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Nerve Entrapment Syndromes

  • Author: Amgad Saddik Hanna, MD; Chief Editor: Brian H Kopell, MD  more...
 
Updated: Nov 11, 2015
 

Background

The brain and spinal cord receive and send information through muscles and sensory receptors. The information sent to organs is transmitted through nerves. The nerves travel to the upper and lower extremities and traverse the 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.

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.

This article summarizes some basic principles of entrapment neuropathies, and, within each section, the specifics of the most common entrapment syndromes are outlined. Together, this information should provide the reader with a solid basis for further investigation.

Carpal tunnel syndrome

In a survey by the American Society for Surgery of the Hand of 716 hand surgeons regarding 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 being the most common forms of postoperative pain management, at 61%.[1, 2]

For excellent patient education resources, see eMedicineHealth's patient education article Carpal Tunnel Syndrome.

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History of the Procedure

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).

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Problem

Entrapment neuropathies are a group of 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.

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Epidemiology

Frequency

Neurosurgeons, among other surgical specialists, treat these entrapment neuropathies, which can account for 10-20% of the practice’s cases. Orthopedic and plastic surgeons also perform these types of surgery.

Carpal tunnel syndrome (CTS), compression of the median nerve at the wrist, is the most common entrapment neuropathy. Cubital tunnel syndrome is the second most common and is caused by a compression at the elbow. Other rare nerve entrapment syndromes include the suprascapular nerve, which accounts for approximately 0.4% of upper girdle pain symptoms, and meralgia paresthetica, which is a compression of the lateral femoral cutaneous nerve [LFCN] in the groin.

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Etiology

Nerve entrapment syndromes result from chronic injury to a nerve as it travels through an osseoligamentous tunnel; the compression is typically between the ligamentous canal and bony surfaces. Other potential anatomical sites 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.

In cases of nerve entrapment, at least one portion of the compressive surfaces is mobile. This results in either a repetitive "slapping" insult or a "rubbing/sliding" compression against sharp, tight edges, with motion at the adjacent joint that results in a chronic injury. Immobilization of the nerve with a splint or lifestyle adjustments may therefore 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 in the spinoglenoid notch, and microtrauma in elite athletes.[3]

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Pathophysiology

Repetitive injury and trauma to a nerve may result in microvascular (ischemic) changes, edema, injury to the outside layers of the nerve (myelin sheath) that aid in the 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 permanent fibrotic changes in the neuromuscular junction that may prevent full reinnervation and restoration of function.

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Presentation

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

  • Irritative 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 nerves, 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 ulcerations

Most entrapment syndromes involve mixed sensory and motor nerves and, thus, conform to the aforementioned pattern. Some exceptions are 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.

  • Relevant anatomy
    • Median nerve compression at the wrist is 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 and then fans out to the soft tissue of the palmar skin as the palmar aponeurosis. The combined layers of the TCL and proximal palmar fascia form the flexor retinaculum.
    • The palmaris longus tendon inserts in 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 people, the nerve is beneath a fascial membrane between the flexor carpi radialis and the 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 arise from the ulnar aspect of the median nerve, and an accessory motor branch may even emerge proximal to the flexor retinaculum.[4]
    • 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 injury during carpal tunnel surgery, either directly or indirectly (eg, from retractor pressure).
  • Clinical presentation [5, 6]
    • Patients note a dull, aching pain at the wrist that may extend up the forearm to the elbow. Often, it 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." The pain is typically worse at night and disturbs their sleep. As the symptoms worsen, sensation may be decreased at the volar pads of the thumb, index, middle, and ring fingers. The symptoms are the result of compression of the median nerve as it passes through the wrist and carpal tunnel.
    • 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 more proximally located.
    • In more chronic or severe cases, weakness in the hand or atrophy may be present. The median nerve at the wrist supplies the following functions to the 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) is typically dually innervated by both the 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 also 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).

