Median nerve.

In the upper arm, there are no motor branches, but in some instances of a deficient musculocutaneous nerve, there may be branches to the coracobrachialis, biceps brachii, and brachialis muscles. Awareness of this anatomical variation is important when dissecting the motor fascicles to the biceps and brachialis during distal nerve transfers to restore elbow flexion for brachial plexus injury. Communicating branches from the median and musculocutaneous nerve can be encountered. This can explain loss of arm flexor function or weakness in the event of a high median nerve injury.

At the level of the lacertus fibrosus and into the cubital fossa, the median nerve, brachial artery, and biceps tendon are closely related. ^, In the antecubital fossa, the nerve is anterior to the brachialis insertion and medial to the biceps tendon. As the nerve continues distally, there are posterior branches to the flexor pronator group of muscles arising from the medial epicondyle innervating the pronator teres (PT), flexor carpi radialis (FCR), palmaris longus (PL), and flexor digitorum superficialis (FDS). Most commonly, there is one branch to the PT, but there may be separate branches to the superficial and deep heads. Although anatomical variability is present, there is typically one fascicle to the FCR and two fascicles to the FDS and PL.

In the forearm, the median nerve continues distally between the superficial (humeral) and deep (ulnar) heads of the PT. The course is anterior to the ulnar artery, with these structures typically separated by the deep head of the PT. Distal to the PT, the nerve passes deep to the fibrous arch of the FDS and superficial to the flexor digitorum profundus (FDP). Approximately 5 cm distal to the medial epicondyle and just distal to the FDS arch, the anterior interosseous nerve (AIN) branches from the dorsal–radial aspect of the median nerve innervating the FDP of the index and middle finger and the flexor pollicis longus (FPL) ( Fig. 19.1 ). The AIN continues distally with the anterior interosseous artery along the interosseous membrane and innervates the pronator quadratus. The terminal portion provides sensory innervation to the wrist capsule. ^, Traumatic (typically neurapraxic) injury to the AIN may occur with fractures about the elbow (most commonly, extension-type pediatric supracondylar humerus fractures). Also of note, the AIN fascicles can be dissected (internally neurolysed) from the median nerve proper as proximal as the distal third of the upper arm. This is important when performing a nerve transfer from the brachialis branch of the musculocutaneous nerve to the AIN.

(A) Course of the median nerve in the upper extremity and motor innervation of muscles in the forearm and hand. (B) Sensory innervation of the median nerve in the palmar and dorsal hand.

(Courtesy of Jin Bo Tang).

After the AIN branch, the median nerve continues distally between the FDS and FDP and medial to the FPL. The palmar cutaneous branch of the median nerve (PCBMN) is the last branch in the forearm. At approximately 5 cm proximal to wrist crease, the median nerve becomes more anterior/superficial in the axial plane, between the FDS and FCR, but remains deep to the PL (if present). In the coronal plane, it remains ulnar to the FCR. At this level, the internal topography of the nerve is consistent. The motor fascicles are typically situated along the radial and central portions of the nerve, whereas the sensory portions are anterior/superficial and ulnar.

In the hand, the median nerve enters passing through the carpal tunnel. The recurrent motor branch arises from the radial aspect of the median nerve to innervate the abductor pollicis brevis, flexor pollicis brevis, and opponens pollicis. Following the origin of the recurrent motor branch, the median nerve proper continues distally, providing sensory innervation through the common and proper digital nerves and motor branches to the first and second lumbrical muscles. The sensory innervation includes the palmar side of the thumb, the index and middle finger, and the radial half of the ring finger and the dorsal aspect of the respective digits distal to the proximal interphalangeal (PIP) joints, including the nail beds ( Fig. 19.1 ). ^,

The PCBMN provides sensation to the radial aspect of the palm. It typically originates approximately 4 to 7 cm proximal to the wrist crease and runs between the median nerve (ulnarly) and FCR (radially) for 16 to 25 mm before piercing the antebrachial fascia 2 cm proximal to the wrist crease. After crossing the wrist crease, the PCBMN courses palmar and ulnar to the FCR tendon and reaching the skin just radial to the confluence of the thenar and hypothenar muscles. The PCBMN is at risk during anterior approaches to the distal radius. The PCBMN typically runs alongside the ulnar aspect of the FCR (but not within its sheath), but variations in the course of the PCBMN in the distal forearm have been described, including a course within the FCR sheath. The PCBMN is also at risk during carpal tunnel release. Several surface anatomical landmarks of varying reliability have been described to minimize risk to the PCBMN during skin incision placement for carpal tunnel release. Anatomical variations of the PCBMN at the wrist crease and base of the palm are also relevant to deeper dissection during carpal tunnel release. The PCBMN can branch through the PL tendon proximal to the palmar fascia and through antebrachial fascia proximal to the wrist crease. It can also pierce the transverse carpal ligament or palmar carpal ligament. These variations emphasize the importance of direct visualization during release of the carpal tunnel, Guyon’s canal, or the distal antebrachial fascia.

Connections between the median and ulnar nerve have been described in the forearm ( Martin-Gruber and Marinacci connections ) and in the hand ( Riche-Cannieu and Berrettini connections ). In Martin-Gruber connections , a branch from the median nerve may travel with the ulnar nerve in the forearm. This branch may then innervate the thenar muscles and median intrinsics only (as expected), or it can innervate both median and ulnar motor distributions in the hand (thenars, median intrinsics, and ulnar intrinsics). The reverse may also be true—a branch from the ulnar nerve may travel with the median nerve in the forearm. This branch may then innervate the ulnar intrinsics alone (as expected) or with the ulnar intrinsics, thenar muscles, and median intrinsics. These connections may account for remaining motor function despite an anticipated deficit after a peripheral nerve lesion—for example, remaining thenar motor function after a low median nerve injury due to a Martin-Gruber connection in the forearm. The Marinacci connection is a reverse Martin-Gruber anastomosis, in which the communicating nerve fibers run from the ulnar nerve to the median nerve in the forearm. In the hand, connections between the motor branches ( Riche-Cannieu connections ) and sensory branches ( Berrettini connections ) of the median and ulnar nerves may have similar implications. In rare cases, a Riche-Cannieu connection may explain atypical and unexpected clinical deficits, such as first dorsal interosseous weakness in the setting of carpal tunnel syndrome without evidence of ulnar nerve compression.

