Nerve Entrapment Syndromes of the Lower Extremity


Nerve entrapment syndromes of the lower extremity can involve the following nerves and branches thereof:

  • Iliohypogastric nerve
  • Ilioinguinal nerve
  • Genitofemoral nerve
  • Femoral nerve
  • Lateral femoral cutaneous nerve
  • Saphenous nerve
  • Obturator nerve
  • Common peroneal nerve
  • Superficial peroneal nerve
  • Deep peroneal nerve
  • Tibial nerve
  • Plantar nerves
  • Digital nerves

The genitofemoral nerve or its branches (genital or femoral) can be entrapped throughout its course. Nerve injury occurs most commonly as a complication of surgical procedures involving the lower abdomen.

Injury or entrapment of the lateral femoral cutaneous nerve, also known as meralgia paresthetica (from the Greek words mēros [“thigh”] and algos [“pain”]), is a syndrome of paresthesia and pain in the lateral and anterolateral thigh. This syndrome is seen most commonly in individuals aged 20-60 years, but it can occur in people of all ages.

Entrapment of the tibial nerve or one of its branches gives rise to tarsal tunnel syndrome, which is the most common entrapment neuropathy in the foot and ankle area. This entrapment typically occurs within or distal to the tarsal canal, resulting in pain or sensory disturbance on the plantar aspect of the foot. Patients typically present with intractable heel pain.

Historically, tarsal tunnel syndrome was defined as entrapment of the tibial nerve in the fibro-osseous tunnel behind the medial malleolus, and it was considered rare. [123In time, however, the lateral plantar nerve and its branches were noted to be a more common site of entrapment. Accordingly, some authors have used the following terms to differentiate the location of entrapment:

  • Proximal tarsal tunnel syndrome - Entrapment of the tibial nerve in the fibro-osseous tunnel behind the medial malleolus
  • Distal tarsal tunnel syndrome - Entrapment of the distal branches (ie, the medial and lateral plantar nerves)

In addition, others have more specifically identified entrapments involving the first branch of the lateral plantar nerve and the calcaneal nerves. Nevertheless, the term tarsal tunnel syndrome continues to be frequently used to define all entrapments of the tibial nerve or its branches, starting from posterior to the medial malleolus and extending distally. [4]

Some studies of tarsal tunnel syndrome suggest a slight female predominance, and the range of patient ages has been reported to be 14-80 years. This condition is common in nonathletes, though Baxter initially noted it in long-distance runners. [5]

Interdigital neuritis—also referred to as Morton neuroma, [6interdigital neuroma, Morton metatarsalgia, or interdigital nerve compression—results from entrapment of a plantar interdigital nerve as it passes under the transverse metatarsal ligament. [7It is defined as a perineural fibrosis of the involved interdigital nerves, and true neuromatous involvement is not seen.

Interdigital neuritis is most common in the second or third interspace, but occurrences in the first and fourth interspace have been reported; double neuromas occurring in the second and third interspace are not uncommon. This condition is more common in women than in men. Although it can occur in persons of all ages, it is most common in middle-aged individuals.

For patient education resources, see Knee PainBursitis, and Electromyography (EMG).


Iliohypogastric nerve

The iliohypogastric nerve arises primarily from the ventral primary rami of L1 and occasionally with a twig from T12. Its pathway resembles that of the intercostal nerves in the thoracic region.

The iliohypogastric nerve traverses the psoas major, piercing the lateral border of the muscle anterior to the quadratus lumborum and posterior to the kidney to traverse the lateral abdominal wall. It penetrates the transversus abdominis near the iliac crest, coming between it and the internal oblique muscle. The nerve supplies the lower fibers of the transversus abdominis and the internal oblique muscle and divides into lateral and anterior cutaneous branches.

The anterior cutaneous branch of the iliohypogastric nerve continues anteriorly between the internal oblique muscle and the transversus abdominis muscle, then pierces the internal oblique muscle and becomes cutaneous through an opening in the fascial aponeurosis of the external oblique muscle, approximately 2-3 cm cephalad to the superficial inguinal ring. The distribution of the cutaneous sensation is a small region just superior to the pubis.

