CHAPTER 74 MANAGEMENT OF NERVE INJURIES AND COMPRESSIVE NEUROPATHIES OF THE UPPER EXTREMITY
SCOTT A. MITCHELL AND KODI AZARI
PERIPHERAL NERVE INJURY
The peripheral nerve is a hierarchical structure in which the axon is the basic subunit. The endonerium surrounds individual myelinated axons or groups of unmyelinated axons. Collections of axons are gathered into fascicles by a layer of perineurium. The fascicle is the smallest subunit of peripheral nerve that can be surgically dissected. Within most peripheral nerves, fascicles are grouped together by condensations of internal epineurium. For instance, as the ulnar nerve approaches the wrist, distinct fascicular groups bound for the dorsal sensory, deep motor, and superficial sensory branches may be identified. The outermost layer of connective tissue, the external epineurium, encases the fascicular groups to form the peripheral nerve. The epineurium is typically surrounded by loose areolar tissue permitting nerve excursion with joint motion.
Common etiologies of peripheral nerve injury include penetrating trauma, traction, compression, electrical, and thermal injuries. Many injuries reflect a combination of these mechanisms. A variety of secondary processes, including infection, ischemia, and fibrosis, may contribute to further damage. Although the peripheral nerve may be injured in a variety of manners, it has a limited arsenal of responses. There are two basic pathophysiologic responses to trauma—demyelination and axonal degeneration. This primary distinction forms the basis for most classifications of nerve injuries. Mild injuries result in local demyelination along otherwise intact axons. Repair of the myelin sheath by residing Schwann cells typically restores function. More severe injuries affect the axons themselves, resulting in degeneration of the axons distal to the site of injury through the process of Wallerian degeneration. Regeneration of injured axons and re-innervation of distal targets are required to restore function.
Classification of Nerve Injury
There are two commonly used classification schemes for peripheral nerve injuries (see chapter 36). Seddon divided peripheral nerve injuries into three subtypes: neurapraxia, axonotmesis, and neurotmesis.1 Neurapraxia refers to a conduction block in which axons remain in continuity. In its mildest form, temporary neural ischemia produces a reversible physiologic conduction block. More severe forms result from focal demyelination at the site of injury. Axons remain anatomically intact but are unable to conduct across the injured segment. Prognosis for spontaneous recovery is typically good, although with more significant injuries remyelination may require several weeks. In the absence of secondary injury, full functional recovery can be expected within 2 to 3 months.
Axonotmesis refers to the loss of continuity of the axons within a peripheral nerve; however, all layers of the connective tissue architecture, including the endoneurial tubes, remain intact. Wallerian degeneration, a programmed involution of axonal segments, occurs distal to the site of injury. This process clears the endoneurial tubes of axonal and myelin debris in preparation for axonal regeneration. Axonal regrowth begins near the site of injury and progresses under ideal conditions at a rate of 1 mm/day. As the endoneurial tubes remain intact to guide regeneration, prognosis for recovery is favorable and functional recovery is anticipated.
Neurotmesis implies complete nerve transection with disruption of axons and all layers of investing connective tissue. There is degeneration of all axons distal to the site of injury as well as a physical separation of the nerve ends. Scar tissue formation within the intervening gap blocks advancement of the regenerating axons and results in a neuroma. Recovery will not occur unless the transected stumps are surgically coapted.
Sunderland expanded Seddon’s classification to delineate five degrees of nerve injury.2 First- and second-degree injuries are analogous to Seddon’s neurapraxia and axonotmesis, respectively. With third-degree injury, there is loss of continuity of the axons as well as the endoneurial tubes. The fascicular architecture and investing perineurium remain intact. Axonal regeneration will occur; however, specificity of reinnervation is compromised due to endoneurial disruption and prognosis is less favorable than with second-degree injuries. Fourth-degree injury refers to loss of continuity of the axons, endoneurial tubes, and perineurium, with only the outer epineurium remaining intact. This degree of injury often produces a neuroma in continuity due to intra-neural scaring that precludes significant spontaneous recovery. Fifth-degree injury, analogous to Seddon’s neurotmesis, refers to complete nerve transection.
During the early clinical evaluation of patients with traumatic peripheral nerve injuries, it is not possible to distinguish among these subtypes. The mechanism of injury may provide some guidance. Penetrating trauma tends to produce neurotmesis injuries. The zone of injury is typically small with sharp lacerations but may be more extensive with dull lacerations as stretching and tearing of tissues become more prominent. Traction tends to produce axonotmesis with a relatively extensive zone of injury. Acute compression generally produces neurapraxia due to local contusion. The surrounding inflammatory response, however, can contribute to subsequent scarring, chronic compression, and eventual axonal injury.
Electrodiagnostic Studies. Electrodiagnostic studies are useful objective tests to classify nerve injuries and identify early stages of recovery. Testing consists of two components: nerve conduction studies (NCSs) and electromyography (EMG). NCSs measure signal transmission along large myelinated axons, whereas EMG measures spontaneous and induced electrical activity within target muscles.
