Injuries of the Brachial Plexus
Scott H. Kozin
ANATOMY
Brachial Plexus
The origin of the brachial plexus is from the ventral rami of the fifth through eighth cervical (C5 through C8) and the first thoracic (T1) spinal nerves.95,146 Small contributions may originate from the fourth cervical (C4) and second thoracic (T2) nerves, known as prefixed and postfixed contributions, respectively. The dorsal and ventral rootlets (six to eight rootlets per level) exit the spinal cord, merge to form the spinal nerves, which leave the intervertebral foramina, and quickly divide into dorsal and ventral rami (Fig. 32-1). The small dorsal rami travel posterior to innervate the skin and muscles of the neck and upper back and are not part of the brachial plexus. The ventral rami emerge between the anterior and middle scalene muscles and are designated as the nerve roots of the brachial plexus (Fig. 32-2). The cervical roots (C5 through C8) descend toward the first rib, whereas the T1 root must ascend over the first rib to form the brachial plexus. Sympathetic fibers join the nerve roots as they traverse between the scalene muscles. C5 and C6 receive fibers from the middle sympathetic cervical ganglion, and C7, C8, and T1 acquire fibers from the cervicothoracic (stellate) ganglion. These sympathetic fibers control blood-vessel smooth-muscle contraction (vasoconstriction) and sweat gland activity.
The motor cell bodies of the nerve roots for the brachial plexus are located within the ventral horn of the spinal cord gray matter (see Fig. 32-1). In contrast, the sensory cell bodies are positioned outside the spinal cord within the dorsal root ganglia. The dorsal root ganglia transfer afferent fibers to the spinal cord through the dorsal rootlets. The knowledge of the difference in anatomic location of cell bodies between motor and sensory fibers is important for the accurate diagnosis and treatment of proximal brachial plexus injuries.
 FIGURE 32-1. Artist schematic of spinal cord with motor and sensory (dorsal root ganglion) cell bodies. |
The ventral rami of C5 and C6 combine to form the upper trunk, the C7 ramus continues alone as the middle trunk, and C8 and T1 unite to form the lower trunk (see Fig. 32-2). The trunks are located in the posterior triangle of the neck, enclosed by the posterior border of the sternocleidomastoid muscle, anterior border of the upper trapezius, and clavicle. The spinal accessory nerve (cranial nerve XI) crosses the posterior triangle to innervate the trapezius muscle. This nerve divides the posterior triangle into nearly equivalent upper and lower parts. The lower portion of the triangle contains the brachial plexus, with the upper and middle trunks superior to the omohyoid muscle and the lower trunk inferior to it. Each trunk divides into anterior and posterior divisions and proceeds behind the clavicle. The divisions then merge into three cords named in relation to the axillary artery. The anterior divisions of the upper and middle trunks combine to form the lateral cord. The three posterior divisions of the upper, middle, and inferior trunks converge to form the posterior cord. The anterior division of the lower trunk continues as the medial cord.
The cords proceed behind the pectoralis minor muscle into the axilla. Each cord divides into two terminal branches (Fig. 32-3). The lateral cord terminates as the musculocutaneous nerve and a branch to the median nerve. The musculocutaneous nerve perforates and supplies the coracobrachialis
muscle and then becomes the principal motor nerve of the flexor compartment of the arm. The posterior cord divides into the axillary and radial nerves. At the level of the glenohumeral joint, the axillary nerve, along with the posterior humeral circumflex vessels, travels inferior to the subscapularis muscle and across the upper border of the teres major to enter the quadrangular space for innervation of the deltoid and teres minor muscles. Compression of the nerve or artery can occur at the quadrangular space from hypertrophy or anomalies of the bordering muscles. The radial nerve is the largest branch of the brachial plexus and passes inferior to the teres major muscle to enter the posterior arm between the long head of the triceps and humerus via the triangular interval. The medial cord continues as the ulnar nerve and a branch to the median nerve, which contains the vast majority of median motor fibers. The ulnar nerve travels down the arm medial to the brachial artery, pierces the medial intermuscular septum, and enters the cubital tunnel. The median nerve forms anterior to the axillary artery from the union of the medial and lateral and medial cord branches and descends into the arm.
muscle and then becomes the principal motor nerve of the flexor compartment of the arm. The posterior cord divides into the axillary and radial nerves. At the level of the glenohumeral joint, the axillary nerve, along with the posterior humeral circumflex vessels, travels inferior to the subscapularis muscle and across the upper border of the teres major to enter the quadrangular space for innervation of the deltoid and teres minor muscles. Compression of the nerve or artery can occur at the quadrangular space from hypertrophy or anomalies of the bordering muscles. The radial nerve is the largest branch of the brachial plexus and passes inferior to the teres major muscle to enter the posterior arm between the long head of the triceps and humerus via the triangular interval. The medial cord continues as the ulnar nerve and a branch to the median nerve, which contains the vast majority of median motor fibers. The ulnar nerve travels down the arm medial to the brachial artery, pierces the medial intermuscular septum, and enters the cubital tunnel. The median nerve forms anterior to the axillary artery from the union of the medial and lateral and medial cord branches and descends into the arm.
 FIGURE 32-2. Artist schematic of brachial plexus from roots to branches. |
Several branches arise from the roots, trunks, and cords of the brachial plexus (see Fig. 32-2). The status of these intermediate nerves provides valuable information about the location of nerve injury. At the root level, the dorsal scapular nerve arises from C5, pierces the middle scalene to enter the posterior triangle of the neck, and innervates the levator scapulae and rhomboid muscles. The long thoracic nerve arises from C5, C6, and C7 just distal to the intervertebral foramina and travels behind the brachial plexus along the chest wall to supply the serratus anterior muscle. The phrenic nerve originates at the root level from C3, C4, and C5 and crosses the anterior scalene muscle to enter the thorax. The phrenic nerve may be injured in nerve root injuries, which results in hemidiaphragm paralysis.
At the trunk level, the suprascapular nerve arises from the upper trunk to travel across the posterior cervical triangle to the suprascapular notch. Often, the origin is a trifurcation consisting of the anterior division of the upper trunk, posterior division of the upper trunk, and the suprascapular nerve. The suprascapular nerve advances through the suprascapular notch, inferior to the ligament, to innervate the supraspinatus and infraspinatus muscles. Common sites of compression of this nerve occur at the suprascapular notch, affecting both the supraspinatus and infraspinatus muscles, or distal to the notch secondary to labral pathology, affecting only the infraspinatus muscle.
There are no branches from the plexus at the division level. At the cord level, multiple branches are present. From the lateral cord, the lateral pectoral nerve arises to pass anterior to the axillary artery, to perforate the clavipectoral fascia, and to innervate the clavicular part of the pectoralis major. The posterior cord supplies three branches: the upper subscapular, the thoracodorsal, and the lower subscapular nerves. The upper subscapular nerve innervates the upper portion of the subscapularis muscle. The lower subscapular nerve innervates the lower subscapularis and the teres major muscle. The
thoracodorsal nerve originates between the upper and lower subscapular nerves, passes behind the axillary artery, and supplies the latissimus dorsi muscle. The medial cord provides one motor and two sensory branches. The medial pectoral nerve traverses and innervates the pectoralis minor muscle and then continues to supply the sternocostal portion of the pectoralis major muscle. The medial brachial and medial antebrachial cutaneous nerves are the only sensory branches to arise directly from the plexus and supply the arm and forearm, respectively. These large sensory nerves can be utilized as a source of nerve grafts in lower trunk injuries, especially in infants as sural nerves have limited length.
thoracodorsal nerve originates between the upper and lower subscapular nerves, passes behind the axillary artery, and supplies the latissimus dorsi muscle. The medial cord provides one motor and two sensory branches. The medial pectoral nerve traverses and innervates the pectoralis minor muscle and then continues to supply the sternocostal portion of the pectoralis major muscle. The medial brachial and medial antebrachial cutaneous nerves are the only sensory branches to arise directly from the plexus and supply the arm and forearm, respectively. These large sensory nerves can be utilized as a source of nerve grafts in lower trunk injuries, especially in infants as sural nerves have limited length.
