Traumatic peripheral neuropathies

INTRODUCTION — Traumatic peripheral nerve injuries may cause significant disability and have a serious impact on the patient's life. Early diagnosis, accurate and timely management, and close follow-up are warranted. This topic discusses the classification and evaluation of traumatic injury to peripheral nerves and briefly outlines treatment considerations.

Traumatic plexopathies are discussed in detail separately. (See "Brachial plexus syndromes", section on 'Traumatic plexopathies' and "Surgical treatment of brachial plexus injuries" and "Lumbosacral plexus syndromes", section on 'Trauma'.)

Neurologic deficits associated with specific nerve injuries are discussed more fully elsewhere. (See "Overview of upper extremity peripheral nerve syndromes" and "Overview of lower extremity peripheral nerve syndromes".)

ANATOMY AND PHYSIOLOGY — The peripheral nerve consists of myelinated and unmyelinated nerve fibers. Unmyelinated axons are surrounded by the plasma membrane of a supporting cell called the Schwann cell. Myelinated axons are surrounded by a myelin sheath, a specialized structure of the Schwann cell that wraps around the axon and insulates it with layers of cell membrane. Gaps in myelin occur at regular intervals, called the nodes of Ranvier. The segments of axon covered by myelin between the gaps are called the internodal segments [1,2]. The myelin sheath has a low capacitance and a high resistance to electrical current, so that current flow is directed longitudinally along the axon, rather than transversely across the axon membrane. Ion channels within the axon membrane are differentially distributed at the node of Ranvier and under the myelin sheath. The differential expression of ion channels and the insulating properties of the myelin sheath result in a rapid mode of nerve transmission called saltatory conduction.

TRAUMA MECHANISMS — Traumatic nerve injury results from the application of kinetic energy to the nerve, with consequent compressive or tensile forces applied to the nerve. Examples include injuries from a sudden stretch of a limb, a laceration from a sharp object, and a gunshot wound with associated cavitation effect produced by the bullet moving through tissue with a high velocity [3]. (See "Severe upper extremity injury in the adult patient" and "Severe lower extremity injury in the adult patient".)

Neuropathies caused by trauma produce signs and symptoms that relate to the specific location and severity of the injury. However, trauma is unique from other causes of neuropathy in several respects. The sudden nature of the event leads to a well-defined sequence of abnormalities on clinical neurophysiologic evaluation, and recovery is strongly related to the type and severity of injury. A single nerve, nerve group, or multiple nerves in different body regions may be injured simultaneously, depending on the traumatic mechanism. Therapy is directed to individual anatomic reconstruction rather than disease modification.

Most commonly, nerve injury occurs from traction/stretch, laceration, compression, or ischemia. The nerve dysfunction results primarily from the direct mechanical forces applied to it and secondarily from the vascular compromise that follows, with consequent ischemic nerve damage.

Traction/stretch — Peripheral nerves can accommodate a significant degree of tension before developing internal/external structural damage. This is due in part to length redundancy that allows the nerve to adapt to stretches that may result from normal changes in body position (eg, the ulnar nerve at the elbow). In addition, the natural resting tension permitted by the amount of the elastin and collagen present in the perineural layer of nerve allows for stretch up to 10 to 20 percent with no traumatic consequences. However, when these mechanisms of compensation are exceeded, internal and external nerve damage occurs [4,5]. In addition to direct neural injury, the vasa nervorum may be ruptured, causing bleeding into the nerve sheath and consequent compressive hematomas resulting in ischemia. Specific nerves are more susceptible than others to trauma from stretch due to their location and level of resting tension [6].

Contusion/compression — External pressure can injure the nerve by being either continuously applied for hours at a time, such as occurs with compressive radial neuropathy ("Saturday night palsy"), or repeatedly applied with cumulative effect, such as in habitual leaning on the elbow. More commonly, the nerves can be chronically compressed by abnormal neighboring structures, or while passing through fibro-osseous spaces (eg, the cubital tunnel or carpal tunnel) [7].

Nerve laceration/transection — A nerve can be lacerated or completely transected as a consequence of a traumatic injury. This is more likely to be related to a penetrating injury mechanism (eg, knife wound, gunshot), rather than a blunt injury mechanism. (See "Severe upper extremity injury in the adult patient" and "Severe lower extremity injury in the adult patient".)

Combined injury mechanisms — Most nerve injuries due to trauma involve a combination of the above mechanisms. Sports- and motor vehicle-related injuries are predominantly due to stretch/traction, although both contusion and laceration may also occur. Missile-related injuries (eg, gunshot wounds) may cause nerve contusions or transection. Even when nerve continuity is maintained, the cavitation effect produces significant intraneural damage. Compression injuries are often iatrogenic and relate to body positioning during anesthesia; the mechanism of injury in such cases is usually a combination of contusion and ischemia. Injuries from sharp objects are often lacerations, though significant soft tissue damage can cause swelling with subsequent compression.

