Peripheral nerve injury in sports.

Review Article

Peripheral Nerve Injury in Sports Brian W. Hainline, MD, FAAN ABSTRACT Purpose of Review: The purpose of this review is to discuss peripheral nerve injuries in sport and to discuss such injuries within the context of their mechanisms of action. Recent Findings: This review is based on the author’s personal experience combined with analysis of pertinent articles and reviews. Peripheral nerve injuries are uncommon in sport, but represent a potentially serious cause of morbidity to the athlete. Although making a diagnosis of the involved peripheral nerve is not necessarily difficult for the practicing neurologist, it is critical to always place peripheral nerve injury in sport within the context of sports medicine. Nerve injuries do not occur in isolation, but rather are intertwined with the conditioning of the athlete, the biomechanics of the sport, and the use of protective equipment. Summary: In assessing peripheral nerve injuries in sport, it is not enough to simply make a diagnosis of the involved nerve; the physician must also assess whether the nerve became injured through a process of direct acute compression or stretching, repetitive compression and stretching over time, or another mechanism such as ischemia or laceration. Diagnosing sports-related peripheral nerve injuries within the context of their mechanism of action better allows for the possibility of functional rehabilitation.

Address correspondence to Dr Brian W. Hainline, National Collegiate Athletic Association, PO Box 6222, Indianapolis, IN 46206, [email protected]. Relationship Disclosure: Dr Hainline reports no disclosure. Unlabeled Use of Product/Investigational Use Disclosure: Dr Hainline reports no disclosure. * 2014, American Academy of Neurology.

Continuum (Minneap Minn) 2014;20(6):1605–1628.

INTRODUCTION Peripheral nerve injury may develop during sport training and competition through a variety of mechanisms. The incidence of peripheral nerve injury in sport is not known because of a paucity of longitudinal studies addressing this issue; Hirasawa and Sakakida estimated that peripheral nerve injury accounts for less than 0.5% of sports-related injuries.1 Peripheral nerve injuries may present as any combination of pain, numbness, loss of motor function, and loss of functional movement. It is often a small decrement in performance or the inability to improve despite a progressive regimen of training that first alerts the sports clinician to the possibility of peripheral nerve injury in an athlete. Nerve injuries are classically categorized as neurapraxia, axonotmesis, or Continuum (Minneap Minn) 2014;20(6):1605–1628

neurotmesis.2 Neurapraxia is the mildest of nerve injuries and is characterized by temporary motor paralysis with or without sensory loss. Focal demyelination is present, with sparing of the axon. Because of preserved structural integrity, full nerve recovery is the rule as myelin is restored. Axonotmesis is a moderate nerve injury that is characterized by complete motor, sensory, and autonomic dysfunction. The axon is damaged, but structural integrity of the endoneurium, perineurium, and epineurium, which form the surrounding support structure of the nerve, remains. Recovery is slow and may be incomplete. Axonal regeneration occurs at a rate of 1 mm to 7 mm per day, and such regeneration may ultimately reach its target because regeneration is directed along the nerve support structure. www.ContinuumJournal.com

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

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Peripheral Nerve Injury KEY POINTS

h Nerve injuries do not occur in isolation, but rather are intertwined with the conditioning of the athlete, the biomechanics of the sport, and the use of protective equipment.

h Peripheral nerve injuries may present as any combination of pain, numbness, loss of motor function, and loss of functional movement.

h Overuse injuries develop when cumulative repetitive force is greater than that which a specific tissue is able to withstand.

Neurotmesis is the most severe nerve injury, with complete destruction of the nerve distal to the site of injury. Motor, sensory, and autonomic dysfunction are complete, with no hope of spontaneous recovery because of complete interruption of the structural integrity of both the nerve and its surrounding support structure. Recovery may only occur through direct surgical intervention. In addition to classifying nerve injury, it is important to define peripheral nerve injury in sport as acute versus subacute or chronic. Acute injuries are the result of immediate compressive, stretch, or laceration forces applied to the nerve. Although acute lesions may result from faulty athletic technique or biomechanics, they more often result from a sudden mishap (eg, a fall) or a sudden extrinsic force for which the athlete is not prepared (eg, a blindsided tackle). Subacute and chronic injuries, on the other hand, are best placed in the category of overuse injury. Overuse injuries develop when cumulative repetitive force is greater than that which a specific tissue is able to withstand. 3 Most authors refer to repetitive microtrauma as the defining characteristic of overuse injuries.

Schematic of periodization. Periodization requires a combination of overreaching and recovery to achieve peak performance. Overreaching is a normal process of training in which the accumulation of training and nontraining stressors leads to a short-term decrease in performance. Recovery is the body’s ability to return to a state of readiness following a physical or mental challenge.

FIGURE 5-1

Reprinted with permission from Kovacs M, United States Tennis Association Youth Symposium.4

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To understand overuse injuries, the discerning clinician must be aware of a multitude of factors, including the athlete’s training regimen, the biomechanics involved in training that are specific to the sport, relevant equipment, and periodization. Periodization is the systematic training of athletic activity that allows for a combination of cyclical peak performance and appropriate recovery. From a periodization perspective, it is critical to understand how the athlete recovers. Recovery must be defined on a daily, weekly, and longerterm calendar basis. Without proper recovery, the body is exposed to excessive forces from which it is not allowed time to repair. Training involves a process of overreaching, which leads to a temporary diminution in function (Figure 5-14). With proper recovery, the body can move to a state of supercompensation and an improved baseline of function. This process is repeated over time as athletes attempt to improve through regular training and targeted periodization. For the training regimen, it is important to understand if the athlete is simply training within his or her specified sport, or if the athlete is also performing strength training and conditioning in addition to the specified sport. If training is simply within the sport, then the athlete’s body may not have enough strength, endurance, or flexibility to withstand repetitive sport-specific forces. For sport biomechanics, it is important to understand if the athlete is properly utilizing the full kinetic chain continuum. The kinetic chain continuum means that forces are sequentially applied from the legs and torso to the upper body in order to generate speed and power. For example, in overhead sport activities, such as pitching in baseball, serving in tennis, and playing volleyball, at least 75% of the overhead force should be

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generated from the legs and torso. If dysfunction exists in this part of the kinetic chain, then excessive force generationVand overuse injury riskVwill occur in the region of the shoulder and upper arm. Case 5-1 demonstrates how peripheral nerve injuries resulting from overuse involve a complicated yet logical kinetic chain continuum. DIAGNOSIS Diagnosing a peripheral nerve injury requires a solid grounding in nerve anatomy and the relationship of peripheral nerves to surrounding soft tissue. This is especially true in subacute and chronic nerve injuries because the mechanism of injury invariably involves

repetitive compression/traction from the soft tissue. The following steps are usually required in making a peripheral nerve injury diagnosis. Localize the Lesion As in all of neurology, it is important to define anatomically the site of the lesion. For peripheral nerve injuries, the lesion may be at the spinal nerve root level or at the most distal segment of the nerve. It does not suffice to simply name the nerve that is involved, eg, ulnar nerve dysfunction. Rather, it is important to localize the site of the lesion along the nerve pathway through a careful neurologic examination. Because there may be differing motor and sensory innervation along the pathway

Case 5-1 A 25-year-old right-handed male tennis player was referred for further evaluation of his inability to hit a backhand volley. The patient had played competitive tennis most of his life, but noticed increasing difficulty hitting a high backhand volley over a period of 4 months because of loss of strength. One year earlier he had sustained a left ankle sprain, for which he rested and then returned to normal training, without any specific rehabilitation for the ankle injury. The musculoskeletal examination revealed scapular dyskinesis (a repetitive overuse pattern of abnormal motion of the scapula during coupled scapulohumeral movements) and poor left leg stabilization relative to the right leg. The neurologic examination revealed mild atrophy of the right infraspinatus muscle with associated infraspinatus weakness. (The backhand volley in tennis is dependent on infraspinatus function.) The diagnosis was suprascapular nerve injury at the spinoglenoid notch, likely as a result of repetitive compression and stretching from abnormal scapular movement. Further evaluation included an analysis of the patient’s service motion, which was noteworthy for a paucity of lower extremity force generation because of an unstable left ankle. This led to a compromised and excessive force-generating motion around the scapula and shoulder, which caused a pattern of inconsistent muscle firing. Treatment involved rest, followed by functional rehabilitation of the left ankle and the scapular support muscles, followed by improved serve biomechanics. The full rehabilitation involved a multidisciplinary team approach with the neurologist, physical therapist, strength and conditioning specialist, and personal coach. The patient made a full recovery without surgery. Comment. This case highlights the importance of not simply making a diagnosis based on lesion location, but also making a functional diagnosis that includes a thorough understanding of the concept of overuse injuries before making a treatment recommendation that is sport- and training-specific to the athlete. Continuum (Minneap Minn) 2014;20(6):1605–1628

