Nerve Entrapment Around the Elbow

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Chapter 31 Nerve Entrapment Around the Elbow

Mike Hayton, Sumedh Talwalkar

Introduction

The elbow is a common site of nerve entrapment syndromes. The reasons for this are multifactorial, and this chapter will identify the more common causes and their management, with an emphasis on our personal approach.

The three major nerves of the upper limb (ulnar, median and radial) pass from the arm into the forearm in close proximity to the elbow joint. The ulnar nerve passes between the two heads of flexor carpi ulnaris (FCU) with the median nerve passing between the two heads of pronator teres. The radial nerve or, more accurately, its posterior interosseous motor branch, passes between the two heads of the supinator muscle. Each nerve and its branches can be compressed, giving rise to well-described nerve entrapment syndromes.

Background/aetiology

The nerves that cross the elbow are either purely sensory, purely motor or contain mixed sensory and motor fibres. When nerve entrapment occurs the classical presentation involves loss of sensation and motor power. The modalities of sensation travel in the larger diameter fibres and are often the first and most severely affected by compression. These include light touch and fine discrimination. Smaller diameter fibres that convey pain are well preserved until severe prolonged compression occurs. Loss of motor power is identified in the specific muscle groups that are supplied by the compressed nerve. Macroscopic loss of power can be noticed within the large muscle groups, including the forearm flexors and extensors. These may manifest themselves as finger drop, loss of grip strength or generalized weakness. Weakness in the ulnar innervated muscles of the hand may be detected before wasting is seen if a careful clinical history is obtained. Patients often describe progressive clumsiness in the hand with loss of the normal fine motor control. This is followed by wasting of the small muscles of the hand that is easily visualized due to the lack of fat in this region or by comparison of asymmetry with the opposite limb.

Clinical examination of the hand may also reveal trophic changes. These include healing burns, scalds and lacerations that the patient may not have noticed until the damage had been done. A thorough history and clinical examination should enable an appropriate differential diagnosis of the possible sites of compression. These include the anterior horn cell, the spinal canal, the intervertebral foramen and the thoracic outlet together with the elbow, wrist and hand. In addition to a careful assessment of the nerves around the elbow, physical examination should include a general neurological assessment with examination of the legs for any long tract signs that may suggest a lesion in the spinal cord or canal.

The clinician should also be aware that occasionally a ‘double-crush’ phenomenon may occur. This was first described by Upton and McComas ¹ in 1973 who stated that ‘neural function was impaired because single axons, having been compressed in one region, become especially susceptible to damage at another site’. When this occurs in the upper limb the peripheral nerves become hypersensitized by proximal compression in the neck and are more susceptible to an otherwise well-tolerated level of compression.

Clinical Pearl 31.1

In the assessment of nerve entrapment around the elbow, clinical examination should include the sensory and motor supply of the ulnar, median and radial nerves together with a careful examination of the cervical spine and lower limbs. The clinician should also be aware of the possibility of a ‘double crush’.

The causes of compression can vary widely and are given below.

• Anatomical

The anatomical structures around the elbow and, in particular, the various fibro-osseous tunnels and fibrous arches can cause rigid borders against which nerves may be compressed. The large range of elbow flexion will produce longitudinal traction on the nerves lying within the extensor compartment whilst compressive forces are applied to the nerves on the flexor surface. The ulnar nerve for example is subjected to longitudinal traction during terminal flexion. In addition it has been reported that 5.1 mm of ulnar nerve excursion is needed for elbow motion from 10° to 90°.² This alone may compromise nerve function, but when combined with a second local insult such as a fibrous band or impinging osteophyte there is an increased likelihood of nerve irritation.

• Congenital

Congenital abnormalities can also produce nerve entrapment. The median and very occasionally the ulnar nerve may be compromised by the ligament of Struthers. This arises from a supracondylar spur on the medial border of the distal humeral shaft and extends obliquely to the medial epicondyle (Fig. 31.1).

• Inflammatory

Figure 31.1 (A) Supracondylar process: anteroposterior view. (B) Supracondylar process: lateral view.

Inflammatory processes, particularly rheumatoid arthritis, have been implicated in nerve entrapment at the elbow. Posterior interosseous nerve palsy secondary to radiocapitellar synovitis, can give rise to a lag in finger extension and lead to a misdiagnosis of tendon rupture at the wrist. Careful clinical assessment will distinguish the palsy from a tendon rupture or subluxed extensor tendons in the metacarpophalangeal joint gutters.

• Traumatic

Transient ulnar nerve palsy may occur from a direct blow to the nerve in its relatively unprotected medial epicondylar groove. More serious is tardy ulnar nerve palsy that is usually the result of excessive cubitus valgus deformity. This occurs most frequently after non-operatively treated displaced lateral humeral condylar fractures of childhood.

• Metabolic

A number of metabolic conditions are well-recognized causes of peripheral nerve entrapment syndromes. These include pregnancy, thyroid disease, diabetes and sarcoidosis. The symptoms of nerve compression may resolve once the underlying medical cause is treated although this is not always the case.

