Sarah A. Eby
Jeffrey G. Jenkins
Eric J. Buchner
Trauma to peripheral nerves is a rare but important cause of sport-related injuries in the athlete (27).
The type of peripheral nervous system (PNS) injury that occurs can vary based on numerous factors including type of sport, level of competition, and age of athlete (53).
The segment of the PNS affected by injury, including nerve root, plexus, and peripheral nerve, also varies.
It is important for the physician to be aware of the presentation, diagnosis, prognosis, and treatment of common peripheral nerve injuries associated with certain sports and athletic participation in general.
This chapter will provide an overview of peripheral nerve anatomy and nerve injury diagnosis, classification, and prognosis, and identify common peripheral nerve injuries that will likely be encountered in the athletic population.
PERIPHERAL NERVE ANATOMY
Cell body: Located in the anterior horn of the spinal cord for motor neurons or in the dorsal root ganglion for sensory neurons
Axon: Projection from the cell body involved in propagation of an action potential and transport of cell nutrients. Axons may be myelinated or unmyelinated.
Myelin: Substance produced by Schwann cells, layered to form a myelin sheath around axons, that acts as insulation for the conduction of current.
Epineurium: Loose connective tissue that surrounds the entire nerve and protects it from compression.
Perineurium: Strong layer of connective tissue surrounding fascicles or bundles of nerve fibers.
Endoneurium: Connective tissue that surrounds an individual axon.
Etiology of peripheral nerve injury includes stretch or traction, compression, vibration, laceration, and ischemia (11).
Most traumatic peripheral nerve injuries occur in the upper extremity, with the ulnar nerve most frequently injured (11).
Seddon Classification of Nerve Injury
Neurapraxia denotes injury to myelin alone, with electrodiagnostic findings of conduction block and, later, conduction velocity slowing along the involved segment of nerve.
Axonotmesis describes injury to axons resulting in wallerian degeneration. Early electrodiagnostic findings include loss of nerve conduction across the site of the injury (indistinguishable from neurapraxia). Later findings of decreased or absent evoked potential amplitudes distal to the site of injury are seen as wallerian degeneration occurs.
Neurotmesis is complete disruption of the nerve, with injury to axons and wallerian degeneration as well as disruption of the supporting connective tissue. This type of injury carries a poor prognosis for recovery and usually requires urgent surgical intervention.
Electrodiagnostic testing cannot differentiate between complete axonotmetic lesions and neurotmesis because the difference between these types of lesions is in the integrity of the supporting structures, which have no electrophysiologic function.
Sunderland Classification of Nerve Injury
Organizes injury type based on the nerve anatomy involved.
Class 1: Injury to myelin alone (i.e., neurapraxia). Prognosis for recovery is excellent.
Class 2: Axonotmesis with injury to axons with intact endoneurium, perineurium, and epineurium. Prognosis is good in general but varies depending on percentage of axons injured and distance of lesion from muscle.
Class 3: Axonotmesis with injury to the endoneurium and sparing of the perineurium and epineurium. Prognosis is poor. Surgery may be required.
Class 4: Axonotmesis with injury to the endoneurium and perineurium and sparing of the epineurium. Prognosis is poor. Surgery is required to restore nerve continuity.
Class 5: Neurotmesis. Complete transection of the peripheral nerve. Surgery is required to restore nerve continuity. Prognosis for recovery is particularly poor (38).
DIAGNOSIS OF PERIPHERAL NERVE INJURY
Electrodiagnostic testing with nerve conduction studies (NCSs) and electromyography (EMG) is necessary to determine location, severity, and prognosis of nerve injury.
Timing of Electrodiagnostic Testing
Timing of testing depends on the question being asked.
Immediate to 7 days: Localization of injury with NCS, identifying conduction block versus axonotmesis (2,38).
1-2 weeks: Distinguishes complete lesions from incomplete lesions. May also distinguish axonal from demyelinating lesions (axonotmesis and neurotmesis from neurapraxia) (2).
3-4 weeks: Able to characterize lesion as EMG becomes useful. A single study at this point will yield the most information (2). Although EMG cannot accurately quantify axonal damage, it is the most sensitive indicator that axonal damage has occurred.
Prognosis is based on severity and type of damage to the nerve. Although purely neurapraxic (demyelinating) lesions have an excellent prognosis for fast and complete recovery, axonotmetic and neurotmetic lesions have variable outcomes based on the number of axons injured.
