Entrapment Neuropathies Beyond Carpal Tunnel Syndrome: A Clinical Review for the Internist

Dr Neeraj Manikath , claude.ai

Abstract

Entrapment neuropathies represent a significant yet often underdiagnosed cause of peripheral nerve dysfunction in clinical practice. While carpal tunnel syndrome dominates clinical attention, numerous other compression neuropathies can cause substantial morbidity and diagnostic confusion. This review focuses on clinically important entrapment neuropathies excluding carpal tunnel syndrome, emphasizing diagnostic pearls, anatomical considerations, and management strategies relevant to internists and trainees. Understanding these conditions requires integration of anatomical knowledge, pattern recognition, and systematic clinical examination—skills that define excellence in internal medicine.

Keywords: Entrapment neuropathy, ulnar neuropathy, peroneal neuropathy, meralgia paresthetica, thoracic outlet syndrome, peripheral nerve compression

Introduction

Entrapment neuropathies occur when peripheral nerves are compressed at anatomically vulnerable sites, resulting in focal dysfunction. The incidence of these conditions ranges from 1-3% in the general population, with certain occupational and metabolic risk factors substantially increasing prevalence. While carpal tunnel syndrome accounts for approximately 90% of all entrapment neuropathies, internists must maintain vigilance for less common but clinically significant compression syndromes that can mimic systemic neurological disorders, radiculopathies, or even central nervous system pathology.

The diagnostic challenge lies in recognizing characteristic patterns while excluding mimics such as polyneuropathy, radiculopathy, mononeuritis multiplex, or focal CNS lesions. This review addresses entrapment neuropathies that internists are likely to encounter, providing practical diagnostic and management guidance.

Ulnar Neuropathy at the Elbow

Clinical Anatomy and Pathophysiology

The ulnar nerve is the second most commonly entrapped nerve after the median nerve. Compression typically occurs at two sites: the cubital tunnel (formed by the medial epicondyle, olecranon, and arcuate ligament) or the more distal Guyon's canal at the wrist. Cubital tunnel syndrome represents the most common ulnar entrapment, with an incidence of 25 per 100,000 person-years.

The ulnar nerve is particularly vulnerable at the elbow because it traverses a tight fibro-osseous tunnel where it can be compressed during elbow flexion (which increases pressure by up to 20-fold), subjected to traction forces, or subluxate anteriorly over the medial epicondyle. Chronic compression leads to segmental demyelination and, if prolonged, axonal degeneration.

Clinical Presentation: Pearls and Oysters

Classic Features:

Paresthesias in the fifth digit and ulnar half of the fourth digit
Weakness of intrinsic hand muscles (interossei, lumbricals to digits 4-5, adductor pollicis)
Clawing of the ring and little fingers (hyperextension at MCP, flexion at IP joints)
Positive Tinel's sign at the cubital tunnel
Froment's sign (compensatory thumb IP flexion when attempting lateral pinch due to adductor pollicis weakness)

Pearl #1: The "Wartenberg Sign" Observation of persistent abduction of the little finger at rest indicates weakness of the third palmar interosseous muscle and is an early, often overlooked sign of ulnar neuropathy.

Pearl #2: Differentiating Cubital Tunnel from C8 Radiculopathy Unlike C8 radiculopathy, ulnar neuropathy spares:

The flexor digitorum profundus to digits 2-3 (median nerve)
The extensor indicis proprius
Sensory function over the dorsal forearm (posterior cutaneous nerve of forearm)
The abductor pollicis brevis (median nerve, T1 innervation)

Oyster #1: The "Paradoxical" Ulnar Neuropathy Lesions proximal to the mid-forearm spare the flexor digitorum profundus to digits 4-5, preventing severe claw deformity. More distal lesions cause greater clawing because the long flexors remain functional while intrinsics are paralyzed—the "ulnar paradox."

Oyster #2: Delayed Presentation Patients may present years after initial injury (trauma, fracture) with progressive symptoms, a phenomenon termed "tardy ulnar palsy." Always inquire about remote elbow trauma.