Cubital tunnel syndrome (ulnar nerve)

Most patients who present with cubital tunnel syndrome have no identifiable aetiology for their compression although in a minority a cause can be recognized, and these include:

• lateral condylar fractures with malunion, leading to a cubitus valgus and secondary tardy ulnar palsy (Fig. 31.2)

• osteoarthritis of the elbow with osteophyte formation in the cubital tunnel

• compression by the anconeus epitrochlearis muscle that passes from the medial epicondyle to the medial border of the olecranon

• medical conditions such as diabetes, sarcoidosis, pregnancy and thyroid disease

• radiotherapy for malignancy resulting in neural scarring

• iatrogenic. Some of the most severe cases of cubital tunnel syndrome that we have seen have been caused by iatrogenic injury. Unconscious patients who have been inadequately nursed on intensive care units or during prolonged surgery will suffer direct ulnar nerve compression if their elbows are not appropriately protected.

Figure 31.2 Ulnar nerve lesion: wasting of first dorsal interosseous muscle.

Background and aetiology

The ulnar nerve at the level of the elbow is a large mixed motor and sensory nerve. It provides sensation to the ulnar one and a half digits of the hand, the volar and dorsal aspect of the hand and the medial aspect of the forearm. It is the motor supply to FCU, flexor digitorum profundus (FDP), palmaris brevis, adductor pollicis, the deep head of flexor pollicis brevis, seven interossei, three hypothenar muscles and the lumbricals to the little and ring fingers. With severe ulnar nerve compression at the elbow, the commonest site of muscle wasting, is the first dorsal interosseous muscle (Fig. 31.3).

Figure 31.3 Cubitus valgus deformity.

The intraneural anatomy of the ulnar nerve at the elbow is organized into a layered formation of fibres.³ Sunderland showed that the sensory supply to the hand was present in the most superficial layer beneath which was found the innovation of the intrinsic muscles. The motor branches to the long flexor tendons were present in the deepest portion of the nerve. This patterning explains the early onset of sensory symptoms in the hand and why weakness of the long flexor tendons occurs at a much later stage with more significant compression.

The ulnar nerve blood supply is segmental and is a major concern during anterior transposition when the nerve is solely dependent on its intraneural supply. Prevel et al ⁴ in a study on the extrinsic blood supply showed that the ulnar nerve receives two constant major pedicels from the superior ulnar collateral artery proximally and the posterior ulnar recurrent artery distally. In a cadaveric study they demonstrated by measuring total vessel length and distance to the medial epicondyle that the extrinsic vascular supply could be preserved during anterior transposition of the ulnar nerve, even after the nerve had been extensively mobilized. Simple decompression, however, has the advantage of leaving the nerve in situ with its surrounding vascular supply.

The ulnar nerve can be compressed at four main sites around the elbow:

• The most proximal site of compression is where the ulnar nerve passes from the anterior to the posterior compartment of the arm.

• A second site of compression is the arcade of Struthers.⁵ This is a band of thickened fascia that extends from the medial head of triceps (approximately 10 cm proximal to the medial epicondyle) to the medial intermuscular septum. It may represent a variant of a supracondylar spur which, in its full form, is a bony bar arising from the medial shaft of the humerus and extending to the medial condyle. The spur is often incomplete and may only have a proximal bony spur from the humeral shaft continuing distally as a fibrous band.

• The commonest site of compression at the elbow is Osborne’s fascia. This connects the two heads of FCU, beneath which the ulnar nerve passes into the forearm. The cubital tunnel is formed by a groove on the dorsal surface of the medial epicondyle proximally, and the posterior and oblique portions of the ulna collateral ligament distally. The roof of the cubital tunnel is formed by a fibro aponeurotic band ⁶ (Fig. 31.4). The nerve may be subject to simple compression by the fascia but may additionally be compressed due to the change in shape of the cubital tunnel with elbow movement. In full extension of the elbow the cross-section of the cubital tunnel is smooth and circular. However, on flexion this changes to a flattened triangle with reduction in the cross-sectional area by as much as 55%.⁷ It has also been suggested⁷ that the ulnar nerve is stretched by approximately 47 mm from full extension to full flexion. This traction effect often reproduces symptoms. The change in shape of the tunnel and traction on the ulnar nerve in flexion explains the increasing symptoms that occur when the elbow is flexed. The flexion compression test makes use of this finding (see later).

• The ulnar nerve may also be compressed distally by the fascia of FCU and the fascia over the proximal edge of flexor digitorum superficialis.⁸ The fibres supplying FDP and FCU are relatively protected as they lie centrally whereas the fibres supplying sensation and those supplying the small muscles of the hand are more vulnerable as they have a more superficial position in the nerve. Thus hand signs manifest sooner than other features of ulnar nerve compression.⁸

Figure 31.4 Osborne’s fascia.

