Nerve Entrapment Syndromes

Updated: Jan 04, 2023
Author: Amgad Saddik Hanna, MD; Chief Editor: Brian H Kopell, MD 


Practice Essentials

Entrapment neuropathies are disorders of the peripheral nerves that are characterized by pain and/or loss of function (motor and/or sensory) of the nerves as a result of chronic compression. The brain and the spinal cord receive and send information through muscles and sensory receptors, and information sent to organs of the body is transmitted through the nerves. These nerves travel to the upper and lower extremities and traverse various joints along their paths. Unfortunately, these nerves can become compressed or entrapped at various regions of the extremities, especially at "tunnel" regions, where they may be predisposed or vulnerable to compression.

Neurosurgeons, among other surgical specialists (eg, orthopedists, plastic surgeones), treat these entrapment neuropathies, which can account for 10-20% of cases in a practice. The first operations or decompressions for different nerve entrapments were performed more than a century ago, but the disorders were described even earlier by such pioneering physicians as Sir Astley Cooper (1820s) and Sir James Paget (1850s).

Repetitive injury and trauma to a nerve may result in microvascular (ischemic) changes, edema, injury to outside layers of the nerve (myelin sheath) that aid in transmission of the nerve’s messages, and structural alterations in membranes at the organelle levels in both the myelin sheath and the nerve axon. Focal segmental demyelination at the area of compression is a common feature of compression syndromes. Complete recovery of function after surgical decompression reflects remyelination of the injured nerve. Incomplete recovery in more chronic and severe cases of entrapment is due to Wallerian degeneration of the axons and to permanent fibrotic changes in the neuromuscular junction that may prevent full reinnervation and restoration of function.

Nerve entrapment syndromes result from chronic injury to a nerve as it travels through an osseoligamentous tunnel; compression is typically evident between the ligamentous canal and bony surfaces. Other anatomic sites with potential for entrapment include the muscular arcade of the supinator (also known as the arcade of Frohse), the posterior interosseous nerve (PIN), and the thoracic outlet for the lower trunk of the brachial plexus.[1]

In cases of nerve entrapment, at least 1 portion of the compressive surface is mobile. This results in a repetitive "slapping" insult or "rubbing/sliding" compression against sharp, tight edges with motion at the adjacent joint, resulting in a chronic injury. Immobilization of the nerve by means of a splint or lifestyle adjustments may resolve the symptoms. Entrapment neuropathies can also be caused by systemic disorders such as rheumatoid arthritis, pregnancy, acromegaly, or hypothyroidism.

Suprascapular nerve entrapment may cause 2% of all cases of chronic shoulder pain. Of the many reported causes of suprascapular nerve entrapment, the most common are para-labral cysts, usually found in the spinoglenoid notch, and microtrauma among elite athletes.[2]

Carpal tunnel syndrome (CTS), defined as compression of the median nerve at the wrist, is the most common entrapment neuropathy.[3]  Cubital tunnel syndrome, the second most common, is caused by compression at the elbow.[4] Other rare nerve entrapment syndromes involve the suprascapular nerve and account for approximately 0.4% of upper girdle pain symptoms; meralgia paresthetica is compression of the lateral femoral cutaneous nerve (LFCN) within the groin.[5]

(An ulnar nerve transposed at the elbow is shown in the image below.)

Ulnar nerve (U) transposition at the elbow. A: The Ulnar nerve (U) transposition at the elbow. A: The medial intermuscular septum (arrows) is resected to prevent compression of the transposed nerve. Vasoloops are around the ulnar nerve and a vascular pedicle between the nerve and the septum that has been preserved. B: After subcutaneous transposition, the ulnar nerve is observed lax in elbow flexion. The ulnar nerve and its distal branches are surrounded by vasoloops.

Anterior cutaneous nerve entrapment syndrome is a frequent cause of abdominal wall pain due to trapped thoracic intercostal nerves between abdominal muscles. History and bedside Carnett's sign can elicit the diagnosis. Injection of local anesthetics with steroids in the junction between rectus sheath and abdominal muscle under ultrasound guidance can provide sustained pain relief.[6]

Cauda equina syndrome (CES) involves compression of some or all of the lumbar and sacral peripheral nerve roots.The literature reveals timing to surgical decompression, severity of symptoms at the time of onset, and involvement of bladder dysfunction as prognostic indicators of CES.[7]

The American College of Radiology (ACR) has published the following guidelines for thoracic outlet syndrome[8] :

  • Radiography of the chest and either MRI without and with IV contrast of the chest or MRI without IV contrast of the chest are usually appropriate for the initial and follow-up imaging after surgery or intervention for patients with neurogenic thoracic outlet syndrome (nTOS). MRI without IV contrast is an acceptable alternative to MRI without and with IV contrast (ie, only one procedure will be ordered to provide the clinical information to effectively manage the patient’s care).
  • Radiography of the chest and US duplex Doppler of the subclavian artery and vein, CT with IV contrast of the chest, or catheter venography of the upper extremity are usually appropriate for the initial and follow-up imaging after surgery or intervention for patients with venous thoracic outlet syndrome (vTOS). US duplex Doppler, CT with IV contrast, and catheter venography are equivalent alternatives (ie, only one procedure will be ordered to provide the clinical information to effectively manage the patient’s care).
  • Radiography of the chest and CTA with IV contrast of the chest, MRA without and with IV contrast of the chest, US duplex Doppler of the subclavian artery and vein, or arteriography of the upper extremity are usually appropriate for the initial and follow-up imaging after surgery or intervention for patients with arterial thoracic outlet syndrome (aTOS). CTA with IV contrast, MRA without and with IV contrast, US duplex Doppler, and arteriography of the upper extremity are equivalent alternatives (ie, only one procedure will be ordered to provide the clinical information to effectively manage the patient’s care).



Symptoms of nerve compression vary based on the particular nerve involved. In general, however, the temporal sequence of neurologic manifestations is as follows:

  • Irritation or inflammation (sensory nerves): pain, paresthesia

  • Ablative symptoms: numbness (sensory nerves), weakness and atrophy (motor nerves)

In a major mixed nerve (both sensory and motor) such as the sciatic or median nerve, signs of sympathetically mediated features may be prominent in chronic cases. These changes manifest as the following:

  • Dry, thin, hairless skin

  • Ridged, thickened, cracked nails

  • Recurrent skin ulceration

Most entrapment syndromes involve mixed sensory and motor nerves and thus conform to the aforementioned pattern. Exceptions include the deep branch of the ulnar nerve at Guyon canal and PIN (both predominantly motor) and the lateral femoral cutaneous nerve (LFCN; pure sensory) near the anterior superior iliac spine (ASIS).