Axonal loss results in decreased evoked potential amplitudes. The best determination for degree of axonal loss is comparison to asymptomatic contralateral amplitude. A side-to-side amplitude difference of 50% is generally indicative of significant axonal loss.
EMG can determine complete versus partial functional denervation based on the absence or presence of motor unit action potentials. EMG can also demonstrate evidence of reinnervation based on the amplitude, phases, and duration of motor unit action potentials.
Most prognostication for motor recovery after peripheral nerve injury is extrapolated from a study of injured facial nerve compound motor action potential amplitudes in comparison with the asymptomatic contralateral side (45). Results indicated:
0%-10% amplitude of contralateral side: poor prognosis
10%-30% amplitude of contralateral side: good prognosis
> 30% amplitude of contralateral side: excellent prognosis
Mechanism of injury also contributes to prognosis, with avulsion-type injuries having the worst prognosis and compression injuries having the best prognosis (38).
Treatment of Nerve Injury
Early treatment is focused on pain control to allow for passive range of motion of the affected joint and limb.
Neuropathic pain is best managed with anticonvulsants, such as gabapentin, tricyclic antidepressants, and selective norepinephrine and serotonin reuptake inhibitors. Topical anesthetics and transcutaneous electrical nerve stimulation are good adjunct therapies (11,16,25).
Pain refractory to these medications and modalities can be managed with opioids, nonsteroidal anti-inflammatory medications, or in severe cases, a peripheral nerve or spinal block (11,25).
Desensitization techniques are important to reduce hypersensitivity and allodynia.
Function and range of motion are also preserved with static or dynamic splinting.
Surgical management of nerve injury is dependent on the nerve injured, the type of injury, and the timing of injury (11,44,48).
Acute surgery (within 72 hours of injury) is indicated when there is a sharp nerve transection or laceration, or a hematoma or pseudoaneurysm is compressing the nerve (38).
Early surgery (within several weeks of injury) is indicated when there was blunt transection or avulsion of the nerve or when complete nerve lesions are noted during initial vascular repair surgery or on imaging (38).
Delayed surgery (3-6 months from injury) is indicated in most cases when degree of nerve damage is uncertain. Because patients with incomplete nerve lesions have better outcomes without surgery, appropriate management involves watching and waiting for clinical or electrodiagnostic evidence of recovery (11).
Surgical techniques for nerve repair include external neurolysis, which involves removal of the damaged epineurium, end-to-end nerve anastomosis, and nerve transfer or grafting (11,48).
Repair to reinnervate the muscle must be performed before 12-18 months after injury, when irreversible damage to the denervated muscle occurs (11).
Procedures such as tendon and muscle transfer can restore function when the primary muscle is irreversibly damaged.
PERIPHERAL NERVE INJURY IN NONCONTACT SPORTS
PNS injuries make up a small percentage of all sport-related traumas. However, there are certain relatively safe sports in which peripheral nerve injuries comprise a large proportion of all injuries incurred. These are volleyball, cycling, and racquet sports.
Peripheral nerve injuries are unfortunately common in volleyball, with the most common being suprascapular nerve entrapment at the spinoglenoid notch.
This presents as painless weakness and atrophy of the infraspinatus in the dominant serving arm of the player.
Prevalence has been documented to range from 33% to 45% of symptomatic international-level players and to be 12% in asymptomatic players at the same level (17,19,53).
EMG reveals isolated infraspinatus denervation and motor unit loss (32,53). Possible etiologies of this specific nerve entrapment related to volleyball serving include increased shoulder range of motion and impingement of the infraspinatus branch of the suprascapular nerve between the edge of the spine of the scapula and the medial tendinous margin between the infraspinatus and supraspinatus muscles (40,53).
Cycling is commonly associated with two peripheral nerve injuries: ulnar neuropathy at the wrist, or “cyclist’s palsy,” and pudendal neuropathy.
Cyclist’s palsy presents as numbness and paresthesias in the ulnar distribution of the hand (small finger and ulnar half of the ring finger) and weakness of hand intrinsic muscles (24).
Ulnar neuropathy at the wrist is highly prevalent in long-distance cyclists and is independent of handlebar design (24,34)
Injury is due to compression of the ulnar nerve at the wrist. NCSs have demonstrated significantly increased distal motor latencies in the deep branch of the ulnar nerve after a long-distance cycling event, suggesting the possibility of acute trauma (1,24).
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