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Nerve Repair Manual: A Practical Approach to Injury and Repair in the Brachial Plexus and Upper Extremity, Scott H. Kozin, MD, Brian O’Doherty, photographer, checkpointsurgical.com

Nerve Repair Manual:

A Practical Approach to Injury and Repair in the Brachial Plexus and Upper Extremity

Scott H. Kozin, MD

Brian O’Doherty, photographer

checkpointsurgical.com


The Checkpoint® Nerve Stimulator/Locator is a single-use, sterile device intended to provide electrical stimulation of exposed motor nerves or muscle tissue to locate and identify nerves and to test nerve and muscle excitability.

Do not use the Checkpoint Nerve Stimulator when paralyzing anesthetic agents are in effect, as an absence or inconsistent response to stimulation may result in inaccurate assessment of nerve and muscle function.

For a complete list of warnings and precautions regarding the use of the Stimulator, please see www.checkpointsurgical.com

This manual is designed to guide the diagnosis and treatment of nerve injuries. The manual is not intended to replace sound clinical judgment or meticulous surgical technique.

© Copyright 2016 Checkpoint Surgical Inc. All rights reserved.


Preface

Why make a manual solely devoted to nerve repair in the brachial plexus and upper extremity? This answer is simple; find a perplexing problem and simplify it. The diagnosis of nerve injury produces confusion, myth, and misperception. The field of nerve injury crosses many specialties including neurology, neurosurgery, plastic surgery, physiatry, orthopedic surgery, and therapy. These areas of medicine publish in different arenas and present in dissimilar venues. These specialties infrequently interact and therefore critical information that may enhance the diagnosis and treatment of nerve injuries is not shared. In addition, the quagmire of misinformation and the magnitude of unsubstantiated treatment modalities are overwhelming for clinicians and patients. The unvetted material on the internet has potentiated the problem of "publishing" unreliable information. Hence, unproven and unsupported treatment regimens are propagated and applied to treat patients with nerve injuries. These modalities often delay treatment and miss a window of opportunity to intervene and truly improve outcome.

The goal of this manual is to simplify and demystify nerve injuries based upon our current understanding of anatomy, injury, treatment, and outcome. This knowledge is derived from the credible peer reviewed literature and twenty years of experience examining, treating, and operating on patients with nerve injuries. These patients have been informative and vital to enlighten my understanding of nerve injuries from diagnosis thru treatment. Their participation in the "practice of medicine" has been invaluable and instrumental in my learning during my career as a nerve surgeon. Their contributions must be recognized and appreciated as their willingness to discuss, interpret, and express their thoughts has been priceless.

The goal of this project is to produce a readable and dependable multi-disciplinary manual based upon what we "know now" (circa 2016). As the knowledge base expands and innovation progresses forward, the information and recommendations will change over time. As Socrates said "the only true wisdom is knowing that you know nothing" and I expect this manual to evolve over time as our knowledge of nerve injury and pathophysiology is supplanted by ongoing research and new discoveries. The ultimate goal is to eventually provide discrete guidelines and apply innovative techniques to improve the lives of patients with nerve injuries.

Scott H. Kozin, MD Signature

Scott H. Kozin, MD

Introduction

Nerve injuries are devastating to the patient and challenging to the clinician. The anatomy can be perplexing as the nerves course from the spinal cord to supply their respective muscles. The nerves also provide critical sensation to the limb that differs from their muscle innervation. The physical examination of specific nerves requires diligence and a keen understanding of sensory and muscle innervation. Following nerve injury, the pathoanatomy contains puzzling terminology such as neurapraxia, axonotmesis, and neurotmesis. The treatment following nerve injury is confounded by numerous factors that lead the clinician astray and obscure the time to intervene. Ancillary studies such as electrodiagnostic testing, magnetic resonance, or ultrasound may provide valuable information or produce indeterminate information that add further confusion and further delays intervention. Nerve surgery can be complicated with the variety of available options including neurolysis, direct repair, conduit interposition, grafting (allograft or autograft) and nerve transfer. This manual will demystify nerve injuries and provide a practical approach to anatomy, injury, examination, and treatment that will give the clinician the knowledge and confidence necessary to diagnose and manage nerve injuries.

Anatomy

Central Nervous System

The central and peripheral nervous system is an array of neural connections that allow transmission of a purposeful thought into an immediate action. The central nervous system transmits efferent signals from the brain (somatosensory motor cortex) to the spinal column. These signals leave the brain and travel to the anterior horn cells within the spinal column (motor cell bodies) and exit via the brachial plexus to control all movement in the shoulder girdle and the entire upper extremity. Similarly, afferent sensory signals travel back from the limb into the spinal cord via the dorsal root ganglion (sensory cell body) that resides in the intervertebral foramina. The signal continues into the spinal cord and up to the brain to perceive pain, temperature, pressure, proprioception, and touch.

Brachial Plexus

The brachial plexus is a vexing complex of nerves that can be simplified into basic anatomical elements. There are certainly variations in brachial plexus anatomy; however, this description applies to the vast majority of persons and this simplified explanation can be relayed to patients and their families when describing the anatomy and injury (Figure 1). The brachial plexus is structurally similar to tree roots that provide the foothold for the tree that

Stretch Injuries: Neuropraxia, Axonotmesis, Neurotmesis (Rupture), Avulsion - 20,000 Fibers per Root, Upper Trunk (C5/6): Shoulder, Biceps; Middle Trunk (C7): Triceps, Finger Extension, Wrist Extension; Lower Trunk (C8/T1): Finger flexion

Figure 1: Simplified diagram of the brachial plexus with relevant anatomy that is explainable to patients and families. (Courtesy of Dan A. Zlotolow, MD)

subsequently outlet into branches. There are five roots (four cervical, one thoracic) labeled C5, C6, C7, C8, and T1: the acronym C refers to cervical or neck and T for thoracic or chest. The T1 nerve root, however, originates from the spinal cord and travels above the clavicle. Hence, all five nerve roots are in the neck. From these five nerve roots, three trunks (upper, middle and lower) are formed. The upper trunk is the combining of the C5 and C6 nerve roots. The lower trunk is the conjoining of the C8 and T1 nerve roots. The middle trunk is continuation of the C7 nerve root. The trunks pass beneath the clavicle and travel into the arm sending nerve branches along the way to innervate the muscles within the shoulder girdle. Ultimately, the trunks terminate into major peripheral nerves that supply fundamental movement and sensation to the arm, forearm, and hand. Each root is analogous to an internet cable with insulation on the outside (myelin sheath) and fiber optic cables (axons) on the inside. Each root contains approximately 20,000 axons (fiber optic cables) for a total of 100,000 axons (five roots x 20,000 axons/root).

The diagram of the brachial plexus may be necessary to pass a medical school test, but does not depict the anatomic innervation related to the crisscrossing of nerve fibers. A simplified and practical approach is the best method to understand the contributions of the upper, middle, and lower trunks with respect to limb movement. The upper trunk (C5, C6) controls shoulder (glenohumeral joint) movement, primarily rotator cuff and deltoid muscles, that governs shoulder abduction, external rotation, and internal rotation. The upper trunk also controls elbow flexion, forearm supination, and contributes to wrist extension. The middle trunk (C7) primarily manages elbow extension, forearm pronation, wrist extension, finger extension, and thumb extension. The lower trunk (C8, T1) is critical for hand function and governs grasp and all fine motor tasks, such as crossing one’s fingers and touching the tip of the thumb to the tip of the small finger (opposition).

This basic understanding of "trunk" function can be expanded into more detail. The upper trunk provides primarily nerve and muscle input into the axillary nerve (deltoid and teres minor muscles), suprascapular nerve (supraspinatous and infraspinatous muscles), and musculocutaneous nerve (biceps and brachialis muscles). The upper trunk also contributes to the radial nerve to innervate the brachioradialis, supinator, and extensor carpi radialis longus muscles. The middle trunk provides the primarily nerve and muscle input into the radial nerve (triceps, extensor carpi radialis brevis, extensor digitorum communis, extensor indicis propious, extensor digiti minimi, and extensor carpi ulnaris). The middle trunk also contributes to the median nerve to innervate the pronator teres and flexor carpi radialis muscles. The lower trunk provides the primary nerve and muscle input into ulnar nerve (flexor digitorum profundus, flexor carpi ulnaris, interossei, hypothenars, and adductor pollicis). The lower trunk also contributes to the median nerve via the anterior interosseous nerve (pronator quadratus, flexor pollicis longus, and flexor digitorum profundus to the index finger) and the recurrent motor nerve (thenar muscles).

