Brachial Plexus Injuries

MAJ Ean Saberski MD

Neither Dr. Saberski nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this chapter.

This chapter is adapted from Rhee PC, Shin AYS: Brachial plexus injuries, in Krajbich JI, Pinzur MS, Potter BK, Stevens PM, eds: Atlas of Amputations and Limb Deficiencies: Surgical, Prosthetic, and Rehabilitation Principles, ed 4. American Academy of Orthopaedic Surgeons, 2016, pp 389-407.

ABSTRACT

Traumatic brachial plexus injuries present with devastating deficits of upper extremity utility. These deficits ultimately result in lifelong functional, occupational, social, and psychological consequences. Predictable injury patterns aid in the localization of traumatic lesions, but further evaluation is required for prognostication and treatment planning. Serial examination, advanced imaging, and electrodiagnostic studies all are critical elements in the evaluation of brachial plexus injuries, and with these tools the appropriate treatment is determined. In many cases, brachial plexus exploration and reconstruction with intraplexus or extraplexus nerve transfers results in excellent restoration of function. In other cases, plexus reconstruction is not feasible, and secondary reconstruction with free functional muscle transfer or amputation leads to improved upper extremity utility. In all cases, co-management of these complex patients between a multidisciplinary team optimizes outcomes and minimizes patient suffering.

Introduction

Brachial plexus injuries (BPIs) disrupt the function of the upper extremity and result in devastating long-term disability. Patients confront a wide scope of morbid issues including loss of function, psychological distress, chronic pain and dysesthesias, and aesthetic disappointment. BPIs are common in high-energy activities and misadventures, and are globally on the rise.¹^,²^,³^,⁴^,⁵^,⁶

Epidemiology

Males between the ages of 15 and 25 years are the most likely demographic to sustain BPI.⁶^,⁷^,⁸ BPIs most commonly result from motor vehicle accidents, and of these accidents 70% involve motorcycles or bicycles.⁹ The most common injury pattern is a supraclavicular injury with at least one root avulsion, and the most common root avulsions are the lower roots.⁹^,¹⁰

Both blunt and penetrating trauma can result in traumatic BPI. Closed BPI due to blunt trauma results in a traction injury between the mobile units of the neck, shoulder, arm, and torso (Figure 1). Penetrating injuries can result from any variety of trauma, including both high-energy and low-energy sources such as gunshot wounds and stab wounds.

Pathoanatomy

Five cervical nerve roots coalesce to form the brachial plexus, typically C5, C6, C7, C8, and T1. Contributions from C4 and T2 also have been described.¹¹ In the presence of a C4 or T2 contribution, the brachial plexus is termed prefixed or postfixed, with incidences of 28% to 62% and 16% to 73% in cadaver specimens, respectively. The brachial plexus has five sections: roots, trunks, divisions, cords, and terminal branches (Figure 2).

The dorsal and ventral nerve rootlets converge to form the spinal root as it passes through the spinal foramen. The cell bodies for motor nerves that course within the ventral rootlets originate from the anterior horn cells of the spinal cord. Conversely, the cell bodies for the sensory nerves that travel within the dorsal rootlets reside in the dorsal root ganglion (DRG), which is protected within the spinal canal and foramen (Figure 3, A).

The anatomic location of nerve injury in relation to the DRG has prognostic value. When the spinal rootlets are injured proximal to the DRG, a preganglionic injury has occurred (Figure 3, B). Preganglionic BPIs can be further differentiated into central avulsions in which the rootlets are avulsed directly off the spinal cord and intradural ruptures in which the rootlets rupture proximal to the DRG. Injuries to the brachial plexus distal to the DRG result in postganglionic injury¹⁰ (Figure 3, C and D). Although the dorsal and ventral rootlets are both avulsed in most cases, either rootlet can be avulsed in isolation in as many as 10% of cases.¹²^,¹³^,¹⁴ Distinguishing a preganglionic from a postganglionic injury is imperative because spontaneous recovery cannot occur with a preganglionic BPI. In addition, the technique for brachial plexus reconstruction is markedly different for the two types of injuries.

FIGURE 1 Illustration depicting one common mechanism (a fall from a motorcycle) that can result in a closed, traumatic brachial plexus injury. The arrow represents the direction of the force causing the nerve avulsions and ruptures. (Courtesy of the Mayo Foundation for Medical Education and Research, Rochester, MN.)

FIGURE 2 Illustration of the brachial plexus nerves. LSS = lower subscapular, MABC = medial antebrachial cutaneous, MBC = medial brachial cutaneous, TD = thoracodorsal, USS = upper subscapular. (Courtesy of the Mayo Foundation for Medical Education and Research, Rochester, MN.)