CLASSIFICATION AND PATHOPHYSIOLOGY — Seddon proposed a classification of nerve injury in 1942 that is still in use today [8]. Injuries are defined as neurapraxia, axonotmesis, and neurotmesis (table 1) based upon the severity and extent of injury to the structural components of the peripheral nerve, including Schwann cells, axons, and surrounding connective tissue [9,10].

A second classification was proposed in 1990 by Sunderland [5,9], who divided nerve injuries in five grades (table 1). Grade I corresponds to neurapraxia; II to axonotmesis; and III, IV, and V to neurotmesis. Grades III, IV, and V are distinguished by the extent to which perineural and epineural tissues are disrupted, so that the prognosis for recovery is better for Grade III lesions. Grade V lesions correspond to severed nerves, or nerves disrupted by scar tissue to the extent that no significant regeneration can occur across the area of injury.

Neurapraxia — Neurapraxia is usually caused by a mild injury (eg, ischemia, mechanical compression, metabolic or toxic factors) that results in focal demyelination, but no loss of axonal integrity in the region of injury. Weakness and sensory loss are due to conduction block; this may be confirmed with electrodiagnostic studies. The axon distal to the injury is intact, and there is nerve continuity across the site of injury. Excellent recovery is expected, and may occur within hours, days, weeks, or, at the maximum, a few months.

Axonotmesis — Axonotmesis typically occurs as a result of crush injuries, nerve stretch injuries (eg, motor vehicle accidents, falls), or percussion injuries (eg, gunshot wounds). The axon is locally but irreversibly damaged, and the myelin sheath is similarly involved. However, the surrounding stroma, including the endoneurium and perineurium, remains intact. Proximal to the lesion, the cell body undergoes changes including swelling and chromatolysis, which resolve with time. Distal to the lesion, the axon degenerates and the myelin sheath involutes; this process is known as Wallerian degeneration. In the first week after the injury, the distal nerve segment undergoes swelling with disappearance of neurofibrils, and then complete digestion of the axon and myelin components ensues. The proximal nerve segment also undergoes retrograde degeneration up to a few centimeters. Neuromuscular junction failure occurs five to six days after a neurotmetic lesion, even though any weakness caused by the injury is noted immediately [11]. Muscle atrophy occurs in the weeks after [3,6,12,13]. However, because the Schwann cells maintain their continuity, subsequent axonal regrowth may proceed along the bands of Büngner (representing Schwann cell proliferation) [12,14].

Prognosis depends upon several factors, including the degree of internal disorganization in the nerve, the distance to the end organ, anatomic particularities of a given nerve (nerves with simple branching patterns are more likely to reinnervate the target), and functional complexity of the nerve (pure sensory and pure motor nerves are more successful at reaching their target than mixed nerves).

Overall, partial recovery is the expected outcome, but the time course is significantly protracted as compared with neurapraxia.

Neurotmesis — Neurotmesis most often occurs in association with severe lesions, such as sharp injuries, traction injuries, percussion, or exposure to neurotoxic substances. The axon, myelin sheath, and surrounding stroma are all irreversibly damaged. The external continuity of the injured nerve is usually disrupted. No significant regeneration occurs with such a lesion, unless surgical reconstruction is performed.

Mechanisms of functional recovery — Despite the clear pathophysiologic distinctions described above, nerve lesions in most traumatic injuries are mixed. Thus, a single traumatic event will cause a combination of neurapraxia, axonotmesis, and neurotmesis in various degrees. The final outcome depends on the ratio between the individual components of the injury (ie, the predominant pathophysiologic feature), which may be difficult to assess clinically.

Mechanisms of peripheral nerve recovery include resolution of conduction block (in neurapraxic lesions), distal axonal sprouting (in axonotmetic lesions), and axonal regeneration (in axonotmetic and neurotmetic lesions) [3]. Not surprisingly, the speed and completeness of recovery depends on which process predominates.

●In a neurapraxic lesion, resolution of the conduction block is the mechanism promoting recovery of function after a nerve injury. Improvement is expected to be quick if the cause is ischemia, whereas improvement may take months if the cause is demyelination (depending upon the severity of the lesion and the length of the demyelinated segment).