Ulnar nerve at the elbow (cubital tunnel)

See the list below:

  • Relevant anatomy
    • 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 exist 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 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.
  • Pathophysiology
    • Ulnar neuropathy at the elbow may be from a posttraumatic or nontraumatic etiology. Trauma may be caused by a single event or, more typically, 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.
    • 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 the 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 by the rubbing action against or over the bony surfaces (ie, medial epicondyle).
  • Symptoms in 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 in the ring and little fingers
    • Hand weakness, especially with gripping objects
  • Signs of ulnar compression include the following:
    • 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
      • Two-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 and profound weakness and atrophy of the intrinsic hand muscles.
    • Weakness of finger abductors and adductors (interossei) and adductor of the thumb (adductor pollicis) may be detected whereas thumb abduction is normal.
    • An ulnar claw hand may be present with extension of the little and ring fingers.
    • Extension at the metacarpophalangeal joints and flexion at the intraphalangeal joints is caused by the 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)

See the list below:

  • Relevant anatomy [7, 8]
    • 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.
    • 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 – The deep branch
      • Zone 3 – The superficial branch or branches
    • These anatomic zones correlate with clinical symptomatology. Patients with zone 1 compression can present with motor, sensory or mixed lesions; those with zone 2, motor lesions, and 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 the most common and usually occurs at the level of the fibrous arch of the hypothenar muscles. The distal canal is also the 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 ulnar half of the ring finger. Its only motor fibers are to the palmaris brevis, which wrinkles the hypothenar skin to cup the palm.
  • Causes
    • 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
  • Clinical presentation
    • The classic presentation is a young man with painless atrophy of the 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, which has the sensation affected 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).
    • 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

See the list below:

  • Relevant anatomy
    • At mid arm, the radial nerve descends behind the humerus, deep to the long head of the triceps, and then spirals around the humerus in 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 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 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, 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, extensor carpi ulnaris, and the extensor digitorum communis medially and the extensor indicis proprius, extensor pollicis longus and brevis, and abductor pollicis longus laterally.
    • PIN compression is most commonly associated with tendinous hypertrophy of the arcade of Frohse and 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 a 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.
    • In the authors' opinion, so-called spontaneous PIN “compression” is probably often due to brachial plexitis (inflammation) rather than true entrapment. Brachial plexitis tends to have more diffuse involvement affecting certain sites more commonly (nb, electromyography may be especially helpful). However, brachial plexitis may present affecting one nerve territory only; in these cases, distinction of plexitis from an entrapment may be difficult.
    • The clinical picture is as follows:
      • The PIN is predominately 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 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 of the 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 because of irritation of the nervi nervorum of the PIN.

Suprascapular nerve entrapment

See the list below:

  • Relevant anatomy [9, 10]
    • 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.[11]
    • 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 of the syndrome. The syndrome often afflicts athletes, particularly those involved in basketball, volleyball, weightlifting, and gymnastics.
  • Clinical presentation
    • Pain symptoms
      • Pain with insidious onset
      • Deep, dull aching pain in the posterior part of the shoulder and upper periscapular region
      • Noncircumscribed pain
      • No neck or radicular symptoms
      • Shoulder weakness
    • Signs
      • Weakness is confined to the supraspinatus, which initiates shoulder abduction and/or the infraspinatus, which externally rotates the arm. This pattern of weakness must be distinguished from rotator cuff disease and C5 radiculopathy.
      • Atrophy can manifest 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)

See the list below:

  • Relevant anatomy
    • 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 in the pelvis over the iliacus muscle deep to the iliacus fascia. Just medial to the ASIS, the nerve exits the pelvis by passing through the 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 then it 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 an anterior and posterior branch, 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 relaxed with flexion. Extension also tenses the deep fascia and may add to the compression from the front. The nerve may also be compressed directly by tight belts or pants, or pressure with a patient prone in spine surgery.
  • Clinical presentation
    • The main symptoms are an uncomfortable numbness, tingling, and painful hypersensitivity in the distribution of the LFCN, usually in the anterolateral thigh down to the upper patella region. The symptoms are often accentuated by walking down slopes and stairs; prolonged standing in the erect posture; and, sometimes, lying flat in bed. The patient learns to relieve symptoms by placing a pillow behind the thighs and 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. The resulting anesthesia over the sensory territory of the LFCN should be concomitant with the complete cessation of pain and tingling. Differential diagnosis includes lumbar disc herniation at the L2/L3 levels, which may require an MRI.