Ulnar nerve.

In the upper arm, the ulnar nerve courses inferiorly under the pectoralis minor muscle. At approximately the mid-humerus level, it passes posteriorly through the medial intermuscular septum and deep to the internal brachial ligament if the ligament is present. At the level of the supracondylar ridge, the inferior ulnar collateral artery joins the ulnar nerve as it passes into the retrocondylar groove on the posterior aspect of the distal humerus. Frequently, the first branch of the ulnar nerve originates at or above the medial epicondyle to innervate the elbow joint before its entrance into the cubital tunnel.

As the ulnar nerve crosses the elbow joint, it passes under Osborne’s ligament—a band of fibrous tissue that spans the area between the origin of the humeral head of the flexor carpi ulnaris (FCU) from the medial epicondyle and ulnar head of the FCU from the olecranon. The cubital tunnel is bound by Osborne’s ligament proximally and the deep fascia of the flexor pronator mass distally as the nerve exits deep to the two heads of the FCU. The FCU aponeurosis and two heads of the FCU form the roof of the cubital tunnel, and the posterior band of the medial collateral ligament of the elbow forms the floor. As the position of the elbow changes from extension to flexion, the volumetric dimensions of the cubital tunnel change from ovoid to elliptical, causing effacement of the ulnar nerve. Branches to the FCU (mean 3, range 1–6) originate at a mean 25 mm distal to the medial epicondyle (range 6 mm proximal to 73 mm distal).

The ulnar nerve exits the cubital tunnel underneath the deep fascia of the flexor pronator mass, surrounded by the FCU medially, the median-innervated FDS muscle anterolaterally, and the FDP muscle posterolaterally ( Fig. 19.3 ). The ulnar nerve innervates the FCU. In addition, the ulnar nerve typically provides a single motor branch to the medial half of the FDP at a mean 3 cm distal to the medial epicondyle. It continues between the FCU and FDS muscle bellies in the proximal and middle thirds of the forearm and along a deep intermuscular septum between these two muscles. In the distal third of the forearm, the ulnar nerve courses between the FDS and FDP muscle bellies and then becomes more superficial, traversing distally under the antebrachial fascia directly medial to the ulnar artery and radial to the FCU. A nervi vasorum (the nerve of Henle) originates from the ulnar nerve 16 cm proximal to the pisiform to provide sympathetic innervation to the ulnar artery in the forearm, which may have a key role in pathologic vasospasm or Raynaud’s phenomenon.

(A) Course of the ulnar nerve in the upper extremity (lower image) , with a focused view of the structures over the ulnar nerve in the elbow region (upper image) . In the forearm, the ulnar nerve innervate the flexor carpi ulnaris (FCU) and the ulnar-half flexor digitorum profundus (FDP) muscles to the ring and little fingers. (B) Course of the ulnar nerve and its innervated muscles in the hand: hypothenar muscles (the abductor digiti minimi, opponens digiti minimi, and flexor digiti minimi), the palmar and dorsal interossei muscles, the third and fourth lumbricals, thenar muscles (adductor pollicis and the deep head of flexor pollicis brevis)

(A. Courtesy of Martin Langer. B. Courtesy of Julia Ruston).

The dorsal cutaneous branch of the ulnar nerve (DCBUN) originates approximately 5 to 9 cm proximal to the distal articular surface of the ulna, pierces the deep fascia running deep to the FCU tendon, and eventually becomes midaxial at the level of the ulnocarpal joint. The DCBUN commonly divides into two to four branches, which provide cutaneous sensory innervation to the dorsomedial hand, long, ring, and small fingers ( Fig. 19.2 ). Because of its location at the distal forearm and at the wrist, the DCBUN is particularly at risk of injury during arthroscopy as well as with other ulnar-sided wrist procedures.

(A) Course of the radial nerve in the upper arm. (B) Motor innervation of extensor muscles of the forearm by the radial nerve and the posterior interosseous nerve (PIN). The PIN is the radial nerve after it sends off the superficial radial nerve (SRN). (C) Sensory innervation of the radial nerve in the dorsal radial hand. (D) Sensory innervation of the palmar and dorsal aspect of the hand by the ulnar nerve.

(Courtesy of Jin Bo Tang).

At the palmar wrist crease, the ulnar nerve passes together with the ulnar artery deep to the flexor retinaculum in the Guyon’s canal. The ulnar nerve traverses together with the ulnar artery on its radial side. The distal ulnar tunnel is approximately 4 cm in length, originates 2 cm proximal to the pisiform, and terminates 1 cm distal to the pisiform. Most commonly, this corresponds to the level of the bifurcation of the ulnar nerve into the deep motor branch and a terminal superficial branch. Three anatomical zones are areas proximal to the bifurcation (zone I), the deep motor branch (zone II), and the superficial branch (zone III). The deep motor branch typically descends deep to and radial to the superficial branch, passes over the pisohamate ligament, and under the fibrous leading edge of the hypothenar muscles. The nerve then passes between the flexor digiti minimi and abductor digiti minimi, innervating both before piercing through and innervating the opponens digiti minimi. It then passes distally around the ulnar aspect of the hook of the hamate, running deep to the flexor tendons to innervate the third and fourth lumbricals, the dorsal interossei, the palmar interossei, the adductor pollicis, and the deep head of the flexor pollicis brevis. The terminal superficial branch gives off two branches to innervate the palmaris brevis before dividing into a digital nerve to the ulnar side of the small finger and a common digital nerve to the web space between the ring and small finger ( Fig. 19.3 ).

Variations within Guyon’s canal have been described and include more proximal branching points and the formation of a separate distinct branch to the abductor digiti minimi. The motor branch (along with the ulnar artery) may be found radial to the hook of the hamate (increasing risk of iatrogenic injury during carpal tunnel release). Innervation of the hypothenar muscles from anomalous median nerve branches or connections both in the forearm (Martin-Gruber connections) and at the level of the carpal tunnel has been described and may explain “nonanatomical” clinical findings.