●In an incomplete axonotmetic lesion, two forms of regeneration facilitate recovery. First, distal axonal sprouting from intact neighboring motor axons starts within four days after nerve injury. The sprouts may start at the distal nodes of Ranvier (nodal sprouts) or from nerve terminals (terminal sprouts). For axons that have undergone Wallerian degeneration, the proximal nerve stump begins to sprout regenerating axons that would start to penetrate the area of injury. In minor axonotmetic lesions, with preservation of the endoneurial tubes, the axons can traverse the segment of injury in 8 to 15 days and then regenerate along the distal nerve segment at a rate of 1 to 5 mm/day. The regeneration rate depends on location of the injury (faster for more proximal lesions) and type of injury (faster for crush injuries than for sharp lacerations) [3,13]. As an example, after a crush injury, the rate of axonal regeneration is approximately 8 mm/day in the upper arm, 6 mm/day in the upper forearm, 1 to 2 mm/day at the wrist, and 1 to 1.5 mm/day in the hand. After a nerve laceration, the axonal regeneration is expected at a rate of 1 to 2 mm/day [7]. In more severe axonotmetic lesions, with distortion of the endoneurial tubes and scarring formation, the axons penetrate the injury area more slowly. The regenerating axons may be misdirected, resulting in aberrant reinnervation, possibly never reaching their end organ, or reaching a "wrong" end organ (eg, resulting in facial synkinesis following an idiopathic facial nerve palsy). Axonal regeneration may also occur in a partial axonotmetic lesion along with distal axon sprouting, resulting in dually innervated muscle fibers.

●With complete neurotmesis, such as in a nerve transection, disruption of the axon as well as its supporting structures occurs. Spontaneous reversal of the changes is impossible as the nerve regenerates in a disorganized proliferation of axons, Schwann cells, and perineural cells within a collagenous stroma called a neuroma (picture 1). With surgical intervention (scarring debridement and approximation of the nerve ends or interposing of a nerve graft), the axon may grow along the endoneurial tubes of the distal segments. This process may take months to years until useful function is achieved. In neurotmesis, muscle recovery can only occur by axonal regeneration.

Recovery also depends on the integrity of the muscle when the nerve reaches it. The result of a nerve repair is likely to be poor if the denervation interval extends beyond the time that muscle fibrosis develops, typically one to two years [3,13,15]. However, this interval may be longer when a presentation is mixed or partial because some component of neuromuscular integrity can delay fibrosis by maintaining motor end plates.

These mechanisms of nerve regeneration affect motor and sensory fibers in a similar fashion. However, as the end organs for the sensory fibers do not degenerate (as the muscle does) the sensory recovery may continue for longer periods of time than motor system recovery [3].

COMMON LOCATIONS — This section will focus on describing the common locations of nerve injuries in relation to different mechanisms of trauma for median, ulnar, radial, sciatic, peroneal, tibial, and femoral neuropathies [7].

Traumatic brachial and lumbosacral plexopathies are discussed separately. (See "Brachial plexus syndromes", section on 'Traumatic plexopathies' and "Surgical treatment of brachial plexus injuries" and "Lumbosacral plexus syndromes", section on 'Trauma'.)

Median neuropathies — Median neuropathies caused by trauma most commonly occur at the wrist (carpal tunnel syndrome) and occur in a variety of situations, including crush injury of the hand and distal radius or carpal bone fractures. (See "Carpal tunnel syndrome: Pathophysiology and risk factors" and "Carpal tunnel syndrome: Clinical manifestations and diagnosis".)

The median nerve also can be injured at several levels across the arm, and different mechanisms of trauma are described at each location. Proximally in the axilla, the median nerve may be injured by compression due to prolonged use of crutches, missile injuries, stabbing wounds, and anterior shoulder dislocation. The resulting injury can be complex, involving multiple nerves including the ulnar and radial nerves (ie, triad neuropathy).

In the upper arm, the nerve may be injured by fractures of the humerus, stab wounds, or prolonged compression due to placement of a tourniquet. At the elbow and in the forearm, the most frequent causes for traumatic median neuropathy include fractures of the humerus (supracondylar and medial condyle), elbow dislocation, and injection injuries. Anterior interosseous nerve injury (branch of the median nerve in the forearm) may occur with midshaft fracture of the radius [7].

Ulnar neuropathies — Ulnar syndromes caused by trauma occur most often at the elbow and the wrist (see "Ulnar neuropathy at the elbow and wrist", section on 'Localization and etiology'). This is due to the anatomic vulnerabilities of the ulnar nerve at these locations. As an example, the ulnar nerve at the elbow traverses the extensor surface of the joint, which makes it susceptible to trauma.

The ulnar nerve may be injured in the axilla by use of crutches and in the upper arm by tourniquets applied to the upper arm. The nerve can be similarly injured during coma. Nerve injury may develop with supracondylar fractures of the humerus and by misplaced injections.

At the elbow, at the condylar groove, and at the cubital tunnel, different mechanisms of nerve injury are described: old fractures (medial and lateral epicondyles, supracondylar fractures of humeral shaft) with consequent development of tardy ulnar palsy, acute trauma, anesthesia (external pressure upon the ulnar nerve at the condylar groove, or prolonged flexion), and repetitive minor trauma that involves multiple episodes of pressure associated with elbow flexion (eg, leaning of the elbow on a desk). Rarely, in the forearm, the nerve may be injured as a complication of arteriovenous shunt placed for dialysis.

At the wrist and hand, ulnar neuropathies are commonly caused by chronic, repeated external pressure with cumulative effect, such as occupational use of the tools that press into the base of the hand, bicycle riding, pizza cutting, and others. However, acute trauma (eg, blunt trauma/laceration) as a mechanism for nerve injury may be encountered as well [7].