There are a few muscles that have segmental innervation from numerous nerve roots. The pectoralis major receives innervation from C5 thru T1 moving from top (clavicle origin) to bottom (ribs). The subscapularis muscle receives innervation from upper and lower subscapular nerves (C5 thru C7) moving from upper to lower. The latissimus dorsi receives innervation from C6 thru C8 with C7 inputting the strongest contribution. The serratus anterior muscle receives segmental innervation from C5 thru C7 from upper to lower. The sensory examination is distinctly different than the motor examination. The upper trunk provides sensation to the radial sensory (first web space and radial dorsum of hand) and median nerves (palmar aspect of thumb and index fingers). The middle trunk inputs sensation into the median nerve that supplies the long finger (palmar aspect of long finger). The lower trunk provides sensation into the ulnar nerve (ulnar dorsum of hand and palmar aspect of ring and small fingers).

Practical Anatomy for Brachial Plexus Injury Pattern

Trunk (Roots)

Muscles

Sensation

Upper Trunk
(C5 & C6)

Shoulder (rotator cuff and deltoid)

Forearm supination (biceps & supinator)

Elbow flexion (biceps, brachialis, brachioradialis)

Wrist extension (extensor carpi radialis longus)

Median nerve sensibility thumb & index finger

Middle Trunk
(C7)

Elbow extension (triceps)

Latissimus dorsi Forearm pronation (pronator teres)

Wrist extension (extensor carpi radialis longus)

Digital extension (MCP joints)

Wrist flexion (flexor carpi radialis)

Median nerve sensibility long finger

Lower Trunk
(C8 & T1)

Forearm pronation (pronator quadratus)

Extrinsic finger and thumb flexors (flexor digitorum profundus and flexor pollicis longus)

Wrist flexion (flexor carpi ulnaris)

Digital extension (IP joints)

Intrinsic muscles (interossei, thenars, hypo thenars, ad-ductor pollicis

Ulnar nerve sensibility (ring and small fingers)

Evaluation

Understanding the brachial plexus and peripheral anatomy facilitates and simplifies the physical examination. The nerve-motor evaluation should be concise, focused, and relatively brief in the majority of cases. This succinctness is especially important when examining children who have a short attention span and are easily distracted. In acute isolated nerve injuries, passive and active movements are performed and documented. Passive movement should be full and painless. The lack of painless full passive movement is a harbinger of another underlying problem, such as fracture or dislocation. Over time, passive movement can decrease and a joint contracture can develop without therapeutic interventions, such as stretching and splinting. Cardinal active movements are performed to illustrate and document specific motions that demonstrate a functional or nonfunctional nerve. The table below lists those active movements elicited and their respective peripheral nerve and primary nerve root basis.

Table: Cardinal Movements and Nerve Innervation

Movement

Peripheral Nerve- Muscle(s)

Nerve Root(s)

Shoulder abduction

Axillary nerve- deltoid

C5, C6

Suprascapular nerve- supraspinatous

C5, C6

Shoulder external rotation

Suprascapular nerve- infraspinatous

C5, C6

Axillary nerve- teres minor

C5, C6

Shoulder internal rotation

Subscapular nerves- subscapularis

C5, C6, C7

Elbow flexion

Musculocutaneous nerve-biceps, brachialis

C6

Radial nerve-brachioradialis

C6

Elbow extension

Radial Nerve- triceps

C7

Forearm supination

Musculocutaneous nerve- biceps

C6

Radial nerve- supinator

C6

Forearm pronation

Median nerve- pronator teres

C7

Median nerve (AIN)- pronator quadratus

C8,T1

Wrist extension

Radial nerve- extensor carpi radialis longus

C6

Radial nerve- extensor carpi radialis brevis

C7

Wrist flexion

Median nerve- flexor carpi radialis

C7

Ulnar nerve- flexor carpi ulnaris

C8

Long finger flexion

Median and ulnar- flexor digitorum profundus

C8, T1

Long finger and thumb flexion

Median- flexor pollicis longus

C8, T1

Finger MCP joint extension

Radial nerve- extensor digitorum communis

C7

Finger IP joint exten- sion

Ulnar nerve- dorsal and palmar interossei

C8,T1

Finger abduction and adduction

Ulnar nerve- dorsal and pal- mar interossei, respectively

C8,T1

Thumb abduction and adduction

Median- abductor pollicis

C8,T1

Ulnar- adductor pollicis

C8,T1

AIN = anterior interosseous nerve

Video 1: Intrinsic versus Extrinsic

Patient can cross fingers on left hand but not on right.

Figure 2A: Inability to cross fingers. 17 year-old who sustained a right ulnar nerve laceration above the elbow.

Certain cardinal movements require additional clarification to fully understand nerve injury. The movements about shoulder, elbow, forearm, and wrist are more easily understood. The hand movements require further enlightenment. Digital (thumb and finger) opening requires metacarpophalangeal and interphalangeal joint extension. The primary metacarpophalangeal joint extensor muscles originate in the forearm (extrinsic muscles) and are the extensor digitorum communis, extensor indicis proprious, and extensor digiti minimi muscles innervated by the radial nerve (C7). The primary interphalangeal joint extensor muscles originate in the hand (intrinsic muscles) and are the interossei innervated by the ulnar nerve (C8, T1). Digital (thumb and finger) closing or grasping requires both metacarpophalangeal and interphalangeal joint flexion. The primary interphalangeal joint flexor muscles originate in the forearm (extrinsic muscles) and are the flexor digitorum profundus, flexor digitorum superficialis, and flexor pollicis longus muscles innervated by the median (C8, T1) and ulnar nerves (C8, T1). The primary metacarpophalangeal joint flexor muscles originate in the hand (intrinsic muscles) and are the interossei and adductor pollicis innervated by the ulnar nerve (C8, T1). Hence, full digit extension and flexion of the digits requires a coordinated effort between the extrinsic and intrinsic muscles innervated by different nerves. This synchronized task is disrupted by injury to the radial (C7) or ulnar (C8, T1) nerve or nerve roots (Video 1). This harmonized motion is also necessary for crossing fingers, as this seemingly simple task is anything but simple. Full metacarpophalangeal and interphalangeal joint extension coupled with interossei adduction and abduction is necessary to complete this complicated task.

Special Tests

Patient's two thumbs holding paper.

Figure 2B: Positive Froment’s sign.

There are a variety of tests that are valuable in discerning nerve injury patterns. As discussed, crossing one’s fingers is a synchronized task that requires full metacarpophalangeal and interphalangeal joint extension coupled with interossei adduction and abduction. This infers functioning radial (C7) and ulnar (C8, T1) nerves or nerve roots (C7,C8,T1) (Figure 2A). The Froment’s sign tests for adductor pollicis muscle function and distal ulnar nerve (C8, T1) function. In other words, the adductor pollicis is essential for lateral pinch and functions similar to a palmar interossei. The adductor pollicis adducts the thumb, flexes the metacarpophalangeal joint and extends the interphalangeal joint. This combined movement produces lateral pinch. The Froment’s sign is assessed by asking the patient to forcefully perform lateral pinch to a piece of paper using both hands (Figure 2B). An absent or weak adductor pollicis is unable to generate enough force for lateral pinch and the paper can be easily pulled from the affected side. In addition, the flexor pollicis longus is recruited during lateral pinch, which results in unopposed interphalangeal joint flexion and feeble pinch (Froment’s sign). Another maneuver to assess lower trunk function is asking the patient to form a "table top" with their fingers (Finger 2C). Specifically, full metacarpophalangeal flexion and interphalangeal joint extension indicates intact ulnar nerve or nerve roots (C8, T1).

Patient can perform table top with left hand but not with right.

Figure 2C: Unable to perform a table top with their fingers, specifically, full metacarpophalangeal flexion and interphalangeal joint extension at the same time.

There are also a variety of simple valid tasks that assess specific peripheral nerves. Asking the patient to make an OK sign requires flexion of the thumb and index interphalangeal joints (Figure 3). This indicates intact anterior interosseous nerve function, which receives its input from the median nerve and C8 and T1 nerve roots. Patients often enjoy extending the index and small fingers while grasping the second and third fingers with the thumb (Figure 4). This maneuver demonstrates functioning extensor indicis propious and extensor digiti minimi muscles innervated by the posterior interosseous branch of the radial nerve (C7).

Sensory Examination

Hand making 'Ok' sign.

Figure 3: OK sign requires flexion of the thumb and index interphalangeal joints and indicates intact anterior interosseous nerve function (median nerve and C8 and T1 nerve roots).

Patient extending index and small fingers while curling second and third fingers.

Figure 4: Asking the patients to extend their index and small fingers while grasping the second and third fingers demonstrates functioning extensor indicis propious and extensor digiti minimi muscles (posterior interosseous branch of the radial nerve (C7).