Radial nerve.

In the upper arm, the radial nerve passes posteriorly through the triangular interval. Before it enters the spiral groove of the humerus, the radial nerve gives off a branch to the long head of triceps, the upper branch to the medial head of the triceps, the lower branch to the medial head of the triceps and anconeus, and the upper branch to the lateral head of the triceps. At the medial border of the humerus (entrance of spiral groove), the lower lateral brachial cutaneous nerve arises from the radial nerve. The radial nerve obliquely courses across the posterior surface of the humeral shaft from medial to lateral, giving off another cutaneous nerve (posterior cutaneous nerve of the forearm). These two cutaneous nerves with sensory distributions may also arise from a common trunk from the radial nerve at the level of the deltoid tuberosity, crossing the lateral head of the triceps before dividing. After reaching the lateral portion of the humeral shaft, the radial nerve pierces the lateral intermuscular septum, 8 to 12 cm proximal to the lateral epicondyle, and passes from the posterior to anterior compartment. When passing the distal third of the humeral shaft, there are only a few fibers of the brachioradialis muscle separating the radial nerve from the humerus until the level of the metaphyseal flare, when the muscle belly of the brachialis is interposed between the radial nerve and the humerus. The middle to distal third humeral shaft fractures are often associated with radial nerve injuries. Proximal to the lateral epicondyle, the radial nerve provides variable innervation to the lateral brachialis, followed by consistent innervation of the brachioradialis and ECRL. ^,

The radial nerve crosses the elbow in the interval between brachialis and brachioradialis muscles. At the level of the radiocapitellar joint (3 cm proximal to the supinator muscle), it divides into its terminal branches: the superficial radial nerve (SRN) continuing deep to the brachioradialis and the posterior interosseous nerve (PIN) ( Fig. 19.2 ). There is a variability of innervation to the ECRB, including branches from the PIN, SRN, or an independent branch from the radial nerve proper. This variability has implications for the planning of nerve transfer surgery, emphasizing the importance of direct visualization during surgical dissection.

The PIN courses within the supinator muscle. The location of the PIN changes after injuries of the proximal radius. After exiting the supinator, the PIN travels in the deep interval between the abductor pollicis longus (APL) and extensor carpi ulnaris (ECU) and provides motor branches to the ECU, extensor digitorum communis (EDC), and extensor digiti minimi (EDM). The last set of branches arising from the PIN are to the APL, extensor pollicis brevis (EPB), and either to the extensor pollicis longus (EPL) or the extensor indicis proprius (EIP). The PIN lies deep to the fourth extensor compartment on the posterior interosseous membrane and terminates as a sensory branch to the wrist joint. It is a potential donor for nerve grafts between its final motor branch and its nodular termination with a length of 5 to 10 cm.

Regarding the SRN, 9 cm (7–11 cm) proximal to the radial styloid, the SRN pierces the brachioradialis to enter the subcutaneous tissue in the plane between brachioradialis and ECRL. The distal branching pattern of the dorsal and palmar branches of the SRN have tremendous variability. The main palmar branch of the SRN supplies the dorsal/radial digital nerve of the thumb with interconnections from the terminal portions of the lateral antebrachial cutaneous nerve. The main dorsal branch of the SRN supplies the dorsal/ulnar digital nerve of the thumb, the dorsal/ulnar and dorsal/radial digital nerves of the index finger, and the dorsal/radial digital nerve of the long finger.

Median nerve.

The loss of sensation in the palmar and dorsal surfaces of the lateral three-and-a-half digits is a typical symptom after complete laceration of the median nerve. The symptoms can range from paresthesia to complete loss of the sensation of these areas. The decrease in touch sensation upon clinical examination is the primary sign leading to the diagnosis ( Box 19.2 ).

With decrease or loss of different muscles innervated by the median nerve, median nerve injuries can be classified as high or low, corresponding to the lesion proximal or distal to the origin of the AIN. In low injuries, the thenar intrinsic muscles innervated by the median nerve, usually the abductor pollicis brevis (APB), opponens pollicis, and superficial head of the flexor pollicis brevis (FPB), are paralyzed. In high injuries, the pronator teres, FCR, all the finger superficiales, index and middle finger profundi, FPL, and pronator quadratus muscles are also paralyzed ( Box 19.2 ).

The prime muscle of thumb opposition is the APB, although both the opponens pollicis and FPB also produce some opposition. The adductor pollicis and the two extrinsic thumb extensors cause thumb retroposition, whereas the FPL can act as a muscle of either opposition or retroposition, depending on the position of the thumb. Thumb abduction and opposition are frequently retained after isolated median nerve injury as a result of preserved ulnar nerve function. Jensen considered that opponensplasty was required in only 14% of median nerve injuries, and it is my experience (Esther Vögelin) that reasonable opposition is commonly retained in complete median nerve transections, if an adequate FPL function is present.

In high median nerve paralysis, all the muscles in the forearm flexor compartment apart from the ulnar-innervated FCU and the profundi to the little and ring fingers are paralyzed. However, the working part of the profundus muscle often provides a full, although weak, range of middle finger flexion ( Box 19.2 ). Again, my enthusiasm for reconstructive surgery is tempered by my belief (Esther Vögelin) that sensation is the prime determinant of hand function and because I believe that sensory recovery after a high median nerve repair in adults is mostly poor and is even worse if a nerve graft is required.

Ulnar nerve.

Complete loss of sensation, or numbness and tingling in the palmar aspect of the little finger and ulnar part of the ring finger, with weakness or loss of coordination of the fingers are common findings after ulnar nerve injury, which usually can lead to diagnosis. In the first few weeks after ulnar nerve injury, claw finger deformity does not present, but weeks or months after injury, the ring and little finger typically present claw finger deformity. In incomplete ulnar nerve injury, decrease in the muscle power of the forearm or intrinsic muscle in the hand may not be obvious. Claw finger deformity may not be visible, but sensory disturbance of the ulnar nerve innervated area in the hand should lead to suspicion or diagnosis of incomplete ulnar nerve laceration.