Ilioinguinal nerve

The ilioinguinal nerve arises from the fusion of T12 and L1 nerve roots and emerges from the lateral border of the psoas muscle; it traverses the anterior abdominal wall to the iliac crest just inferior to the hypogastric nerve.

Adjacent to the anterior margin of the iliac crest, the ilioinguinal nerve pierces the transversus abdominis and the internal oblique muscle (providing neural branches to these) and sending neural branches to the iliohypogastric nerve. It then supplies sensory branches to supply the pubic symphysis, the superior and medial aspect of the femoral triangle, and either the root of the penis and anterior scrotum (in males) or the mons pubis and labia majora (in females).

Genitofemoral nerve

The genitofemoral nerve arises from the L1 and L2 ventral primary rami, which fuse in the psoas muscle. It pierces the anterior surface of the psoas major at the level of L3-4 and descends on the fascial surface of the psoas major past the ureter. The nerve then splits into genital and femoral branches near the inguinal ligament.

The genital branch of the genitofemoral nerve continues along the psoas major to the deep inguinal ring and enters the inguinal canal. In males, it supplies the cremaster muscle, spermatic cord, scrotum, and adjacent thigh. In females, it travels with the round ligament of the uterus and provides cutaneous sensation to the labia majora and adjacent thigh.

The femoral branch of the genitofemoral nerve lies lateral to the genital branch on the psoas major and travels lateral to the femoral artery and posterior to the inguinal ligament to enter the proximal thigh. There, it pierces the sartorius distal to the inguinal ligament and supplies the proximal portion of the thigh about the femoral triangle, just lateral to the skin that is innervated by the ilioinguinal nerve.

Femoral nerve

The femoral nerve arises from the posterior divisions of the ventral primary rami of L2, L3, and L4 within the psoas major. These nerves join to form the largest branch of the lumbar plexus. The femoral nerve emerges from the lateral border of the psoas major and courses inferiorly in the intermuscular groove between this muscle and the iliacus. It passes under the inguinal ligament lateral to the femoral artery and vein and then divides into multiple branches within the femoral triangle.

In the proximal thigh, the femoral nerve divides into sensory branches, which innervate the upper and anterior thigh, and muscular branches, which innervate the quadriceps. One of the major branches is the lateral femoral cutaneous nerve (see below). [8Probably the best-known cutaneous nerve arising from the femoral nerve is the saphenous nerve (see below).

Another important branch of the femoral nerve is the medial femoral cutaneous nerve, which originates just distal to the inguinal ligament, descends on the sartorius muscle, and penetrates the deep fascia about the distal third of the thigh, at which point it splits into two terminal nerve branches.

One branch of the medial femoral cutaneous nerve innervates the skin covering the medial aspect of the distal thigh and knee joint region. The second branch supplies the skin superior to the patella and shares several communicating branches with the saphenous nerve. The posterior branch of the medial cutaneous nerve travels along the medial border of the sartorius and pierces the deep fascia about the knee, also communicating with the saphenous nerve in providing cutaneous sensation to the patellar region.

Lateral femoral cutaneous nerve

The lateral femoral cutaneous nerve arises from the ventral primary rami of L2-4, where they divide into anterior and posterior branches. The dorsal portions fuse to form the lateral femoral cutaneous nerve in the midpelvic region of the psoas major. The nerve then courses over the iliacus toward the anterior superior iliac spine (ASIS). It travels posterior to the inguinal ligament and superior to the sartorius at the iliac crest region and divides into anterior and posterior branches.

The anterior branch of the lateral femoral cutaneous nerve comes off 10 cm distal to the inguinal ligament, in line with the ASIS, and supplies cutaneous sensation to the lateral thigh, including the area just proximal to the patella; it then communicates with cutaneous branches of the femoral nerve and the saphenous nerve to form the patellar plexus. The posterior branch of the nerve pierces the fascia lata posteriorly and laterally and divides into multiple small branches that supply the skin from the greater trochanter to the midthigh. [9]

Saphenous nerve

The saphenous nerve is the terminal branch (and the longest branch) of the femoral nerve. It is a pure sensory nerve that is made up of fibers from the L3 and L4 spinal segments. Because of its long course, it can become entrapped in multiple locations, from the thigh to the leg.