Diagnostic Approach

Clinical Examination Hacks:

Elbow flexion test: Sustained elbow flexion for 60 seconds reproducing symptoms has 75% sensitivity
Pressure provocation test: Direct pressure over cubital tunnel for 60 seconds (91% sensitivity)
Scratch collapse test: Light scratch over the cubital tunnel followed by resisted shoulder external rotation; collapse indicates nerve irritation

Electrodiagnostic Studies: Nerve conduction studies demonstrating focal slowing across the elbow segment (>10 m/s decrease compared to forearm segment) or conduction block confirm the diagnosis. Normal median sensory responses help exclude polyneuropathy. Needle EMG identifies denervation in ulnar-innervated muscles while sparing median and radial territories.

Imaging: MRI or ultrasound can identify structural causes (ganglion cysts, accessory muscles like anconeus epitrochlearis, osteophytes) and demonstrate nerve swelling or signal change.

Management Strategies

Conservative Management:

Activity modification avoiding prolonged elbow flexion
Nocturnal elbow splinting in 30-45° flexion
NSAIDs for symptom control
Vitamin B12 supplementation if deficient (cofactor in myelin synthesis)

Surgical Intervention: Indicated for progressive motor weakness, failed conservative therapy >3 months, or evidence of axonal loss. Options include simple decompression, medial epicondylectomy, or anterior transposition. Outcomes are better when surgery is performed before severe axonal loss develops.

Common Peroneal (Fibular) Neuropathy

Clinical Anatomy and Pathophysiology

The common peroneal nerve, most vulnerable of all peripheral nerves to compression, wraps around the fibular neck where it is subcutaneous and fixed against bone. Compression occurs from:

Leg crossing or prolonged squatting
Tight casts or orthotic devices
Rapid weight loss (loss of protective fat padding)
Prolonged surgical positioning
Direct trauma
Mass lesions (ganglion cysts, most commonly)

The nerve divides into superficial (foot eversion, lateral leg sensation) and deep (foot/toe dorsiflexion, first web space sensation) branches just distal to the fibular head.

Clinical Presentation: Pearls and Oysters

Classic Features:

Foot drop with steppage gait
Weakness of ankle dorsiflexion and toe extension
Weakness of foot eversion (distinguishes from L5 radiculopathy where inversion is also weak)
Sensory loss over dorsum of foot and lateral leg
Preserved ankle reflex (unlike S1 radiculopathy)

Pearl #3: The "Inverted Ankle Jerk" In severe L5 radiculopathy, tibialis posterior (L5 > S1) may be weak, but plantar flexion (S1) is preserved, creating an "inverted" response. This is absent in peroneal neuropathy where plantar flexion remains brisk.

Pearl #4: Foot Position at Rest With peroneal neuropathy, the foot assumes an equinovarus position (plantarflexed and inverted) due to unopposed action of posterior tibial and gastrocnemius muscles. This differs from an L5 radiculopathy where the foot typically maintains neutral position.

Oyster #3: The Painless Foot Drop Unlike L5 radiculopathy which usually presents with back and leg pain, peroneal neuropathy at the fibular head is typically painless or minimally painful. Pain suggests alternative diagnosis or dual pathology.

Oyster #4: Bilateral Presentation Bilateral peroneal neuropathy suggests systemic causes: hereditary neuropathy with liability to pressure palsies (HNPP), vasculitis, or habitual leg crossing. Always consider HNPP in patients with recurrent or multiple entrapment neuropathies.

