6.10 Peripheral nerve entrapment

The term ‘peripheral nerve entrapment’ implies nerve compression based on impingement by adjacent soft tissue or bony structures, usually occurring in well-defined locations in the upper extremity. However, other factors frequently play a role in the onset of symptoms. Inflammation of the surrounding or adjacent structures can apply direct pressure to the nerve itself or increase pressure within a confined space. Systemic conditions, such as pregnancy, diabetes, and disorders of thyroid function, alter symptom manifestation and pressure applied to the nerve. Appropriate epineural blood supply also appears to be critical in the production of symptoms. Direct trauma to the nerve, although a relatively uncommon cause, can produce symptoms based on swelling, haematoma formation, or direct axonal injury. Similarly, abnormal tethering of the nerve can restrict its normal gliding motion leading to a traction phenomenon which impairs physiological function.

Peripheral nerve entrapment has several stages (Box 6.10.1):

Historically, peripheral nerve entrapment has been seen in the middle-aged and elderly population, more commonly in females than males, with a predictable and gradual progression of numbness and tingling. Patients with long-standing compression often presented with dense impairment of sensibility, with or without atrophic muscles, and with a poor prognosis for recovery after decompression. During the last 10–15 years, there have been increasing presentations from younger industrial or clerical workers undertaking repetitive hand tasks or using vibratory tools. The reasons remain unclear, although greater awareness of these conditions in the general population has contributed. The increase of workers’ compensation claims for peripheral nerve entrapment has complicated the diagnosis and treatment of these conditions.

Nerve compression usually occurs gradually. Paraesthesia occurring at night or in response to specific activities is typical. Acute nerve compression is rare; patients note immediate symptoms of dense numbness and tingling in the appropriate distribution, often after a defined traumatic event. Bleeding and haematoma formation secondary to the injury are the most common cause and patients with these findings are often best treated by immediate surgical decompression.

Since the clinical manifestations of impaired nerve function (sensory symptoms and muscle weakness or wasting) are projected to the distal terminations of the peripheral nerves, the site of the nerve lesion may, in theory, be deduced from the distribution of the symptoms. This is not always reliable. Assessment of the patient requires a careful interpretation of patient history and physical examination, as well as a thorough knowledge of the neural anatomy of the upper extremity. In most patients, clinical signs point to involvement of a single nerve. Once the affected nerve is identified, the site of compression can be localized by a combination of specific symptoms, physical signs, and electrodiagnostic testing. One should always be alert to unusual causes of peripheral nerve compression such as tumour surrounding the brachial plexus, radiation plexopathy, and the possibility of a double-crush phenomenon involving two sites of compression in the same nerve at different levels.

Sensibility testing can also provide valuable information although is rarely used in routine clinical practice. The Semmes–Weinstein monofilament test and vibration tests that examine the threshold for neural stimulation (a reflection of the function of single nerve fibres supplying one or more receptors) are more effective early since conventional sensory tests often show no abnormality in early and intermediate stages of neural entrapment. These are, in practice, only used in research. In contrast, static and moving two-point discrimination which test innervation density reflect the interpretation of signals from many overlapping receptor fields and require a considerable drop-out of fibres before performance is impaired. These tests are most frequently used to plot recovery after nerve repair.

Electrodiagnostic testing remains the most objective method available for investigating peripheral nerve compression (Table 6.10.1). The general assumption that electrodiagnostic testing is highly reproducible and completely accurate is incorrect. These tests are operator dependent, rely on the establishment of ‘normal’ values for each laboratory, and are affected by environmental conditions such as patient temperature, room temperature, and electromagnetic interference.

A summary of the physical signs and usefulness of electrodiagnostic testing in peripheral nerve compression

Carpal tunnel syndrome is compression of the median nerve beneath the transverse carpal ligament in the wrist. It is the most common peripheral nerve entrapment syndrome, affecting about one in 1000 of the population per year, but its frequency of presentation may be increasing in parallel with greater community awareness.

The classical clinical picture is of nocturnal paraesthesiae that wake the patient and are relieved by shaking the hands or hanging them in a dependent position. In severe cases, patients wake several times each night. In milder cases, patients will often note numbness and tingling upon waking in the morning, with fine motor activities of the hand, or when gripping the hand for extended periods of time (e.g. holding a steering wheel while driving a car). Numbness and tingling should be related to the median nerve distribution involving the thumb, index, and middle fingers, and the radial half of the ring fingers. Possible proximal causes of numbness and tingling, such as thoracic outlet syndrome, cervical radiculopathy, or pronator syndrome, should always be considered.