The roots merge to form the upper trunk (C5 and C6), middle trunk (C7), and lower trunk (C8 and T1). The site at which C5 and C6 unite (the point of Erb) marks the location where the suprascapular nerve emerges.¹⁰ The trunks divide into anterior and posterior divisions as the brachial plexus passes beneath the clavicle (Figure 4). The posterior divisions coalesce to form the posterior cord; the anterior divisions of the upper and middle trunk form the lateral cord. The anterior division from the lower trunk continues as the medial cord. The cords are named based on their location relative to the axillary artery (Figure 4).

FIGURE 3 A, Illustration of spinal rootlets and the dorsal root ganglion within the spinal canal. Illustrations depict avulsion (B), stretch (C), and rupture (D) brachial plexus injuries. (Courtesy of the Mayo Foundation for Medical Education and Research, Rochester, MN.)

FIGURE 4 Illustration of the brachial plexus in relation to the clavicle and the axillary artery. (Courtesy of the Mayo Foundation for Medical Education and Research, Rochester, MN.)

Many terminal branches of the brachial plexus originate from the cords (Figure 2). The lateral cord splits into the musculocutaneous nerve and the lateral cord contribution to the median nerve. The medial cord parts to form the ulnar nerve and the medial cord contribution to the median nerve. The posterior cord divides into the axillary and radial nerves.

Terminal branches can arise in various sites within the brachial plexus. The phrenic, dorsal scapular, and a contribution to the long thoracic nerve branches off the C5 nerve root. The suprascapular nerve and the nerve to the subclavius muscle originate from the upper trunk. The lateral pectoral nerve originates from the lateral cord; the medial pectoral, medial brachial cutaneous, and medial antebrachial cutaneous nerves form from the medial cord. The thoracodorsal and upper and lower subscapular nerves emerge from the posterior cord.

In addition to root avulsions causing BPIs, traumatic BPIs can occur when the neural elements are stretched or ruptured (Figure 3, C and D). Lesions that remain in continuity (stretch) have the potential for spontaneous recovery based on the degree of neural injury (neurapraxia or axonotmesis).¹⁵ A rupture (neurotmesis) of the neural elements can occur at any site distal to the DRG to the terminal branches. Ruptures most commonly occur at the root or peripheral nerve levels.

BPIs can be described by the nerve root level involved, by the location of the injury, or in relation to the DRG. Common patterns of injury based on the neural level involved include the upper trunk, upper and middle trunk, lower trunk, and panplexus (complete) BPIs. A panplexus BPI affects all neural elements of the brachial plexus with similar or varied degrees of injury. Otherwise, the location of the BPI can be described in reference to the clavicle as supraclavicular (root and trunk), retroclavicular (division), and infraclavicular (cords and terminal branches). Similarly, the location of injury relative to the DRG can be expressed as preganglionic or postganglionic.

BPIs usually occur at sites where the nerve is relatively fixed, restrained by surrounding structures, or changes direction. Examples include the suprascapular nerve within the suprascapular notch, the axillary nerve within the quadrilateral space, or the musculocutaneous nerve as it penetrates the coracobrachialis.¹⁵ In general, supraclavicular injuries are more common than infraclavicular injuries. Of the supraclavicular injuries, a panplexus BPI is the most common injury pattern. In addition, upper trunk lesions are more common than lower trunk injuries.

Physical Examination

A thorough physical examination can aid in the accurate diagnosis of a BPI. On inspection, any traumatic or surgical wounds are noted. The resting position of the hand, wrist, elbow, and shoulder girdle can help elucidate the dysfunctional motor units. Percussion along the course of the nerve can elicit paresthesias in the distribution of the nerve root that can help distinguish between preganglionic and postganglionic injuries. Pain over a percussed nerve typically indicates a rupture, whereas lack of pain can indicate an avulsion.¹⁰ An advancing Tinel sign suggests a recovering nerve lesion and should be serially examined over time.¹³

A systematic motor examination of the entire affected upper extremity is imperative to localize the BPI (Figure 5). Motor strength can be graded based on the modified British Medical Research Council system, with useful motor function defined as grade 3 or higher. To assign grade 3 strength to a muscle, the muscle unit tested needs to have motion against gravity in the full arc of passive range of motion. Grade 3 strength cannot be obtained if active motion is unequal to passive motion, no matter how strong the muscle is in the lesser arc of motion. In addition, the integrity of cranial nerve XI should be assessed with strength testing of the upper, middle, and lower trapezius, because the spinal accessory nerve can be used as a donor nerve for nerve transfers or the trapezius tendon can serve as a donor for shoulder tendon transfers.

