<!-- Deleted image removed: right|thumb|350px|Neurapraxia is a disorder of the [[peripheral nervous system. The disorder involves a compression of the nerve, which results in a blockage of conduction. Temporary damage be to the myelin sheath is also exhibited in neurapraxia.]] -->

Neurapraxia is a disorder of the peripheral nervous system in which there is a temporary loss of motor and sensory function due to blockage of nerve conduction, usually lasting an average of six to eight weeks before full recovery. Neurapraxia is derived from the word apraxia, meaning “loss or impairment of the ability to execute complex coordinated movements without muscular or sensory impairment”.

This condition is typically caused by a blunt neural injury due to external blows or shock-like injuries to muscle fibers and skeletal nerve fibers, which leads to repeated or prolonged pressure buildup on the nerve. As a result of this pressure, ischemia occurs, a neural lesion results, and the human body naturally responds with edema extending in all directions from the source of the pressure. This lesion causes a complete or partial action potential conduction block over a segment of a nerve fiber and thus a reduction or loss of function in parts of the neural connection downstream from the lesion, leading to muscle weakness.

Neurapraxia results in temporary damage to the myelin sheath but leaves the nerve intact and is an impermanent condition; thus, Wallerian degeneration does not occur in neurapraxia. In order for the condition to be considered neurapraxia, according to the Seddon classification system of peripheral nerve injury, there must be a complete and relatively rapid recovery of motor and sensory function once nerve conduction has been restored; otherwise, the injury would be classified as axonotmesis or neurotmesis. Thus, neurapraxia is the mildest classification of peripheral nerve injury.

Neurapraxia is very common in professional athletes, especially American football players, and is a condition that can and should be treated by a physician.

Signs and symptoms

A variety of nerve types can be subjected to neurapraxia and therefore symptoms of the injury range in degree and intensity. Common symptoms of neurapraxia are disturbances in sensation, weakness of muscle, vasomotor and sudomotor paralysis in the region of the affected nerve or nerves, and abnormal sensitivity of the nerve at the point of injury. It has been observed that subjective sensory symptoms include numbness, tingling, and burning sensations at the site of the injury. Objective sensory symptoms are generally minimal in regards to touch, pain, heat, and cold. 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. 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. 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.

  • Axonotmesis occurs when the majority of the supporting structures of the nerve are preserved, but disruption of the nerve fibers is still observed. Wallerian degeneration often occurs in the near the proximity of the injury site. Typical episodes of transient neurapraxia only last a few seconds and symptoms dissipate entirely.

American football

Cervical cord neurapraxia among American football players is commonly observed in athletes playing positions involving high-speed collisions and open-field tackling. Cases of neurapraxia in the National Football League were first described in 1986 by Joseph Torg, M.D., founder of the National Football Head and Neck Injury Registry (established in 1975). The cervical spine cannot properly absorb the force of a collision when the head is even slightly lowered as is the case in spearing. In addition to outlawing acts such as spearing, prevention of neurapraxia on the football field relies on instruction and reinforcement of proper tackling technique by coaches and trainers.

In M*A*S*H Season 4 Episode one, Benjamin "Hawkeye" Pierce claims that Walter "Radar" O'Reilly has neurapraxia as an excuse for driving past a military checkpoint. Hawkeye lies about the causes and treatments to keep them from getting into trouble. When questioned by Radar if it was a real disease, he answered "Yes, but only people that bite their nails can get it" (which Radar was currently doing).

See also

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References