Peripheral nerves consist of a mixture of myelinated and unmyelinated axons. Motor, sensory, and sympathetic fibers often travel together in a single nerve. Axons are grouped in bundles termed fascicles, which are surrounded by perineurium. The fine connective tissue between axons within a fascicle is called endoneurium. Fascicles are held together as a nerve by the epineurium. Nerves are considered monofascicular, oligofascicular, or polyfascicular, depending on the number of fascicles. The relationship between fascicles changes along the longitudinal course of the nerve. The degree of fascicular change decreases distally. The mesoneurium, which is the connective tissue surrounding the epineurium, facilitates longitudinal gliding of the nerve.
After a nerve is injured, a number of changes occur. The somatosensory cortex reorganizes so the area represented by the injured nerve diminishes. The cell body of the lacerated axon increases in size. The production of materials for repair of the cytoskeleton is increased, and the production of neurotransmitters decreases. At the proximal segment of the injured axon, further proximal degeneration occurs based on the severity of the injury. In the axon distal to the laceration, Schwann cells phagocytose the axon, allowing the surrounding myelin tube to collapse.
Within 24 hours of injury, axonal sprouting occurs from the proximal stump. Multiple axons in a fascicle form a regenerating unit. The number of axons in the unit decreases with time. Longitudinal growth of the regenerating nerve depends on the ability of the axons to adhere to trophic factors in the basal lamina of the Schwann cell. Changes also occur at the distal end of the nerve. At the motor endplate, the muscle fibers atrophy. The sensitivity and number of acetylcholine receptors increase as their location expands from pits to the entire length of the muscle fiber. If the muscle fiber is reinnervated, both old and new motor endplates become active. The recovery of strength is greatest after primary nerve repair, less vigorous after repair with nerve grafting, and weakest after direct implantation of the nerve end into muscle. Muscle reinnervation occurs only if the axon reaches the muscle within a year. In contrast, sensory receptors may be effectively reinnervated years after injury.
Nerve injures are classified into three types. (1) Neurapraxia is a conduction block that occurs without axonal disruption. Recovery is usually complete within days to a few months. (2) Axonotmesis describes an injury in which axonal disruption occurs, with the endoneurial tube remaining in continuity. The intact endoneurial tube provides the regenerating sprouting axons with a well-defined path to the end organs. Because axonal growth occurs at approximately 1 mm/day, recovery is good but slow. (3) Neurotmesis refers to transection of the nerve. Unless the nerve is repaired, the regenerating axons cannot find a suitable path and recovery does not occur. The frustrated sprouting axons form a neuroma at the distal end of the proximal segment of the lacerated nerve.
Preoperative and postoperative assessment of motor and sensory function include quantitative measurement of pinch and grip strength, static and moving two-point discrimination, and vibration and pressure measurements. Two-point discrimination reflects innervation density, whereas vibration and pressure measurements gauge innervation threshold.
Nerve repair should be carried out with magnification and microsurgical technique. A tension-free repair provides the ideal environment for nerve regeneration. Tension at the repair site may be diminished by advancement of the nerve (ie, anterior transposition of the ulnar nerve for proximal forearm ulnar nerve laceration) or by limitation of joint motion. If a tension-free repair is impossible, nerve grafting is necessary to bridge the defect in the nerve. Frequently used donor nerves include the sural nerve, the anterior branch of the medial antebrachial cutaneous nerve, and the lateral antebrachial cutaneous nerve. Nerve defects of 2 cm or less may be managed by placing and securing the severed ends of the nerve within a conduit or adjacent vein that permits the uninterrupted regeneration of axons from the proximal nerve end.
Primary repair is preferred to nerve grafting because the latter procedure requires two sites of nerve coaptation. Epineurial repair is usually performed under magnification, using 8-0 or 9-0 suture (Figure 9–22A). When a particular fascicular group (eg, motor branch of the median nerve) is recognized as mediating a specific function, it may be repaired separately (Figure 9–22B). Postoperative therapy may include motor and sensory reeducation to maximize the clinical result.