Diagnostic Approach

Clinical Examination Hacks:

The "toe extension test": Inability to extend the great toe specifically suggests deep peroneal involvement
"Heel walk test": Inability to walk on heels demonstrates dorsiflexion weakness
Tinel's sign at the fibular head (present in 85% of cases)

Key Differentiation from L5 Radiculopathy:

Feature	Peroneal Neuropathy	L5 Radiculopathy
Back pain	Absent	Usually present
Foot inversion	Normal	Weak
Hip abduction	Normal	May be weak
Sensory loss	Dorsal foot, lateral leg	Lateral leg, medial foot
Ankle jerk	Normal	Normal

Electrodiagnostic Studies: Demonstrate focal slowing or conduction block across the fibular head. Must demonstrate normal tibial responses and normal peroneal responses above the fibular head to exclude sciatic neuropathy. EMG of paraspinal muscles helps exclude radiculopathy.

Imaging: MRI or ultrasound to identify mass lesions, particularly ganglion cysts arising from the tibiofibular joint (present in 10-15% of cases). Lumbosacral spine MRI if radiculopathy suspected.

Management Strategies

Conservative Management:

Ankle-foot orthosis (AFO) to prevent ankle contracture and facilitate ambulation
Avoidance of leg crossing and pressure
Physical therapy focusing on strengthening tibialis anterior and maintaining ankle range of motion
Serial examinations; 60-80% recover spontaneously within 3-6 months if neuropraxic injury

Surgical Intervention: Indicated for mass lesions (ganglion cyst excision), failure to improve after 3 months with complete denervation on EMG, or progressive weakness. Nerve decompression with or without cyst excision shows good outcomes when performed early.

Meralgia Paresthetica (Lateral Femoral Cutaneous Neuropathy)

Clinical Anatomy and Pathophysiology

The lateral femoral cutaneous nerve (LFCN), a pure sensory nerve arising from L2-L3 roots, becomes entrapped where it passes under or through the inguinal ligament near the anterior superior iliac spine. Risk factors include obesity, tight clothing, pregnancy, diabetes, and rapid weight changes. Iatrogenic injury during anterior iliac crest bone graft harvest or hip surgery is increasingly recognized.

Clinical Presentation: Pearls and Oysters

Classic Features:

Burning pain, tingling, or numbness over anterolateral thigh
Symptoms worsen with standing, walking, or hip extension
Relief with sitting or hip flexion
No motor weakness (pure sensory nerve)
Hyperalgesia or allodynia in affected region

Pearl #5: The "Reverse Lasègue" or "Pelvic Tilt Test" With the patient prone, passive hip extension reproduces symptoms by stretching the nerve at the inguinal ligament. Sensitivity approaches 95%.

Pearl #6: Obesity and the "Belt Line Sign" Look for skin indentation or hyperpigmentation along the belt line in obese patients—a visual clue to chronic compression etiology.

Oyster #5: The Bilateral Presentation Bilateral meralgia paresthetica should prompt consideration of:

Retroperitoneal pathology (hematoma, tumor, abscess)
Ascites
Pregnancy
Excessive lumbar lordosis
Systemic causes (diabetes, hypothyroidism)

Oyster #6: The Psychological Comorbidity Chronic neuropathic pain in meralgia paresthetica frequently coexists with anxiety and depression. Screen for psychological distress and address comprehensively.

Diagnostic Approach

Clinical Examination Hacks:

Direct pressure test: Firm pressure just medial to the ASIS reproduces symptoms
Sensory mapping: Carefully map the sensory deficit; involvement limited to anterolateral thigh without posterior or medial thigh involvement confirms LFCN
Motor examination: Normal hip flexion, knee extension, and hip adduction exclude lumbar plexopathy or radiculopathy

Electrodiagnostic Studies: Generally not required for diagnosis but can be confirmatory. Comparison of LFCN sensory nerve action potentials between affected and unaffected sides showing amplitude reduction or absence supports diagnosis. However, technical difficulty limits utility.

Imaging: Usually unnecessary unless atypical features (bilateral, progressive, associated motor findings) suggest alternative diagnosis. Consider CT or MRI of pelvis to exclude mass lesions or retroperitoneal pathology.