There are numerous methods to assess the status of sensation or sensibility. Options include two-point discrimination, vibratory testing, Semmes Weinstein monofilament testing, ten test, and sharp/dull perception. I never perform sharp/dull perception as you will quickly lose rapport with the patient, especially children. Two- point is my preferred method of assessment in the office setting as it is quick and efficient. A caliper or paper clip can be used as the discriminator. The finger is touched with enough pressure to blanch the skin. The patient always starts with their eyes open and their non-injured limb to ensure understanding of the test. Subsequently, their eyes are closed and the test completed on the non-injured and injured limb. The test is performed on the tip of the thumb (median and C6), long finger (median and C7), and small finger (ulnar and C8). Two-point discrimination greater than 15 millimeters after sharp injury infers nerve laceration. The ten test (TT) is simple, reliable, and requires no test equipment. The subject reports his/ her light touch perception of the skin during simultaneous stroking of the normal contralateral part and the area under examination. The patient rates their sensation between 0/10 and 10/10 with 0 being no sensation and 10 perfect sensation. The TT requires patient cooperation and comprehension, which may be challenging for some patients.

Sensory examination in children is more difficult. Two-point discrimination is unreliable until about six to eight years of age. There are other signs of absent sensibility in children. One clinical clue is that children will bypass or ignore digits without sensation. Another sign is dryness of the finger as nerve supply is necessary for moisture. Lastly, water immersion will not produce wrinkling of the fingers ("pruney fingers") without an intact nerve supply.

Ancillary Testing

Ancillary testing that may be helpful include imaging modalities and electrodiagnostic testing. Imaging studies include ultrasound, magnetic resonance imaging (MRI), and computerized tomography (CT) myelography. Ultrasound and MRI can visualize peripheral nerve continuity versus frank discontinuity. However, neither imaging modality can discriminate between a neuroma-in-continuity that will recover versus a neuroma in-discontinuity that will not recover. Imaging studies may be useful in brachial plexus injuries, especially adult injuries for assessment of potential nerve root avulsion. Following nerve root avulsions, a meningeal pouch filled with cerebrospinal fluid (pseudomeningocele) forms outside the intervertebral foramen. CT myelography and MRI can visualize these pseudomeningoceles (Figure 5). However, there are false- positive and false-negative results with both imaging modalities. More advanced techniques are under development to improve the diagnostic accuracy but their validity remains to be established. Magnetic resonance imaging currently offers the best evaluation of the brachial plexus trunks and cords with potential identification of a neuroma. Unfortunately, the MRI is unable to assess whether the neuroma has axons in-continuity (axonotmesis) or there is complete discontinuity (neurotmesis).

MRI of head, neck, and shoulder region.

Figure 5: Coronal MRI reveals right sided pseudomeningoceles that have formed outside the intervertebral foramen indicative of nerve avulsion injury.

Electrodiagnostic testing consists of two distinct assessments: nerve conduction and electromyography (direct testing of muscle integrity). Nerve conduction studies across an injured nerve segment will be abnormal immediately after injury. However, the conduction loss can be from a neurapraxia, axonotmesis, or neurotmesis. A neurapraxia type injury does not compromise the axons and the electromyography assessment will always be normal. Following more severe axonotmesis or neurotmesis injuries, an immediate assessment with electromyography will also be normal. However, as Wallerian degeneration ensues, the presence of denervation potentials (fibrillation potentials and positive sharp waves) within the affected muscles will become evident with electromyography. The presence or absence of muscle denervation cannot be determined until Wallerian degeneration is complete, which occurs one to four weeks following injury. The standard algorithm for assessment with electromyography is to wait until at least three weeks after injury. Denervation potentials, however, do not discriminate between an axonotmesis versus neurotmesis. Hence, early electrodiagnostic testing can never truly discriminate between an axonotmesis that has the potential for spontaneous recovery versus a nerve transection or neurotmesis that has no chance of spontaneous recovery.

Nerve conduction studies can be helpful in determining nerve root avulsions. The dorsal root ganglion (sensory cell body) remains attached to the spinal nerve while the motor cell body is separated from the distal downstream axons. The sensory loop is still able to conduct neuron signals. The sensory nerve conduction is preserved and normal in the absence of clinical sensation. This finding is pathognomonic of nerve root avulsion.

Intraoperative Assessment

Nerve identification and intraoperative assessment are paramount factors to optimize surgical outcome. Proper nerve identification can be confirmed by nerve stimulation, especially during nerve transfer surgery. In addition, confirming preoperative physical examination and findings from electrodiagnostic testing can be enhanced with intraoperative stimulation. The Checkpoint Nerve Stimulator provides a valuable tool with its stimulation specifications, variable parameters, and reliability, to enhance intraoperative decision-making. The device can safely stimulate either continuously or repeatedly without fear of diminished nerve and muscle response. The ability to control pulse duration at each amplitude assures stimulation delivery through varying tissues that surround the nerve and assists in preventing "false negative" assessment of nerve integrity.

Injury

There are numerous mechanisms that can result in nerve injury. The most common etiologies are laceration, traction, and compression. Less common causes include infection (e.g., leprosy), idiopathic (Parsonage Turner syndrome or Neuralgic amyotrophy), radiation, electric shock, and tumor (e.g., schwannomas or neurofibromas). This manual will focus on nerve injuries related to open or closed traumatic injuries, specifically laceration and traction. Laceration can be caused by penetrating trauma (e.g., knife or gunshot wound), fracture, and iatrogenic mechanisms. Traction injuries can result from a myriad of events such as athletic endeavors, motorcycle accidents, and during delivery of a baby (brachial plexus birth palsy).

Nerve laceration can be complete or partial involving only a segment of the nerve. Complete transection injuries are relatively straightforward to diagnose. There is complete loss of movement in those muscles innervated by the nerve and there is absent sensation in the skin innervated by the lacerated nerve. Timely surgery is required and the repair techniques will be discussed under the section entitled Nerve Surgery. Partial lacerations are much more difficult to diagnose and treat. There is incomplete loss of movement and/or sensation. A comprehensive physical examination, clinical suspicion, and electrodiagnostic testing are necessary to confirm the diagnosis. A useful sign to detect injured axons is the acute TineI’s sign. Gentle tapping over the cut nerve will elicit an electrified response from the exposed axons and sends the sensation of tingling or pins and needles into the sensory distribution of the injured nerve. This sign is decisive in the evaluation of a child with a potential nerve injury. The child will describe electric shocks and their heightened response when the cut nerve is tapped is often dramatic. Treatment requires exploration and a split nerve repair technique that is discussed under Nerve Surgery.

Video 2: Advancing Tinel’s sign after axonotmesis injury to the median nerve.

Closed traction injuries are more of a dilemma to diagnose and treat. The traction induces strain (change in length) that injures the nerve. The amount of ultimate strain has numerous components that affect the extent of nerve damage including the magnitude of the force and the vector along the nerve. The injury represents a continuum with progressive injury to the nerve. Mild stretch disrupts the myelin sheath and interrupts nerve conduction without loss of continuity of the axon (neurapraxia). Recovery takes place via remyelination without Wallerian degeneration. Ongoing stretch exceeds the elastic limit of the nerve and damages the myelin sheath and the underlying axons with loss of axon continuity (axonotmesis). The connective tissue of the nerve is preserved (epineurium, perineurium, and endoneurium). The entire nerve distal to the injury undergoes Wallerian degeneration that usually begins within 24–36 hours after injury and is complete one to four weeks later. The axonal degeneration is followed by degradation of the myelin sheath and infiltration by macrophages. The debris within the distal stump is removed to allow for regeneration. The motor and sensory cell bodies transition from their normal role as signaling centers to nerve cell growth promoting centers with upregulation and an increase in cellular activity. The cell body actively increases its synthesis of structural proteins necessary for axonal repair and regeneration. Axonal sprouts emerge just proximal to the injury (first node of Ranvier) and venture into the distal nerve stump. Many axon collateral sprouts (5-20) enter the stump and those collateral sprouts that make incorrect target contact are pruned. Ultimately, accurate motor neurons project their axons into muscle and accurate sensory neurons reach their sensory receptors. Axonal regeneration occurs at a rate of one to three millimeters per day. This axonal regeneration is a staggered response toward the motor and sensory cell targets. There will be an advancing Tinel’s sign as the nerve regenerates in a distal direction. In other words, tapping over leading edge of the regenerating nerve will elicit tingling or pins and needles into the sensory distribution of the injured nerve (Video 2). This advancing Tinel’s sign is a barometer for the location of distal regeneration and will advance as the nerve regenerates toward its motor end plates and sensory receptors. The extent of recovery is related to the robust response of the axonal sprouting and the distance to the motor end plate. Longer distances prognosticate lesser recovery as the motor end plates within the muscle undergo irreversible end plate demise between 18 and 24 months. Subsequent to this demise, additional nerve regeneration will be ineffective in reinnervating the muscle.

Venn Diagram showing Neurapraxia as a separate circle, with Axonotmesis and Neurotmesis as overlapping circles.

Continual stretch leads to complete disruption of the nerve including the sheath, axon, and encapsulating connective tissue (epineurium, perineurium, and endoneurium). This injury is referred to as a neurotmesis and results in irreversible intraneural scarring. The prognosis for recovery is bleak without surgical reconstruction. The intervening scar must be resected and nerve reconstruction performed to allow for nerve regeneration. Another surgical option is nerve transfers distal to the injury that bypass the neurotmesis altogether. These transfers are discussed under the Nerve Surgery section.