Physical examination includes tests of median nerve function (sensibility and thenar muscle power) and provocative tests. The two classic manoeuvres are Phalen’s test and Tinel’s test. In Phalen’s test (generally performed on both hands simultaneously), the wrist is held fully flexed for up to 60s, noting the onset of paraesthesiae in the median nerve distribution. For Tinel’s test, the examiner’s finger or a rubber mallet is used to tap over the median nerve within and just proximal to the transverse carpal ligament, proving positive if the patient has distal radiation of ‘electric shocks’ or tingling in the median nerve distribution. Phalen’s test is sensitive but sometimes renders false-positive results. Tinel’s test is more specific but is less sensitive, so that a positive result is informative but a negative one is still consistent with carpal tunnel syndrome. Median nerve compression (the compression or pressure test) can also be used. The median nerve is compressed/pressed upon by the examiner’s finger just proximal to the carpal canal. Like Phalen’s test, if positive there is usually a response in 20s but it may be necessary to press for 60s.

Electrodiagnostic testing is the single best test in diagnosing carpal tunnel syndrome, and is especially invaluable when the clinical impression is inconsistent with the typical history and physical signs of the syndrome. Although this test provides the most objective examination of the median nerve, it should used in conjunction with the clinical signs and symptoms.

Conservative management includes use of a neutral-position wrist splint to be worn at night and during repetitive activities of the hands, and occasionally the use of oral anti-inflammatory medications. Steroid injections can offer two benefits in patients with a relatively short duration of symptoms: a cure (in less than half of patients) and diagnostic confirmation if there is a response even transiently.

Most patients eventually require surgical release of the transverse carpal ligament. Operative treatment is indicated in patients who have fixed neurological symptoms, i.e. thenar atrophy or constant sensory impairment (implying severe compression), although relief of symptoms may be incomplete. The carpal ligament can be divided open or with the newer techniques of endoscopic or mini-open ligament release. Open techniques are safer, with less chance of injury to the median nerve, common digital nerves, and flexor tendons, and a lower recurrence rate; however, increased palmar tenderness is a drawback (Figure 6.10.1). Though pillar pain is certainly not eliminated, endoscopic release provides the benefit of less palmar tenderness.

Postoperative splinting is not required routinely, and the outcome of splinting does not significantly differ from that of soft dressing. Concomitant internal or external neurolysis of the median nerve do not help and increase the risks, and so are not routinely performed.

Entrapment of the median nerve in the proximal forearm is rare. Although called the pronator syndrome, compression may occur at various sites. Occasionally, patients will present with compression of the median nerve under a ligament of Struthers arising from a supracondylar process of the humerus. Alternative sites of compression as it passes through the proximal forearm and elbow region include the lacertus fibrosus, the origin of the pronator teres, and the arch of the flexor digitorum superficialis muscle distally. Patients classically complain of numbness in the radial three and a half digits and occasional thenar weakness. Unlike carpal tunnel syndrome, nocturnal paraesthesiae and tingling are generally absent with paraesthesiae chiefly occurring with forearm muscle contraction. Patients can complain of pain in the volar aspect of the proximal forearm. Phalen’s test is generally negative. The pronator compression test, involving compression applied at the junction of the pronator heads with resulting dysaesthesiae and tingling in the median nerve distribution, may support this diagnosis. Flexing the elbow with the forearm in supination while simultaneously applying resistance can indicate compression at the lacertus fibrosus. If paraesthesiae occur while resisting forearm pronation with full elbow extension, the pronator site is indicated. The occurrence of median nerve tingling while the examiner resists isolated proximal interphalangeal joint flexion of the middle finger can indicate entrapment of the median nerve below the arch of the flexor digitorum superficialis muscle. Electrodiagnostic testing is essential.

Conservative treatment is to modify forearm and wrist musculature activity, possible through the use of a volar neutral position wrist splint. Occasionally heat and massage, as well as non-steroidal anti-inflammatory medications, can improve the condition. Surgical release of the median nerve in the proximal forearm may be required. Of the four sites which should all be checked during surgery after the median nerve is identified, the lacertus fibrosus and arch of the flexor digitorum superficialis appear to be most commonly associated with visual compression of the median nerve. The large blood vessels immediately adjacent to the median nerve should be protected during surgery (Figure 6.10.2). If a patient has had a previous carpal tunnel release without symptom relief, pronator syndrome should be considered but is still rare.