Radial neuropathies — Radial neuropathies caused by trauma commonly develop in the mid-upper arm. At this level, the nerve is especially vulnerable to trauma due to its proximity with the shaft of the humerus. Compression of the nerve main trunk may occur in the spiral groove or just proximally or distally. (See "Overview of upper extremity peripheral nerve syndromes", section on 'Radial neuropathy at the spiral groove'.)

Like traumatic median and ulnar neuropathies, the mechanism of injury differs based upon location. Causes of radial neuropathies in the upper arm include fractures of the humerus, blunt injuries, compression by prolonged tourniquet use, and misplaced injections. One of the common causes is prolonged external compression of the nerve during sleep, which can occur if the patient's head lies on the medial aspect of the upper arm, or when the arm hangs over the edge of a bench. Sedation or inebriation may prevent the patient from being wakened by the warning sign of paresthesia in the arm, leading to the term "Saturday night palsy" for this type of radial nerve injury. Similarly, the nerve may be compressed during general anesthesia or during coma.

Injury of the posterior interosseous nerve, a branch from the radial nerve in the proximal forearm, can be caused by fractures or dislocations of the radius, given the proximity of the nerve to the head and proximal shaft of the radius. In addition, secondary injury to the posterior interosseus nerve may accompany traumatic radial neuropathy associated with fractures of the humeral shaft [16].

Similar to the occurrence of the tardy ulnar neuropathy, a posterior interosseous neuropathy may occur years after a poorly healed elbow fracture, by exposure of the nerve to prolonged stretching and angulation forces [7]. (See "Overview of upper extremity peripheral nerve syndromes", section on 'Posterior interosseous neuropathy'.)

Sciatic neuropathies — Sciatic neuropathy caused by trauma occurs most often in the gluteal region, given its close proximity to the hip joint, associated with pelvic and hip joint fractures or with hip surgery. (See "Overview of lower extremity peripheral nerve syndromes", section on 'Sciatic nerve'.)

Similar to the other neuropathies described above, additional causes of sciatic neuropathy include missile wounds, external compression (eg, from coma, bicycling, prolonged assumed yoga "lotus" position), internal compression from deeply situated masses (eg, endometriosis, hematoma), and misplaced injections. In the thigh, the sciatic nerve is less often injured; most cases occur as a result of missile wounds. However, fractures of the femur, lacerations, and external compressions are possible mechanisms for trauma.

From a clinical perspective, the symptoms and signs of a traumatic sciatic neuropathy are the same as for other etiologies. However, sciatic nerve lesions are frequently incomplete, and often mimic common peroneal neuropathy. Proximal lesions can therefore be mistakenly diagnosed as a more distal neuropathy. Predominance of findings suggesting peroneal pathology are thought to be due to the greater vulnerability of the lateral trunk (common peroneal nerve) given the anatomic characteristics of the nerve, which is firmly fixed at the sciatic notch and fibular neck and contains fewer but larger fascicles and less supporting connective tissue when compared with the medial trunk (tibial nerve) [7].

Peroneal neuropathies — Peroneal neuropathies caused by trauma most frequently occur at the fibular head. This is explained by the close proximity of the nerve to the fibular head and its passage through the fibular tunnel, which is a tendinous tunnel between the edge of the peroneus longus muscle and the fibula. The common situations that are associated with nerve damage are external compression, such as during anesthesia, coma, prolonged leg-crossing, squatting, and compression from braces or plaster casts. In addition, direct trauma, such as blunt injuries, fractures of the fibula, knee dislocations, or traction injuries, may represent mechanisms for nerve injury [6,7,17]. (See "Overview of lower extremity peripheral nerve syndromes", section on 'Fibular (peroneal) nerve' and "Foot drop: Etiology, diagnosis, and treatment".)

Tibial neuropathies — Tibial neuropathies caused by trauma may occur at different levels. The most characteristic location is at the tarsal tunnel, where the damage may occur to the tibial nerve or its branches, the median and lateral plantar nerves (figure 1). External pressure (eg, tight shoes, casts), fractures at the ankle, twisting of the ankle, and post-traumatic fibrosis (occurring years after the initial injury) are some of the traumatic causes for nerve damage at this location [7]. (See "Overview of lower extremity peripheral nerve syndromes", section on 'Tibial nerve'.)

Femoral neuropathies — The location of the femoral nerve in the pelvis and upper leg renders it susceptible to a variety of iatrogenic injuries. In a systematic review, compression and ischemic injuries resulting from pelvic surgery were frequently reported [18]. Injury during hip surgery can also occur. Local trauma can lead to an iliopsoas hematoma that compresses the femoral nerve [19,20]. In a review of seven consecutive cases referred to a large electromyography center, six resulted from hip arthroplasty and one from a high femoral fracture [21]. (See "Overview of lower extremity peripheral nerve syndromes", section on 'Femoral nerve' and "Nerve injury associated with pelvic surgery".)