Neurapraxia is an entity separate and distinct from the more severe injuries of axonotmesis and neurotmesis. Traction axonotmesis and neurotmesis lesions, however, are a continuum with an overlap similar to a Venn diagram. Complex nerve injuries, such as brachial plexus injuries often have elements of each type of injury that may be intertwined. In reality, a trunk may have axonotmesis and neurotmesis within the zone of injury, complicating terminology and decision-making to determine which nerve will spontaneously recover and which will not recover. The clinician may interpret these injuries as "partial ruptures" or " incomplete neurotmesis," terms that add ambiguity into the delineation of the exact injury pattern.

Another confounding factor in brachial plexus injuries is the location of injury. The vast majority of brachial plexus injuries are supraclavicular (above the clavicle). Axonotmesis typically occur at the level of the trunk within the neck. Neurotmesis injury can occur at the level of the trunk and is called a rupture. This injury separates the motor and sensory cell bodies from their distal downstream connections. Neurotmesis can also occur when the spinal nerve is pulled from the spinal cord and is called an avulsion; similar to pulling a plug from the wall and disconnecting the wire (spinal nerve) from the plug (spinal cord). This injury separates the motor cell body from the distal downstream axons. In contrast, this injury is proximal to the dorsal root ganglion (preganglionic) and the sensory distal downstream axons are not separated from their cell body (located in the dorsal root ganglion) and downstream axons. The sensory loop is disrupted from the spinal cord, but preserved in its connection to the periphery. The sensory loop is unaware of its disconnection, which preserves its ability to conduct neuron signals back and forth. As discussed previously, an electrodiagnostic study of sensory conduction will demonstrate preservation of signal conduction in the absence of clinical sensation. The physical finding of absent sensation combined with the electrodiagnostic findings of normal sensory conduction is pathognomonic of root avulsion. As of 2016, there is no reliable technique to restore continuity between an avulsed nerve root and the spinal cord. The injury is similar to a spinal cord injury with limited ability to recover notwithstanding surgical alternatives. Surgery can bypass the injury discussed under nerve repair techniques, but no direct repair to the spinal cord is possible.

Treatment Principles

Timing

The timing of intervention is based upon fundamental principles of nerve regeneration and muscle viability. Nerve regeneration is slow with a rate between one to three millimeters per day. In addition, muscles do poorly without nerve input. Visual examination can assist in determining viable muscle. A healthy muscle with an intact nerve supply has a bright red color. When a muscle loses its nerve supply, the color degrades to pale and a chronically denervated muscle has even poorer color and lacks contractibility. This lack of contractibility can be confirmed during surgery, using the Checkpoint Nerve Stimulator at the 20mA muscle testing setting. If the muscle innervation is intact, the stimulator can be placed directly on muscle tissue at the 20mA setting and increasing the pulse width slider switch should demonstrate a proportional increase in muscle contraction. A chronically denervated muscle will have minimal to no contractibility at the 20mA muscle testing setting.

The reconstructive goal is to avoid the pale non-contractile muscle that occurs following prolonged denervation and irreversible endplate demise 18 to 24 months after injury. Chronically denervated muscle eventually becomes fibrotic and electrically inactive. In contrast, the encapsulated sensory receptors retain their capacity for reinnervation for many years. When making a decision regarding surgical intervention, application of these essential principles guides treatment. The objective is to intervene as soon as possible in neurotmesis to allow ample time for nerve regeneration and muscle reinnervation. The obstacle is deciphering an axonotmesis with ample spontaneous recovery from a neurotmesis that necessities surgical intervention.

Potential ancillary testing to enhance accurate diagnosis was discussed previously. The underlying problem is that no test is 100% accurate in distinguishing an axonotmesis from a neurotmesis without obvious discontinuity on an imaging study. Clinical signs that infer an axonotmesis are an advancing Tinel’s sign and recovery of the most proximal muscle that is distal to the nerve injury. As the nerve regenerates via axonal sprouting, this muscle would be reinnervated first. A useful ancillary test that can detect early signs of recovery following axonotmesis is electromyography. Axonal regeneration leads to the formation of nascent potentials that are low in amplitude, polyphasic in configuration, and variable in duration. These initial immature nascent potentials may precede clinical recovery as they are incapable of generating a detectable contraction or force. This finding may obviate the need for surgical intervention as they prognosticate additional functional recovery over time.

Nerve Surgery

Lacerated left median nerve and palmar cutaneous branch.

Figure 6A: 6 year-old who lacerated left median nerve and palmar cutaneous branch (Courtesy of Allan Peljovich, MD).

There are a variety of nerve surgeries depending upon the injury pattern, time from injury, extent of injury, and available surgical options. The surgical team needs to be prepared with ample equipment including magnification (loupes and/or microscope), nerve stimulator, micro suture and/or fibrin glue. This section will discuss the various possibilities from simple to complex.

Nerve Repair

Primary nerve repair with gently coaptation of the cut nerve ends.

Figure 6B: Primary nerve repair with gentle coaptation of the cut nerve ends.

The most straightforward surgical option is direct repair following a sharp laceration, such as a knife. The surgical approach always begins outside the zone of injury to identify uninjured nerve based upon the normal anatomy. The uninjured nerve is traced toward the injury from both a proximal and distal direction. The sharply transected nerve is identified and mobilized to allow a tension free repair or coaptation. The orientation of the nerve is essential to approximate sensory to sensory and motor to motor proximal and distal fascicles. The vaso nervorum (vessels located on the epineurium) can guide the surgeon to correctly orient the nerve and the size of the group fascicles. In acute injuries, the Checkpoint Nerve Stimulator can identify motor fascicles on the distal transected nerve and facilitate orientation. The epineurium should be gently approximated to coapt the cut nerve ends ensuring that the nerve ends are not too tight (strangulated) or too loose (Figure 6 A&B). We equate nerve repair to kissing your mother versus kissing your girlfriend. A gentle kiss on the cheek will afford the best possible condition for nerve regeneration. Tightly squeezing the nerve ends will "bunch" the axons and impede nerve regeneration. The coaptation can be secured with a few microsutures and/ or fibrin glue dependent upon the surgeon preference; the results following sutures and glue are similar. There have been numerous attempts to perform individual group fascicle repair to directly coapt the motor to motor and sensory to sensory fascicles. However, these techniques have not been shown to be superior to epineurial repair and lead to increased scarring within the repair.

Neurolysis

The role of neurolysis following nerve injury is debatable. A recovering nerve should be left alone as neurolysis may cause additional scarring, disrupt circulation, and diminish functional recovery. The primary role of neurolysis is outside of the nerve itself and is to remove extrinsic compression such as encasing bone or enveloping cicatrix. Other indications are crush injuries or Volkmann’s ischemic contracture whereby subsequent fibrosis may squeeze the nerve thus compounding the initial injury. In these cases, the Checkpoint Nerve Stimulator can assist in locating the nerve within the scar and to evaluate nerve function. The Checkpoint Nerve Stimulator probe can be placed directly on the scarred area at 0.5 mA and the pulse width slowly increased with ongoing assessment of any motor response. If no motor response is appreciated after reaching the maximum 200 microseconds, the process can be repeated at the 2.0 mA amplitude. Once identified, the nerve location and its course can be mapped by sweeping the probe across the tissue observing the motor response.

Intraoperative Nerve Assessment

The concept of intraoperative nerve assessment via nerve action potential across the neuroma is controversial regarding the ability to predict a neuroma in-continuity that will recovery (axonotmesis) versus a neuroma in- discontinuity (neurotmesis). Authorities debate as to whether a less than 50% conduction across a neuroma-in- continuity should be treated with neuroma resection and grafting, versus a less severe nerve injury with greater than 50% conduction across the neuroma could be treated with neurolysis alone. Currently, the answer is unknown and we rely on our preoperative examination and assessment of functional recovery.

The Checkpoint biphasic stimulation has variable stimulation parameters that may add additional information during the decision making process. In addition, the Checkpoint Nerve Stimulator is invaluable during nerve surgery such as nerve transfer procedures. The device has three amplitude settings, 0.5, 2.0 and 20 mA. The stimulator also has a variable pulse duration slider switch that adjusts from 0 to 200 microseconds, allowing variable output at each amplitude, much like a dimmer switch controlling the output from a wall switch. The device employs a fixed frequency of 16 Hz enabling the device to produce a tetanic contraction of muscle. Most importantly, the Checkpoint’s biphasic waveform, unlike other stimulators, employs waveform that has no direct current. The stimulator excites the nerve while maintaining recruiting efficiency via a large fast pulse (cathode phase or "stimulating phase") that stimulates the nerve and follows that stimulation by a smaller amplitude anode phase or "recovery phase" that lasts longer and recovers all the charge introduced by the larger fast pulse. In essence, the biphasic waveform removes the same amount of energy that it’s introducing, thus delivering a net zero charge to the tissue. The Checkpoint Nerve Stimulator has a design that is inherently safe and cannot deliver any net direct current to the patient and most importantly, the Checkpoint can be used to deliver stimulus current to nerve tissue indefinitely without risk of tissue damage.