Presentation, investigations and treatment options

Presentation

Patients present with an insidious onset of altered sensation in the ulnar nerve distribution. The sensory loss on the dorsum of the hand helps differentiate compression of the ulnar nerve at the elbow from compression within Guyon’s canal at the wrist. Compression in Guyon’s canal spares sensory changes on the dorsum of the hand due to the fact that the dorsal sensory branch to the back of the hand arises proximal to the wrist.

Initial sensory symptoms are often reported as a ‘cotton wool’ feeling. Pins and needles occur in the same distribution and may lead to a gradual progressive loss of sensation. Symptoms are usually worse at night but are less classical than those that occur with carpal tunnel syndrome. The nocturnal symptoms occur in our opinion due to the loss of the muscle pumps at night and pooling of interstitial fluid in the peripheries.

Patients may also report motor symptoms and these should be taken seriously as muscle wasting can occur quickly. An early warning of impending motor loss is the feeling of clumsiness in the hand. Functional activities of daily living with the affected hand such as hair drying, brushing hair, driving and telephone use are all aggravated by elbow flexion.

In the early stages of cubital tunnel syndrome there may be few if any physical signs. Inspection may reveal excessive cubitus valgus. The normal elbow has approximately 7° of physiological valgus although this varies between individuals. The key is an asymmetrical valgus deformity. Careful questioning may identify a childhood fracture. Inspection may also reveal a deformed elbow joint consistent with osteoarthritis. Muscle wasting may be observed in the ulnar flexor forearm and in the hand. Wasting of the first dorsal interosseous muscle is very easily identified when present. The hand may take on a guttered appearance with intermetacarpal wasting of the interossei.

Palpation of the elbow may reveal ulnar nerve tenderness in the cubital tunnel, coexisting medial epicondylitis or an ulnar nerve which subluxes anteriorly on flexion. Tinel’s test may be positive anywhere along the nerve and in our experience it is more sensitive than when performed at the wrist for carpal tunnel syndrome. The test involves gently tapping along the course of the nerve from distal to proximal. An unpleasant sensation is felt at the site of entrapment.

Froment’s sign is also useful in the assessment of ulnar nerve function. It involves placing a piece of paper between the patient’s adducted thumbs and index fingers of both hands. The patient is then asked to resist extraction of the paper by the examiner. With normal power, the first dorsal interosseous and adductor muscles will prevent removal of the paper from between the digits. However, with ulnar nerve palsy these muscles are weak and the patient subconsciously recruits the flexor pollicis longus (FPL) tendon (anterior interosseous nerve supply). The thumb interphalangeal joint flexes to pinch the paper and prevent its extraction. Additional evidence of ulnar nerve dysfunction is the patient’s inability to cross their fingers symmetrically.

Our favoured provocation manoeuvre is the flexion compression test. In this test the patient is asked to fully flex the elbow while the examiner applies digital pressure over the cubital tunnel. A positive test is associated with the development of ulnar nerve symptoms within 30 seconds of applying digital pressure.

Clinical Pearl 31.2

The commonest site of muscle wasting with severe ulnar nerve compression at the elbow is the first dorsal interosseous muscle.

Investigations

Patients suspected of bony abnormalities, including cubitus valgus or osteoarthritis, should undergo anteroposterior and lateral plain radiographs centred on the elbow. In addition a cubital tunnel view is useful to visualize the medial epicondylar groove. This comprises a posteroanterior radiograph taken with the elbow in full flexion. A plain anteroposterior radiograph in full elbow extension will demonstrate valgus alignment. If this is greater than 7° a simple ulnar nerve decompression may be unsuccessful in relieving the patient’s symptoms and an anterior transposition is the preferred option.

Electro-physiological investigations are of value in clinically equivocal scenarios or where the site of the compression is in doubt or in the setting of a possible polyneuropathy or double crush syndrome.

An ultrasound scan may be a useful test to visualize the ulnar nerve in cases of suspected subluxation in the larger obese patient. It will also reveal the lack of nerve excursion and movement on flexion and will show sites of tethering and compression. In addition it may indicate neural swelling proximal to the site of compression.⁵

Treatment options

Non-operative treatment

The non-surgical management of ulnar neuropathy should be restricted to mild to moderate entrapment.⁹ Simple analgesics and non-steroidal antiinflammatory drugs may be useful for some patients. Others find splints beneficial although rigid devices are often poorly tolerated by both the patient and their bed-time partner. As a short-term measure we advise the patient to make a hole at the far end of a pillowcase. The hand can be passed through the pillowcase, alongside the pillow exiting on its far side through a small window that has been cut in the seam. During rest at night, flexion of the elbow, which often accompanies patients who sleep in the fetal position, is prevented. The elbow is unable to flex due to the bulky pillow. Patients often find this useful and more comfortable than other types of splint. In our experience, however, spontaneous resolution of symptoms is unlikely if the nerve entrapment syndrome is secondary to osteoarthritis, if there is a significant bony deformity such as cubitus valgus; or, if the compression appears to be severe, with significant motor wasting or sensory loss.

