Traumatic Brachial Plexus Injury

Abstract
A 24 year old gentleman with a traumatic left brachial plexus injury. He showed no clinical improvement after initial physiotherapy and observation. A neurotisation was performed with a satisfactory outcome.
Keywords: Brachial plexus injury, neurotisation,
Introduction
Traumatic brachial lexus injury is not uncommon. It results in variable loss of upper extremity function. The restoration of this function requires good stability if the involved shoulder and elbow flexion of adequate strength and range of motion. A proper understanding and evaluation of brachial plexus lesions is a prerequisite to any reconstructive procedure.
Narakas developed his rule of "seven seventies" in his experience over 18 years with 1068 patients.1 Approximately 70% were motor vehicle accidents (MVAs). Of the MVAs, 70% were motorcycles or bicycles. Of the cycle riders, 70% had multiple injuries. Of the multiple injuries in cycle riders, 70% were supraclavicular injuries. Of the supraclavicular injuries, 70% had at least one root avulsed. Of the avulsed roots, 70% were lower C7, C8, T1.  Of the 70% avulsed roots, 70% of those were associated with chronic pain.

Case Report
A 50 year old gentleman was involved in a road traffic accident. He was riding a motorcycle on a slippery road. He collided with a car and was thrown off his motorcycle. He was brought to the emergency department with bruises over his left shoulder and a flail left upper limb. Physical examination revealed absent power of his left shoulder abduction and flexion and elbow flexion without evidence of penetrating trauma to the neck, shoulder, or axilla. Wrist and hand movement and sensation were intact, whereas sensation was diminished in the shoulder and proximal arm. Pulses were intact in the left arm. The left glenohumeral joint showed full passive range of motion. X-rays of the cervicothoracic spine, ribs, left shoulder, humerus, forearm, or hand demonstrated no evidence of fracture.
A computed tomographic (CT) scan of the head showed no intracranial haemorrhage, mass effect, or midline shift; a CT scan of the cervical spine was negative for fracture, subluxation, and malalignment but was positive for left-sided paravertebral soft tissue swelling.
The diagnosis of upper root brachial plexus injury was made and the patient was admitted for observation. He was subsequently discharged with an arm sling and an electrodiagnostic study was obtained 3 weeks later.
He was seen in the Hand clinic approximately 6 weeks after his initial trauma. The patient noted that he had a complete inability to activate the left deltoid and biceps muscles without improvement and experienced 9/10 pain radiating from his left neck down to his fingers as well as numbness and tingling in the same distribution. On neurological examination, the patient was a well-appearing man holding his left arm at his side. His mental status and cranial nerves were normal, including no evidence of Horner's syndrome. On motor evaluation, the patient had a mild amount of left scapular winging with normal trapezius function and was 0/5 on direct testing of the supra- and infraspinatus, deltoid, biceps, and brachioradialis muscles. Rhomboid function was present but moderately weak, triceps were 3/5, the latissimus dorsi and pectoralis major sternal head were 4/5, pectoralis major clavicular head was 0/5, supinator was 3/5, and all other muscle groups were 5/5. He had absent deep tendon reflexes at the biceps and brachioradialis on the left side and had numbness to light touch in a C5 and C6 dermatomal distribution on the left. There was evidence of mild subluxation of the glenohumeral joint and some atrophy of his biceps, and deltoid muscles.
The patient was informed regarding the nature of his injury and poor recovery as evidenced by no clinical improvement and EMG documentation of complete denervation of muscles in a C5, C6 distribution. It is likely that he would not regain significant function without surgical intervention. The patient was informed that the recovery process would take months to years and likely would not be complete. A comprehensive pain management program as well as physical and occupational therapy will be prescribed, particularly to avoid contracture formation in his shoulder and elbow.
He continued the physical and occupational therapy for 4 months without showing any improvement. After considering the recommendations, the patient elected to pursue surgery.
A supraclavicular approach was used to identify the phrenic nerve which was located on the anterior surface of the anterior scalenus muscle. The integrity of the nerve was confirmed by a nerve stimulator. The nerve was dissected and transacted at the upper margin of the clavicle just before its entry into the thoracic cavity. It was the mobilised laterally for transfer. The next step was the isolation of the MCN via infraclavicular approach. The musculocutaneous nerve (MCN) was dissected proximally inside the lateral cord before it was cut. The sural nerve autograft was passed deep to the clavicle and was sutured to the phrenic nerve and MCN. Next, the location of the distal accessory nerve and the suprascapular nerve at the suprascapular notch were identified. After the skin incision, the trapezius muscle was splitted and a blunt dissection was carried out over the supraspinatus muscle to the superior border of the scapula. The superior scapular ligament was identified and divided under direct vision. The suprascapular nerve was revealed in the adispose tissue below the divided ligament. The nerve was dissected as proximal as possible. Subsequently, a medial dissection was made to locate the accessory nerve. The nerve was then dissected as far distally as possible. The suprascapular nerve is divided sharply proximally, and the accessory nerve is divided distally, and the proximal end of the accessory nerve is sutured to the distal end of the suprascapular nerve with interrupted 9-0 nylon.
The patient was discharged with an arm sling and continued his physical therapy and rehabilitation as outpatient.


