The long thoracic nerve originates directly from C5–C7 roots, before the formation of the brachial plexus. It innervates the serratus anterior muscle and has no cutaneous sensory representation (Fig. 65-2). Weakness of the serratus anterior is debilitating, because it stabilizes the scapula for pushing movements and elevates the arm above 90 degrees. This is the most common cause of scapular winging; it is best recognized by having the patient push against a wall. The inferior medial border is the most prominently projected away from the body wall. A dull shoulder ache may accompany this neuropathy. When severe acute pain occurs with the onset of scapular winging, brachial plexus neuritis should be considered.

Figure 65-2 Neuropathy about Shoulder.

The long thoracic nerve may be damaged by mechanical factors, including repetitive or particularly forceful injuries to the shoulder or lateral thoracic wall and by surgical procedures including first rib resection, mastectomy, or thoracotomy. It is one of the most common nerves to be affected by acute brachial neuritis, solely or in combination with others.

Scapular winging can also be related to scapular fracture and avulsion. Because they are surgically correctable, it is important to distinguish them from a primary long thoracic nerve injury. Furthermore, scapular winging can be caused by weakness of the trapezius (resulting from injury of the spinal accessory nerve) or the rhomboid muscles (resulting from a dorsal scapular nerve lesion). Inspection of the posterior shoulder region can provide diagnostic clues. Although the scapula is typically displaced medially in long thoracic nerve lesions, lateral deviation points to weakness of the trapezius or rhomboids. Scapular winging is a predominant feature in patients with facioscapulohumeral muscular dystrophy, where its bilateral representation and the other associated clinical features distinguish it from long thoracic nerve palsy.

Suprascapular Neuropathies

Clinical Vignette

A 25-year-old right-handed woman was evaluated for dull right shoulder pain and weakness. The symptoms were most noticeable during overhead activities. She had no sensory loss, and no injury had preceded the onset of her symptoms. Examination disclosed tenderness to palpation at the spinoglenoid notch. Shoulder position was normal; range of motion was full. Motor examination was significant for weakness of external shoulder rotation and mild atrophy of the infraspinatus muscle overlying the scapula. Reflexes and sensory examination were normal. These findings of infraspinatus atrophy, weak external rotation of the shoulder, and point tenderness over the spinoglenoid notch were consistent with a focal suprascapular neuropathy. Electromyography (EMG) demonstrated active denervation changes confined to the infraspinatus muscle consistent with the clinical diagnosis. A magnetic resonance image (MRI) of the right shoulder revealed a cystic lesion at the spinoglenoid notch, which was confirmed by surgical exploration.

The suprascapular nerve emerges from the upper trunk of the brachial plexus, receiving fibers from C5 and C6 roots. It does not have any cutaneous innervation. The suprascapular nerve first provides innervation to the supraspinatus muscle, a shoulder abductor, and then to the infraspinatus, a shoulder external rotator (see Fig. 65-1). The suprascapular nerve may be injured at the suprascapular notch, before the innervation of the supraspinatus muscle, or distally at the spinoglenoid notch, affecting the infraspinatus alone (see Fig. 65-2). The most common site of entrapment is at the suprascapular notch, under the transverse scapular ligament. Acute-onset cases result from blunt shoulder trauma, with or without scapular fracture, or from forceful anterior rotation of the scapula. The suprascapular nerve may also be affected by brachial plexus neuritis in isolation or with other nerves. Suprascapular neuropathies of insidious onset often occur subsequent to callous formation after fractures, from entrapment at the suprascapular or spinoglenoid notch, by compression from a ganglion or other soft tissue mass, or by traction caused by repetitive overhead activities such as volleyball or tennis.

Axillary Neuropathies

Clinical Vignette

A 72-year-old man had pain and weakness of the right arm following a fall. Evaluation in the emergency room disclosed an anterior dislocation of the right shoulder, which was reduced. Despite treatment, the patient continued to have difficulty raising the arm above the head. Electrodiagnostic testing several weeks later showed reduced recruitment pattern of motor unit action potentials in the right deltoid and teres minor muscles. The EMG was suggestive of stretch injury with demyelinating nerve injury without evidence of axon loss. The patient recovered spontaneously over the course of the following month.