Isolated compression of the anterior interosseous nerve branch of the median nerve occurs but, again, rarely. The condition results in loss of motor function without sensory loss, usually seen with the loss of the ability actively to flex the distal interphalangeal joint of the index finger and the interphalangeal joint of the thumb (loss of the OK or ring sign). Patients may also experience non-specific aching and discomfort in the volar proximal forearm. Occasionally, the pronator quadratus can be deemed weak by testing resisted pronation with the elbow fully flexed to reduce the effect of the proximal pronator teres.

Anterior interosseous nerve syndrome is generally treated conservatively for 3–6 months, since most patients will recover spontaneously. If patients present with pain in both forearms or with symptoms extending proximally in the limb, transient brachial neuritis or Parsonage–Turner syndrome should be considered. The indication for surgical release of the anterior interosseous nerve is the lack of active flexion return in the distal interphalangeal joint of the index finger and that of the thumb, but the timing of surgery is controversial and almost always can be avoided. On rare occasions, only one of the thumb or index finger is involved, generally indicating a more distal compression of the anterior interosseous nerve; one must be careful not to confuse this diagnosis with that of an isolated tendon rupture to either the flexor pollicis longus or the flexor digitorum profundus of the index finger especially in rheumatoid patients who can have isolated rupture of the flexor pollicis longus tendon. Flexion of the interphalangeal joint of the thumb when pressure is applied firmly to the flexor pollicis longus muscle belly in the forearm confirms that the tendon is intact.

Cubital tunnel syndrome, or entrapment of the ulnar nerve at the medial elbow region, is the second most common peripheral nerve entrapment syndrome. The most common complaint is numbness and tingling in the little finger and ulnar half of the ring finger, commonly aggravated by repeated elbow flexion and extension, or by sleeping in a ‘fetal position’ with the elbows flexed. Weakness of the ulnar-innervated intrinsic muscles is a sign of severe or long-standing compression. Several other conditions may mimic cubital tunnel syndrome, though examination generally excludes cervical root entrapment, cervical rib or band, radiation plexopathy, and peripheral nerve tumours. If sensory symptoms involve the medial aspect of the forearm, the cause is probably proximal to the cubital tunnel.

Cubital tunnel syndrome can be distinguished from the much less common compression of the ulnar nerve at the wrist (Guyon’s canal compression syndrome) by involvement of the dorsal sensory branch of the ulnar nerve, by weakness of the flexor digitorum profundus muscle of the small finger and flexor carpi ulnaris muscle, and by localization of Tinel’s test to the cubital tunnel.

Conservative management includes a night elbow extension splint or, alternatively, wrapping a pillow with tape around the elbow in the fashion of a ‘doughnut’ to prevent elbow flexion during sleep. Steroid injection use at the cubital tunnel is best avoided due to a high incidence of fat necrosis, and non-steroidal anti-inflammatories are ineffective. Surgical decompression is indicated if conservative treatment fails or if muscle weakness or wasting is present.

The various operative procedures used for treatment of cubital tunnel syndrome all appear to provide 85–90 % improvement of symptoms. Surgical procedures include simple decompression of the cubital tunnel, decompression with partial medial epicondylectomy, and transposition of the ulnar nerve anteriorly. Simple decompression alone is generally indicated if Tinel’s sign over the ulnar nerve at the elbow is localized to the cubital tunnel and the origin of the flexor carpi ulnaris. After simple decompression, the ulnar nerve must not sublux with elbow flexion and extension. If this does occur, partial medial epicondylectomy should be performed. Anterior transposition of the ulnar nerve is performed very variably depending upon surgeon preference. Indications include patients exhibiting significant involvement of the ulnar nerve with evidence of atrophy or weakness (Figure 6.10.3), especially in patients with fixed flexion deformities of the elbow. Since the nerve is being transposed anterior to the medial epicondyle, the medial intermuscular septum should be completely resected to avoid any ‘tenting’ of the ulnar nerve over this structure following transposition. The cubital tunnel release should be complete around the medial epicondyle, and the fascia, both deep and superficial overlying and within the flexor carpi ulnaris, needs to be completely released to prevent any further ‘kinking’ of the ulnar nerve distally. Transposition of the ulnar nerve can either be to the subcutaneous tissues above the fascia of the flexor pronator group, within the musculature of the flexor pronator group itself with the fascia repaired, or beneath the flexor pronator group with the origin repaired to the medial epicondyle. This is dictated by surgeon preference rather than scientific evidence.