Surgical technique and rehabilitation

Although cubital tunnel surgery is usually performed under general anaesthesia as a day case, it can be performed under local anaesthesia in patients with comorbidities that prevent the safe use of a general anaesthetic. It is unwise, however, to use local anaesthesia in patients with bulky arms, excessive subcutaneous adipose tissue or in patients who may require an anterior transposition.

We position the patient in the lateral decubitus position, with a narrow, high tourniquet. The arm is supported over a narrow gutter and is exsanguinated. For a simple in situ release a 5 cm skin incision is made over the cubital tunnel. For an anterior transposition an 8–10 cm incision is made 2 cm anterior to the medial epicondyle. The greater length of this incision is required to allow the nerve, once fully released and anteriorly transposed, to have a straight course without any kinks at its proximal or distal margins.

Following the skin and dermal incision blunt dissection is performed down to the deep fascia. This prevents inadvertent division of the medial antebrachial nerve that passes obliquely across the operative field to supply skin over the olecranon.

Simple decompression

Simple decompression is adequate for the vast majority of patients and can be performed through a relatively small incision that preserves the vascular bed of the nerve. The ulnar nerve is identified proximal to the elbow on the medial aspect of the arm. It can be felt as a rubbery cord. Having mobilized the skin edges, the nerve can be released for 10–15 cm proximal to the skin incision using appropriately angled retractors. Osborne’s fascia is then released between the two heads of the FCU (Fig. 31.5). In simple decompressions the medial intermuscular septum is not excised or released. Having completed the decompression the tourniquet is released, bleeding controlled and the wound closed with a subcuticular suture.

Figure 31.5 (A) Intermuscular septum. (B) Intermuscular septum held. (C) Intermuscular septum incised. (D) Intermuscular septum excised.

In our experience, many of the ulnar nerves that we have successfully decompressed, with complete resolution of symptoms, have a relatively normal appearance at the time of surgery. The normal intraneural vascular markings are easily identified along the length of the nerve and if the tourniquet is released prior to closure, the nerve returns to its deep pink colouration. However if the compressed nerve has become narrowed, fibrosis in the epineurium and between the individual fascicles reduces the chance of a successful surgical outcome.

Subcutaneous anterior transposition

Having positioned the patient and undertaken the incision as previously described the ulnar nerve is identified as it passes beside the medial intermuscular septum. A 4 cm strip of the septum is then excised in order to allow the nerve to remain in the anterior compartment once it has been transposed. Distally the ulnar nerve is released for 5 cm as it passes down between the two heads of the FCU. The nerve can then be mobilized from its bed, preserving its longitudinal blood supply. The new bed for the ulnar nerve is then prepared. The fat is mobilized off the common flexor fascia for approximately 8–10 cm anterior to the medial epicondyle. A fascial strip is then elevated, as shown in Figure 31.6A. The nerve is transposed anteriorly and the fascial strip (Fig. 31.7) looped around the nerve and sutured back onto itself, securing the nerve in its anteriorly transposed position (Fig. 31.8). It is of vital importance that the ulnar nerve does not travel through any sharp angles, proximally, distally or underneath the fascial loop. In particular, the fascial loop should be loose and not cause any compression of the nerve. The transposed nerve should be tension free. The tourniquet is released, haemostasis achieved and the wound closed with a subcuticular suture.

Figure 31.6 (A) Fascial strip fashioned from flexor pronator expansion. (B) Fascial strip dissected to fashion sling.

Figure 31.7 Nerve passed anterior to sling.

Figure 31.8 Sling used to stabilize nerve anteriorly.

Submuscular anterior transposition

Submuscular transposition allows the anteriorly transposed nerve to be placed in a vascular bed deep to muscle.¹⁰ The nerve is exposed, as for a simple subcutaneous anterior transposition. The common flexor origin is reflected from the medial epicondyle, leaving a rim of tissue, to allow a meticulous repair following transposition. Having elevated the common flexor origin a space is created anterior to the medial epicondyle into which the nerve can be placed in a tension-free and smooth-running line (Fig. 31.9). The common flexor origin is then repositioned in its anatomical footprint and repaired to the remaining cuff of tissue. The wound is closed with a subcuticular absorbable suture. On the second postoperative day the patient’s dressings are reduced and early mobilization permitted to encourage neural gliding.

Figure 31.9 Submuscular transposition.

Partial medial epicondylectomy

The nerve is exposed as for a simple decompression, through a 5 cm incision. The common flexor origin is incised and elevated from the medial epicondyle. The medial epicondyle is then exposed subperiosteally and an osteotomy performed removing a small part of the epicondyle. Any sharp edges of bone are smoothed off with bone nibblers and the nerve anteriorly transposed. The common flexor origin is then reconstructed by suturing it to the surrounding periosteum (Fig. 31.10). It is important during this procedure that only a small part of the medial epicondyle is excised since excessive bone removal will violate the anterior bundle of the medial collateral ligament at the elbow causing significant valgus instability. O’Driscoll et al¹¹ reported in a laboratory study, that only 19% of the width of the medial epicondyle should be removed in order to prevent damage to the underlying ligament. Having performed the epicondylectomy, haemostasis is achieved and the wound closed with a subcuticular suture. Early mobilization is encouraged, after 2 days.