Common peroneal nerve entrapment

See the list below:

  • Relevant anatomy
    • 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 fibula, it lies superficial to the lateral head of gastrocnemius. It winds around the lateral aspect of the neck of fibula deep to the peroneus longus (fibular tunnel), where it divides into superficial peroneal, deep peroneal, and articular branches. Entrapment occurs where the nerve is in close relationship to the neck of fibula.
    • In the thigh, it supplies the short head of 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
  • Clinical presentation
    • 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 toes, and eversion of 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.[12]

  • Relevant anatomy
    • 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:
      • The tibialis posterior tendon
      • The flexor digitorum longus tendon
      • The posterior tibial artery and vein
      • The tibial nerve
      • The flexor hallucis longus tendon.
    • The tibial nerve has 3 terminal branches. It bifurcates into the medial and lateral plantar nerves within 1 cm of the malleolar-calcaneal axis in 90% of cases; in the other 10% of cases, the medial and plantar nerves are 2-3 cm proximal to the malleolus.
    • The calcaneal branch 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 the sensation over the medial plantar surface of the foot inclusive of at least the first 3 toes. The lateral branch supplies all of the 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.
  • Clinical presentation
    • Early symptoms are burning, tingling, and dysesthetic pain over the plantar surface of the foot. Characteristically, the 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 the 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

See the list below:

  • Relevant anatomy [13]
    • 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.
    • Structures crossing on top of the first rib, from anterior to posterior: 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.
  • Clinical presentation
    • Neural syndrome: Typically, patients present with pain and paresthesias along the ulnar aspect of the forearm, hand, and medial 2 fingers. These symptoms are often exacerbated with overhead activities. Patients with neurogenic symptoms often have no objective neurologic deficits clinically or electrophysiologically. On rare occasion, true neurologic loss may be present with clinically apparent weakness and atrophy as well as electrophysiological 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 has atrophy affecting thenar and hypothenar eminences.
    • Venous syndrome: Patient presents with arm swelling, cyanosis, and pain.
    • Arterial syndrome: Episodic muscle cramping, coldness, and blanching of the hand, especially with arm elevation occur.
  • Diagnosis [14, 15]
    • Provocative maneuvers include 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 ninety degree abduction in external rotation stress test. Upper limb tension test of Elvey: the arms are abducted at 90 degrees and the wrists are dorsiflexed, the head is tilted to the contralateral side. Pulse obliteration with provocative maneuvers could occur in 9-53% of normal people. Tenderness with percussion over the lower elements of the brachial plexus in the supraclavicular fossa may be present.
    • 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.
    • Electrodiagnostic studies
    • Vascular laboratory studies including Doppler ultrasonography combined with provocative maneuvers
    • MRI/MRA
    • Angiography is rarely indicated.
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Contributor Information and Disclosures
Author

Amgad Saddik Hanna, MD Assistant Professor, Department of Neurosurgery, University of Wisconsin School of Medicine and Public Health

Amgad Saddik Hanna, MD is a member of the following medical societies: American Association of Neurological Surgeons, Central Neuropsychiatric Association, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

Coauthor(s)

James S Harrop, MD Associate Professor, Departments of Neurological and Orthopedic Surgery, Jefferson Medical College of Thomas Jefferson University

James S Harrop, MD is a member of the following medical societies: American Association of Neurological Surgeons, American College of Surgeons, American Spinal Injury Association, North American Spine Society, Congress of Neurological Surgeons, Cervical Spine Research Society

Disclosure: Received consulting fee from Depuy spine for consulting; Received none from Geron for none; Received none from Neural Stem for none; Received ownership interest from Axiomed for none; Received honoraria from Stryker Spine for none.

Robert J Spinner, MD The Burton M Onofrio, MD, Professor of Neurosurgery, Professor of Orthopedics and Anatomy, Mayo Medical School; Co-Director, Brachial Plexus Clinic, Consultant, Department of Neurologic Surgery, Mayo Clinic

Robert J Spinner, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association for the Advancement of Science, American Association for Hand Surgery, American Association of Neurological Surgeons, American College of Surgeons, American Medical Association, American Orthopaedic Association, American Association of Clinical Anatomists, Congress of Neurological Surgeons, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

George M Ghobrial, MD Resident Physician, Department of Neurological Surgery, Thomas Jefferson University Hospital

Disclosure: Nothing to disclose.