 FIGURE 32-3. Artist schematic of brachial plexus behind the clavicle pectoralis minor muscle. |
The vascular anatomy of the brachial plexus centers about the subclavian and axillary vessels. The subclavian artery originates from the arch of the aorta on the left side and from the brachiocephalic artery on the right. The subclavian artery ascends over the first rib to reside between the anterior and middle scalene muscles, with the roots and trunks of the brachial plexus. In contrast, the subclavian vein is located anterior to the anterior scalene muscle. The subclavian vessels cross the first rib and become the axillary vessels with the vein medial to the artery. The axillary vessels accompany the brachial plexus behind the pectoralis minor muscle to enter the axilla. The axillary vessels become the brachial vessels beyond the axilla.
There is variability and asymmetry in the neural and vascular anatomy of the brachial plexus.95,146,216 The commonly cited neural anatomy involving C5 to T1 occurs in 75% of people. A prefixed plexus is present when there is a relatively large contribution from C4 and a small allotment from T1, which occurs in 22% of the population. In contrast, a post-fixed plexus has substantial contribution from T2 with little from C5. There are also variations in cord separation and peripheral branching patterns of nerves that may or may not affect segmental innervation. Branches may occasionally arise from divisions instead of their usual origin from trunks or cords. The vascular relation to the plexus can also be altered, with the axillary artery or vein shifted in position or even piercing a nerve.134 The subclavian vein can travel with the artery and brachial plexus posterior to the anterior scalene muscle.147 Anomalies in nerve and/or vascular anatomy should be considered when clinical, diagnostic, and surgical findings do not correspond.
Thoracic Outlet Anatomy
The thoracic outlet begins just distal to the intervertebral foramina and extends to the coracoid process. The outlet is surrounded by anatomic constraints that encompass the brachial plexus and associated vessels (subclavian and axillary).
These structures include muscles (anterior and middle scalene muscles), skeleton (first rib, cervical ribs, clavicle, and coracoid), and fascia or fibrous bands. The most common sites of compression in thoracic outlet syndrome are at the superior thoracic outlet, the scalene interval or triangle, the costoclavicular space, or the subcoracoid area (Fig. 32-4 Table 32-1).6,149,166,176 This compression can be static or dynamic (i.e., dependent on posture and activity).115
These structures include muscles (anterior and middle scalene muscles), skeleton (first rib, cervical ribs, clavicle, and coracoid), and fascia or fibrous bands. The most common sites of compression in thoracic outlet syndrome are at the superior thoracic outlet, the scalene interval or triangle, the costoclavicular space, or the subcoracoid area (Fig. 32-4 Table 32-1).6,149,166,176 This compression can be static or dynamic (i.e., dependent on posture and activity).115
The anterior border of the superior thoracic outlet is the sternum; the lateral boundary is the first rib, and the posterior limit is the thoracic vertebrae.230 The lower trunk must ascend from the intervertebral foramina to navigate over the first rib. A post-fixed brachial plexus must climb even higher to exit from the thorax. The lower trunk can be compressed or stretched over the first rib in this area.
The scalene triangle is formed by the anterior and middle scalene attachments on the first rib. These muscles originate from similar transverse processes of the upper and middle cervical vertebrae and diverge to their insertion sites. The scalene triangle has a narrow base (approximately 1 to 2 cm) and elongated sides.45,97,166 The upper roots (C5 through C7) descend, whereas the lower roots (C8 and T1) and subclavian artery must ascend to pass through the scalene triangle. The presence of a cervical rib or a fibrous band extending from an incomplete cervical rib to the first rib can reduce the dimensions of the triangle by elevation of its base. This forces the lower roots and subclavian artery to further ascend to enter the scalene triangle. Cervical ribs are present in 0.5% to 1% of individuals and occur bilaterally 50% to 80% of the time.6,115,162,191 The width of the scalene triangle can be narrowed by anterior or middle scalene muscle abnormalities, which can precipitate thoracic outlet compression.45,91,203
 FIGURE 32-4. Artist schematic of thoracic outlet compression sites. |
TABLE 32-1 Sites of Compression in Thoracic Outlet Syndrome | ||||||||||
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The costoclavicular interval is between the clavicle and the first rib. Depression of the clavicle reduces this space and can compress the brachial plexus and subclavian vessels. A hypertrophied subclavius muscle or a fractured clavicle with abundant callus formation can narrow the costoclavicular space. The subclavian vein is also susceptible to compression within the costoclavicular interval.
The subcoracoid area can compress the brachial plexus. The coracoid provides a fulcrum across the plexus during abduction and external rotation of the arm. The pectoralis minor and conjoined tendon (short head of the biceps and coracobrachialis) prevents slippage of the plexus from behind
the coracoid. Excessive arm elevation can lead to a traction or compressive neuropathy along the coracoid process.197
the coracoid. Excessive arm elevation can lead to a traction or compressive neuropathy along the coracoid process.197
ADULT BRACHIAL PLEXUS INJURIES
Numerous etiologies of adult brachial plexus injuries exist, the most common causes being vehicular trauma, athletic endeavors, domestic violence, and systemic disease. These etiologies can be divided into trauma (penetrating and nonpenetrating), entrapment, and infection (Table 32-2). There are other less common etiologies of brachial plexopathy related to tumors, neuropathies (e.g., Parsonage-Turner syndrome), and iatrogenic causes.6,79,89,128,132
PATHOPHYSIOLOGY
The most common cause of brachial plexus injury is traction which occurs from pulling the extremity, forcible head rotation from the shoulder, or direct depression of the shoulder girdle.197 Traction causes injury via stretching or straining of the nerve beyond its physiologic limits. There is a direct correlation between strain and reduction of intraneural blood flow. A 15% elongation of the nerve reduces blood flow by approximately 80% to 100%35,118,228 The extrinsic vascular system (longitudinal vessels in the epineurium) appears to be more susceptible to stretch than the intrinsic circulation (endoneurial vascular network).99 Continued elongation will cause overt ischemia and disruption of nerve metabolism. Persistent traction will ultimately disrupt nerve fiber and/or sheath continuity. Therefore, traction can cause a spectrum of nerve injury ranging from a temporary disruption in nerve fiber conduction to functional discontinuity of the nerve fibers and sheath.
TABLE 32-2 Etiology of Brachial Plexus Injuries | ||||||||||||||||||||||||||||||||||||||||
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Various factors determine the portion of the plexus injured and the extent of damage incurred. These determinants include the local anatomy, magnitude and duration of the force applied, and the position of the extremity and head at the time of the accident.197 The upper roots descend beneath the clavicle, whereas the lower roots ascend over the first rib. Therefore, the upper plexus is taut with the arm dangling at the side, and the lower plexus is taut with the arm abducted and elevated. As a result, the upper roots and trunk are most susceptible to traction that increases the distance between the head and neck. In contrast, the medial, lateral, and posterior cords pass beneath the coracoid, which act as a pulley. Excessive arm abduction can elevate the coracoid pulley and places preferential tension across the cords of the brachial plexus.
