Peripheral Nerve Compression Syndromes

Introduction

Peripheral nerve compression syndromes — entrapment neuropathies — are common conditions in which a peripheral nerve is compressed at a specific anatomical site, producing characteristic sensory and motor deficits in the nerve’s distribution. The compression may be acute (rare, typically traumatic) or chronic (the great majority of clinical cases). The chronic compression syndromes are produced by anatomical narrowness of fibro-osseous tunnels, by hypertrophied retinacular structures, by inflammatory or fibrotic tissue, by mass lesions, by repetitive mechanical forces, or by combinations of these factors. Successful management requires accurate diagnosis (based on anatomical knowledge of the typical compression sites, clinical examination, and selective use of electrodiagnostic studies), conservative measures appropriate to the specific syndrome, and surgical decompression when indicated. This chapter, synthesizing content from Apley & Solomon’s, Miller’s Review, Dutton’s Orthopaedic Examination, and Netter’s Examination, addresses the principal upper-limb compression syndromes (carpal tunnel, cubital tunnel, radial tunnel, posterior interosseous, anterior interosseous, Guyon’s canal, thoracic outlet syndrome), the lower-limb compression syndromes (tarsal tunnel, common and superficial peroneal nerve compression, meralgia paresthetica, piriformis syndrome), and the principles of evaluation and management.

General Principles

The pathophysiology of nerve compression follows a stereotyped sequence. Initially, increased pressure on the nerve impairs venous outflow, producing intraneural edema and increased endoneurial fluid pressure. Continued compression compromises arterial inflow and produces nerve ischemia. With sustained compression, there is segmental demyelination at the compression site, followed by axonal injury (Wallerian degeneration) of progressively more axons. The earliest physiological consequence is reduced conduction velocity across the compression site; later, conduction block and reduction in compound muscle action potential amplitude develop. Initially the changes are reversible with relief of compression; with prolonged compression, the axonal damage produces irreversible deficits. The clinical presentation reflects this sequence: the earliest symptoms are intermittent paresthesias and dysesthesias in the nerve distribution, often nocturnal or activity-related; progressively, the symptoms become continuous, with persistent numbness and motor weakness; in established disease, atrophy of the innervated muscles develops. The investigation of suspected nerve compression includes: focused clinical examination of the nerve’s sensory and motor distribution; provocative tests (Tinel, Phalen, and various nerve-specific maneuvers); assessment for muscle wasting; assessment of the differential diagnosis (cervical or lumbar radiculopathy, more proximal nerve injury, neurological disease, systemic causes of polyneuropathy); and selective use of electrodiagnostic studies (nerve conduction studies and EMG, with the principal diagnostic features being slowed conduction velocity and prolonged latency at the compression site, with denervation

potentials in the innervated muscles in advanced disease). Imaging (ultrasound, MRI) is increasingly used in selected cases.

Carpal Tunnel Syndrome

Anatomy and Etiology Carpal tunnel syndrome (CTS) is compression of the median nerve at the wrist beneath the transverse carpal ligament (flexor retinaculum). The condition is the commonest peripheral nerve compression syndrome, with a lifetime prevalence of approximately 10%. The carpal tunnel contains nine flexor tendons (four FDP, four FDS, one FPL) plus the median nerve, with the transverse carpal ligament forming the volar boundary and the carpal bones forming the dorsal and lateral boundaries. The volume of the tunnel is fixed; any increase in tendon volume (tenosynovitis) or in fluid content (fluid retention) raises the pressure on the median nerve. Risk factors include female sex (3:1 ratio), age 40-60 years, pregnancy and lactation, diabetes mellitus, rheumatoid arthritis, thyroid disease, obesity, occupational repetitive hand use (controversial as an isolated risk factor), and various uncommon causes including amyloidosis (particularly in dialysis patients) and acromegaly. Clinical Features The classical presentation is of intermittent paresthesia, numbness, and pain in the median nerve distribution of the hand (the palmar aspect of the thumb, index, middle, and radial half of the ring finger), typically worst at night and waking the patient from sleep. The patient often describes a need to shake the hand to relieve the symptoms (“flick sign”). Activities that maintain the wrist in flexion or extension (reading a book, driving, using a phone) provoke symptoms. As the condition progresses, the symptoms become more constant, with persistent numbness and reduced sensation. In advanced disease, motor symptoms develop with weakness of thumb abduction and opposition (the thenar muscles supplied by the recurrent motor branch) and visible thenar atrophy. Examination findings include: positive Tinel sign at the volar wrist (percussion over the median nerve producing distal paresthesia in the nerve distribution); positive Phalen test (sustained wrist flexion for 60 seconds producing distal paresthesia); positive carpal compression test (sustained pressure over the volar wrist producing paresthesia); reduced two-point discrimination in the median nerve distribution (a later finding); thenar atrophy and reduced abductor pollicis brevis strength (advanced disease). Investigations Electrodiagnostic studies are the gold-standard objective test, demonstrating slowed conduction velocity and prolonged latency across the carpal tunnel. Sensory studies are more sensitive than motor studies for early disease. Ultrasound demonstrates median nerve swelling proximal to the carpal tunnel (cross-sectional area >9-12 mm²) and is increasingly used as an alternative to electrodiagnostic studies.

