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 : axonotmesis, neurapraxia and neurotmesis.
Axonotmesis is part of Seddon's classification scheme used to classify nerve damage. It 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.
It 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 spleens 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. 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. For regeneration requires a number of weeks.
In this case there is an interruption in conduction of the impulse down the nerve fiber, and recovery takes place without wallerian degeneration. This is the mildest form of nerve injury. This is probably a biochemical lesion caused by a concussion or other shock-like injuries to the fiber. In the case of the role nerve, neurapraxia is brought about by compression or relatively mild, blunt blows, including some low-velocity missile injuries close to the nerve. There is a temporary loss of function which is reversible within hours to months of the injury ( the average is 6-8 weeks ). There is frequently greater involvement of motor than sensory function with autonomic function being retained.
Neurotmesis is the most severe lesion with potential of recovering. It occurs on severe contusion, stretch, laceration, or Local Anesthetic Toxicity. Not only the axon, but the encapsulating connective tissue lose their continuity. The last (extreme) degree of neurotmesis is transsection, but most neurotmetic injuries do not produce gross loss of continuity of the nerve but rather than internal disruption of the architecture of the nerve sufficient to involve perineurium and endoneuruim as well as axons and their covering. Denevertion changes recorded by EMG are the same as those seen with axonotmetic injury. There is a complete loss of motor, sensory and autonomic function. If the nerve loss has been completely divided, axonal regeneration causes a neuroma to form in the proximal stump. For neurotmesis, it is better to use a new more complete classification called Sunderland System.