Tristan B Fried Student Medical Researcher, Thomas Jefferson Hospital; Student Researcher (STAR), Department of Dermatology, Hahnemann University

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Ryszard M Pluta, MD, PhD Associate Professor, Neurosurgical Department Medical Research Center, Polish Academy of Sciences, Poland; Clinical Staff Scientist, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH); Fishbein Fellow, JAMA

Ryszard M Pluta, MD, PhD is a member of the following medical societies: Polish Society of Neurosurgeons, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Brian H Kopell, MD Associate Professor, Department of Neurosurgery, Icahn School of Medicine at Mount Sinai

Brian H Kopell, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, International Parkinson and Movement Disorder Society, Congress of Neurological Surgeons, American Society for Stereotactic and Functional Neurosurgery, North American Neuromodulation Society

Disclosure: Received consulting fee from Medtronic for consulting; Received consulting fee from St Jude Neuromodulation for consulting; Received consulting fee from MRI Interventions for consulting.

Additional Contributors

Michael G Nosko, MD, PhD Associate Professor of Surgery, Chief, Division of Neurosurgery, Medical Director, Neuroscience Unit, Medical Director, Neurosurgical Intensive Care Unit, Director, Neurovascular Surgery, Rutgers Robert Wood Johnson Medical School

Michael G Nosko, MD, PhD is a member of the following medical societies: Academy of Medicine of New Jersey, Congress of Neurological Surgeons, Canadian Neurological Sciences Federation, Alpha Omega Alpha, American Association of Neurological Surgeons, American College of Surgeons, American Heart Association, American Medical Association, New York Academy of Sciences, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Dachling Pang, MD, FRCS(C), FACS Professor of Pediatric Neurosurgery, University of California, Davis, School of Medicine; Chief, Regional Center for Pediatric Neurosurgery, Kaiser Permanente Hospitals of Northern California

Dachling Pang, MD, FRCS(C), FACS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, American College of Surgeons, Congress of Neurological Surgeons, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Kamran Sahrakar, MD, FACS Clinical Professor, Department of Neurosurgery, University of California at San Francisco

Kamran Sahrakar, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, American Medical Association, California Medical Association, Florida Medical Association, and Nevada State Medical Association

Disclosure: Nothing to disclose.

References
  1. Munns JJ, Awan HM. Trends in carpal tunnel surgery: an online survey of members of the American Society for Surgery of the Hand. J Hand Surg Am. 2015 Apr. 40 (4):767-71.e2. [Medline].

  2. Lane LB, Starecki M, Olson A, Kohn N. Carpal tunnel syndrome diagnosis and treatment: a survey of members of the American Society For Surgery of the Hand. J Hand Surg Am. 2014 Nov. 39 (11):2181-87.e4. [Medline].

  3. Clavert P, Thomazeau H. Peri-articular suprascapular neuropathy. Orthop Traumatol Surg Res. 2014 Dec. 100 (8 Suppl):S409-11. [Medline].

  4. Lanz U. Anatomical variations of the median nerve in the carpal tunnel. J Hand Surg Am. 1977 Jan. 2(1):44-53. [Medline].

  5. Ball C, Pearse M, Kennedy D, Hall A, Nanchahal J. Validation of a one-stop carpal tunnel clinic including nerve conduction studies and hand therapy. Ann R Coll Surg Engl. 2011 Nov. 93(8):634-8. [Medline].

  6. Bland JD, Weller P, Rudolfer S. Questionnaire tools for the diagnosis of carpal tunnel syndrome from the patient history. Muscle Nerve. 2011 Nov. 44(5):757-62. [Medline].

  7. Gross MS, Gelberman RH. The anatomy of the distal ulnar tunnel. Clin Orthop Relat Res. 1985 Jun. 238-47. [Medline].

  8. Ruder JR, Wood VE. Ulnar nerve compression at the arch of origin of the adductor pollicis muscle. J Hand Surg Am. 1993 Sep. 18(5):893-5. [Medline].