Failure to achieve good results with these techniques may result from inadequate decompression, failure to ensure that the nerve is stable during elbow flexion/extension, or that it is free from compression in its new position.

Compression of the ulnar nerve at Guyon’s canal (ulnar tunnel syndrome) is rare. Its numerous causes include space-occupying lesions (e.g., ganglion cysts), anomalous muscles, fractures of the hook of the hamate, thrombosis of the ulnar artery, repeated trauma to the heel of the hand (hypothenar hammer syndrome), and long-distance cycling. Symptoms may be motor, sensory, or both, depending on the location of the compressive lesion relative to the ulnar nerve branches. It can be difficult to differentiate from more proximal compression, i.e. at the elbow. The signs of proximal compression as noted earlier should be looked for, as should local nerve irritability, i.e. a positive Tinel’s sign over the ulnar nerve at the wrist.

The Allen test can often detect occlusion of the ulnar artery. Radiographic examination (e.g. computed tomography scanning) may identify a fracture of the hook of the hamate, while magnetic resonance imaging can define the nature and location of ganglia and other lesions.

Conservative management with rest and splintage is appropriate when compression arises from repeated local trauma or pressure. Since space-occupying lesions are so often the cause of compression within Guyon’s canal, operative treatment is commonly needed. No matter the compression site, the ulnar nerve must be traced through the entire tunnel so as to ensure complete decompression, a process that generally yields good results.

Occasionally patients are seen who have carpal tunnel and Guyon’s canal compression syndrome simultaneously. These patients can be treated by release of the carpal tunnel alone, since the procedure relaxes Guyon’s canal. Alternatively, the vertical septa to Guyon’s canal can be released through the same incision.

Entrapment of the posterior interosseous nerve produces two separate clinical pictures. In the first, a mass lesion around the neck of the radius may cause painless paralysis of the muscles supplied by the posterior interosseous nerve (see later). The second, termed radial tunnel syndrome, is a dynamic form of entrapment of the posterior interosseous nerve that cannot be unequivocally diagnosed following clinical and electrodiagnostic examinations.

Though a number of compressive sites have been described, the three most consistent are the fibrous edge of the extensor carpi radialis brevis muscle, the proximal edge of the supinator muscle (the arcade of Frohse), and the recurrent leash of radial vessels (the leash of Henry) that cross superficial to the posterior interosseous nerve (Figure 6.10.4). Patients complain of a deep-seated aching in the proximal forearm after strenuous muscle activity. Deep palpation where the posterior interosseous nerve enters the supinator muscle will produce marked tenderness, sometimes with radiation to the proximal forearm. Radial tunnel syndrome should be differentiated from lateral epicondylitis since these conditions can coexist. Pain with resisted wrist extension is generally directed towards the lateral epicondyle itself, and focal pain directly over the lateral epicondyle is typically indicative of lateral epicondylitis. Pain on resisted middle finger extension is occasionally seen in patients with radial tunnel syndrome. An injection of local anaesthetic that abolishes the pain and gives a temporary wrist drop provides further evidence to support the diagnosis. Electrodiagnostic studies, although extremely helpful if positive, are frequently normal in this dynamic compression syndrome.

Conservative management involves modification of upper-limb activity for 4–6 weeks and may be augmented by neutral wrist splinting. If conservative management fails, surgical decompression of the radial nerve, including the distal posterior interosseous nerve and sensory branch of the radial nerve, may be undertaken. Decompression should ensure release of the fascial tissues superficial to the radiocapitellar joint, coagulation and release of the recurrent radial artery known as the leash of Henry (ligating each vessel independently and sequentially), release of the fibrous edge of the extensor carpi radialis brevis, and, most importantly, release of the proximal edge of the supinator (the arcade of Frohse). In rare instances in which tenderness is also noted at the distal portion of the supinator preoperatively, release of the entire supinator or the distal edge may be required. Blunt finger probing along the radial nerve proximally and distally will exclude other areas of compression. The results of decompression of the radial tunnel have been quite variable. Coincidental undiagnosed lateral epicondylitis can lead to ‘failure’ of radial tunnel decompression so the lateral epicondyle should be addressed surgically if signs of lateral epicondylitis are present.