With neurapraxic or demyelinating lesions, NCSs demonstrate a conduction block across the zone of injury. With complete injuries, when the nerve is stimulated proximal to the lesion, distal potentials are absent. With incomplete injuries, a characteristic feature of demyelination is slowing of conduction across the lesion. When stimulated below the site of injury, however, conduction along the distal nerve segments remains normal. EMG demonstrates decreased voluntary motor unit action potentials. A defining feature of neurapraxic lesions on EMG is that no fibrillations or denervation changes develop regardless of the time since injury.
With axonal injury, including axonotmesis and neurotmesis, conduction both above and below the site of injury is disrupted due to axonal damage. Conduction abnormalities in the distal segment are not present acutely but develop over the first 1 to 2 weeks as axonal degeneration ensues. A characteristic feature of axonal damage on NCS in cases of incomplete lesions is decreased amplitude of distal potentials with normal conduction velocity. EMG demonstrates denervation potentials and fibrillations in affected muscles 3 to 4 weeks following injury. Their presence identifies axonal injury but does not discriminate between axonotmesis and neurotmesis lesions.
Clinical Management. Initial treatment decisions are based primarily upon injury mechanism and presumptive classification of the nerve lesion. Neurologic deficits in the context of penetrating trauma, even if incomplete, are assumed to represent neurotmesis injuries. Early surgical exploration is recommended. Primary repair is ideally performed within 72 hours of injury. For sharp, clean lacerations with minimal contusion of the nerve ends, primary repair may be performed at the time of initial exploration. If significant crush or avulsion is identified or in cases with unstable wounds, the nerve ends should be grossly approximated to prevent retraction. Definitive reconstruction should be delayed for 2 to 3 weeks to allow demarcation of the extent of nerve injury. Nerve grafts or conduits are typically required to span the resultant nerve gap.
For closed injuries in which nerve continuity is uncertain, an initial period of observation is recommended. Treatment decisions are based on the assumption that neurapraxic and axonotmetic lesions will recover spontaneously and these lesions are best treated nonoperatively. As early as 1 to 2 weeks following injury, electrodiagnostic studies can distinguish neurapraxic from axonal injuries. With neurapraxia, conduction distal to the site of injury remains intact, whereas with axonal injury, distal conduction is impaired due to axonal degeneration. Early studies may also determine whether a lesion is complete or incomplete. The presence of even a small number of motor units under voluntary control defines an incomplete lesion. This indicates that the nerve has not been completely transected and that surgery is less likely to be required.
Electrodiagnostic studies are traditionally repeated 4 to 6 weeks following traumatic injury. EMG evidence of target muscle denervation identifies the presence of axonal injury. However, the only way to differentiate axonotmesis from neurotmesis injuries, aside from surgical exploration, is to monitor the patient for signs of recovery. This critical distinction relies on the return of motor unit potentials following axonal regeneration, confirming the presence of an axonotmesis lesion. However, this is a retrospective diagnosis and intervention cannot be delayed indefinitely. There are a number of temporal factors to consider in determining the optimal timing of intervention for non-recovering deficits. With neurapraxic injuries, remyelination may require up to 8 to 12 weeks. With axonotmesis injuries, axonal regeneration proceeds at a rate of 1 mm/day under ideal conditions. Depending on the site of injury and distance to the nearest target muscle, evidence of early re-innervation will often become apparent within 3 to 6 months. However, a competing process occurs during this time that must also be considered. Irreversible atrophy gradually occurs in denervated muscle (estimated rate of loss of 1% per week) such that significant motor recovery is unlikely beyond 12 to 18 months. For this reason, if there is no clinical or electrodiagnostic recovery evident by 3 to 6 months after injury, surgical exploration is generally recommended. For chronic nerve injuries presenting beyond the 12- to 18-month window, tendon transfers should be considered.
Two common clinical scenarios deserve special mention. Gunshot wounds are considered apart from other penetrating traumas. Most deficits are secondary to concussive effects rather than direct laceration. The potential for spontaneous recovery is favorable and a period of observation as with closed injuries is recommended. Nerve deficits occurring in association with fractures are managed primarily based on the fracture. With closed fractures, 70% to 80% of nerve deficits are neuropraxic and may be managed nonoperatively. However, if internal fixation is indicated, nerve exploration may be reasonably performed during fracture exposure. The incidence of nerve laceration increases with open fractures. Early nerve exploration at the time of wound debridement is recommended. Definitive reconstruction should await fracture repair and stable wound coverage.
COMPRESSIVE NEUROPATHIES OF THE UPPER LIMB
Compressive neuropathies are among the most common clinical problems encountered in the upper limb. Each of the major peripheral nerves demonstrates a predilection for entrapment in specific anatomic regions. Although presentations vary based on the affected nerve and site of entrapment, the common pathophysiologic pathway reflects the mechanical and ischemic effects of chronic compression. In their early phases, compressive neuropathies resemble focal neurapraxias. With short-term compressive pressures of 30 mm Hg, there is disruption of intra-neural blood flow and loss of slow axonal transport.3 This manifests clinically as temporary paresthesias and muscle weakness. Increased vessel permeability following an episode of compression also causes intra-neural edema, which leaves the nerve more susceptible to further insults.3 More prolonged compression affects the myelin sheath, leading to focal demyelination beginning with large diameter sensory and motor fibers. In their chronic forms, compressive neuropathies are characterized by a mixture of demyelination and axonal loss. It is thought that the inflammatory reaction to compressive episodes, in conjunction with chronic ischemia and impaired axonal transport, ultimately lead to progressive fibrosis and axonal damage. The critical pressure or duration of compression required to produce axonal injury remains unknown.