Median nerve at the wrist (carpal tunnel syndrome)

Carpal tunnel syndrome (CTS) is the most commonly encountered nerve entrapment condition. Median nerve compression at the wrist is seen at the transverse carpal ligament (TCL), which attaches to and arches between the pisiform and hamate on the ulnar side and the scaphoid and trapezium on the radial side. The palmar fascia is fused to the TCL proximally, then fans out to the soft tissue of the palmar skin as the palmar aponeurosis. Combined layers of the TCL and the proximal palmar fascia form the flexor retinaculum.

The palmaris longus tendon inserts into the palmar aponeurosis and lies directly over the median nerve just proximal to the TCL but is absent in approximately 15% of individuals. In these patients, the nerve can be found beneath a fascial membrane between the flexor carpi radialis and flexor digitorum superficialis tendons.

The palmar cutaneous branch originates from the radial side of the median nerve proximal to or just deep to the flexor retinaculum, then transverses superficially to the flexor retinaculum to innervate the thenar eminence (thumb) and the palm, roughly up to the vertical line overlying the fourth metacarpal.

The recurrent motor branch to the thenar muscles leaves the median nerve radially just beyond the distal edge of the flexor retinaculum, but variant nerves may pierce through the flexor retinaculum or may arise from the ulnar aspect of the median nerve, and an accessory motor branch may even emerge proximal to the flexor retinaculum.[9]

Occasionally, the ulnar nerve (10%) and artery (4%) lie radial to the hook of the hamate superficial to the flexor retinaculum, placing them at risk for direct or indirect injury during carpal tunnel surgery (eg, from retractor pressure).

Patients note a dull, aching pain at the wrist that may extend up the forearm to the elbow. Often, this pain is associated with distressing paresthesias in the thumb and index finger, particularly upon awakening. Typically, patients rub their wrists or shake their hands to try to "get the blood back into their wrists."[10] The pain is typically worse at night and disturbs the patient's sleep. As symptoms worsen, sensation may be decreased at the volar pads of the thumb and index, middle, and ring fingers. These symptoms are the result of compression of the median nerve as it passes through the wrist and the carpal tunnel.[11, 12]

Sensation in the palmar surface of the lateral 3.5 fingers is often affected; however, the palm is supplied by the palmar cutaneous branch, which does not travel through the carpal tunnel. Therefore, if palmar sensation is lost, the nerve injury is most likely located more proximally.

In more chronic or severe cases, weakness in the hand or atrophy may be evident. The median nerve at the wrist supplies the following functions to LOAF muscles in the hand:

  • L: Lumbricals 1 and 2 are affected.

  • O: Opponens pollicis is affected.

  • A: Abductor pollicis brevis (APB) loss results in weakness and atrophy, causing thinning of the lateral contour of the thenar bulk.

  • F: Flexor pollicis brevis (FPB) typically is dually innervated by both median and ulnar nerves; therefore, compression of only the median nerve does not usually cause appreciable symptoms because of the ulnar nerve contribution.

Forced wrist flexion causes increasing paresthesia and pain (Phalen test), as does extreme wrist extension (reverse Phalen test), due to compression of the nerve in the carpal tunnel. Symptoms can be elicited by applying steady pressure with the thumbs over the flexor retinaculum (compression test). Gentle tapping of the median nerve over the flexor retinaculum (wrist) produces paresthesias (percussion test).

Acute carpal tunnel syndrome is a surgical emergency that requires decompression. Progressively worsening pain and sensory disturbances in the median nerve distribution distinguish acute carpal tunnel syndrome from the less severe median nerve neurapraxia. Neuropathy can occur primarily at the time of injury, as the result of unreduced fracture fragments or callus, or following prolonged immobilization in palmar flexion. Prompt diagnosis and treatment of acute injury to the median nerve after wrist trauma are key to a successful outcome.[13]

Ulnar nerve at the elbow (cubital tunnel)

The ulnar nerve travels on the medial side of the brachial artery in the upper arm, pierces the medial intermuscular septum at mid arm, and continues toward the elbow on the medial head of the triceps. At the elbow, it passes through the cubital tunnel—a groove between the medial humeral epicondyle and the olecranon. The nerve travels beneath the aponeurotic arcade between the 2 heads of the flexor carpi ulnaris and down the forearm between the deep and superficial finger flexors.

The following 5 potential areas of ulnar nerve entrapment are found within its course into and out of the elbow:

  • The arcade of Struthers (present in 70% of the population; differs from the ligament of Struthers, which can compress the median nerve) stretches from the medial head of the triceps to insert into the medial intermuscular septum. It is located approximately 6-8 cm above the medial epicondyle. It can be a factor in ulnar nerve compression after ulnar nerve transposition.

  • The medial intermuscular septum presents a sharp edge that can indent the nerve (particularly after anterior transposition) in which the nerve may be kinked.

  • The cubital tunnel is floored by the medial collateral ligament of the elbow and is roofed by the arcuate ligament (cubital tunnel retinaculum) that stretches between the medial humeral epicondyle and the medial aspect of the olecranon.

  • The arching band of aponeurosis between the 2 heads of the flexor carpi ulnaris (so-called Osborne band) may compress the nerve, especially during repetitive contraction of the muscle.

  • The aponeurotic covering between the flexors digitorum profundus and superficialis is occasionally a site of compression.

Ulnar neuropathy at the elbow may result from a posttraumatic or nontraumatic etiology. Trauma may be caused by a single event or, more typically, may be due to mild repetitive injuries. The resulting pathophysiologic basis for the traumatic neuropathy is likely due to scarring and adhesion at the cubital tunnel, compression at the heads of the flexor carpi ulnaris aponeurosis, or both.[14]

Patients with an ulnar neuropathy from a nontraumatic etiology often perform activities that require repetitive elbow flexion or prolonged resting of the elbow on a hard surface. Elbow flexion creates narrowing of the cubital tunnel as a result of traction on the arcuate ligament and bulging of the medial collateral ligament. Elbow flexion may also contribute to the injury by increasing intraneural pressure. With scarring and adhesion on the epineurium, elongation accentuates the tethering effect on the axons. These effects may be accentuated at night when the patient sleeps with the elbow in flexion.