Nonpenetrating Trauma
Nonpenetrating trauma is the leading cause of upper brachial plexus injuries. Most brachial plexus injuries result from motor vehicle accidents, especially motorcycle misadventures.145,178 The injury is more frequently seen in areas where motorcycles are the principal mode of transportation.32 It is estimated that there is a 2% incidence of brachial plexus injury following motorcycle accidents, with a prevalence in young males.143,145 Interestingly, the incidence has recently increased and is probably related to mandatory helmet regulations and better transportation of trauma patients who previously would have succumbed to their injuries.143 Associated injuries are common, including head trauma and fractures or dislocations of the cervical spine, shoulder, forearm, and hand.145,178
Automobile, bicycle, sporting, and pedestrian accidents are much less common causes of brachial plexus injuries, as are shoulder dislocations or fractures (proximal humerus, clavicle).83,128 Although, the incidence of brachial plexus injury is rising in adolescents who participate in extreme sports. Minor stretch injuries of the plexus (i.e., burners or stingers) are common in contact sports, especially football, because tackling drives the shoulder downward and forcibly flexes the neck toward the contralateral side.83 The athlete experiences burning pain and paresthesias that radiate from the supraclavicular area into the arm. Transient weakness and sensory abnormalities may also be present. The vast majority of burners are upper plexus traction injuries with signs and symptoms that usually resolve spontaneously over a few minutes. There should not be concomitant neck pain or restricted neck mobility. Incomplete neurologic recovery or restricted neck motion requires further diagnostic evaluation as the impact could have caused a cervical spine fracturedislocation or a profound brachial plexus injury. Failure to make a timely diagnosis of cervical spine injury can result in subsequent quadriplegia.
Shoulder dislocations are often related to sporting accidents and can produce nerve injuries of the axillary,
suprascapular, or musculocutaneous nerves.4 These injuries are usually (80% of the time) temporary lesions that resolve over 4 to 6 months and are covered in Chapter 33. We have seen permanent injuries affecting various cords and cautious optimism is the rule in plexus injuries following shoulder dislocation.
suprascapular, or musculocutaneous nerves.4 These injuries are usually (80% of the time) temporary lesions that resolve over 4 to 6 months and are covered in Chapter 33. We have seen permanent injuries affecting various cords and cautious optimism is the rule in plexus injuries following shoulder dislocation.
Penetrating Trauma
Penetrating trauma to the brachial plexus is often secondary to gunshot wounds or stabbings. Gunshot wounds occur at the time of war and during domestic violence.100,152 Bullet injuries act as projectile missiles that cause neural injury by means of a blast effect, or less commonly, direct nerve transection.18,100,152 The shock wave (temporary cavity) reverberates causing a variable degree of nerve injury with the extent of blast correlating with the deformation, fragmentation, orientation, and velocity of the bullet. The part of the plexus injured depends upon the entrance and exit passageway.
Infection
Infection is an uncommon cause of brachial plexopathy. The exact etiology remains unclear, with both viral pathogens and secondary immunologic factors proposed as possibilities. There are a number of reported antecedent events that may serve as triggers including viral infections, immunizations, strenuous exercise, and surgery (perioperative and peripartum periods).199 This brachial neuritis is also known as neuralgic amyotrophy or Parsonage-Turner syndrome. Patients usually present with acute onset of intense pain about the shoulder girdle without antecedent trauma.156 Weakness of the muscles innervated by the affected nerves develops after the initial pain subsides. The upper brachial plexus is most commonly involved; specifically, the suprascapular or long thoracic nerve (Fig. 32-5). Varying parts of the plexus can be involved, however, and the distribution can be patchy. Electromyographic abnormalities of the denervated muscles are apparent 3 to 4 weeks after the initial pain response, with positive sharp waves and fibrillation potentials indicative of acute denervation. The treatment is conservative management with observation and serial examinations as the natural history of brachial neuritis is resolution of the pain followed by improvement in motor function. However, prolonged recovery time (1 to 2 years) and persistent weakness is not uncommon years after the brachial neuritis.83,121,139,207 In children, there is a rare hereditary form of neuralgic amyotrophy that is autosomal-dominant and recurrent (Fig. 32-6). Mutations in the gene septin 9 on chromosome 17q23 have been found in several families with the hereditary form of the condition.110
 FIGURE 32-5. A 14-year-old female with neuralgic amyotrophy affecting the right long thoracic nerve. (Courtesy of Shriners Hospital for Children, Philadelphia.) (A) Right scapular winging exacerbated by pushing against wall. (B) Side view with marked winging. This patient awoke with intense shoulder pain and subsequent scapula winging from isolated long thoracic nerve involvement in Parsonage-Turner syndrome. |
 FIGURE 32-6. A 10-year-old male with recurrent hereditary neuralgic. (Courtesy of Shriners Hospital for Children, Philadelphia.) (A) Episode with right-sided weakness. (B) Typical fascial features with considerable hypotelorism. (C) Decreased shoulder abduction and wrist drop. (D) Limited ability to grasp. |
CLASSIFICATION OF BRACHIAL PLEXUS INJURY
The lesion in brachial plexus injury is classified according to the anatomic location and extent of nerve involvement. Supraclavicular lesions affect the roots, trunks, and divisions, whereas infraclavicular injuries involve the cords and branches. Approximately 75% of brachial plexus injuries are classified as supraclavicular lesions. A supraclavicular injury can disrupt the rootlet connection with the spinal cord resulting in an avulsion. The mechanism of an avulsion is usually secondary to traction along the affected root(s) and separates the motor cell body in the spinal cord from its axons. In contrast, the sensory cell body is located in the dorsal root ganglion and remains connected to its axons (see Fig. 32-1). Therefore, the motor portion of the nerve undergoes Wallerian degeneration, with degradation of the axons and myelin sheaths, whereas the sensory fibers are spared from Wallerian degeneration, but have been irrevocably detached from the spinal cord. The injury will cause a clinical motor and sensory loss; however, electrodiagnostic studies will reveal the abnormal motor findings with intact sensory conduction. In other words, the dorsal root is still functioning and is unaware that it is disconnected from the spinal cord.
The injury can also interrupt nerve continuity at the trunk level causing a rupture. Ruptures separate both motor and sensory cell bodies from their axons resulting in Wallerian degeneration across all fibers. The differentiation between avulsion and rupture is a decisive element in the treatment algorithm of brachial plexus traction injuries. Discontinuity by rupture can be treated by various surgical techniques to reestablish nerve continuity, whereas avulsion injuries are irreparable and require alternative techniques to restore function. The differentiation can be difficult as traction can cause ruptures and avulsions at different levels, which confounds accurate diagnosis.
Supraclavicular lesions are subdivided into groups according to the pattern of involvement (Table 32-3).5,138 The ErbDuchenne palsy involves C5 and C6, or the upper trunk, and is characterized by loss of elbow flexion, and weakness of shoulder abduction and external rotation.49,57 Sensory deficit is apparent in the corresponding dermatomes (radial side of forearm, thumb, and index). A C7 injury can accompany an Erb’s palsy (a.k.a. extended upper brachial plexus lesion) and adds paralysis of elbow extension, wrist extension (extensor carpi radialis brevis), and finger extension (extensor digitorum communis and proprius). The Dejerine-Klumpke palsy involves C8 and T1, or lower trunk, and is characterized by absent intrinsic hand musculature and finger flexors (flexor digitorum profundus) with intact shoulder, elbow, and wrist function.102 Sensory deficit is present over the ulnar side of the forearm and hand. This isolated lower plexus palsy is uncommon in both adults and children.63,81 Lastly, the injury can involve the entire plexus (C5, C6, C7, C8, and T1), which causes a flail and anesthetic limb.
