300px To assess the location and severity of a peripheral<unk> , clinical assessment is commonly combined with electrodiagnostic tests.<unk> es to the myelin are usually the least severe (neuropraxia), while<unk> es to the axons and supporting structures are more severe (axonotmesis is moderate<unk> , while neurotmesis is severe<unk> . It may be difficult to differentiate the severity by clinical findings due to common neurological impairments, including motor and sensory impairments distal to the lesion. Neurapraxia Nerve compression in neurapraxia Neurapraxia is the least severe form of<unk> , with complete recovery. In this case, the axon remains intact, but there is myelin damage causing 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<unk>  (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. In electrodiagnostic testing with nerve conduction studies, there is a normal compound motor action potential amplitude distal to the lesion at day 10, and this indicates a diagnosis of mild neurapraxia instead of axonotmesis or neurotmesis. Axonotmesis This is a more severe<unk>  with disruption of the neuronal axon, but with maintenance of the epineurium. This type of nerve damage may cause paralysis of the motor, sensory, and autonomic, and is mainly seen in crush<unk> . 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 the interruption of the axon and its covering of myelin, but with 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 4 weeks later shows fibrillations and denervation potentials in musculature distal to the<unk>  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<unk>  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. Neurotmesis Neurotmesis is the most severe lesion with no potential of full recovery. It occurs on severe contusion, stretch, or laceration. The axon and encapsulating connective tissue lose their continuity. The last (extreme) degree of neurotmesis is transsection, but most neurotmetic<unk> es do not produce gross loss of continuity of the nerve but rather internal disruption of nerve structures sufficient to involve perineurium and endoneurium as well as axons and their covering. Denervation changes recorded by EMG are the same as those seen with axonotmetic<unk> . There is a complete loss of motor, sensory and autonomic function. If the nerve 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 the Sunderland System.
Nerve injury
Accessory nerve disorder
Neurocristopathy
Catastrophic injury
Enthesopathy
Neuromuscular disease
Nerve compression syndrome
Spinal disease