Discussion
Anatomy
Brachial plexus is a network of nerves originating from the ventral rami of C5 to T1 nerve roots. In more than half of the cases, the C4 give branch to the C5. The second thoracic nerve (T2) also contributes directly to the plexus via intrathoracic precostal communication with the T1. The ventral rami emerge between the scalenius anterior and the scalenius medius muscles in the posterior triangle of the neck and descend toward the anterior portion of the first rib. Immediately after entering the posterior triangle, the C5 and C6 nerve roots join to form the upper trunk, the C7 continues as the middle trunk and the C6 and C7 join to form the lower trunk. The suprascapular nerve arises from the upper trunk at which point it is also known as Erb’s point. Just proximal to the clavicle, the trunks split into anterior and posterior divisions. The three cords are formed by combinations of the anterior and posterior divisions and named according to their relation to the second part of the axillary artery. The lateral cord is formed by the union of anterior division of upper and middle trunks (C5-C7), the medial cord is formed by anterior division of the lower trunk and the posterior cord is formed by the posterior division of all trunks.
The lateral cord passes superficial and lateral to the second part of the axillary artery and gives off three nerves: the lateral pectoral nerve, the lateral cord contribution of the median nerve and the musculocutaneous nerve. The medial cord emerges between the axillary artery and vein and descends medial to the artery, where it gives off the medial pectoral nerve, the medial brachial cutaneous nerve, the medial antebrachial cutaneous nerve, the medial cord contribution to the median nerve, and the ulnar nerve. The posterior cord originates superior and lateral to the axillary artery and passes posterior to it. From the posterior cord arise the two subscapular nerves, the thoracodorsal nerve, the axillary nerve, and the radial nerve.


Etiology and classification
Traumatic brachial plexus injury has a wide variety of etiologic factor and can be divided into causative mechanism:
  1. Closed injury.
  • Traction injury.
  • Compression.
  • Combined lesion.