Figure 31.10 Medial epicondylectomy.

Clinical Pearl 31.3

If a partial medial epicondylectomy is performed it is important that only a small part of the epicondyle is excised otherwise there is a risk of damage to the medial collateral ligament resulting in instability of the elbow.

Rehabilitation

We prefer to use a subcuticular absorbable suture, supplemented by Steri-Strips to the wound edges. This method of closure has the advantage of a more cosmetic scar that we feel is important since scars in this area can become hypertrophic. Patients should be warned regarding this possibility preoperatively.

At the end of the surgical procedure a wool and crepe bandage is applied with the elbow in 90° of flexion. A polysling-type support is used by the patient for the first 1–2 days. At approximately 2 days the bulky dressing is reduced and the patient encouraged to mobilize the elbow in order to promote neural gliding. We do not routinely use physiotherapy unless the patient is having difficulty achieving full elbow flexion and extension.

Outcome including literature review

Dellon and Coert ¹² in a retrospective study of 121 consecutive patients (161 extremities) treated by submuscular transposition of the ulnar nerve reported excellent results in 65%, good results in 23%, fair results in 4%, failure in 7.5% and recurrence of symptoms in 0.5%. The authors showed significant improvement in function in terms of both sensory and motor components of the ulnar nerve. Nouhan and Kleinert,¹³ using the same grading system as Dellon and Coert, presented the results of submuscular anterior transposition in 33 extremities with a mean duration of follow-up of 49 months. They reported good to excellent results in 97% (36%: excellent, 61%: good). Kaempffe and Farbach¹⁴ showed improvement in 93% of patients who had undergone medial epicondylectomy, which compares favourably with the results of other investigators.¹⁵^–²⁰

More recently a meta-analysis of randomized controlled trials has been published comparing simple decompression of the ulnar nerve with anterior transposition. The study identified four randomized controlled trials, two of which had subcutaneous transpositions whilst the other two had submuscular transpositions. The results suggested that there was no difference in motor nerve conduction velocities or clinical outcome between simple decompression and subcutaneous or submuscular anterior transposition of the ulnar nerve.²¹

Complications of treatment

Anatomical variations can adversely affect the results of anterior submuscular transposition.²² These include a high origin of the superficial head of the pronator teres (20%), failure to divide a thick common flexor origin concealed within the flexor pronator mass and the presence of a periosteal origin of the FCU that is more medial than the origin of the common flexor mass and must be resected.²²

Other complications of anterior submuscular transposition include neuroma formation (2%),²³ reflex sympathetic dystrophy (2%)¹³ and loss of elbow extension. Care must also be taken with mobilization and repair of the common flexor mass as rupture has been reported in 4% of cases.¹² The commonest complication following subtotal medial epicondylectomy is pain and tenderness at the osteotomy site. Kaempffe and Farbach¹⁴ reported medial epicondylar tenderness in 44% of their patients at 11 months’ follow-up.

Medial epicondylectomy may also result in medial elbow instability secondary to damage to the anterior band of the medial collateral ligament. This is usually due to over-generous excision of the epicondyle. Studies by Dinh and Gupta,¹⁵ however, have shown that if the procedure is performed properly instability does not occur. This has also been noted by Heithoff,¹⁶ who reported a 1% incidence of instability in a review of 350 cases. Amako et al¹⁷ and Froimson and colleagues¹⁸ on the other hand found a 74% incidence of instability in their patients, 20% of whom were symptomatic. Flexor/pronator weakness can also occur following the procedure. Heithoff and colleagues¹⁹ showed a 10% loss of grip strength with a 5% loss of pinch strength at a 2.3-year follow-up.

Reattachment of the flexor pronator mass and prolonged immobilization can result in elbow stiffness. Kaempffe and colleagues ¹⁴ reported an average loss of 19° of extension in 15% of their patients. In a study of 160 cases, Seradge and Owen²⁰ found that over a 10-year period the rate of recurrence was 13%. The recurrence rate in women was noted to be twice that of men (18% vs. 10%). This doubled in patients with ipsilateral carpal tunnel symptoms.

Personal view

Our management of cubital tunnel syndrome is to advise conservative treatment for patients with mild sensory symptoms of recent onset. This involves the use of non-steroidal antiinflammatory drugs together with night splintage. If when examined, the patient also has any evidence of early motor abnormality our preferred treatment option is in situ decompression. This we have found effective for the majority of patients with mild disease although we accept that it does not address tensile forces on the ulnar nerve generated by elbow flexion.²⁴

For patients with more severe symptoms we prefer to perform an anterior transposition of the ulnar nerve making sure that there are no locally compressive forces on the nerve and that the nerve has a straight course at the end of the procedure. If the patient may require bony elbow surgery in the future (OK procedure, total elbow arthroplasty) we perform a subcutaneous transposition otherwise we undertake a submuscular transposition. We acknowledge that the study by Zlowodski et al ²⁴ would suggest that simple decompression of the nerve will give equally good results when compared to anterior transposition but we feel that in patients with severe symptoms it is helpful to relieve both the compressive and tensile forces on the nerve during elbow flexion.