A: Schematic diagram of epineurial repair technique. B: Group fascicular repair technique. (Reproduced, with permission, from Mackinnon SE, Dellon AL: Surgery of the Peripheral Nerve. New York: Thieme; 1988.)
Primary nerve repair is indicated after a sharp nerve division occurs. After avulsion injuries, repair even by nerve grafting cannot be performed until the proximal and distal extent of injury is known. When closed nerve injury occurs, sensory and motor function is closely monitored. If no recovery is seen within 3 months, electrodiagnostic studies are carried out. If no electrical evidence of recovery is documented, the nerve is explored, and neurolysis, secondary nerve repair, or nerve grafting is accomplished.
Compressive neuropathies are a group of nerve injuries that have common pathophysiology factors and occur at predictable sites of normal anatomic constraint. Nerve dysfunction is the result of neural ischemia in the compressed segment. Symptoms may resolve after release of the anatomic structures producing pressure on the nerve, particularly when compression is neither severe nor long standing.
Compression of the median nerve within the carpal tunnel is the most common upper extremity compressive neuropathy. The carpal tunnel is that space along the palmar aspect of the wrist anatomically bounded by the scaphoid tubercle and the trapezium radially, the hook of the hamate and the pisiform ulnarly, the capitate dorsally, and the transverse carpal ligament palmarly (Figure 9–23).
The Guyon canal and carpal tunnel and contents. (Cross section of supinated right wrist, viewed from proximal to distal.) Note the relationship between the transverse carpal ligament and the volar carpal ligament (partially resected). (Reproduced, with permission, from Reckling FW, Reckling JB, Mohn MP: Orthopaedic Anatomy and Surgical Approaches. St. Louis: Mosby-Year Book; 1990.)
Carpal tunnel syndrome is most often idiopathic. It is associated with pregnancy, amyloidosis, flexor tenosynovitis, acute or chronic inflammatory conditions, traumatic disorders of the wrist, endocrine disorders (diabetes mellitus and hypothyroidism), and tumors within the carpal tunnel.
Differential diagnosis includes compression of the median nerve or cervical roots in other anatomic locations. Diabetic neuropathy may produce symptoms similar to those of carpal tunnel syndrome, and patients with diabetic neuropathy may develop concomitant carpal tunnel syndrome.
Most patients complain of numbness in the thumb and index and middle fingers, though many note that the entire hand feels numb. Pain rarely prevents the affected individual from falling asleep but characteristically awakens the patient from sleep after a number of hours. After a period of moving the fingers, most patients are able to return to sleep. Many patients complain of finger stiffness upon arising in the morning.
Discomfort or numbness, or both, may be incited by activities in which the wrist is held in a flexed position for a sustained period of time (eg, holding a steering wheel, telephone receiver, book, or newspaper). Discomfort and pain may radiate from the hand up the arm to the shoulder or neck. The patient may complain of clumsiness when trying to perform tasks such as unscrewing a jar top and may experience difficulty in holding on to a glass or cup securely.
Atrophy of muscles innervated by the median nerve is visible in severe long-standing cases but is uncommon in most cases of recent onset. Weakness of the abductor pollicis brevis muscle may be detected by careful manual muscle testing.
Three provocative tests, the Phalen maneuver, the Tinel sign, and the wrist compression test, are helpful in establishing the diagnosis of carpal tunnel syndrome.
The Tinel sign is elicited by percussing the skin over the median nerve just proximal to the carpal tunnel; when it is positive, the patient complains of an electric or tingling sensation radiating into the thumb, index, middle, or ring fingers.
The Phalen wrist flexion sign, or Phalen maneuver, is usually positive in patients with carpal tunnel syndrome and is thought by many to be even more diagnostic than the Tinel sign. When this maneuver is performed, the elbow should be maintained in extension while the wrist is passively flexed (Figure 9–24). The time is then measured from initiation of wrist flexion to onset of symptoms; onset within 60 seconds is considered supportive of the diagnosis of carpal tunnel syndrome. Both the time to onset and the location of paresthesias should be recorded.
Phalen maneuver. (Reproduced, with permission, from American Society for Surgery of the Hand: The Hand: Examination and Diagnosis, 2nd ed. Philadelphia: Churchill Livingstone; 1983.)