KEY POINTS

h To understand overuse injuries, the discerning clinician must be aware of a multitude of factors, including the athlete’s training regimen, the biomechanics involved in training that are specific to the sport, relevant equipment, and periodization. Periodization is the systematic training of athletic activity that allows for a combination of cyclical peak performance and appropriate recovery.

h Without proper recovery from an overuse injury, the body is exposed to excessive forces from which it is not allowed time to repair.

h Diagnosing a peripheral nerve injury requires a solid grounding in nerve anatomy and the relationship of peripheral nerves to surrounding soft tissue.



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h The athlete may perceive weakness that is muscle-specific even though the examiner may not detect frank weakness through oppositional motor testing.

h Localizing the nerve injury and then defining the surrounding soft tissue becomes the foundation for a more thoughtful analysis of kinetic chain continuum forces that affect that particular area of the body. The kinetic chain continuum means that forces are sequentially applied from the legs and torso to the upper body in order to generate speed and power.

h The musculoskeletal examination may include a multidisciplinary approach with a physical therapist and coach, especially with regard to kinetic chain function.

h Needle EMG studies for peripheral nerve injuries should not be performed within the first 3 weeks of nerve injury, as they may be normal until wallerian degeneration is more complete.

of the nerve, the examination must be detailed with regard to motor and sensory function. Additionally, some athletes possess considerable strength relative to nonathletes, so the motor examination must take this into consideration. The athlete may perceive weakness that is muscle-specific even though the examiner may not detect frank weakness through oppositional motor testing. As an example of the importance of localization, the ulnar nerve is commonly injured in baseball pitchers in the region of the cubital tunnel. Localizing nerve dysfunction to the cubital tunnel allows for a focused evaluation of this region, which may lead to a musculoskeletal diagnosis of any combination of ulnar nerve compression at the cubital tunnel, ulnar nerve stretch injury from subluxation at the elbow, ulnar nerve compression from bone spurs in the ulnar groove, and ulnar nerve stretch injury from excessive valgus forces. Localizing the nerve injury and then defining the surrounding soft tissue becomes the foundation for a more thoughtful analysis of kinetic chain continuum forces that affect that particular area of the body (Case 5-2). For example, repetitive baseball pitching coupled with poor biomechanics can lead to a repetitive valgus force that pushes the forearm and hand toward the lateral side of the elbow, which leads to repetitive stress of the ulnar collateral ligament and subsequent stretch injury of the ulnar nerve. Define the Pathophysiology Acute injuries are easy to define pathophysiologically. They usually result from a direct, severe compressive force, laceration, stretch injury from a bone fracture or dislocation, or ischemic insult as a secondary response to a compartment syndrome. In each case, the acute event is noted and attempts are made to

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relieve any further nerve injury by surgery or immobilization. Subacute and chronic nerve injuries occur in the setting of musculoskeletal overuse, with the nerve undergoing repetitive compression, traction/stretch, or both. Over time, such repetitive microtrauma overwhelms the nerve’s ability to compensate in the setting of progressive soft tissue pathology. It is not enough to simply state that the pathology is from repetitive compression or traction, but rather the mechanism of action of such compression or traction must be identified. Defining pathophysiology requires a detailed musculoskeletal examination, something that is not often taught during a traditional neurology residency. The musculoskeletal examination includes a combination of assessing for the possibility of chronic compression or traction as a result of muscle imbalance, joint laxity, joint deformity, or kinetic chain dysfunction. Such an examination also requires a working knowledge of the athlete’s sport, because sportspecific movements may be the root cause of overuse injuries. The musculoskeletal examination may also include a multidisciplinary approach with a physical therapist and coach, especially with regard to kinetic chain function. ELECTRODIAGNOSTIC STUDIES The electrodiagnostic examination is an extension of the physical examination and can aid in precisely localizing the site and type of the lesion. The most common electrodiagnostic studies for peripheral nerve injuries include nerve conduction studies and EMG. Needle EMG studies should not be performed within the first 3 weeks of nerve injury, as they may be normal until wallerian degeneration is more complete.5 The EMG does not replace a careful neurologic examination; indeed, it should be an extension of a detailed



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KEY POINT

Case 5-2

h EMG can detect subtle

A 17-year-old right-handed male presented with symptoms of progressive elbow pain, medial hand numbness, and decreased ability to grip the baseball while pitching. The patient had played competitive baseball most of his life, and had specialized year-round as a baseball pitcher for the past 2 years with the hope of obtaining a college scholarship. He frequently pitched more than 80 pitches per game, and he played in different leagues throughout the year. Many times he rested only 2 or 3 days after pitching a game. He did very little off-field strengthening and conditioning. Examination revealed pain at the right cubital tunnel, with exacerbation of symptoms following prolonged elbow flexion. He had diminished two-point discrimination in the fifth digit of his right hand and subtle weakness of the flexor profundus (ulnar innervated). Nerve conduction study revealed slowing across the elbow; EMG was normal. Dynamic ultrasound revealed right ulnar nerve swelling at the elbow and subluxation of the nerve with full elbow flexion. Functional movement analysis revealed extreme inflexibility of the entire thoracic torso, with resultant compensatory valgus stress (force that pushes the forearm and hand toward the lateral side of the elbow, which can lead to repetitive stress of the ulnar collateral ligament and subsequent stretch injury of the ulnar nerve) at the elbow during pitching motion. Treatment included rest, followed by a serious educational intervention regarding periodization and the importance of functional movement. (Periodization is the systematic training of athletic activity that allows for a combination of cyclical peak performance and appropriate recovery.) The patient engaged in progressive physical therapy and improved his thoracic mobility considerably. He then changed his pitching motion, gaining considerable kinetic chain momentum from his legs and thoracic spinal region. (The kinetic chain continuum means that forces are sequentially applied from the legs and torso to the upper body in order to generate speed and power.) He recovered completely and ultimately played varsity college baseball. Comment. This case demonstrates some key points: (1) year-round sport specialization can lead to overuse injuries; (2) competing at an advanced level requires off-field training; (3) periodization is a critical part of normal recovery; (4) interruptions in the kinetic chain continuum lead to excessive force generation distal to the point of kinetic chain interruption; and (5) full recovery is possible if functional movement and periodization become incorporated into rehabilitation.

examination. It is the clinical examination that directs the EMG. However, EMG can detect subtle signs of motor dysfunction that are not noticeable through oppositional muscle testing, especially in well-trained athletes. Therefore, it is important to listen carefully to the athlete’s concerns, as he or she may be unable to perform at an expected functional level, suggesting underlying muscle weakness, although the physical examination may not deContinuum (Minneap Minn) 2014;20(6):1605–1628

signs of motor dysfunction that are not noticeable through oppositional muscle testing, especially in well-trained athletes.

tect the muscle weakness. In this case, the EMG study may detect motor unit configuration changes that help to confirm the diagnosis. Somatosensory evoked potentials are sometimes a useful adjunct to nerve conduction studies and EMG, especially for proximal nerve lesions that are difficult to assess by conventional nerve conduction studies, eg, brachial and lumbar plexus lesions or lesions of the lateral femoral cutaneous nerve. www.ContinuumJournal.com


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h Acute traumatic injuries may require imaging studies to assess the degree of soft tissue damage and to aid in making a decision regarding surgical intervention.

h Ultrasound is an often overlooked and underutilized imaging modality of peripheral nerve injury in sport.

h Not only can ultrasound detect abnormal nerve movement in a dynamic state, but it can also reveal nerve entrapment with joint movement.

