a short period of time immediately following the injury. However, in severe cases of neurapraxia, symptoms can persist for weeks or months at a time. Causes The cause of neurapraxia is a neural lesion which causes a temporary block of nerve conduction without transection of the axon. A conduction block is classified as a 40% reduction in action potential amplitude over a short distance on the nerve, or a 50% reduction for a longer distance on the nerve. In neurapraxia, stimulation to the injured nerve results in a greater reduction in the action potential amplitude on the proximal site of the injury as opposed to the distal site. Anatomy Neurapraxia occurs in the peripheral nervous system typically in the ulnar, median, and radial nerves of the upper body and in the sciatic and peroneal nerves of the lower body. Peripheral nerves are myelinated, relatively large, spatially complex cells whose size and connectivity typically make them more susceptible to damage and compromise their capacity to self-repair, although this is not the case in neurapraxia. Microscopic evidence has shown that there is damage to the myelin sheath, but not to the axon. Therefore, distal nerve fibers do not degenerate and the myelin damage can be repaired. Order of pathology The order of pathology within the first 24 hours after injury follows a general pattern of nerve injury. The first physical manifestation of the injury is focal swelling adjacent to the site of the injury. In the cellular dimension, a fragmentation of neurotubules and neurofilaments occurs as a result of pressure exerted on the nerve. Axons swell at some sites and are compressed at others, leading to a beaded appearance. Mechanisms of injury There are several mechanisms of nerve injury including mechanical lesions, ischemia, immunologic attack, metabolic disorder, toxic agents, and exposure to radiation. The most common mechanism of injury is nerve compression in which external pressure causes decreased blood flow to the nerve and deformation of the nerve fibers. Repeated or prolonged compression of the nerve results in ischemia and ultimately edema above and below the source of the pressure (I). The thinning of myelin sheaths or focal demyelination are the main consequences of the injury that lead to conduction blockage. Diagnosis Seddon classification There are three distinct classifications and degrees of nerve injury: Neurotmesis is the most serious degree of nerve injury. It involves the disruption of the nerve and the