The saphenous nerve branches from the femoral nerve just distal to the inguinal ligament and courses with the superficial femoral artery to enter the adductor (Hunter’s) canal in the distal third of the thigh. This canal extends proximally from the apex of the femoral triangle to the inferomedial aspect of the thigh in the adductor magnus tendon, just proximal to the femoral condyle. The canal is somewhat triangular and lies between the vastus medialis laterally and the adductor magnus and adductor longus medially.

The roof of the adductor canal is a dense bridge of connective tissue extending between these muscle groups. The saphenous nerve exits the canal by piercing the roof and becomes subcutaneous about 10 cm proximal to the medial epicondyle of the femur. The nerve may also pierce the sartorius. Once it becomes subcutaneous, the nerve branches to form the infrapatellar plexus, while the main branch continues along the medial leg and foot.

Obturator nerve

The obturator nerve is formed by the fusion of anterior branches of the anterior primary rami of L2, L3, and L4. The largest contribution is from L3, and the smallest contribution typically is from L2. The rami fuse in the substance of the psoas and emerge from the medial border of the psoas beneath the common iliac vessels just lateral to the sacrum.

The obturator nerve then travels along the lateral wall of the lesser pelvis to enter the obturator foramen. Just anterior to the internal obturator muscle and before entering the thigh, the nerve divides into an anterior branch and a posterior branch. The anterior branch travels superficial to the internal obturator muscle but deep to the pectineus and the adductor longus, then travels superficial to the adductor brevis.

The obturator nerve terminates at the distal aspect of the adductor longus, forming a subsartorial plexus by communicating with the anterior cutaneous branches of the femoral and saphenous nerves. The nerve then gives off its motor branches to the muscles and extends its articular branches to the hip joint. The motor branches arise distal to the obturator foramen to supply the adductor brevis, adductor longus, and gracilis.

Rarely, a terminal cutaneous branch may emerge from the inferior aspect of the adductor longus and follow the medial border of the sartorius to the medial knee region, where it supplies the skin of the medial and distal thigh region.

Tibial nerve

The tibial nerve (L4-S3) is a branch of the sciatic nerve. After entering the lower leg between the two heads of the gastrocnemius, it runs deep to the soleus in the deep posterior compartment of the leg. In the upper leg, the nerve lies between the tibial muscle and the flexor digitorum longus; in the lower leg, it is between the flexor digitorum longus and the flexor hallucis longus.

The tibial nerve then travels behind the medial malleolus, through the proximal tarsal tunnel, where it divides into its terminal branches, the medial and lateral plantar nerves. Havel et al have shown that in 93% of cases, this bifurcation occurs within 2 cm of an imaginary line drawn between the middle of the medial malleolus and the mid calcaneus. [10Calcaneal branches, which have a highly variable anatomy, are present.

Most individuals (79%) have a single calcaneal nerve, usually arising from the tibial nerve but sometimes arising from the lateral plantar nerve. About 21% have multiple calcaneal branches originating from the tibial nerve, the lateral plantar nerve, the medial plantar nerve, or some combination of these. The calcaneal branches travel over the abductor hallucis and supply sensation to the medial heel pad. The medial calcaneal nerve or nerves penetrate the flexor retinaculum and innervate the skin over the medial and posterior heel.

The tarsal tunnel is formed by the medial surface of the talus, the inferomedial navicular, the sustentaculum tali, and the curved medial surface of the calcaneus. The fibrous portion of the canal is the flexor retinaculum, also called the laciniate ligament. The retinaculum is formed by the deep and superficial aponeurosis of the leg and is attached closely to the sheaths of the posterior tibial, flexor digitorum longus, and flexor hallucis tendons.

Typically, a fibrous septum courses between the calcaneus and the deep fascia of the abductor hallucis and separates the medial and lateral plantar nerves just beyond their division from the tibial nerve.