  1. Open injury.
  • Sharp.
  • Gunshot.
  • Radiation.

Traction lesion results from forceful separation of the neck and shoulder or upper arm and trunk. The nerve pathology occurs between the two anchoring points. The proximal anchoring point is at the spinal cord and nerve root junction, and the distal point is at the neuromuscular junction. The coracoid process is regarded as a temporary lever in forceful hyperabduction of the shoulder. It is not only the direction of the applied force to brachial plexus that determines the severity of the nerve damage, but also the speed of the application of the traction force. High-velocity traction injury is the overall leading cause of brachial plexus injury in nearly all reports.2,3 The majority of traction injuries are a result of motor vehicle accidents. The clavicle serves as a strongest link between the shoulder and neck. If it is broken, all of the traction forces are transmitted through the neurovascular bundle. This mechanism of injury causes the greatest damage to the upper roots. Whereas hyperabduction of the shoulder mostly affects C8 and T1 nerve root. The high-velocity traction injury can cause nerve root avulsion from the spinal cord, nerve ruptures, or stretch injuries (Fig. 2).
Traction forces can result in preganglionic or postganglionic injuries. Preganglionic injuries refer to lesions proximal to the dorsal root ganglion, which is in the spinal canal, and foramen. Preganglionic ruptures may be central or direct from the spinal cord or intradural. Preganglionic lesions do not cause Wallerian degeneration or neuroma formation because the axons remain in continuity with the cell bodies in the dorsal root ganglion. Postganglionic lesions are defined as any lesions distal to the spinal ganglion and are physiologically similar to other peripheral nerve injuries.

Figure 2: Level of nerve injury.

The compression lesions may occur when a traumatic force is applied on the shoulder in the cephalocaudal direction. The brachial plexus may also be compressed in between the clavicle and the first rib. Any fractures of the surrounding bones may compress the brachial plexus. Chronic compression from carrying heavy weights on shoulders may cause a temporary brachial plexus lesion.
In traction and compression injury, the injury is usually diffuse, from nerve roots through terminal branches, and disruption of brachial plexus can be found on more than one site. This injury is usually associated with vascular damage.

Open injuries of the brachial plexus are much less common in normal practice. The injury only involves part of the brachial plexus and carries a good prognosis. Associated vascular and intrathoracic injuries are commonly found.
Radiation brachial plexus injury is usually found in patients several years after radiation therapy to the ipsilateral breast or axilla for the treatment of breast cancer.4 Patients usually present with progressive motor and sensory deficits that may be caused by radiation, compression of recurrent neoplasm, or both.
Clinical evaluation
A complete understanding of the nature and mechanisms of injury is important in evaluating patients with a brachial plexus injury. Knowing the exact neck and arm position at the moment of injury greatly assists in predicting the site of the brachial plexus lesion. Extension of the arm in 90-degree abduction of the shoulder puts maximum tension on the C7 root of the brachial plexus, but with increased force, all nerve roots may be affected. Previous radiation therapy to the neck, upper chest, and axilla can cause radiation brachial plexitis or fibrosis.
Patients usually present with a slowly advancing motor and sensory deficit associated with pain. Pain over a nerve is common with rupture, as opposed to percussion tenderness with avulsion. Paresthesia and dysesthesia of the involved limb is common. The patient may also present with weakness or heaviness in the extremity. A vascular injury may accompany traction injury. It may present with a diminished pulse.
Iatrogenic compression injuries to the brachial plexus can occur because of improper positioning in the operating room.

General Physical Examination
Contusion and ecchymosis at the suprascapular or deltopectoral area indicate the site of injury in compression lesions of the brachial plexus. Abrasions on the ipsilateral shoulder and cheek suggest traction lesions of the brachial plexus incurred in motorcycle accidents. A winged scapula with an intact spinal accessory nerve is highly suggestive of a C5-C6-C7 avulsion, whereas the presence of Horner’s syndrome (enophthalmos, myosis, ptosis, and absence of facial sweating on the affected side) suggests a cervical or T1 root avulsion and interruption of sympathetic innervations.5 A sensory-sweating dissociation in an anesthetic and flail arm also suggests root avulsion.6 A paralyzed diaphragm, as determined by inspiratory/expiratory chest x-rays or fluoroscopic studies, suggests a high plexus lesion.7