Spontaneous subluxation or dislocation of the ulnar nerve out of the cubital tunnel occurs in up to 15% of the population, occasionally aggravating symptoms of entrapment through a rubbing action against or over the bony surfaces (ie, medial epicondyle).[15]

Signs and symptoms of the clinical presentation include the following:

  • Pain typically presents as a deep ache around the elbow region.
  • Pain is exacerbated when the medial elbow is impacted.
  • Intermittent paresthesias and numbness may occur in the ring finger and in the little finger.
  • Hand weakness may be noted, especially with gripping objects.
  • Sensation over the palmar portion of the fifth digit and the ulnar half of the fourth digit specifically is decreased to the following stimuli: pinprick, light touch, and 2-point discrimination
  • Sensory loss can also be detected along the dorso-ulnar aspect of the hand (due to involvement of the dorsal cutaneous branch of the ulnar nerve, which arises proximal to the wrist).
  • Late symptoms include dense numbness, profound weakness, and atrophy of intrinsic hand muscles.
  • Weakness may be detected in finger abductors and adductors (interossei) and in the thumb (adductor pollicis), whereas thumb abduction is normal.
  • An ulnar claw hand may be present with extension of little and ring fingers.
  • Extension at the metacarpophalangeal joints and flexion at the intraphalangeal joints is caused by loss of lumbricals 3 and 4.
  • Provocative tests: A gentle tapping of the nerve at and around the cubital tunnel elicits distressing electrical shock, tingling, or both, down into the ulnar fingers (percussion test). Sustained elbow flexion combined with gentle digital pressure on the cubital tunnel causes paresthesias and pain.

Ulnar nerve compression at the wrist (Guyon canal)

At the wrist, the ulnar nerve runs above the flexor retinaculum lateral to the flexor carpi ulnaris tendon and medial to the ulnar artery. At the proximal carpal bones, it dips between the pisiform and the hook of the hamate at the entrance to the Guyon canal, roofed over by an extension of the TCL between these 2 bones.[16, 17]

Three zones of the ulnar nerve within the distal ulnar tunnel have been defined as follows:

  • Zone 1 – Ulnar nerve proximal to the bifurcation

  • Zone 2 – Deep branch

  • Zone 3 – Superficial branch or branches

These anatomic zones correlate with clinical symptoms. Patients with zone 1 compression can present with motor, sensory, or mixed lesions; those with zone 2, motor lesions, and with zone 3, sensory.

After entering the Guyon canal, the deep (motor) branch first supplies the abductor digiti minimi (ADM), then crosses under one head of the flexor digiti minimi (FDM), supplies this muscle, and crosses over to supply the opponens digiti minimi (ODM) before rounding the hook of the hamate to enter the mid palmar space and supply other hand muscles. Depending on the exact site of compression within the Guyon canal, the ADM or both the ADM and the FDM may be spared. The ODM is always affected, together with the interossei, lumbricals 3 and 4, and the adductor pollicis.

Compression of the deep branch is most common and usually occurs at the level of the fibrous arch of the hypothenar muscles. The distal canal is also a common site for ganglions arising from the wrist.

The superficial branch supplies sensation to the hypothenar skin ulnar to the vertical line at the base of the ring finger and ends as the 2 ulnar digital nerves for the little finger and the ulnar half of the ring finger. Its only motor fibers extend to the palmaris brevis, which wrinkles the hypothenar skin to cup the palm.

Patients typically have repeated trauma or compression at the wrist. Examples of this are as follows:

  • Paraplegics who use hand crutches that have a horizontal bar across the palm, or those using wheelchairs

  • Motorcyclists or bicyclists who firmly grasp the handlebar

  • Operators of pneumatic drills

  • Carpenters who perform repetitive activities such as hammering

The classic presentation is a young man with painless atrophy of hypothenar muscles and interossei with sparing of the thenar group. Sensory loss and pain involving the ulnar 1.5 digits may be present.

This site can be differentiated from ulnar compression at the elbow, in which sensation over the dorsum of the ulnar half of the ring finger and the little finger (from the dorsal cutaneous branch, which leaves the ulnar nerve prior to entering Guyon canal, approximately 6-8 cm proximal to the wrist) is affected.

A positive Phalen test and percussion tenderness over the course of the ulnar nerve at the wrist may be present.

Radial nerve in the proximal forearm – posterior interosseous nerve syndrome

At mid arm, the radial nerve descends behind the humerus, deep to the long head of the triceps, then spirals around the humerus between the medial and lateral heads of the triceps in the spiral groove. Approximately 5-10 cm above the lateral humeral epicondyle, the nerve pierces the lateral intermuscular septum to gain the anterior compartment of the arm. Here, it immediately enters the deep, muscular groove bordered medially by the biceps and the brachialis and laterally by the brachioradialis, the extensor carpi radialis longus (ECRL), and the extensor carpi radialis brevis (ECRB). The nerve then courses immediately in front of the radiocapitellar joint capsule, where it divides into the (motor) deep branch of the radial nerve and the sensory superficial radial nerve (SRN).

Branches to the brachioradialis and ECRL come off before the bifurcation, and the nerve to the ECRB comes off the deep branch of the radial nerve. A leash of arterial branches (of Henry) that arises from the recurrent radial artery cross over the deep branch of the radial nerve just before the arcade of Frohse. This nerve continues as the PIN in the radial tunnel. The PIN traverses a musculo-tendinous arcade—the arcade of Frohse, which is formed by the upper free border of the superficial head of the supinator. Within the tunnel, the PIN rests on the deep head of the supinator.

After emerging from the radial tunnel beneath the supinator, the PIN lies posteriorly to the interosseous membrane of the forearm and innervates the extensor digiti minimi, the extensor carpi ulnaris, and the extensor digitorum communis medially, as well as the extensor indicis proprius, the extensor pollicis longus and brevis, and the abductor pollicis longus laterally.

PIN compression is most commonly associated with tendinous hypertrophy of the arcade of Frohse and with fibrous thickening of the radiocapitellar joint capsule. Vascular compression by the leash of Henry has been reported. Lesions such as lipoma, synovial cyst, rheumatoid synovitis, and vascular aneurysm have been found in some cases. Hobbies or occupations associated with repetitive and forceful supination predispose the individual to PIN neuropathy. Chronic trauma to the flexion surface of the forearm likewise causes problems. For example, the constricting rings of the Canadian crutches, which exert direct pressure over the supinator surface, typically cause PIN neuropathy in patients with paraplegia.

Brachial plexitis tends to have more diffuse involvement affecting certain sites more commonly (nb, electromyography may be especially helpful). However, brachial plexitis may affect only 1 nerve territory; in these cases, distinction of plexitis from entrapment may be difficult.

The PIN is predominantly a motor nerve. It has pain fibers supplying the wrist but has no cutaneous innervation of the skin. Paralysis of the extensor muscles is heralded by a feeling of fatigue during finger extension and elbow supination. The extension in the metacarpophalangeal joints is weakened, but it is not weakened in the interphalangeal joints because the lumbricals are intact.

The index and fifth fingers receive both their own extensor tendon and the tendon branch from the common extensor and are less affected than the extension of the third and fourth digits. Thus, in the early stage of entrapment, the hand exhibits a characteristic pattern upon finger extension, in which the middle 2 fingers fail to extend, while the index and little fingers can be extended ("sign of horns").

Progression of paralysis eventually causes weakness in all finger extensors and in thumb abduction. Radial wrist extensors are intact because of the proximal innervation of the extensor carpi radialis muscles. No sensory symptoms are present. Dull, aching pain is sometimes present over the front of the elbow, and palpation over the radiohumeral joint often aggravates the pain, probably via irritation of the nervi nervorum of the PIN.