The first branch of the lateral plantar nerve travels between the deep fascia of the abductor hallucis and the medial fascia of the quadratus plantae, then continues deep to the flexor digitorum brevis. Although the anatomy is somewhat variable, this branch typically provides a sensory branch to the medial calcaneal tuberosity, motor branches to the flexor digitorum brevis, and sometimes a motor branch to the quadratus plantae. It then provides a sensory branch to the lateral heel and a motor branch to the abductor digiti quinti.

Various anomalies have been reported, including the direct origination of all branches of the medial and lateral plantar nerves from the tibial nerve.

The medial plantar nerve provides sensation to the medial half of the foot and the medial three and one half digits. The nerve provides motor branches to the abductor hallucis, the flexor digitorum brevis, and the flexor hallucis brevis, as well as to the first lumbrical.

Common peroneal nerve

The common peroneal nerve arises from the sciatic nerve at approximately the middle to distal third of the thigh region. At this point, it descends to the popliteal fossa, innervating the short head of the biceps femoris. [11It travels along the lateral aspect of the distal thigh beneath the cover of the long and short heads of the biceps femoris to the region of the fibular head.

Proximal to the fibular head, the common peroneal nerve gives off two branches: the sural communicating branch, which assists in the formation of the sural nerve with a branch provided by the tibial nerve, and the lateral cutaneous nerve of the calf, which provides cutaneous sensation to the proximal and lateral aspect of the leg. It also supplies the knee joint via its articular branches.

The common peroneal nerve then courses around the fibular neck and passes through the fibro-osseous opening in the superficial head of the peroneus longus. This opening can be quite tough and can cause the nerve to pass through it at an acute angle. Also, significant fibrous connective tissue secures the nerve to this proximal portion of the fibula, potentially compromising the nerve. Distal to this fibular tunnel, the common peroneal nerve divides into the superficial and deep peroneal nerves (see below).

Superficial peroneal nerve

The superficial peroneal nerve, one of the branches of the common peroneal nerve, travels in the lateral compartment and supplies the peroneus longus and peroneus brevis. In most individuals, it pierces the deep fascia and emerges into the subcutaneous fat at approximately the level of the middle and lower third of the leg and at an average of about 10-15 cm above the tip of the lateral malleolus. [12]

At an average of 4-6 cm proximal to the ankle joint, the superficial peroneal nerve divides into a large (2.9 mm) medial dorsal cutaneous nerve and a smaller (2 mm), more laterally located intermediate dorsal cutaneous nerve.

In 28% of patients, the superficial peroneal nerve branches more proximally. In these cases, the medial dorsal cutaneous branch usually follows the more common track of the superficial peroneal nerve and emerges into the subcutaneous tissues in the distal lateral leg. The intermediate dorsal cutaneous nerve penetrates the crural fascia more distally, either anterior or posterior to the fibula and at an average of 4-6 cm proximal to the ankle joint.

At the level of the malleoli, in most patients, the medial dorsal cutaneous nerve is located at approximately half of the distance from the lateral malleolus to the medial malleolus, and the intermediate dorsal cutaneous nerve is located at approximately one third of this distance.

The medial dorsal cutaneous nerve supplies the skin of the dorsomedial aspect of the ankle, the medial aspect of the hallux, and the second and third digits (except for the first webspace). The intermediate dorsal cutaneous nerve supplies the skin on the dorsolateral part of the ankle and gives off dorsal digital nerves for the third, fourth, and fifth toes.

Accessory branches of the superficial peroneal nerve have been reported to cross over the lateral malleolus, where they have been entrapped by fascial bands. An accessory motor branch of the superficial peroneal nerve has also been found to innervate the extensor digitorum brevis in some patients. [13]

Deep peroneal nerve

The deep peroneal nerve, the other branch of the common peroneal nerve, originates just distal to the fibular head, [14entering the anterior compartment in front of the interosseous membrane. It courses lateral to the anterior tibial muscle, traveling along with the anterior tibial artery and vein. In the proximal third of the leg, the nerve courses between the anterior tibial muscle and the extensor digitorum longus; in the middle third, it runs between the anterior tibial muscle and the extensor hallucis longus anterior to the anterior tibial vessels.

