Peripheral nerve entrapment: how to diagnose and when to refer

Peripheral nerve entrapment (entrapment neuropathy) can affect any peripheral nerve in the body. Entrapment may occur when nerves pass through narrow, rigid tunnels, traverse highly mobile joints, pass along hypertrophied muscles or fibrous bands, or are subject to extrinsic pressure from certain limb postures. Such compressions are more likely with repetitive activity, presence of tissue swelling, trauma, and generalised polyneuropathies such as diabetic neuropathy, or in some inherited neuropathies such as hereditary neuropathy with liability to pressure palsies.1

While there are some 50 described different entrapment neuropathies,2,3 here we discuss some of the more common entities, and outline an approach to clinical diagnosis, investigation and management (Box 1 and Box 2). It is important that the treating practitioner perform a focused clinical assessment before referral for investigations, so that the appropriate test is performed in a timely manner. For most entrapments, symptoms are more prominent than overt signs unless the process is advanced; muscle wasting is usually a late sign. Commonly, entrapment neuropathies are confused with radiculopathies or more diffuse neuropathies, and patients may therefore be inappropriately referred for spinal imaging.

Diagnostic considerations

Each entrapment or compression neuropathy is recognised by sensory symptoms (pain and/or numbness and paraesthesia in the anatomical distribution of that nerve) and in more severe cases, weakness and muscle wasting confined to muscles innervated by that nerve. Although pain may extend more diffusely, the sensory loss is limited to the known anatomical nerve territory. Objective signs or neurophysiological evidence of sensory or muscle involvement outside that territory should suggest an alternative (or additional) diagnosis. Hence, a working knowledge of peripheral nerve anatomy is crucial in these assessments. Increasingly, ultrasound or magnetic resonance imaging studies are being used in the assessment of peripheral nerve injuries. They may be particularly helpful in the more disputed entities.4

Electrophysiological studies are useful to provide objective evidence of localised nerve dysfunction, to exclude various mimics, assess severity and gauge prognosis. Typical nerve conduction changes are localised slowing or conduction block at the site of compression, reduced motor or sensory responses in distal segments of the nerve, normal findings in adjacent nerves, and in more severe cases, electromyography (EMG)‐recorded denervation in muscles distal to the compression.

Many upper limb mononeuropathies can be mimicked or be caused by brachial neuritis (also known as neuralgic amyotrophy or Parsonage–Turner syndrome), an acute onset inflammatory neuritis presenting with severe regional pain and subsequent weakness and wasting in various territories, typically in the shoulder girdle.5 Restricted forms resembling suprascapular neuropathy, anterior interosseous neuropathy, long thoracic neuropathy or upper brachial plexopathy can be difficult to differentiate from entrapment clinically and sometimes even with EMG. The nerves of the upper limb are shown in the Supporting Information.

Upper limb

Carpal tunnel

The most common entrapment neuropathy involves the median nerve at the wrist (carpal tunnel syndrome), which classically presents with nocturnal sensory symptoms, relieved by shaking the hand. Symptoms affect the lateral digits, sometimes the whole hand, and pain may radiate into the forearm but rarely to the shoulder. In these atypical presentations, it is essential to consider the differential diagnosis. Similar hand numbness may also result from C6 or C7 radiculopathy, with or without upper limb weakness. Conversely, thenar wasting or weakness is also a feature of C8/T1 radiculopathy or lower trunk brachial plexopathy; however, these present with thenar and hypothenar weakness, and sensory loss in the ulnar side of the hand. Thenar wasting can also result from local arthritis and mimic carpal tunnel syndrome. The diagnosis should always be confirmed with nerve conduction studies, looking for localised slowing of sensory or motor conduction at the distal median nerve across the carpal tunnel. Mild sensory disturbance is managed with nocturnal wrist splints. More persistent symptoms may improve in the short term with local steroid injection,6 but in patients with hand weakness or failed conservative treatment, referral for surgical decompression is indicated.

Cubital tunnel

Ulnar nerve entrapment at the elbow (cubital tunnel syndrome) is the second most common entrapment neuropathy. It may result from habitual elbow flexion or leaning on elbows, and can be associated with nerve subluxation at the elbow, prolonged bed rest or general anaesthesia, but may also occur decades following elbow trauma. Symptoms, signs and differential diagnoses are listed in Box 1. Clinically C8/T1 radiculopathy or lower trunk brachial plexopathy (thoracic outlet syndrome) will affect thenar muscles in addition to ulnar‐innervated intrinsic hand muscles. More extensive weakness and fasciculations should raise concern about motor neuron disease.

Electrodiagnostic features include localised slowing of motor or sensory conduction across the elbow segment, sometimes with localised conduction block or reduction of distal ulnar motor and sensory responses. Needle EMG helps identify significant muscle denervation seen in more severe cases, with changes confined to ulnar muscles.

Mild sensory disturbance is managed with hand therapy with or without elbow splints, and avoidance of provoking postures; weakness or failed conservative treatment may require surgical decompression (neurolysis or anterior transposition7).

