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 cases of motor neuron neurapraxia, symptoms consist of flaccid paralysis of the muscles innervated by the injured nerve or nerves.Symptoms are often transient and only last for 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. 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 nerve sheath.
- 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.
- Neurapraxia is least serious form of nerve injury.
Treatment and recovery
The entire nerve is involved in the response to traumatic injuries. The outcome of nerve repair is dependent on the degree of the nerve injury and the circumstances at the site of injury. Since neurapraxia is the least serious form of peripheral nerve injury, recovery and treatment are not extensive. Once the cause of neurapraxia is eliminated, recovery of the lesions in the nerve occurs within a short time span.Non-operative treatment
Neurapraxia is often treated and cured by non-operative means. The primary goals of treatment are to maintain the proper nutrition of the paralyzed muscles, prevent contraction by the antagonists of the paralyzed muscles, and to consistently keep the joints mobile. A splint is often used in cases of neurapraxia because it is able to maintain a relaxed position of the paralyzed muscle. The splint prevents the paralyzed muscle from being overstretched either by the force of gravity or by other non-paralyzed antagonists. During the recovery period of neurapraxia, it is essential that the joints constantly undergo passive movement in order to preserve proper mobility. If joints are kept mobile, the limb has the best possible chance of benefit from the return of nervous function. Non-steroidal anti-inflammatory medications can also help to reduce swelling at the injury site. In addition to these non-operative remedies, it is suggested that muscles affected by neurapraxia be kept warm at all times. Circulation in the limb is stimulated with the use of heat.Once voluntary movement has returned to the muscle, recovery and treatment continues by the participation in active exercises. Physical Therapy and Occupational Therapy are common sources of treatment during these early stages of restoration of active movement. Almost all cases of neurapraxia can be completely treated by non-operative means.