Ulnar nerve injuries are classified as high or low according to the muscles involved. Low injuries occur distal to the origins of the motor branches to the FCU and ring and little finger FDP muscles. Strength of the extrinsic hand muscles is unaffected, but sensation is lost on the ulnar border of the hand and in the ring and little fingers, and the ulnar-innervated intrinsic muscles are paralyzed. This results in weakness of thumb pinch, claw deformity, loss of the normal pattern of finger flexion, and significant loss of hand dexterity and strength. ^,

High injuries occur above the origins of the motor branches to the FCU and ring and little finger FDP muscles. In this situation, loss of distal interphalangeal (DIP) joint flexion of the ring and little fingers and wrist flexion compound the aforementioned findings, although, paradoxically, the claw deformity tends to be less severe. The ulnar nerve usually innervates the hypothenar muscles (ADM, flexor digiti minimi, opponens digiti minimi), all the interosseous muscles of the fingers, the lumbricals for the ring and little fingers, and the adductor pollicis muscle. In addition, the FPB muscle frequently (79% of cases) has a dual median and ulnar innervation.

The motor branch of the ulnar nerve can be lacerated in the palm of the hand after it has given off its branches to the hypothenar muscles, and this results in paralysis of the adductor pollicis muscle and the interossei for the index, middle, and ring fingers, whereas the hypothenar muscles retain normal function and sensation in the ring and little fingers is preserved. The motor branch of the ulnar nerve can also be damaged or compressed in the distal portion of Guyon’s canal, such that ring and little finger sensation is normal but there is loss of function in all the ulnar-innervated intrinsic muscles, including those of the hypothenar eminence.

Ulnar nerve laceration or compression in the proximal portion of Guyon’s canal causes loss of sensation in the palmar aspects of the hypothenar eminence and ring and little fingers, as well as loss of function in all the ulnar-innervated intrinsic muscles. However, sensation is preserved in the dorsal ulnar aspect of the hand because this is provided by the dorsal branch of the ulnar nerve, which arises in the distal forearm and perforates the deep fascia 6 to 8 cm proximal to the wrist.

Only ulnar nerve injuries in or above the cubital tunnel cause loss of function in the FCU and the ring and little finger FDP muscles. The characteristic deformity of ulnar nerve palsy is clawing of the two ulnar digits, because their lumbrical and interosseous muscles are innervated by the ulnar nerve, whereas the lumbricals of the index and middle fingers are supplied by the median nerve and continue to function.

A low ulnar nerve palsy demonstrates more severe clawing of the ring and small fingers than a high palsy because of unopposed interphalangeal (IP) joint flexion of the FDP. There are many clinical signs and specific tests for loss of ulnar nerve motor function ( Box 19.2 ). Clawing, with hyperextension at metacarpophalangeal (MP) joints and flexion at IP joints, is the characteristic resting posture of the ring and little fingers ( Duchenne’s sign ). Bouvier’s maneuver is used to test the integrity of the central slip and the lateral bands of the extensor expansion. Hyperextension of the clawed finger MP joints is blocked, and the MP joints are held in slight flexion. Attempted extension of the fingers results in full active extension of the PIP and DIP joints if the normal anatomy of the extensor expansion is preserved.

A sensitive way to detect mild as well as severe loss of ulnar nerve function is to place the patient’s hand flat on a tabletop with the fingers abducted. Then, ask the patient to abduct the middle finger from side to side ( Pitres-Testut sign ). This allows the strength of radial and ulnar abduction to be assessed (testing second and third dorsal interosseous muscle strength); in addition, if the patient is asked to move the middle finger from side to side as fast as possible, the coordination and ease of this maneuver can be compared with the normal hand to reveal subtle loss of motor function.

Another sign of loss of ulnar nerve function is the inability to cross the middle finger dorsally over the index finger, or the index finger over the middle finger (a test of the first palmar interosseous and second dorsal interosseous muscles). Froment’s sign —marked thumb IP joint flexion when pinching sheets of paper between the thumb and index finger—indicates paralysis of the adductor pollicis and first dorsal interosseous muscles, with replacement of their pinch function by the FPL.

Wartenberg’s sign is the inability to adduct the extended little finger to touch the extended ring finger. This is due to the EDM abducting the little finger (despite paralysis of the hypothenar muscles), unopposed by the third palmar interosseous, which is also paralyzed. In addition to the static claw deformity, loss of intrinsic muscle function may affect the normal dynamics of finger movement. In a normal hand, the MP joints flex before the IP joints when gripping an object, such that the object is drawn into the palm of the hand. In ulnar paralysis, however, the DIP joints flex first, followed by the PIP joints and then the MP joints, such that the object is not guided into the palm but is pushed out of the palm by the fingertips.

Radial nerve.

The most typical finding after radial nerve injury is that the patient cannot actively extend the MP joints of the fingers and thumb and has great difficulty in grasping objects ( Fig. 19.4 ), which usually leads to diagnosis. If the laceration is above the elbow, the patient may not be able to actively extend the wrist. Sensory disturbance after radial nerve injury is mainly on the dorsal hand, especially the dorsal first web area and dorsal aspect of the radial three digits proximal to the DIP joint level.

Radial nerve injury. (A) Lower injury (distal to the elbow); after radial nerve injury at the left forearm, the left hand cannot extend the metacarpophalangeal (MP) joints, and the right side is normal. (B) High injury causes wrist dropping leads to wrsit dropping. In both injuries, the patient cannot actively extend the MP joint of the fingers, but in high injury, the patient cannot actively extend the wrist as well, presenting typical wrist dropping.

(copyright of Jing Chen).

Perhaps more importantly, the loss of active wrist extension robs the patient of the mechanical advantage that wrist extension provides for grasp and power grip. With trauma to the upper extremity, most injuries of the radial nerve occur distal to the branches to the triceps in the upper arm. The radial nerve innervates the brachioradialis (BR) and ECRL before it divides into its two terminal branches, the posterior interosseous (motor) and superficial (sensory) branches.