The axillary nerve, along with the radial nerve, is a terminal branch of the posterior cord of the brachial plexus. It innervates the deltoid and the teres minor and provides sensory innervation to the lateral upper part of the shoulder via the superior lateral brachial cutaneous nerve of the arm (Figs. 65-1 and 65-3). In lesions of the axillary nerve, shoulder abduction is weakened and cutaneous sensibility of the lateral shoulder diminishes, overlapping the C5 dermatome. Because the teres minor is not the predominant external rotator of the shoulder, clinical isolation and testing are difficult. EMG may be necessary to define neurogenic injury to this muscle. Most axillary neuropathies are traumatic, related to anterior shoulder dislocations, humerus fractures, or both. Recognition of nerve injury may be delayed because of the shoulder injury. Acute axillary neuropathies can result from blunt trauma or as a component or sole manifestation of brachial plexus neuritis.

Figure 65-3 Cutaneous Innervation of the Upper Limb.

Musculocutaneous Neuropathies

Clinical Vignette

A 43-year-old woman presented to the laboratory for routine blood work after her annual physical examination. During phlebotomy in the right antecubital fossa, she experienced a sharp pain, radiating from the elbow to the wrist, which persisted for several days. She then developed numbness of the right lateral forearm. She had no weakness. Nerve conduction studies showed an absent sensory nerve action potential of the lateral antebrachial cutaneous nerve. The needle examination was normal.

The musculocutaneous nerve originates directly from the lateral cord of the brachial plexus. It innervates the coracobrachialis, biceps brachii, and brachialis muscles and terminates in its cutaneous branch, the lateral antebrachial cutaneous nerve. Isolated musculocutaneous neuropathies are rare. They have been reported in weight lifters, after surgery, and after prolonged pressure during sleep. Damage to the musculocutaneous nerve results in weakness of forearm flexion and supination and sensory loss of the lateral volar forearm (see Fig. 65-2). The biceps reflex is diminished, but the brachioradialis reflex (same myotome, different nerve) is preserved. More commonly, injury to this nerve occurs as part of a more widespread traumatic injury, usually involving the proximal humerus. The musculocutaneous nerve can also be preferentially involved in acute brachial plexus neuritis. Distal lesions of the lateral antebrachial cutaneous nerve may result from attempted cannulation of the basilic vein in the antecubital fossa. Rupture of the biceps tendon is a significant differential diagnostic consideration of musculocutaneous neuropathy.

Differential Diagnosis

The most common etiologies of shoulder pain are injuries to glenohumeral, subacromial, and acromioclavicular regions. Pain often may be reproduced by local pressure or provocative movements and positions. Rotator cuff tears can mimic nerve injury because of apparent weakness of shoulder abduction (supraspinatus) and external rotation (teres minor and infraspinatus). Motor neuron disease may begin in the shoulder region. It must be considered in the differential diagnosis of weakness without associated pain or sensory signs and symptoms. C5 radiculopathy also enters the differential diagnosis in patients reporting shoulder pain sometimes extending into the upper arm with weakness and numbness. This pain might originate within the scapular region and not the neck. Having patients flex their neck laterally in the direction of the symptomatic limb may reproduce the pain. Patients with C5 weakness have problems with shoulder abduction (deltoid and supraspinatus muscles), external rotation (infraspinatus), and arm flexion (biceps brachii). The biceps stretch reflex is often diminished. Paresthesias or sensory loss occurs in a discrete patch on the lateral proximal arm overlying the deltoid muscle.

Diagnostic Approach

EMG is the primary diagnostic tool in the evaluation of suspected shoulder mononeuropathies. It is particularly helpful to identify mononeuropathies affecting the shoulder girdle for several reasons. Neurogenic injury may go unsuspected because pain is the predominant symptom. Weakness may be hidden by the observation of normal strength within unaffected muscles performing similar functions, for example, supraspinatus weakness obscured by normal deltoid function. Conversely, nerve injury may be suspected because of apparent weakness caused by tendon rupture, only to be refuted by the absence of denervation on needle EMG. Although theoretically nerve conduction studies can be performed on the musculocutaneous and axillary nerves, their value is limited by technical factors. These nerves are typically accessible at only one stimulation site, precluding the determination of conduction velocities and accurate identification of conduction block. However, demyelination with conduction block may be suspected when a normal compound muscle action potential is obtained from a weak muscle; often, this finding portends an excellent prognosis. This conclusion should be reached cautiously because the same pattern may result from axon loss when the study is performed within the first week after injury, before wallerian degeneration has taken place.