Treatment Initial management is conservative: night-time wrist splinting in neutral position (which prevents the wrist flexion-extension that exacerbates symptoms); activity modification; oral or injected corticosteroids (with corticosteroid injection providing dramatic short- term relief in many cases, although the long-term outcomes are often disappointing without addressing underlying factors); and management of contributing systemic conditions. Surgical management — carpal tunnel release — is indicated for symptoms refractory to conservative care, for the presence of motor symptoms or thenar atrophy, and for advanced disease. Two techniques are used: Open carpal tunnel release: A small palmar incision over the carpal tunnel, with direct visualization and complete transection of the transverse carpal ligament. Excellent outcomes, low complication rate, and substantial decompression of the median nerve. Endoscopic carpal tunnel release: A 1-2 portal endoscopic approach to the carpal tunnel from proximal to distal, with a specialized blade transecting the transverse carpal ligament under endoscopic visualization. Theoretical advantages include smaller incision and faster recovery; disadvantages include the small but real risk of incomplete release or injury to the median nerve or palmar cutaneous branch. Outcomes are generally excellent with either technique, with substantial symptom relief in 80-95% of patients and high patient satisfaction. The principal predictors of poor outcome are advanced disease with established axonal damage (thenar atrophy at presentation) and the presence of confounding conditions (cervical radiculopathy, systemic neuropathy).

Cubital Tunnel Syndrome

Cubital tunnel syndrome is compression of the ulnar nerve at the elbow, specifically beneath the cubital tunnel retinaculum (the arcuate ligament of Osborne) connecting the medial epicondyle to the olecranon. The ulnar nerve passes through the cubital tunnel and is uniquely vulnerable to compression because of its superficial position behind the medial epicondyle and its passage through a narrow fibrous tunnel. Clinical features include numbness and paresthesia in the ulnar nerve distribution (the dorsal and palmar aspects of the little finger and the ulnar half of the ring finger), worse with elbow flexion (which stretches and compresses the ulnar nerve); medial elbow pain; and, in advanced disease, weakness of the ulnar-innervated intrinsic hand muscles with characteristic “claw hand” deformity (hyperextension at the MCP joints of the ring and little fingers with flexion at the PIP and DIP joints) and weakness of grip and pinch. The Tinel sign at the cubital tunnel and the elbow flexion test (sustained elbow flexion reproducing symptoms) support the diagnosis. The Froment sign (substitution of the adductor pollicis by the FPL during key pinch, producing flexion of the thumb IP joint) demonstrates weakness of the ulnar-innervated adductor pollicis.

Treatment is initially conservative: avoidance of sustained elbow flexion, particularly during sleep (with night-time elbow extension splinting or simple wrapping of a towel around the elbow to prevent flexion), NSAIDs, and physiotherapy. Surgical treatment is indicated for refractory disease or progressive motor deficit. Options include: Simple decompression (in situ release of the cubital tunnel retinaculum): The simplest procedure; good results in mild to moderate disease. Anterior transposition (subcutaneous, intramuscular, or submuscular): The ulnar nerve is moved from its position behind the medial epicondyle to a position anterior to it, eliminating the dynamic stretch with elbow flexion. Submuscular transposition (beneath the flexor-pronator origin) is preferred for revision procedures. Medial epicondylectomy: Resection of part of the medial epicondyle to allow the ulnar nerve to translate anteriorly without formal transposition. Outcomes vary substantially with severity at presentation, with mild disease having excellent outcomes and advanced disease with established motor deficit having less reliable improvement.

