Peripheral Nerve Injuries 

Updated: Dec 01, 2020
Author: Stefanos F Haddad, MD; Chief Editor: Murali Poduval, MBBS, MS, DNB 


Practice Essentials

Peripheral nerve injuries may result in loss of motor function, sensory function, or both.[1, 2]  Such injuries may occur as a result of trauma (blunt or penetrating) or acute compression.

Paul of Aegina (625-690) was the first to describe approximation of the nerve ends with wound closure. Hueter (1871, 1873) introduced the concept of primary epineurial nerve suture, and Nelaton described secondary nerve repair in 1864. Even at an early time, the idea of decreasing tension on the nerve suture was important.

In 1882, Mikulicz described sutures that reduced tension, and Loebke described bone shortening to decrease nerve tension in 1884. In 1876, Albert described grafting nerve gaps. A great deal of information regarding the evaluation and treatment of traumatic nerve injuries came with the experience of treating wartime injuries.

The future in peripheral nerve injuries lies in maximizing motor and sensory recovery after nerve injury. Strategies to maintain the neuromuscular junction are important for permitting muscle reinnervation after prolonged muscle denervation, as well as decreasing injury to the cell body.

In traumatic nerve injury with large nerve gaps, nerve allografts have been described. However, because of the morbidity associated with immunosuppression, the use of the nerve allograft has been stringently limited to otherwise unreconstructable injuries. Investigations to decrease the antigenicity of the allograft or induce tolerance to the nerve allograft are ongoing, and success in these investigations will permit the use of nerve allografts without immunosuppression.


A nerve is composed of neural tissue (axon) and connective tissue. In myelinated nerve fibers, each axon is surrounded by the endoneurium. Groups of nerve fibers are surrounded by the perineurium to form fascicles, and groups of fascicles are surrounded by the internal and external epineurium. For optimal outcome after surgery, knowledge of motor and sensory fascicular topography within the nerve is essential to ensure correct alignment of the motor and sensory fascicles.


Peripheral nerve injury may result in demyelination, axonal degeneration, or both. Clinically, both demyelination and axonal degeneration result in disruption of sensory function, motor function, or both in the injured nerve. Depending on the severity and degree of nerve injury, recovery of function occurs with remyelination and with axonal regeneration and reinnervation of the sensory receptors, motor end plates, or both.[1, 2]


Limited reported data are available to determine the incidence of peripheral nerve injuries. In North America, data taken from a trauma population in Canada revealed that approximately 2-3% of patients had a major nerve injury.[3] In New South Wales, Australia, 2% of patients were reported to have a major nerve injury. In a study of the US National Inpatient Sample database, Lad et al reported higher rates of median, ulnar, and radial nerve injuries as compared with brachial plexus injuries.[4]  


With closed traumatic injuries or restoration of nerve continuity, axons may regenerate and thus reinnervate the motor end plates and sensory receptors. Depending on the severity of nerve injury, recovery of motor and sensory function is variable.

When the nerve injury is very proximal (eg, in brachial plexus injury or sciatic nerve injury), nerve regeneration may not occur quickly enough to permit muscle reinnervation. For example, in a lower trunk brachial plexus injury, reinnervation of the ulnar nerve intrinsic hand muscles is not possible due to the long period of muscle denervation because of the long distance necessary for nerve regeneration.

If, however, surgery is performed within 3-6 months after the nerve injury was sustained, the patient can be expected to recover the use of most muscles, excluding muscles in the hand or foot in injuries at the trunk level or higher. Distal nerve transfers are used to recover distal extremity motor function.

A cross-sectional study evaluated the biomedical and psychosocial factors associated with disability after upper-extremity nerve injury (follow-up period, 6 months to 15 years).[5]  In this study, disability, as assessed on the basis of DASH (Disabilities of the Arm, Shoulder, and Hand) Questionnaire scores, was predicted by pain catastrophizing, sensitivity to cold, time elapsed since injury, employment status, intensity of pain, older age, and the presence of brachial plexus injury.

Additional studies have shown that peripheral nerve injury, particularly in the upper extremity, has a major impact on function and employment, resulting in significant healthcare costs. Both proximal and distal nerve injuries can lead to long-term disability, subsequent sick leave, and (in 30%) permanent disability pension.[6]



History and Physical Examination

The clinical appearance following nerve injury varies according to the nerve affected (sensory, motor, or combined). Injury to a motor nerve results in loss of muscle function, whereas injury to a sensory nerve results in loss of sensation to the affected nerve's sensory distribution, neuromatous or causalgia pain, or both.[1, 2]


Classification of nerve injury was described by Seddon in 1943[7]  and by Sunderland in 1951.[8]  The classification of nerve injury described by Seddon comprised neurapraxia, axonotmesis, and neurotmesis. Sunderland expanded this classification system to include five degrees of nerve injury, as described below.

