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Brachial plexus injuries comprise approximately one-third of all peripheral nerve injuries and are seen in just more than 1% of patients presenting to a trauma facility. They usually affect younger patients, with a median age of 34. Because of the association of such injuries with violent trauma and contact sports, males are affected more frequently than females. By the same line of reasoning, they are also often associated with injuries in other organ systems that are life-threatening. It was estimated that as many as 80% of patients with severe traumatic brachial plexopathy had multiple traumas to the head and skeletal system. Hence there can be a delay in the diagnosis and treatment of brachial plexus injuries while the management of the other injuries is given priority.
The brachial plexus can be injured in several ways. The most common etiology is trauma, which can result in open or closed injuries. Among the closed injuries, the most common is caused by stretch or contusion, usually secondary to motor vehicular accidents involving motorcycles. Sports such as football, cycling, and skiing, among others, can also cause such injuries. Regardless of the setting, the mechanism is the same: the head and neck are usually forcefully pushed in one direction and the shoulder and arm in another. This results in severe stretching of the soft tissues, including the plexal elements and less frequently, the blood vessels. As for open injuries, the common etiologies are gunshot wounds and lacerations with knives or glass. Iatrogenic injuries may be open or closed. Nontraumatic causes of brachial plexus injuries include thoracic outlet syndrome and nerve sheath tumors, which cause injury by compression of plexal elements. In a survey of 1019 brachial plexus lesions by Kim et al., the most common type of brachial plexus injury was due to stretch or contusion (50%), followed by thoracic outlet syndrome (16%) and nerve sheath tumors (16%). Gunshot wounds (12%) and lacerations (7%) complete the list. Because the majority of brachial plexus injuries are due to stretch/contusion, this chapter will focus on the diagnosis and management of such injuries.
Injury patterns can also be classified into supraclavicular and infraclavicular injuries. The supraclavicular plexus refers to the C5-T1 spinal nerves and the upper, middle, and lower trunks with their branches and divisions. On the other hand, the infraclavicular plexus refers to the cords and the nerves. In the series reported by Kim, 72% of brachial plexus stretch injuries are supraclavicular and 28% are infraclavicular. Of the supraclavicular injuries, C5-T1 palsy is the most frequent injury pattern, followed by C5-C7 then C5-C6. In terms of spontaneous recovery rate, C5-C6 has the best prognosis, with 30% of patients regaining significant function by 3 to 4 months. This compares favorably with C5-C7 palsy, where approximately 16% recover spontaneously in the early months, and C5-T1 (pan-plexus palsies), with only 4% incidence of spontaneous recovery.
Supraclavicular plexus injuries are more likely (52%) to come to surgery due to the severity of these injuries, with up to two-thirds having avulsion of at least one spinal nerve. The infraclavicular lesions are less likely (17%) to be operated on, with half sustaining only neurapraxic injuries. Of the supraclavicular plexus injuries requiring surgery due to the lack of clinical recovery, two-thirds will have at least some involvement of lower plexal (C8 and T1 spinal nerve) elements. The majority of these with panplexal involvement will have avulsed one or more spinal nerves, and exceedingly few will regain any useful function without intervention. On the contrary, when lower plexal elements are spared, and the primary injury thus less extensive, up to 25% may still make a good functional recovery of involved elements after neurolysis alone, without nerve repair.
The brachial plexus originates at the level of the spine and usually includes the C5, C6, C7, C8, and Tl spinal nerves, the three trunks of the plexus, and their anterior and posterior divisions ( Fig. 184.1A ). Spinal nerves and trunks are supraclavicular, whereas divisions tend to lie behind the clavicle. Lateral, posterior, and medial cords are infraclavicular, as are their origins for the major nerves of the upper extremity (see Fig. 184.1B ).