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IMAGING STUDIES MRI may sometimes provide a useful adjunct to both diagnosis and prognosis of peripheral nerve injury in sport. This includes evaluating the suspected site of injury and the degree of muscle damage as a result of the injury. Acute traumatic injuries may require imaging studies to assess the degree of soft tissue damage and to aid in making a decision regarding surgical intervention. Additionally, MRI may provide early evidence of nerve dysfunction that is not detectable by electrodiagnostic studies. Nerve hyperintensity can be detected on T2-weighted MRI images within 24 hours of a nerve lesion. Muscle edema can be detected in subacute denervation.6 However, MRI alone does not provide meaningful information apart from the entire clinical picture regarding prognosis in acute nerve injury in sport. MRI may have a place in diagnosing subacute and chronic nerve injuries in sport. Although MRI will not normally provide more information than a careful clinical and electrodiagnostic examination with regard to nerve injury localization, it may provide useful information regarding the surrounding soft tissue. This is especially true in peripheral nerve injuries that are refractory to conventional treatment of rest and rehabilitation. In this case, MRI may detect other causes of nerve dysfunction, such as a cyst, frank nerve entrapment, or a nerve tumor. Ultrasound is an often overlooked and underutilized imaging modality of peripheral nerve injury in sport. In the author’s personal experience, ultrasound is used much more extensively in Europe than in the United States as an adjunct in the diagnosis and management of peripheral nerve injury in sport. Indeed, for over 10 years, ultrasound has been considered a routine clinical tool in the player treatment rooms of the French Open Tennis

Championships. Ultrasound imaging can be done immediately within the office, and because of technologic improvements, peripheral nerves can be imaged in a dynamic setting. For example, in the case of ulnar nerve dysfunction at the elbow, the ulnar nerve can be viewed with elbow flexion and extension, and ultrasound may reveal nerve subluxation.7 Not only can ultrasound detect abnormal nerve movement in a dynamic state, but it can also reveal nerve entrapment with joint movement. Furthermore, ultrasound can be used as a guide for therapeutic injections that are aimed at relieving perineural inflammation. However, ultrasound imaging is not part of traditional neurology residency or subspecialty fellowship training. Given its practical usefulness, ultrasound should become increasingly incorporated into the toolbox of the sports neurologist who manages peripheral nerve injuries. CLINICAL PRESENTATIONS Shoulder and Upper Extremity Injuries Stingers. A stinger (also known as a burner) is defined as transient neurologic dysfunction resulting from direct collision and subsequent pain or paresthesia, with or without weakness, of one upper extremity. Stingers occur commonly as acute injuries in American football and have also been described in basketball, bodybuilding/weightlifting, boxing, hockey, and wrestling. Typically, the athlete has undergone direct impact to the neck or shoulder and presents immediately with any combination of burning pain, numbness, tingling, and weakness of the upper extremity. Pain is often diffuse and nondermatomal. The mechanism of action is debated, and, in part, the mechanism of action must be placed within the context of the collision. When an athlete sustains a blow that results in downward displacement of the ipsilateral shoulder and



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contralateral neck flexion, the mechanism of action of neurologic dysfunction in the stinger is likely a traction injury to the brachial plexus. However, when the neck is flexed or rotated toward the affected upper extremity, the mechanism of action of neurologic dysfunction is likely from neural foraminal narrowing and compression of the exiting nerve root. Even sudden compression of a single nerve root may result in neurologic symptoms that are not confined to a single dermatome. No return-to-play guidelines exist for stingers. As they are commonplace in American football, the prevailing culture is for players to return to competition when symptoms resolve; some players return to play when they are still somewhat symptomatic. The issue for neurologists is to first define the mechanism of action of symptoms in the affected athlete and then to develop return-to-play guidelines as appropriate. If possible, it is important to understand the biomechanics of the inciting trauma to help distinguish brachial plexus from nerve root injury. Further management must also include assessing the functional strength of the ipsilateral shoulder and the scapulothoracic support. If an athlete develops recurring stingers as a result of suspected brachial plexus traction injury, then a problem with technique in blocking or tackling, shoulder/scapulothoracic support, or both likely exists, and these issues should be addressed as part of the athlete’s return-to-play considerations. If nerve root compromise is suspected, cervical spine imaging studies, including dynamic plain films, are indicated. Stingers need to be differentiated from cervical cord neurapraxia, which likely develops from sudden neck extension during collision in an athlete with a narrow spinal canal. Symptoms may vary, and unilateral symptoms of transient numbness or weakness may be difficult Continuum (Minneap Minn) 2014;20(6):1605–1628

to distinguish from nerve root or brachial plexus injury. Symptoms in more than one limb must be assumed to be from cervical cord injury. The likely mechanism is from sudden cervical spine shortening, buckling of the ligamentum flavum, subarachnoid space narrowing, and subsequent diminished blood flow or direct spinal cord pressure with subsequent neurologic dysfunction.8 Spinal accessory nerve injury. The spinal accessory nerve (cranial nerve XI) is a pure motor nerve that innervates the trapezius and sternocleidomastoid muscles. The spinal accessory nerve lies superficially in the neck, just posterior to the scalene muscles in the posterior triangle. Because of its superficial location, the spinal accessory nerve is vulnerable to either direct blows to the neck or traction injuries from contact that depress the shoulder with the head rotated in the contralateral direction (Figure 5-2).

FIGURE 5-2

KEY POINTS

h When an athlete sustains a blow that results in downward displacement of the ipsilateral shoulder and contralateral neck flexion, the mechanism of action of neurologic dysfunction in a stinger is likely a traction injury to the brachial plexus.

h If possible, it is important to understand the biomechanics of the inciting trauma of stingers to help distinguish brachial plexus from nerve root injury.

Superficial location of the spinal accessory nerve in the neck. The spinal accessory nerve is vulnerable to blunt trauma and traction injuries because of its superficial location in the neck. Printed with permission. B 2014 Cheryl Reynon.



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h Because of its superficial location, the spinal accessory nerve is vulnerable to either direct blows to the neck or traction injuries from contact that depress the shoulder with the head rotated in the contralateral direction.

h Because the long thoracic nerve is somewhat superficial and has considerable length, it may be susceptible to repeated traction injuries associated with abnormal shoulder movement.

h A winged scapula is not pathognomonic for long thoracic nerve injury and may result from dysfunction of other scapula-stabilizing muscles.

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Spinal accessory nerve injury has been described primarily as an acute injury in judo, karate, kickboxing, football, lacrosse, and hockey. Athletes present with difficulty elevating or shrugging the shoulder. The sternocleidomastoid is not involved because injury occurs distal to the site of sternocleidomastoid innervation. Most athletes have motor weakness for more than 3 months. Return-to-play guidelines are driven by recovery of motor function. Initial treatment includes physical therapy that focuses on maintaining range of motion while strengthening the shoulder and scapulothoracic support musculature. If recovery has not begun in 6 weeks, then nerve conduction studies and EMG are indicated. Electrodiagnostic studies may reveal denervation of the trapezius muscles. If reinnervation is not evident on EMG and motor weakness persists, surgical exploration may be considered. The athlete should not return to play until shoulder shrug strength and function have returned to normal.9 Long thoracic nerve injury. The long thoracic nerve is a pure motor nerve that innervates the serratus anterior. The long thoracic nerve travels laterally beneath the clavicle and then along the anterolateral aspect of the chest wall. Because the long thoracic nerve is somewhat superficial and has considerable length, it may be susceptible to repeated traction injuries associated with abnormal shoulder movement. Case series do not provide a definitive mechanism of action of injury. Acute injury may occur from sudden trauma to the lateral thoracic wall. More commonly, the clinical presentation is the result of chronic overuse injury in sports such as archery, bodybuilding, judo, karate, shooting, tennis, volleyball, wrestling, golf, and bowling. The mechanism of action of nerve injury likely results from some combination of repetitive hyperabduction of the shoulder, arm extension,