DIAGNOSIS — The diagnosis of a traumatic peripheral neuropathy is clinical and is based upon the presence of neurologic symptoms and signs consistent with a nerve injury along with a history of or suspicion for acute or repetitive trauma as the probable cause. To address these questions, a thorough clinical history and physical examination should be completed. For some patients, symptoms and signs may reveal overt sensorimotor loss corresponding to a specific nerve. For other patients, the clinical findings may be more subtle. As examples, patients with sensory loss may report symptoms of a dull ache. Those with a radial nerve compression of the forearm may report only vague shoulder pain.

The laboratory evaluation to support the clinical diagnosis of nerve injury includes electrodiagnostic studies, somatosensory evoked potentials, magnetic resonance imaging (MRI), magnetic resonance neurography, and ultrasound techniques.

Once a traumatic neuropathy is clinically diagnosed, the classification (ie, pathophysiology and severity) of the lesion should be determined, which often requires serial physical examinations and testing over time for closed nerve injury [22].

Evaluation — Clinicians evaluating patients with traumatic nerve injury are confronted with the following questions:

●Is there a single nerve lesion, or does the injury involve multiple nerves, plexus, or nerve roots?

●Is the pathophysiology one of neurotmesis, neurapraxia, axonotmesis, or a combination? (See 'Classification and pathophysiology' above.)

●How severe is the injury?

●What is the likelihood for recovery?

The symptoms and signs of traumatic peripheral neuropathies do not differ from their presentation associated with other etiologies. (See "Overview of upper extremity peripheral nerve syndromes" and "Overview of lower extremity peripheral nerve syndromes" and "Carpal tunnel syndrome: Clinical manifestations and diagnosis" and "Ulnar neuropathy at the elbow and wrist".)

However, some patients with severe injury may be unable to provide a reliable history or participate in a neurologic examination due to pain, sedative medications, or impaired alertness from concomitant head trauma. The approach to the evaluation for these patients is discussed in greater detail separately. (See "Severe upper extremity injury in the adult patient" and "Severe lower extremity injury in the adult patient".)

Electrodiagnostic testing is almost always indicated as part of the evaluation. In addition, imaging and ultrasound are useful adjunctive techniques when there is uncertainty after clinical and electrodiagnostic evaluation.

Electrodiagnostic testing — Electrodiagnostic testing with nerve conduction studies and electromyography provides information regarding localization, severity, and prognosis of the nerve injury [23-25]. (See "Overview of nerve conduction studies" and "Overview of electromyography".)

Electrodiagnostic testing may be performed early, at 7 to 10 days post-injury, to obtain a baseline study and information regarding localization. However, conduction block cannot be distinguished from axonotmesis or neurotmesis for up to one week, and evidence of muscle denervation is often not present until approximately three weeks post-injury. Thus, repeat electrodiagnostic testing at three weeks post-injury is often indicated to determine the pathophysiology of the injury.

Evidence for nerve regeneration may be sought any time after two months. Six months is usually regarded as the latest time for successful surgical anastomosis with complete neurotmesis, and is a useful time for reevaluation to assess nerve recovery [26].

Neurapraxic lesion — On nerve conduction studies, the hallmark of a neurapraxic lesion is the presence of a conduction block, which is characterized by preserved compound motor action potential (CMAP) amplitudes when the nerve is stimulated distal to the site of the injury and smaller or absent CMAP amplitude when the stimulation site is proximal to the injury [10]. In addition, neurapraxic lesions often cause slowing of conduction velocity across the lesion. Similar findings are obtained when recording from sensory nerves, but determining the presence of partial conduction block for sensory nerves is more complex than for motor nerves. Therefore, in a neurapraxic lesion, the localization of the injury is usually determined by motor nerve conduction studies. Electrophysiologic findings often parallel improvement of clinical symptoms, so that ongoing nerve conduction studies may be superfluous.

In neurapraxic lesions with conduction block, the only electromyographic finding may be decreased motor unit action potential (MUAP) recruitment when the lesion is incomplete or absent motor unit potentials with complete lesions. These changes are recorded immediately after the injury. As there is no associated axonal loss with neurapraxia, there will be no change in MUAP morphology. In addition, because there is no disruption of the neuromuscular junction and no denervated muscle fibers, no spontaneous activity such as fibrillation potentials or positive waves is expected.

Axonotmetic and neurotmetic lesions — The initial electrophysiologic changes in an axonotmetic lesion are similar to those found in a neurapraxic one, as the process of the Wallerian degeneration starts approximately at day 3 and is completed by days 5 through 8 for motor fibers and by days 7 through 10 for sensory fibers [6,10,27-29].

