Uncommon Nerve Entrapment Syndromes

Nerve entrapment syndromes are a group of conditions in which peripheral nerves are damaged, through compression or repeated trauma. This session will look at conditions which cause compression of three nerves:

• Suprascapular nerve
• Lateral femoral cutaneous nerve (meralgia paraesthesia)
• Tibial nerve at the ankle (tarsal tunnel syndrome)

The pathological process is similar in each case. Therefore, the general principles of treatment are similar.

The generic features will be considered first. Each nerve-specific syndrome will then be reviewed, the anatomy described and specific treatments discussed.

Median nerve at the wrist (carpal tunnel syndrome), ulnar nerve at the wrist and elbow and radial nerve in the forearm are examined in the Learning Zone session: on Common Entrapment Syndromes.

Nerve entrapment syndromes are caused by chronic injury to a nerve as it travels through a bony or ligamentous tunnel.

Repetitive compression, rubbing or sliding of the nerve within the canal, or against a bony prominence, results in chronic injury to the nerve. Immobilisation of the affected area with a splint can reduce this form of damage.

Entrapment neuropathies can also be caused by systemic disorders such as rheumatoid arthritis, pregnancy, acromegaly, or hypothyroidism.

Repetitive injury to a nerve may result in ischaemia, oedema and damage to the myelin sheath of the nerve.

Focal segmental demyelination at the area of compression is the key patho-physiological feature of all nerve entrapment syndromes.

Complete recovery of function after surgical decompression reflects re-myelination of the injured nerve.

Incomplete recovery in more chronic and severe cases of entrapment is due to Wallerian degeneration of the axons and permanent fibrotic changes in the neuromuscular junction. These changes prevent re-innervation and restoration of function.

The symptoms of nerve entrapment syndromes are dependent on the nerve involved, but some generalisation of nerve entrapment syndromes can be made.

The symptoms can be identified as irritative symptoms of pain and paresthesia, which affect sensory nerves and follow a temporal sequence.

If these symptoms are not treated, ablative symptoms, such as numbness of sensory nerves, and weakness and atrophy of motor nerves follow. These changes may be irreversible.

The initial management involves:

• Analgesia
• Reducing the aggravating movement (splinting or change of activity)

If this fails, surgical decompression may be required.

Introduction

Where does the suprascapular nerve originate from?

The suprascapular nerve arises from the upper trunk of the brachial plexus and travels with the suprascapular artery across the posterior triangle of the neck (Fig 1).

The artery and nerve dip under the trapezius and pass through the suprascapular notch on the superior border of the scapula. The nerve then passes through the suprascapular fossa, supplying supraspinatus muscles before tracing along the base of the spine of the scapula to supply the infraspinatus muscle. This nerve also supplies sensation to the posterior aspect of the shoulder joint.

The suprascapular ligament crosses the upper margin of the suprascapular notch and can cause entrapment of the suprascapular nerve, particularly if the notch is tight.

Compression of the sensory fibres causes an ill-localised, dull shoulder pain.

Athletes, especially those involved with shoulder movement, such as gymnasts, weightlifters and basketball players, are particularly at risk.

Pathophysiology

The suprascapular nerve can be injured in several places.

• The suprascapular notch. The nerve is apposed to the inferior margin of the superior transverse scapular ligament.
• Between the spine of the scapula and the tendinous margin of the infraspinatus and supraspinatus muscles during extreme abduction and external rotation of the shoulder.
• Compression at any point by a mass, most commonly a ganglion cyst.

Investigations

As with most nerve entrapment neuropathies, the diagnosis is normally clinical.

MRI images display a high signal intensity in the affected nerve segment at the site of the compression because of the presence of oedema in the myelin sheath and perineurium.

MRI is also very good at detecting masses causing compression, and can detect muscle atrophy.

Electromyographic (EMG) studies may show signs of denervation of supraspinatus and infraspinatus, but are invasive and technique dependant.

Treatment and Prognosis

Conservative measures consist of educating the patient to adopt avoidance behaviours. However, this seldom works in young, physically-active patients, especially if symptoms are occupation related.

Conditioning exercises, and periodically injecting the nerve with bupivacaine and dexamethasone, may accord long-term relief.

Surgery is recommended for physically-active patients and those with severe and long-standing symptoms or weakness.

Prognosis

Symptomatic improvement is expected in 95% of patients who undergo decompression, often within days of the surgery.