Patients with upper radial nerve injury (above the elbow) cannot extend the wrist, but patients with low radial nerve injury (the injury to PIN) usually can extend the wrist; all these patients cannot extend the MP joints of the affected hand ( Box 19.2 ) ( Fig. 19.4 ). Patients with PIN palsy have at least one strong radial wrist extensor intact, resulting in radial deviation of the wrist with extension, which may be marked in some patients.

Unless a patient has a painful neuroma, the sensory part of the radial nerve can usually be ignored. Loss of sensibility on the radial side of the dorsum of the hand may be bothersome, but rarely a disability. Occasionally, a patient with a complete radial nerve palsy has no demonstrable sensory deficit because, in some patients, the superficial branch of the radial nerve is absent, and its function is replaced by the lateral antebrachial cutaneous nerve.

Timing of direct repair.

Direct end-to-end repair of a lacerated nerve is ideally performed in the acute setting (within 3 days). The advantages of acute repair include the ability to perform intraoperative nerve stimulation, to optimize motor nerve recovery within its narrow time frame, and to adequately gain exposure and mobilize nerve ends with only minimal scar tissue formation. Nerve ends seem to still contain neurotransmitters within 72 hours of injury. From a histopathologic standpoint, nerve ends have clear and symmetrically apposed fascicles immediately after transection, which then become increasingly difficult to match, as Schwann cell proliferation, fibrosis, and angiogenesis occur at each end.

Numerous studies have reported that a well-performed primary nerve repair results in a significantly better outcome than either delayed end-to-end repair or delayed nerve grafting. The importance of an early repair has been reported for many upper-extremity peripheral nerves, including the median, radial, ulnar, and musculocutaneous nerves.

However, if a primary repair or reconstruction is not possible, it must be of high priority to guide motor neurons to their target muscles before neuromuscular endplates degrade after 18 months. After that time, only salvage procedures such as tendon transfers remain a possibility to achieve functional improvement. For reconstruction of pure sensory nerve lesions, there is a longer period and at least protective sensation can be achieved up to 2 to 3 years.

Indications for direct repair.

Primary suture repair of a peripheral nerve laceration is indicated when healthy, nonscarred nerve ends can be directly aligned in a tension-free manner. Excessive mobilization of the nerve ends from the intact tissue should be avoided.

After debridement of damaged nerve tissue and trimming nerve stumps, direct coaptation may still be possible. There are three different end-to-end repair types: epineurial repair; group fascicular repair; and fascicular repair. There is, however, a lack of consensus as to which technique is superior, especially when discussing group fascicular and epineurial repair. Clinical studies have shown no differences in these techniques. Therefore, epineurial repair is often performed.

Surgical methods and techniques of direct nerve repair.

Adequate visualization of relevant neural, vascular, and musculoskeletal structures is required for precise end-to-end nerve repair. Although large nerves can be repaired under high-powered loupe magnification (at least 3.5×), smaller branches usually benefit from the use of a microscope (12–15× magnification). Surgical tips are given in ( Box 19.3 ).

• 1.
  

  Nerve end resection: Injured nerve end resection up to healthy nerve tissue facilitates fascicle apposition and optimizes functional outcome. More resection length is required as the time from injury increases.

  
  
• 2.
  

  Length of resection: How much nerve tissue has to be resected because of neuroma and/or damage is controversial and ultimately based on the surgeon’s experience and preference. Common methods used are external and internal visualization (e.g., fascicular structure and bleeding under the microscope), palpation, pliability, intraoperative histology, and intraoperative nerve studies (nerve action potential and somatosensory evoked potential) in larger or proximal mixed sensory-motor nerves. (The author’s threshold for adequate nerve health is at least 50%–75% preservation of fascicular architecture; the more proximal the lesion, the more crucial but difficult the decision —Esther Vögelin.)

  
  
• 3.
  

  Resection of scar tissue around the nerve: External neurolysis of the involved nerve ends from the surrounding scar tissue bed without further damaging the nerve ends is mandatory. A well-vascularized tissue bed is essential.

  
  
• 4.
  

  Repair tension: No or minimal tension of the nerve repair is important. However, minimal tension in a fresh nerve laceration always exists because of the elastic nature of nerves. Failure to hold an end-to-end repair with a single 9-0 suture in a small nerve branch and with a single 8-0 suture in a mixed sensory-motor nerve is a sign of undue tension. The nerve suture must withstand extension and flexion of the wrist and elbow extension <30 degrees without epineural tearing.

  
  
• 5.
  

  Epineural repair: Epineural repair is preferred to align the nerve ends only to avoid greater dissection and trauma to the fascicles of the nerve (in the case of perineural repair) and intraneural scar formation. No difference between fascicular and epineural repair has been demonstrated in peripheral nerve injuries.

  
  
• 6.
  

  After performing a nerve repair, a protecting soft-tissue envelope intuitively seems to minimize the chances of ischemia and scar formation impeding neural regeneration. Ideally, a barrier consists of no inflammatory reaction and sufficient porosity to facilitate the diffusion of nutrients, avoiding axonal escape and scar-induced ischemia as well as promoting nerve gliding. Available barriers range from synthetic and xenograft materials to autologous vein wrapping and pedicled/free tissue coverage.

For direct nerve repair in an acute nerve laceration with a minimal gap, nerve ends are easily mobilized after minimal resection and minimal repair tension without restricted joint range of motion. An operating microscope is usually used for all nerve repairs as it aids in precise placement of epineural sutures and minimizes damage to nerve tissue. A few epineural sutures are placed ( Fig. 19.5 ), the preferred suture material being nylon with a caliber typically 9-0 (or 8-0 for a corner suture). Repair the nerve ends at 12 and 6 o’clock first, in the epineurium in a slightly loose fashion, barely touching the fascicles. No fascicles should escape the repair site. Minimal trimming of escaping fascicles is an option.