Pressure over the median nerve proximal to the wrist provokes symptoms within 30 seconds. The test is confirmatory to other physical signs of median nerve compression.
Two-Point Discrimination Test
Two-point discrimination is often diminished in the finger pulps of patients with carpal tunnel syndrome. Sensation in the radial aspect of the palm should be normal, however, because the palmar cutaneous branch of the median nerve does not pass through the carpal tunnel.
Imaging studies are not routinely indicated for the management of carpal tunnel syndrome. MRI may be considered if a space-occupying lesion or tumor is suspected.
Nerve conduction velocities and electromyography help localize nerve compression to the wrist and evaluate residual neural and motor integrity. Nerve conduction velocity and electromyogram studies are indicated for patients who have failed conservative care and are considered candidates for surgery. A distal motor latency greater than 3.5–4.0 ms is the best indicator of carpal tunnel syndrome.
Because the pressure within the carpal tunnel increases if the wrist is held in sustained flexion (usual sleep posture) or sustained extension, the initial treatment of carpal tunnel syndrome should include a splint that maintains the wrist in a neutral position at night. Clinical improvement with this simple measure adds further support to the diagnosis of carpal tunnel syndrome. Activities that provoke symptoms may be modified with simple measures such as adjustment of keyboard height and rotation of repetitive job activities.
Injection of steroids into the carpal tunnel often decreases the inflammatory response around the flexor tendons and diminishes symptoms. To inject the carpal tunnel, a 25-gauge 1.5-inch needle is placed at the palmar wrist crease just ulnar to the palmaris longus tendon. If the palmaris longus is absent, a line along the radial border of the ring finger is drawn to the wrist crease. Before placing the needle, patients are told they may experience an electric shock sensation in the fingers. If this sensation occurs, the needle may be in the median nerve, and the injection should not be given. The needle is withdrawn and placed a few millimeters ulnar. When inserting the needle, first the skin is punctured, then a pop is felt as the needle passes through the transverse carpal ligament. A mixture of a short-acting anesthetic and steroid is injected. Transient relief of symptoms after injection suggests a greater likelihood of a favorable result after surgical decompression.
Patients unresponsive to conservative measures may benefit from surgical division of the transverse carpal ligament. This division may be accomplished through either direct open exposure or through an endoscopic approach. The open incision is made in the palm over the transverse carpal ligament, staying ulnar to the axis of the palmaris longus, along the longitudinal axis of the radial border of the ring finger. This incision avoids injury to the palmar cutaneous branch of the median nerve. After incising the palmar fascia longitudinally, the transverse carpal ligament is identified and sectioned longitudinally under direct observation. Endoscopic division of the transverse carpal ligament avoids a potentially tender palmar incision with either a single wrist portal proximal to the palm or with a combined proximal portal and short midpalmar portal along the axis of the open incision. Although some studies noted an earlier return to work activities after endoscopic release, the incidence of iatrogenic nerve and tendon injuries and late recurrence of symptoms from incomplete ligament division may be higher with endoscopic release than with open release. Both types of procedures are effective ways of treating carpal tunnel syndrome. The decision of which technique to use is based on the surgeon's experience. Endoscopic carpal tunnel release should not be used for treatment of recurrent carpal tunnel syndrome.
Patients are encouraged to actively move their fingers from the first postoperative day. Wrist motion is begun within the first week. Incisional tenderness often prevents patients from fully using their hands and returning to unrestricted work for the first 4–8 weeks. If patients have difficulty with hand function 3–4 weeks after surgery, a therapy program is prescribed consisting of desensitization, ROM, and strengthening.
The median nerve may be compressed in the proximal forearm by one or more of the following structures: ligament of Struthers, lacertus fibrosus, pronator teres muscle, or proximal fibrous arch on the undersurface of the flexor digitorum superficialis muscle.
Patients with pronator syndrome complain of pain that is usually more severe in the volar forearm than in the wrist or hand. Pain usually increases with activity. Complaints of numbness in the thumb, index, middle, and ring fingers may initially suggest the possibility of carpal tunnel syndrome. Night symptoms, however, are unusual in cases of isolated pronator syndrome.