Needle EMG can identify even subtle axon loss by the detection of fibrillation potentials. The evaluating physician and the electromyographer should always examine the patient and consider every potential neuropathic cause of shoulder pain. Otherwise, uncommon neuropathies can easily be overlooked.

A common clinical dilemma occurs with patients who have nontraumatic shoulder girdle mononeuropathies. It is difficult to differentiate a primary idiopathic lesion from a limited form of brachial plexus neuritis and to determine whether entrapment or a related process necessitating surgical exploration is involved. A thorough clinical and electrodiagnostic examination is thus required. Subtle clinical or electrodiagnostic evidence of involvement of muscles innervated by a different nerve usually suggests that a conservative approach is indicated, as this constellation of findings speaks against compression of a single nerve.

Routine radiographs are useful to detect scapular fractures secondary to acute injuries, which sometimes predispose patients to suprascapular neuropathies or serratus anterior dehiscence from the scapula. MRI can define insidious-onset neuropathies that may be caused by expanding masses, for example, a ganglion cyst in the spinoglenoid notch.

Management and Prognosis

Unfortunately, shoulder bracing provides little benefit to patients with shoulder girdle weakness. Exercises to strengthen other shoulder girdle muscles may provide partial functional compensation. If nerve transection from acute penetrating injury is suspected, surgical exploration and primary anastomosis should be considered, although results are mixed. In acute nonpenetrating injury, exploration can be considered after 3–6 months, provided no clinical or electrodiagnostic evidence of reinnervation exists. Nerve grafting is an option if unanticipated nerve transection is found. For insidious-onset neuropathies without defined cause, imaging should be considered to exclude ganglion cysts or other masses. If no mass is demonstrable and the patient shows no evidence of improvement, exploration may be considered, particularly at potential sites of entrapment such as the suprascapular or spinoglenoid notches.

Despite apparent axonal injury in brachial plexus neuritis, there is a good prognosis for functional recovery. Unfortunately, this recovery typically takes 6 months to 2 years. The prognosis for direct compressive injury is less predictable and probably depends on reinnervating distance, patient age, and attendant comorbidities. Stretch injuries and entrapment have the highest likelihood of a significant demyelinating component, with excellent outcome being the rule, particularly if entrapment is recognized and removed before significant axon loss occurs.

Median Mononeuropathies

The anatomy of the median nerve is important in understanding the signs and symptoms of entrapment lesions at the level of the wrist, versus the more proximal lesions. The median nerve provides essential motor and sensory function to the lateral aspect of the hand (Fig. 65-4). It supplies the intrinsic hand muscles of most of the thenar eminence and innervates several forearm muscles. Its major sensory role is to provide innervation for the thumb, index, and middle fingers and the lateral half of the ring finger.

Figure 65-4 Median Nerve.

The median nerve is formed by lateral and medial cord fibers of the brachial plexus. The lateral cord carries mainly sensory fibers from C6–C7 roots and provides the sensory innervation to the thumb and the first two and a half fingers. It also contains motor fibers from the C6-C7 roots, which contribute to the innervation of the forearm muscles. The medial cord carries motor fibers from the C8-T1 roots that innervate the thenar eminence. The distal median nerve at the wrist is the primary site of clinical involvement in carpal tunnel syndrome. More proximal lesions at the elbow are far less common.

Distal Median Entrapment

Clinical Vignette

A 45-year-old factory worker presented with a 3-year history of intermittent right hand tingling. Initially, this had occurred only in the morning on awakening. In recent months, his symptoms had awoken him at night, interfering with his sleep. He reported that “all” digits were affected and that the paresthesias were sometimes accompanied by aching of the wrist and forearm. Shaking of the hand relieved the discomfort. There was no decline of hand strength. Neurologic examination disclosed minimal weakness of right thumb abduction without loss of thenar eminence bulk. Results of reflex and sensory examinations were normal, including 2-point discrimination and graded monofilament touch. The symptoms were reproduced by nerve percussion over the median nerve at the wrist (Tinel sign).

Etiology and Epidemiology

Carpal tunnel syndrome (CTS) is common and associated with high economic costs. The lifetime risk of acquiring CTS might be as high as 10%, with an approximate annual incidence of 0.3% and a peak in the 6th decade. CTS is more than three times more prevalent in women than in men and often affects both hands. The incidence is substantially increased in the working population, particularly blue-collar workers. Carpal tunnel syndrome has been associated with numerous other conditions, such as pregnancy, endocrine disorders (hypothyroidism, acromegaly, diabetes), rheumatoid arthritis, sarcoid, hemodialysis, and amyloidosis. However, most of the cases are idiopathic, related to repeated stress to the nerve, followed by edema, ischemia, and demyelination of the median nerve at the wrist. If the trauma is severe or prolonged enough, axonal loss ensues.