COMPRESSIVE NEUROPATHIES OF THE MEDIAN NERVE
Carpal Tunnel Syndrome
The carpal tunnel refers to the fibro-osseous canal bounded by the concave bony arch of the carpus and the transverse carpal ligament (TCL). Although the tunnel is open-ended both proximally and distally, it behaves much like a closed compartment physiologically. Contents of the carpal canal include the median nerve and tendons of the flexor digitorum superficialis (FDS) and flexor digitorum profundus (FDP), and the flexor pollicis longus (FPL). The median nerve typically runs in a superficial and radial position (Figure 74.1). Near the distal aspect of the carpal tunnel, the median nerve divides into sensory branches to the thumb, index, middle, and radial ring fingers and the recurrent motor branch to the thenar musculature. Anatomic variations in the course of the recurrent motor branch are classified as extraligamentous, subligamentous, and transligamentous patterns, the latter being most vulnerable to injury during carpal tunnel release. The palmar cutaneous nerve arises 5 cm proximal to the wrist crease. It passes superficial to the TCL to supply the skin over the thenar eminence.
FIGURE 74.1. The median nerve in the carpal tunnel. (A) Note the superficial and radial position of the median nerve beneath the transverse carpal ligament. (B) The nearby ulnar neurovascular bundle passes superficial to the transverse carpal ligament as it courses through Guyon’s canal.
Carpal tunnel syndrome (CTS) represents the most common compressive neuropathy encountered clinically. Common comorbid conditions associated with increased risk of developing CTS include advanced age, female gender, obesity, diabetes, and pregnancy. A variety of additional etiologic conditions have been implicated, including hypothyroidism, rheumatologic and autoimmune diseases, alcoholism, and renal failure. Compression may also result from space-occupying lesions within the canal such as proliferative tenosynovitis, hematoma, tumors, or ganglion cysts. Displaced distal radius or carpal injuries may also diminish canal volume. Although CTS is often viewed as an occupational disorder, a causative relationship underlying the commonly cited association with cumulative or repetitive work activity such as keyboarding has not been objectively demonstrated.
The history and physical examination are cornerstones for diagnosis. Patients classically report intermittent numbness and paresthesias in the radial digits. Symptoms may be exacerbated with activities involving prolonged wrist flexion or extension and are characteristically relieved by shaking the hand. Nocturnal symptoms are considered a hallmark of CTS, and their absence should invite suspicion for alternate causes. In more severe cases, numbness and/or paresthesias become constant. Frequent dropping of objects and loss of coordination in the hand may be reported and likely reflect the combination of thenar weakness and impaired sensibility in the radial digits.
Examination may demonstrate decreased light touch sensation in the median innervated digits. Objective threshold tests including Semmes-Weinstein monofilament testing are more sensitive to detect early sensory loss compared with innervation density tests such as two-point discrimination. With advanced disease, weakness and atrophy of the thenar musculature develop. Several examination maneuvers have been described to aid in the diagnosis of CTS. Tinel’s nerve percussion test, Phalen’s wrist flexion test, and Durkan’s nerve compression test are among the most common tests. Provocative tests should reproduce paresthesias in the median nerve distribution.
Electrodiagnostic studies remain the primary objective test to diagnose CTS and are considered by many to represent the reference standard. The hallmark findings of compressive neuropathies on NCSs are an increase in distal latency and a decrease in conduction velocity. Although standards vary, distal motor latencies of greater than 4.5 ms and/or distal sensory latencies of more than 3.5 ms are generally considered diagnostic. A decrease in amplitude of distal potentials, indicative of axonal loss, may be seen in more severe cases. EMG may also demonstrate increased insertional activity, fibrillations, and denervation potentials in the thenar musculature with advanced disease.
Treatment decisions are based upon the duration and severity of symptoms, etiology, and patient preference. Nonsurgical measures include night splinting and corticosteroid injection. Both are more likely to be successful in patients with mild or recent-onset symptoms. Corticosteroid injection offers transient relief in 80% of patients; however, only 20% are expected to be symptom free 1 year later.4Injections may also be used diagnostically when alternative etiologies are being considered. A favorable response confirms the diagnosis and predicts successful outcome with surgical release. Nonoperative measures are less likely to benefit patients with prolonged symptoms or advanced disease with evidence of median nerve denervation. Surgical release should be considered in these cases.
Surgical release of the TCL is the most effective treatment for CTS.5 Release may be performed through either open or endoscopic approaches. Open release involves placement of a 2 to 4 cm incision in the base of the palm. The palmar fascia and TCL are incised longitudinally to expose the median nerve. Division is performed along the ulnar margin of the TCL to avoid injury to the motor branch. Release is carried distally to the superficial arch. Proximally, the deep antebrachial fascia is divided for a variable distance above the wrist crease. Adjunctive procedures including epineurotomy, internal neurolysis, routine tenosynovectomy, and reconstruction of the TCL have not been found to improve outcomes. Endoscopic techniques aim to minimize the problems of scar tenderness, pillar pain, and prolonged recovery that may be observed following open releases. Endoscopic procedures have been associated with shorter recovery time and a more rapid return to work.6 However, long-term outcomes are not substantially different from open decompression.