(A) 90% division of a median nerve. (B) After microsurgical repair.

After completion of the repair, minimal tension at the repair site is checked, when the involved body part is put through passive range of motion on the operating table. The repair is usually augmented with fibrin glue (Tisseel® 2 mL, Baxter, Glattpark, Switzerland). Postoperative immobilization of the repair site without tension for 3 weeks is applied.

Indications of nerve grafting and donor sites.

If direct repair is not feasible (no tension-free repair, delayed presentation, presence of a segmental defect), nerve grafting is considered. The gold standard graft material remains the autograft. The advantages of autograft, as a graft material, include preserved nervous architecture and biology (i.e., Schwann cells and vasculature). In addition, autograft remains the preferred graft option (as opposed to allograft or conduits) for motor and mixed nerves and defects >3 cm. The disadvantages of autografts include potential donor site morbidity (from surgical harvest itself and/or resulting nerve deficit or painful stump neuroma formation) and limited availability.

Higgins and colleagues examined the suitability of several donor site options for digital nerve segments based on fascicle number and cross-sectional area. Distal to the common digital nerve bifurcation, the lateral antebrachial cutaneous nerve was most similar. From the wrist to the common digital nerve bifurcation, the sural nerve was most appropriate based on these two criteria (i.e., fascicle number and cross-sectional area).

In the major nerves of the upper extremity (i.e., axillary, radial, ulnar, median, and musculocutaneous nerves, nerve roots), often cable grafts, i.e., bridging a nerve gaps with multiple nerve cables, are needed. The sural nerve in combination with thin allografts (2–3 mm) is the preferred donor nerve choice of one author (Esther Vögelin). For smaller sensory nerve defects (<3 cm), the ipsilateral posterior interosseous cutaneous nerve of the wrist or allografts can be used ( Table 19.1 ).

Surgical techniques for graft repair.

Surgical tips are given in ( Box 19.3 ). After nerve resection back to healthy proximal and distal ends ( Fig. 19.6 ), the defect is measured. Donor nerve grafts are harvested at a length 20% longer than the defect size. When the recipient site is completed, the donor nerve is harvested and prepared. If multiple strands of nerve graft are needed, they may be fixed together with fibrin glue (Tisseel 2 mL, Baxter, Glattpark, Switzerland) to enable easy transfer and positioning. All nerve grafts have to be set in a retrograde orientation. This is important to ensure that every ingrowing axon is completely guided through the graft and into the distal nerve. If antegrade positioning is used, the risk of losing axons is high—especially in long nerve grafts, giving off several branches on their way.

(A) A scarred nerve defect. (B) Nerve resection to healthy ends. (C) Harvesting sural nerve graft. (D) Three incisions (arrows) . (E) Endoscopic harvest behind the medial malleolus (Courtesy of A.O. Grobbelaar). (F) Preparation of nerve cables. (G) *Fibrin sealant (Tisseel) at neurorrhaphy site. **Nerve autograft cables.

A no-tension repair should be achieved. At the completion of the repair, it is imperative that there is also only minimal tension on the repair site when the involved body part is put through passive range of motion on the operating room table ( Fig. 19.7 ). Postoperatively, the limb can be immobilized for a short time, but some surgeons do not immobilize and allow for free gliding.

A nerve graft is used to repair a defect. Nerve connectors (Axogen®) around proximal and distal graft repair sites.

Selections of graft methods.

Epineurial repair is the current preferred method for nerves in the upper arm, elbow, forearm, and hand. It is a general finding that a longer defect (3–5 cm) leads to a worse outcome no matter what methods are used. Allografts appear to be the choice of increasingly more colleagues.

Proximal to the hand, median, ulnar, and radial nerves are all mixed nerves. After the repair of mixed or motor nerves, such as the median and ulnar nerves, studies have demonstrated that autograft repair results in meaningful recovery in 60% to 80% of radial and median nerves and in 57% to 60% of ulnar nerves. For median nerve repairs up to 50 mm, 75% of patients experienced meaningful recovery, and for ulnar nerve repairs of similar criteria, up to 67%. Furthermore, in a more recent study of the author (Esther Vögelin) and colleagues, Leckenby et al reported a motor recovery rate of ∼67% was appreciated across a variety of repaired nerve defects up to 30 mm. Therefore studies are ongoing to establish if mixed or motor nerve defects less than 30 mm can be repaired equally well using processed nerve allografts compared to autografts. As reviewed in greater detail by Rbia and Shin, there is still insufficient evidence at this time to support their widespread use as alternatives to autografts for repair of mixed or motor nerve defects.

In the study of the author (Esther Vögelin) and colleagues, processed nerve allografts used to repair nerve defects between 30 and 49 mm yielded ∼75% meaningful sensory recovery but only 38% motor recovery. Similarly, defects greater than 50 mm yielded 53% sensory recovery, but only 10% recovery of meaningful motor function. Hoben et al postulate that longer grafts show increased accumulation of senescent markers, delayed angiogenesis, and environmental imbalance. Clinical findings indicate a larger defect in motor nerves is more difficult to recover..

For pure sensory nerve of a small defect, such as digital nerves, any method seems to work, but conduits are less popular than decades ago and allografts have become more popular, although the choices are very different among colleagues in different countries.

Later in this chapter, functional recovery after repair of different nerves and unsolved problems are detailed.

Proximal nerve defects: Nerve grafting and nerve transfers.

In proximal nerve defects, nerve autografts are used for the above-mentioned three reasons in combination with distal nerve transfers ( Table 19.2 ) ( Box 19.4 ).

Long nerve defects >6 cm.

Long nerve defects after tumor resection or injuries may be reconstructed with vascularized sural nerve grafts; 38 cm of vascularized medial sural nerve and 21 cm lateral sural nerve graft may be harvested as a vascularized nerve free flap. The free vascularized sural nerve graft combined with a fasciocutaneous posterior calf flap pedicled on the superficial sural artery offers a reliable solution for complex tissue and nerve defects.

Nerve connectors.