With occurrence of the Wallerian degeneration, the amplitudes of the CMAP and sensory nerve action potential (distally and proximally recorded) decline. The speed of this process depends on the length of the distal axon segment. Because there is no focal slowing or conduction block, it is difficult to localize the site of injury along the nerve-by-nerve conduction studies. In this situation, analyzing the denervation pattern by electromyographic sampling of the muscles may help determine the localization of the injury.

With incomplete lesions, the decreased number of axons manifests initially on electromyography as decreased recruitment. Over time, the motor unit territory of the surviving axons increases, as a consequence of the process of nerve sprouting, and the morphology of the MUAP changes, with increases in amplitude, duration, and number of phases (ie, typical neurogenic changes) [10].

With complete lesions, unstable motor unit potentials and nascent potentials (the earliest sign of reinnervation) may be recorded if the axon successfully regenerates and new neuromuscular junctions are formed. The nascent potentials usually precede any sign of clinical improvement. Fibrillation potentials may develop as soon as at 10 to 14 days, depending upon the length of the distal axon stump, with full development between 21 to 30 days.

Most nerve injuries present as mixed lesions (neurapraxia and axonotmesis) associating conduction block with partial axonal loss. The degree of axonal loss may be determined by comparing the distal motor response amplitude in the affected limb with that obtained in the contralateral limb. To further assess the degree of conduction block, the motor response amplitudes obtained distal to the lesion should be compared with those obtained proximal to the lesion [3,26].

Somatosensory evoked potentials — In cases when neuronal continuity is in question, somatosensory evoked potentials can provide important information regarding the axonal functional continuity. Occasionally, dermatomal somatosensory evoked potentials are useful when symptoms are in a distribution not well represented by commonly studied peripheral nerves [30,31].

Radiography — Certain nerve injuries are associated with different types of fractures, which are usually diagnosed by radiographs. For example, humeral fractures might be associated with radial nerve injuries, ulnar/radius fractures may be associated with ulnar and median nerves injuries, hip fractures are associated with sciatic nerve injuries, and distal femur fractures are associated with peroneal/tibial nerve injuries [4,13].

Magnetic resonance imaging — MRI techniques allow evaluation of the nerve in cross-section, and assessment of muscle changes in response to denervation [32].

Imaging features suggestive of peripheral nerve injury include nerve hyperintensity, perineural fibrosis, loss of fascicular pattern, bulbous enlargement, and discontinuity. Although all of these signs can be seen in the setting of a high-grade nerve injury, nerve discontinuity is the most specific predictor of severity [33].

Muscle denervation can be documented by certain MRI sequences (eg, short-tau inversion recovery) earlier than by electromyography. Reportedly, the MRI changes may become obvious as soon as four days post-injury and revert slowly as reinnervation develops. However, soon after an injury, neither MRI nor electrodiagnostic testing can differentiate between a neurapraxic and an axonotmetic lesion [34,35].

Magnetic resonance neurography (a refined MRI technique developed to improve image resolution) is a useful tool to evaluate proximal nerve involvement and complex nerve injuries and to monitor nerve recovery, as reversion of the MRI changes correlates with clinical improvement [36-38]. In chronic nerve injuries, neurography can also provide important information regarding the viability of the remaining muscle tissue and therefore the likelihood that it can be reinnervated [4,39]. Another method, magnetic resonance diffusion tensor imaging with tractography, is a quantitative technique that holds promise for visualizing peripheral nerve pathways [40-42]. Potential applications include distinguishing axonotmetic from neurotmetic nerve damage and monitoring recovery by demonstrating axonal regeneration (picture 2).

Ultrasound — Ultrasound can provide information regarding the neural pathology (eg, nerve caliber, presence of the distal nerve end, presence of neuroma) and extraneural pathology (eg, soft tissue involvement, such as scar tissue, hematoma), therefore allowing evaluation of the level, extent, and severity of the nerve lesion [32,43]. As an example, in one series of 98 patients with suspected traumatic nerve injury, findings from ultrasound modified the diagnostic and therapeutic approach in 65 patients (58 percent), including the distinction between nerve continuity or discontinuity, determination of etiology, and demonstration of multiple sites of injury [44].

This type of information can complement the data obtained through electrodiagnostic testing, proving valuable for management decisions. Also, the technique may be used in follow-up to assess nerve recovery. However, the utility of this modality may be limited because ultrasonographers with expertise in peripheral muscle and nerve evaluation are not always available [45,46]. (See "Diagnostic ultrasound in neuromuscular disease".)

TREATMENT OVERVIEW — After determining the type and severity of a traumatic neuropathy, the treatment approach is either surgical or conservative with close follow-up. Early mobilization, supervised physical therapy, and pain management are indicated. Referral to a multidisciplinary nerve injury program is indicated where available [47].

When approaching a traumatic neuropathy, the first decision is whether the treatment should be surgical or nonsurgical. Treatment differs based on whether there is evidence or high suspicion for nerve transection versus less severe injuries (algorithm 1) [4,47]. Surgical repair is typically pursued for patients with suspected nerve transection. For patients monitored serially with conservative management, surgical intervention is indicated if there are no clinical or electrodiagnostic signs of recovery by 6 to 12 months.