  9. Fritz RC, Helms CA, Steinbach LS, Genant HK. Suprascapular nerve entrapment: evaluation with MR imaging. Radiology. 1992 Feb. 182(2):437-44. [Medline].

  10. Rengachary SS, Neff JP, Singer PA, Brackett CE. Suprascapular entrapment neuropathy: a clinical, anatomical, and comparative study. Part 1: clinical study. Neurosurgery. 1979 Oct. 5(4):441-6. [Medline].

  11. Bigliani LU, Dalsey RM, McCann PD, April EW. An anatomical study of the suprascapular nerve. Arthroscopy. 1990. 6(4):301-5. [Medline].

  12. Cimino WR. Tarsal tunnel syndrome: review of the literature. Foot Ankle. 1990 Aug. 11(1):47-52. [Medline].

  13. Birch R, Bonney G, Wynn Parry CB. Entrapment neuropathy. Surgical disorders of the peripheral nerves. Churchill Livingstone; 1998. 245-291.

  14. Nord KM, Kapoor P, Fisher J, et al. False positive rate of thoracic outlet syndrome diagnostic maneuvers. Electromyogr Clin Neurophysiol. 2008 Mar. 48(2):67-74. [Medline].

  15. Sanders RJ, Hammond SL, Rao NM. Diagnosis of thoracic outlet syndrome. J Vasc Surg. 2007 Sep. 46(3):601-4. [Medline].

  16. Wininger YD, Buckalew NA, Kaufmann RA, Munin MC. Ultrasound combined with electrodiagnosis improves lesion localization and outcome in posterior interosseous neuropathy. Muscle Nerve. 2015 Jul 22. [Medline].

  17. Dellon AL, Hament W, Gittelshon A. Nonoperative management of cubital tunnel syndrome: an 8-year prospective study. Neurology. 1993 Sep. 43(9):1673-7. [Medline].

  18. Pirela-Cruz MA, Omer GF. Surgical exposure of the peripheral nerves of the upper extremity. Benzel EC, ed. Practical Approaches to Peripheral Nerve Surgery. American Association of Neurological Surgeons; 1992. 139-142.

  19. Palmer DH, Paulson JC, Lane-Larsen CL, Peulen VK, Olson JD. Endoscopic carpal tunnel release: a comparison of two techniques with open release. Arthroscopy. 1993. 9(5):498-508. [Medline].

  20. Bartels RH, Verhagen WI, van der Wilt GJ, Meulstee J, van Rossum LG, Grotenhuis JA. Prospective randomized controlled study comparing simple decompression versus anterior subcutaneous transposition for idiopathic neuropathy of the ulnar nerve at the elbow: Part 1. Neurosurgery. 2005 Mar. 56(3):522-30; discussion 522-30. [Medline].

  21. Biggs M, Curtis JA. Randomized, prospective study comparing ulnar neurolysis in situ with submuscular transposition. Neurosurgery. 2006 Feb. 58(2):296-304; discussion 296-304. [Medline].

  22. Gabel GT, Amadio PC. Reoperation for failed decompression of the ulnar nerve in the region of the elbow. J Bone Joint Surg Am. 1990 Feb. 72(2):213-9. [Medline].

  23. Manske PR, Johnston R, Pruitt DL, Strecker WB. Ulnar nerve decompression at the cubital tunnel. Clin Orthop Relat Res. 1992 Jan. 231-7. [Medline].

  24. Osterman AL, Davis CA. Subcutaneous transposition of the ulnar nerve for treatment of cubital tunnel syndrome. Hand Clin. 1996 May. 12(2):421-33. [Medline].

  25. Learmonth JR. Technique for transplantation of the ulnar nerve. Surg Gynecol Obstet. 1942. 75:792-3.

  26. Cravens G, Kline DG. Posterior interosseous nerve palsies. Neurosurgery. 1990 Sep. 27(3):397-402. [Medline].

  27. McGillicuddy JE, Harrigan MR. Meralgia Paresthetica. Techniques in Neurosurgery. 2000. 6(1):50-56.

  28. de Ruiter GC, Kloet A. Comparison of effectiveness of different surgical treatments for meralgia paresthetica: Results of a prospective observational study and protocol for a randomized controlled trial. Clin Neurol Neurosurg. 2015 Jul. 134:7-11. [Medline].