Nerve Graft

A delay in surgical intervention following a sharp laceration results in additional obstacles for successful repair. A complete laceration results in nerve retraction and subsequent neuroma formation as the nerve attempts to regenerate. Surgical exploration reveals retraction coupled with proximal and distal neuromas. Resection of the hard "woody" neuromas is necessary to expose unscarred viable axons that can regenerate. This resection increases the intervening gap. Primary repair is no longer possible as the nerve ends cannot be approximated with a tension free repair. The intervening gap must be bridged by a scaffold to allow nerve regeneration across the defect. There are a variety of options to bridge the gap including autograft, allograft, and synthetic conduits. The gold standard is autograft, although the use of conduits and allografts are viable options. Conduits are best for short gaps as the regenerating nerve can navigate across the defect. Larger defects, especially major peripheral nerves, require better guidance. I prefer sural nerve allograft in the vast majority of cases and reserve conduits and allografts for deficits that cannot be bridged by available autograft. However, I do recognize that ongoing research into the perfect conduit or allograft may one day supersede the use of autograft especially as nerve growth factors that promote nerve regeneration are identified and incorporated into the product. A conduit or allograft laced with these nerve factors may ultimately be superior to nerve autograft, avoid the potential donor morbidity, and save operating room time.

Pre-Reduction and Post-Reduction x-rays of arm.

Figure 7A&B: 9 year-old fell off slide six months ago sustaining a left both bone forearm fracture. Treated with hematoma block and closed reduction. Subsequently developed absent median motor and sensation in hand. Nerve conduction studies revealed median absent sensory and motor conduction.

The technique of nerve grafting across the brachial plexus or a peripheral nerve requires meticulous technique to maximize outcome (Figure 7A&B). The neuroma is resected and the proximal and distal segments are sharply cut until viable nerve ends are visible (Figure 7C-H). The extremity or neck is positioned to maximize the gap between the proximal and distal nerve ends. This positioning avoids any tension along the grafts once the extremity or neck is repositioned following the reconstruction. For autograft, the primary donor is the sural nerve for large gaps. However, depending upon the injury and need for graft material, other alternatives may be available such as the medial antebrachial cutaneous and radial sensory nerves. The defect between the proximal and distal nerve ends is measured. The grafts are cut to size and positioned across the defect to obtain a similar graft diameter as the cut nerve ends (Figure 7I). The grafts are carefully secured with microsutures and/ or glue (Figure 7J). Conduits or nerve connectors can be used to facilitate nerve alignment at the proximal and distal coaptation sites. Conduits or nerve connectors should not cover the entire cable graft as imbibition (absorption of nutrients) and inosculation (vessel ingrowth) occur from the recipient bed.

Nerve exploration revealing nerve entering and exiting fracture site.

Figure 7C: Nerve exploration revealing nerve entering and exiting fracture site. Checkpoint Nerve Stimulator showed no distal response.

Nerve cut proximal with nerve cutting device.

Figure 7D: Nerve cut proximal with nerve cutting device.

Nerve cut distal with nerve cutting device.

Figure 7E: Nerve cut distal with nerve cutting device.

Intervening neuroma removed.

Figure 7F: Intervening neuroma removed.

Good proximal axons.

Figure 7G: Good proximal axons.

Good distal axons.

Figure 7H: Good distal axons.

3 cm defect bridged with sural nerve cable grafts augmented by nerve connectors to facilitate alignment.

Figure 7I: 3 cm defect bridged with sural nerve cable grafts augmented by nerve connectors to facilitate alignment.

Fibrin glue applied to secure coaptation sites.

Figure 7J: Fibrin glue applied to secure coaptation sites.

Partial Nerve Injuries

Acute partial nerve laceration treated by repair of the cut portion while protecting the undamaged segment.

Figure 8: Acute partial nerve laceration treated by repair of the cut portion while protecting the undamaged segment (Courtesy of Dan A. Zlotolow, MD).

Partial nerve injuries are difficult to diagnose and challenging to treat. Within the injury, there are intact and disrupted fascicles. Acute partial nerve laceration is managed by repair of the cut portion while protecting the undamaged segment. The unharmed segment prevents nerve retraction, which facilitates a tension free repair (Figure 8).

Video 3: Split nerve grafting

Delayed partial nerve injuries, especially the combination of axonotmesis and neurotmesis within the zone of injury, are puzzling to diagnose. Careful deliberation coupled with a thorough comprehensive examination is necessary to make an accurate diagnosis. The axonotmesis section will recover at a rate of one to three millimeters per day and will produce an advancing Tinel’s sign. The neurotmesis portion will form a neuroma and will not regenerate. Hence, an odd recovery pattern will develop over time with reinnervation of only those muscles innervated by the regenerating axons. A key clinical sign is a non- anatomical or unexplainable recovery as the nerve regenerates. For example, an axonotmesis injury to the radial nerve above the elbow should result in reinnervation of the brachioradialis (elbow flexor) followed by the wrist extensor muscles (extensor carpi radialis and extensor carpi brevis) followed by the finger extensors (extensor digitorum communis). Recovery of finger extensor before wrist extensor infers a partial nerve injury with axonotmesis and neurotmesis subdivisions. Delayed partial nerve lacerations are treated with preservation of the intact nerve and resection of the damaged segment (Video 3). A biphasic nerve stimulator (Checkpoint Nerve Stimulator) is crucial during dissection of the partially cut nerve to discriminate intact functional axons from lacerated non-functional scar that requires resection. A biphasic waveform allows for repeated stimulation and contact with the nerve without the concern of nerve injury or fatigue. The visual motor response can be continually monitored. The defect across the lacerated non-functioning nerve is bridged via nerve grafting techniques discussed previously. Delayed partial nerve lacerations can also be treated with nerve transfers that completely bypass the injured segment.

Nerve Transfers

The concept, indications, and techniques of nerve transfers have expanded greatly over the last decade. The concept of nerve transfer involves taking a non-critical normal donor nerve (part or whole) and transferring this donor nerve into a non-functioning recipient nerve to provide motor and/or sensory innervation. The general principles for the selection of donor nerves are similar to tendon transfers. The donor nerve must be normal, expendable, and preferably synergistic. Normal implies uninjured and not a reinnervated nerve. Expendable means the patient can function without the donor nerve. Synergistic infers the donor nerve fires in phase with the recipient nerve/ muscle. In addition to these motor nerve transfers, sensory nerve transfers are also available and follow similar principles of normal and expendable. Any loss of sensation from the donor sensory nerve must be acceptable to the patient. From a surgical perspective, the donor and recipient nerves should be in close proximity to avoid any intervening graft and to allow a tension free coaptation.

There are distinct advantages of nerve transfers compared to nerve grafting. Nerve transfer involves motor to motor and sensory to sensory coaptation avoiding potential misdirected fibers. Because nerve transfers are typically performed distal to the site of injury, the motor nerve transfer is closer to the muscle end plate and reinnervation is quicker. However, the regeneration rate is still one to three millimeters per day and and motor end plate viability degrades at 18 to 24 months. Nerve transfers are particularly applicable to proximal injuries, such as brachial plexus injuries or major peripheral nerves above the elbow, as the slow rate of nerve regeneration often precludes muscle recovery before irreversible motor end plate demise. Nerve transfers are also invaluable in late presenting nerve injuries that have missed the window of opportunity for repair or reconstruction but still have adequate time for regeneration via nerve transfer that is closer to the motor endplates.

The donor options for motor nerve transfers have expanded over the last decade with research and investigation into possible donors. The donor list is likely to grow and increase the available options. The nerve transfer can be end-to-end or end-to-side into the recipient nerve. In most circumstances, end-to-end repair is preferred as the results are superior. In my practice, end- to-side transfers are reserved for dire straits where there are no other options. There are two distinct types and techniques of nerve transfer. In the more straightforward procedure, an expendable donor nerve is cut as distal as possible (donor distal) and the recipient is cut as proximal as possible (recipient proximal) to provide adequate length of nerve for the transfer and coaptation. Subsequently, the cut nerve ends are repaired end-to-end without tension (e.g., spinal accessory to suprascapular nerve transfer).

Available Donor Motor Nerves via Distal Dissection

Nerve

Descriptor

Caveats

Spinal accessory nerve

Distal to upper trapezius muscle function.