Examination may reveal sensory and motor deficits similar to those seen in carpal tunnel syndrome, but significant differences may be detected on careful evaluation. Dysesthesia may include the distribution of the palmar cutaneous nerve. The Tinel sign is positive at the forearm level rather than at the wrist. The Phalen maneuver does not provoke symptoms. Patients may experience pain with resistance to contraction of the pronator teres or flexor digitorum superficialis muscles tested by resistance to forearm pronation or to isolated flexion of the proximal interphalangeal joints of the long and ring fingers.
Evaluation of symptomatic patients should include electrodiagnostic studies if a 6-week course of immobilization fails to effect improvement. Surgical treatment requires generous decompression of all potentially constricting sites.
Anterior Interosseous Syndrome
The anterior interosseous nerve branch divides from the median nerve 4–6 cm below the elbow. This branch of the nerve innervates the flexor pollicis longus, flexor digitorum profundus of the index and middle fingers, and pronator quadratus muscles. The anterior interosseous nerve may be compressed by the deep head of the pronator teres, the origin of the flexor digitorum superficialis, a palmaris profundus, or the flexor carpi radialis. In addition, accessory muscles connecting the flexor digitorum superficialis to the flexor digitorum profundus proximally and Gantzer muscle (the accessory head of the flexor pollicis longus) may impinge on the anterior interosseous nerve.
Patients affected with anterior interosseous nerve syndrome complain of inability to flex either the thumb interphalangeal joint or the index-finger distal interphalangeal joint. In contrast to those with pronator syndrome, these patients do not complain of numbness or pain.
Surgical decompression of the anterior interosseous nerve may be indicated when the syndrome does not spontaneously improve. All potentially compressing structures must be exposed and released.
The ulnar nerve is most commonly compressed at the cubital tunnel, along the medial side of the elbow. Compression may occur between the ulnar and humeral origins of the flexor carpi ulnaris or at the proximal border of the cubital tunnel because the nerve is tethered anteriorly with elbow flexion (Figure 9–25).
Points of constriction of the ulnar nerve at the elbow. (From Amadio PC: Anatomic basis for a technique of ulnar nerve transposition. Surg Radiol Anat 1986;8:155; used, with permission, from Mayo Foundation.)
Patients affected with cubital tunnel syndrome most often complain of paresthesia and numbness involving the ring and little fingers. Because symptoms may be aggravated or provoked by sustained elbow flexion, patients may complain of increased symptoms while talking on the telephone. Many patients complain of being awakened at night by the symptoms, most often when sleeping with the elbows flexed. Patients whose exam demonstrates weakness of muscles innervated by the ulnar nerve may note clumsiness and lack of dexterity.
A positive Tinel sign is noted when percussion over the ulnar nerve at the elbow provokes paresthesias along the ulnar forearm and hand. The nerve may be noted to sublux over the medial epicondyle as the arm is brought into flexion.
Motor strength should be assessed both in intrinsic muscles innervated by the ulnar nerve (first dorsal interosseous muscle) and in extrinsic muscles innervated by the ulnar nerve (flexor digitorum profundus of the little finger).
With weakness of the ulnar nerve–innervated adductor pollicis muscle, a positive Froment sign may be observed. As the patient tries to hold a piece of paper placed between the thumb and the index finger, the thumb interphalangeal joint flexes in an attempt to substitute flexor pollicis longus activity for inadequate adductor pollicis strength.
The ulnar nerve may be rendered symptomatic by fully flexing the elbow with the wrist in the neutral position. The elbow flexion test, a provocative maneuver, is considered positive if paresthesia is elicited in the ring and little fingers within 60 seconds. The location of the paresthesia and the time between initiation of elbow flexion and the onset of symptoms should be recorded.
Conservative treatment may include the use of an elbow pad to protect the nerve from trauma or a splint holding the elbow at approximately 45 degrees of flexion. The splint may be worn continuously or at night only, depending on the frequency and intensity of symptoms.
Electrodiagnostic studies should be obtained if conservative treatment does not alleviate the symptoms, particularly if motor weakness is evident. The reliability of nerve conduction studies at the elbow depends on the ability of the electromyographer to measure the length of the ulnar nerve accurately.