Partial or complete loss of posterior interosseous nerve function may occur because of compression by a mass lesion within or at either end of the supinator muscle, most commonly caused by lipomas around the radial neck and rheumatoid synovial cysts. The diagnosis of a complete palsy is based on the loss of finger and thumb extension with weak and radial-directed extension of the wrist under the influence of extensor carpi radialis longus. Incomplete lesions, sometimes producing loss of extension of one or two digits, are easily confused with the much more common extensor tendon rupture. Operatively, the removal of the mass should be approached anterior to the proximal part of the supinator or posterior to the distal part.

Compression of the radial nerve sensory branch in the middle and distal forearm is very uncommon. The sensory branch of the radial nerve normally courses underneath the muscle belly of the brachioradialis and emerges from below its tendinous portion in the distal third of the forearm (Figure 6.10.5), where irritation, compression, or tethering may occur. Occasionally, a tingling or shocking sensation in the territory of the sensory branch can be provoked by forcefully pronating the forearm for up to 60s. The most useful sign is a positive Tinel’s test directly over the sensory branch of the radial nerve as it enters under or exits from underneath the brachioradialis. Injection of a local anaesthetic can confirm the diagnosis. This condition is found more proximal than de Quervain’s stenosing tenovaginitis, which occurs at the radial styloid level.

Conservative management involves the use of a volar neutral position wrist splint to try to reduce inflammation. Surgical management generally involves release of any fascial and constricting fibres at the junction of the extensor carpi radialis longus and brachioradialis. Careful release of the sensory branch of the radial nerve through a ‘no-touch’ technique should be undertaken to ensure complete removal of compression. Occasionally, the edge of the brachioradialis pushes into the sensory branch of the radial nerve itself, requiring resection of half of the brachioradialis tendon to decompress the sensory branch of the radial nerve and provide a blunter edge with less overall constriction. Early mobilization is generally used in these patients to stop secondary adhesions. The results of surgery have been variable.

On occasion, patients present with symptoms that have persisted or recurred after surgical decompression for three possible reasons: incorrect original diagnosis; incomplete previous decompression; or psychological concerns related to issues of compensation in the workplace. In this case, psychological factors as well as the peripheral nerves and musculoskeletal system (to exclude further causes of entrapment) must be examined. If these examinations are unsuccessful, the area can be re-explored to ensure that the original decompression was complete. The results of such surgery may be disappointing unless the surgeon is able to release a tight structure that was missed at the first operation. Symptoms may recur because of new or recurrent pathological changes in the areas of compression. In general, patients who have had a period of excellent relief of symptoms followed by recurrence fare better with a secondary surgical decompression than those whose symptoms were never relieved.

The two common examples of recurrent compression, although fortunately rare, are following carpal tunnel and cubital tunnel release. Patients who have undergone open carpal tunnel release will generally have good relief of symptoms but after several years can suffer a recurrence, especially if there are underlying pathological changes, such as amyloid deposition in chronic haemodialysis or diabetes. Frequently, these patients can be treated successfully by open revision surgery.

Failure following decompression of the ulnar nerve at the cubital tunnel region can occur after any procedure. Commonly, the release of the ulnar nerve was incomplete at the first operation or other structures were not dealt with adequately (most importantly the medial intermuscular septum and fascia of the flexor carpi ulnaris). Revision surgery is typically performed by transposing the ulnar nerve anteriorly.

Entrapment of the peripheral nerves is a common cause of symptoms in the upper extremity. Isolating the exact area of entrapment involves taking a careful history and a thorough physical examination to identify the nerve involved and to locate the site of compression. Conservative management can result in modest successes, especially if symptoms are of short duration and activities inciting the symptomatology can be curtailed for a period of time. Fortunately, surgical decompression also has met with a relatively high success rate if the diagnosis is accurate. Electrodiagnostic studies are an extremely helpful adjunct in establishing the diagnosis, but they can neither replace a careful history and physical examination nor make the diagnosis on their own. Isolated electrodiagnostic findings are not themselves an indication for surgery unless the diagnosis is supported by clinical evidence from the history and examination. With careful thought and planning, successful treatment of patients suffering from peripheral nerve entrapment is the rule rather than the exception.