Nerve compression syndrome

Last revised by Joshua Yap on 20 May 2023

Nerve compression syndromes or nerve entrapment neuropathies are a group of several nerve disorders associated with sensory and/or motor loss resulting from nerve compression.

Nerve compression syndromes are common 1-5 and can account for 10-20% of cases in specialist clinics of neurosurgeons, orthopedic and plastic surgeons treating those cases. The most common nerve entrapment neuropathy is carpal tunnel syndrome 1-3 followed by cubital tunnel syndrome 1.

Predisposing factors that increase the risk of nerve compression syndromes include the following 3:

Nerve compression syndromes are associated with the following conditions 2:

The diagnosis of most nerve entrapment neuropathies can be made on clinical grounds. Electrodiagnostic tests as nerve conduction studies and electromyography can help to confirm the clinical diagnosis 4. A local nerve block by injecting a local anesthetic can also confirm the diagnosis.

Symptoms of nerve entrapment syndromes will mostly depend on the location and the nerve involved and generally include pain, paresthesia numbness, muscular weakness and atrophy in specific distribution territory of the affected nerve. Clinical testing might include altered reflexes or sensory testing including decreased mechanosensitivity 3.

In major mixed nerves, symptoms might also include dry skin, cracked nails and recurrent skin ulcerations.

Some nerve entrapment syndromes will predominantly or only feature either motor or sensory symptoms.

Acute injury or chronic repetitive trauma and compression are thought to cause edema and microvascular ischemic changes of the myelin sheath 3,4. This can result in structural alterations such as fibrosis, focal or segmental demyelination, degeneration and inflammatory changes of the myelin sheath and possibly the nerve axons at the site of compression further leading to alterations in axonal transport and decreased mechanosensitivity 3,4.

The majority of peripheral nerve compression injuries can be classified as grade 1 nerve injuries or neuropraxia and are characterized by focal demyelination at the compression site without associated axonal or connective tissue damage 5,6.

Nerve compression syndromes often develop at specific sites, where nerves travel through narrow anatomical openings such as fibrous, fibro-osseous or muscular tunnels and rub at tight edges or get compressed during motion.

A multifactorial origin is considered in which the occurrence of an acute or chronic repetitive stress due to fixed or dynamic compressive forces are important factors 6. However, beyond that, the exact etiology of nerve compression syndromes seems to be largely unknown 2,3.

Nerve entrapment neuropathies can be categorized by their location and include the following 4,7-13:

Under the microscope chronic nerve compression injuries are usually feature the following 5,6:

  • normal axonal morphology and neuromuscular junctions

  • thin degraded myelin sheath (increase in g-ratio: axon/fiber diameter)

  • decreased internodal length

  • Schwann cell proliferation with an increase in Schmidt Lanterman incisures

Ultrasound is useful in the assessment of peripheral entrapment neuropathies such as carpal tunnel syndrome or cubital tunnel syndrome and might demonstrate an increase in cross-sectional area or mass-like enlargement, a decrease in echogenicity and hyperemia of the affected nerve segment 9-11. Ultrasound might also show increased echogenicity of affected muscle groups 9.

MRI might be acquired especially in more proximal entrapment neuropathies 3 and might show alterations in signal intensity and morphology at the area of the affected nerve segment 12. It might show signs of denervation of the affected muscle groups like muscle edema, muscle atrophy and/or fatty degeneration and can identify mass lesions such as cysts or tumors compressing a specific nerve 12.

Nerves can be directly assessed with T2-weighted neurography by using sequences with long echo times (≥90 ms), frequency-selective fat suppression and radiofrequency saturation for signal suppression of the adjacent vessels 12. Unlike in tendons, magic angle phenomena can persist at higher echo times in peripheral nerves (up to 70 ms) and on STIR secquences 12.

  • T1: iso or hypointense

  • T2: hyperintense

  • T2SPAIR/STIR: hyperintense

  • T1 C+ (Gd): enhancement

The radiological report should include a description of the following features:

  • signal alterations or enhancement of the affected nerve

  • morphological nerve changes

  • denervation changes in muscles

  • possible etiologies (e.g. mass occupying lesions)

Management depends on the site and etiology and usually initially includes conservative measures and surgery in refractory or longstanding cases 13. Nerve compression syndromes due to lifestyle or occupational conditions might be initially treated behavioral modifications, manual exercises, splinting and local corticosteroid therapy 3,5.

Pregnancy-related nerve compression syndromes as meralgia paraesthetica might become asymptomatic after delivery and weight loss. Nerve compression syndromes associated with systemic conditions as autoimmune or thyroid disease might be managed by treating the underlying systemic disorder.

Surgical decompression is an option in patients with longstanding symptoms that are refractory to conservative measures or motor deficits as weakness. Prognosis varies slightly with the specific nerve compression syndrome and the underlying etiology. Surgical decompression is usually effective. Recurrences occur in 10-30% depending on the specific type of nerve entrapment.

If left untreated nerve compression syndromes can lead to axonal Wallerian degeneration and permanent fibrotic changes with functional loss, muscular atrophy and fatty degeneration.

Descriptions of nerve compression syndromes go back to the early 19th century, where they were mentioned by Sir Astley Cooper in the 1820s and Sir James Paget in the 1850s 7. The first decompression surgery a transverse carpal ligament release was performed by Dr Herbert Galloway in 1924 on a patient whose wrist was crushed by a falling window 7.

The differential diagnosis of nerve entrapment syndromes depends on the location of nerve entrapment. Beyond that they include the following:

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