Numerous procedures are described to relieve ulnar nerve compression at the elbow. These include simple decompression of the ulnar nerve within the cubital tunnel or decompression with anterior transposition of the nerve subcutaneously, intramuscularly, or submuscularly into the flexor pronator mass. When the nerve is transposed, great care must be taken to excise the medial intermuscular septum proximally and to release the aponeurosis between the humeral and ulnar origins of the flexor carpi ulnaris distally, to avoid creating a new area of impingement.
An alternative surgical strategy involves decompression of the nerve and medial epicondylectomy. This technique removes the prominence against which the ulnar nerve is tethered with elbow flexion. After surgery, initial rehabilitation focuses on regaining elbow ROM. Strengthening begins at 4–6 weeks, and the patient is usually able to return to unrestricted work at 8–12 weeks.
The ulnar nerve passes from the forearm into the hand through the Guyon canal (see Figure 9–23). The anatomic borders of the Guyon canal are the pisiform and pisohamate ligament ulnarly, the hook of the hamate and insertion of the transverse carpal ligament radially, and the volar carpal ligament forming the roof of the tunnel.
Examination should document ulnar nerve sensory and motor integrity. In contrast to the findings in cubital tunnel syndrome, the Tinel sign is positive at the wrist rather than at the elbow. Extrinsic motor function is normal. The region of compression should be delineated by electrodiagnostic studies. In some cases, MRI studies demonstrate a space-occupying lesion such as a ganglion compressing the nerve within the Guyon canal.
When splinting is ineffective, surgical decompression should be considered. When symptoms exist in tandem with carpal tunnel syndrome, release of the transverse carpal ligament favorably alters the shape and size of the Guyon canal. Postoperative care is the same as following carpal tunnel release.
The radial nerve may be rendered symptomatic if compressed in the region of the radial tunnel. Points of impingement along the radial tunnel, located at the level of the proximal radius, include fibers spanning the radiocapitellar joint, the radial recurrent vessels, the extensor carpi radialis brevis, the tendinous origin of the supinator (arcade of Frohse), and the point at which the nerve emerges from beneath the distal edge of the supinator.
Because radial tunnel syndrome often occurs in combination with lateral epicondylitis, the two diagnoses are frequently confused. Patients with radial tunnel syndrome experience pain over the midportion of the mobile wad (brachioradialis, extensor carpi radialis longus, and extensor carpi radialis brevis muscles), whereas the pain experienced by patients with lateral epicondylitis is located at or just distal to the lateral epicondyle. Patients with radial tunnel syndrome experience pain when simultaneously extending the wrist and fingers while the long finger is passively flexed by the examiner (positive long-finger extension test). Patients with radial tunnel syndrome often also experience pain with resisted forearm supination.
Conservative treatment of radial tunnel syndrome includes measures to avoid forceful extension of the wrist and fingers. The wrist is splinted in dorsiflexion while the forearm is immobilized in supination. Persistent symptoms in spite of splinting may be treated by surgical decompression of the radial nerve. Concomitant lateral epicondylitis should be treated surgically at the same time that the radial nerve is decompressed.
Posterior Interosseous Nerve Syndrome
The radial nerve splits into the posterior interosseous nerve and the superficial sensory branch of the radial nerve after passing anteriorly to the radiocapitellar joint. The posterior interosseous nerve then passes beneath the origin of the extensor carpi radialis brevis, radial recurrent artery, and arcade of Frohse. The posterior interosseous nerve is most commonly entrapped at the proximal edge of the supinator, although entrapment may also occur at either the middle or the distal edge of the supinator muscle.
In contrast to radial tunnel syndrome, patients with posterior interosseous nerve syndrome experience extrinsic extensor weakness. Pain may be less than that of patients with radial tunnel syndrome.
Paralysis may be either partial or complete. Because the brachioradialis, extensor carpi radialis longus, supinator, and often extensor carpi radialis brevis are innervated by the radial nerve proximal to the posterior interosseous nerve branch, these muscles are spared. Digital extension at the metacarpophalangeal joint is the principal deficit from loss of extensor digitorum communis, extensor indicis proprius, and extensor digit quinti function.