In most cases, upper trunk injury results in a predictable loss of shoulder abduction, external rotation, and elbow flexion. Additional damage to the C7 nerve root in an upper trunk BPI can be indicated by triceps, pronator teres, and/or wrist and finger extensor muscle weakness. An isolated lower trunk injury often manifests as loss of hand function (intrinsic and extrinsic) with preserved shoulder and elbow function. In T1 nerve root avulsions, disruption of the sympathetic outflow to the head and neck can occur because of the intimate relationship of the sympathetic ganglion for T1 and the adjacent nerve root. This can be clinically evident with Horner syndrome (miosis, ptosis, and anhidrosis) (Figure 6). Similarly, certain findings on clinical examination can suggest a preganglionic BPI within the upper trunk (Table 1).

A comprehensive neurologic examination must be performed to identify a coexistent spinal cord injury (SCI). A prevalence of 12% has been reported for a concomitant SCI in patients with a BPI.¹⁶ Patients with a combined BPI/SCI who have sustained a preganglionic injury at one or more root levels are more likely to exhibit Horner syndrome and phrenic nerve dysfunction than a patient with an isolated BPI. Theoretically, a shared mechanism of injury results in a combined SCI/BPI. Therefore, a neurologic examination of the contralateral upper limbs and bilateral lower limbs should be performed, including sensory levels and the presence of increased reflexes or pathologic reflexes.¹⁰

A vascular examination is performed because injury to the axillary artery is not uncommon with infraclavicular BPIs or in cases of scapulothoracic dissociation. The status of the axillary artery is also important because the thoracoacromial trunk is a common target vessel for free-functioning muscle transfers (FFMTs).

Imaging Studies

The radiographic priority in evaluating BPI is to define the bony anatomy with plain radiographs. These images will reveal associated trauma to the cervical spine, shoulder, and chest. Beyond illustrating the extent of the injury complex, the plain radiographs may give insight to the underlying brachial plexus lesion. Cervical transverse process, spinous process, and vertebral body fractures are known to have an association with root avulsions at their corresponding levels.¹⁰ Shoulder radiographs demonstrate the competency of the shoulder joint, and loss of deltoid and rotator cuff muscle tone may be revealed by inferior subluxation of the humeral head from the glenoid.

CT is the modality of choice for detecting root avulsions. With avulsion, the dural sac can rupture and subsequently heal, producing a pseudomeningocele, which is characteristic of a preganglionic injury¹⁵ (Figure 7). Fine-cut postmyelographic CT has a reported sensitivity and specificity between 80% and 90% in the detection of both pseudomeningoceles and the diagnosis of root avulsions.¹²^,¹³^,¹⁷^,¹⁸^,¹⁹ However, immediately after a preganglionic BPI, a hematoma can be present within the pseudomeningocele that can displace the dye used for myelography, producing a false-negative result.¹⁰ Therefore, CT myelography should be performed 3 to 4 weeks after BPI to allow blood clots to disperse and pseudomeningoceles to fully form. Ultimately, the invasive technical process and the inability to fully characterize brachial plexus injuries limit the clinical utility of CT myelography.

MRI demonstrates variable success in illustrating root avulsions, but it has many advantages over CT myelography when evaluating patients with a BPI.¹⁸^,²⁰^,²¹^,²² MRI is particularly useful in evaluating the postganglionic plexus through multiple levels of potential plexus injury. MRI can visualize the entire brachial plexus, which allows identification of neuromas, inflammation, edema, and mass lesions within or adjacent to the brachial plexus.²³

Electrodiagnostic Studies

Electrodiagnostic studies are a critical tool in defining brachial plexus lesions. Electromyography (EMG) is commonly used for the outpatient evaluation of brachial plexus lesions. EMG studies are not useful in the immediate postinjury period because of the lag of wallerian degeneration. The first clinically revealing data are usually observed by EMG by week 4 after injury. EMG can detect nuanced findings that allow for the determination of acutely denervated muscles. Motor unit action potentials (MUAPs) during EMG study can be used to help delineate the degree of injury. Absent MUAPs correlate with a greater degree of injury and ultimately guide toward a higher level of reconstruction. MUAPs are particularly useful for patients in whom serial examinations are required because of their qualitative and quantitative metrics (Table 2).

FIGURE 5 Image of the brachial plexus physical examination form. (Courtesy of the Mayo Foundation for Medical Education and Research, Rochester, MN.)

FIGURE 6 Clinical photograph of a patient with Horner syndrome, which consists of miosis, ptosis, and anhidrosis. (Courtesy of the Mayo Foundation for Medical Education and Research, Rochester, MN.)

Sensory nerve action potentials are also critically useful. Studies showing disruption of sensory nerve action potentials suggest a postganglionic injury, and studies showing preserved sensory nerve action potentials suggest a preganglionic injury. This phenomenon is expected because of the axonal arc through the dorsal root ganglion.