Supraclavicular lesions can also be isolated to peripheral branches, such as the suprascapular or long thoracic nerve. This can be secondary to trauma, infection (neuralgic amyotrophy), surgical positioning, or iatrogenic.
Infraclavicular lesions are less common (approximately 25%) and usually represent stretch injuries from an associated shoulder dislocation or fracture.4 These injuries represent peripheral nerve lesions of the plexus. The axillary nerve is particularly susceptible to traction because it is securely anchored as it traverses the quadrangular space. The majority of these injuries are covered in Chapter 33.
Supraclavicular and infraclavicular nerve injuries can also be characterized by their severity, regardless of the location of injury and extent of plexus involvement. The gradation of nerve injury begins with neuropraxia, extends to axonotmesis, and culminates in neurotmesis (Table 32-4).186 A neuropraxiais a segmental demyelination with maintenance of intact nerve fibers and axonal sheath. A temporary conduction block follows, without axonal damage and Wallerian degeneration. Complete recovery usually occurs over the ensuing days to weeks as remyelinization is completed. Electrodiagnostic studies demonstrate a decrease in nerve conduction without electromyographic changes of denervation within the muscle.22 An axonotmesis is a disruption of nerve fiber integrity with preservation of the epineural sheath and framework. Wallerian degeneration and nerve fiber regeneration are necessary for recovery. Electrodiagnostic studies exhibit a decrease in nerve conduction velocity and electromyographic changes of muscle denervation (insertional activity, fibrillations, and positive sharp waves).22 Wallerian degeneration is characterized by the proliferation of Schwann cells that phagocytose myelin and axon debris. The axons distal to the injury degrade from lack of
nutrition and loss of blood supply. Regeneration of the axons occurs at a rate of approximately 1 mm/day or 1 inch/month. This slow regeneration delays recovery and means that distal nerve injuries have a better prognosis because the extent of Wallerian degeneration is decreased and the proximity to the motor endplates is increased. Prolonged denervation (greater than 18 to 24 months) results in irreversible motor endplate degradation and muscle fibrosis. In contrast, the encapsulated sensory receptors retain their capacity for reinnervation for many years. These factors portend the overall prognosis for axonotmesis as variable and guarded, which is vital information to relay to the patient.
nutrition and loss of blood supply. Regeneration of the axons occurs at a rate of approximately 1 mm/day or 1 inch/month. This slow regeneration delays recovery and means that distal nerve injuries have a better prognosis because the extent of Wallerian degeneration is decreased and the proximity to the motor endplates is increased. Prolonged denervation (greater than 18 to 24 months) results in irreversible motor endplate degradation and muscle fibrosis. In contrast, the encapsulated sensory receptors retain their capacity for reinnervation for many years. These factors portend the overall prognosis for axonotmesis as variable and guarded, which is vital information to relay to the patient.
Table 32-3 Patterns of Brachial Plexus Injuries | ||||||||||||||||||
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Table 32-4 Seddon’s Classification of Nerve Injury | |||||||||||||||
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A neurotmesis is a disruption of the nerve fiber and axonal sheath. Transection is the classic example of this injury, but severe traction or contusion can produce a similar injury with irreversible intraneural scarring. The prognosis is bleak without surgical resection of the intervening scar and nerve coaptation by direct repair or graft interposition to allow for nerve regeneration. A severe brachial plexus injury often represents a combined lesion, with elements of neuropraxia, axonotmesis, and neurotmesis, thus complicating accurate diagnosis and predictions for recovery.
EVALUATION OF ADULT BRACHIAL PLEXUS INJURY
The clinical evaluation of the patient with a brachial plexus injury begins with a careful history and detailed examination. Severe pain in an anesthetic extremity is a worrisome finding that suggests deafferentation and avulsion injuries. The examination should include the head and neck, thorax, injured extremity, and neurovascular systems. Knowledge of brachial plexus anatomy and concomitant muscle innervation is a prerequisite to accurate diagnosis. A thorough physical examination is the foundation that will dictate the treatment algorithm. Imaging studies and electrodiagnostic tests provide supplemental information to further clarify the extent of injury. The goal of this evaluation is to precisely define the location and extent of nerve injury. This information will direct treatment, which may range from continued observation to prompt surgical intervention.
Adult brachial plexus injuries are usually not evaluated in the acute setting, but rather referred after treatment of any life-threatening injuries. An inquiry into the mechanism of injury and degree of energy involved is important. The force applied (direction, magnitude, and duration), position of the extremity, and concomitant injuries (fractures, dislocations, visceral damage, head trauma, and vascular damage) are important details. Unfortunately, the particulars of the accident are often obscured by loss of consciousness, associated injuries, or amnesia.143 In sharp penetrating trauma, the timing of neurologic deficit is important. An instantaneous deficit implies nerve laceration, whereas a delayed onset indicates a compressive neuropathy by an expanding hematoma or false aneurysm.18,51 Important past medical history includes overall general health before the accident, hand dominance, occupation, and hobbies.
The physical examination begins with observation of the extremity’s posture and the manner by which the patient uses the extremity as these are important indicators of the segment of the brachial plexus involved. Motor and sensory deficits determined by the physical examination should be correlated with the ancillary studies to define the extent and pattern of injury to the plexus. The basis of the evaluation is to perform a detailed examination to determine the specific motor and sensory deficits. An inventory of the muscles innervated by the brachial plexus is imperative to accurately define the injury and provides a baseline to assess recovery. Physical findings should be recorded on a data sheet, including gradation of muscle strength according to the international muscle scoring system (Grades 1 to 5), and the presence or absence of sensory deficits (Table 32-5).2 Sensibility is assessed using two-point discrimination or Semmes-Weinstein monofilament testing. This extensive documentation method eliminates inadvertent omission of important elements of the examination and allows serial examinations to be performed by different individuals.
Careful examination of the muscles innervated by the proximal branches from the brachial plexus will help define the proximity of the plexus lesion to the spinal cord (Table 32-6). Disruption of the dorsal rami (paraspinal muscles), dorsal scapular (rhomboids and levator scapulae), and long thoracic (serratus anterior) nerves are suggestive of an avulsion injury. The presence of a Horner’s syndrome, a drooped eyelid, constricted pupil, sunken globe, and sweating deficiency along the affected side of the face, usually implies an avulsion injury at C8 and T1 (Fig. 32-7). However, the false-positive response rate for a Horner’s syndrome is 10% and the false-negative rate is 28%.82 Percussion of the supraclavicular and infraclavicular
plexus is performed to assess for the presence or absence of a Tinel’s sign. A positive Tinel’s sign is indicative of a postganglionic injury (e.g., rupture), whereas this sign will be absent in a preganglionic lesion (e.g., avulsion) because the link to the spinal cord and brain has been disrupted.
plexus is performed to assess for the presence or absence of a Tinel’s sign. A positive Tinel’s sign is indicative of a postganglionic injury (e.g., rupture), whereas this sign will be absent in a preganglionic lesion (e.g., avulsion) because the link to the spinal cord and brain has been disrupted.