or shoulder protraction.9 In the author’s experience, scapular dyskinesia (a repetitive overuse pattern of abnormal motion of the scapula during coupled scapulohumeral movements) may be a predisposing factor. Athletes with long thoracic nerve injury present with discomfort around the shoulder girdle, poor active shoulder motion, and a winged scapula, especially during forward-pushing movements. A winged scapula is not pathognomonic for long thoracic nerve injury and may result from dysfunction of other scapula-stabilizing muscles. Nerve conduction studies and EMG should be performed to confirm isolated long thoracic nerve dysfunction versus other causes of scapular winging, including dysfunction of the trapezius and rhomboids. Treatment includes physical therapy, with a particular focus on scapular stabilization. Once scapular stabilization begins to return, the sportspecific biomechanics of the athlete should be assessed. No strict return-toplay guidelines have been established for long thoracic nerve injury, and full return of strength may take up to 2 years because of the length of the nerve. The important factor to consider is for the athlete to have functional scapular movement. Suprascapular nerve injury. The suprascapular nerve arises from the superior trunk of the brachial plexus and is a mixed sensory-motor nerve. The sensory branches cover the coracohumeral and coracoacromial ligaments, subacromial bursa, and the acromioclavicular and glenohumeral joints. The motor branch innervates the supraspinatus and infraspinatus muscles. Suprascapular nerve entrapment can lead to shoulder pain and posterior shoulder/scapular weakness. The suprascapular nerve courses through the posterior triangle of the neck and the trapezius muscle and passes through the suprascapular



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notch under the transverse scapular ligament (Figure 5-3). A branch to the supraspinatus arises at or just proximal to the transverse scapular ligament. The nerve then courses toward the spinoglenoid notch and around the scapular spine, passing through the spinoglenoid ligament and terminating in the infraspinatus muscle. Many variations in anatomy exist that have not been linked with certainty to suprascapular nerve entrapment. Although the suprascapular nerve may be injured from direct trauma, most often the nerve is injured through repetitive overhead motion. At the level of the suprascapular notch, the suprascapular nerve is susceptible to a sling effect, which is accentuated with scapular depression and retraction (from hyperabduction of the shoulder). The nerve is also susceptible at the spinoglenoid notch from repetitive overhead activity, especially in athletes who are baseball pitchers or fencers or who play volleyball or tennis. Athletes with suprascapular nerve injury report deep shoulder pain, and clinical examination reveals weakness, often with atrophy, of the infraspinatus muscle and sometimes the supraspinatus muscle, depending on the site of compression. Point tenderness and cross-adducting the arm across the chest can accentuate pain. Other rotator cuff muscles and proximal arm muscles are not involved. Electrodiagnostic studies can demonstrate both increased latency from Erb point to fixed locations in the supraspinatus and infraspinatus muscles, plus denervation in the affected muscles. Imaging studies (ultrasound and MRI) can outline the course of the nerve to rule out a ganglion cyst of the nerve and provide anatomic detail of muscle atrophy. Management of overuse causes of suprascapular nerve dysfunction initially includes rest, followed by rehabilitation. Rehabilitation of suprascapular nerve Continuum (Minneap Minn) 2014;20(6):1605–1628

FIGURE 5-3

Path of the suprascapular nerve. The nerve is most vulnerable to injury at the suprascapular and spinoglenoid notches. Printed with permission. B 2014 Cheryl Reynon.

injury must include an analysis of the athlete’s biomechanics and functional movement of overhead activity. Improper overhead technique may be causative, and this is usually coupled with scapular dyskinesia, which results from poor scapulothoracic stabilization. Poor scapulothoracic stabilization leads to faulty movement of the entire scapula, which may then predispose to repetitive stretch/compression of the nerve. Operative treatment for refractory cases includes release of the transverse scapular ligament for a proximal entrapment or release of the spinoglenoid ligament for distal lesions. Operative success is more often achieved for proximal lesions. With any approach, failure to address biomechanics and functional movement will lead to incomplete or no recovery.10 Axillary nerve injury. The axillary nerve arises from the posterior cord of the brachial plexus just before the posterior cord becomes the radial nerve (Figure 5-4). The axillary nerve courses posterior to the proximal radius; the nerve innervates the deltoid and teres minor muscles and supplies sensation to the lateral aspect of the

KEY POINTS

h Although the suprascapular nerve may be injured from direct trauma, most often the nerve is injured through repetitive overhead motion.

h Rehabilitation of suprascapular nerve injury must include an analysis of the athlete’s biomechanics and functional movement of overhead activity.



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h Axillary nerve injury presents acutely as a result of trauma from a direct blow, anterior shoulder dislocation, or humerus fracture.

h The musculocutaneous nerve is more commonly injured in the distal arm, with entrapment of the lateral cutaneous nerve between the distal biceps tendon and brachialis muscle.

FIGURE 5-4

The brachial plexus and formation of the major nerves of the upper extremity. The brachial plexus is formed from multiple cervical nerve roots and is the source of the major nerves of the upper extremity. Printed with permission. B 2014 Cheryl Reynon.

proximal arm. Axillary nerve injury presents acutely as a result of trauma from a direct blow, anterior shoulder dislocation, or humerus fracture. Athletes present with weakness of arm abduction, but rarely notice the small area of numbness in the upper arm, which can be detected by careful clinical examination. Electrodiagnostic studies can differentiate partial from complete injuries. Partial injuries will usually respond to rest and rehabilitation, which should include shoulder stabilization. Complete injuries require attempts at surgical repair of the nerve. The athlete’s return to play is guided by restoration of functional movement of the shoulder. Musculocutaneous nerve injury. The musculocutaneous nerve arises from the lateral cord of the brachial plexus (Figure 5-4), passes beneath the coracoid process, and travels down the

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medial aspect of the arm. It innervates the coracobrachialis, biceps, and brachialis muscles, and provides sensation to the radial/volar forearm through its terminal branch as the lateral cutaneous nerve of the forearm. Proximal nerve injury is relatively uncommon and results from repetitive overuse with hypertrophy of the coracobrachialis muscle and subsequent entrapment. Athletes present with elbow flexion weakness. Treatment in this case includes rest and a change in training; local injection or surgical release may be required for more refractory entrapment. The musculocutaneous nerve is more commonly injured in the distal arm, with entrapment of the lateral cutaneous nerve between the distal biceps tendon and brachialis muscle. In this scenario, the common mechanism of action is repetitive overuse that includes elbow extension and concomitant



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forearm pronation, eg, in athletes who play racket sports. Athletes present with any combination of pain, numbness, and paresthesia in the forearm that is exacerbated upon ball contact with the racket.11 Treatment of this type of presentation includes rest, followed by physical therapy and an analysis of sportspecific mechanics. A change in technique becomes the most effective longterm treatment, with specific attention to correcting an overreliance on power generation from the arm versus power generation through a proper kinetic chain continuum. Median nerve injury. The median nerve is formed from both the medial and lateral cords of the brachial plexus (Figure 5-4), travels across the medial aspect of the arm, and crosses between the two heads of the pronator teres as it enters the forearm (Figure 5-5).

FIGURE 5-5

At this level, the median nerve runs beneath the lacertus fibrosis and under the flexor digitorum superficialis arch. More distally, the median nerve gives rise to the anterior interosseous nerve, which specifically innervates the flexor pollicis longus, pronator quadratus, and flexor digitorum profundus. The median nerve innervates all flexor muscles in the forearm except the flexor carpi ulnaris and the medial two digits of the flexor digitorum profundus (both innervated by the ulnar nerve). Sensory branches innervate the palmar/lateral aspect of the hand, including the first three and a half digits. The main trunk of the median nerve courses more distally through the carpal tunnel, which is an enclosed space formed by the carpal wrist bones and the transverse carpal ligament. In the hand, the median nerve that traverses the carpal tunnel innervates the lumbricals (1 and 2),

Course of the median nerve. Note the relationship to the pronator teres in the forearm, a common source of entrapment. Printed with permission. B 2014 Cheryl Reynon.