Each individual spinal nerve or root of the plexus originates as multiple sensory rootlets from the dorsal root entry zone of the posterolateral sector of the spinal cord and usually as one ventral or motor rootlet from the ventrolateral portion of the cord. The dorsal rootlets combine to form one dorsal root per spinal segment before entering the foramen. Within the foramen, the course of the roots varies between 10 and 16 mm. The dorsal root ganglion is located at an intraforaminal level and usually at its midpoint. Shortly distal to this, the anterior and posterior roots blend together to form the (mixed) spinal nerve. Posterior primary branches or rami then go to the paraspinal muscles and the much larger anterior ramus contributes to the brachial plexus.
Within the foramen, the C5 spinal nerve gives rise to a dorsal scapular nerve branch, which supplies the rhomboids. In addition, a branch that contributes to the long thoracic nerve exits the foramen posterior to the spinal nerve. The C4 spinal nerve may also make a small contribution to the plexus. Rarely, this may be substantial and thus represent a prefixed plexus. C6 blends with C5 to form the upper trunk. Usually, the long thoracic nerve arises from the dorsal surface of the distal portion of C6, just before it melds into the upper trunk. The C7 spinal nerve blends imperceptibly into the middle trunk with little to differentiate the two. C8 combines with Tl to form the lower trunk. It is at this level that rami communicantes are most likely seen coming and going from the spinal nerve. These rami and their ganglia form the cervical sympathetic chain, whose largest ganglion is usually found posterior to the vertebral artery close to the latter’s division from the subclavian artery. Occasionally, T2 or a contribution from it may combine with T1 or its junction with the lower trunk to help form the latter.
The upper and middle trunks are the most readily identified portions of the supraclavicular plexus. The upper trunk is usually adherent to and sometimes partially covered by the anterior scalene muscle. As one proceeds distally along the lateral edge of the trunk, the suprascapular nerve (SSN) is encountered arising from the dorsolateral surface of the distal upper trunk, just as it forms anterior and posterior divisions. This trident-like structure, with SSN, posterior and anterior divisions (from lateral to medial) is an excellent landmark for the termination of the upper trunk (see Fig. 184.1A ).
The middle trunk is found beneath the anterior scalene and is often covered by some muscular connections between the anterior and medial scalene or with scar tissue resulting from injury. It is usually smaller in caliber than either the upper or lower trunk. The posterior division of the middle trunk combines with its counterpart from the upper and lower trunks to form the posterior cord deep and just distal to the clavicle. The middle trunk anterior division combines with that from the upper trunk to form the lateral cord.
The lower trunk is usually relatively short and lies somewhat behind the subclavian artery. Exposure is aided by skeletonizing the inferior surface of the subclavian artery so that it can be gently elevated by a vein retractor. The posterior division of the lower trunk blends with the corresponding divisions from the other trunks to help form the posterior cord. The bulk of the lower trunk proceeds directly through its anterior division to form the medial cord.
Although each trunk has an anterior and a posterior division as outlined previously, they can blend with other divisions before forming cords. Sometimes one or more divisions trade bundles of nerve fibers back and forth several times. In addition, the site at which cords begin distal to the clavicle can vary from patient to patient. Separating divisions in cases in which there has been a stretch injury, gunshot wound, or prior vascular dissection can be quite difficult. The surgeon works from trunks in a distal direction and cords in a proximal one to expose the divisions.
These are named, by convention, in relation to the axillary artery at the level of the coracoid. The lateral cord is usually superficial to the artery and is the first major neural element encountered after section of the pectoralis minor muscle as one begins dissection in the infraclavicular region. It terminates in a contribution to the median nerve and an oblique takeoff running laterally to form the musculocutaneous nerve (MCN) (see Fig. 184.1B ). The latter dives immediately between the two heads of the biceps muscle but usually gives off one or more coracobrachialis branches first.