Other experts advocate for early surgical exploration of any traumatic nerve injuries, whether open or closed using intraoperative monitoring to determine if further surgical repair is necessary. The reason for an early approach is an easier exploration (due to less scaring) and possible improved outcomes for earlier compared with later repair [47].

Suspected nerve transection — For patients with a transected nerve or those with traumatic injuries where nerve transection is highly suspected (eg, bone fracture with clinical and imaging evidence suggestive of nerve discontinuity), surgical nerve repair is typically indicated, but the timing differs according to the mechanism of trauma [4,47]:

●For patients with sharp laceration/transection, immediate (eg, <72 hours) primary repair with tension-free end-to-end suturing may be performed.

●For patients with blunt transection, delayed surgical repair after acute inflammation resolves may be required to allow clear delineation of the healthy nerve ends. Surgery involves resection of the intraneural scar segment and subsequent nerve repair with or without a nerve graft or nerve transfer.

Nerve not likely transected — For patients with traumatic injuries where nerve transection is not suspected, immediate surgical exploration is usually not indicated. We suggest initial conservative medical management with close follow-up using serial clinical examinations, electrodiagnostic testing, and magnetic resonance neurography to monitor recovery (algorithm 1).

●For patients with electrodiagnostic evidence of axonal integrity at the site of the injury (neurapraxia), a conservative medical approach is advised because the prognosis is excellent, with expected recovery in weeks.

●More severe closed nerve injuries should be assessed with serial examinations and electrodiagnostic studies after four to six weeks. Severe crush or extreme traction injuries can disrupt nerve continuity producing either axonotmetic lesions that may recover with conservative treatment or neurotmetic lesions that do not.

•For patients with an absent nerve response across a traumatic nerve lesion in continuity (neurotmesis), a surgical approach with resection of the intraneural scar and graft repair is often performed.

•For patients with some nerve recovery either clinically (eg, paresthesia that migrate during sequential examinations) or electrodiagnostically (eg, polyphasic potentials and increases in nerve conduction amplitudes), continued conservative treatment with close follow-up every one to three months is pursued.

Surgical intervention is usually not indicated if there is electrodiagnostic evidence of axonal regeneration and muscle reinnervation and the nerve is demonstrated to be in continuity. However, surgical exploration prior to 6 to 12 months post-injury is often pursued if no recovery is documented [48-50]. In a study of 95 patients with traumatic radial nerve injury, electrodiagnostic testing was able to identify severe injury (no motor unit potentials) in 96 percent by four months [51].

Surgical techniques — The main goal of surgery is to restore motor and sensory neurologic function [15,52]. Different surgical techniques are used based on the type of nerve injury (algorithm 1).

For nerve lesions that are not in continuity, primary or secondary end-to-end anastomosis or repair using a nerve graft is required. For nerve lesions apparently in continuity, the surgical approach differs based on the results of direct intraoperative monitoring. External or internal neurolysis is the preferred approach if nerve action potentials are recorded. Split repair or resection of neuromas followed by end-to-end suture or graft repair is to be performed if no nerve action potentials are recorded. Reportedly, the most favorable results are achieved (in decreasing order) by performing neurolysis, suture repair, and graft repair [53-57].

Surgical techniques and management of upper and lower extremity nerve injury are reviewed in greater detail separately. (See "Surgical reconstruction of the upper extremity", section on 'Nerve repair/reconstruction' and "Surgical reconstruction of the lower extremity", section on 'Nerve repair/reconstruction' and "Surgical treatment of brachial plexus injuries", section on 'Techniques for managing traumatic injuries' and "Foot drop: Etiology, diagnosis, and treatment", section on 'Surgical management'.)

PROGNOSIS — The long-term outcome of a traumatic neuropathy varies according to patient age, the mechanism of trauma, the type and location of the nerve injury, the gap length, the pathophysiology of the injury (usually mixed), and the type and timing of surgery. Therefore, the prognosis of the injury may be difficult to predict. However, the prognosis can be estimated based upon the pathophysiology of the injury [3,23].

●Neurapraxic lesions (ischemia and focal demyelination) should resolve in up to three months.

●Mixed neurapraxic and axonotmetic injuries (demyelinating plus axonal) have a biphasic or bimodal recovery: the neurapraxic component resolves quickly, followed by a slower recovery of the axonal component that depends upon distal axonal sprouting, axonal regeneration from the site of the lesion, and the location of the injury. With strengthening exercises, muscle fiber hypertrophy may develop, providing additional recovery a few weeks after the injury. Typically, patients with this type of injury experience a relatively rapid but incomplete recovery, followed by slower further recovery that may continue for 18 months or longer [10]. Sensory recovery may continue after the motor (strength) recovery has reached a plateau.

●Partial axonotmetic (axonal loss) lesions may also have a bimodal recovery, with early incomplete recovery that is dependent upon distal axon sprouting and a later recovery phase that is driven by axonal regeneration.