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h The pronator syndrome is synonymous with median nerve entrapment in the forearm and results from repetitive overuse, specifically at the elbow and forearm.

h Carpal tunnel syndrome is common in athletes and nonathletes.

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opponens pollicis, abductor pollicis brevis, and flexor pollicis brevis. The pronator syndrome is synonymous with median nerve entrapment in the forearm and results from repetitive overuse, specifically at the elbow and forearm.12 The nerve can become entrapped by the two heads of the pronator teres (provoked on examination by resisted pronation of the extended forearm) or from either the lacertus fibrosis (provoked on examination by resisted elbow flexion and forearm supination) or flexor digitorum superficialis arch (provoked on examination by resistance to flexion of the third proximal interphalangeal joint).4 Athletes present with proximal forearm pain; numbness may occur in the hand if the median nerve is compressed, but will not occur if the anterior interosseous nerve (which is purely motor) is compressed. There may be weakness in forearm pronation, wrist flexion, and grip strength. The provocative tests described above are usually more helpful than electrodiagnostic studies in making a diagnosis. Dynamic ultrasound imaging can help to localize the site of compression. Pronator syndrome has been described in archery, baseball, weightlifting, and racket sports. Treatment includes rest and physical therapy, with a focus on functional restoration and proper sport-specific mechanics, again with an emphasis on proper kinetic chain force generation. Ultrasound-guided injections may alleviate pain. For refractory cases, surgical decompression may be necessary. Carpal tunnel syndrome is common in athletes and nonathletes.11 Athletes who apply excessive pressure over the palmar aspect of the hand are at risk, especially cyclists and wheelchair athletes. Carpal tunnel syndrome has also been described in archery, bodybuilding, weightlifting, football, golf, wrestling, and tennis. Athletes often present with numbness or pain in the lateral three and a half digits

of the palm, possibly with hand grip weakness. Prolonged wrist flexion can exacerbate symptoms because of venous backflow through the carpal tunnel, and shaking the hands may help to alleviate such symptoms. Treatment includes splinting the wrist in a neutral position, possibly coupled by a corticosteroid injection in the carpal tunnel space. Rehabilitation should focus on an assessment of functional sport-specific biomechanics. Surgical decompression of the carpal tunnel may be necessary for more refractory cases. Ulnar nerve injury. The ulnar nerve is formed from the medial cord of the brachial plexus (Figure 5-4). The ulnar nerve travels in the medial arm and traverses posteriorly between the medial head of the triceps and the overlying arcade of Struthers. The nerve then passes behind the medial epicondyle in the ulnar groove and enters the forearm under the flexor carpi ulnaris in the cubital tunnel, which is formed from the two heads of the flexor carpi ulnaris and the arcuate ligament (Figure 5-6). The ulnar nerve innervates the flexor carpi ulnaris and the flexor digitorum profundus (fourth and fifth digits). Sensation includes the palmar aspect of the fifth digit and half of the fourth digit, plus the palmar/medial aspect of the hand. More distally, the ulnar nerve enters the hand through the Guyon canal, which is a space formed by the pisiform and hamate carpal bones and the carpal ligament. Within the hand, the ulnar nerve innervates the hypothenar muscles, medial lumbrical muscles, dorsal interossei, palmar interossei, adductor pollicis, deep head of the flexor pollicis brevis, and palmaris brevis. The ulnar nerve can be injured acutely from a direct blow to the back of the elbow in contact sports. More commonly, ulnar nerve injury results from traction or compressive forces at the elbow in the setting of repetitive



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FIGURE 5-6

The ulnar nerve and cubital tunnel. Traction and compression injuries are common at the cubital tunnel in the elbow. Printed with permission. B 2014 Cheryl Reynon.

overuse. Ulnar nerve dysfunction may be caused by excessive elbow valgus forces, especially from pitching in baseball (Case 5-2); compression at the cubital tunnel from repetitive stress; or spur formation in the ulnar groove with subsequent nerve compression.5,11 Athletes present with numbness/ discomfort in the fifth digit and half of the fourth digit (provoked by forced elbow flexion), sometimes accompanied by pain in the same distribution and loss of grip strength. Nerve conduction studies and EMG can localize the site of the ulnar nerve entrapment. Dynamic ultrasound can demonstrate both ulnar nerve thickening at the elbow and nerve subluxation/compression. Treatment includes rest and functional rehabilitation, which must address proper sport-specific biomechanics. A localized corticosteroid injection may provide relief of symptoms. Surgical transposition of the ulnar nerve or simple decompression may be required for more refractory cases. Distal ulnar nerve compression can occur at the wrist (Guyon canal) as a direct compressive injury and has been described in wheelchair athletes, bicyclists, cross-country skiers, and snowmobilers. Treatment in this Continuum (Minneap Minn) 2014;20(6):1605–1628

case focuses on relieving the site of compression, either through supportive braces/specialized gloves or a change in technique. Radial nerve injury. The radial nerve is an extension of the posterior cord of the brachial plexus (Figure 5-4). The radial nerve courses in the posterior compartment of the upper arm and enters the radial sulcus on the humerus (Figure 5-7). From there, the nerve enters the anterior compartment of the arm between the brachialis and brachioradialis muscles.13 At the elbow, the radial nerve branches into a sensory nerve and the posterior interosseous nerve. The posterior interosseous nerve begins after the radial nerve travels through the supinator muscle through the arcade of Fro ¨hse, which is a potential site of entrapment. In the proximal arm, the radial nerve innervates the triceps, extensor carpi radialis longus, extensor carpi radialis brevis, and the brachioradialis muscles. The posterior interosseous nerve innervates the extensor muscles of the hand and the abductor pollicis longus. The sensory branch of the radial nerve supplies the dorsolateral hand, including the first three and a half digits.

KEY POINTS

h Ulnar nerve injury commonly results from traction or compressive forces at the elbow in the setting of repetitive overuse.

h Dynamic ultrasound can demonstrate both ulnar nerve thickening at the elbow and nerve subluxation/compression.

h Distal ulnar nerve compression can occur at the wrist (Guyon canal) as a direct compressive injury and has been described in wheelchair athletes, bicyclists, cross-country skiers, and snowmobilers.



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h Proximal radial nerve injury has been described as resulting from forceful, repetitive elbow extension.

h Athletes with posterior interosseous nerve entrapment present with forearm pain that is worsened with supination resistance with the elbow at 90 degrees.

FIGURE 5-7

Course of the radial nerve. This nerve is an extension of the posterior cord of the brachial plexus. Printed with permission. B 2014 Cheryl Reynon.

Radial nerve palsy has been described as an acute injury from inadvertent compression as the nerve courses along the triceps muscle, but this is rare in sports. Proximal radial nerve injury has been described as resulting from forceful, repetitive elbow extension.

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Athletes present with brachioradialis and extensor wrist/finger weakness with sensory loss along the dorsolateral hand. The posterior interosseous nerve is susceptible to repetitive overuse injury in the proximal fibrous origin of the supinator muscle, within the arcade



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of Fro ¨ hse; other sites include the fibrous bands from the radiocapitellar joint and the tendinous origin of the extensor carpi radialis brevis.5,11 The mechanism of action is repetitive pronation and supination, as occurs in racket sports, especially tennis. Although faulty technique has not been described as causative, it is the author’s opinion that overreliance on the forearm for force generation can be causative. Athletes with posterior interosseous nerve entrapment present with forearm pain that is worsened with supination resistance with the elbow at 90 degrees. No sensory loss occurs with a posterior interosseous nerve lesion. Weakness is observed in the finger extensors with radial wrist deviation upon extension. Treatment includes rest and functional physical therapy, with a focus on the kinetic chain and stroke mechanics. For refractory cases, surgical release of the forearm entrapment may be indicated. Lower Extremity Injuries Ilioinguinal and iliohypogastric nerve injuries. The ilioinguinal and iliohypogastric nerves run a similar course through the lower abdomen and are commonly overlooked as sources of repetitive overuse injury in sport.14 They are more commonly associated with inadvertent injuries from surgery in the lower abdominal and inguinal region. Because these nerves run a similar course and are not well described in the sports medicine literature, they will be considered together. The ilioinguinal nerve is a branch of the first lumbar nerve that passes along the lateral psoas muscle and then travels obliquely across the quadratus lumborum and iliacus to perforate the transversus abdominis. The ilioinguinal nerve innervates the lowest portions of the transversus abdominis and internal oblique muscles. The sensory branches supply the pubic Continuum (Minneap Minn) 2014;20(6):1605–1628

symphysis, the superior and medial aspect of the femoral triangle, and the root of the penis/anterior scrotum in the male and the mons pubis/labia majora in the female. The iliohypogastric nerve also arises from the first lumbar nerve, traverses the psoas muscle and lateral abdominal wall, and courses through the transversus abdominis muscle at the margin of the internal oblique musculature (Figure 5-8). The iliohypogastric nerve innervates the lower fibers of the transversus abdominis and internal oblique muscles. The sensory branches supply a small region just superior to the pubis.