Clinical Presentation and Testing

Median nerve entrapment at the wrist commonly presents with intermittent symptoms, including pain and paresthesias in the hand and forearm. The symptoms tend to occur on awakening or at night, and they are often provoked by certain postures or activities such as reading or driving (Fig. 65-5). The perception that paresthesias may affect all digits (rather than just the lateral three and a half innervated by the median nerve) is likely related to the greater cortical representation of the thumb and first two fingers. As CTS progresses, persistent numbness ensues, alerting the patient that the precise sensory distribution involves the volar surface of the first three and a half digits. The neurologic examination, particularly in mild CTS cases, may offer few clues. It is helpful in severe cases, in which atrophy of the thenar eminence is common. Median hand functions, primarily thumb abduction and opposition, are weak. Having the patient supinate the forearm so the palm is flat, and then raise the thumb vertically against resistance, tests the abductor pollicis brevis muscle. Forearm muscles supplied by the median nerve proximal to the flexor retinaculum are spared in CTS.

Figure 65-5 Carpal Tunnel Syndrome–I.

Provocative tests offer supportive but not diagnostic evidence in suspected CTS (Fig. 65-6). A positive Tinel sign consists of an electric, shooting sensation (not just local discomfort) radiating into the appropriate digits with wrist percussion. Tinel and Phalen maneuvers (reproduction of paresthesias on forceful flexion of the wrist) should be performed with nonleading questions to improve response credibility. It is recommended that the Phalen maneuver be maintained for at least 1 minute before determining that the result is negative. The pressure test may be the most reliable of the three maneuvers; pressure is placed over the carpal tunnel (proximal palm, not wrist) for 20–30 seconds, attempting to reproduce paresthesias in a median nerve distribution.

Figure 65-6 Carpal Tunnel Syndrome–II.

Differential Diagnosis

Diagnosis of CTS is usually straightforward, although other conditions may mimic CTS. The assessment of the patient needs to incorporate clinical and electrophysiologic data, as more than 10% of the asymptomatic general population might have abnormal nerve conduction parameters suggestive of CTS. The most common differential diagnosis is a C6–C7 radiculopathy, in which numbness occurs in a similar distribution, that is, digits 1 through 3. Patients with a radiculopathy usually have neck or radicular pain. Nerve conduction studies and needle EMG can differentiate these entities. Although the muscles of both thenar and hypothenar eminence originate from the C8 root, its sensory territory is confined to the medial aspect of the hand and arm. The C8 root also innervates the flexor digitorum profundus of digits 4 and 5 and the extensor indicis proprius muscles via the ulnar and radial nerves, respectively. Ulnar neuropathies have an entirely different pattern of motor and sensory loss.

Carpal tunnel syndrome virtually never presents with predominant motor symptoms. If thumb abduction is weak, evidence of other motor involvement should be sought to confirm a different lesion. Weakness and atrophy confined to the median forearm muscles suggest a proximal median nerve lesion, particularly at the elbow (pronator syndrome). If more widespread weakness is demonstrated, with the absence of sensory signs or symptoms, motor neuron diseases or multifocal motor neuropathy require diagnostic consideration.

A more widespread polyneuropathy should be excluded. This can occur particularly in patients with diabetes, who may not be as aware of sensory loss in their feet compared with their hands. Clinical examination and EMG usually clarify this issue. Plexopathies typically produce motor and sensory dysfunction within multiple nerve distributions in a single extremity and pain in the shoulder region. They rarely enter the CTS differential diagnosis. Although it is uncommon for CNS disorders to produce sensory signs and symptoms within the distribution of a single peripheral nerve, occasionally cervical spinal cord lesions, such as cervical spinal stenosis or intrinsic cord tumors, and very rarely focal frontoparietal brain lesions, may mimic CTS. Vitamin B₁₂ deficiency and syringomyelia are considerations in patients with bilateral hand numbness.

Management

Data regarding the natural history of CTS is scarce. Twenty to 30% of hands appear to improve spontaneously over 1–2 years, but this might in part be due to lifestyle changes, and long-term follow-up is not available. There are few randomized controlled trials comparing different treatment modalities. Treatment recommendations are further complicated by conflicting data as to whether clinical features or electrophysiological parameters can predict treatment outcome.