Lateral Femoral Cutaneous Nerve Entrapment

What type of nerve entrapment is lateral femoral cutaneous nerve entrapment?

The lateral femoral cutaneous nerve originates directly from the lumbar plexus and has root innervation from L2-3.

The nerve runs through the pelvis along the lateral border of the psoas muscle to the lateral part of the inguinal ligament.

Here, it passes to the thigh through a tunnel formed by the lateral attachment of the inguinal ligament and the anterior superior iliac spine.

This is the most common site of entrapment.

Entrapment causes a painful mononeuropathy of the lateral femoral cutaneous nerve (LFCN).

It is a purely sensory nerve, innervating the anterolateral thigh.

The clinical history, and examination, is usually sufficient to make the diagnosis.

The image illustrates the path of the lateral cutaneous nerve showing area of compression.

Clinical Presentation

The patient typically complains of numbness and paraesthesia of the upper lateral thigh, which may be painful.

The symptoms are usually unilateral and may be aggravated by walking or standing, and helped by sitting.

Examination reveals numbness of the anterolateral thigh in the area of paraesthesia.

Tapping over the upper lateral inguinal ligament, or extending the hip may make the paraesthesia worse. Motor strength should be normal.

It is associated with pregnancy, tight-fitting clothing and obesity.

It is more common in diabetics and, rarely, may be caused by a tumour or iliopsoas haemorrhage.

The image illustrates the clinical presentation of meralgia paraesthesia.

The entrapment of the lateral femoral cutaneous nerve causes may be intrapelvic, extrapelvic or mechanical.

Differential Diagnosis

Differential diagnoses for meralgia paraesthesia include:

• Femoral mononeuropathy
• Lumbosacral disc compression

Treatment and Prognosis

The diagnosis is normally clinical.

Nerve conduction studies are technically difficult to perform.

The diagnosis can be confirmed by resolution of symptoms after the injection of 0.5% bupivacaine, one finger breadth below the anterior superior iliac spine.

The condition resolves on its own in at least 25% of cases.

Removing the cause is the best treatment by losing weight or wearing loose-fitting clothing.

When pain is severe, a steroid injection may temporally relieve symptoms.

If symptoms persist, surgical decompression may be required.

Prognosis

The pain typically resolves slowly over time, but the numbness in the distribution of the LFCN may persist.

Tarsal Tunnel Syndrome

What is tarsal tunnel syndrome (TTS)?

The flexor retinaculum extends posteriorly and distally from the medial malleolus. The tibial nerve passes behind the medial malleolus and beneath the flexicular retinaculum bifurcating into calcaneal and plantar branches.

Several factors may contribute to the development of tarsal tunnel neuropathy:

• Soft tissue masses, for example lipomas, within the tendon sheath may cause compression neuropathy of the posterior tibial nerve
• Bony prominences and exostoses may also contribute to the disorder
• Valgus deformity of the hind foot may contribute to the neuropathy, by increasing the tensile load on the tibial nerve

Clinical Presentation

Findings of pain, paresthesias, and numbness are not uncommon, but symptoms generally subside with rest; although they may not fully disappear.

In some cases, atrophy of the intrinsic foot muscles may be noted, although this may be clinically difficult to ascertain.

Eversion and dorsiflexion may cause symptoms to increase at the endpoint range of motion.

Differential Diagnosis

Differential diagnoses for TTS include:

• Plantar fasciitis
• Stress fractures of the hind foot
• Herniated vertebral disc
• Peripheral neuropathies, for example from diabetes or alcoholism, and inflammatory arthritides, such as Reiter’s syndrome or rheumatoid arthritis

Investigations

Nerve conduction studies are a useful adjunct to clinical examination, but TTS is possible with normal nerve conduction studies.

It should also be noted that in normal elderly patients, sensory responses may be absent.

MRI and ultrasound may be useful in diagnosis if soft tissue masses, or a space occupying lesion, are considered the cause for the nerve compression.

Plain radiography may be useful for diagnosis of fractures, bony masses and osteophytes, which may cause the nerve compression.

Treatment and Prognosis

Conservative treatment includes the use of local anaesthetics and soluble steroids, which may aid in the reduction of the patient’s pain.

The use of night splints with the foot in plantar flexion and varus may be considered in patients with a valgus foot.

When medical therapies fail, surgical decompression may be required.

Prognosis

Studies demonstrate that approximately 75% of patients who undergo surgical decompression have appreciable pain relief, and 25% obtain little or no relief.

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