Compression syndromes

Etiology and pathogenesis

Compression, or tunnel, neuropathies are pathological conditions that develop due to mechanical impact on peripheral nerves. This impact can be either single or repetitive.

The main pathogenetic mechanism of the disease consists in chronic compression of nerve trunks in narrow anatomical spaces—the so-called tunnels (canals).

Among the key causes leading to the development of compression are:

• Various limb injuries.
• Nerve compression by surrounding soft tissues.
• Bone fractures disrupting the anatomy of the canal.
• Formation of hematomas that physically reduce the tunnel volume and put pressure on the nerve.

Clinical presentation and diagnostics

Clinical manifestations of tunnel syndromes develop in a strict sequence. It is important to remember that sensory disturbances always appear first. This is explained by anatomical features: thick sensory nerve fibers are significantly larger than motor ones, which is why they react faster to ischemia and mechanical pressure.

• Initial symptoms: patients complain of paresthesia, hyperesthesia (increased sensitivity), or hypesthesia (decreased sensitivity). Pain syndrome is also characteristic, and the pain can be localized either strictly in the innervation zone of the affected nerve or spread far beyond it.
• Late symptoms: indicate significant damage to nerve fibers. At this stage, motor and autonomic-trophic disorders join, and muscle weakness and hypotrophy of the innervated muscles occur.

An absolutely pathognomonic sign is Tinel's sign. It manifests as increased sensitivity, soreness, or paresthesia upon percussion (tapping) at the site of suspected nerve compression.

To confirm the diagnosis and accurately assess the degree of damage, the following are used:

1. ENMG (electroneuromyography): the key method for studying the conduction velocity of electrical excitation along sensory and motor fibers.
2. EMG (electromyography).
3. Ultrasound of the peripheral nerve to visualize the structure.
4. MRI (used when available for a detailed assessment of soft tissues).

Epidemiology of frequent mononeuropathies

• Median nerve neuropathy: most commonly proceeds in the form of carpal tunnel syndrome. This is the most prevalent pathology, accounting for up to 2/3 of all cases of tunnel neuropathies.
• Ulnar nerve neuropathy at the elbow level: the second most common compression-ischemic neuropathy after median nerve lesion. Interestingly, in 75% of cases, the compression localization is in the retroepicondylar groove, and only in 25% in the cubital canal itself. Because of this, the term "cubital tunnel syndrome" is considered anatomically inaccurate for most patients. It is preferable to say "ulnar nerve neuropathy at the elbow level," although some authors still include the groove in the canal structure.
• Radial nerve neuropathy: is also one of the most frequent compression-ischemic neuropathies. The incidence ranges from 1.5 to 3 cases per 100,000 adult population, with the pathology being more common in men. In frequency, it is second only to carpal and cubital syndromes, as well as Morton's metatarsalgia and Meralgia Paresthetica (lateral femoral cutaneous nerve neuropathy).

Principles of treatment

Patient management tactics depend on the stage of the disease.

Conservative treatment (in early stages):

• First of all, it is necessary to eliminate the etiological factor, i.e., treat the underlying disease.
• It is important to exclude provoking factors: the patient is forbidden to stay in an uncomfortable posture for a long time and perform monotonous stereotyped movements.
• Orthopedic correction using special bandages and splints is applied.
• As local therapy, the introduction of corticosteroids directly into the corresponding anatomical canal is effective.

Symptomatic pharmacotherapy: If the patient is bothered by severe pain and paresthesia, non-steroidal anti-inflammatory drugs (NSAIDs) and non-narcotic analgesics are prescribed. Anticonvulsants (pregabalin, gabapentin, carbamazepine) are used to relieve neuropathic pain.

Surgical treatment: Indicated in cases where conservative therapy proves ineffective (which is common in clinical practice). The main goal of the operation is to perform surgical decompression of the compressed nerve.

Features of the treatment of neuropathies involving facial muscles: In some cases (for example, in neuropathies where the role of herpes simplex virus is proven), the treatment regimen is expanded:

• Glucocorticosteroids: Prednisolone is prescribed at a dose of 60–80 mg/day in the first 5–7 days. Then the dosage is gradually reduced over 10–14 days. This regimen ensures faster functional recovery.
• Antiviral therapy: Acyclovir is used orally 400 mg 5 times a day (7-day course) OR Valacyclovir 1 g 3 times a day (7-day course).
• Non-drug treatment (from the first days): special gymnastics of facial muscles is indicated. Adhesive tape patches are used to prevent overstretching of the affected muscles.
• Prevention of complications: if the patient has lagoftalmus (incomplete eyelid closure), artificial tear preparations are mandatory. This is critically important to prevent corneal damage.

Class and exam questions

What else to study on this topic

• Technique of performing and interpreting ENMG and EMG results
• Anatomy of the retroepicondylar groove and cubital canal
• Morton's metatarsalgia and Meralgia Paresthetica: clinical picture
• Regimens for using anticonvulsants in neuropathic pain
• Indications and methods of surgical decompression of peripheral nerves

Other topics in the "Additional Topics" section

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