Management Strategies

Conservative Management (First-line, 90% success rate):

Weight loss if obese
Loose-fitting clothing
Postural modification
Local injection with corticosteroid and local anesthetic (diagnostic and therapeutic)
Neuropathic pain medications (gabapentin, pregabalin, duloxetine, amitriptyline)

Interventional/Surgical Management: Reserved for refractory cases. Options include:

Nerve blocks (pulsed radiofrequency ablation)
Surgical decompression (70-80% success rate)
Neurectomy as last resort (risk of painful neuroma)

Radial Neuropathy (Saturday Night Palsy)

Clinical Anatomy and Pathophysiology

The radial nerve is vulnerable to compression in the spiral groove of the humerus, where it lies directly against bone. Classic scenarios include:

"Saturday night palsy": prolonged arm compression during deep sleep (alcohol intoxication, sedatives)
"Honeymoon palsy": partner's head resting on arm during sleep
Improper crutch use ("crutch palsy")
Humeral fractures

The radial nerve innervates the triceps (high lesions only), brachioradialis, wrist extensors, finger extensors, and thumb extensors/abductors. It provides sensory innervation to the posterior arm, forearm, and dorsal first web space.

Clinical Presentation: Pearls and Oysters

Classic Features:

Wrist drop (inability to extend wrist)
Weakness of finger extension at MCP joints
Weakness of thumb extension and abduction
Preserved finger IP joint extension (intrinsic muscles)
Sensory loss over dorsal first web space (often minimal)
Preserved triceps function in spiral groove lesions (nerve branches to triceps arise proximally)

Pearl #7: The "Test of Three" Three key examination findings confirm radial neuropathy: weak wrist extension, weak finger MCP extension, preserved finger IP extension (interossei/lumbricals via ulnar and median nerves).

Pearl #8: Minimal Sensory Loss Despite extensive sensory territory, sensory loss is often confined to a small patch over the dorsal first web space due to overlap with other nerves. Don't exclude radial neuropathy based on absent sensory symptoms.

Oyster #7: The "Pseudo-Ulnar Claw" With complete wrist drop, patients cannot generate tension in the finger extensors, causing the fingers to assume a flexed position that may superficially resemble ulnar clawing. Passive wrist extension eliminates this "pseudo-claw."

Oyster #8: High vs. Low Lesions High radial nerve lesions (axilla) involve triceps weakness and sensory loss over posterior arm. Spiral groove lesions spare triceps but involve brachioradialis. Posterior interosseous nerve (PIN) lesions spare brachioradialis and sensation entirely, causing isolated finger/thumb extension weakness.

Diagnostic Approach

Clinical Examination Hacks:

Brachioradialis test: Have patient flex elbow against resistance with forearm in neutral position—visible/palpable muscle contraction indicates lesion is distal to spiral groove
Finger abduction test: With wrist passively extended, inability to abduct fingers distinguishes radial (normal) from ulnar (weak) neuropathy
Tinel's sign along the spiral groove

Electrodiagnostic Studies: Demonstrate focal slowing, conduction block, or reduced amplitude across the spiral groove. EMG shows denervation in radial-innervated muscles with normal median and ulnar territories. Timing: wait 3 weeks for denervation potentials to appear.

Management Strategies

Conservative Management:

Wrist/hand splint (cock-up splint) to prevent contracture and facilitate hand function
Most cases (70-90%) recover spontaneously within 2-4 months
Physical therapy to maintain passive range of motion
Avoid further compression

Surgical Intervention: Indicated for:

Complete nerve transection (open fractures, penetrating injury)
Failure to show recovery by 3-4 months with complete denervation
Progressive weakness despite conservative management

Thoracic Outlet Syndrome (TOS)

Clinical Anatomy and Pathophysiology

TOS encompasses compression of the brachial plexus and/or subclavian vessels as they traverse the thoracic outlet—the space bordered by the first rib, clavicle, and scalene muscles. Three subtypes exist:

Neurogenic TOS (95%): Lower trunk (C8-T1) compression causing hand intrinsic muscle weakness and sensory symptoms
Venous TOS (3-4%): Subclavian vein compression causing arm swelling
Arterial TOS (1%): Subclavian artery compression causing arm ischemia

True neurogenic TOS is rare and often overdiagnosed. Many cases labeled "disputed TOS" lack objective findings and represent myofascial pain or cervical spine pathology.