Conservative therapies should be considered first, as carpal tunnel release surgery carries a risk of potentially serious complications, such as reflex sympathetic dystrophy (complex regional pain syndrome), injury to the median palmar cutaneous branch, and hypertrophic scar. Ergonomic workplace alterations and avoidance of offending activities or positions are generally recommended. Neutral wrist splints, typically worn at night, initially help more than 50% of patients by maximizing the carpal tunnel diameter and minimizing nerve pressure, which is better than the natural remission rate. Local steroid injections may provide temporary pain relief with an initial success rate almost as good as surgical therapy. However, this is rarely a permanent solution, as there are frequent relapses requiring repeated injections, and there is the possible risk of flexor tendon rupture. Nonsteroidal anti-inflammatory drugs, vitamin B₆, and diuretics are of no proven benefit.

Surgical decompression is offered to patients with increasingly annoying sensory symptoms and progressive abnormalities on neurologic examination and electrophysiological testing (see Fig. 65-6). Although published success rates vary significantly, the average surgical success rate is 75%; 8% of patients may worsen after surgery. Long duration of symptoms, increasing age, and the presence of workers compensation claims appear to be associated with poorer outcome. Patients with moderate electrophysiological abnormalities appear to do best, and the success rate of surgery in the absence of nerve conduction abnormalities is only 51%. Occasionally, patients present with end-stage CTS and absent motor responses on nerve conduction studies. Resolution of pain is the only realistic goal of surgical intervention for these patients. Meaningful return of thenar strength is less likely this late in the course of the neuropathy. Endoscopic techniques are being used in carpal tunnel decompression but the relative benefit of this technique compared with traditional decompressive surgery is not known.

Proximal Median Neuropathies

Clinical Vignette

A 36-year-old secretary complained of difficulty holding a pen and snapping her fingers to music for 6 months. The onset of weakness had been preceded by an aching pain in the volar forearm. There was no sensory loss. The patient had delivered healthy twins 3 months prior to presentation. Neurologic evaluation demonstrated weakness of the flexor pollicis longus muscle and the median-innervated portion of the flexor digitorum profundus, manifested by the inability to flex the distal phalanx of the thumb and the index and long fingers.

EMG confirmed active and chronic denervation in the flexor pollicis longus, flexor digitorum profundus 2 and 3, and pronator quadratus muscles. MRI of the forearm showed evidence of atrophy in the muscles supplied by the anterior interosseous nerve, but no other abnormalities were detected. Surgical exploration revealed entrapment of the anterior interosseous nerve by the deep head of the pronator teres muscle.

Median neuropathies arising rostral to the most proximal muscle innervated by the median nerve (the pronator teres) occur at a frequency of less than 1% of that of CTS. In a very small proportion of the population, there is a bony spur that originates from the shaft of the medial humerus, proximal to the medial epicondyle. A tendinous band called the ligament of Struthers stretches between these two structures and may represent a site of compression for the median nerve. More distally, in the antecubital fossa, the median nerve may become entrapped beneath the lacertus fibrosus, a fibrous band that runs between the tendon of the biceps and the proximal flexors of the forearm. Even more distally, the nerve can become entrapped in the substance of the pronator teres muscle or beneath the sublimis bridge of the flexor digitorum superficialis muscle (pronator teres syndrome).

The clinical and electrophysiologic recognition of weakness in the distribution of the forearm muscles innervated by the median nerve is the diagnostic key (Fig. 65-7). When the median nerve lesion is most proximal, the pronator teres muscle is involved and may be atrophied. Clinical features also include pain in the volar forearm exacerbated by physical activity. There is weakness of thenar muscles and sensory loss in the thumb, index finger, long finger, and lateral aspect of the ring finger.

Figure 65-7 Proximal Compression of Median Nerve.

Mechanical lesions within the axilla, secondary to shoulder dislocation or penetrating injury, may also affect the proximal median nerve, although concomitant injury of other nerves often exists. More distal lesions of the proximal median nerve include humeral fractures, elbow dislocations, tourniquet compression, and forms of penetrating trauma, such as catheterization of the antecubital veins.

EMG is the crucial initial study. Imaging studies, particularly MRI of the elbow region, are indicated when EMG results are positive. Focal lesions, such as the bony origin of a ligament of Struthers or a venous infarction secondary to tourniquet compression, may be defined on neuroimaging.