Suprascapular nerve entrapment

The suprascapular nerve arises from the lateral aspect of the upper trunk of the brachial plexus, runs across the posterior triangle of the neck together with the suprascapular artery and the omohyoid muscle, dips under the trapezius, and then passes through the suprascapular notch at the superior border of the scapula. As the nerve enters the supraspinous fossa, it supplies the supraspinatus muscle, then curls tightly around the base of the spine of the scapula, enters the infraspinous fossa, and supplies the infraspinatus.[18, 19, 20]

A stout, strong suprascapular ligament closes over the free upper margins of the suprascapular notch. Suprascapular nerve entrapment is caused by this ligament, often in conjunction with a tight, bony notch. The only sensory fibers in the suprascapular nerve supply the posterior aspect of the shoulder joint. These articular fibers are the source of the ill-localized, dull shoulder pain associated with the syndrome. The syndrome often afflicts athletes, particularly those involved in basketball, volleyball, weightlifting, and gymnastics.

Signs and symptoms include the following:

  • Pain with insidious onset

  • Deep, dull aching pain in the posterior portion of the shoulder and in the upper periscapular region

  • Non-circumscribed pain

  • Lack of neck or radicular symptoms

  • Shoulder weakness

  • Weakness confined to the supraspinatus, which initiates shoulder abduction, and/or to the infraspinatus, which externally rotates the arm. This pattern of weakness must be distinguished from rotator cuff disease and C5 radiculopathy.

  • Atrophy manifesting as hollowing of the infraspinous fossa and prominence of the scapular spine. Supraspinatus atrophy may not be obvious because of the overlying trapezius. Deep pressure over the midpoint of the superior scapular border may produce discomfort.

Lateral femoral cutaneous nerve (meralgia paresthetica)

The lateral femoral cutaneous nerve (LFCN) arises from the ventral rami of the L2 and L3 nerve roots. This purely sensory nerve is formed just deep to the lateral border of the psoas muscle, then descends into the pelvis over the iliacus muscle deep to the iliacus fascia. Just medial to the ASIS, the nerve exits the pelvis by passing through deep and superficial bands of the inguinal ligament as they attach to the ASIS. The nerve is almost horizontal while still within the pelvis before it traverses the inguinal ligament, but it then takes a vertical course out to the surface of the thigh.

This almost 90º kink of the nerve is often exaggerated by a thickened ridge in the iliacus fascia, where it attaches to the posterior aspect of the inguinal ligament. Beyond the groin, the nerve quickly enters the fascial covering of the sartorius, which originates from the ASIS. The most constant relationship of the LFCN is with the medial border of the sartorius about 2-5 cm distal to the ASIS. After this, the nerve usually crosses over the muscle and divides into anterior and posterior branches, supplying sensation to the anterolateral surface of the thigh down to the top of the patella.

A protruding, pendulous abdomen, as seen in obesity and pregnancy, compresses the inguinal ligament downward and onto the nerve, causing it to be kinked. This angulation of the nerve is further exaggerated with extension of the thigh and is relaxed with flexion. Extension also tenses the deep fascia and may add to compression from the front. The nerve may also be compressed directly by tight belts or pants, or by pressure when a patient is prone in spine surgery.

The main symptoms include uncomfortable numbness, tingling, and painful hypersensitivity in the distribution of the LFCN, usually in the anterolateral thigh down to the upper patellar region. Symptoms are often accentuated by walking down slopes and stairs; by engaging in prolonged standing in the erect posture; and, sometimes, by lying flat in bed. The patient learns to relieve symptoms by placing a pillow behind the thighs and by assuming a slightly hunched posture while standing.

Decreased appreciation of pinprick is elicited, together with a hyperpathic reaction to touch and even an after-discharge phenomenon of persistent, spontaneous tingling after the touch. Deep digital pressure medial to the ASIS may set off shooting paresthesia down the lateral thigh. The diagnosis is confirmed with a nerve block using 0.5% bupivacaine injected a finger's breadth medial to the ASIS. Resulting anesthesia over the sensory territory of the LFCN should be concomitant with complete cessation of pain and tingling. Differential diagnosis includes lumbar disc herniation at L2/L3 levels, which may require magnetic resonance imaging (MRI).

Common peroneal nerve entrapment

The common peroneal nerve is 1 of the 2 terminal divisions of the sciatic nerve. It is smaller and lateral to the tibial nerve. It descends obliquely along the lateral side of the popliteal fossa medial to the tendon of the biceps femoris. Posterior to the head of the fibula, it lies superficial to the lateral head of the gastrocnemius. It winds around the lateral aspect of the neck of the fibula deep to the peroneus longus (fibular tunnel), where it divides into superficial peroneal, deep peroneal, and articular branches. Entrapment occurs when the nerve is in close relationship to the neck of the fibula.

In the thigh, it supplies the short head of the biceps femoris and contributes to the sural nerve. In the leg, it supplies the muscles of the lateral and anterior compartments of the leg and sensation on the dorsum of the foot.

Signs and symptoms include the following:

  • Pain radiating from the knee region to the dorsal aspect of the foot

  • Sensory loss on the dorsum of the foot

  • Foot drop (loss of dorsiflexion of the foot) and loss of extension of the toes, as well as eversion of the ankle (this is differentiated from an L5 radiculopathy, in which posterior tibialis function [inversion in plantar flexion] is affected)

  • Tinel sign at the fibular neck: The differential diagnosis is broad, and lumbar radiculopathy (L4 or L5) must be considered.

Tarsal tunnel syndrome

Compression of the tibial nerve behind the medial malleolus, or tarsal tunnel syndrome (TTS), is an uncommon entrapment neuropathy.[21]

The roof of the tunnel is formed by the flexor retinaculum stretched between the medial malleolus and the calcaneus. The tarsal bones are the floor. Numerous fibrous septae between the roof and the floor subdivide the tunnel into separate compartments at various points. The contents of the tarsal tunnel at its proximal end are, from front to back, as follows:

  • Tibialis posterior tendon

  • Flexor digitorum longus tendon

  • Posterior tibial artery and vein

  • Tibial nerve

  • Flexor hallucis longus tendon.

  • Tibial nerve with 3 terminal branches. It bifurcates into medial and lateral plantar nerves within 1 cm of the malleolar-calcaneal axis in 90% of cases; in the other 10%, the medial and plantar nerves are found 2-3 cm proximal to the malleolus.