First-degree nerve injury

A first-degree injury or neurapraxia involves a temporary conduction block with demyelination of the nerve at the site of injury. Electrodiagnostic study results are normal above and below the level of injury, and no axonal degeneration or denervation muscle changes are present. No Tinel sign is present. Once the nerve has remyelinated at that area, complete motor and sensory recovery occurs. Recovery may take up to 12 weeks.

Second-degree nerve injury

A second-degree injury or axonotmesis results from a more severe trauma or compression. This causes wallerian degeneration distal to the level of injury and proximal axonal degeneration to at least the next node of Ranvier. In more severe traumatic injuries, the proximal degeneration may extend beyond the next node of Ranvier.

Electrodiagnostic studies of motor nerve injuries demonstrate denervation changes in the affected muscles, and in cases of reinnervation, motor unit potentials (MUPs) are present. Axonal regeneration occurs at the rate of 1 mm/day or 1 in./month and can be monitored with an advancing Tinel sign. The endoneurial tubes remain intact, and recovery therefore is complete, with axons reinnervating their original motor and sensory targets.

Third-degree injury

The third degree of injury was introduced by Sunderland to describe an injury more severe than second-degree injury. As with a second-degree injury, wallerian degeneration occurs, and electrodiagnostic studies demonstrate denervation changes with fibrillations in the affected muscles. In cases of reinnervation, MUPs are present.

Regeneration occurs at a rate of 1 mm/day, and progress may be monitored with an advancing Tinel sign. However, with the increased severity of the injury, the endoneurial tubes are not intact, and regenerating axons therefore may not reinnervate their original motor and sensory targets.

The recovery pattern is mixed and incomplete. Reinnervation of sensation occurs only if sensory fibers reach their sensory end organs; similarly, muscle reinnervation occurs if motor nerve fibers reach their muscle targets. Even within a sensory nerve, recovery can be mismatched if sensory fibers reinnervate a different area within the nerve's sensory distribution. If the muscle target is far from the injury site, nerve regeneration may occur, but the muscle may not be reinnervated, because of the long period of denervation and irreversible muscle degeneration.

Fourth-degree injury

A fourth-degree injury results in a large area of scar at the site of nerve injury and precludes any axons from advancing distal to the level of nerve injury. Electrodiagnostic studies reveal denervation changes in the affected muscles, and no MUPs are present. A Tinel sign is noted at the level of the injury, but it does not advance beyond that level. No improvement in function is noted, and surgery is required to excise the neuroma and restore neural continuity, thus permitting axonal regeneration and motor and sensory reinnervation.

Fifth-degree injury

A fifth-degree injury is a complete transection of the nerve. Like a fourth-degree injury, it requires surgery to restore neural continuity. Electrodiagnostic findings are the same as those for a fourth-degree injury.

Sixth-degree injury

The category of sixth-degree injury was introduced by Mackinnon to describe a mixed nerve injury that combines the other degrees of injury.[2] This type of injury commonly occurs when some fascicles of the nerve are working normally while other fascicles may be recovering, and other fascicles may require surgical intervention to permit axonal regeneration.



Imaging Studies

Imaging studies are appropriate in cases of suspected nerve tumors, though false-negative and false-positive findings are possible in magnetic resonance imaging (MRI) evaluation of nerve tumors.

Imaging studies are appropriate in cases of suspected brachial plexus avulsion injury to evaluate for avulsion of the nerve roots from the spinal cord. Computed tomography (CT) myelography can be used to investigate for suspected brachial plexus avulsion injury, though it has largely been replaced with MRI in this setting.

Other Tests

Electrodiagnostic studies are useful in detecting nerve injury, nerve compression, or both, as well as in identifying early stages of recovery.[9]

Electromyography (EMG) is performed at least 4 weeks after nerve injury. EMG testing done earlier than this may yield false-negative findings because it takes 4-6 weeks for muscle fibrillations to become apparent. Evidence of denervation is indicated by the presence of fibrillations in the muscle. Reinnervation is signaled by the presence of motor unit potentials (MUPs).

Nerve conduction studies are particularly useful in identifying secondary compression sites that may be present. If the nerve is compressed at an entrapment site, such as the carpal tunnel or the cubital tunnel, axonal regeneration may be impeded and thus limit reinnervation. In cases of brachial plexus injury, nerve conduction studies can help determine the presence of an avulsion injury. Intact normal distal sensory nerve conduction and motor denervation are diagnostic of an avulsion injury.