In nerve reconstructions with auto-/allografts, neurorrhaphy protectors (nerve tubes) may assist nerve regeneration. There are many commercially available products to promote nerve repair ( Table 19.3 ). In acute nerve repair and reconstructions with auto- and allografts, I have used veins in small sensory nerve repairs or porcine small intestine submucosa (collagen 1 and 3) as a nerve wrap to protect the neurorrhaphy site (Esther Vögelin). The advantage of the latter material is that it retains its ability to serve as an extracellular matrix scaffold remodeling the epineurium for the regenerating nerve. Vein connectors are natural barriers and have also been used to protect the neurorrhaphy site ( Table 19.3 ).

Surgical techniques for nerve connectors.

A synthetic nerve tube (e.g., Chitosan-material) (10 mm in length, 2.1 mm in diameter) or a small intestinal submucosa derived nerve connector (10 mm × 2–3 mm) is positioned at the proximal or distal site of the severed sensory nerve. Two to four 9-0 stitches are performed for the neurorrhaphy, and then the connector is pulled over the neurorrhaphy site and fixed by an additional 9-0 single stitch on each side. Alternatively, a nerve protector (open 10 × 10 mm folded around the nerve to form a tube) is wrapped around the neurorrhaphy site after the coadaptation. The tubes are irrigated with saline ( Fig. 19.7 ).

Outcomes and limitations of nerve connectors.

Sadek et al reported that patients with saphenous vein wrapping of ulnar nerve repairs had improved motor, sensory, and electrophysiological recovery compared with unmatched historical controls. Amniotic membrane wraps have also been described as a barrier to perineural fibrosis in chronic scarred nerve lesions. The most commonly reported improvements of coaptation aids ( Table 19.3 ) are improved sensory outcomes, reduced tenderness or pain at the coaptation site, and reduced operative time. The current clinical evidence data suggest that there is a better functional outcome in the short term, especially in sensory nerve repairs.

Treatment choices for nerve defects vary in regions and countries. However, in many regions worldwide it is considered that a short gap in a sensory nerve may be repaired with a connector with good recovery. Therefore the use of a connector is often for a short gap (<0.5–1 cm) in a sensory nerve. A connector is used for wrapping the surgically repaired nerve more often. Commonly, a longer defect is still repaired with a nerve autograft or allograft. The options, methods and indications of reconstruction are summarized in Table 19.1 .

Nerve transfers.

Nerve transfers provide the possibility of reanimating the muscles that normally perform a movement. The transfers are usually carried out near target muscles and therefore may be successful later after injury than direct nerve repair. However, they rely on nerve regeneration, which inevitably takes several months and is not predictable. Tendon transfer can give earlier return of function. The speed of recovery that the patient needs should therefore be taken into account. Other factors that should be considered include whether suitable nerve or tendon transfers are available, the age of the patient as nerve regeneration is more reliable in younger patients, and whether the nerve transfers will compromise secondary tendon transfer if unsuccessful.

For radial nerve injury, recommended nerve transfers comprise the FDS branch of the median nerve to the nerve to extensor carpi radialis brevis (ECRB) for wrist extension and the branch to the FCR to the posterior interosseous nerve for finger and thumb extension ( Table 19.2 ) ( Fig. 19.9 ). ^, This combination denervates the FCR and therefore reduces options for later tendon transfer. Ray and Mackinnon reported results in 19 patients who underwent nerve transfer at a mean of 6 months after injury. MRC grade 4 or 5 wrist extension was restored in 18 and grade 4/5 finger and thumb extension in 12, although additional tendon transfer for wrist extension was performed in nine patients. Although tendon transfer is generally reliable at improving function, Bertelli noted a limited range of digital extension and restricted wrist flexion after tendon transfer in comparison to nerve transfer.

The flexor digitorum superficialis (FDS) branch of the median nerve is cut and transferred to the nerve to the extensor carpi radialis brevis (ECRB) for wrist extension and the branch to the flexor carpi radialis (FCR) to the posterior interosseous nerve (PIN) for finger and thumb extension.

For high median nerve injury, branches of the radial nerve may be used to restore median nerve function. Transfer of the ECRB branch of the radial nerve is used to restore PT function and the supinator branch to restore AIN function ( Table 19.2 ), or the ECRB branch of the radial nerve is used to restore AIN function ( Fig. 19.10 ). An anterior forearm incision with step lengthening of the PT and release of the deep head facilitates the exposure. After identifying the donor and recipient, one branch to the ECRB is used for the pronator. The radial nerve branch to the ECRB can also be transferred to the AIN ( Fig. 19.10 ). This transfer has the advantage of allowing the synergistic motion of wrist extension and finger flexion, while preserving the synergistic motion of the ECRL and ECU to maintain wrist extension. Grip strength may be regained with transfer of the radial nerve branch to the supinator to the FDS. The nerve transfer to the AIN appears to have advantages over traditional tendon transfers, because one transfer may allow restoration of several functions and no postoperative immobilization is necessary. The nerve to the brachialis can be used to restore AIN function as well.

The transfer of the extensor carpi radialis brevis (ECRB) branch to anterior interosseous nerve (AIN) for median nerve function. (A) Before transfer: donor nerve is marked with green . (B) The AIN is cut at the site of branching from the median nerve and then connected to the transferred nerve. PIN, Posterior interosseous nerve.

For high ulnar nerve injury, besides surgical repair of the transected ulnar nerve at or proximal to the elbow, the terminal branch of the AIN can be dissected out and connected to the ulnar nerve at the wrist level in an end-to-side fashion by some surgeons ( Fig. 19.11 ). Some surgeons may prefer end-to-end anastomosis of the AIN to the motor branch of the ulnar nerve repair distally after the motor branch of the ulnar nerve (located in ulnar side of the nerve at the wrist level) is dissected out. This may shorten the time to innervate the intrinsic muscles of the hand. End-to-side anastomosis is also preferred by some surgeons, as this does not interfere with possible recovery of the ulnar nerve, especially its sensory recovery. Outcomes after nerve transfer for high ulnar nerve injury, particularly the AIN to the ulnar motor branch, are reported to outperform both isolated primary nerve repair and nerve grafting. ^, Questions remain regarding the mechanism of nerve regeneration of the end-to-side anastomosis, and outcomes of the transfer through end-to-side anastomosis are hard to evaluate. Nevertheless, it is a safe option as the ulnar nerve is not transected.