Nerve can be harvested via anterior or posterior approach

Intercostal nerves

 

Phrenic nerve must be working

Radial nerve branch to triceps

Medial, lateral, or long head branch

 

Brachialis motor nerve

 

Biceps must be functioning

Medial pectoral nerve

Dissect from medial cord

Upper and/or lower pectoral nerves must be working

Thoracodorsal nerve

Distal branch

 

Flexor digitorum superficialis motor nerve

 

Flexor digitorum profundus must be working

Extensor carpi radialis brevis motor nerve

 

Extensor carpi radialis longus must be working

Anterior interosseous nerve

Distal at level of pronator quadratus

Pronator teres should be working

Flexor carpi ulnaris motor nerve

 

Flexor carpi radialis should be working

Flexor carpi radialis motor nerve

 

Flexor carpi ulnaris should be working

The ulnar nerve is carefully separated into group fascicles via intra-fascicular dissection to identify appropriate donor group fascicle.

Figure 9: The ulnar nerve is carefully separated into group fascicles via intra-fascicular dissection to identify appropriate donor group fascicle.

In the more complex nerve transfer, a proximal nerve with redundant motor fibers is carefully separated into group fascicles via intra-fascicular dissection (Figure 9). The Checkpoint biphasic wave form nerve stimulator on low amplitude (0.5 milliamps) and low pulse duration selectively stimulates each group fascicle and the motor response noted. A redundant group fascicle, preferably with synergistic movement, is selected and cut distal (donor distal) to the recipient nerve. The recipient motor nerve is cut as proximal as possible (recipient proximal) and the nerve ends are repaired end-to-end without tension. The differences between these techniques are illustrated in the videos.

Available Donor Motor Nerves via Intra-fascicular Dissection

Nerve

Descriptor

Caveats

Ulnar motor fascicle

 

Lower trunk must be working

For elbow flexion, select a fascicle that innervates the flexor carpi ulnaris for synergistic movement

Median motor fascicle

 

Lower trunk must be working

Avoid anterior interosseous nerve harvest

Medial pectoral nerve

Can dissect directly from middle trunk

Upper and/or lower pectoral nerves must be working

The numerous nerve transfer options prevent an all-encompassing description of every technique and the surgeon should fully understand the technique prior to performing the procedure. The nerve transfer options can be divided according to the function to be restored.

Nerve Transfer Options for Particular Motor Function

Function

Nerve transfer options

Shoulder

Spinal accessory to suprascapular nerve

Triceps branch to axillary nerve

Pectoral fascicle to long thoracic nerve

Thoracodorsal to long thoracic nerve

Pectoral fascicle to spinal accessory nerve

Elbow flexion

Median/ulnar fascicles to biceps/brachialis motor nerves

Elbow extension

Ulnar fascicle to triceps motor nerve

Axillary branch (posterior division) to triceps motor nerve

Forearm pronation

Flexor digitorum superficialis to pronator teres nerve

Extensor carpi radialis brevis to pronator teres nerve

Wrist extension

Median (flexor carpi radialis and flexor digitorum superficialis) to radial (posterior interosseous nerve and extensor carpi radialis brevis) nerve

Fingers and thumb flexion (Median nerve)

Flexor digitorum superficialis to anterior interosseous nerve

Brachialis to anterior interosseous nerve

Extensor carpi radialis brevis to anterior interosseous nerve

Extensor carpi radialis brevis to pronator teres and supinator to anterior interosseous nerve

Fingers and thumb extension (Posterior interosseous nerve)

Median (flexor carpi radialis/ flexor digitorum superficialis) to radial (posterior interosseous/ extensor carpi radialis brevis) nerve

Supinator nerve to posterior interosseous nerve

Hand intrinsic function (Ulnar nerve)

Anterior interosseous to ulnar motor nerve

Nerve Transfer Options For Hand Sensation

Diagram of sensory nerve transfer in the hand.

Figure 10: Sensory nerve transfer in a median nerve injury that sacrifices the ulnar nerve sensation to the ring- small interspace to regain sensation to the ulnar side of the thumb and the radial side of the index sensory nerves
(Courtesy of Dan A. Zlotolow, MD).

Nerve transfers to restore hand sensation utilize non-critical sensory territories to reinnervated critical sensory regions. These critical areas include the thumb-index finger for object manipulation and the ulnar border of the hand for protection. The donor nerve depends upon availability. In a median nerve injury, the most common transfer sacrifices the ulnar nerve sensation to the ring-small interspace by transferring these sensory nerves to the ulnar side of the thumb and the radial side of the index sensory nerves (Figure 10). In an ulnar nerve injury, the sensory nerve to the long-ring interspace third web space is transferred to the ulnar digit nerve of the small finger. Other transfers have been described using the superficial radial nerve, lateral antebrachial cutaneous nerve, and dorsal cutaneous branch of the ulnar nerve as donor nerves. Different from motor nerve transfers, sensory nerve transfers are not time sensitive and sensation may be restored many years after injury as sensory receptors remain viable.

Selected Techniques of Nerve Transfer

This section will highlight currently common motor nerve transfer procedures. Nerve transfers to restore shoulder and elbow function are frequently performed. Nerve transfer to restore intrinsic muscle function after proximal ulnar nerve injury is also gaining popularity. Therefore, these techniques will be described in this inaugural manual.

Nerve Transfers to Restore Shoulder Function

Video 4: Anterior approach for spinal accessory to suprascapular nerve transfer.

Video 5: Spinal Accessory to suprascapular nerve transfer

Incision drawn on skin.

Figure 11A: Incision drawn for posterior approach for spinal accessory to suprascapular nerve transfer.

The trapezius muscle revealed and elevated, close up of suprascapular nerve.

Figure 11B&C: B: Trapezius muscle elevated from scapular spine and suprascapular nerve identified entering scapular notch. C: Close up of suprascapular nerve.

Spinal accessory nerve.

Figure 11D: Spinal accessory nerve isolated deep to trapezius muscle and traced in a distal direction.

Nerve transfer spinal accessory, close-up of nerve coaptation.

Figure 11E&F: E: Nerve transfer spinal accessory to suprascapular secured with suture and fibrin glue. F: Close-up of nerve coaptation.

Nerve transfers to restore shoulder function should address the deficits in both rotator cuff function (suprascapular nerve) and deltoid function (axillary nerve). Therefore, two donor nerves are necessary. The spinal accessory nerve is the preferred donor for the suprascapular nerve and a branch of the radial nerve to the triceps the preferred donor for axillary nerve. The spinal accessory nerve can be harvested via an anterior supraclavicular approach or a posterior approach along the scapular spine. The anterior approach is preferred during brachial plexus exploration as the incision and locale is the same (Video 4). The posterior approach is preferred during isolated nerve transfer surgery as the donor is more distal and the recipient nerve closer to the muscle end plate. In addition, the superior transverse scapular ligament can be divided to decompress the suprascapular notch and eliminate any potential site of compression on the regenerating nerve.

The posterior approach is performed with the patient in the lateral decubitus or prone position (Figure 11A)(Video 5). Lateral decubitus is preferred as concomitant nerve transfers for elbow flexion can be performed without repositioning the patient. The affected hemithorax and arm are prepped and draped. An incision is performed just above the scapula spine that extends from medial to the scapula to the acromion. The underlying trapezius muscle is elevated from the spine of the scapula with electrocautery. The underlying supraspinatous muscle is identified. A rake retractor is placed into the supraspinatous muscle and pulled in an inferior direction while the trapezius muscle is elevated in a superior direction.

This combination of retraction opens up the space above the scapula. The superior border of the scapula is palpated and the superior transverse scapular ligament and suprascapular notch identified just lateral to the omohyoid muscle’s insertion into the scapula. The ligament is incised while protecting the underlying suprascapular nerve (Figure 11B &C). The nerve is then traced in a proximal direction and ultimately cut (recipient proximal).

Attention is then directed to identifying the spinal accessory nerve (Figure 11D). The undersurface of the trapezius muscle is explored just medial to the scapular border. The nerve resides between the midline (spine) and the border of the scapula. The nerve is verified using the Checkpoint Nerve Stimulator and traced in a distal direction to gain length. The nerve is transected as distal as possible (donor distal). The spinal accessory and suprascapular nerves are brought in proximity along the superior border of the scapula. Tension free coaptation is performed with microsutures and/or fibrin glue. (Figure 11E & F)

Axillary inscision drawn and dissection of incision.

Figure 12A&B: A: Axillary incision drawn for radial to axillary nerve transfer for elbow flexion. B: Axillary incision and deep dissection to identify radial and axillary nerve.

Axillary nerve divided and traced.

Figure 12C: Axillary nerve divided into group fascicles and traced in a proximal direction.

Radial nerve traced.

Figure 12D: Radial nerve traced in a distal direction.

Radial to axillary nerve transfer.

Figure 12E: Radial to axillary nerve transfer.