The posterior cord is deep or posterior to the axillary artery. Several subscapular branches (upper and lower) usually arise from the posterior cord and run inferiorly and obliquely. A relatively sizable branch, the thoracodorsal, runs from its posterior aspect almost directly posteriorly to supply the latissimus dorsi. The cord then divides into its two major branches, the axillary and the (larger) radial nerves. After coursing inferiorly and slightly laterally, the axillary nerve dives down to reach the quadrilateral space and eventually the deltoid muscle in the posterior arm. The major posterior cord outflow is the radial nerve, which runs inferiorly toward the humeral groove to wind around the humerus. A very important anatomic landmark is the medial relation between the radial nerve and the profundus branch of the axillary artery. This can be used to locate the proximal radial and differentiate it from the more lateral axillary nerve.
The medial cord sends a major contribution to the median nerve that wraps around the medial and superior side of the axillary artery. As this contribution is given off, so are the ones to the ulnar nerve and the medial brachial and antebrachial branches. These neural structures remain medial to the brachial artery as they begin their descent down the arm. Be aware that stretch injury can change the positions of trunks, cords, and nerves and their proximal to distal positions in relation to the usual anatomic landmarks of the arm.
It is important to obtain a good clinical history with regard to the mechanism of injury and the deficits incurred. In general, a high-velocity motor vehicular accident would result in a higher risk of root avulsion. The evolution, or lack thereof, of the patient’s motor and sensory symptoms over time is extremely helpful. Worsening of the symptoms may indicate an ongoing compressive lesion such as a hematoma, whereas improvement over time suggests spontaneous recovery and possibly, nonoperative management. Other accompanying injuries, specifically vascular and musculoskeletal, along with any surgical intervention performed for these, must be elicited by the examiner.
A comprehensive physical examination begins with inspection. Typical positioning of the limb suggests involvement of the upper or lower plexus elements or both. For example, upper plexus palsy (Erb palsy) has the characteristic “waiter’s tip” position, a lower plexus palsy (Klumpke palsy) typically results in a “claw hand,” and a panplexus palsy usually results in a flail arm. One then proceeds to perform an assessment of the shoulders, neck, and high back from behind with the patient standing. One can readily spot asymmetry of the shoulder girdles, drooped shoulder, or laterally rotated scapula. In addition, the parascapular area is inspected for rhomboid atrophy, winging of the scapula, or atrophy of supraspinatus, infraspinatus, or deltoid muscles. Muscular atrophy can be a true neurogenic type secondary to muscle denervation or, at times, from disuse. The mechanics of shoulder abduction and internal and external rotation of the upper arm should be viewed from behind, as can the response of latissimus dorsi to a deep cough. If there is a question of diaphragmatic paralysis, the chest can be percussed from behind, matching inspiratory tympani with that on expiration. Then, standing at the patient’s side, one can recheck internal and external rotation of the arm as well as adduction of the arm by the pectoralis and other muscles. Biceps/brachialis and brachioradialis can then be tested as elbow flexors and triceps as an elbow extensor. With the elbow fully extended, pronation and supination are tested, followed by wrist extension and flexion.
Hand muscle function is best tested with both the subject and the examiner seated and facing each other. The patient’s hands can be placed palm up on the knees for finger flexion testing and palm down on the knees or on a flat surface to test for extension. Each hand can then be held and manipulated to test for fine muscle hand intrinsic function, presence or absence of sweating, and sensory testing. For motor testing, the British Medical Research Council (MRC) grading system (0 to 5) is most commonly used. Degrees of active and passive range of motion should also be documented.
After inspecting and testing these muscles, the examiner’s attention is directed to the front of the patient’s body. The neck is also inspected and palpated. Associated findings such as Horner syndrome should be looked for. Scars in supraclavicular, infraclavicular, and axillary spaces should be inspected and palpated. Deep tendon reflexes are ascertained and compared with the contralateral extremity, followed by a sensory exam.