The transfer of the anterior interosseous nerve (AIN) to motor branch of the ulnar nerve. The AIN is identified and divided deep to pronator quadratus muscle and connected to the motor branch (located in the ulnar side) of the ulnar nerve. FDP, Flexor digitorum profundus; FDS, flexor digitorum superficialis.

Sensory transfer of the dorsal cutaneous branch of the ulnar nerve to the first and second web-space fascicles of the median nerve may help restore sensation of the median nerve. The third web-space fascicle of the median nerve and distal stump of the dorsal cutaneous ulnar branch (DCU) are coapted end-to-side to the ulnar nerve to recover protective sensation ( Fig. 19.12 ).

The third web-space fascicle of median nerve and distal stump of the dorsal cutaneous ulnar branch (DCU) are coapted end-to-side to the ulnar nerve to recover protective sensation. (A) Before transfer. (B) After transfer; insertion is the amplified view of the connection made.

Nerve transfer is used by only a small number of hand surgeons currently. Its benefits and limitations are not well defined yet. Especially for those patients of delay in repair or failure of recovery 1 year after surgery, tendon transfer is a conventional and reliable method to restore some useful function of the affected muscles. Tendon transfers are used by almost all hand surgeons. Therefore we suggest that readers learn about the timing and evidence of nerve transfers carefully before performing such surgery as this is still under investigation. Readers should also decide whether to perform tendon transfers versus nerve transfers.

Tendon transfers.

Many hand surgeons would regularly perform tendon transfer for these patients. The timing of tendon transfer is ideally 1 year after nerve repair or reconstruction. It is also often said to be 9–12 months or 6-18 months after nerve repair or grafting depending on the level of injury. A longer delay in tendon transfer would not affect the outcomes of tendon transfers. Nerve transfer should rarely be performed more than 1 year after nerve repair or reconstruction as nerve transfer aims to reinnervate the targeted muscles, which requires a viable end-plate of the nerve in the muscle, and avoid prolonged muscle atrophy. The timing should be taken into the careful consideration of the surgeons.

It is worth noting that tendon transfers are preferred by not few surgeons at an early time (e.g., immediately after injury) for the patients with a high nerve transection (proximal to the elbow), because the motor recovery is usually unpredictable or poor in these patients. It is reasonable to perform earlier tendon transfers to ensure function of the hand, not waiting for motor recovery of the repaired or reconstructed nerve. For these patients, it is advised that the direct repair or reconstruction should also be done, to offer some degrees of sensory recovery of the hand, because a hand after tendon transfers would not work well if there is no any sensation. Nerve repair or reconstruction may restore some degrees of sensation in the hand even the motor recovery of the nerve repair is not sufficient for hand function. These thoughts and advices are worth knowing and considering when one treats a patient with complete transection of a nerve trunk. For a nerve trunk partially transected proximal to the elbow, motor and sensory recovery is much better, which are not considered for early tendon transfer.

The principles and methods of tendon transfers are given in Chapter 21 solely for tendon transfers. Readers can refer to those contents for their decision on tendon transfer for failed nerve repair and reconstruction. We highlight some of these transfers later in this chapter (In-Depth Advice).

Digital nerves.

Digital nerves are commonly divided in the digits or palm of the hand as a result of lacerations. There may be associated damage to tendons and other structures. Outcomes can be assessed in terms of return of sensation in the area innervated by the affected nerve, usually the pulp of a digit (distal to the DIP joint). Outcomes of repair of single digital nerves are difficult to assess as improvement in sensation is possible due to crossover from the other digital nerve in a digit. In general, sensation rarely returns to normal in adults. In a systematic review of outcomes of digital nerve repair in adults, only level IV evidence was found. ^, Although protective sensation returned in most cases after nerve repair, normal or approaching normal sensation was regained in less than 25%.

Age is an important factor with younger patients doing better. In a series of secondary repairs of 254 digital nerves in 95 patients, Kallio et al found useful sensation (MRC grade S3 or S4) at long-term follow-up in 80% of nerves that were sutured and 56% of those grafted. All patients under age 15 years regained useful sensation, but only 26% of those over age 40. The outcomes were better after repairs performed less than 3 months from injury. The length of nerve graft was a factor, with only 15% of those with a graft over 5 cm gaining useful recovery.

Digital nerve repair may be complicated by painful neuroma formation. Dunlop et al found an overall incidence of 4.6% in the studies included in their review. There is a risk of hyperesthesia or unpleasant sensation, with Goldie et al reporting this in 12 of 30 digits. Cold intolerance is common, reported in a third of patients after 2 years.

Controversies exist about whether a single digital nerve needs repair; some consider the repair is to prevent painful neuroma. However, a digital nerve cut around the DIP joint does not need repair, as at this level it is small and cross-innervation to the pulp would occur.

Median and ulnar nerves.

The median and ulnar nerves are most often injured at the wrist or in the forearm commonly as a result of lacerations. Birch reported a large series of median and ulnar nerve repairs using the grading system described by Birch and Raji ( Tables 19.9 and 19.10 ). Outcomes are clearly better after primary suture compared with delayed suture or nerve grafting. Overall, these results suggest that about two-thirds of patients who have had primary repair have muscle power of at least MRC grade 4, can accurately localize touch, can recognize objects, and have 2PD of less than 8 mm on the fingertips.

TABLE 19.9

Results of Repair of 119 Median Nerves in Tidy Wounds from Distal Wrist Crease to Elbow Crease (Adults, Age 16 to 65 Years Old)

(Birch et al).

	NUMBER OF NERVES REPAIRED
Outcome	Primary Repair	Delayed Suture	Graft	Total
Excellent	5	1	0	6
Good	27	9	12	48
Fair	12	14	25	51
Poor or bad	2	7	5	14
Total	46	31	42	119

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