myelin degenerate, followed within 3 to 5 days by failure to generate and conduct a nerve action potential.
The axon may regrow within the architecture provided by the basement membrane of Schwann cells, but the degree and efficiency of regrowth depend on good approximation of the nerve ends.
2. Segmental demyelination
Segmental demyelination develops after damage to the myelin sheath or Schwann cell.
Because the muscle is not denervated, no atrophy develops. Prognosis for complete recovery is good.
3. Axonal degeneration
Axonal degeneration develops from damage to the axon resulting in distal dying of the axon and subsequent loss of myelin.
Once the distal nerve dies, the muscle is denervated; hence, muscle atrophy develops.
The denervated muscle fibers can be reinnervated by surrounding nerves, but recovery may not be complete.
Neuronopathy develops when damage to the cell body of the neuron results in the breakdown of the entire nerve, peripherally and centrally, involving the anterior horn cell or dorsal root ganglion.
In acute nerve injuries, the extent and degree of damage can be graded using Sunderland’s classification Grade I-V or Seddon’s classification of neurapraxia, axonotmesis, and neurotmesis.
Neurapraxia (Grade I) occurs when the myelin alone has been damaged with good prognosis for recovery within hours to weeks.
Axonotmesis (Grades II-IV) refers to varying degrees of damage to the axons and surrounding connective tissues.
Neurotmesis (Grade V) involves injury to the entire nerve including the epineurium (e.g., in a nerve transection).
Usually both axonotmesis and neurotmesis result in incomplete or no recovery of function.