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.

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.

A nerve contains sensory fibers, motor fibers, or both. Sensory fibers lesions cause the sensory problems below to the site of injury. Motor fibers injuries may involve lower motor neurons, sympathetic fibers, and or both.

Assessment items include:

- Sensory fibers that send sensory information to the central nervous system.

- Motor fibers that allow movement of skeletal muscle.

- Sympathetic fibers that innervate the skin and blood vessels of the four extremities.

In assessment, sensory-motor defects may be mild, moderate, or severe. Damage to motor fibers results in paralysis of the muscles. Nervous plexus injuries create more signs and symptoms from sensory-motor problems (such as brachial plexus injuries). In these cases, the prognosis depends on the amount of damage and the degree of functional impairment.

Axonotmesis is an injury to the peripheral nerve of one of the extremities of the body. The axons and their myelin sheath are damaged in this kind of injury, but the endoneurium, perineurium and epineurium remain intact. Motor and sensory functions distal to the point of injury are completely lost over time leading to Wallerian Degeneration due to ischemia, or loss of blood supply. Axonotmesis is usually the result of a more severe crush or contusion than neurapraxia.

Axonotmesis mainly follows a stretch injury. These stretch injuries can either dislocate joins or fracture a limb, due to which peripheral nerves are severed. If the sharp pain from the exposed axon of the nerve is not observed, one can identify a nerve injury from abnormal sensations in their limb. A doctor may ask for a Nerve Conduction Velocity (NCV) test to completely diagnose the issue. If diagnosed as nerve injury, Electromyography performed after 3 to 4 weeks shows signs of denervations and fibrillations, or irregular connections and contractions of muscles.

Symptoms of neurotmesis include but are not limited to pain, dysesthesias (uncomfortable sensations), and complete loss of sensory and motor function of the affected nerve.

Peripheral nerve injuries can be classified in two different ways. Neurotmesis is classified under the Seddon system which is defined by three grades of nerve injury. The mildest grade is referred to as neurapraxia and is characterized by a reduction or complete blockage of conduction across a segment of nerve while axonal continuity is maintained and nerve conduction is preserved. These injuries are almost always reversed and a recovery takes place within days or weeks. The second classification of the Seddon system is referred to as axonotmesis which is a more severe case of peripheral nerve injury. Axonotmesis is classified by an interruption of the axons, but a preservation of the surrounding connective tissues around the axon. These injuries can heal themselves at about 1mm/day, therefore resulting in recovery to be possible but at a slower rate than neurapraxia. The last and most severe case of peripheral nerve injury is known as neurotmesis, which in most cases cannot be completely recovered from even with surgical repair.

The second classification of nerve injury is known as the Sunderland classification which is more complex and specific. This classification uses five different degrees of nerve injury, the first one being the least severe and the equivalent to neurapraxia and the most severe being the fifth degree and having the same classification as neurotmesis. The second through fourth degrees are dependent on the variance of axon discontinuity and are classified under Seddon’s classification of axonotmesis.

This is the least severe form of nerve injury, 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 injury (the average is 6–9 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 neuropraxia instead of axonotmesis or neurotmesis.

Nerve injury is injury to nervous tissue. There is no single classification system that can describe all the many variations of nerve injury. In 1941, Seddon introduced a classification of nerve injuries based on three main types of nerve fiber injury and whether there is continuity of the nerve. Usually, however, (peripheral) nerve injury is classified in five stages, based on the extent of damage to both the nerve and the surrounding connective tissue, since supporting glial cells may be involved. Unlike in the central nervous system, neuroregeneration in the peripheral nervous system is possible. The processes that occur in peripheral regeneration can be divided into the following major events: Wallerian degeneration, axon regeneration/growth, and nerve reinnervation. The events that occur in peripheral regeneration occur with respect to the axis of the nerve injury. The proximal stump refers to the end of the injured neuron that is still attached to the neuron cell body; it is the part that regenerates. The distal stump refers to the end of the injured neuron that is still attached to the end of the axon; it is the part of the neuron that will degenerate but that remains in the area toward which the regenerating axon grows. The study of peripheral nerve injury began during the American Civil War and has greatly expanded to the point of using growth-promoting molecules.

Based on the location of the nerve damage, brachial plexus injuries can affect part of or the entire arm. For example, musculocutaneous nerve damage weakens elbow flexors, median nerve damage causes proximal forearm pain, and paralysis of the ulnar nerve causes weak grip and finger numbness. In some cases, these injuries can cause total and irreversible paralysis. In less severe cases, these injuries limit use of these limbs and cause pain.

The cardinal signs of brachial plexus injury then, are weakness in the arm, diminished reflexes, and corresponding sensory deficits.

1. Erb's palsy. "The position of the limb, under such conditions, is characteristic: the arm hangs by the side and is rotated medially; the forearm is extended and pronated. The arm cannot be raised from the side; all power of flexion of the elbow is lost, as is also supination of the forearm".

2. In Klumpke's paralysis, a form of paralysis involving the muscles of the forearm and hand, a characteristic sign is the "clawed hand", due to loss of function of the ulnar nerve and the intrinsic muscles of the hand it supplies.

Signs and symptoms may include a limp or paralyzed arm, lack of muscle control in the arm, hand, or wrist, and lack of feeling or sensation in the arm or hand. Although several mechanisms account for brachial plexus injuries, the most common is nerve compression or stretch. Infants, in particular, may suffer brachial plexus injuries during delivery and these present with typical patterns of weakness, depending on which portion of the brachial plexus is involved. The most severe form of injury is nerve root avulsion, which usually accompanies high-velocity impacts that commonly occur during motor-vehicle collisions or bicycle accidents.