TABLE 32-5 Brachial Plexus Examination Sheet | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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TABLE 32-6 Indicators of Avulsion Injuries and Poor Prognosis for Recovery | ||||||||||||||||||||||||
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 FIGURE 32-7. A 30-year-old woman involved in a motor vehicle accident with avulsions of C8, T1, and ruptures of C5, C6, C7. Persistent subtle left Horner’s syndrome years after injury. |
Postganglionic injuries are further localized by examination of the intermediate and terminal branches. The status of the suprascapular (supraspinatus and infraspinatus), thoracodorsal (latissimus dorsi), upper and lower subscapular (subscapularis and teres major), and medial and lateral pectoral (pectoralis major and minor) nerves will further define the injury. Examination of the pectoralis major muscle is particularly helpful because of its dual segmental innervation from the lateral pectoral (C5, C6, C7) and medial pectoral (C8, T1) nerves from the lateral and medial cords, respectively. Selective atrophy of the clavicular head (lateral pectoral) or sternocostal head (medial pectoral) facilitates diagnosis, whereas complete atrophy implies a global injury. Over time, we have developed a rapid methodology to evaluate which nerve roots of the brachial plexus are injured by examination of key muscles that are innervated by specific roots (Table 32-7).
A peripheral vascular examination with palpation of the radial and ulnar pulses is a fundamental component of the evaluation, as damage to the axillary or subclavian vessels can occur at the time of initial injury. Decreased or absent peripheral pulses, a delayed neurologic deficit (expanding hematoma), and penetrating trauma warrant magnetic resonance imaging (MRI) angiography, computed tomography (CT) angiography, or arteriography.18,51,61,198
TABLE 32-7 Practical Examination for Brachial Plexus Injury Pattern | ||||||||
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IMAGING STUDIES
Brachial Plexus Injury
Imaging studies are an important part of the evaluation as they provide valuable information about the level of injury. Plain X-ray films of the cervical spine, clavicle, shoulder, and chest are routinely obtained. Various findings are suggestive of particular levels of plexus injury (Table 32-8). The bone and/or ligament injury often represents a failure of the supporting and protective structures about the brachial plexus. For example, a transverse process fracture or scapulothoracic dissociation implies a preganglionic avulsion injury while a shoulder dislocation infers a postganglionic nerve injury. Scapulothoracic dissociation is a devastating injury that can cause rapid exsanguination from an avulsion of the subclavian artery. If the patient survives the injury, the nerve damage is usually extensive with avulsions across the plexus. The prognosis for return of nerve function is bleak and extensive methods of nerve reconstruction are often required to restore some nerve continuity.52
Hemidiaphragm paralysis may occur from injury to the adjacent phrenic nerve at the time of brachial plexus injury. This paralysis may not be apparent on a static chest X-ray, therefore a dynamic study, such as fluoroscopy or ultrasound, during breathing is required for diagnosis of phrenic nerve injury.
Angiography is indicated if there is any question of the vascular status of the extremity or integrity of the subclavian or axillary vessels. Palpable radial or ulnar pulses may be present (secondary to collateral flow) despite proximal injury.18 Penetrating trauma or an expanding hematoma requires MRI angiography, CT angiography, or arteriography.18,51,61,198
TABLE 32-8 Radiographic Findings in Injuries to the Brachial Plexus | ||||||||||||||||||||||||
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 FIGURE 32-8. Artist schematic of pseudomeningocele associated with avulsion injuries of the brachial plexus. |
Myelography is used to define the presence or absence of a pseudomeningocele, a meningeal pouch filled with cerebrospinal fluid that extends through the intervertebral foramen into the paraspinal area (Fig. 32-8). This pouch represents an extraction of the dural and arachnoidal sleeve through the intervertebral foramen that often occurs during a root avulsion injury. The inability to visualize the nerve root on the myelogram further supports the diagnosis of an avulsion injury. However, false-positive pseudomeningoceles have been found in patients in whom the rootlets were intact with isolated dura rupture, and false-negative results have been reported during surgical exploration.36,63,81 Methods recommended to improve the diagnostic accuracy of myelography are to delay the test for 4 to 6 weeks after injury to allow for resolution of local swelling and intradural blood clots and utilization of CT myelography to visualize small pseudomeningoceles.143,174 Newer sophisticated techniques, including MR myelography (FIESTA-fast imaging employing steady-state acquisition), diffusion-weighted neurography, and Bezier surface reformation have been developed, but the current gold standard remains CT myelography.66
Magnetic resonance imaging has become the primary imaging modality in some institutions, based on the scanner available and specialization of the radiologist.151,154 The study provides multiplanar imaging to assess the various components of the brachial plexus.151 Strong magnetic gradients (≥1 T) and flexible surface coils improve image quality. Varying the pulse sequence will provide high-resolution images that will facilitate identification of plexus pathology. Magnetic resonance imaging currently offers the best evaluation of the trunks and cords, with potential identification of a neuroma (Fig. 32-9).151 Unfortunately, the MRI is unable to assess whether the neuroma has axons incontinuity or there is complete discontinuity.
ELECTRODIAGNOSTIC STUDIES
Electrodiagnostic testing plays an integral part in the diagnosis and treatment of brachial plexus lesions.46 Methods employed to evaluate these lesions include electromyography, nerve conduction velocity measurements, somatosensory-evoked potentials (SEPs), and nerve action potentials (NAPs). It is imperative that the surgeon and neurophysiologist have a dependable relationship with reciprocal communication. Serial electrodiagnostic studies, performed in conjunction with serial physical examinations, identify reinnervation (active polyphasic motor units, the emergence of nascent potentials, and a decrease in the number of fibrillation potentials) or persistent denervation.190 The results of neurophysiologic testing performed preoperatively, intraoperatively, and postoperatively may directly affect the decision-making process.142
Electromyography
Electromyography (EMG) records the electrical activity of muscle fibers at rest and during activation. This signal is recorded by the insertion of EMG needles into the muscle. The normal muscle is silent at rest and active during contraction with progressive recruitment of motor units. A denervated muscle will exhibit spontaneous electrical discharge (fibrillations and positive sharp waves) when the EMG needle is inserted.22,46 These findings are not present until 2 to 4 weeks after denervation. A reinnervated muscle will begin to show reinnervation or nascent potentials (polyphasic low-amplitude recordings). These electrical changes of muscle regeneration will precede the clinical detection of muscle activity. Therefore, the EMG examination of the muscles innervated by the brachial plexus can provide valuable information about the degree of injury and early recovery. The dilemma with EMG interpretation,
however, is the inability to quantify electrical recordings with extent of recovery. In other words, return of electrical activity may not correlate with return of active motion, especially in birth palsies.123,212
however, is the inability to quantify electrical recordings with extent of recovery. In other words, return of electrical activity may not correlate with return of active motion, especially in birth palsies.123,212
 FIGURE 32-9. A 16-year-old female injured while snowboarding. (Courtesy of Shriners Hospital for Children, Philadelphia.) (A) Subluxation of shoulder and no active motion. (B) MRI reveals pseudomeningocele at C5 indicative of root avulsion. |
An EMG evaluation of the more proximal branches from the brachial plexus can help differentiate an avulsion injury from a rupture (see Table 32-6). For example, fibrillations and positive sharp waves of the paraspinal muscles (innervated by the dorsal rami from the spinal nerve) or serratus anterior (innervated by the long thoracic nerve) imply an avulsion injury, whereas preservation of a normal electrical signal suggests a more distal lesion. The EMG is also useful to differentiate the degree of intraneural injury (neuropraxia, axonotmesis, and neurotmesis) and to follow the progress after injury. A neuropraxia can be differentiated from a more severe nerve injury by the absence of fibrillation potentials and positive sharp waves. An axonotmesis or neurotmesis will exhibit these denervation findings on EMG approximately 2 to 4 weeks after injury. Serial EMG evaluations can infer an axonotmesis injury by the spontaneous return of nascent units or reinnervation potentials that will precede clinical recovery of function. A neurotmesis injury will not exhibit EMG signs of spontaneous recovery.