  • Calcaneal branch, which usually comes off the lateral plantar fascicles (but around 30% leave the main nerve trunk just proximal to the tunnel). Distally, the medial and lateral plantar nerves travel in separate fascial compartments. The medial branch supplies the intrinsic flexors of the great toe, the first lumbrical, and sensation over the medial plantar surface of the foot inclusive of at least the first 3 toes. The lateral branch supplies all interossei and the lateral 3 lumbricals, as well as sensation over the lateral plantar surface of the foot. The calcaneal branch, which traverses its own tunnel, provides sensation to the heel.

Early symptoms include burning, tingling, and dysesthetic pain over the plantar surface of the foot. Characteristically, pain is set off by pressing or rubbing over the plantar skin, sometimes with after-discharge phenomenon. Percussion tenderness (Tinel sign) is often evident over the course of the main nerve or its branches, and pain may be aggravated by forced eversion and dorsiflexion of the ankle.

In advanced cases, the intrinsic flexors of the great toe are weak and atrophied, producing hollowing of the instep. The lateral toes may also show clawing due to paralysis of the intrinsic toe flexors. The calcaneal branch may be spared because of its proximal takeoff.

Thoracic outlet syndrome

Thoracic outlet syndrome is a rare condition (1-3 per 100,000) caused by neurovascular compression at the thoracic outlet. This disorder can be classified as neurogenic, arterial, or venous based on the compressed structure(s). Patients develop an objectively verifiable form of thoracic outlet syndrome secondary to congenital abnormalities such as cervical ribs or fibrous bands originating from a cervical rib. Neck trauma or repeated work stress can cause scalene muscle scarring or dislodging of a congenital cervical rib that can compress the brachial plexus. Nonsurgical treatment includes anti-inflammatory medication, weight loss, physical therapy/strengthening exercises, and botulinum toxin injections. The most common surgical treatments include brachial plexus decompression, neurolysis, and scalenotomy with or without first rib resection.[22]

The first thoracic ventral ramus joins the eighth cervical ventral ramus to form the lower trunk of the brachial plexus. This runs near the subclavian artery on top of the pleural apex to enter the axilla between the clavicle anteriorly and the first rib posteriorly.[23]  Structures crossing on top of the first rib, from anterior to posterior, include subclavian vein, scalenus anterior, subclavian artery, lower trunk of brachial plexus, and scalenus medius. The lower trunk and/or the subclavian artery could be compressed by different structures: fibrous bands deep to the scalenus anterior muscle, thickened suprapleural membrane (Sibson fascia), a cervical rib (bony or fibrous), or an elongated transverse process of C7.

In the neural syndrome, patients typically present with pain and paresthesias along the ulnar aspect of the forearm, hand, and medial 2 fingers. Symptoms are often exacerbated by overhead activities. Patients with neurogenic symptoms often have no objective neurologic deficits clinically or electrophysiologically. On rare occasions, true neurologic loss may be seen with clinically apparent weakness and atrophy, as well as electrophysiologic denervation of finger and hand muscles supplied by the lower trunk (C8 and T1). The Gilliatt-Sumner hand characteristic of the neurogenic thoracic outlet syndrome consists of atrophy affecting thenar and hypothenar eminences.

In the venous syndrome, patients present with arm swelling, cyanosis, and pain; in the arterial syndrome, episodic muscle cramping, coldness, and blanching of the hand, especially with arm elevation, may occur.[24]

Provocative maneuvers include the Adson test (obliteration of the pulse with chin elevation and head turning to the ipsilateral side). Although this was Adson’s original description, pulse obliteration could occur more frequently with head rotation to the contralateral side. In 1966, Roos popularized the 90º abduction in external rotation stress test. In the upper limb tension test of Elvey, the arms are abducted at 90º and the wrists are dorsiflexed, while the head is tilted to the contralateral side. Pulse obliteration with provocative maneuvers could occur in 9-53% of normal people. Tenderness with percussion may be noted over the lower elements of the brachial plexus in the supraclavicular fossa.[25, 26]

Other tests include electrodiagnostic studies; vascular laboratory studies, including Doppler ultrasonography combined with provocative maneuvers; magnetic resonance imaging (MRI)/magnetic resonance angiography (MRA); and, rarely, angiography.

(Chest radiographs could show a cervical rib, as depicted in the image below, or prolonged transverse process of C7.)

Chest PA radiograph showing a right cervical rib ( Chest PA radiograph showing a right cervical rib (arrows), a possible cause of thoracic outlet syndrome.




Imaging Studies

Magnetic resonance imaging (MRI) using the short inversion imaging recovery (STIR) technique displays high signal intensity in the affected nerve segment at the site of compression, probably due to edema in myelin sheath and perineurium. Magnetic resonance neurography is evolving as an important tool in sorting out various painful limb syndromes involving forearm and shoulder. This technique has been incorporated by some groups into treatment of patients with routine entrapment syndromes (eg, carpal and cubital tunnel syndrome). MRI and other imaging modalities are used with atypical presentations of common disorders or with recurrent symptoms after previous operation, as well as with suspected rare entrapment. For example, MRI is especially helpful in identifying a mass lesion in patients with a lesion compressing the suprascapular nerve, the ulnar nerve at the wrist, or the posterior interosseous nerve (PIN).

Diagnostic Procedures

The diagnosis of most entrapment neuropathies can usually be established on clinical grounds alone. For typical cases of carpal tunnel and ulnar cubital syndromes, electrodiagnostic tests (nerve conduction study and electromyography) are not always necessary. Still, they provide useful information: confirming the clinical diagnosis and localization, grading the lesion, identifying an underlying or superimposed peripheral neuropathy, and distinguishing other entities. Additionally, a baseline electrodiagnostic study may allow comparison with a postoperative study in patients with persistent symptoms.

In more unusual entrapment neuropathies such as those involving the suprascapular nerve, the ulnar nerve at the wrist, or the posterior interosseous nerve (PIN), electrodiagnostic tests may be invaluable. For PIN syndrome, electrodiagnostic studies combined with neuromuscular ultrasound can guide accurate electrode localization and can provide diagnostic information about lesion location.[27, 28]

Local nerve block with a local anesthetic agent is useful in confirming the diagnosis of certain entrapments such as meralgia paresthetica.



Medical Therapy

Conservative measures should be tried first in most cases of entrapment neuropathy. Meralgia paresthetica secondary to pregnancy and obesity and intrapartum median nerve compression at the wrist may become completely asymptomatic after delivery or weight loss. Compression neuropathies secondary to systemic disease such as thyroid disease and autoimmune conditions may be effectively managed with treatment of etiologic factors.

In uncomplicated, nonsystemic cases, conservative management mainly consists of educating the patient to adopt avoidance behaviors. This seldom is practical in young, physically active patients, especially if symptoms are occupation related. In cases of posterior interosseous nerve entrapment at the elbow caused by certain kinds of prosthetic devices (eg, Canadian crutches), redesigning or substituting the device may result in relief. Wrist splints for CTS are commonly prescribed but rarely provide long-term control.[29]

Conditioning exercises and periodic injections around the nerve with bupivacaine and dexamethasone may accord long-term relief. Surgery is recommended for patients with symptoms refractory to nonoperative measures and/or for those with severe and long-standing symptoms or weakness.