Conservative treatment consists of rest and anti-inflammatory medications. In patients with severe symptoms and electrodiagnostic evidence of axonal loss, surgical exploration of the median nerve in the proximal forearm should be considered.

Anterior Interosseous Neuropathies

The anterior interosseous nerve is the largest motor branch of the median nerve. It does not supply any sensory innervation to the skin, but does carry sensory fibers to the muscles of the forearm and interosseous membrane. It arises about 5–6 cm below the elbow. The muscles supplied by the anterior interosseous nerve are flexor pollicis longus, flexor digitorum profundus to the second and third digits and pronator quadratus. Possible etiologies for anterior interosseous neuropathy are aberrant fibrous bands, fractures, compression by the deep head of the pronator teres muscle, pregnancy, brachial plexus neuritis, which might present as a multifocal neuropathy, or idiopathic.

Anterior interosseous neuropathy usually presents with nonspecific pain in the proximal forearm. The motor symptoms include weakness of forearm pronation with the elbow flexed and weakness of distal phalanx flexion of the thumb, the index finger, and the long finger. Affected persons cannot form a circle by pinching their thumb and index finger. This presentation is similar to more proximal median neuropathies but without involvement of the pronator teres. Furthermore, there is no sensory involvement.

The treatment, depending on etiology, may be nonsurgical or surgical. Rest, anti-inflammatory medications, and splints can help. Surgical treatment includes exploration of the nerve.

Ulnar Mononeuropathies

The ulnar nerve primarily innervates intrinsic hand muscles, including all hypothenar muscles (Fig. 65-8). The muscles of the thenar eminence supplied by the ulnar nerve are the adductor pollicis and part of the flexor pollicis brevis. Only two forearm muscles have ulnar innervation, the flexor carpi ulnaris and the medial part of the flexor digitorum profundus. The ulnar nerve also supplies sensation to the medial one and a half fingers (the medial aspect of digits 4 and 5), on the dorsal surface sometimes the medial two and a half fingers (see Figs. 65-3 and 65-8). Manifestations of ulnar neuropathies vary with location and severity. Progressive motor deficits lead to the classic “claw hand,” with hyperextension of the fourth and fifth metacarpophalangeal joints and flexion of the proximal and distal interphalangeal joints (Fig. 65-9). This is most pronounced when the patient is asked to open the hand because of the unopposed action of radial nerve–innervated muscles. Similar to its median counterpart, the ulnar nerve is typically affected at two anatomic loci, the elbow and wrist, however, in reverse frequency. The majority of ulnar nerve lesions occur at the elbow (Fig. 65-10).

Figure 65-8 Ulnar Nerve.

Figure 65-9 Ulnar Tunnel Syndrome.

Figure 65-10 Compression of Ulnar Nerve.

Proximal Lesions

Clinical Vignette

A 55-year-old man presented to the emergency room afraid he was having a heart attack. He had suddenly experienced sharp, shooting pain radiating from the left elbow distally, associated with tingling of the hand. Upon further questioning, the patient mentioned occasional tingling of digits 4 and 5 of the left hand for several years. He was an avid reader and frequently read with his elbows resting on his desk.

The neurologic examination revealed decreased light touch in the left ring finger and little finger, splitting the ring finger. There was minimal weakness of finger abduction, and a Tinel sign at the left elbow was present.

Electrodiagnostic testing showed a demyelinating left ulnar neuropathy at the elbow.

Proximal ulnar neuropathies are second only to CTS in frequency. Etiologies include external compression or entrapment at the elbow after remote elbow trauma (tardy ulnar palsy), and entrapment just distal to the elbow joint (cubital tunnel syndrome, Fig. 65-11).

Figure 65-11 Cubital Tunnel Syndrome.

Numbness and paresthesias of the fifth and sometimes half of the fourth digit are the rule and may be provoked by having the patient maintain a fully flexed elbow posture for 30 to 60 seconds. Sensory signs or symptoms should not extend proximal to the wrist, in which case a C8 radiculopathy has to be considered in the differential diagnosis. Weakness of the intrinsic muscles of the hand is more common in ulnar neuropathies than in CTS. Clinically apparent involvement of ulnar forearm muscles is rarely detected. Sometimes, there is associated aching of the elbow or forearm pain. The diagnosis is confirmed by EMG. High-resolution sonography can be helpful, when precise localization of the lesion by EMG is difficult, but is not routinely performed.