  29. Humphreys DB, Novak CB, Mackinnon SE. Patient outcome after common peroneal nerve decompression. J Neurosurg. 2007 Aug. 107(2):314-8. [Medline].

  30. Mackinnon SE, Dellon AL. Lower extremity nerves. Kline DG, Hudson AR. Nerve Injuries: Operative Results for Major Nerve Injuries, Entrapments, and Tumors. 1st ed. WB Saunders Co: 1995. 389-394.

  31. Morimoto D, Isu T, Kim K, Sugawara A, Yamazaki K, Chiba Y, et al. Microsurgical Decompression for Peroneal Nerve Entrapment Neuropathy. Neurol Med Chir (Tokyo). 2015. 55 (8):669-73. [Medline].

  32. Yassin M, Garti A, Weissbrot M, Heller E, Robinson D. Treatment of anterior tarsal tunnel syndrome through an endoscopic or open technique. Foot (Edinb). 2015 Sep. 25 (3):148-51. [Medline].

  33. Orlando MS, Likes KC, Mirza S, Cao Y, Cohen A, Lum YW, et al. A decade of excellent outcomes after surgical intervention in 538 patients with thoracic outlet syndrome. J Am Coll Surg. 2015 May. 220 (5):934-9. [Medline].

  34. Kuschner SH, Brien WW, Johnson D, Gellman H. Complications associated with carpal tunnel release. Orthop Rev. 1991 Apr. 20(4):346-52. [Medline].

  35. Filler AG. Piriformis and related entrapment syndromes: diagnosis & management. Neurosurg Clin N Am. 2008 Oct. 19(4):609-22, vii. [Medline].

  36. Tiel RL. Piriformis and related entrapment syndromes: myth & fallacy. Neurosurg Clin N Am. 2008 Oct. 19(4):623-7, vii. [Medline].

  37. Dellon AL. Neurosurgical prevention of ulceration and amputation by decompression of lower extremity peripheral nerves in diabetic neuropathy: update 2006. Acta Neurochir Suppl. 2007. 100:149-51. [Medline].

  38. Elliott R, Burkett B. Massage therapy as an effective treatment for carpel tunnel syndrome. J Bodyw Mov Ther. 12/2012. 17(3):[Medline].

  39. Galardi G, Amadio S, Maderna L, et al. Electrophysiologic studies in tarsal tunnel syndrome. Diagnostic reliability of motor distal latency, mixed nerve and sensory nerve conduction studies. Am J Phys Med Rehabil. 1994 Jun. 73(3):193-8. [Medline].

  40. Kline DG, Hudson AR. Vertebral artery compression. J Neurosurg. 1995 Oct. 83(4):759. [Medline].

  41. Kureshi SA, Friedman AH. Carpal Tunnel Release: Surgical consideration. Techniques in Neurosurgery. 2000. 6(1):5-13.

  42. LeRoux PD, Ensign TD, Burchiel KJ. Surgical decompression without transposition for ulnar neuropathy: factors determining outcome. Neurosurgery. 1990 Nov. 27(5):709-14; discussion 714. [Medline].

  43. Ochoa JL. Genesis of the structural pathology of myelinated fibers in median nerve entrapment. Muscle Nerve. 2012. 46(6):978. [Medline].

  44. [Guideline] Tubbs RS, Mortazavi MM, Farrington WJ, Chern JJ, Shoja MM, Loukas M, et al. Relationships Between the Posterior Interosseous Nerve and the Supinator Muscle: Application to Peripheral Nerve Compression Syndromes and Nerve Transfer Procedures. J Neurol Surg A Cent Eur Neurosurg. May/2013. EPub ahead of print:13. [Medline].

  45. Yalcin E, Unlu E, Akyuz M, Karaahmet OZ. Ultrasound diagnosis of ulnar neuropathy: Comparison of symptomatic and asymptomatic nerve thickness. J Hand Surg Eur Vol. 4/2013. [Medline].

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