In the distal arm, the median nerve and brachial artery course between the biceps and brachialis muscles. The median nerve enters the forearm between the superficial humeral and deep ulnar heads of the pronator teres (Figure 74.2). It then passes beneath the proximal arch of the FDS to travel between the FDS and FDP muscles through the forearm. The anterior interosseous nerve (AIN) branches from the median nerve in the antecubital fossa roughly 4 cm distal to the medial epicondyle. The AIN typically arises from the radial aspect of the nerve and passes beneath both the deep head of the pronator teres and the FDS arch to course along the interosseous membrane in the forearm.
Proximal compressive neuropathies of the median nerve are very uncommon relative to CTS. Pronator syndrome refers to a constellation of signs and symptoms resulting from compression of the median nerve around the elbow. This syndrome was initially attributed to entrapment by the pronator teres muscle. Several additional potential sites of compression have been identified, including the ligament of Struthers (a fibrous band extending from an anomalous supracondylar process of the distal humerus to the medial epicondyle), the proximal fibrous arch of the pronator teres, intramuscular aponeurotic bands within the pronator, the proximal arch of the FDS, and by the leading edge of the bicipital aponeurosis.7
Clinically, patients with pronator syndrome present with aching pain in the proximal forearm and antecubital fossa accompanied by numbness and paresthesias radiating into the radial digits. These sensory complaints may be mistaken for CTS. Unlike CTS, however, symptoms primarily occur during activity and are rare at night. Distal sensibility may be diminished in the radial digits and over the thenar eminence in the palmar cutaneous nerve distribution. The latter is spared with CTS. Characteristically, motor weakness is absent in pronator syndrome. Tenderness to palpation in the antecubital fossa and a Tinel sign over the course of the nerve in this region further differentiate pronator syndrome from CTS. The pronator compression test involves manually compressing the median nerve at the proximal aspect of the pronator muscle for 30 seconds. Other provocative tests include resisted forearm supination, resisted forearm pronation with the elbow extended, and resisted middle finger proximal interphalangeal flexion. Positive tests should reproduce paresthesias in the median distribution. Electrodiagnostic tests are obtained primarily to exclude CTS or more proximal compression. However, abnormalities are present in only 30% to 50% of patients.
FIGURE 74.2. The course of the median nerve through the antecubital fossa. Common sites of compression include the bicipital aponeurosis, pronator teres, and fibrous proximal arch of the flexor digitorum superficialis (FDS).
Nonoperative treatment measures are recommended. The combination of rest, activity modification, anti-inflammatory medication, and temporary splinting relieves symptoms in approximately 50% of patients. In refractory cases, release is performed through a curvilinear incision across the antecubital fossa. All potential sites of compression from the ligament of Struthers through the pronator and FDS arcades are released. The AIN is also identified and decompressed through its passage beneath the deep head of the pronator and FDS arch.
Anterior Interosseous Nerve Syndrome
The AIN innervates the FPL, FDP to the index and middle fingers, and pronator quadratus. Patients with AIN syndrome present with loss of motor function in these muscle groups. FPL weakness and difficulty with pinch are often the most noticeable. Pain in the antecubital fossa may be present. However, because the AIN is a motor nerve, the paresthesias and distal sensory loss typical of carpal tunnel and pronator syndrome are absent. Patients have difficulty flexing the thumb interphalangeal (IP) joint and index finger distal interphalangeal (DIP) joint when asked to make an “OK” sign. Weakness of the long finger DIP joint flexion is typically less severe than in the index finger. Pronator quadratus weakness will not be apparent if tested with the elbow extended due to the strength of the pronator teres but may be unmasked if tested with the elbow in full flexion to relax the pronator teres.
Debate continues as to whether this rare entity represents a compression neuropathy or a peripheral neuritis akin to Parsonage-Turner syndrome. The latter should be considered if symptom onset was sudden and accompanied by severe antecedent pain. Attritional ruptures of the FPL and FDP tendons as seen with rheumatoid arthritis may also mimic the motor deficits of AIN syndrome. The presence of intact thumb and index finger tenodesis with wrist motion confirms tendon integrity.
Most patients with AIN syndrome improve without surgical intervention.8 An extended period of observation (3 to 6 months) has been recommended given this favorable natural history. The surgical approach for patients who have not demonstrated improvement during this period is similar to that described for pronator syndrome. The median nerve is identified proximally, and all potential constrictive sites across both the median nerve and AIN are released through the pronator muscle and FDS arcade.