Intraoperative use of electrodiagnostic studies is integral to surgical decision making. Commonly used techniques include nerve action potentials, somatosensory evoked potentials, and motor evoked potentials. The presence of a nerve action potential across a nerve lesion indicates intact (preserved or regenerating) axons and suggests that nerve recovery will occur with neurolysis alone in 90% of patients.²⁴ The presence of a somatosensory evoked potential or a motor evoked potential indicates an intact connection between the central and peripheral nervous system through a preserved dorsal or ventral rootlet, respectively. Therefore, both somatosensory evoked potentials and motor evoked potentials are absent in postganglionic BPIs and in combined preganglionic and postganglionic BPIs.

TABLE 1 Physical Examination Findings That Suggest Preganglionic Brachial Plexus Injuries

Clinical Entity	Muscles Affected	Nerve	Spinal Level
Horner syndrome	NA	T1 sympathetic ganglia	C8-T1
Scapular winging	Serratus anterior	Long thoracic	C5-C7
NA	Levator scapulae	Dorsal scapular	C3, C4, C5
NA	Rhomboids	Dorsal scapular	C4, C5
NA	Cervical paraspinal	Dorsal rami	C4-T1
NA = not applicable

FIGURE 7 Coronal (A) and axial (B) CT myelograms of the spine show pseudomeningoceles and root avulsions. (Courtesy of the Mayo Foundation for Medical Education and Research, Rochester, MN.)

TABLE 2 Degree of Nerve Injury and Associated Electrodiagnostic Findings

Sunderland Classification	Fibrillations	MUAPs	Surgical Intervention
I (neurapraxia)	–	+ (normal)	None
II (axonotmesis)	+	+^a	Initial observation, and if necessary, neurolysis
III (partial neurotmesis)	+	+^a	Initial observation, and if necessary, neurolysis
IV (partial neurotmesis)	+	–	Nerve reconstruction
V (complete neurotmesis)	+	–	Nerve reconstruction
Reproduced with permission from Hill JR, Lanier ST, Brogan DM, Dy CJ: Management of adult brachial plexus injuries. J Hand Surg Am 2021;46(9):778-788, Table 1; adapted with permission from Ferrante MA, Wilbourn AJ: The electrodiagnostic examination with peripheral nerve injuries, in Mackinnon SE, ed: Nerve Surgery, ed 1. Thieme, 2015, Table 3.1, p 59.
^aEarly (8 to 12 weeks), collateral sprouting; late, axonal regeneration.

Fundamentals of Surgical Management for BPI

The tenets of brachial plexus reconstruction revolve around patient selection, timing of surgery, and the priority of restoring function within the upper limbs.¹⁰ Patients are indicated for surgery in the absence of clinical or electrodiagnostic evidence of recovery on serial examinations or when recovery is impossible (root avulsions).

The timing of surgery depends largely on the mechanism of injury. In penetrating injuries with sharp transection of the brachial plexus, immediate exploration and primary repair is warranted to facilitate direct nerve coaptation before the onset of perineural scarring. Penetrating injuries from a blunt object can be treated in a subacute manner (3 to 4 weeks) to facilitate further demarcation of the neural zone of injury that can be adequately identified and resected at the time of surgery. Gunshot wounds are managed based on the projectile velocity; BPIs resulting from low-velocity gunshot wounds often cause neurapraxia, and spontaneous recovery can be expected. However, in cases of high-velocity gunshot wounds, surgical exploration is often necessary because of the magnitude of associated soft-tissue damage.¹⁰

For closed BPIs, the timing of surgery depends largely on the type of nerve injury. For root avulsions, early surgery is recommended at 3 to 6 weeks after injury, whereas presumed ruptures and stretch injuries should be explored at 3 to 6 months after serial examinations with demonstration of inadequate or absent reinnervation. Typically, brachial plexus exploration and reconstruction should be performed by 6 months after injury.¹⁵ Poor outcomes can be expected in patients who undergo brachial plexus reconstruction beyond 6 to 9 months after injury because motor end plates degenerate before the regenerating nerves can reach the target muscles.¹⁰ After 1 year, brachial plexus reconstruction is not advised because of progressive neural death and irreversible muscle atrophy.¹⁵

The priority of brachial plexus reconstruction is to restore elbow function, obtain shoulder abduction and stability, regain hand sensibility, provide wrist flexion and finger extension, and establish hand intrinsic function.¹⁰ These functions can be obtained with primary and secondary brachial plexus reconstruction. Primary brachial plexus reconstruction refers to the initial surgical management to include neurolysis, direct nerve repair, nerve grafting, nerve transfers, and FFMTs. Secondary brachial plexus reconstruction is performed to improve the gains achieved with primary reconstruction or if earlier attempts at reconstruction have failed; examples include tendon/muscle transfers, FFMTs, arthrodesis, and corrective osteotomies.¹⁰^,²⁵

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