Conduction Velocity
The integrity of the peripheral nerve is determined by the measurement of the conduction velocity. The motor or sensory latency can be measured utilizing the compound motor action potential (CMAP) or the sensory nerve action potential (SNAP) recordings, respectively. The conduction velocity (CV) is the distance between two sites of stimulation divided by the time for the NAP to travel from proximal to distal.22 The terms antidromic and orthodromic impart directionality to the stimulation. Antidromic sensory testing is when the stimulation is proximal (e.g., the wrist) and the recoding is distal (e.g., fingers). Orthodromic sensory testing would be stimulation at the fingertips and recording at the wrist. A severed nerve will lose the capability to conduct a sensory or motor action potential distal to the lesion as the nerve degenerates. However, the distal portion of the nerve may be able to conduct for several days after injury prior to degeneration. Therefore, early measurement of conduction velocities can produce a false-positive result for nerve continuity. Electrodiagnostic testing is often delayed for 3 weeks to allow time for loss of conduction and denervation changes in muscle.
The status of the SNAP and corresponding sensory nerve conduction velocity is helpful in differentiating preganglionic avulsion injuries from postganglionic lesions. The presence of a normal sensory CV in an anesthetic part of the arm indicates a preganglionic injury. This occurs because the sensory nerve is not separated from its cell body, which is located in the dorsal root ganglion. However, the sensory nerve is separated from the spinal cord and sensation cannot be processed within the central nervous system. In contrast, the CMAP or motor nerve conduction velocity is absent in both preganglionic and postganglionic injuries and is not a distinguishing factor.
Somatosensory-Evoked Potentials
SEPs and motor-evoked potentials (MEPs) are electrical responses of the brain and spinal cord to stimulation of peripheral sensory fibers. SEPs and MEPs are typically used at the time of surgery. SEPs record conduction from the stimulating
electrode to the central nervous system and can detect lesions within the sensory system. This technique can be employed to assess conduction across the brachial plexus to define irreparable nerve root avulsions. The absence of SEPs recorded over the spinal cord or somatosensory cortex on nerve root stimulation indicates a dorsal root avulsion and is a contraindication for nerve grafting.111,142 MEPs are recorded from muscles following stimulation of the motor cortex. Recordings are obtained as neurogenic potentials in the brachial plexus or as myogenic potentials from the muscle. The absence of MEPs via stimulation of the motor cortex indicates a ventral root avulsion and is a contraindication for nerve grafting.
electrode to the central nervous system and can detect lesions within the sensory system. This technique can be employed to assess conduction across the brachial plexus to define irreparable nerve root avulsions. The absence of SEPs recorded over the spinal cord or somatosensory cortex on nerve root stimulation indicates a dorsal root avulsion and is a contraindication for nerve grafting.111,142 MEPs are recorded from muscles following stimulation of the motor cortex. Recordings are obtained as neurogenic potentials in the brachial plexus or as myogenic potentials from the muscle. The absence of MEPs via stimulation of the motor cortex indicates a ventral root avulsion and is a contraindication for nerve grafting.
Nerve Action Potentials
NAPs are used intraoperatively to assess lesions in continuity. Stimulating and recording of a nerve proximal and distal to a neuroma can identify the presence or absence of axonal continuity.100 The presence of NAPs indicates propagation of an action potential along viable nerve fibers. This finding may help the surgeon decide between neurolysis or excision and interposition grafting.100 However, this technique does not provide quantitative data nor does it have the capacity to distinguish motor from sensory axons. Technical modifications to record the CMAP in innervated muscles or tetanic stimulation may provide better guidelines for surgical decision making.46,100,112
NONOPERATIVE TREATMENT
The vast majority of adult brachial plexus injuries are initially treated without surgery. Trauma resuscitation, repair of visceral damage, reconstitution of vascular flow, and stabilization of fractures dominate the acute management period. It is important to recognize that brachial plexus injuries with concomitant upper extremity fractures are best treated by fracture fixation because of the high nonunion rate (almost 50%) and the need for early mobilization to prevent contracture, edema, and stiffness.17 The initial goal of the post-injury period is to precisely define the location and extent of the brachial plexus injury. This task is accomplished by a thorough examination and supplemented by the imaging studies previously described.
Following stabilization of the patient, the brachial plexus injury has certain features that require specific management (Fig. 32-10). Range of motion exercises and anti-edema measures are required to prevent swelling and stiffness that will develop in the flail limb. Passive motion is necessary to maintain supple joint structure and to avoid contractures that will limit functional recovery. A sling may be applied to support the shoulder, but must be removed multiple times a day for range of motion exercises. Electrical stimulation to diminish muscle wasting during nerve regeneration may be implemented, but its long-term efficacy is unclear.
Brachial plexus injury may result in neurogenic pain, which may be present after preganglionic and postganglionic injuries (Fig. 32-11).21 Preganglionic pain may be unbearable and constant, with a burning or crushing sensation. In some patients, this debilitating pain persists and requires multidisciplinary pain management. This type of pain is often recalcitrant to narcotics and alternative medications may be helpful, including anticonvulsants, tricyclic antidepressants, and serotonin inhibitors. Refractory pain may require desperate measures, such as implantable pumps or central nervous stimulators and ablation of the dorsal root entry zone (DREZ). Unfortunately, 5% of patients exhibit persistent intractable pain.21,182 Amputation of the affected arm, however, will not relieve recalcitrant neurogenic pain.190,223 Postganglionic pain is from afferent signals that can still travel to the central nervous system. This pain can also be severe, but usually dissipates over time to a manageable intensity.
Serial examinations are performed to further define the injury and to evaluate for signs of early recovery. X-rays of the chest, cervical spine, and shoulder girdle are evaluated for radiographic signs associated with a brachial plexus injury (see Table 32-9). Persistent deficits 3 to 4 weeks after injury warrant additional study. Options include advanced imaging studies (e.g., CT myelogram and/or MRI) and electrodiagnostic testing. Baseline electrodiagnostic studies are performed to assess for muscle denervation and the possibility of nerve rootlet avulsions (see Table 32-6).
Nonoperative management is usually continued for 3 months during which therapy is necessary to maintain passive motion and supple joints. Serial examinations are performed at monthly intervals and repeat electrodiagnostic tests are performed 3 months after injury. At this time, the clinical information and the ancillary studies are combined to define the level and extent of injury. The prognosis for recovery is also calculated. This observation period of 3 months is often sufficient time to adequately assess the injury and to decide whether or not spontaneous recovery is possible. The surgeon must also decide if the injury is amenable to surgical repair or reconstruction. Progressive recovery that follows a sequential pattern warrants continued observation and negates the need for exploration.