COMPRESSIVE NEUROPATHIES OF THE ULNAR NERVE
Cubital Tunnel Syndrome
The ulnar nerve is a terminal branch of the medial cord of the brachial plexus. In the proximal arm, the nerve courses medial to the axillary artery in the anterior compartment. At the level of the mid-humerus, the nerve pierces the medial intramuscular septum and enters the posterior compartment. It then passes posterior to the medial epicondyle of the distal humerus and enters the cubital tunnel, bounded by the medial epicondyle, olecranon process of the proximal ulna, and the overlying arcuate ligament (Osborne’s ligament). The nerve then enters the forearm between the two heads of the flexor carpi ulnaris (FCU) and courses distally between the FCU and FDP muscle bellies.
Ulnar nerve compression at the elbow is the second most frequently encountered compressive neuropathy in the upper limb. Although multiple potential sites of compression across the elbow have been identified, the cubital tunnel proper is the most common. The floor of this fibro-osseous tunnel is formed by the medial epicondyle of the humerus and the olecranon process of the ulna. The roof is formed by Osborne’s ligament. Distally, this ligament is confluent with the proximal aponeurotic arcade spanning the two heads of the FCU origin. Within this tunnel, the ulnar nerve is subject to both longitudinal traction and direct compression. Due to the course of the nerve posterior to the axis of elbow motion, the nerve itself stretches 5 mm with full elbow flexion.9 The shape of the tunnel also changes dramatically with elbow motion. It transitions from a round contour in elbow extension to a flattened triangle with elbow flexion, reducing its cross-sectional area by over 50%.9
Multiple additional sites of compression of the nerve across the medial elbow have been identified and must be considered during surgical release (Figure 74.3). The most proximal site of potential compression is the arcade of Struthers, located on average 8 cm proximal to the medial epicondyle. This arcade is formed by an aponeurotic band extending obliquely from the medial head of the triceps fascia to the medial intermuscular septum. Hypertrophy of the medial triceps may exacerbate compression in this region. The intermuscular septum thickens and flares distally as it inserts onto the medial epicondyle and may be a site of potential compression. Most commonly, this is iatrogenic due to kinking of the nerve over its edge following anterior transposition. Compression at the medial epicondyle or retrocondylar groove may occur as a consequence of bony trauma, elbow arthritis, or valgus deformity. Instability of the ulnar nerve allowing subluxation out of the groove or frank dislocation over the epicondyle with elbow flexion may also cause neuritis. The most distal site of potential compression occurs 4 to 5 cm distal to the medial epicondyle as the ulnar nerve penetrates the deep flexor-pronator aponeurosis to course between the FDP and FDS muscles.
Patients with cubital tunnel syndrome present with intermittent numbness and paresthesias in the small and ring fingers. Symptoms are exacerbated by prolonged elbow flexion or direct pressure on the posteromedial elbow. Because the ulnar nerve has a relatively high proportion of motor fibers, motor dysfunction will predominate in more severe cases. The hand intrinsic muscles tend to be most affected. Early fatigue with repetitive activities, weakness of grip and pinch, and loss of dexterity may be noted.
FIGURE 74.3. The course of the ulnar nerve across the elbow. Note the five common sites of compression: arcade of Struthers, medial intermuscular septum, medial epicondyle, Osborne’s ligament, and deep flexor-pronator aponeurosis.
Examination characteristically reveals diminished light touch sensation in the small and ulnar ring fingers. Sensory loss over the dorsoulnar hand in the distribution of the dorsal sensory branch of the ulnar nerve distinguishes ulnar nerve compression at the elbow versus the wrist. The bulk and strength of the first dorsal interosseous should be compared with the contralateral side. Wartenberg sign, an abducted posture of the small finger most notable with finger extension, may be an early presenting sign of motor weakness. With more advanced disease, weakness of thumb pinch (due to both adductor pollicis and first dorsal interosseous dysfunction) may result in Froment’s sign (flexion of the thumb IP joint) or Jeanne’s sign (hyperextension of the thumb metacarpophalangeal [MP] joint) with attempted forceful pinch. Extrinsic weakness may be apparent in the FDP to the small finger, though FCU weakness is seldom encountered. With chronic severe compression, weakness and atrophy of the intrinsic musculature may produce clawing of the ring and small fingers.
The elbow is assessed for tenderness, deformity, crepitus, or loss of motion suggestive of bony or articular pathology. Instability of the nerve, defined as either subluxation or frank dislocation of the nerve from the epicondylar groove with elbow flexion, is assessed. Provocative tests include the presence of a Tinel sign over the course of the ulnar nerve and the elbow flexion test in which the elbow is placed in maximal flexion for up to 60 seconds. A combined elbow flexion-compression test, in which direct pressure is applied to the cubital tunnel proper during elbow flexion, enhances sensitivity of this maneuver. These maneuvers are considered positive if they reproduce paresthesias in the ulnar distribution. These provocative tests may cause paresthesias in 10% to 15% of normal individuals, and correlation with clinical symptoms is necessary.
Electrodiagnostic studies are helpful to confirm the diagnosis when symptoms or clinical findings are equivocal or if the site of compression is uncertain. Results are typically reported as conduction velocities rather than distal latencies as are standard in carpal tunnel testing. Motor conduction velocity of less than 50 m/second represents absolute slowing. Relative slowing by more than 10 m/second across the elbow compared with conduction through the forearm is also considered diagnostic. A drop in amplitude of compound muscle action potentials in the hypothenar and first dorsal interosseous muscles with stimulation of the nerve indicates axonal damage. EMG studies may demonstrate fibrillations, denervation potentials, and increased insertional activity in the ulnar innervated intrinsics with advanced disease.