On presentation, an attempt is made to localize the injury to the involved plexus elements based on the history and physical examination, supplemented by electrodiagnostic and imaging investigations. During assessment, functional loss of each element is graded as complete, incomplete, or none. In general, the clinical deficits with truncal, cord, and cord-to-nerve level injuries are relatively constant, the exception being the wrist and finger function that remain after combined middle and lower trunk damage. In addition, lower trunk loss sometimes involves more than hand intrinsic muscle and ulnar distribution sensory loss. C7 injuries can result in surprisingly few deficits, often only partial triceps weakness, because other spinal nerves carry input to the muscles supplied by this element. At the division level, injuries can have different patterns of loss, depending on which truncal outflows are involved and the proportion of anterior and posterior division loss. The typical motor and sensory involvement for each spinal nerve and truncal element are summarized in Table 184.1 .
Structure Involved | Distribution of Loss |
---|---|
C5 | Supraspinatus and infraspinatus, deltoid; rhomboids and serratus anterior also if injury is very proximal |
C6 | Biceps, brachialis, brachioradialis, supinator |
C7 | Triceps, pronator teres, some latissimus dorsi |
C8 | Wrist and finger flexors, finger and thumb extensors, some hand intrinsics |
T1 | Hand intrinsics |
Upper trunk (C5-6) | Supra- and infraspinatus, deltoid, biceps and brachialis, brachioradialis, supinator |
Middle trunk | Same as C7 |
Lower trunk (C8-T1) | All hand intrinsics, some wrist and finger flexor and extensor loss |
A 56-year-old, right-handed man was involved in a motorcycle accident and dislocated his right shoulder joint. He noticed numbness of his radial three fingers and was unable to abduct his shoulder or flex his elbow. Initially he also had difficulty extending his wrist, fingers, and elbow. His shoulder dislocation was reduced, and he was evaluated by a neurosurgeon 6 weeks later. Atrophy of his deltoid and biceps muscles was evident. No contraction of his deltoid, supraspinatus, infraspinatus, biceps, or brachioradialis muscles could be appreciated, but his elbow, wrist, and finger extension had recovered to MRC grade 4. His wrist and finger flexors and hand intrinsic muscles functioned normally. Clinically, he presented predominantly with an Erb palsy. Electrodiagnostic studies confirmed denervation of his biceps, deltoid, and supraspinatus muscles with reduced activation of triceps and pronator teres. Positive radial nerve sensory nerve action potentials (SNAPs) were recorded with stimulation at his insensate thumb, suggestive of a preganglionic lesion.
Four months after the injury, there was still no sign of deltoid, supraspinatus, or biceps contraction, but his elbow, wrist, and finger extension strength had returned to close to normal. A magnetic resonance imaging (MRI) study of his cervical spine demonstrated the appearance of a pseudomeningocele at the C4/C5 level on the right side and asymmetry of the rootlets, suggestive of a proximal injury to the C5 spinal nerve.
Five months post injury, he underwent right brachial plexus exploration and was found to have a preganglionic injury at C5 and C6, indicative of avulsion injury. Nerve transfers (accessory to SSN, triceps branch to axillary nerve, and ulnar fascicle to biceps branch of MCN) were performed in an attempt to restore the patient’s shoulder abduction and elbow flexion.
Although a thorough physical examination is paramount, well-selected electrical and imaging studies play an important role in the assessment of brachial plexus lesions.
For supraclavicular palsies, the major question to be answered is how far proximal or medial the injury extends along the spinal nerves and roots. Special electromyography (EMG) studies are of some help in this regard. Muscles that can be tested include the paraspinal, serratus anterior, and rhomboid muscles, because their innervation is very proximal. EMG studies of the other muscles supplied by the brachial plexus may help the clinician to ascertain the location and extent of a plexus lesion and may suggest the possibility of recovery even if there is no clinical evidence of this.
After serious plexus injury, it may take several months for certain electrical signs of recovery to occur. However, with some injuries, recovery in the distribution of one or more elements may become evident in the early months. This makes repeated electrical as well as clinical study worthwhile. Nevertheless, electrical studies must always be interpreted in the context of the clinical findings and can never substitute, even in part, for a thorough clinical examination.
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