Anterior interosseous nerve syndrome and pronator syndrome

The anterior interosseous nerve branches from the median nerve immediately after the proximal margin of the flexor digitorum superficialis about 4 cm distal to the medial epicondyle of the humerus. It arises from the posterolateral aspect of the median nerve and is a pure motor nerve to FDP of the index and middle finger, FPL and pronator quadratus. The long flexor of the thumb and the FDP of the ring and middle fingers are supplied by multiple nerve branches along the medial and lateral edges of these muscles.²⁵

A number of anatomical variations exist including the Martin Gruber anastomosis in the forearm, which may alter the clinical presentation of any associated syndrome. In addition variations have been described in relation to the passage of the anterior interosseous nerve through the pronator teres. Beaton and Anson ²⁶ showed that in 82% of cases the nerve passed between the deep and superficial heads of the pronator teres, deep to the ulnar head in 7% and through the superficial head in 2% of cases. In 9% of cases the deep head was absent.

Gantzer’s muscle (accessory head of the FPL) may also cause neurological compression. It lies under the deep head of the pronator teres and primarily arises from the medial epicondyle of the humerus (85%). al-Qattan ²⁷ found this muscle in over half of the 25 specimens he examined.

A supracondyloid process over the distal humerus may have attached the ligament of Struthers which can cause compression of the median nerve as it passes beneath it.²⁸ Median nerve compression can either present as a motor palsy (anterior interosseous nerve syndrome) or with diffuse pain over the forearm and hand easily confused with carpal tunnel syndrome (pronator syndrome).

Anterior interosseous nerve syndrome

Background and aetiology

Turner and Parsonage ²⁹ originally reported anterior interosseous nerve syndrome in relation to brachial neuritis. However it was Kiloh and Nevin³⁰ who first described the specific features of the condition with isolated paralysis of the FPL and the median innervated FDP. The anterior interosseous nerve can be compressed at the following sites around the elbow:

• Between the two heads of pronator teres

• Underneath the fibrous arch of flexor digitorum superficialis

• Underneath an accessory bicipital aponeurosis

• By Gantzer’s muscle.

Presentation, investigations and treatment options

Presentation

The commonest presentation is weakness of pinch with an inability to pick up objects or difficulty in writing. Often there is a history of forearm pain followed by weakness of the hand. A history of transient shoulder pain following a viral illness preceding the development of upper limb weakness usually points to brachial neuritis (Parsonage–Turner syndrome).²⁹

The patient will lose motor power to FPL (interphalangeal joint of the thumb) and FDP (distal interphalangeal joint) to the index and middle finger. Pronator quadratus is also affected but is difficult to test and the patient is usually not aware of the motor loss associated with this muscle.

Patients with an anterior interosseous nerve syndrome are unable to perform the classic ‘O’ sign achieved by pinching together the tips of the index finger and thumb. For this to be possible active flexion is required in the index and thumb distal interphalangeal joints. Patients with an anterior interosseous nerve deficit have a more oval shaped pinch grip.

Clinical Pearl 31.4

The commonest presentation of anterior interosseous nerve syndrome is weakness of pinch grip with an inability to make an ‘O’ sign by pinching together the tip of the thumb and index finger.

Pronator syndrome

Background and aetiology

Pronator syndrome is a controversial condition characterized by vague discomfort in the forearm that results from compression of the median nerve. It is usually chronic in nature although occasionally it may occur acutely secondary to a crush injury or bleeding within the flexor compartment of the forearm.

Presentation, investigations and treatment options

Presentation

Patients with pronator syndrome present with diffuse pain over the proximal forearm along the course of the median nerve. The symptoms may resemble those of carpal tunnel syndrome. In both conditions there is pain and paraesthesia over the radial three and a half digits that is made worse with certain repetitive tasks. Nocturnal symptoms tend to be more common with carpal tunnel syndrome with pain relief occurring on shaking the fingers. Patients with pronator syndrome often report weakness of pronation, but do not usually notice weakness or paralysis of the small muscles of the hand innervated by the median nerve. They do occasionally report that the thumb feels clumsy.

In pronator syndrome there may be sensory loss over the thenar aspect of the palm that is supplied by the palmar cutaneous branch of the median nerve the origin of which is proximal to the carpal tunnel. Phalen’s test is usually negative, however, there are three specific provocation tests that are helpful in identifying the site of nerve compression:

• If compression is at the level of pronator teres resisted forearm pronation, with the elbow in flexion and with gradual extension of the arm will reproduce the symptoms.

• Compression under the bicipital aponeurosis can be assessed by resisted forearm flexion, with the arm in supination. This manoeuvre should increase the patient’s discomfort.