●Neurotmetic lesions have the worst prognosis. The recovery depends only upon axonal regeneration. As mentioned before, the axonal regeneration rate depends on location of the injury and is generally faster for more proximal lesions. It also depends on the type of injury, and is usually faster for crush injuries than for sharp lacerations (see 'Mechanisms of functional recovery' above). Therefore, we recommend waiting two to four months and looking for evidence for reinnervation in previously denervated muscles close to the injury. Lesions with some spontaneous recovery, demonstrated by the presence of reinnervation, are treated conservatively. Lesions with no evidence for axonal regeneration should be addressed surgically.

The follow-up period for traumatic neuropathies should be individualized. Nerve recovery can be monitored for at least three years, if needed.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Severe blunt or penetrating extremity trauma".)

SUMMARY AND RECOMMENDATIONS

●Mechanisms of injury – Nerve injury due to trauma occurs from traction/stretch, laceration, compression, or ischemia. The nerve dysfunction results primarily from the direct mechanical forces applied to it and secondarily from the vascular compromise that follows, with consequent ischemic nerve damage. Most nerve injuries due to trauma involve a combination of the above mechanisms. (See 'Trauma mechanisms' above.)

●Classification – Nerve injuries are classified as neurapraxia, axonotmesis, and neurotmesis (table 1). (See 'Classification and pathophysiology' above.)

•Neurapraxia – Neurapraxia is usually caused by a mild injury that results in focal demyelination but no loss of axonal integrity.

•Axonotmesis – Axonotmesis typically occurs as a result of crush, stretch, or percussion injuries. The axon is locally but irreversibly damaged, and the myelin sheath is similarly involved. However, the surrounding stroma, including the endoneurium and perineurium, remains intact.

•Neurotmesis – Neurotmesis most often occurs in association with severe lesions, such as sharp injuries, traction injuries, percussion, or exposure to neurotoxic substances. The axon, myelin sheath, and surrounding stroma are all irreversibly damaged.

●Common sites of injury – Common locations of nerve injuries caused by trauma include the following:

•Median nerve – Median neuropathies most commonly occur at the wrist (see 'Median neuropathies' above)

•Ulnar nerve – Ulnar syndromes occur most often at the elbow and the wrist (see 'Ulnar neuropathies' above)

•Radian nerve – Radial neuropathies commonly develop in the mid-upper arm (see 'Radial neuropathies' above)

•Sciatic nerve – Sciatic neuropathies occur most often in the gluteal region (see 'Sciatic neuropathies' above)

•Peroneal nerve – Peroneal neuropathies most frequently occur at the fibular head (see 'Peroneal neuropathies' above)

•Tibial nerves – Tibial neuropathies most often occur at the tarsal tunnel. (see 'Tibial neuropathies' above)

●Diagnosis – The diagnosis of a traumatic peripheral neuropathy is clinical and is based upon the presence of neurologic symptoms and signs consistent with a nerve injury along with a history of or suspicion for acute or repetitive trauma as the probable cause. Electrodiagnostic testing provides information regarding localization, severity, and prognosis of the nerve injury. Imaging and ultrasound are useful adjunctive techniques when there is uncertainty after clinical and electrodiagnostic evaluation. (See 'Diagnosis' above.)

●Treatment – The treatment approach is either surgical or conservative with close follow-up. Early mobilization, supervised physical therapy, and pain management are indicated. The decision to pursue surgical treatment is based on whether there is evidence of or high suspicion for nerve transection (algorithm 1). (See 'Treatment overview' above.)

•Suspected nerve transection – For patients with a transected nerve or those with traumatic injuries where nerve transection is highly suspected (eg, bone fracture with clinical and imaging evidence suggestive of nerve discontinuity), surgical nerve repair is typically indicated (algorithm 1). (See 'Suspected nerve transection' above.)

•Nerve not likely transected – For patients with traumatic injuries where nerve transection is not suspected, we suggest initial conservative medical management with close follow-up using serial clinical examinations, electrodiagnostic testing at four to six weeks, and/or magnetic resonance neurography to monitor recovery (algorithm 1). (See 'Nerve not likely transected' above.)

-For patients with electrodiagnostic evidence of axonal integrity at the site of the injury (neurapraxia), a conservative medical approach is advised because the prognosis is excellent, with expected recovery in weeks.

-For patients with an absent nerve response across a traumatic nerve lesion in continuity (neurotmesis), a surgical approach with resection of the intraneural scar and graft repair is often performed.

-For patients with some nerve recovery either clinically or electrodiagnostically, continued conservative treatment with close follow-up every one to three months is pursued. Surgical intervention is usually not indicated if there is electrodiagnostic evidence of axonal regeneration and muscle reinnervation and the nerve is demonstrated to be in continuity. However, surgical exploration prior to 6 to 12 months post-injury is often pursued if no recovery is documented.