FIGURE 5-8

The lumbar plexus. The lumbar plexus arises from lumbar and sacral nerve roots, and is the source of the major nerves of the lower extremity. Printed with permission. B 2014 Cheryl Reynon.



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h The ilioinguinal and iliohypogastric nerves may be injured in association with repetitive microtrauma and scarring of the transversus abdominis or internal oblique muscles.

h Lateral femoral cutaneous nerve injury can develop acutely through blunt trauma in the inguinal region, especially in contact/collision sports such as football and rugby.

FIGURE 5-9

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The ilioinguinal and iliohypogastric nerves may be injured in association with repetitive microtrauma and scarring of the transversus abdominis or internal oblique muscles. The author has evaluated several athletes who presented with lower abdominal dysesthesia and referred pain in the pubic or genital region. Pain may be reproduced upon palpation in the lateral inguinal region and with provocative resistance to selective muscle contraction of the transversus abdominis and internal oblique muscles. It is often difficult to isolate these muscles in confrontational testing, but ultrasound is very useful in guiding the athlete to selective muscle contraction. Athletes with injuries to the ilioinguinal or iliohypogastric nerves note an inability to fully engage their core musculature, especially in eccentric loading during hyperextension. Although muscle weakness is difficult to discern, dynamic ultrasound often reveals subtle tears of the transversus abdominis muscle, sometimes with associated scar tissue and lack of muscle activation (Figure 5-9). Diagnosis is confirmed with demonstration of sen-

Ultrasound of core musculature. Ultrasound is a valuable tool to identify dynamic images of core musculature.

sory loss in the appropriate distribution. Treatment includes rest and functional physical therapy. In particular, athletes learn to sequentially activate their core musculature while avoiding an overreliance on the midline rectus abdominis muscles. Lateral femoral cutaneous nerve injury. The lateral femoral cutaneous nerve is a pure sensory nerve derived from the L2 and L3 nerve roots (Figure 5-8). The lateral femoral cutaneous nerve courses through the midpelvic region over the iliacus toward the anterior superior iliac spine, where it then travels posterior to the inguinal ligament and superior to the sartorius muscle at the iliac crest region (Figure 5-10). Sensory innervation is in a fairly well-circumscribed region of the anterolateral thigh, not conforming to the traditional L2 or L3 sensory distribution. Lateral femoral cutaneous nerve injury can develop acutely through blunt trauma in the inguinal region, especially in contact/collision sports such as football and rugby. Athletes develop pain, numbness, and paresthesia over the anterolateral thigh following contact, and symptoms may persist for hours to months, depending on the extent of nerve injury. Repetitive overuse injury of the lateral femoral cutaneous nerve develops in one of two mechanisms: (1) following repetitive flexion and extension of the hip, especially in jumping sports such as gymnastics; or (2) following compression from external gear, eg, scuba diving in a tight wetsuit or mountain climbing with a low-lying backpack that attaches across the groin (Case 5-3).15 Symptoms may develop more insidiously, with numbness and paresthesia over the anterolateral thigh. Athletes often report burning pain, and symptoms frequently worsen with hip extension or lying supine.



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KEY POINT

h The diagnosis of lateral femoral cutaneous nerve injury is straightforward if the clinician is thinking about this possibility, and the sensory examination will confirm the diagnosis.

FIGURE 5-10

Femoral and lateral femoral cutaneous nerves. The pure sensory lateral femoral cutaneous nerve is more commonly injured in sport than the femoral nerve. Printed with permission. B 2014 Cheryl Reynon.

The diagnosis of lateral femoral cutaneous nerve injury is straightforward if the clinician is thinking about this possibility, and the sensory examination will confirm the diagnosis. Traditional nerve conduction studies and EMG are unremarkable, although somatosensory evoked potentials of the lateral femoral cutaneous nerve may demonstrate a peripheral delay. Treatment includes rest, possibly with a localized corticosteroid injection in the inguinal region of the nerve. Because some athletes develop more significant burning pain, medications such as anticonvulsants or antidepressants may be necessary.16 Treatment should also include a review of equipment utilization and Continuum (Minneap Minn) 2014;20(6):1605–1628

technique with regard to hip hyperextension. This syndrome is often referred to as meralgia paresthetica and is frequently misdiagnosed as a lumbar radiculopathy. Femoral nerve injury. The femoral nerve arises from the ventral rami of L2, L3, and L4 and forms the largest branch of the lumbar plexus (Figure 5-8). The femoral nerve passes along the lateral border of the psoas muscle, adjacent to the iliacus muscle, and travels under the inguinal ligament, where it divides into multiple branches within the femoral triangle (Figure 5-10). Motor innervation is to the quadriceps. Sensory innervation includes the anterior and medial thigh; the nerve continues as www.ContinuumJournal.com


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h Femoral nerve injury is unusual in sport and results from an acute traumatic injury following sudden collision, often with hip hyperextension.

h Because femoral nerve injury in sport is posttraumatic, patients should undergo MRI of the pelvis to rule out a tear or hemorrhage of the iliopsoas muscle.

Case 5-3 A 40-year-old woman presented with concerns of left thigh numbness and pain. She developed symptoms following a 1-week scuba diving trip, during which she rented equipment and dove daily. She sustained no acute trauma, but noticed vague numbness and a ‘‘sunburn-like’’ sensation over her left anterolateral thigh. Her symptoms worsened on a daily basis, but there was no evidence of sunburn or other skin discoloration. She denied low back pain or leg weakness. She had undergone outside treatment with her primary physician and an orthopedic surgeon, both of whom diagnosed sciatica. MRI of the lumbar spine, ordered by her orthopedic surgeon, revealed degenerative disc changes from L2 through L4, with multilevel foraminal narrowing but without disc herniation or central lumbar stenosis. Lumbar epidural corticosteroid injections and transforaminal injections at L2 and L3 had not relieved her symptoms. The patient sought an additional opinion when spinal surgery was recommended. The musculoskeletal examination was notable for pain provocation with palpation in the inguinal region. There was no inguinal fullness or mass. Her lumbar spine range of motion was unremarkable. Neurologic examination revealed mild allodynia with associated sensory loss in the left anterolateral thigh, conforming to the distribution of the lateral femoral cutaneous nerve. Motor examination and reflexes were normal. Following the diagnosis of a lateral femoral cutaneous nerve injury, a therapeutic corticosteroid injection was delivered in the left inguinal region, adjacent to the pathway of the nerve. The patient obtained good relief, and a second injection 3 weeks later led to long-lasting relief of her symptoms. A review of the patient’s scuba diving equipment revealed that the gear was rather tight-fitting in the inguinal ligament region. Indeed, she noticed much more severe pain when wearing her equipment during the last 2 days of diving. Comment. This patient had classic sensory symptoms of lateral femoral cutaneous nerve injury and sport participation that provided a logical mechanism of action for her symptoms.

the saphenous nerve, which provides sensation to the anteromedial leg below the knee. Femoral nerve injury is unusual in sport and results from an acute traumatic injury following sudden collision, often with hip hyperextension. Femoral nerve injury has been described in gymnastics, football, dancing, long jumping, basketball, ballet dancing, bodybuilding, and cross-country skiing.5,11,15 Athletes present with inguinal pain, thigh numbness, and leg weakness, specifically leg buckling from quadriceps weakness. Examination findings are noticeable for provocation of pain with hip extension. Neurologic examination reveals patchy numbness in the thigh, quadriceps weakness, and a diminished