Distal Lesions

Clinical Vignette

A 40-year-old jackhammer operator noted progressive wasting of muscle bulk in the right hand. He had no pain or sensory loss. He had read about his symptoms on the Internet, and he became concerned he might have Lou-Gehrig’s disease.

On neurologic examination, the patient had difficulty holding a piece of paper between the right thumb and index finger. While attempting to do so, he flexed the distal phalanx of the thumb (Froment sign). There was atrophy of the first dorsal interosseous muscle, and fasciculations were observed within this muscle. Abduction of the little finger was of normal strength, and no sensory deficits were demonstrated.

Electrodiagnostic testing was consistent with a distal left ulnar neuropathy involving only the deep motor branch. The patient regained some strength after switching jobs.

Ulnar neuropathies at the level of the wrist or palm are less common than proximal lesions. The nerve might become entrapped at the level of the ulnar tunnel or the Guyon canal. Common causes are trauma, ganglion cysts, rheumatoid arthritis, and wrist fractures. Depending on the exact site of injury, there may or may not be associated sensory symptoms (see Fig. 65-9). Sensory loss on the dorsal aspect of the medial hand points to a more proximal ulnar neuropathy with involvement of the dorsal ulnar cutaneous nerve.

Ulnar neuropathies in the palm distal to the Guyon canal present with weakness confined to the ulnar muscles on the lateral aspect of the hand, particularly thumb adduction. This is secondary to weakness of the adductor pollicis, the only thenar muscle not primarily innervated by the median nerve. The first dorsal interosseous muscle is also affected, whereas abduction of the little finger may be preserved. The accompanying intrinsic muscle atrophy and the lack of sensory deficits sometimes prompt consideration of motor neuron disease. Lesions in the palm usually result from local trauma and repetitive injury, for example, from bicycling or from occupations that use tools requiring significant intermittent pressure over the distal ulnar motor fibers (i.e., electricians, clam or oyster shuckers, and pizza cutters). EMG is essential for diagnosis. When the pressure is discontinued, significant recovery of function can occur.

Differential Diagnosis

Motor neuron disease is a primary consideration in patients presenting with asymmetric painless atrophy of the hand intrinsics. One key differentiating feature between motor neuron disease and an ulnar nerve lesion is the frequent involvement of the abductor pollicis brevis muscle in motor neuron disease; this is innervated by the median nerve.

Lower brachial plexus injuries are accompanied by motor and sensory dysfunction in the distribution of multiple peripheral nerve territories within a single extremity. Historically, thoracic outlet syndrome, a distal T1 radiculopathy or proximal lower trunk brachial plexopathy, was considered a common cause of upper extremity neurologic symptoms. Thoracic outlet syndrome is now recognized as a rare condition that is more likely to mimic an ulnar neuropathy than CTS. Perhaps many cases of CTS were erroneously diagnosed and treated as thoracic outlet syndrome before the recognition of the frequency of CTS in the late 1950s and early 1960s. EMG defined the relative frequency of these lesions.

C8 radiculopathies are less common than C7 or C6 radiculopathies but can easily be confused with an ulnar neuropathy because of their overlapping sensory territory. Medial forearm numbness and weakness of non–ulnar innervated C8 muscles (i.e., the thenar eminence, the flexor pollicis longus, and the extensor indicis proprius) provide the major diagnostic distinctions.

Management

Conservative treatment consists of avoiding the stretch produced by a fully flexed elbow via a padded splint that prevents further direct nerve pressure. More than 50% of patients with mild nerve compression might recover with conservative therapy, although data on long-term outcome is limited. Surgical management of ulnar lesions is not as well defined as with CTS. It is even less clear who is likely to benefit from surgery, and there is no consensus on which surgical procedure is appropriate. Persistent pain, progressive motor deficits, and to a lesser extent failure to improve after 3–6 months of conservative management are reasons to consider surgery. Once sensory ulnar nerve conductions can no longer be obtained, recovery of sensory function after surgery becomes less likely. With tardy ulnar palsy, surgeons typically transpose the nerve away from the offending epicondylar groove, often with concomitant epicondylectomy (see Fig. 65-11). This procedure is associated with some risk, particularly in patients with diabetes, because the microvasculature of the nerve can be easily compromised. For cubital tunnel lesions in the absence of trauma or prior surgical procedure involving the elbow, anterior transposition seems to offer no advantage over simple decompression of the nerve.