The radial to axillary nerve transfer has two possible approaches: posterior or axillary. Both approaches accomplish the transfer and the choice is based upon concomitant procedures and surgeon preference. An axillary incision with medial extension down the arm is currently preferred (Figure 12A & B). This approach allows for a radial to axillary nerve transfer along with a single or double fascicular transfer for elbow flexion. The patient is placed in the lateral decubitus and the affected hemithorax including the arm is prepped and draped. The axillary incision is designed within a skin fold from the posterior acromion to the mid-axilla. The incision is then extended down the medial aspect of the arm over the intermuscular septum. Dissection is performed through the fat and fascia to identify the following muscles from anterior to posterior: latissimus dorsi, teres major, long head of the triceps, and deltoid. The axillary nerve resides deep to the latissimus dorsi and teres major muscles and is isolated anterior (emanating from the posterior cord) and posterior (toward the deltoid) to these muscles (Figure 12C). The motor and sensory parts of the axillary nerve must be separated. There are typically three group fascicles within the axillary nerve. The most superior group fascicle follows the posterior humeral circumflex vessel and innervates the anterior and middle deltoid. This group fascicle is the recipient nerve. The middle group fascicle branch innervates the posterior deltoid. The inferior group fascicle branch innervates the teres minor. Vessels loops are placed proximal and distal to the intended area of microdissection. Elevation of the vessels loops places tension across the nerve and eases dissection. The epineurium is gently opened by spreading with micro forceps and the underlying group fascicles are exposed. The Checkpoint Nerve Stimulator set at 2.0 milliamps may facilitate identification by stimulating any remaining muscle fibers visualized as slight twitching of the deltoid. Lack of stimulation requires distal dissection to directly identify fascicles entering the deltoid muscle (motor) versus entering the skin (sensory).

Attention is next directed at identifying the radial nerve just anterior to the latissimus dorsi and teres major tendons (Figure 12D). The radial nerve and the branches to the triceps muscle are isolated. The Checkpoint Nerve Stimulator on low amplitude (0.5 milliamps) is used to stimulate the individual triceps branches. Occasionally, a common trunk from the radial nerve divides into three individual branches (long head, lateral head, and medial head). This anatomic variation requires intrafascicular dissection to ensure preservation of elbow extension after nerve transfer.

The branch to the long, lateral, or medial head can be selected as the donor depending upon nerve caliber, location, and ease of dissection. The medial head branch provides more distal length (donor distal); however, the long or lateral are suitable options. Once an appropriate sized radial nerve branch to the triceps is identified, the branch is dissected in a distal direction to gain donor nerve length. The adjacent group fascicle of the axillary nerve (usually the group fascicle to the anterior deltoid) is dissected in a proximal direction (recipient proximal). After adequate proximal recipient and distal donor dissection have been achieved, the group fascicles are cut. The recipient axillary nerve branch to the deltoid and donor radial group fascicle nerve, are then brought in proximity and a tension-free coaptation performed with microsutures and/or fibrin glue (Figure 12E).

Nerve Transfers to Restore Elbow Flexion

Video 6: Ulnar to musculo-cutaneous nerve transfer.

Video 7: Median to musculo-cutaneous nerve transfer.

Nerve transfers to restore elbow flexion can address the deficit in brachialis and/or biceps muscle function. The standard donor for the biceps motor nerve is a group fascicle from the ulnar nerve (Video 6). The standard donor for the brachialis is a group fascicle from the median nerve (Video 7). A single or double fascicular transfer can be performed.

Right arm with medial incision.

Figure 13A: Right arm with medial incision. Red vessel loop is around biceps motor branch from musculocutaneous nerve, yellow vessel loop is around ulnar nerve.

Motor branch from musculocutaneous nerve to biceps muscle.

Figure 13B: Motor branch from musculocutaneous nerve to biceps muscle.

Longitudinal epineurotomy.

Figure 13C: A longitudinal epineurotomy along the ulnar nerve to identify the individual group fascicles and to isolate an expendable motor component. Adjacent parallel nerve is medial antebrachial cutaneous.

Group fascicle of ulnar nerve.

Figure 13D: Group fascicle of ulnar nerve to extrinsic muscles is divided and transferred toward the biceps motor branch.

Surgery is performed with the patient supine and the arm extended. A medial arm incision is performed along the intermuscular septum (Figure 13A). The basilic vein and medial antebrachial cutaneous nerve are isolated and protected. The musculocutaneous nerve is identified deep to the biceps muscle (Figure 13B). The biceps motor nerve is proximal to the brachialis motor nerve. The location of the biceps motor nerve is heralded by a vascular leash. The motor nerve is identified and traced in a proximal direction using intra-fascicular dissection to gain length. If a double fascicular transfer is planned, the musculocutaneous nerve is traced in a distal direction to identify the brachialis motor nerve that is dissected in a similar fashion. After both recipients are identified, attention is directed toward the donor nerves.

The ulnar nerve adjacent to the biceps motor nerve and the median nerve opposite the brachialis motor nerve are isolated. Vessel loops are placed proximal and distal to the intended area of microdissection to simplify the dissection. Elevation of the vessels loops places tension across the nerve and eases dissection. The epineurium is gently opened by spreading with micro forceps and the underlying group fascicles are exposed (Figure 13C). Using the Checkpoint Nerve Stimulator on low amplitude (0.5 milliamp), the group fascicles are individually stimulated. For the ulnar nerve, the group fascicle that yields primarily extrinsic function and preferably wrist flexion (flexor carpi ulnaris) is chosen. For the median nerve, the group fascicle that yields primarily extrinsic function (flexor carpi radialis, flexor digitorum superficialis, or palmaris longus) is selected and care is taken to preserve anterior interosseous nerve. The donor group fascicle is dissected in a distal direction (donor distal) to gain nerve donor length. Once adequate proximal recipient and distal donor dissection has been achieved, the group fascicles are cut (Figure 13D). The recipient and donor nerves are brought in proximity and a tension free coaptation performed with microsutures and/or fibrin glue.

Nerve Transfers to Restore Elbow Extension

Video 8: Ulnar motor to triceps motor nerve transfer.

This nerve transfer is similar in dissection to the transfer for elbow flexion. The difference is in the selection of the recipient nerve being a radial nerve branch to the triceps. The ulnar nerve is typically used as the donor nerve (Video 8). Another option is using the posterior branch of the axillary nerve as the donor nerve. This transfer is gaining popularity in persons with spinal cord injury. There are typically three group fascicles within the axillary nerve. The most superior group fascicle follows the posterior humeral circumflex vessel and innervates the anterior and middle deltoid. This group fascicles should be preserved. The middle group fascicle branch innervates the posterior deltoid and is the donor nerve. The inferior group fascicle branch innervates the teres minor.

Using the ulnar nerve as the donor nerve, the Checkpoint Nerve Stimulator on low amplitude (0.5 milliamp) verifies the group fascicle that yields primarily extrinsic function. Subsequently, an appropriate sized radial nerve branch to the triceps is identified and dissected in a proximal direction to gain length. The adjacent group fascicle of the ulnar nerve is dissected in a distal direction (donor distal). After adequate proximal recipient and distal donor dissection has been achieved, the group fascicles are cut. The recipient radial nerve branch to the triceps and donor ulnar group fascicle nerves are then brought in proximity and a tension free coaptation performed with microsutures and/or fibrin glue.

Nerve Transfer to Restore Intrinsic Function

Video 9: Anterior interosseous nerve to ulnar motor nerve transfer.

Surgery is performed with the patient supine and the arm extended (Video 9). Under tourniquet control, an incision is performed from the distal ulnar forearm into the palm across Guyon’s canal. Skin flaps are raised and the ulnar neurovascular structures isolated deep to the flexor carpi ulnaris. The ulnar neurovascular structures are traced in a distal direction. The volar carpal ligament is divided to open Guyon’s canal. The deep motor branch of the ulnar nerve is identified and dissected in a proximal direction separating the motor nerve from the sensory branches. The dissection proceeds into the forearm. The anterior interosseous nerve is isolated proximal to the pronator quadratus and traced into the muscle to gain length. Since the pronator quadratus will be denervated following the transfer, the muscle is simply divided by bipolar electrocautery. The anterior interosseous nerve is traced as distal as possible (donor distal). After adequate proximal recipient and distal donor dissection has been achieved, the group fascicles are cut. The recipient deep motor branch of the ulnar nerve and the anterior interosseous nerve are brought in proximity and a tension free coaptation performed with microsutures and/or fibrin glue.

Nerve Reconstruction versus Nerve Transfer versus Tendon Transfer

A discussion regarding the choice between nerve reconstruction (repair or graft), nerve transfer, and tendon transfer is necessary. The chosen procedure depends on the clinical scenario with consideration of numerous patient and injury factors including patient age, time from injury, extent of injury, available donors, and surgeon preference. These procedures are not mutually exclusive and can be used in combination. For example, an ulnar nerve laceration proximal to the elbow may be treated with nerve grafting for sensation and extrinsic muscle recovery (flexor carpi ulnaris and flexor digitorum profundus) and nerve transfer for intrinsic muscle recovery. Another example would be a radial nerve laceration proximal to the elbow treated with tendon transfer for wrist extension and nerve transfer to the posterior interosseous nerve for distal recovery (thumb and finger extension). There are often multitudes of plausible surgical options; however, all must abide to the principles previously detailed. Tendon transfer remains the gold standard for chronic nerve lacerations that have passed the window of opportunity for nerve reconstruction.