Neurologic Examination
Every muscle of the affected upper extremity innervated by the brachial plexus must be examined and graded according to the Medical Research Council score.8 It has a scale of 0 to 5 of which 5 is the normal muscle strength, whereas 0 is a flail muscle. Brachial plexus root avulsions may be associated with spinal cord injury, therefore examination of the lower extremity muscle power is also required to detect the presence of long tract sign.
A complete sensory examination should include both subjective and objective sensory changes. Objective tests of all sensory modalities are performed on each dermatome of the cervical and brachial plexus. Pain, temperature, touch, vibratory sense, and two-point discrimination are tested and recorded. Pain is a complex and difficult feature of the brachial plexus injury. It can be divided into neuralgic pain and causalgic pain. Neuropathic pain in brachial plexus injury may be present with avulsion lesion of the lower roots. The deafferentiation pain from root avulsion usually appears a few weeks after injury. The causalgic pain has no precise distribution and appears immediately after injury.
The examination of the sympathetic nervous system is important as the avulsion of the lower roots or a high lesion of the corresponding spinal nerves can compromise the ipsilateral sympathetic preganglionic fibers. Vasomotor disturbances, cyanosis, edema of the soft tissues, and trophic lesions should be observed. Anhydrosis of the anesthetic area suggests a postganglionic lesion. The presence of Horner's syndrome (anhydrosis, miosis, ptosis, and enophthalmos) is a bad prognostic feature and is associated with T1 root avulsions.

Vascular Examination
Vascular examination should be performed during initial evaluation. Major vascular injury is found in association with brachial plexus injury in 10% to 16% of cases.9 Progressive loss of motor and sensory function of the affected extremity suggests an expanding hematoma or aneurysm compressing the adjacent neural structure. An angiography is indicated in any abnormal vascular examinations, widened mediastinum and first rib fracture.

Musculoskeletal Examination
The majority of brachial plexus injuries are caused by falls from motorcycles, therefore musculoskeletal injuries are commonly found concomitant with brachial plexus trauma. The associated injuries of the upper extremity can include clavicular fracture, acromioclavicular joint separation, scapula fracture, first rib fracture, cervical transverse process fracture, humeral fracture, glenohumeral dislocation, and scapulothoracic dissociation. Fracture and dislocation around the clavicle indicate a bad prognostic sign.10 Because the clavicle is the only solid structure connecting the shoulder girdle to the neck, its fracture allows all of the traction force to be directed at the underlying soft structures (i.e., brachial plexus and subclavian vessels). Cervical transverse process fractures are commonly found with high ruptures or avulsions of the corresponding nerve roots. Scapulothoracic dissociation is often associated with multiple root avulsions. First rib fracture is often associated with lesion of the lower roots as well as vascular injuries. Fracture of the coracoid process is often found with lateral cord injury, whereas scapular and humeral neck fractures are associated with posterior cord lesion.
Investigations
Plain radiography of the shoulder girdle, cervical spine, and chest should be made for patients with traumatic brachial plexus lesions. Chest radiography is obtained to determine whether there is a widened superior mediastinum, which suggests major vascular injury.
Myelography is indicated in traction brachial plexus lesions presenting with a persistent complete or partial neurologic deficit. The dural tear usually healed in three weeks. Myelography should not be performed no sooner than 3 weeks, otherwise the leakage from the nerve root avulsion may obscure the visualisation. Myelography in combination with computed tomography (CT-myelography) improves visualization of the spinal cord and nerve root lesions.11 R.W. Marshall and R.D. De Silva, Computerised axial tomography in traction injuries of the brachial plexus. J Bone Joint Surg Br 68 5 (1986), pp. 734–738
Magnetic Resonance Imaging (MRI) provides a better image of the extraforaminal brachial plexus structures. It is non-invasive, relatively quick, requires no contrast medium, provides multiple projections, and is comparable in diagnostic ability to the more invasive , time consuming techniques of conventional myelography and CT myelography.12,11
Early interest in the use of MRI in brachial plexus injuries was directed at the post-ganglionic plexus. MRI can detect post-injury fibrosis and neuroma formation in the post-ganglionic plexus.13 However, MRI cannot identify the precise site of injury or the severity of the injury due to the complexity of the anatomy of the post-ganglionic brachial plexus.14 The current focus on the use of MRI is on the pre-ganglionic plexus with the aim of providing a non invasive means of detecting nerve root avulsion.15,16
Ultrasound has been proposed as a possible technique for examining the post-ganglionic brachial plexus in cases of injury. 21. C. Martinoli, S. Bianchi, E. Santacroce, F. Pugliese, M. Graif and L.E. Derchi, Brachial plexus sonography: a technique for assessing the root level. AJR Am J Roentgenol 179 (2002), pp. 699–702. View Record in Scopus | Cited By in Scopus (33)It has obvious potential advantages, in terms of high soft-tissue resolution and the ability to follow each component of the plexus as it passes in an oblique plane through the base of the neck.17
Electromyography gives objective information on motor dysfunction, especially when clinical examination of motor function is difficult. Electromyography is used during the first week after injury to determine whether the lesion is a continuity lesion. The presence of motor unit action potentials across the affected site, in spite of a complete paralysis, indicates a partial lesion.
Exploration is the most accurate investigation of the supraclavicular plexus. If this inspection is undertaken in the first week after injury, the effect of trauma on the anatomical structures is easily identified and understood. However, there are arguments for and against early surgery. Arguments for early exploration include allows ease of diagnosis because tissue planes are open, fibrosis and scarring are absent and the nerve in continuity is assessed visually. Surgery is not destructive and carries little morbidity or penalty and allows early repair, avoiding increased target organ decay. It allows early prognosis for patient and consequent early decisions about future employment, rehabilitation and resettlement. Arguments against early exploration include spontaneous recovery may occur without surgery. The lesion-in-continuity may or may not recover and the surgeon is occasionally unable to determine this at surgery.