Clinical Presentation: Pearls and Oysters

Classic Features (True Neurogenic TOS):

Weakness and atrophy of hand intrinsic muscles (particularly thenar)
Pain in ulnar forearm and hand
Sensory loss in ulnar distribution
Symptoms worsen with arm elevation or overhead activities
Gilliatt-Sumner hand: severe thenar and hypothenar atrophy with finger clawing

Pearl #9: The "True TOS Triad" True neurogenic TOS requires all three: (1) medial arm/forearm pain, (2) hand intrinsic muscle weakness, (3) sensory loss in ulnar distribution. Isolated pain without objective findings suggests alternative diagnosis.

Pearl #10: Vascular TOS Presentation Venous TOS presents acutely with arm swelling, cyanosis, and prominent veins (Paget-Schroetter syndrome), often after vigorous arm exercise. Arterial TOS causes arm claudication, coolness, color changes, or digital ischemia/emboli.

Oyster #9: The "Disputed TOS" Dilemma Many patients diagnosed with "TOS" have normal examinations and electrodiagnostic studies. Symptoms are often positional pain without weakness or atrophy. These cases represent myofascial pain syndromes, postural dysfunction, or cervical spine pathology rather than true TOS.

Oyster #10: Provocative Tests Are Non-Specific Classic tests (Adson's, Wright's, Roos) have poor specificity (positive in 50% of asymptomatic individuals). Never diagnose TOS based on provocative testing alone without objective neurological or vascular findings.

Diagnostic Approach

Clinical Examination Hacks:

Elevated arm stress test (EAST/Roos test): Sustained arm elevation with repeated fist clenching for 3 minutes reproducing symptoms suggests TOS, but specificity is low
Measure arm circumferences: >2 cm difference suggests venous TOS
Look for vascular signs: coolness, color change, absent pulses, supraclavicular bruit, digital emboli

Electrodiagnostic Studies: In true neurogenic TOS, show reduced ulnar (and occasionally median) sensory amplitudes with normal latencies, and EMG evidence of C8-T1 denervation. Normal studies argue strongly against true neurogenic TOS.

Imaging:

Chest X-ray: identify cervical ribs, elongated C7 transverse processes, or first rib anomalies
MRI/MRA: exclude mass lesions (Pancoast tumor, lymphadenopathy, aneurysm)
Venography (venous TOS) or arteriography (arterial TOS) to demonstrate vascular compression

Management Strategies

Conservative Management (First-line for Neurogenic TOS):

Physical therapy: postural training, scalene/pectoralis minor stretching, shoulder girdle strengthening
Avoid provocative positions
Weight loss if obese
Pain management

Surgical Intervention: Reserved for:

True neurogenic TOS with progressive weakness despite conservative therapy
Venous TOS (first rib resection + venous reconstruction)
Arterial TOS (surgical decompression + arterial repair)

Surgical outcomes for "disputed TOS" are poor, with high reoperation rates and patient dissatisfaction. Avoid surgery without objective findings.

Tarsal Tunnel Syndrome

Clinical Anatomy and Pathophysiology

The posterior tibial nerve passes through the tarsal tunnel, bounded by the medial malleolus, calcaneus, and flexor retinaculum. Compression causes plantar foot symptoms. Etiologies include:

Space-occupying lesions (ganglion cysts, lipomas, varicosities)
Trauma/ankle fractures
Posterior tibialis tenosynovitis
Biomechanical factors (pes planus, hindfoot valgus)
Systemic diseases (diabetes, hypothyroidism, rheumatoid arthritis)

Clinical Presentation: Pearls and Oysters

Classic Features:

Burning pain, tingling, or numbness on plantar surface of foot
Symptoms worse with standing, walking, or at night
Relief with rest or leg elevation
Weakness of toe flexion (late finding)
Tinel's sign over tarsal tunnel

Pearl #11: The "Tinel's Paradox" Tinel's sign in tarsal tunnel syndrome radiates distally (towards toes), unlike in other entrapment neuropathies where it may radiate proximally. This helps confirm the diagnosis.