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or absent knee reflex. Because femoral nerve injury is posttraumatic, patients should undergo MRI of the pelvis to rule out a tear or hemorrhage of the iliopsoas muscle. This injury can usually be managed without surgery, even in the setting of a hematoma. Return to play is guided by restoration of both quadriceps and iliopsoas function. In particular, functional movement of the iliopsoas should be addressed if this muscle was injured during the trauma. Sciatic nerve injury. The sciatic nerve is formed from the anterior and posterior ventral rami of L4-S2 and the anterior ventral ramus of S3. The sciatic nerve courses through the pelvis and exits at the greater sciatic foramen lateral



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to the ischial tuberosity and beneath the piriformis muscle (Figure 5-11). The sciatic nerve innervates the hamstring muscles proximally. The nerve divides into the laterally placed common fibular (previously known as the peroneal) nerve17 and medially placed tibial nerve; bifurcation occurs at variable levels, but most often just proximal to the popliteal fossa.

FIGURE 5-11

Fibular motor innervation controls foot and ankle extension and ankle eversion; tibial motor innervation controls ankle and foot flexion and ankle inversion. Sciatic nerve injury is unusual in sports, and results from major trauma such as a fall, with or without fracture of the hip or proximal tibia. Athletes present with variable sensory loss in the distal leg, sparing the saphenous nerve distribution,

KEY POINT

h Sciatic nerve injury is unusual in sports, and results from major trauma such as a fall, with or without fracture of the hip or proximal tibia.

Course of the sciatic nerve. The sciatic nerve branches into the fibular (peroneal) and posterior tibial nerves. Printed with permission. B 2014 Cheryl Reynon.




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Peripheral Nerve Injury KEY POINT

h Common fibular nerve injury can develop as an acute traumatic event or as part of an overuse injury.

FIGURE 5-12

with variable weakness of foot and ankle extension and flexion. There may be preferential weakness of the fibular or tibial branch, depending on the site of trauma. All patients should undergo leg imaging (plain x-rays and MRI as warranted) to assess the extent of damage.

Course of the fibular nerve. The common fibular nerve gives rise to the superficial and deep fibular nerves. Printed with permission. B 2014 Cheryl Reynon.

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The piriformis syndrome is a controversial clinical condition in sports medicine. Theoretically, sciatic nerve entrapment or irritation develops from compression at the level of the piriformis secondary to piriformis hypertrophy, although evidence is lacking regarding actual nerve entrapment.18 Patients may present with variations of gluteal and referred leg pain. Because the role of piriformis hypertrophy and nerve entrapment is poorly documented, piriformis syndrome is also referred to as deep gluteal syndrome.18 Fibular nerve injury. The common fibular nerve is a continuation of the lateral sciatic nerve (Figure 5-11). The common fibular nerve descends through the popliteal fossa and passes behind the head of the fibula, turning obliquely around the fibular neck (Figure 5-12). The common fibular nerve divides into the superficial and deep fibular nerves after traveling through the peroneus longus muscle. The superficial fibular nerve innervates the peroneus longus and brevis muscles (ankle eversion) and supplies sensation to the dorsum of the foot. The deep fibular nerve innervates the tibialis anterior muscle and all toe extensors, while providing sensation to a well-circumscribed area in the first webspace of the foot. Common fibular nerve injury can develop as an acute traumatic event or as part of an overuse injury. Because of the superficial location of the common fibular nerve, it is susceptible to blunt trauma, especially in sports such as hockey, soccer, and football.11 In these cases, athletes may present with sudden numbness in the foot with associated partial or complete footdrop. In many cases, blunt trauma causes a neurapraxic injury that recovers in minutes to days. Return to play is guided by functional recovery of ankle movement.



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The fibular nerve may be injured in conjunction with adduction knee injuries or lateral ankle sprains. In this setting, traction is applied to the nerve, and athletes present with variable foot numbness and weakness of ankle and foot extension and eversion. Fibular nerve injury may be overlooked in ankle sprains, and poor recovery may be incorrectly attributed to incomplete ankle rehabilitation.19 It is for this reason that the clinician should have a heightened awareness of possible fibular nerve injury in ankle sprains; ankle weakness will not only prevent proper rehabilitation, but will also render the athlete susceptible to further ankle sprains. Nerve conduction studies and EMG will document fibular nerve injury. Treatment is focused on physical therapy and functional restoration of leg and ankle movement. The fibular nerve is susceptible to repetitive stress, especially in runners.20 The common fibular nerve may be irritated along the fibular neck as the nerve travels through the peroneus longus muscle; at this level, the nerve may be compressed by a tight fascial band. Athletes are normally not symptomatic at rest or with walking. Upon running, symptomatic athletes report pain, paresthesia, and footdrop. Nerve entrapment can be confirmed by nerve conduction studies and EMG, including prerunning and postrunning. The literature is scant regarding biomechanical predisposition to entrapment, such as hypermobility of the fibular head or hyperadduction with running, and no reasonable studies have been conducted on the effect of footwear and orthotics on this condition. Surgical release at the fascial band has been reported to alleviate symptoms.11 Runners and other athletes may also be susceptible to compression or ischemia of the deep fibular nerve and superficial fibular nerve as a manifestaContinuum (Minneap Minn) 2014;20(6):1605–1628

tion of a compartment syndrome.21 A compartment syndrome is caused by increased pressure in a closed area as a manifestation of unyielding fascial enclosure of musculature. As pressure in the compartment increases in the setting of exercise, direct pressure effects, ischemia, or both cause nerve dysfunction. The anterior compartment includes the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius muscles. The lateral compartment includes the peroneus brevis and peroneus longus muscles. Similar to compression at the fibular neck, runners are asymptomatic at rest and develop progressive symptoms with running. Runners report pain and paresthesia in the anterior or lateral compartment extending into the foot that become progressively worse with prolonged running. In more extreme cases, runners will develop footdrop with deep fibular nerve involvement or ankle instability with superficial fibular nerve involvement. Diagnosis is confirmed through a careful history and examination prerunning and postrunning. The examination should include compartment pressure measurements using a wick or slit catheter technique (commonly performed by an orthopedic surgeon) and may also include nerve conduction studies and EMG.5 Aside from unyielding fascia, excessive plantar flexion and inversion forces may contribute to the development of compartment syndrome with fibular nerve injury. Treatment includes rest and gradual restoration of running, but may require fasciotomy. Some literature support exists for evaluating and possibly changing the athlete’s running technique.22 The deep fibular nerve is also susceptible to injury as it traverses the ankle into the foot. Improperly fitting ski boots, ice skates, or inline skates can compress the deep fibular nerve, and athletes will report localized ankle pain

KEY POINTS

h Fibular nerve injury may be overlooked in ankle sprains, and poor recovery may be attributed to incomplete ankle rehabilitation.

h The fibular nerve is susceptible to repetitive stress, especially in runners.

h Improperly fitting ski boots, ice skates, or inline skates can compress the deep fibular nerve, and athletes will report localized ankle pain plus paresthesia in the first webspace of the foot.



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h Tarsal tunnel syndrome refers to posterior tibial nerve entrapment at the level of the tarsal tunnel.

h A functional assessment of ankle movement should be performed in athletes with tarsal tunnel syndrome, with a goal of restoration of full ankle stability with repetitive running, jumping, and landing movements.

