There is no single classification system that can describe all the many variations of nerve injury. Most systems attempt to correlate the degree of injury with symptoms, pathology and prognosis. In 1943, Seddon introduced a classification of nerve injuries based on three main types of nerve fiber injury and whether there is continuity of the nerve. The three types are : neurapraxia, axonotmesis and neurotmesis.
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There is no single classification system that can describe all the many variations of nerve injury. Most systems attempt to correlate the degree of injury with symptoms, pathology and prognosis. In 1943, Seddon introduced a classification of nerve injuries based on three main types of nerve fiber injury and whether there is continuity of the nerve. The three types are : neurapraxia, axonotmesis and neurotmesis.
Neurapraxia
This is the least severe form of nerve injury, with complete recovery. In this case, the actual structure of the nerve remains intact, but there is an interruption in conduction of the impulse down the nerve fiber. Most commonly, this involves compression of the nerve or disruption to the blood supply (ischemia). There is a temporary loss of function which is reversible within hours to months of the injury (the average is 6-8 weeks). Wallerian degeneration does not occur, so recovery does not involve actual regeneration. There is frequently greater involvement of motor than sensory function with autonomic function being retained.
Axonotmesis
This is a more severe nerve injury with disruption of the neuronal axon, but with maintenance of the myelin sheath. This type of nerve damage may cause paralysis of the motor, sensory, and autonomic. Mainly seen in crush injury.
If the force creating the nerve damage is removed in a timely fashion, the axon may regenerate, leading to recovery. Electrically, the nerve shows rapid and complete degeneration, with loss of voluntary motor units. Regeneration of the motor end plates will occur, as long as the endoneural tubules are intact.
Axonotmesis involves loss of the relative continuity of the axon and its covering of myelin, but preservation of the connective tissue framework of the nerve ( the encapsulating tissue, the epineurium and perineurium, are preserved ). Because axonal continuity is lost, Wallerian degeneration occurs. Electromyography ( EMG ) performed 2 to 3 weeks later shows fibrillations and denervation potentials in musculature distal to the injury site. Loss in both motor and sensory spines is more complete with axonotmesis than with neurapraxia, and recovery occurs only through regenerations of the axons, a process requiring time.
Axonotmesis is usually the result of a more severe crush or contusion than neurapraxia, but can also occur when the nerve is stretched (without damage to the epineurium). There is usually an element of retrograde proximal degeneration of the axon, and for regeneration to occur, this loss must first be overcome. The regeneration fibers must cross the injury site and regeneration through the proximal or retrograde area of degeneration may require several weeks. Then the neuritis tip progresses down the distal site, such as the wrist or hand. Proximal lesion may grow distally as fast as 2 to 3 mm per day and distal lesion as slowly as 1.5 mm per day. Regeneration occurs over weeks to years.