Suprascapular nerve

Suprascapular nerve neuropathy, caused by entrapment at the suprascapular notch, beneath the suprascapular ligament, presents with non‐specific shoulder region pain and limitation of the use of the arm above shoulder level; it may present in people performing overhead activities, and in bodybuilders. Weakness usually presents later, following the shoulder pain. It can be difficult to separate from primary shoulder pathology, C5 or C6 radiculopathy (Box 1), and brachial neuritis,5 all of which produce shoulder pain, weakness and wasting. Rotator cuff degeneration is recognised by painful restriction of passive shoulder movements, in addition to pain‐related weakness with voluntary action. EMG shows denervation changes confined to the supraspinatus and infraspinatus muscles in suprascapular nerve palsy, whereas C5 and C6 radiculopathy are recognised by more widespread EMG abnormalities. Early management is conservative; however, prolonged symptoms, or significant weakness or wasting necessitate surgical decompression at the suprascapular notch.

Anterior interosseous nerve

The anterior interosseous nerve branch of the median nerve supplies the flexor pollicis longus, flexor digitorum profundus and pronator quadratus but has no cutaneous component. Anterior interosseous nerve entrapment deep to the forearm flexor muscles is rare, and many suspected entrapments are thought to be restricted forms of brachial neuritis.8 Differentiation from median neuropathy and C8 radiculopathy can be determined clinically (Box 1).

Electrodiagnostic features include denervation isolated to anterior interosseous nerve‐innervated muscles, with normal findings on standard median nerve conduction, and normal EMG of other median, ulnar and radial C8 muscles. Management commences with a trial of rest and physiotherapy, but failure of improvement should prompt consideration of surgical decompression.8

Posterior interosseous nerve

The posterior interosseous nerve is the terminal, purely motor branch of the radial nerve, distal to the branches to brachioradialis and extensor carpi radialis longus. Posterior interosseous nerve entrapment at the arcade of Frohse (tendinous arch of the supinator) is often confused with lateral epicondylitis. The presenting features may be differentiated from radial neuropathy and C7 radiculopathy by sensory changes and more proximal weakness (Box 1). Imaging may be helpful to identify structural lesions.

Electrodiagnostic features include EMG findings confined to posterior interosseous nerve muscles, with normal radial nerve conduction studies and normal EMG in proximal radial and C7‐ or C8‐innervated muscles. Failure of a trial of rest or steroid injection favours referral for surgical decompression at the arcade of Frohse.

Lower limb

Common peroneal nerve

The common peroneal nerve is typically compressed at the fibular neck; this may occur spontaneously, after prolonged squatting or habitual leg crossing, knee trauma, or pressure from ganglion cysts or plaster/bandages. The foot drop of peroneal nerve palsy differs from L5 radiculopathy by sparing ankle inversion weakness.

Neurophysiological diagnostic features include localised nerve conduction slowing or block across the fibular neck, and reduction in peroneal sensory responses, with denervation on EMG confined to the common peroneal nerve muscles. EMG abnormalities above the knee indicate a more proximal site of injury. Early and later management options are listed in Box 2, but avoidance of provoking postures and use of ankle splints for footdrop should not be forgotten.

Tarsal tunnel

The tarsal tunnel is a fibro‐osseous space on the medial side of the ankle where the posterior tibial nerve can be compressed, especially with ankle deformity. There are anatomical similarities with the carpal tunnel, but tarsal tunnel syndrome is not simply the lower limb analogue of carpal tunnel syndrome, as axonal loss pathology predominates over localised slowing. Compression typically produces plantar pain, numbness and tingling aggravated by weight‐bearing. The clinical presentation and extensive differential diagnoses (Box 2) often result in delayed diagnosis, although dispute remains regarding the optimal diagnostic and treatment options.9 Nerve conduction studies and EMG are less useful than in carpal tunnel syndrome, but in more severe cases show absent sensory and slowed motor responses in the plantar nerves. They have a greater role in exclusion of generalised sensory polyneuropathy and EMG changes of S1 radiculopathy.

Meralgia paraesthetica

Meralgia paraesthetica is the syndrome of entrapment of the lateral femoral cutaneous nerve where it traverses the inguinal ligament medial to the anterior superior iliac spine. Lateral thigh numbness, tingling or dysaesthesia may be intermittent or constant, often occurring with hip extension. The main differential diagnoses are mid‐lumbar radiculopathies, lumbar plexopathy or femoral neuropathy, which are distinguished by additional involvement of quadriceps muscles and knee reflex (Box 2).

Conclusion

This article addresses some of the more common entrapment neuropathies. It is evident that timely diagnosis requires a clear appreciation of functional anatomy, and consideration of various differential diagnoses, including radiculopathies, rheumatic conditions, and medical neuropathies, including neuralgic amyotrophy in painful, acute‐onset cases. The pattern of the reported pain or numbness and distribution of weakness should be consistent with a single nerve territory before attributing the presentation to a focal entrapment. Considerable extra localising information can be gained from properly performed electrophysiological studies, which are useful in confirming the diagnosis, assessing severity and prognosis. The determinants of functional outcome are multifactorial, including severity and duration of compression, patient age and comorbidities, and timely diagnosis and management.