Pearl #12: The "Valvus Stress Test" Passive eversion of the heel stretches the posterior tibial nerve and reproduces symptoms, supporting the diagnosis.

Oyster #11: Distinguishing from Plantar Fasciitis Plantar fasciitis causes heel pain worse with first steps in morning. Tarsal tunnel syndrome causes burning/tingling over the entire plantar surface, worse with prolonged standing. Sensory examination distinguishes the two.

Oyster #12: Incomplete Syndromes The posterior tibial nerve divides into medial plantar, lateral plantar, and calcaneal nerves. Compression can selectively involve individual branches, causing localized symptoms that may not fit the classic picture.

Diagnostic Approach

Electrodiagnostic Studies: May show prolonged motor latencies to abductor hallucis (medial plantar nerve) or abductor digiti minimi (lateral plantar nerve), or reduced sensory amplitudes. However, technical difficulty and high false-negative rates limit sensitivity (50-60%).

Imaging: MRI identifies space-occupying lesions in 60-80% of cases and is critical for surgical planning. Ultrasound is increasingly used for dynamic assessment.

Management Strategies

Conservative Management:

Orthotic devices to correct biomechanical abnormalities
Corticosteroid injection (diagnostic and therapeutic)
NSAIDs and neuropathic pain medications
Activity modification

Surgical Intervention: Indicated for identifiable space-occupying lesions or failed conservative therapy. Outcomes are best when structural causes are identified and addressed. Success rates range from 44-91%, with better outcomes when surgery is performed early and specific pathology is identified.

Anterior Interosseous Syndrome

Clinical Anatomy and Pathophysiology

Anterior interosseous nerve (AIN), a pure motor branch of the median nerve arising in the proximal forearm, innervates the flexor pollicis longus (FPL), flexor digitorum profundus (FDP) to digits 2-3, and pronator quadratus. Compression occurs due to:

Fibrous bands (Gantzer's muscle)
Direct trauma
Vigorous arm exercise (spontaneous AIN syndrome)
Inflammatory neuritis (Parsonage-Turner variant)

Clinical Presentation: Pearls and Oysters

Classic Features:

Inability to flex thumb IP joint
Inability to flex index finger DIP joint
No sensory loss (pure motor nerve)
Pain in proximal forearm (50% of cases)
Characteristic "pinch sign" or "OK sign" abnormality

Pearl #13: The "Pinch Sign" Attempting to make an "OK" sign results in thumb IP and index DIP extension rather than flexion, creating a triangle rather than a circle. This pathognomonic sign immediately suggests AIN syndrome.

Pearl #14: The "Pronator Drift" Subtle weakness of pronator quadratus can be detected by comparing resisted pronation strength with the forearm in various positions of elbow flexion. Weakness suggests AIN involvement.

Oyster #13: AIN Palsy vs. FPL Tendon Rupture FPL tendon rupture (trauma, rheumatoid arthritis) mimics AIN palsy. Key distinction: palpable FPL contraction with attempted thumb flexion indicates nerve (AIN) problem; absent contraction suggests tendon rupture.

Oyster #14: The "Spontaneous" AIN Syndrome Many cases occur spontaneously after vigorous arm use without identifiable compressive lesion. These may represent a focal neuritis (neuralgic amyotrophy variant) and have good spontaneous recovery (70-80% by 12 months).

Management Strategies

Conservative Management: Most spontaneous cases recover within 6-12 months. Monitor clinically and with serial EMG. Avoid surgery during this period.