• When compression occurs beneath the fibrous arcade of the FDS, resisted flexion of the proximal interphalangeal joints, forced forearm pronation or elbow flexion against resistance will all aggravate the patient’s symptoms.

Palpation may indicate tenderness over the proximal forearm along the course of the nerve with Tinel’s sign being most prominent at the main site of compression. This could be at the ligament of Struther, the lacertus fibrosus or the fibrous arcade of the FDS. Local pressure over pronator teres in the proximal forearm may increase discomfort.

Summary Box 31.2 Pronator syndrome provocation tests

Site of compression	Provocation tests
Pronator teres	Symptoms reproduced by resisted forearm pronation with the elbow in flexion and with gradual extension of the forearm
Bicipital aponeurosis	Symptoms increased by resisted forearm flexion with the arm in supination
Fibrous arcade of flexor digitorum superficialis	Symptoms increased by resisted flexion of the proximal interphalangeal joints, forced forearm pronation or elbow flexion against resistance

Investigations

Electrophysiological tests and, in particular, needle electromyograms (EMGs) can be useful to confirm the diagnosis.

Treatment options

Conservative treatment with rest, the avoidance of exacerbating activity and the use of non-steroidal antiinflammatory drugs are appropriate measures for the majority of patients. Only if symptoms persist would surgical decompression of the nerve usually be considered.

Surgical technique and rehabilitation

The operative treatment of pronator syndrome and rehabilitation is identical to that described for anterior interosseous nerve syndrome.

Outcome including literature review

Over 50–70% of patients with pronator syndrome respond to conservative treatment.^35,³⁶ Following failure of conservative management, surgical treatment has been shown to have a 90% success rate.^37,³⁸

Radial tunnel syndrome

Michele and Krueger ³⁹ first described radial tunnel syndrome (RTS) as radial pronator syndrome in 1956, however Roles and Maudsley⁴⁰ were the first to coin the term radial tunnel syndrome having defined the anatomical boundaries of the region and identified the structures that could cause compression of the posterior interosseous nerve.

Radial tunnel syndrome is a clinical entity that is difficult to diagnose due to the diffuse nature of its symptoms, and as a result there has been debate about its very existence.

Weitbrecht and Navickine ⁴¹ noted an incidence of 1% in a large series of compression neuropathies of the upper limb. This relatively low figure may reflect the difficulty in making an accurate diagnosis with many cases being wrongly labelled as resistant tennis elbow.^40,⁴²

Cravens and Kline ⁴³ reported RTS secondary to repetitive activities associated with musicians swimmers and tennis players.

Background and aetiology

The radial nerve is a branch of the posterior cord of the brachial plexus and carries fibres from C6, C7 and C8. In the arm it supplies the triceps and runs within the spiral groove before entering the anterior aspect of the arm by piercing the lateral intramuscular septum some 12 cm proximal to the lateral epicondyle. It travels between the brachialis and biceps tendon medially, and the mobile wad laterally. The nerve passes over the anterior aspect of the elbow at the level of the radiocapitellar joint. Just distal to this the nerve divides into the purely motor posterior interosseous nerve and the superficial radial nerve. The posterior interosseous nerve passes beneath the arcade of Frohse and between the two heads of the supinator muscle. The superficial radial nerve passes superficial to the supinator muscle on the deep surface of brachioradialis. Recurrent vessels of the radial artery cross perpendicular to the radial nerve and may be a cause of dynamic compression of the superficial radial nerve.

The radial nerve can be compressed at a number of levels as described by Konjengbam and Elangbam:⁴⁴

• Leading edge of the extensor carpi radialis brevis

• Radiocapitellar arthrosis

• Ligament of Frohse

• Between the two heads of supinator ⁴⁵

• As it exits from under the brachioradialis (handcuff neuritis).

Presentation, investigations and treatment options

Presentation

The presenting symptoms of radial tunnel syndrome are rarely severe enough to cause significant muscle weakness and as a consequence it is often difficult to make the diagnosis. Clinically there is considerable overlap and similarity between the presentation of RTS and lateral epicondylitis.

Patients with radial tunnel syndrome may report an aching sensation, extending from the volar aspect of the forearm to the radial aspect of the hand. Pure motor loss is rare although patients often have a deep-seated aching of the supinator muscle and some subjective feeling of weakness.

A useful examination technique is the rule of nine described by Loh et al.⁴⁶ In Figure 31.12 the three medial pressure areas should not be painful and serve as controls. The proximal of the three middle circles misses the nerve and if painful usually indicates biceps tendonitis. The two more distally are in line with the median nerve and if painful may indicate a high median nerve lesion. The specific test for RTS is a pain response over the two lateral proximal circles.

Figure 31.12 Radial and median nerves and their relation to pressure areas denoted by circles.

(Courtesy of Professor J. Stanley.)