In a study of 50 women with CTS who were randomly assigned to manual therapy or surgery for treatment, researchers concluded that neither treatment resulted in changes in cervical range of motion.[30]


Operative Details

The general principle of operative intervention involves decompression of the nerves in zones of compression. In some cases, surgical beds may be improved, or nerves can be transposed.[31]

Carpal tunnel syndrome

Anesthesia may be local, regional, or general. Use of a tourniquet is optional. The surgical incision should be made directly over the palmaris longus tendon in line with the radial aspect of the ring finger, roughly coinciding with the longitudinal midpalmar crease. A 3-cm palmar incision may be used over the extent of the TCL. The distal extent of the incision can be approximated by the intersection of a line from the abducted thumb to the hook of the hamate and the flexed ring finger. The proximal extent of the TCL is the distal wrist crease. A small opening is made in the ulnar portion of the TCL, and an elevator is passed beneath the ligament. The ligament is sharply incised ulnarly. The recurrent branch is not routinely visualized.

Fat surrounding the superficial palmar arch should be visualized at the distal extent of the decompression. Under direct visualization, a portion of the antebrachial fascia should be released proximally. Shorter or longer skin incisions can be used, each with potential advantages and disadvantages. A shorter incision may decrease postoperative pain but may make complete visualization more challenging. A longer incision crossing the wrist crease allows identification of the median nerve beneath the antebrachial fascia before it passes under the ligament; however, healing of this portion of the incision may be slower.

Care should be taken not to injure (1) cutaneous branches during superficial exposure, (2) the ulnar neurovascular bundle with the blade of the retractor, (3) the median nerve itself, (4) its recurrent and palmar cutaneous branches by staying ulnar during carpal tunnel release, or (5) the digital branches (and interconnections) during the distal portion of the dissection.

The tourniquet, if used, is often released by surgeons prior to wound closure.

Use of the endoscopic retinaculotome via the 2-portal or single-portal technique has been advocated, with reports indicating that more rapid recovery (including faster return to work) and less postoperative pain are achievable compared to open surgery.[32] Benefits are short lived and must be counted against a higher complication rate of injury to ulnar and median nerves, and to the superficial palmar (arterial) arch in some series.

In a survey of 716 hand surgeons conducted by the American Society for Surgery of the Hand to examine carpal tunnel surgery, 90% said they used electrodiagnostic testing at least occasionally. IV sedation with local anesthesia was the most common practice (used by 43%), followed by Bier block (at 18%). About 50% did not administer preoperative antibiotics at the time of surgery. A mini-open incision was most commonly used (50%). Postoperative pain management was variable, with hydrocodone and derivatives the most commonly used forms of postoperative pain management (at 61%).[33, 34]

Ulnar entrapment at the elbow

Five surgical procedures can be used to correct ulnar entrapment at the elbow, but according to the literature, the specific indications for each are far from clear. In most instances, the surgeon's preference and expertise should influence the selection.[35, 36, 37, 38, 39]

In situ decompression

An incision is made posterior to the medial humeral epicondyle overlying the ulnar nerve. Various techniques exist. In theory, the cubital tunnel is unroofed in the vicinity of the cubital tunnel retinaculum and the proximal portion of the flexor carpi ulnaris. This limited approach can be performed under local anesthesia via a short incision. The nerve is identified proximal to the medial epicondyle and is decompressed distal to the medial epicondyle for several centimeters. Proximal potential anatomic sites of compression are not addressed. Some surgeons and authors do decompress more proximally, addressing the medial intermuscular septum and the arcade of Struthers. Still others perform circumferential neurolysis. More extensive proximal decompression and neurolysis make the ulnar nerve more apt to dislocate with elbow flexion.

The nerve is not circumferentially dissected out, which presumably avoids devascularization and damage to slender muscular branches to the flexor carpi ulnaris. This procedure works well with milder, less chronic forms of the disease. Many surgeons are performing this procedure because of published findings of randomized studies demonstrating equal efficacy and decreased complications compared to other transposition techniques. In cases of spontaneous nerve subluxation or in cases of excessive scarring or osteophyte formation within the cubital tunnel, the authors believe that the nerve should be anteriorly transposed.

Medial epicondylectomy

The nerve is first decompressed in situ. The medial epicondyle is subperiosteally exposed and removed without disturbing the common flexor origin of the pronator teres. Then, the soft tissues over the osteotomy bed are carefully approximated.

Anterior subcutaneous transposition

After neurolysis, the nerve is circumferentially dissected and mobilized from its cubital tunnel bed. Sensory fibers to the elbow joints are severed. Twigs that supply the upper fibers of the flexor carpi ulnaris should be preserved and carefully dissected away from the epineurium to gain length to allow the nerve to be moved onto the anterior surface of the elbow flexor muscles in front of the medial epicondyle.

To avoid kinking the nerve at both ends of the transposition, a segment of the medial intermuscular septum is removed, and the aponeurosis and the muscle fibers of the flexor carpi ulnaris are split longitudinally between the 2 heads. The nerve is then gently placed in a subcutaneous bed. A fasciodermal flap may be fashioned, or several sutures may be placed between the skin flap and the surface of the pronator teres aponeurosis of the common flexor origin just in front of the medial epicondyle.

(See the image below.)

Common peroneal nerve decompression at the fibular Common peroneal nerve decompression at the fibular neck. A: The common peroneal nerve (P) has been identified and mobilized proximal to the fibular tunnel region, fascia (F) covering peroneus longus. B: The common peroneal nerve has been traced through the fibular tunnel. The fascia overlying the peroneus longus muscle has been divided and the muscle (M) has been retracted. The fascial band overlying the nerve is released.


Intramuscular transposition

Adson originated this procedure, supposedly to lessen the vulnerability of the nerve in a subcutaneous location. After transposition, the nerve is placed in a shallow muscular trough created in the pronator teres and flexor carpi ulnaris.

Submuscular transposition

In 1942, Learmonth described this procedure of placing the nerve in an intermuscular plane lined by muscle fascia, where the nerve can glide with joint motions without being “stuck down,” as in the intramuscular or subcutaneous compartments.[40]

The pronator origin is divided often using a step-cut lengthening format, as is the origin of the flexor carpi ulnaris. The anteriorly transposed ulnar nerve is placed under the divided muscles on a fascial bed over the flexor digitorum superficialis and brachialis parallel to the median nerve. The cut ends of the divided tendons are reapproximated in Z-plasty format so that they are lengthened, in effect to lessen tightness over the underlying nerve bed.

Gentle physical therapy is instituted to gradually return the joint to full extension over 3 weeks.