Approach Considerations

Indications for nerve injury surgery are as follows:

  • Closed nerve injury - If there is no evidence of recovery, either clinically or from electrodiagnostic studies, at 3 months after injury, surgery is recommended; if there is evidence of recovery as indicated by motor unit potentials (MUPs), patients should be assessed to determine the progression of recovery and the possible requirement for surgery
  • Open nerve injury (ie, laceration) - Surgical exploration is recommended as soon as possible; all lacerations with a reported loss of sensation or motor weakness should be surgically explored
  • Crush nerve injury - Surgical exploration of the nerve may be delayed for as long as several weeks; however, if, after 3 months, there is no evidence of reinnervation, either clinically or from electrodiagnostic studies (the absence of MUPs signals the absence of reinnervation), surgical reconstruction with nerve repair, transfer, or grafting is indicated

In contaminated or crush nerve injuries, delayed reconstruction may be indicated.

Nonoperative Therapy

In patients with motor nerve injury, initial therapy involves patient education and protection of the joints, including the surrounding ligaments and tendons, from further stress. Splints, slings, or both may be used in these cases to protect the joint and to augment function. For example, a radial nerve injury results in a loss of wrist and finger extension, a wrist drop. A wrist-resting splint may be used to support the hand in a neutral wrist position and place the hand in a more functional position.

In patients with brachial plexus nerve injuries, particularly when C5-6 is affected, continued downward stress at the glenohumeral joint may cause glenohumeral joint subluxation without the muscle support of the rotator cuff muscles. A sling is helpful to unload this joint, prevent complete shoulder dislocation, and decrease pain.

Physical therapy is started in the early stages after nerve injury to maintain passive range of motion in the affected joints and to maintain muscle strength in the unaffected muscles.

No definitive studies have been done to support the use of electrical muscle stimulation to prevent muscle degeneration. In cases of muscle denervation, galvanic direct current stimulation is necessary to elicit a muscle contraction. The risks of galvanic stimulation include a thermal burn beneath the electrodes, particularly in patients with decreased sensation. Because no studies have shown that electrical muscle stimulation using surface electrodes will stop total degeneration of the muscle fibers, the neuromuscular junction, or both, the authors do not advocate direct current stimulation of denervated muscles. If the nerve does not regenerate in time to reinnervate the muscle, there is no need to stimulate the muscle.

With reinnervated muscle, it is theoretically possible to use alternating current stimulation. However, it is necessary to have a large number of reinnervated muscle fibers to stimulate the muscle with alternating current. The authors recommend exercise and biofeedback strategies to increase the strength of a reinnervated muscle, in combination with sensorimotor reeducation.

Surgical Therapy

Treatment of specific injury types


In patients who have neurologic deficits after a laceration, an operative procedure to explore the nerve should be performed as soon after injury as possible. With clean, sharp injuries to the nerve, a direct repair is performed. Direct nerve repair with microsurgical techniques is a gold-standard method for treatment of axonotmesis and neurotmesis; it provides endurance and continuity between the distal and proximal parts of the nerves.[10] With more crushing or avulsion injuries, the nerve ends are reapproximated so that motor and sensory topography can be aligned. The definitive reconstruction is done at 3 weeks or when the wound permits.[11, 2]

Gunshot or blast wounds

Typically, blast wounds associated with neurologic deficit have good potential for neurologic recovery. Thus, unless an associated vascular or bony problem is present, patients with a neurologic deficit after a gunshot or blast injury are initially managed nonoperatively and monitored with frequent clinical examinations. If, by 3 months after the injury, no evidence of clinical recovery or electrical recovery is noted on electrodiagnostic testing, surgical exploration is recommended.

Closed injuries

In patients with closed traction injuries, surgical intervention is recommended 3-6 months after the nerve injury, depending on patient and injury factors. These patients are reexamined both clinically and with electrodiagnostic studies. If there is no evidence of reinnervation either clinically or on electrodiagnostic studies, surgical intervention is necessary.

Preparation for surgery

When there is no clinical or electrodiagnostic evidence of recovery, surgical exploration is recommended. Preoperative evaluation includes a comprehensive sensory and motor assessment. Initial sensory evaluation includes assessment of protective sensation (thermal), tactile (threshold monofilament) and discriminatory function (two-point discrimination) and pain. In patients with no two-point discrimination, light touch (Ten test) is used.[12, 13]  In the Ten test, simultaneous light touch stimuli are applied to the affected area of sensory compromise and to the contralateral region, and the patient compares the sensation on a scale of 0-10.