Tenderness is often elicited along the line of the radial nerve. In addition tenderness may be reproduced in the extended elbow by passively flexing the wrist with pronation. Alternatively pain may be produced when the wrist is extended or supinated against resistance. The pain occurs in the extensor muscle mass rather than the lateral epicondyle which would be consistent with tennis elbow.

The middle finger test is also thought to be sensitive for detecting radial tunnel syndrome. The patient is asked to hold the elbow, wrist and fingers in full extension whilst the examiner applies counter-pressure to the digits. A positive test occurs when pain is greatest on applying pressure to the middle finger rather than the other digits. It is believed that as extensor carpi radialis brevis inserts into the base of the middle finger metacarpal stress on this tendon causes compression of the posterior interosseous nerve. Resisted and repetitive supination of the extended elbow may also reproduce pain over the radial tunnel and common extensor muscles.

Clinical Pearl 31.5

The presenting symptoms of radial tunnel syndrome are vague with deep seated aching pain in the line of the radial nerve. It is rare for there to be significant muscle wasting.

Investigations

Electrophysiology is often unrewarding in radial tunnel syndrome. Albrecht et al ⁴⁷ have shown that the accuracy of diagnosis can only be improved to 50% even with detailed electromyograms. Differential injections^38,^42,⁴⁸ may help distinguish lateral epicondylitis from RTS while imaging studies are only useful if a mass lesion around the elbow is suspected as the aetiological factor.

Treatment options

Most cases of RTS should be treated non-operatively with simple techniques such as the avoidance of repetitive activities and the use of elbow or wrist splints. Simple analgesics and non-steroidal antiinflammatory agents may also be helpful.

Surgery should be considered only after a minimum 3-month period of conservative management has failed.³⁸

Surgical technique and rehabilitation

The patient is placed supine on the operating table with the symptomatic arm resting on an arm table. A narrow high arm tourniquet is applied.

The incision begins approximately 5 cm proximal to the lateral epicondyle and is extended towards the lateral epicondyle before passing distally around the mobile wad. The plane between the extensor carpi radialis brevis (ECRB) and the extensor digitorum communis (EDC) is identified and developed allowing visualization of the superficial head of the supinator muscle (Fig. 31.13). In order to have adequate exposure it is often necessary to detach the ECRB tendon from the lateral epicondyle.

Figure 31.13 Plane of dissection between ECRB and ECU/EDC fibres.

(Courtesy of Professor J. Stanley.)

After ligating the vessels that constitute the leash of Henry (Fig. 31.14) the superficial radial nerve is identified and traced back to the posterior interosseous nerve which passes under the arcade of Frohse (Fig. 31.15) between the two heads of supinator.

Figure 31.14 (A) A: Leash of Henry; B: Superficial branch of radial nerve; C: Brachioradialis. (B) Ligating the leash of Henry. (C) Superficial and deep branches of radial nerve.

Figure 31.15 (A) Identifying arcade of Frohse. (B) Dissecting arcade from underlying nerve. (C) Decompressing the nerve by incision the arcade.

At our institution we decompress the superficial head of the supinator completely. Occasional aponeurotic bands on the deep surface of the superficial head of the supinator can compress the nerve more distally and it is for this reason that we release the supinator throughout its whole length.⁴²

Outcome including literature review

A systematic review of the literature by Huisstede et al ⁴⁹ found no randomized controlled trials or controlled clinical trials for testing the efficacy of different treatment protocols for RTS. The study indicated that surgical decompression of the radial tunnel might be effective in patients with RTS but the role of conservative management was less clear. Good to excellent relief of symptoms has been reported in 51–92% cases.^50,⁵¹ The results from our institution⁵² show that 70% of patients have a favourable outcome following surgery although like Sotereanos⁵³ we noted that patients who had claims pending did less well. Tsai et al³⁸ suggest that the range of outcomes following surgery is likely to represent the subjective nature of the diagnosis with poor localization of pain, a more chronic presentation leading to permanent changes within the nerve or a more frequent association with compensation claims.

Posterior interosseous nerve palsy

Background and aetiology

At the level of the elbow the posterior interosseous nerve passes beneath the arcade of Froshe and between the two heads of the supinator muscle. It may be compressed by a number of structures.

• Synovitis

Synovitis over the anterior radiocapitellar joint can cause local compression of the posterior interosseous nerve and result in paralysis and finger drop. In rheumatoid patients this can cause a diagnostic dilemma as it may be mistaken for rupture of the extensor tendons at the level of the wrist. The differential diagnosis of loss of digital extension is summarized in Summary box 31.3.

Summary Box 31.3 Differential diagnosis of loss of digital extension

Pathology	Clinical features	Test
Posterior interosseous nerve palsy	Loss of digital and/or wrist extension	Tenodesis effect present
Extensor tendon rupture	Loss of digital extension	Loss of compensatory digital extension on passive flexion of the wrist (tenodesis effect)
Sagittal band rupture	Loss of digital extension	Passive extension of the finger allows centralization of the tendon over the metacarpophalangeal joint thus allowing the patient to maintain digital extension but not initiate it