Radial Nerve and Its Branches

Radial Tunnel Syndrome and Posterior Interosseous Nerve Syndrome The radial nerve at the elbow gives rise to the posterior interosseous nerve (PIN, deep branch) and the superficial radial nerve. Compression of these structures produces two related but distinct syndromes: Radial tunnel syndrome: Compression of the PIN in the radial tunnel at the elbow, with five potential sites of compression — fibrous bands anterior to the radiocapitellar joint, recurrent radial vessels (the “leash of Henry”), the fibrous edge of the ECRB origin, the arcade of Frohse (proximal edge of the supinator), and the distal edge of the supinator. Presentation is principally with pain in the lateral elbow and forearm, often confused with lateral epicondylitis (“tennis elbow”). The diagnosis is made by exclusion of lateral epicondylitis and by the characteristic location of tenderness 3-5 cm distal to the lateral epicondyle. Treatment is initially conservative with avoidance of provoking activities; surgical release of the radial tunnel is reserved for refractory cases. Posterior interosseous nerve syndrome: Compression of the PIN producing motor symptoms — weakness of finger extension (with characteristic preserved wrist extension because the ECRL is innervated proximal to the compression). The sensory distribution is unaffected because the superficial radial nerve is not involved. Treatment is principally surgical with release of the compression sites. Wartenberg Syndrome Wartenberg syndrome is compression of the superficial radial nerve as it emerges from beneath the brachioradialis, producing dorsoradial wrist pain and dysesthesia. Treatment

is conservative with avoidance of tight wristwatches and bracelets; surgical release for refractory disease.

Median Nerve Compression in the Forearm

Anterior interosseous nerve syndrome (Kiloh-Nevin syndrome): Compression of the AIN — a pure motor branch of the median nerve — at the level of the FDS arcade or by other structures in the proximal forearm. Presentation is with weakness of FPL, FDP to the index finger, and pronator quadratus, with the characteristic inability to make the “OK sign” with the thumb and index finger (the patient pinches with the thumb and index in extension at the IP and DIP joints rather than in flexion). Sensory function is preserved. Treatment is initially observational, since spontaneous recovery occurs in many cases; surgical release is considered for failure to improve. Pronator syndrome: Compression of the median nerve in the proximal forearm — at the pronator teres, the FDS arcade, the lacertus fibrosus, or other structures. Presentation is with median nerve symptoms in the hand combined with forearm pain. The distinction from carpal tunnel syndrome is by the location of forearm symptoms, the negative Phalen test (which would be positive in CTS), and electrodiagnostic studies. Treatment is initially conservative; surgical release for refractory disease.

Guyon’s Canal Syndrome

Guyon’s canal syndrome is compression of the ulnar nerve at the wrist in Guyon’s canal — the space between the pisiform medially, the hook of hamate laterally, the volar carpal ligament dorsally, and the palmar carpal ligament volarly. Causes include ganglion cysts (the commonest), hook of hamate fractures, repetitive trauma (handlebar palsy in cyclists, hammer palsy), inflammatory conditions, and other mass lesions. Clinical features depend on the location of compression: compression in zone 1 (proximal to the bifurcation into superficial and deep branches) produces combined sensory and motor symptoms; compression in zone 2 (deep branch alone) produces pure motor symptoms in the ulnar-innervated intrinsics; compression in zone 3 (superficial branch alone) produces pure sensory symptoms. Treatment is conservative when a clear precipitant can be addressed; surgical decompression of Guyon’s canal with addressing of any associated mass lesion is indicated for established or refractory disease.

Thoracic Outlet Syndrome

Thoracic outlet syndrome — covered in the chapter on cervical ribs — is the constellation of neurological, vascular, or combined symptoms produced by compression of the brachial plexus, subclavian artery, or subclavian vein in the thoracic outlet. The condition is summarized briefly here for completeness: • The commonest pattern (>90%) is neurogenic TOS with compression of the lower trunk of the brachial plexus.

• Provocative maneuvers (Roos, Adson) have high false-positive rates. • Imaging includes plain radiographs for cervical ribs, MRI of the brachial plexus, and angiography for vascular TOS. • Initial treatment is conservative with physiotherapy and postural correction; surgical decompression (first rib resection, cervical rib resection, scalenectomy) is reserved for refractory cases or for vascular TOS.