FIGURE 5-13

plus paresthesia in the first webspace of the foot. This injury is usually a selflimiting neurapraxia that is corrected with modification of equipment. Tibial nerve injury. The posterior tibial nerve is a continuation of the sciatic nerve (Figure 5-11). The tibial nerve travels from the popliteal fossa along the posteromedial tibia and is well protected in the deep posterior compartment of the leg. The nerve becomes more vulnerable as it traverses the tarsal tunnel and enters the foot (Figure 5-13). The tarsal tunnel is a fibro-osseous canal at the level of the medial malleolus, made up of bone on the inside and the flexor retinaculum on the outside. The tibial nerve, posterior tibial artery, veins, and tendons travel through the tarsal tunnel. At the level of the tarsal tunnel, the tibial nerve divides into the calcaneal nerve, which is a pure sensory nerve providing sensation along the calcaneus; medial plantar nerve, which supplies sensation along the medial sole and first three and a half toes and innervates the abductor hallucis, flexor digitorum brevis, flexor hallucis brevis, and the first lumbrical muscles; and the lateral plantar nerve, which supplies sensation along the

The tarsal tunnel. The tarsal tunnel is a site of entrapment of the tibial nerve at the medial malleolus. Printed with permission. B 2014 Cheryl Reynon.

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lateral sole and lateral one and a half toes and innervates the quadratus plantae, abductor digiti minimi, adductor hallucis, interossei, and the three lateral lumbrical muscles. Tarsal tunnel syndrome refers to posterior tibial nerve entrapment at the level of the tarsal tunnel.23 Athletes report pain and paresthesia emanating from the medial ankle into the foot, worsened with standing, walking, running, and dynamic pushoff during athletic activities. In more severe cases, there may be reduced ability to push off secondary to motor weakness of the intrinsic foot muscles. Tarsal tunnel syndrome is difficult to diagnose because athletes often have a normal examination at presentation, other than reproduction of symptoms with pressure over the tarsal tunnel. EMG studies are usually normal; nerve conduction studies, combined with somatosensory evoked potentials, sometimes reveal slowing at the level of the tarsal tunnel. Plantar fasciitis, intrinsic foot nerve compression, and Morton neuroma can mimic tarsal tunnel syndrome. The mechanism of action includes repetitive flexion and extension of the ankle with associated tenosynovitis in the tarsal tunnel. Recurring ankle sprains with associated ankle instability and fibrosis at the level of the tarsal tunnel have also been implicated. Management of suspected tarsal tunnel syndrome begins with rest. A therapeutic injection of corticosteroid within the tarsal tunnel may provide symptomatic relief. A functional assessment of ankle movement should be performed in athletes with tarsal tunnel syndrome, with a goal of restoration of full ankle stability with repetitive running, jumping, and landing movements. Right/left differences in stability should be assessed. The role of orthotics is not clear, but should be considered because of the localized nature of this syndrome.24 In refractory cases, tarsal tunnel release and neurolysis should be considered.



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Pudendal nerve injury. The pudendal nerve originates from the S2 to S4 nerve roots and enters the gluteal region through the lower part of the greater sciatic foramen, then reenters the pelvis through the lesser sciatic foramen before coursing through the pudendal (Alcock) canal (Figure 5-14). The pudendal nerve supplies sensation to the anal and genital areas; it innervates the bladder and rectal sphincters, the penis and clitoris, and the

FIGURE 5-14

bulbospongiosus and ischiocavernous muscles, and carries postsynaptic sympathetic fibers that innervate penile erectile tissue. The pudendal nerve may be particularly susceptible to compression from prolonged bicycle riding. Athletes develop numbness or pain in the perineal region. Although symptoms are usually short-lived, athletes may be symptomatic for weeks or even months, and symptoms may include male impotence. The mechanism of action is direct

KEY POINT

h The pudendal nerve may be particularly susceptible to compression from prolonged bicycle riding.

Course of the pudendal nerve. Because of its location, the pudendal nerve may be compressed following prolonged bicycle riding. Printed with permission. B 2014 Cheryl Reynon.




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Peripheral Nerve Injury

compression of the nerve or ischemia as a result of saddle loading on a hard and narrow bicycle seat. Wider bicycle seats support the ischial tuberosities and thus decrease pressure in the perineal area. Treatment includes rest and a biomechanical analysis of the athlete’s saddle loading.25,26 CONCLUSION Peripheral nerve injury in sport can be the result of acute trauma or repetitive overuse. Neurologists caring for athletes with suspected peripheral nerve injuries should always place the nerve injury within the context of sports medicine. Acute injuries usually result from collision or a fall, and may require emergency treatment. Overuse injuries often result from any combination of repetitive microtrauma, an inadequate recovery and periodization schedule, poor conditioning and training, and faulty equipment. Proper diagnosis must take into account the athlete and the sport. Management and rehabilitation must focus on the mechanism of action of the nerve injury and functional restoration of movement. REFERENCES

9. Safran MR. Nerve injury about the shoulder in athletes, part 2: long thoracic nerve, spinal accessory nerve, burners/stingers, thoracic outlet syndrome. Am J Sports Med 2004;32(4): 1063Y1076. 10. Safran MR. Nerve injury about the shoulder in athletes, part 1: suprascapular nerve and axillary nerve. Am J Sports Med 2004;32(3):803Y819. 11. Lorei MP, Hershman EB. Peripheral nerve injuries in athletes: treatment and prevention. Sports Med 1993;16(2):130Y147. 12. Rehak DC. Pronator syndrome. Clin Sports Med 2001;20(3):531Y540. 13. Hazani R, Engineer NJ, Mowlavi A, et al. Anatomic landmarks for the radial tunnel. ePlasty 2008;8:e37. 14. McCrory P, Bell S. Nerve entrapment syndromes as a cause of pain in the hip, groin and buttock. Sports Med 1999;27(4):261Y274. 15. Toth C. Peripheral nerve injuries attributable to sport and recreation. Phys Med Rehabil Clin N Am 2008;26(1):77Y100. 16. Khalil N, Nicotra A, Rakowicz W. Treatment for meralgia paraesthetica. Cochrane Database Syst Rev 2008;(3):CD004159. 17. Marciniak C. Fibular (peroneal) neuropathy: electrodiagnostic features and clinical correlates. Phys Med Rehabil Clin N Am 2013;24(1):121Y137. 18. McCrory P, Bell S. Nerve entrapment syndromes as a cause of pain in the hip, groin and buttock. Sports Med 1999;27(4):261Y274. 19. Hertel J. Functional instability following lateral ankle sprain. Sports Med 2000;29(5):361Y371.

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22. Diebal AR, Gregory R, Alitz C, Gerber JP. Effects of forefoot running on chronic exertional compartment syndrome: a case series. Int J Sports Phys Ther 2011;6(4):312Y321. 23. Kinoshita M, Okuda R, Yasuda T, Abe M. Tarsal tunnel syndrome in athletes. Am J Sports Med 2006;34(8):1307Y1312. 24. Bailie DS, Kelikian AS. Tarsal tunnel syndrome: diagnosis, surgical technique, and functional outcome. Foot Ankle Int 1998;19(2):65Y72. 25. Asplund C, Barkdull T, Weiss BD. Genitourinary problems in bicyclists. Curr Sports Med Rep 2007;6(5):333Y339. 26. Weiss BD. Clinical syndromes associated with bicycle seats. Clin Sports Med 1994;13(1):175Y186.



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Response of the gustatory system to peripheral nerve injury.

Peripheral nerve injury as a complication of axillary arteriography.

Peripheral nerve injury triggers central sprouting of myelinated afferents.

Dynamic regulation of Schwann cell enhancers after peripheral nerve injury.

AlphaB-crystallin regulates remyelination after peripheral nerve injury.

Peripheral nerve injury induces adult brain neurogenesis and remodelling.

Peripheral nerve injury and automatic blood pressure measurement.

Altered expression of pp60c-src induced by peripheral nerve injury.

Fibrillation potential amplitude and muscle atrophy following peripheral nerve injury.

Peripheral nerve injury modulates neurotrophin signaling in the peripheral and central nervous system.

Autophagy Promotes Peripheral Nerve Regeneration and Motor Recovery Following Sciatic Nerve Crush Injury in Rats.

Past, Present, and Future of Nerve Conduits in the Treatment of Peripheral Nerve Injury.

Proliferative effects of melatonin on Schwann cells: implication for nerve regeneration following peripheral nerve injury.

Peripheral nerve regeneration following transection injury to rat sciatic nerve by local application of adrenocorticotropic hormone.