Ulnar nerve entrapment at the wrist

A longitudinal incision is made along the course of the ulnar nerve proximal to the wrist, which curves across the wrist crease and then courses slightly toward the hook of the hamate. The ulnar nerve and vessels are mobilized proximally. The deep and superficial branches are protected and decompressed. The fibrotic arch over the deep branch is released.

Posterior interosseous nerve syndrome

An incision is made on the lateral side of the biceps muscle and is extended across the elbow and along the border of the brachioradialis. The radial nerve is picked up within the groove made by the biceps/brachialis and the forearm extensor group. This groove is held open by self-retaining retractors. The lateral antebrachial cutaneous nerve, if seen, should be protected. The radial nerve is then traced toward the upper border of the supinator. The bifurcation into the deep branch of the radial nerve and the superficial radial nerve (SRN) are readily seen just above and in front of the radiocapitellar joint. The SRN courses deep to the brachioradialis and may be picked up first, in which case it is traced backward to locate the much deeper PIN.[41]

Once the arcade is found, it is divided, together with fibers of the superficial supinator muscle, to expose the entire length of the PIN within the radial tunnel. The fascial thickening associated with the joint capsule also is divided, as is the arterial leash of Henry. The PIN can be exposed through a posterolateral incision with forward reflection of the extensor muscles.

Suprascapular nerve entrapment

The patient is placed prone, preferably in a Mayfield head holder. An incision is made 2 cm above and parallel to the scapular spine. The horizontal trapezial fibers are atraumatically split to expose the constant fat pad that separates the trapezius from the supraspinatus muscle. Digital palpation along the sharp, bony edge of the superior scapular border detects the abrupt change into rubbery springiness of the suprascapular ligament. Blunt dissection by firm, sweeping motion using a “peanut” dissector readily reveals the glistening, taut ligament. The suprascapular artery, which crosses above the ligament, is swept aside. The ligament is cut and the bony notch is enlarged with a Kerrison rongeur, if necessary. The nerve is exposed and decompressed. The operative microscope is often employed.[20]

Meralgia paresthetica

Surgical decompression, when necessary, is very effective, but the recurrence rate is 15-20%. A skin incision is made along the medial border of the sartorius, 2 cm below the ASIS, and extends about 6-7 cm. The fascia over the sartorius is exposed. The fascia is then opened in one location and is carefully extended. The nerve is located at the medial border of the muscle or just behind it. It may be attached to the underside of the fascial sheath, so gentle handling is necessary to avoid accidentally cutting the nerve.[42]

The nerve then is traced proximally toward its exit site just medial to the ASIS. The bands of the inguinal ligament over the nerve are divided. If a sharp ridge is palpable just below the nerve, this should also be divided to completely free the nerve of sharp surfaces. The nerve is then followed into the pelvis for a distance of 2-3 cm to ensure clearance of other iliacus fascial bands.

In spite of the incision on the inguinal ligament (on its lateral side), hernia is extremely rare after this procedure. Recurrence of symptoms can be treated with transection of the nerve. After the nerve is freed at the ASIS and proximally toward the pelvis, gentle downward traction is applied and neurectomy is done proximally. This allows the proximal stump to retract proximally into deep tissues. This is thought to decrease painful neuroma formation on the surface of the thigh afterward. Patients tend to adjust well to the numbness. Several studies have reported excellent long-term control of symptoms with nerve transection as primary treatment.

Various surgical procedures can be applied in the treatment of meralgia paresthetica, with the main ones being neurolysis and neurectomy of the lateral femoral cutaneous nerve. In a study comparing the 2 procedures, pain relief was found to be more successful with neurectomy than with neurolysis. Neurolysis was performed in 8 patients, and neurectomy in 14 patients. Successful pain reduction was achieved in 93.3% after neurectomy versus 37.5% after neurolysis.[43]

Common peroneal nerve entrapment

Decompression can be performed under local anesthesia or with sedation.[44, 45, 46] An incision is made obliquely at the neck of the fibula. The deep fascia is opened, exposing the common peroneal nerve. The nerve is followed proximally along the biceps femoris tendon. Distally, the fascia over the peroneus longus is opened. The muscle is then retracted to expose the fascia deep to the muscle. The latter is divided to completely unroof the nerve and expose the terminal branches. The subcutaneous tissue and skin are then closed.[44, 45]

(See the image below.)

Median nerve (M) after decompression at the wrist; Median nerve (M) after decompression at the wrist; note the congestion from the longstanding compression. The transverse carpal ligament (arrows) has been transected. Fat is observed distally.

Tarsal tunnel syndrome

The incision should begin 2 cm proximal to the medial malleolus to identify the neurovascular bundle. The nerve is then followed distally with release of the flexor retinaculum. Mass lesions or fibrous septa are identified and removed. Each of the plantar nerve canals is opened into the plantar surface. A tight fascial band that arises from the border of the abductor hallucis muscle and roofing over the plantar tunnels is divided. All intersecting septa are resected to convert the tunnels into a single cavity. The calcaneal branch is also decompressed. The ankle is placed in a soft splint and is elevated for 3 days, with minimal weightbearing allowed for an additional week.[21, 47]

Thoracic outlet syndrome

A supraclavicular approach to the brachial plexus is performed. Careful dissection of the brachial plexus roots and trunks is followed by exposure of the subclavian artery. Ample decompression of the artery and the lower trunk of the brachial plexus is achieved by resecting fibrous bands, scalenus anterior, cervical rib, or enlarged transverse process of C7. Decompression of C8 and T1 should be done to the level of their foramina. Some surgeons may perform a transaxillary approach by itself or combined with a supraclavicular approach for scalenectomy, rib resection, and neurovascular decompression.[48]


Most decompressions are performed safely in an outpatient setting. Surgical complications from anesthesia and coexisting medical conditions rarely occur. Damage to surrounding nerves or arteries from manipulation is also unusual.

Postoperative infection may develop, especially among patients with diabetes mellitus; this unfortunately predisposes the patient to recurrence of entrapment.

Outcome and Prognosis

In general, surgical outcomes are excellent in primary cases for improvement of pain and function. In secondary cases, results are fair to good; in these situations, pain relief is often the goal.

Carpal tunnel syndrome

Surgery is associated with a 70-90% rate of improvement in median nerve–related symptoms.[49]

The most common potential complications include the following:

  • Misdiagnosis

  • Incomplete sectioning of the TCL

  • Palmar pain

  • Pillar pain along the thenar and hypothenar eminences (probably related to adjustment of carpal bone alignments)

  • Temporary loss of grip strength secondary to relocation of the origin of the hypothenar and thenar muscles and bowing of flexor tendons through the TCL incision

Most of these complications are transient. Neurovascular complications rarely occur and have been reported with open and endoscopic techniques. Neural injury may affect median and ulnar nerves, digital nerves (or communicating branches), or cutaneous branches, and recurrent motor branch and vascular injury may affect the superficial palmar arch or ulnar artery.