Management
Medical Therapy
Nonoperative treatment of brachial plexus lesions is complex and may best be addressed by an integrated multidisciplinary team that includes a skilled orthotist, occupational therapists, physical therapists, and physicians.
In neglected injuries of the brachial plexus, contracture of the joints often causes more disability than muscular paralysis. All joints should be put in full range of movement several times a day.
Continuous stretching of the paralysed muscle is prevented by appropriate splinting. Daily electrical stimulation will prevent excessive wasting of the paralysed muscle. During the phase of recovery it is essential to re-educate all muscle which are showing feeble voluntary contraction. Prolonged treatment may be necessary, and it is important to allow sufficient time for recovery before considering reconstructive operations.

Surgical Management
Brachial plexus exploration is indicated for patients with complete or partial neurologic deficit after a penetrating injury. An iatrogenic sharp injury to the brachial plexus may occur in any procedures around the neck and supraclavicular region. Sharp injuries to the brachial plexus carry a good prognosis. The injured plexus can usually be treated with neurorrhaphy or nerve grafting.

High-velocity traction injury secondary to a fall from a motorcycle usually causes severe damage to nerve roots. Brachial plexus exploration and surgical repair or reconstructions are indicated in patients who have no spontaneous recovery after 3 months. Time is allowed for the recovery of the low-grade injured neural tissue, subsidence of the swollen surrounding tissue, and completion of the diagnostic investigations. In complete brachial plexus palsy with strong radiologic and electrodiagnostic evidence of complete or multiple root avulsions, early surgery (6 weeks to 3 months after injury) is indicated because the chance of spontaneous recovery is less likely.
The timing of surgery depends on the associated injury involved and the nature of recovery. Immediate surgery of the brachial plexus should only be performed in an associated brachial plexus injury (closed or penetrating) with subclavian or axillary vessel injury. Early surgery (6 weeks to 3 months) should be performed in complete brachial palsy patients with total root avulsion. For incomplete brachial plexus palsy or complete brachial plexus palsy without evidence of root avulsion, exploration should be performed when there is no sign of clinical recovery or the initial recovery stopped after an observation period of 4 to 5 months. The result of operative nerve repair and reconstruction is greatly diminished after a 6-month interval between injury and operation. Six months from the time of injury, free muscle transfers should be considered.
A method of restoration of function in preganglionic injuries can be obtained by the transfer of a functional but less important nerve to a distal but more important denervated nerve. Neurotisation or nerve transfer has become an integral part of brachial plexus reconstructive surgery. A nerve transfer may be performed in cases of postganglionic injury as an alternative to nerve grafting or to power free functioning muscle transfer.
Donor nerves can be classified as either intraplexal (within the brachial plexus) or extraplexal (outside the brachial plexus) and as motor nerves or sensory nerves. Extraplexal donor nerves for nerve transfers include the spinal accessory (cranial nerve XI), intercostals nerves, the phrenic nerve, or the contralateral seventh cervical root. Intraplexal donor nerves include the use of motor fascicles of the ulnar nerve or triceps branch of the radial nerve in cases of partial brachial plexus injury.
The surgeons need to identify the available donor nerves and prioritize functions that they aim to restore in the injured limb. The highest priority is elbow flexion, followed by shoulder stability and abduction. Wrist extension/finger flexion and wrist flexion/finger extension follow next. Intrinsic hand function is the last priority, and it is also the most difficult to obtain. Neurotizations are routinely performed to reanimate denervated muscles for elbow flexion and shoulder abduction.