Radial Neuropathies

Clinical Vignette

An 82-year-old man was seen in urgent consultation for a possible stroke. He had awoken in his chair during the late morning with weakness of the right arm. The night prior, he had taken a sleeping pill for the first time in his life.

The neurologic examination revealed weakness of elbow flexion in the semi-pronated position (brachioradialis muscle), wrist extension, and finger extension. The brachioradialis reflex was absent, whereas the triceps reflex and triceps strength were preserved. There was sensory loss to light touch and pinprick on the dorsal aspect of the forearm and dorsolateral hand.

Electrodiagnostic testing performed on the day of presentation was suggestive of an acute right radial neuropathy at the spiral groove. At the time of his follow-up visit 4 weeks later, the patient had completely recovered.

The radial nerve is formed by fibers from all three trunks of the brachial plexus, hence from roots C5 to T1. It primarily supplies the extensor muscles of the arm, forearm, and fingers and one flexor of the arm, the brachioradialis (see Fig. 65-1). It also provides the sensory innervation to the dorsal arm, the dorsolateral aspect of the hand, and the dorsum of the first three and a half, sometimes two and a half fingers (Fig. 65-12).

Figure 65-12 Radial Nerve in Forearm.

Predominant Motor Radial Neuropathies

Radial neuropathies most commonly occur at the midhumeral level near the spiral groove, secondary to external compression (Fig. 65-13). This can occur as a result of impaired consciousness during anesthesia or due to drug or alcohol intoxication (“Saturday night palsy”). These lesions primarily present with wrist and finger drop but little or no pain. Sensory signs and symptoms are often elusive. Elbow extension is spared because the branches of the triceps originate proximal to the spiral groove. The brachioradialis reflex is typically diminished or lost, whereas the triceps and biceps reflexes are unaffected. A potentially confounding examination feature is apparent weakness of ulnar innervated finger abduction that appears concomitant with wrist drop. The full strength of these ulnar muscles requires at least partial wrist extension. Testing the strength of finger abduction while placing the hand and forearm flat on a hard and flat surface circumvents this problem and prevents false localization.

Figure 65-13 Radial Nerve Compression.

The posterior interosseous nerve is analogous to the anterior interosseous nerve because it is a distal, predominantly motor branch of a major peripheral nerve trunk. Posterior interosseous neuropathies commonly occur with fractures of the proximal radius and sometimes have a delayed onset. The posterior interosseous nerve can also be compromised by soft tissue masses. A syndrome of pain and weakness in the muscles innervated by the posterior interosseous nerve may occur in patients who perform repetitious and strenuous pronation/supination movements, which in some instances leads to intermittent posterior interosseous nerve compression by the fibrous edge of the arcade of Frohse (the proximal aspect of the supinator muscle). Entrapment may also develop secondary to a hypertrophied or anomalous supinator muscle. The extensor carpi radialis longus and brevis and the brachioradialis muscles are innervated by branches exiting the radial nerve before the origin of the posterior interosseous nerve; therefore, finger drop, rather than wrist drop as with a more proximal radial nerve lesion, is the dominant manifestation. The extensor carpi ulnaris, however, is weak, which leads to radial deviation of the hand during wrist extension. There is no sensory loss. Pain near the lateral epicondyle of the humerus, extending distally, may occur, as the posterior interosseous nerve gives off sensory fibers supplying the interosseous membrane and joints of the forearm.

Predominant Sensory Radial Neuropathies

The superficial radial nerve, a primary distal sensory branch, may be injured in isolation with external pressure at the wrist, for example, with handcuff injuries. These lesions are readily recognized by the distribution of sensory symptoms on the dorsolateral portion of the hand. Weakness does not occur.

Management

Radial neuropathies usually result from monophasic external compression. They are almost always treated conservatively and successfully.

Mononeuropathies of the Medial and Posterior Cutaneous Nerves of the Forearm

Isolated injuries of the medial cutaneous nerve of the forearm are rare (see Fig. 65-3). Sensory symptoms in the medial volar forearm are more commonly a result of more proximal injuries to the lower trunk or medial cord of the brachial plexus or to the C8 nerve root. Nerve injuries at these levels are associated with additional clinical findings, particularly hand weakness. Sensory symptoms on the posterior forearm from isolated injuries to the posterior cutaneous nerve of the forearm are equally rare.