For the majority of patients with mild, intermittent symptoms, nonoperative measures are appropriate. In many cases, avoiding provocative activities such as prolonged elbow flexion or resting the elbow on firm surfaces relieves symptoms. Night-time splinting of the elbow in a position of relative extension is commonly recommended. As many as 50% of cases in which symptoms have been present for 6 months or less will improve spontaneously.10 Surgical indications are based on the duration and severity of compression. In patients without objective muscle weakness, nonoperative management for at least 6 to 12 weeks is attempted. Surgery may be considered in patients with refractory symptoms. The development of weakness or atrophy of the intrinsic musculature should prompt surgical release.
A variety of procedures have been advocated including simple decompression (in situ decompression), medial epicondylectomy, and decompression with anterior subcutaneous, intramuscular, or submuscular transposition. Choice of surgical technique remains an intensely debated subject. In situ decompression involves incising Osborne’s ligament and releasing the fascial tunnel between the two heads of the FCU. The nerve is retained in its native bed following release. Advantages of this technique include limited dissection of the nerve and preservation of the surrounding vascular network. With the refinement of endoscopic techniques in recent years, in situ decompression has gained popularity. Relative contraindications include nerve instability or distorted tunnel anatomy such as with bony trauma and elbow arthritis.
Medial epicondylectomy combines decompression of the ulnar nerve with resection of the bony prominence of the medial epicondyle. Often described as a “mini-transposition” this technique allows the nerve to shift anteriorly to a path of least resistance while avoiding the more extensive dissection required for formal transposition. The medial collateral ligament of the elbow originates from the inferior margin of the epicondyle and may be injured with excessive bony resection, potentially resulting in elbow instability.
Anterior transposition addresses both direct compression and the longitudinal traction on the nerve that occurs with elbow flexion. All potential sites of compression are released from the arcade of Struthers through the deep flexor-pronator aponeurosis. The nerve is moved anterior to the medial epicondyle to run in a subcutaneous, intramuscular, or submuscular position relative to the flexor-pronator musculature. By transposing the nerve anterior to the axis of motion, tension is decreased with elbow flexion. Disadvantages include more extensive surgical dissection and potential compromise of the nerve’s blood supply. Submuscular transposition also requires release and repair of the flexor-pronator muscular origin.
Despite the frequency of cubital tunnel syndrome, there remains considerable controversy regarding choice of surgical technique. A common theme in the literature is that results are influenced heavily by the duration and severity of compression. A review of historical series found that all techniques provide similar favorable outcomes for patients with mild compression, but anterior submuscular transposition yielded the most satisfactory results with moderate or severe compression.10 More recent studies, however, suggest that in situ decompression provides similar if not improved outcomes compared to transposition with fewer complications.11
Ulnar Tunnel Syndrome
At the level of the wrist, the ulnar nerve and artery enter the ulnar tunnel, also referred to as Guyon’s canal (Figure 74.1). The roof of this canal is formed by the volar carpal ligament and the floor by the TCL (Figure 74.4). The ulnar border is formed by the pisiform and the radial border by the hook of the hamate. Within the canal, the nerve divides into a superficial sensory branch, supplying the palmar surfaces of the small and ring fingers, and a deep motor branch supplying the intrinsic musculature of the hand. The ulnar tunnel is typically divided into three zones based on this branching. Zone I is located proximal to the bifurcation. Zone II follows the deep motor branch as it dives deep beneath the fibrous arch of the hypothenar muscles and around the hook of the hamate. Zone I follows the superficial sensory branch as it courses along the fascia of the hypothenar musculature.
Compression of the ulnar nerve at the wrist is much less frequent than at the elbow. Ulnar tunnel syndrome most commonly results from either direct trauma or the presence of a space-occupying lesion. The latter are identified in almost half of the cases and include ganglia, anomalous muscle bellies, and benign tumors such as lipomas and neurilemmomas. Repetitive blunt trauma to the ulnar aspect of the palm, the so-called hypothenar hammer syndrome, has been associated with direct nerve injury, hook of hamate fractures, and thrombosis or pseudoaneurysms of the ulnar artery.
FIGURE 74.4. Schematic cross section of the wrist through Guyon’s canal. Note the superficial position of the ulnar neurovascular bundle relative to the carpal tunnel. The transverse carpal ligament forms the roof of the carpal tunnel and the floor of Guyon’s canal.
Presenting symptoms depend on the zone of compression within Guyon’s canal. Lesions in zone I typically cause both motor and sensory symptoms. Compression in zone II results in primarily motor symptoms and within zone III results in primarily sensory symptoms. When sensory involvement is present, a Tinel sign over the affected region will be present. Unlike cubital tunnel syndrome, sensation is spared in the distribution of the dorsal sensory branch of the ulnar nerve due to its takeoff proximal to Guyon canal. Motor involvement mimics that of cubital tunnel syndrome, with weakness of the intrinsic musculature. Examination should assess for tenderness over the hook of the hamate, an abnormal Allen test, or a pulsatile mass over the ulnar artery. Electrodiagnostic tests help distinguish ulnar tunnel syndrome from more proximal compression. Imaging studies include plain radiographs or computed tomography to assess for the hook of hamate fracture and magnetic resonance imaging (MRI) to assess for soft tissue anomalies. Ulnar artery thrombosis or pseudoaneurysm may be confirmed with Duplex ultrasound or angiography.