Restoration of abduction and external rotation are high priorities in the rehabilitation of the upper limb so that reconstruction of more distal targets can follow. Early repair of the suprascapular nerve, usually with direct neurotization from the distal spinal accessory nerve, offers a good opportunity for shoulder stabilization and usually can yield adequate shoulder abduction and external rotation.18 External rotation of the humerus can also be restored dynamically with latissimus dorsi rerouting or statically with rotational osteotomy of the humerus.19
The other goals of treatment are to restore grade M4 or M4+ elbow flexion with a range of motion that will allow the hand to reach the face. The resulting function of elbow flexion must outweigh the deficits caused by transferring functional nerves or muscles. To prevent dissipation of elbow flexion strength, the shoulder must be stable.
Ipsilateral C5 is the strongest motor donor, and if there is no avulsion, the proximal part of the ruptured root can be used as a motor donor for multiple neurotizations with interposition nerve grafts. When the proximal stump of the C6 root is also available, a folded vascularized ulnar nerve graft can connect both roots with peripheral targets using the loop technique.20
When the upper plexus roots (C5 and C6) are avulsed from the spinal cord, reconstruction of shoulder and elbow function can be achieved by means of the ipsilateral C7 root which, if intact, can be sacrificed for higher priority targets. In that case, the distal targets innervated by the C7 root can be neurotized with extraplexus motor donors.21
Deltoid motor function can be restored with transfer of the nerve to the long head of the triceps to the anterior branch of the axillary nerve.22 The nerve of the long head of the triceps is synergistic to the target muscle; it is pure motor nerve, with many axons and a size that is matched to the axillary nerve.
Intercostal nerve transfer is one of the more common methods of reanimating the arm. Typically, the third, fourth, and fifth intercostal nerves are used; however, up to seven unilateral intercostal nerves have been used.23 Candidates for this procedure should have no history of rib fractures, thoracotomies, or chest tube placement in the potential donor nerve region. Sensory reinnervation may be achieved by coapting the intercostal nerve sensory axons, which are located in the superior portion of the nerve, with the sensory axons of the musculocutaneous nerve, which are located in the superior and inferior poles of the nerve. The intercostal nerve motor fibers, which run in the inferior portion of the nerve, are coapted to the motor fibers located in the middle of the musculocutaneous nerve.24 Intercostal nerve transfers is more likely to have a useful result when the spinal accessory nerve was used to stabilize the shoulder by nerve transfer to the axillary or suprascapular nerves.25 A muscle transfer procedure may be used to supplement the biceps if elbow flexion is grade M3 or less. In less than 10 percent of patients, uncontrolled elbow flexion was reported with coughing, sneezing, or yawning, but none had a loss of pulmonary function.26
The spinal accessory nerve is another potential donor to achieve elbow flexion. The segment distal to the trapezius ramus is used to preserve sternocleidomastoid and trapezius function. Advantages include its sole function as a motor nerve and similar functional relationship with the musculocutaneous nerve. However, its use does require a nerve graft and, when needed, it is best saved for shoulder stabilization by nerve transfer. Songcharoen et al.27 showed good results when nerve transfer was undertaken within 6 to 9 months of injury and when patients were younger than 40 years old. Waikakul et al found very good or good power in 83 percent of patients who underwent spinal accessory nerve transfers using sural nerve grafts compared with 64 percent of those who had a transfer of three intercostal nerves without nerve grafts.26