Motor assessment should include pinch and grip strength measurements and evaluation of individual muscle strength, which can be quantified by  using the Medical Research Council (MRC) 0-5 grading scale when appropriate. MRC grades are defined as follows:

  • M0 - No contraction
  • M1 - Flicker contraction
  • M2 - Muscle contraction with active motion with gravity eliminated
  • M3 - Full range of motion against gravity
  • M4 - Full range of motion against gravity with some resistance
  • M5 - Full range of motion against gravity with maximum resistance for that muscle

Operative details

Key technical points include the following:

  • Loupe magnification, preferably ×4.3, is employed with use of the microscope for microneurosurgical repairs or grafts
  • Extremity surgery is performed using tourniquet control
  • Nerve coaptations are performed with 9-0 microsuture and no tension at the repair site
  • Bupivacaine is used at the incision site, and in some cases, it also may be used in an infusion pump to control postoperative pain
  • A Jackson-Pratt drain also may be used in some cases to control postoperative drainage

Nerve repair

Reconstruction of nerve continuity can be performed with direct repair.[2]  This is performed when the distal and proximal ends of the nerve are directly coapted. The repair should be performed without tension; if it cannot be performed without tension, another type of nerve reconstruction should be performed (eg, nerve graft or nerve transfer). If the adjacent joint must be flexed or extended to permit coaptation of the distal and proximal ends of the nerve, another type of reconstruction (eg, nerve graft or nerve transfer) should be used.

Nerve graft

In cases where the proximal and distal nerve segments cannot be approximated without tension or where a gap is present between the proximal and distal end of the nerve, a nerve graft may be recommended.[11, 14, 15, 2, 16]  The use of a donor nerve to reconstruct the nerve gap results in a sensory loss in the distribution of the donor nerve. This area of sensory loss becomes smaller over 1-3 years with collateral sprouting from the surrounding sensory nerves.[17]

There are a number of small noncritical sensory nerves that may be used for nerve grafts. In cases where a large nerve gap is present, the sural nerve is used because of the large length of nerve graft material that can be obtained. The sural nerve can be harvested through a single long incision or through multiple step incisions on the posterior calf.

For shorter nerve gaps, the anterior branch of the medial antebrachial cutaneous (MABC) nerve is a good graft donor because the donor site scar is minimal and the resultant sensory loss is on the anterior aspect of the forearm. The MABC nerve is especially useful for upper-extremity surgical reconstructions because all of the incisions are located in the same extremity. The lateral antebrachial cutaneous (LABC) nerve provides about 6 cm of nerve graft material, but the scar on the forearm is more noticeable than that on the inner upper arm for the MABC.

Nerve transfer

The concept of a nerve-to-nerve transfer utilizes a normal neighboring noncritical nerve that is coapted to the distal end of the injured nerve.[18]  This is a particularly useful approach in cases where a large nerve gap is present, proximal nerve injuries are present, or both.[18, 19, 20, 21, 22, 23, 2]  Excellent results have been shown with proximal brachial plexus injuries and distal median, radial, and ulnar nerve injuries.[24, 25, 26, 27, 28, 29]

Postoperative Care

The patient is immobilized in a bulky dressing for several days postoperatively. The postoperative dressing (including the drain and pain pump, if used) is removed 2-3 days after the procedure.

The area of nerve coaptation then is immobilized for a longer time postoperatively (nerve graft, 10-14 days; nerve repair, 3 weeks; nerve transfer, 7-10 days), though the patient is instructed in range-of-motion (ROM) exercises for the joints proximal and distal to the immobilized region. For example, a median nerve repair at the wrist would be immobilized with a wrist-resting splint, and the patient would continue with ROM for the fingers, elbow, and shoulder.

After the surgical procedure, the patient is referred to the hand therapist, initially for immobilization (eg, splinting), education regarding postoperative care, and exercises. The initial goals of postoperative therapy are to regain passive ROM of the joints and soft tissues that have been immobilized. The patient should be instructed in exercises to maintain strength in the unaffected muscles. In the later stages, sensory and motor reeducation are recommended to maximize the outcome.


Complications of nerve surgery are similar to those of other types of surgery and include infection, hematoma, seroma, and injury to surrounding structures, including vascular structures or nerves, particularly in complex reconstructions involving mixed nerve injuries or scarred regions.

Long-Term Monitoring

Initially, the patient is monitored for postoperative wound healing. After immobilization and once full passive ROM has been regained, the patient is monitored every few months to evaluate for evidence of distal target reinnervation.

With nerve regeneration, a Tinel sign progresses distally along the nerve. With muscle reinnervation, a muscle contraction is visible; and with sensory reinnervation, the patient initially responds to light touch. Depending on the level of injury, the patient may continue to progress for varying periods; with distal injuries, maximal function is reached more quickly than with proximal brachial plexus injuries, which continue to improve 2-3 years after surgery.