Nonoperative treatment should be considered in the absence of an identifiable cause of compression. Provocative activities should be identified and avoided. Wrist splints may also be helpful. Decompression is indicated in patients with refractory symptoms or space-occupying lesions. The ulnar nerve and artery are typically identified proximal to the wrist crease. The volar carpal ligament is divided over neurovascular bundle and the bifurcation of the nerve is identified. The motor branch arises from the deep surface of the nerve and passes beneath the proximal arcade of the hypothenar musculature. This fibrous arch is divided and the floor of the canal around the hook of hamate inspected for ganglions or other masses. The ulnar artery is assessed for thrombosis or aneurysm. If present, ligation or graft reconstruction is performed depending on the status of collateral circulation.
COMPRESSIVE NEUROPATHIES OF THE RADIAL NERVE
The radial nerve begins as a terminal branch of the posterior cord of the brachial plexus. The nerve passes from medial to lateral along the spiral groove of the posterior humerus. The nerve pierces the lateral intramuscular septum 10 to 12 cm proximal to the lateral epicondyle and travels between the brachialis and brachioradialis muscles. At the elbow, the nerve lies just anterior to the radiocapitellar joint. In the antecubital fossa, the radial nerve divides into the posterior interosseous (PIN) and superficial radial sensory (RSN) nerves. The RSN continues distally under the cover of the brachioradialis muscle. The PIN, however, dives deep into the radial tunnel just distal to the bifurcation. It courses beneath the proximal fibrous edge of the supinator as it wraps around the proximal radius to enter the posterior compartment of the forearm (Figure 74.5). As it exits the radial tunnel, the PIN divides into multiple motor branches to supply the extensor compartment musculature.
Compression Syndromes of the Posterior Interosseous Nerve
The radial tunnel refers to the anatomic surroundings of the PIN as it courses from the anterior to posterior compartment of the proximal forearm. Five potential sites of compression of the PIN within this tunnel are described. From proximal to distal, these sites include (1) fibrous or compressive bands anterior to the radiocapitellar joint between the brachialis and brachioradialis, (2) transverse crossing radial recurrent vessels at the level of the radial neck (the vascular leash of Henry), (3) fibrous bands along the proximal edge of the extensor carpi radialis brevis (ECRB), (4) the fibrous arcade formed by the leading edge of the supinator muscle (the arcade of Fröhse), and (5) the distal fibrous edge of the supinator fascia. The arcade of Fröhse is most commonly identified as the primary site of compression. This fibrous arch lies roughly 1 cm distal to the leading edge of the ECRB and is formed by a thickened aponeurotic band extending across the proximal edge of the superficial (humeral) head of the supinator muscle.
FIGURE 74.5. Dorsal approach to the posterior interosseous nerve (PIN) through the radial tunnel. The course of the PIN through the supinator is exposed deep to interval between the extensor digitorum communis (EDC) and ECRB muscles in the proximal forearm. Note the arcade of Fröhse at the proximal margin of the supinator, a common site of PIN compression. ECRL, extensor carpi radialis longus.
There are two distinct conditions that may result from compression of the PIN through the radial tunnel—radial tunnel syndrome (RTS) and PIN syndrome. PIN syndrome refers to a loss of motor function only without pain or sensory loss, whereas RTS refers to a pain-only syndrome without motor loss. Why two divergent syndromes may result from compression of the same nerve in the same anatomic region remains a subject of debate.
Radial Tunnel Syndrome. RTS is characterized by pain in the proximal/lateral forearm. Discomfort worsens with repetitive activity. Unlike most compression neuropathies, distal motor function and sensory function remain intact. This disorder shares many features of tennis elbow and distinguishing between the two disorders may be difficult. The characteristic pain and tenderness of RTS is located beneath the mobile wad 3 to 4 cm distal to that of lateral epicondylitis. Provocative exam maneuvers include pain with resisted forearm supination and pain with resisted middle finger MP joint extension. Electrodiagnostic studies are typically unrevealing in the absence of PIN syndrome. Because RTS is largely a clinical diagnosis without consistent objective findings, it remains a controversial diagnosis. Diagnostic injection of short-acting local anesthetic into the radial tunnel remains a useful test. A properly placed injection should produce a temporary PIN palsy. The relief of pain in conjunction with PIN palsy confirms RTS.
Nonoperative treatment is the standard for RTS and includes activity modification, splinting, stretching, and anti-inflammatory medications. Patients must avoid provocative activities involving prolonged elbow extension, forearm pronation, and wrist flexion. Little has been reported regarding the natural history of RTS or the efficacy of nonsurgical treatment. At least 3 months of nonoperative management is recommended prior to surgical intervention.