Lower-Limb Nerve Compression Syndromes

Tarsal Tunnel Syndrome Tarsal tunnel syndrome is compression of the posterior tibial nerve (or its branches — medial and lateral plantar nerves) behind the medial malleolus in the tarsal tunnel. Causes include space-occupying lesions (ganglia, lipomas, varicose veins, accessory muscles), trauma, foot deformity (pronation increasing tension on the nerve), and systemic conditions. Clinical features include burning, tingling, and numbness in the plantar foot (with the medial sole, lateral sole, or both involved depending on which branch is compressed), worse with prolonged standing or walking. Positive Tinel sign behind the medial malleolus and positive dorsiflexion-eversion test (sustained ankle dorsiflexion with eversion reproducing symptoms) support the diagnosis. Electrodiagnostic studies are less reliable than for upper extremity compression syndromes. Treatment is initially conservative with foot orthotics (correcting any associated pronation), NSAIDs, and corticosteroid injection. Surgical decompression is indicated for refractory cases or for clear mass lesions, with outcomes less reliable than for upper extremity compression releases.

Common and Superficial Peroneal Nerve Compression The common peroneal nerve is vulnerable to compression at the fibular neck — by prolonged sitting with crossed legs, leg crossing during anesthesia, tight casts and dressings, ganglia, or direct trauma. Compression produces weakness of foot dorsiflexion and eversion (“foot drop”) with sensory loss over the dorsum of the foot. Conservative treatment includes avoidance of pressure; surgical release of the fibular tunnel is performed for refractory cases. The superficial peroneal nerve can be compressed as it pierces the deep fascia in the lateral leg, producing the “superficial peroneal nerve entrapment syndrome” with lateral leg and dorsal foot pain. Meralgia Paresthetica Meralgia paresthetica is compression of the lateral femoral cutaneous nerve (LFCN) as it passes beneath the inguinal ligament near the anterior superior iliac spine. Causes include obesity, tight clothing or belts, pregnancy, prior surgery in the area, and various other

factors. Presentation is with burning, tingling, and numbness over the anterolateral thigh — a pure sensory syndrome without motor involvement. Treatment is principally conservative with weight loss, avoidance of provoking activities, NSAIDs, and selective LFCN block or injection. Surgical decompression or neurectomy is reserved for severe refractory disease. Piriformis Syndrome Piriformis syndrome is the compression of the sciatic nerve by the piriformis muscle in the deep gluteal region. The condition produces deep buttock pain with radiation down the posterior thigh, often mimicking lumbar radiculopathy. The diagnosis is challenging and somewhat controversial; some authors question whether the syndrome represents a distinct clinical entity rather than a description of multiple deep gluteal causes of sciatic- like pain. Treatment is principally conservative with physiotherapy stretches, NSAIDs, and corticosteroid injection. Surgical release of the piriformis is performed in selected refractory cases.

Compression in Specific Settings

Compression by Casts and Splints Casts and splints can compress superficial nerves, with the lateral femoral cutaneous nerve, common peroneal nerve, and superficial radial nerve being particularly vulnerable. The prevention is careful padding over bony prominences and known nerve courses, with regular reassessment of cast tightness. Perioperative Positioning Injuries Brachial plexus, ulnar nerve, and common peroneal nerve injuries can occur from prolonged abnormal positioning during surgery. Prevention requires careful padding, avoidance of extreme positions, and regular intraoperative reassessment. Compartment Syndrome Compartment syndrome — increased pressure within a fascial compartment with secondary nerve compression — is discussed in the chapter on compartment syndrome.

Summary and Take-Home Points

The peripheral nerve compression syndromes constitute a major component of orthopedic and hand surgery practice. The fundamental principles include: knowledge of the anatomical compression sites for each major nerve; clinical examination targeting the sensory and motor distribution of each nerve; provocative tests to confirm the suspected level of compression; selective use of electrodiagnostic studies for objective documentation and severity assessment; and a graded approach to management with conservative measures (splinting, activity modification, injection) for early disease and surgical

decompression for refractory disease. The principal upper-limb syndromes — carpal tunnel, cubital tunnel, radial tunnel, posterior interosseous, anterior interosseous, Guyon’s canal — and the lower-limb syndromes — tarsal tunnel, common peroneal compression, meralgia paresthetica — each have characteristic clinical features and specific management. The differential diagnosis with cervical or lumbar radiculopathy, with more proximal nerve injury, and with systemic neuropathic conditions must be considered in atypical presentations. Outcomes of timely intervention are generally excellent, with the principal predictors of poor outcome being advanced disease with established axonal damage at presentation.