Surgical Intervention: Indicated for:

Identifiable compressive lesion on imaging
No recovery after 12 months of observation
Progressive weakness

Diagnostic Algorithm for Entrapment Neuropathies

When evaluating suspected entrapment neuropathy, employ a systematic approach:

Characterize the deficit: Motor, sensory, or mixed? Distribution?
Localize anatomically: Which nerve? Which segment?
Exclude mimics: Radiculopathy, plexopathy, polyneuropathy, CNS lesion?
Identify risk factors: Occupational, metabolic, traumatic, structural?
Electrodiagnostic confirmation: NCS/EMG when diagnosis uncertain
Imaging when indicated: MRI or ultrasound for structural lesions
Screen for systemic diseases: Diabetes, hypothyroidism, vasculitis, hereditary neuropathy

Red flags requiring urgent evaluation:

Rapidly progressive weakness
Associated systemic symptoms
Multiple mononeuropathies (vasculitis)
Bilateral simultaneous onset (systemic cause)
Failure to respond to appropriate treatment

General Management Principles

Conservative Management (Universal First-line)

Activity modification: Avoid provocative positions/activities
Splinting: Immobilization to reduce nerve stress
Therapy: Physical/occupational therapy for strengthening and mobility
Medical management: NSAIDs, neuropathic pain medications (gabapentin, pregabalin, duloxetine)
Metabolic optimization: Control diabetes, correct vitamin deficiencies, manage hypothyroidism
Weight loss: Reduces mechanical stress in obesity-related compressions

Surgical Intervention Principles

Consider surgery when:

Progressive motor weakness despite conservative therapy
Severe axonal loss on EMG
Identifiable structural lesion amenable to surgical correction
Failed adequate conservative trial (typically 3-6 months)
Acute severe injury with nerve transaction

Timing matters: Early surgical intervention (within 6-12 months) yields better outcomes before irreversible axonal loss and muscle atrophy occur.

Special Populations

Diabetic Patients

Diabetes increases entrapment neuropathy risk 2-3 fold through multiple mechanisms: nerve ischemia, metabolic derangements, increased susceptibility to mechanical compression. Consider "double crush" phenomenon where diabetic polyneuropathy predisposes to superimposed focal compression.

Pregnancy

Physiological fluid retention, hormonal changes, and weight gain increase entrapment risk, particularly meralgia paresthetica, carpal tunnel syndrome, and peroneal neuropathy. Most resolve postpartum; conservative management preferred.

Hereditary Neuropathy with Liability to Pressure Palsies (HNPP)

Consider HNPP in patients with:

Recurrent entrapment neuropathies
Multiple simultaneous compressions
Family history of similar problems
Focal neuropathy after minimal trauma

Diagnosis via PMP22 deletion testing. Management focuses on prevention and conservative care; surgery has higher recurrence rates.

Clinical Pearls Summary

Wartenberg Sign indicates early ulnar neuropathy
Ulnar paradox: distal lesions cause more clawing
Inverted ankle jerk distinguishes L5 radiculopathy from peroneal neuropathy
Painless foot drop suggests peroneal over L5 pathology
Reverse Lasègue test for meralgia paresthetica
Obesity belt line sign in meralgia paresthetica
Test of three confirms radial neuropathy
Minimal sensory loss in radial neuropathy
True TOS triad required for neurogenic TOS diagnosis
Provocative tests non-specific in TOS
Tinel's paradox in tarsal tunnel syndrome
Valgus stress test for tarsal tunnel
Pinch sign pathognomonic for AIN syndrome
Spontaneous AIN syndrome recovers without surgery in most cases

Conclusion

Entrapment neuropathies beyond carpal tunnel syndrome represent an important group of conditions that internists must recognize and manage. Success requires anatomical knowledge, careful clinical examination, judicious use of electrodiagnostic studies and imaging, and a systematic approach to excluding mimics. Most entrapment neuropathies respond to conservative management, but timely surgical intervention is crucial when indicated to prevent permanent dysfunction. Maintaining awareness of these conditions, their diagnostic pearls, and potential pitfalls enables internists to provide optimal care for patients with these often-overlooked causes of peripheral nerve dysfunction.

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