Decompression may be performed through either volar or dorsal exposures. All potential sites of compression are addressed. The volar approach utilizes the interval between the brachioradialis and FCR in the antecubital fossa. The dorsal approach uses the interval between the extensor carpi radialis longus (ECRL) and ECRB or between the brachioradialis and ECRL. The volar approach provides improved access to the proximal sites of compression; however, the distal aspect of the supinator may be difficult to reach. Conversely, the dorsal exposure provides excellent access to the PIN through the supinator muscle; however, access to the proximal most sites of compression may be limited. A combined approach working along both margins of the brachioradialis through a single incision may also be used.
Posterior Interosseous Syndrome. The PIN is the motor nerve to the extensor musculature of the dorsal forearm. PIN syndrome results from a compressive lesion causing motor weakness. This functional loss is painless, and sensory disturbances are absent. Patients present with difficulty extending the fingers and thumb. Wrist extension is spared due to more proximal innervation of the ECRL from the radial nerve proper, though radial deviation with wrist extension may be noted due to ECRB and extensor carpi ulnaris weakness. The classic differential diagnosis in a patient presenting with an inability to extend the digits and/or thumb includes attritional extensor tendon ruptures as seen in rheumatoid arthritis. The presence of intact tenodesis (passive MP joint extension with wrist flexion) confirms tendon integrity. Ruptures of the sagittal bands of the extensor mechanism with subluxation of the extensor tendons must also be considered.
In contrast to radial tunnel syndrome, electrodiagnostic abnormalities, including fibrillations and denervation potentials in the extensor musculature, are commonly identified. Imaging studies should also be obtained, including either ultrasound or MRI, as compressive soft tissue masses are often identified. Management in the absence of a space-occupying lesion begins with nonoperative measures for a period of up to 3 months. Supervised therapy and intermittent extension splinting of the MP joints are helpful to maintain passive mobility. If no recovery is evident by 3 months, surgical decompression is recommended. The surgical technique follows that of radial tunnel syndrome. Tendon transfers may be considered in chronic cases or those who fail to improve following decompression.
Wartenberg Syndrome. The superficial radial nerve leaves the cover of the brachioradialis in the distal forearm roughly 9 cm above the radial styloid. It passes through a narrow interval between the ECRL and brachioradialis tendons, as it enters the subcutaneous plane. Although the RSN may be compressed at any point along its course, it is most vulnerable as it passes along the sharp dorsal border of the brachioradialis tendon. Trauma is a common inciting factor for RSN compression. Direct blows, handcuffs, or tight wristbands have been implicated. Along its subcutaneous course, the RSN is also particularly sensitive to injury from surgical dissection or percutaneous hardware. Compression due to scarring around the nerve may contribute to refractory symptoms. Patients typically present with painful dysesthesias along the dorsum of the hand radiating into the thumb index and middle fingers. A Tinel sign localizes the site of compression. Because the RSN is a purely sensory nerve, any motor deficits should draw attention to more proximal sites of compression.
Spontaneous resolution of symptoms is common with Wartenberg syndrome and an extended course of nonoperative management is recommended. Because external compression is a common inciting and/or exacerbating factor, removal of any constrictive wear is essential. Corticosteroid injection may be attempted although efficacy is unpredictable. In refractory cases, surgical decompression may be achieved by division of the fibrous dorsal margin of the brachioradialis tendon.
1. Seddon HJ. A classification of nerve injuries. Br Med J. 1942;2:237-239.
2. Sunderland S. A classification of peripheral nerve injuries producing loss of function. Brain. 1951;74:491-516.
3. Rydevik B, Lundborg G, Bagge U. Effects of graded compression on intraneural blood blow. An in vivo study on rabbit tibial nerve. J Hand Surg Am. 1981;6:3-12.
4. Gelberman RH, Aronson D, Weisman MH. Carpal-tunnel syndrome. Results of a prospective trial of steroid injection and splinting. J Bone Joint Surg Am. 1980;62:1181-1184.
5. Hui AC, Wong S, Leung CH, et al. A randomized controlled trial of surgery vs steroid injection for carpal tunnel syndrome. Neurology. 2005;64: 2074-2078.
6. Trumble TE, Diao E, Abrams RA, Gilbert-Anderson MM. Single-portal endoscopic carpal tunnel release compared with open release: a prospective, randomized trial. J Bone Joint Surg Am. 2002;84-A:1107-1115.
7. Johnson RK, Spinner M, Shrewsbury MM. Median nerve entrapment syndrome in the proximal forearm. J Hand Surg Am. 1979;4:48-51.
8. Miller-Breslow A, Terrono A, Millender LH. Nonoperative treatment of anterior interosseous nerve paralysis. J Hand Surg Am. 1990;15:493-496.
9. Apfelberg DB, Larson SJ. Dynamic anatomy of the ulnar nerve at the elbow. Plast Reconstr Surg. 1973;51:79-81.
10. Dellon AL. Review of treatment results for ulnar nerve entrapment at the elbow. J Hand Surg Am. 1989;14:688-700.
11. Zlowodzki M, Chan S, Bhandari M, Kalliainen L, Schubert W. Anterior transposition compared with simple decompression for treatment of cubital tunnel syndrome. A meta-analysis of randomized, controlled trials. J Bone Joint Surg Am. 2007;89:2591-2598.