A neurotmesis injury with loss of continuity (avulsion, rupture, laceration) or severe intraneural damage will not exhibit evidence of improvement at 3 months. In those reparable lesions, surgery is recommended between 3 and 6 months after injury. This time frame for surgery is important to assure the viability of motor endplates to sprouting axons. A further delay in surgery may jeopardize the integrity of the motor endplates and prevent functional recovery, despite satisfactory nerve repair, grafting, or transfer.190 The longer the muscle is denervated, the less the likelihood of successful reinnervation. There is a trend toward earlier surgery, if a non-recoverable and reparable lesion can be identified, to ensure endplate viability.70 Infraclavicular lesions from fracture or dislocation are treated by prompt reduction of the fracture or dislocation. The nerve injury is often an isolated peripheral lesion and treated by observation. Neuropraxia and axonotmesis injuries are customary and the prognosis for recovery is good. Exploration is reserved for those cases without spontaneous recovery.4,141,143
SURGICAL MANAGEMENT
Indications
Immediate surgical intervention for brachial plexus injuries is uncommon and is primarily performed for concomitant vascular injuries to the axillary or subclavian vessels (see Fig. 32-10). Simultaneous inspection of the plexus can be performed with identification of the injured segments. Immediate exploration
is often frustrating, as the vascular repair cannot be adequately mobilized for fear of disruption. Once the injured nerve segments are identified, the treatment depends upon the status of the damaged segments. Sharp transections can be managed by direct repair or graft interposition. Primary neurorrhaphy requires approximation of the cut ends without excessive tension. 51,136,185 However, primary neurorrhaphy is not recommended for traction or gunshot injuries. Instead, delayed management is preferred to allow demarcation of the zone of injury and extent of nerve damage. Fortunately, most penetrating trauma by missile preserves nerve continuity.18,100,152
is often frustrating, as the vascular repair cannot be adequately mobilized for fear of disruption. Once the injured nerve segments are identified, the treatment depends upon the status of the damaged segments. Sharp transections can be managed by direct repair or graft interposition. Primary neurorrhaphy requires approximation of the cut ends without excessive tension. 51,136,185 However, primary neurorrhaphy is not recommended for traction or gunshot injuries. Instead, delayed management is preferred to allow demarcation of the zone of injury and extent of nerve damage. Fortunately, most penetrating trauma by missile preserves nerve continuity.18,100,152
 FIGURE 32-10. Treatment algorithm for adult brachial plexus injuries. CT, computed tomography; EMG, electromyogram; MRI, magnetic resonance imaging; NAPs, nerve action potentials; NCV, nerve conduction velocity; ROM, SEPs, somatosensoryevoked potentials. |
 FIGURE 32-11. A 20-year-old with left global plexus injury secondary to motor vehicle accident and chronic refractory pain. (Courtesy of Shriners Hospital for Children, Philadelphia.) |
Delayed surgical management is usually performed 3 to 6 months after injury. The decision to operate is based on locating a repairable lesion that would not spontaneously recover. This is determined by the compilation of serial examinations and the extent of nerve injury. The time frame assures the viability of motor endplates to sprouting axons via nerve grafting or transfer. Unfortunately, disruptions of the lower trunk (C8, T1) do not respond to nerve grafting in adults as the distance required for the axons to travel to the motor endplates if too far prior to irreversible endplate demise. In contrast, infants can recover lower trunk function after nerve grafting.164
Surgical Approach
The surgical exploration for brachial plexus injuries requires an extensile exposure of the supraclavicular and/or infraclavicular plexus. The procedure is performed with the patient supine and ample preparation of the injured extremity, neck, hemithorax, and lower leg(s) for sural nerve grafts. Electrophysiologic testing apparatus may be used during surgery. This requires placement of scalp or cervical spine electrodes for SEPs and cortical electrodes for MEPs. Bipolar or tripolar probes can be used for direct intraoperative nerve stimulation to record NAPs across a lesion.
Table 32-9 Hospital for Sick Children Active Movement Scale (AMS) | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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The skin incision varies with the extent of plexus exposure anticipated based on the preoperative findings. Supraclavicular exposure begins with an incision across the upper border of the clavicle (Fig. 32-12). This incision may be extended in a proximal direction parallel to the posterior border of the sternocleidomastoid muscle. Skin flaps are elevated and supraclavicular sensory nerves are mobilized. Next, the subcutaneous platysma muscle is divided and the external jugular vein, which descends across the posterior border of the sternocleidomastoid to pierce the fascia, is usually ligated. Partial release of the sternocleidomastoid muscle from the clavicle may be necessary to widen the medial exposure. Similarly, the trapezius muscle can be partially released from the lateral clavicle to enlarge the lateral exposure. The omohyoid muscle is the “door” to the supraclavicular plexus and must be identified (Fig. 32-12B). It can then be retracted or divided at its intermediate tendon to expose the scalene muscles and plexus (upper and middle trunks). The transverse cervical artery, which crosses from anterior to posterior across the operative field just cephalad to the suprascapular artery, is mobilized and
ligated. Next, the phrenic nerve is identified as it travels on the anterior scalene muscle just anterior to the posterior triangle. The phrenic nerve must be protected throughout the dissection (Fig. 32-12C) but the C5 contribution can be sacrificed to gain more proximal root exposure if necessary. Our next step is to isolate the upper trunk and the C5 and C6 roots between the anterior and middle scalene muscles and look for neuroma (Fig. 32-12D). The middle trunk and C7 is inferior and posterior to the upper trunk, whereas the lower trunk is deep to the subclavian vessels and the clavicle, both of which can impede inferior dissection. Osteotomy of the clavicle and/or infraclavicular exposure may be necessary to enhance lower trunk exposure, especially if a clavicular malunion is present.
ligated. Next, the phrenic nerve is identified as it travels on the anterior scalene muscle just anterior to the posterior triangle. The phrenic nerve must be protected throughout the dissection (Fig. 32-12C) but the C5 contribution can be sacrificed to gain more proximal root exposure if necessary. Our next step is to isolate the upper trunk and the C5 and C6 roots between the anterior and middle scalene muscles and look for neuroma (Fig. 32-12D). The middle trunk and C7 is inferior and posterior to the upper trunk, whereas the lower trunk is deep to the subclavian vessels and the clavicle, both of which can impede inferior dissection. Osteotomy of the clavicle and/or infraclavicular exposure may be necessary to enhance lower trunk exposure, especially if a clavicular malunion is present.
 FIGURE 32-12. A 16-year-old sustained a right brachial plexus injury in a motorcycle accident. (Courtesy of Shriners Hospital for Children, Philadelphia.) (A) Incision across the upper border of the clavicle. (B) The omohyoid muscle is retracted in a cephalad direction to expose the underlying brachial plexus. (C) Phrenic nerve isolated along the anterior scalene muscle. (D) Neuroma of upper trunk. (E) Sharp resection of neuroma back to normal appearing fascicles. (F) Defect between C5/C6 and upper trunk (suprascapular, posterior division, and anterior division). (G) Sural nerve grafting from C5/C6 to upper trunk. |
Combined supraclavicular and infraclavicular exposure necessitates extension of the lateral skin incision downward into the deltopectoral interval. Isolated infraclavicular brachial plexus exposure requires only a deltopectoral incision. The deltoid muscle is retracted in a lateral direction and the pectoralis major in a medial direction. Utilizing the coracoid process as a landmark, the pectoralis minor tendon is identified as this is the “door” to the infraclavicular plexus. The tendon is tagged with a suture and divided. Next, the infraclavicular plexus and axillary artery are isolated. The lateral cord (i.e., musculocutaneous and median nerves) is usually the first structure encountered. Identification of the posterior cord (i.e., axillary and radial nerves) and medial cord (i.e., ulnar nerve) requires mobilization of the axillary artery.