Postoperative infection is reported in approximately 0-5% of patients. Palmar space infection is an extremely serious emergency that can result in permanent adhesive tenosynovitis and recurrent median nerve compression. Open drainage, use of a drain, and high-dose intravenous antibiotics should be instituted immediately.

Ulnar nerve compression at the elbow

Adherence to strict surgical principles results in a good outcome in approximately 80% of patients, regardless of the procedure chosen. Surgical failure may be due to inadequate decompression or secondary compression of the ulnar nerve. One should also consider the possibility of a neuroma of the medial antebrachial cutaneous nerve in a patient with medial, volar forearm pain following previous ulnar nerve surgery. Revision ulnar nerve surgery most commonly employs a submuscular transposition, although this technique is by far the most complex and difficult to perfect.

Posterior interosseous nerve syndrome

Good to excellent outcomes are often achieved in these patients following spontaneous recovery or decompression.

Suprascapular nerve entrapment

Symptomatic improvement is frequently seen in patients who undergo decompression. Often this may be seen within days of surgery, especially with respect to external rotation. However, long-term weakness and atrophy may take many months to improve, and some patients never regain full strength. Early detection is an important predictor of outcome in suprascapular entrapment.

Ulnar nerve compression at the wrist

Improvement is expected in painful cases and in those with mild motor loss. In some cases, severe atrophy may improve due to the relatively short distances for reinnervation from the site of compression to the muscle endplate. Long-standing atrophy likely will not improve.

Meralgia paresthetica

Surgical decompression is very effective, but the recurrence rate is 15-20%.

Tarsal tunnel syndrome

In general, 75% of patients enjoy significant improvement with surgical decompression of the tarsal tunnel. The best surgical results are observed in patients with mass lesions within the tunnel; the worst results are seen in patients who have undergone previous exploration for pain and in those with plantar fasciitis and autoimmune disease.



Guidelines Summary

Carpal tunnel syndrome

In February 2016, the American Academy of Orthopaedic Surgeons released an evidence-based clinical practice guideline on the management of CTS. Recommendations based on strong or moderate evidence included the following[50] :

  • Thenar atrophy is strongly associated with ruling in CTS but is poorly associated with ruling it out.
  • Do not use the Phalen test, Tinel sign, flick sign, or upper limb neurodynamic/nerve tension test (ULNT) criterion A/B as independent physical examination maneuvers to diagnose CTS because alone, each has a poor or weak association with ruling in or ruling out the condition.
  • Do not use the following as independent physical examination maneuvers to diagnose CTS because alone, each has a poor or weak association with ruling in or ruling out the condition: carpal compression test, reverse Phalen test, thenar weakness or thumb abduction weakness or abductor pollicis brevis manual muscle testing, 2-point discrimination, Semmes-Weinstein monofilament test, CTS-relief maneuver, pin prick sensory deficit (thumb or index or middle finger), ULNT criterion C, tethered median nerve stress test, vibration perception (tuning fork), scratch collapse test, Luthy sign, and pinwheel.
  • Do not use the following as independent history interview topics to diagnose CTS because alone, each has a poor or weak association with ruling in or ruling out the condition: sex/gender, ethnicity, bilateral symptoms, diabetes mellitus, worsening symptoms at night, duration of symptoms, patient localization of symptoms, hand dominance, symptomatic limb, age, and body mass index.
  • Do not routinely use magnetic resonance imaging (MRI) for the diagnosis of CTS.
  • Diagnostic questionnaires and/or electrodiagnostic studies can be used to aid the diagnosis of CTS.
  • The following factors are associated with increased risk of developing CTS: perimenopausal status, wrist ratio/index, rheumatoid arthritis, psychosocial factors, distal upper extremity tendinopathies, gardening, American Conference of Governmental Industrial Hygienists (ACGIH) hand activity level at or above threshold, assembly line work, computer work, vibration, tendonitis, and workplace forceful grip/exertion.
  • Physical activity/exercise is associated with decreased risk of developing CTS.
  • Use of oral contraception or female hormone replacement therapy is not associated with increased or decreased risk of developing CTS.
  • Immobilization (brace/splint/orthosis) should improve patient-reported outcomes.
  • Steroid (methylprednisolone) injection should improve patient-reported outcomes.
  • Magnet therapy should not be used for treatment of CTS.
  • No benefit is derived from oral CTS treatments (diuretic, gabapentin, astaxanthin capsules, nonsteroidal anti-inflammatory drugs [NSAIDs], or pyridoxine) over placebo.
  • Oral steroids could improve patient-reported outcomes in comparison with placebo.
  • Ketoprofen phonophoresis could provide pain reduction in comparison with placebo.
  • Surgical release of the transverse carpal ligament should relieve CTS symptoms and improve function.
  • Surgical treatment of CTS should have greater therapeutic benefit at 6 and 12 months in comparison with splinting, NSAID therapy, and a single steroid injection.
  • No benefit is derived from routine postoperative immobilization after carpal tunnel release.
  • No benefit is associated with routine inclusion of the following adjunctive techniques: epineurotomy, neurolysis, flexor tenosynovectomy, and lengthening/reconstruction of the flexor retinaculum (transverse carpal ligament).
  • Buffered lidocaine rather than plain lidocaine should be used for local anesthesia because buffered lidocaine could result in reduced injection pain.
  • No additional benefit is seen with routine supervised therapy over home programs in the immediate postoperative period; no evidence meeting the inclusion criteria was found when the potential benefit of exercise versus no exercise after surgery was assessed.

ACR Appropriateness Criteria imaging in the diagnosis of thoracic outlet syndrome

The American College of Radiology has noted the following regarding diagnosis of thoracic outlet syndrome[51] :

  • TOS is characterized by compression of the neurovascular bundle as it passes from the upper thorax to the axilla. Arterial, venous, and neurogenic forms have been identified.
  • TOS may be congenital or acquired and may be secondary to bony issues such as first rib abnormalities, cervical ribs, and bony tubercles, or to soft tissue anomalies such as fibrous bands or cervical muscle hypertrophy.
  • The goals of further imaging are to confirm the diagnosis of TOS, exclude mimics such as cervical spondylosis or shoulder joint or lung apex pathology, allow accurate classification into neurogenic TOS versus venous (Paget-Schroetter) versus arterial TOS, and guide treatment selection to minimize morbidity and mortality.
  • Abduction of the upper limb has been shown to be relevant in diagnosing TOS and is the postural maneuver of choice for cross-sectional imaging.
  • Digital subtraction angiography, US, CTA, and MRA may allow evaluation of vascular structures and secondary effects of compression, whereas CT and MRI may allow identification and evaluation of surrounding neurologic, soft tissue, and bony structures.