Other nerves that could be used to assist in elbow flexion include phrenic nerve,28 cervical plexus,29 hypoglossal nerve30 and C7 cervical nerve.31 The local and distant muscles that may be transferred and used to provide elbow flexion include the following: flexor-pronator mass, pectoralis major, pectoralis minor, latissimus dorsi, triceps, and sternocleidomastoid and the gracilis, rectus femoris, and latissimus dorsi as free muscle transfers. This may be done alone or in combination with a nerve transfer procedure. Unlike nerve transfers, in which the original elbow flexor, the biceps muscle, is reactivated, muscle transfer procedures alter the biomechanics of elbow flexion. Therefore, at least M4 strength and the creation of at least 90 to 100 degrees of elbow flexion are needed to provide useful function.
Various combinations of nerve and muscle transfers have been proposed. Berger et al. suggest an initial nerve transfer procedure supplemented at least 1 year later by a triceps transfer or flexorplasty to achieve elbow flexion.32 Some author used latissimus dorsi transfers for elbow flexion together with nerve transfers for wrist and finger extension.33
Elbow extension is a very important function because it can give stability to the elbow joint. However some author sacrifices the muscle to use it as a pedicled flap to substitute for biceps function.34
Restoration of protective sensation allows the patient to recognize the position of the extremity in space, to avoid injuries, and to use the hand for grasping. Neurotization of the ulnar nerve and lateral cord contribution to the median nerve from intercostal sensory nerves has been proposed.35,36
Glenohumeral arthrodesis and above-elbow amputation are indicated in flail upper extremity with a poor prognosis for additional recovery. A combination of glenohumeral arthrodesis and above-elbow amputation was first recommended by Yeoman and Seddon in 1961.37 Shoulder arthrodesis eliminates symptomatic instability and places the extremity in a functional position. Some range of motion is still preserved via the scapulothoracic articulation. An above-elbow amputation allows early prosthetic training and functional rehabilitation.38 Other indications for shoulder arthrodesis and above-elbow amputation include failed prior operative treatment, patient dissatisfaction with lack of useful function and/or discomfort of the flail limb, and pain or discomfort secondary to inferior glenohumeral subluxation. Contraindications for these procedures include paralysis of the trapezius, levator scapulae, latissimus dorsi, serratus anterior, or rhomboid muscles. These muscle groups are essential for stabilization of the scapula and for compensatory scapulothoracic motion following glenohumeral arthrodesis. An active infection in the proximal humerus or glenohumeral joint is also a contraindication.
Postoperative rehabilitation is important. Restoration of full ROM is essential to prevent joint and soft tissue contractures. A functional orthosis is applied to reduce shoulder subluxation and to relief traction on repaired or neurotized nerve. Reinnervated muscles need to be re-educated. Regular assessment is important to determine return of function or sensation. Regime of exercises may proceed from isometric to isotonic and gravity eliminated to gravity resisted movement.
Conclusion
The principles guiding brachial plexus reconstruction continue to evolve and the modern management of brachial plexus injuries should focus on early aggressive microsurgical reconstruction. The return of functions of upper extremity depends on the severity of the injury and that the reconstruction may require multiple stages, from simple neurolysis to nerve repairs, nerve transfers, nerve grafting, nerve banking, tendon transfers, muscle transplantations, osteotomies, and bone fusions. The future may bring further advances in nerve rootlet replantation for preganglionic injuries and in free muscle transfer techniques. Research into growth factors that promote nerve regeneration may make nerve grafting and transfers more appealing in the future.

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