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Axonotmesis is a disruption of nerve cell axon, with Wallerian degeneration occurring below and slightly proximal to the site of injury.[1] If axons and their myelin sheath are damaged, but Schwann cells, the endoneurium, perineurium and epineurium remain intact, it is called axonotmesis. Axonotmesis is usually the result of a more severe crush or contusion than neuropraxia.[2] In axonotmesis, the proximal section is repaired by creating a sprout with its growth cone, but in the distal section occurs axonal degeneration. The rate of outgrowth of regenerating nerve fibers is about 1 mm to 2 mm per day, so that the recovery of conduction to a target structure depends on not only regrowth into the appropriate endoneurial tube (endoneurium), but also on the distance involved.[3]


A nerve contains sensory fibers, motor fibers, or both. Sensory fibers lesions cause the sensory problems below to the site of injury. Motor fibers injuries may involve lower motor neurons, sympathetic fibers, and or both.

Assessment items include:

In assessment, sensory-motor defects may be mild, moderate, or severe. Damage to motor fibers results in paralysis of the muscles. Nervous plexus injuries create the more signs and symptoms from sensory-motor problems (such as brachial plexus injuries). In these cases, the prognosis depends on the amount of damage and the degree of functional recovery.

EMG and NCV findings[edit]

Changes in EMG:

Electromyography (EMG) is a medical test performed to evaluate and record the electrical activity (electromyogram) produced by skeletal muscles using an instrument called electromyograph. In axonotmesis, EMG changes (2 to 3 weeks after injury) in the denervated muscles include:

  1. Fibrillation potentials (FP)
  2. Positive sharp waves

Changes in NCV (nerve conduction velocity):

EMG test is often performed together with another test called nerve conduction study, that measures the conducting function of nerves. NCV study shows loss of nerve conduction in the distal segment (3 to 4 days after injury). According to NCV study, in axonotmesis there is an absence of distal sensory-motor responses.


Treatment of axonotmesis consists of:

  • Physical therapy or Occupational Therapy. Physical or Occupational therapy aims include:
    • Pain relief
    • Maintain range of motion
    • Reducing muscular atrophy
    • Patient education
  • Use of assistive devices (Orthotic needs)
  • Surgical treatment (For example, in cases of surrounding scar tissue)


The prognosis is usually good in terms of recovery. Rate of recovery depends on the distance from the site of injury, with axonal regeneration occurring at 1 to 4 mm/day.[4] Nerve regeneration may take several months.

See also[edit]


  1. ^ Otto D.Payton & Richard P.Di Fabio et al. Manual of physical therapy. Churchill Livingstone Inc. ISBN 0-443-08499-8
  2. ^
  3. ^ Carol Mattson Porth. Pathophysiology: concepts of altered health states. Publisher: Lippincott. Third Edition. ISBN 0-397-54723-4
  4. ^ Otto D. Payton & Richard P. Di Fabio et al. Manual of physical therapy. Churchill Livingstone Inc. Page 24. ISBN 0-443-08499-8