Surgical Strategy
The surgery for brachial plexus injury is tedious, as scar envelopes the injured neural elements and eliminates the usual dissection planes. Following exposure of the brachial plexus, the injured and uninjured nerves are identified. The normal anatomy is often distorted and intraoperative nerve stimulation is therefore helpful. Direct stimulation of the nerve and observation of any corresponding muscle contraction assists in proper nerve identification. A biphasic stimulator with variable pulse width and amplitude facilitates stimulation (Checkpoint Stimulator, Checkpoint Surgical LLC, Cleveland, Ohio). The focus of the brachial plexus dissection is to differentiate lesions in continuity from those lesions with loss of continuity. The diagnosis is straightforward when the dissection uncovers a transected nerve or avulsed nerve roots. The differentiation, however, can be difficult when dense scar tissue and/or neuroma formation intervenes between the proximal and distal limbs of a completely disrupted nerve.39 In addition, a neurotmesis lesion can occur from severe intraneural damage without overt transection. This lesion will not recover without excision of the scarred nerve tissue and interposition grafting. Intraoperative use of SEPs, MEPs, and direct NAP can facilitate the diagnosis in these equivocal cases, although their reliability is controversial.
Stimulating a nerve and recording the cerebral cortical response indicates an intact SEP. The presence of recordable response implies nerve continuity, and the absence of a response indicates nerve discontinuity. This technique can be applied to a nerve root to determine the absence or presence of an avulsion injury. The absence of a response from a spinal nerve indicates an avulsion injury and is a contraindication to nerve grafting. The determination of the NAP across the neuroma may be helpful as the NAP is recorded by direct stimulation and recording of nerve proximal and distal to a suspected lesion. Conduction across the lesion confirms some nerve continuity, whereas an absent NAP indicates fiber discontinuity with complete intraneural scarring.101,137,144 As stated previously, the use of NAP is variable amongst brachial plexus centers and the interpretation of NAP requires experience.
Treatment of Avulsion Injuries
Currently, there is no surgical treatment to restore nerve rootlet connection (i.e., an avulsion injury) with the spinal cord.143 Experimental work with reattachment of the rootlets directly to the spinal cord is ongoing.24,25 The current treatment for avulsion injuries is nerve grafting using other viable proximal stumps or nerve transfer from intact adjacent nerves (see Fig. 32-10).
Treatment of Lesions in Continuity
The role of neurolysis for neuromas in continuity remains controversial as the ultimate effect on neurologic recovery is questionable. Neurolysis of a recovering nerve may induce further damage and reduce subsequent recovery. If neurolysis is performed and fascicular anatomy cannot be identified, resection and grafting is indicated.137
Treatment of Lesions without Continuity
After completion of the exposure and preliminary dissection, the lesions with loss of continuity are delineated. The proximal and distal stumps available for nerve reconstruction are defined with exclusion of any avulsions. Next, the neuroma is resected between the proximal and distal nerve stumps until normal nerve consistency and fascicular anatomy is encountered (Fig. 32-12E and F). Histology can be used to ensure viable axons.39,125 The distal stumps are now primed for coaptation with viable inflow for regeneration of axons. It is necessary to utilize some decision-making skills, especially in cases with loss of proximal roots secondary to avulsion, to determine the exact connection of proximal and distal stumps that will be performed. Restoration of continuity can be accomplished by nerve grafting or nerve transfer. Nerve grafting is the placement of intercalary segments that act as scaffolding for regenerating axons (Fig. 32-12G). Nerve transfer is coaptation of an expendable motor nerve into the distal stump to supply motor axons downstream. Nerve transfer can also be coaptation of an expendable sensory nerve into the distal sensory nerve stump to obtain sensibility.106
Nerve Grafting
Nerve grafting is the preferred technique for most lesions with loss of continuity (Fig. 32-13A through G). The interposition of nerve graft links the proximal and distal axons and serves as a conduit to channel the growing axons to the periphery. Autograft donor nerve is usually one or both sural nerves, harvested following brachial plexus exploration. Other potential autograft options include the cervical plexus, the ipsilateral medial antebrachial cutaneous nerve, and/or superficial radial nerves. Recently, the use of allograft has been employed as an alternative or additional conduit. However, the results of allograft are still pending and therefore we currently only use allograft in cases with insufficient autograft.
The donor nerve graft is divided into sections that span the defect until a comparable cross-sectional area is obtained for interposition grafting. Epineural sutures and/or biologic adhesives, such as fibrin glue, are utilized to secure the nerve grafts between the proximal and distal stumps (Fig. 32-13F and G).
51,101,141,143 Our preference is biologic adhesives to decrease operative time.63 The laboratory and clinical data demonstrate that glue is equal to, if not superior to, conventional suture methods with regard to the amount of fibrosis, axonal regeneration, and alignment of fascicles. This is due to the fact that the glue acts a sealant and not a barrier to nerve regeneration. Glue does exhibit less tensile strength compared to suture and should not be used alone when the repair is taut.59,153,201
51,101,141,143 Our preference is biologic adhesives to decrease operative time.63 The laboratory and clinical data demonstrate that glue is equal to, if not superior to, conventional suture methods with regard to the amount of fibrosis, axonal regeneration, and alignment of fascicles. This is due to the fact that the glue acts a sealant and not a barrier to nerve regeneration. Glue does exhibit less tensile strength compared to suture and should not be used alone when the repair is taut.59,153,201
 FIGURE 32-13. A 12-year-old struck bar car sustaining a complete infraclavicular brachial plexus injury. (Courtesy of Shriners Hospital for Children, Philadelphia.) (A) Preoperative examination with good shoulder motion, but no distal function. (B) Infraclavicular exposure with release of pectoralis minor. (C) Severed proximal radial, median (blue background), and ulnar nerves. (D) Distal neuromas of median, ulnar, and radial nerves. (E) Resection of proximal neuromas back to normal appearing fascicles. (F) Proximal nerve grafting using fibrin glue. (G) Distal nerve grafting using fibrin glue. |
 FIGURE 32-13. (Continued) |
The nerve grafts are revascularized by vascular ingrowth (a.k.a. imbibition) from the recipient bed.167,185 Therefore, numerous small-diameter grafts are preferable to a single large-caliber graft that is prone to central necrosis. Tension should be avoided across the proximal and distal coaptation sites because this produces an unfavorable condition for axonal sprouting.135,137 In adults, nerve grafts are best directed toward shoulder and elbow muscles for reinnervation because the distance to the branches is short and axonal regrowth can occur, thus preventing irreversible muscle damage.143
Nerve Transfer
Nerve transfers are indicated in avulsion injuries, large defects of the brachial plexus, and late presentation. The use of nerve transfers for inflow axons increases as the number of avulsed roots multiplies. In addition, long interposition nerve grafts (>7 to 10 cm) have less chance for recovery.9,32,106 Nerve transfer involves the connection of an expendable donor motor nerve to provide an axonal source for regeneration of the distal stump. The donor nerves are coapted to selected distal stumps, preferably specific peripheral nerves to achieve a desired function. Ideally, the nerve being transferred is coapted to its distal stump as close as possible to the motor end plates of the desired muscle to be innervated.106,221 Once the donor neurons reinnervate the muscle, function will require voluntary firing of the transferred nerve. Similar to a tendon transfer, activation of the donor nerve requires a period of training and involuntary muscle activation may occur until this transformation has taken place. For example, coughing or sneezing will initially activate intercostal nerve transfer, but over time this response diminishes. The technique of nerve transfer can be used in tandem with nerve grafting or may be the only available option in complete avulsion injuries.
Nerve transfers utilize a variety of axonal sources depending upon the injury. The number of available nerve transfers is increasing, as our knowledge of muscle innervation and nerve redundancy improves. Options include the spinal accessory nerve, intercostal nerves, a portion of the ulnar, median, or radial nerve, the medial pectoral nerve, the phrenic nerve, and the contralateral C7 nerve root (see Fig. 32-14).12,28,30,32,74,75,106,113,114,130,171,221 An ipsilateral C7 nerve root has also been reported as a potential transfer in cases with isolated avulsions of C5 and C6.73
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