The differential diagnosis in a patient with spontaneous loss of digital extension should include the possibility of multiple tendon ruptures in addition to possible radial neuropathy, particularly in patients with RA. The tenodesis effect, in which the fingers extend as the wrist is passively flexed, is preserved in posterior interosseous nerve syndrome but absent if the extensor tendons are ruptured.
Treatment of posterior interosseous nerve syndrome requires thorough decompression of the nerve. If motor recovery does not occur, tendon transfers restore digital extension.
The brachial plexus exits the base of the neck and upper thorax through the thoracic outlet. Anatomic boundaries of the outlet are the scalenus anterior muscle anteriorly, the scalenus medius muscle posteriorly, and the first rib inferiorly. Thoracic outlet syndrome, usually resulting from irritation of the C8- and T1-derived nerves, may be caused by a cervical rib, a fiber spanning from a rudimentary cervical rib, tendinous bands from the scalenus anterior to the medius muscles, or hypertrophic clavicle fracture callus. Poor posture with slumping shoulders and prolonged military brace position are both implicated as contributing factors.
The symptoms of thoracic outlet syndrome are often vague. Symptoms may include pain in the C8-T1 dermatome, with a variable degree of intrinsic muscle weakness. Patients may experience vascular symptoms if the axillary artery is simultaneously being compressed in the thoracic outlet region.
Physical examination of the patient with suspected thoracic outlet syndrome should include an elevated stress test, in which the patient's shoulders are kept extended and the arm is externally rotated 90 degrees at the shoulder. The patient is then asked to open and close the hands with the arms elevated for 3 minutes. Reproduction of symptoms is suggestive of thoracic outlet syndrome.
The Adson sign and the Wright test may be helpful in detecting vascular compression. In a positive Adson test, the radial pulse is obliterated when the patient holds a deep breath with the arm dependent and the headturned to the affected side. In the Wright test, the pulse is obliterated when the shoulder is abducted, externally rotated, and the head is turned away from the involved shoulder. In addition, this maneuver should reproduce the patient's symptoms. Physical examination should document C8 and T1 nerve root function: sensation along the inner border of the hand and forearm and hand intrinsic muscle strength.
Workup of the symptomatic patient should include radiographs of the cervical spine to rule out a cervical rib, electrodiagnostic studies to assess the function of the lower nerve roots, and Doppler studies of the arm in varied positions to assess compression of the axillary artery.
Initial treatment includes postural exercises. Patients who are unresponsive to conservative treatment or have demonstrable weakness may benefit from surgical resection of a cervical rib, resection of the first rib, or scalenotomy.
Cervical Root Compression
Cervical spine root compression may result in complaints of hand pain or weakness. It is useful to inquire routinely about pain or limitation of motion of the cervical spine. If the patient was involved in an accident involving sudden neck flexion and extension, this should be noted. Cervical root compression may occur from a herniated cervical disk, cervical spondylosis, intervertebral foraminal osteophytes, or, rarely, a cervical cord tumor.
Patients with cervical root compression most often complain of pain in a radicular rather than a peripheral nerve distribution. Despite symptoms involving the hand, most patients, when carefully questioned, are able to distinguish pain that begins in the neck and radiates to the hand from pain that begins in the hand and radiates proximally to the neck. Pain may be exacerbated with neck motion (flexion and extension, lateral bending, or rotation), coughing, or sneezing.
Physical examination of the patient with cervical radiculopathy frequently demonstrates either a decreased range of neck motion or pain with neck motion. Symptoms may be reproduced with axial compression on the patient's head (positive Spurling test). Detailed sensory and motor examination may reveal deficits in the domain of one or more roots.
The occasional simultaneous presentation of cervical radiculopathy with peripheral entrapment neuropathy is termed the double-crush syndrome. Whether compression at one level renders a nerve more vulnerable to compressive forces at a second level or whether such cases simply represent two common entities in the same extremity remains the subject of debate.
If a nerve is compressed at more than one location, the more symptomatic area is usually treated first. If both areas are equally symptomatic, the simpler of the two operations is chosen.
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