Rehabilitation

The initial post-operative protocol following nerve repair, grafting, or transfer are similar. The coaptation site is allowed to heal via immobilization without tension across the repair site. The regimen may vary according to concomitant injuries, such as tendon lacerations. In general, following nerve repair, transfer, or reconstrution, the limb is immobilized for three weeks duration followed by gradual mobilization. The initial goal of therapy is to maintain supple joints and prevent contracture. The inherent imbalance that occurs after motor nerve injury predisposes joints to contracture. Passive range of motion and splinting are essential modalities. In patients with loss of sensation, splint fabrication must be meticulous to avert skin breakdown.

Patient education is an important part of the rehabilitation. Sensory loss can lead to inadvertent injury. The patient needs to be extremely careful with regards to hot and cold temperatures. The patient must be educated about nerve injures and the slow regenerative process. Unfortunately, neither the patient nor therapist can speed up the process of watchful waiting at one to three millimeters per day.

As the nerve regenerates to the motor end plates, the focus on therapy changes to late phase rehabilitation and includes motor and sensory re-education. The patient must reactivate or relearn to move the muscle. Movement can be enhanced using auditory or visual biofeedback. Relearning a direct nerve repair or grafting is a straightforward process. Relearning a nerve transfer is more challenging and the rehabilitative techniques are similar to tendon transfer. An experienced therapist is invaluable as the learning process can be frustrating and difficult. The exact process of relearning after nerve injury/reconstruction is largely unknown, but certainly involves brain plasticity and reorganization of the primary somatosensory cortex to learn how to fire a muscle innervated by a different motor nerve.

Video 10: Desensitization for hyperesthesia using various textures.

As the nerve regenerates to the sensory receptors, the initial sensation may be uncomfortable (e.g. tingly or itchy) and hypersensitive. Tactile hyperesthesia refers to recovery that results in an abnormal increase in sensitivity to touch. The therapist uses sensory reeducation or retraining to improve both the patient’s cognitive and adaptive response to stimulation of the affected skin region (Video 10). The early phase of sensory retraining is aimed at reeducating constant (localization) versus moving touch perceptions. For regions with hyperesthesia, desensitization with gentle touch receptors is performed to lessen the response. In the later phase of retraining, the focus shifts to reeducate the directionality of stroking using various textures and stimulation of A-Beta movement (e.g. left to right or distal to proximal). Over time, the program dampens the tactile hyperesthesia and improves object identification and manipulation. Patients regain the ability to perform various activities of daily living and improve in their stereognosis (ability to recognize an object in their hand without any visual cues).

Child's hand with skin bitten and missing.

Figure 14: Infant with brachial plexus birth palsy biting right index finger.

Tactile hyperesthesia in infants, such as babies with brachial plexus palsies, manifests as biting (Figure 14). The biting can be severe and result in infection and even nibbling away of the affected fingertips. Regrettably, there is no intellectual reasoning with infants and the parents feel horrible about the biting. Numerous medical and home remedies have been tried to no avail as the infants continue to gnaw at their digits. Fortunately, as the sensory recovery progresses and the tactile hyperesthesia lessens, the biting diminishes. The result is often physical scarring to the child and emotional scarring to the parents.

Outcome

The outcome following nerve surgery has numerous confounding factors. The results are difficult to decipher as published reports conglomerate a mixed sample of injuries into a single paper. The best results are in distal sharp lacerations in young persons that are repaired with a tensionless technique. However, that may be similar to searching for a herd of unicorns. In clinical practice, the mechanism of injury is often a combination of sharp and blunt trauma with or without an element of traction. In addition, there may be associated injuries such as tendon laceration, artery transection, or bony fracture. Hence, the number of isolated truly sharp transections is relatively low.

Video 11: 5 year-old s/p acute nerve grafting of radial and ulnar nerves in the arm due to segmental loss.

There are certain variables that improve the chances of success including young age (children), distal injuries closer to the motor end plates, timely repair or reconstruction, and meticulous microsurgical technique using appropriate equipment (magnification, micro forceps, and microsutures) (Video 11). In contrast, poor prognostic factors include older age, proximal injuries far from the motor end plates, delayed presentation, and suboptimal technique with inadequate equipment.

In general, timely nerve repair or reconstruction "works" about 85 to 90 percent of the time to reinnervate downstream muscle fibers and/or sensory end organs. However, the patient may not achieve full function and this expected outcome needs to be conveyed to the patient and family prior to surgery. This discussion frequently modifies their expectations. The concepts of slow regeneration and motor end plate demise must be discussed honestly with the patient and family. The discussion equates the nerve to an internet cable, which imparts colloquial understanding into the complexities of nerve anatomy and nerve surgery. The lengthy time to recovery must also be communicated prior to the surgical procedure along with the possible complications.

Figure 15: 14 year-old male depicted in Figure 11 3 years s/p shoulder nerve transfers (spinal accessory to suprascapular and radial to axillary) and elbow nerve transfers (median to brachialis and ulnar to motor nerve transfers for elbow flexion and forearm supination.

Man touching mouth with left hand.

Figure 15A: Elbow flexion.

Man with both arms flexed.

Figure 15B: Good muscle bulk and elbow flexion.

Man reaching straight up with both arms.

Figure 15D: Overhead motion.

Man with both arms reaching out, elbows at 90-degree angles.

Figure 15C: Shoulder external rotation.

The outcomes following nerve transfer surgery have similar challenges but can overcome the factors related to proximity to sensory receptors or motor end plates (Figure 15). The outcome, however, still relies upon age, timeliness, and meticulous microsurgical technique. Nerve transfer surgery has other numerous benefits including operating out of the zone of injury and preferential direction of nerve fibers (motor fibers to motor fibers and sensory fibers to sensory fibers). Nerve transfer surgery is becoming the preferred technique in many situations especially proximal injuries, such as upper trunk (C5, C6) brachial plexus lesions and proximal peripheral nerve injuries. However, nerve transfer surgery is limited by the number of available expendable donors that is narrowed in patients that have sustained multiple nerve injuries.

Future

The future is bright for advances in nerve surgery from diagnosis to treatment and subsequent rehabilitation. The diagnostic advance will be related to the immediate determination of the extent of the nerve injury. Nerve imaging with or without an injectable substance will discriminate whether the injury is a neurapraxia, axonotmesis, or neurotmesis type injury. This diagnostic advance will obviate the current practice of "watching and waiting " that will become obsolete. The physician will be able to ascertain the diagnosis and recommend the appropriate management without wasting time. The immediate or early diagnosis will allow prompt intervention for neurotmesis avoiding the delay in surgical intervention that jeopardizes motor end plate survival.

The surgical management of nerve injuries will be augmented as the pharmacology of nerve regeneration is better elucidated. Nerve repair or reconstruction will be enhanced by the addition of a local or systemic pharmacologic treatment that will promote nerve regeneration. In addition, a period of intraoperative nerve stimulation following repair or reconstruction may ignite nerve regeneration. These pharmacologic agents and intraoperative modalities will enrich nerve regrowth via superior axonal sprouting to the denervated starving motor end plates and sensory receptors. This augmented regeneration may also stimulate motor to motor and sensory to sensory directionality.

The other impactful scientific advance that will improve nerve surgery and rehabilitation is further understanding the brain. Imaging studies have revealed remarkable rapid changes after nerve injuries or limb loss that can be reversed with nerve recovery or limb replantation. Cortical plasticity and motor relearning play a pivotal role during nerve recovery. Harnessing the plasticity of the brain will directly affect rehabilitation after nerve injury. Techniques such as transcranial magnetic stimulation (TMS), electroencephalography, magnetoencephalography (MEG), functional MRI (fMRI), structural MRI (sMRI), and positron emission tomography (PET) are unveiling the mysteries of human cortical plasticity. Rehabilitation that modulates the processes of pruning of ineffective connections and sprouting of intact afferents from nearby cortical and/or subcortical territories will improve nerve recovery.

How soon will these advances occur? Remember what Albert Einstein said, "I never think of the future- it comes soon enough."

Scott Kozin, M.D.

Scott Kozin, M.D.

Chief of Staff, Shriners Hospital for Children

Clinical Professor, Department of Orthopaedic Surgery, Lewis Katz School of Medicine at Temple University

Adjunct Clinical Professor in the Department of Orthopaedic Surgery, Sidney Kimmel Medical College at Thomas Jefferson University

Dr. Kozin has a financial interest and/or other relationship with Checkpoint Surgical Inc. This manual was funded by Checkpoint Surgical Inc. and is not peer reviewed


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Checkpoint Surgical, LLC, 22901 Millcreek Blvd., Suite 110, Cleveland, Ohio 44122, Toll-free: 877.478.9106, Local: 216.378.9107, Fax: 216.378.9116, Email: info@checkpointsurgical.com, www.checkpointsurgical.com