At approximately 3-5 cm proximal to the ankle mortise, the extensor hallucis longus crosses over the deep peroneal nerve, and the nerve is then seen between the extensor hallucis longus and the extensor digitorum longus in the distal part of the leg, at an average of 1.25 cm above the ankle joint. Occasionally, the nerve does not enter this interval until just distal to the mortise. At this level, it is about 3 mm in size and may be under the extensor retinaculum, because the inferior extensor retinaculum can be at, above, or below the ankle mortise level.

At approximately 1 cm distal to the ankle mortise, the nerve divides into lateral and medial branches. The terminal lateral branch curves laterally and supplies the extensor digitorum brevis, the extensor hallucis brevis, the adjacent tarsal and tarsometatarsal joints (including two to four branches innervating the anterolateral part of the subtalar joint), and, occasionally, the second and third dorsal interosseous muscles.

The terminal medial branch is just medial to the dorsalis pedis artery and just lateral to the first tarsometatarsal joint. It travels between extensor hallucis longus tendon and extensor hallucis brevis muscle on the dorsum of the foot. At approximately the metatarsophalangeal (MTP) joint level, the extensor hallucis brevis crosses over the nerve, and the nerve is then between the extensor hallucis brevis and the extensor digitorum longus to the second toe.

This nerve then divides into the dorsolateral cutaneous nerve of the great toe and the dorsomedial cutaneous nerve of the second toe. It supplies sensation to the web between the first and second toes, the dorsalis pedis artery, and the adjacent MTP and interphalangeal (IP) joints. Usually, it supplies the first dorsal interosseous muscle; occasionally, it supplies the second and third interosseous muscles.

Plantar and digital nerves

The common digital nerves originate from the medial and lateral plantar nerves. The medial plantar nerve divides into three common digital nerves, which in turn bifurcate, supplying cutaneous branches to the medial three and one half digits. The lateral plantar nerve gives rise to two common digital nerves, which supply cutaneous branches to the lateral one and one half digits. As the common digital nerves travel distally, they pass plantar to the transverse intermetatarsal ligament.

Substantial variability has been noted in the cutaneous innervation of the webspace and of the plantar aspect of the foot adjacent to the webspace.

Pathophysiology and Etiology

Iliohypogastric nerve entrapment

The iliohypogastric nerve is rarely injured in isolation. The most common causes of injury are surgical procedures, [15including transverse lower abdominal incisions, as in hysterectomies, and injuries from procedures such as inguinal herniorrhaphy and appendectomy.

Such injuries are most likely to occur if the incision extends beyond the lateral margin of the inferior rectus abdominis fibers. The damage can result from direct surgical trauma, such as occurs when the surgeon passes a suture around the nerve and incorporates it into the fascial repair, or from postoperative entrapment in scar tissue or neuroma formation.

Sports injuries, such as trauma or muscle tears of the lower abdominal muscles, may also result in injury to the nerve. Injury may also occur during pregnancy, owing to the rapidly expanding abdomen in the third trimester. This is called the idiopathic iliohypogastric syndrome and is rare.

Ilioinguinal nerve entrapment

Causes of injury to the ilioinguinal nerve include lower abdominal incisions (Pfannenstiel), pregnancy, iliac bone harvesting, appendectomy, inguinal herniorrhaphy, inguinal lymph node dissection, femoral catheter placement, orchiectomy, total abdominal hysterectomy, and abdominoplasty.

Ilioinguinal nerve injury can also occur idiopathically. The prevalence of such injury with surgery has declined, owing to the use of laparoscopic procedures. Tearing of the lower external oblique aponeurosis may also cause injury to this nerve. This injury has been reported in hockey players.

Genitofemoral nerve entrapment

Injury to the genitofemoral nerve may result from hernia repair, appendectomy, biopsies, and cesarean delivery. It may also result from intrapelvic trauma to the posterior abdominal wall, retroperitoneal hematoma, pregnancy, or trauma to the inguinal ligament. Fortunately, injury to this nerve is rare, even with open herniorrhaphy.

A prospective study was performed to evaluate the genitofemoral nerve electrophysiologically in children with inguinal hernia repair. [16Latency of the genitofemoral nerve was found to be prolonged after inguinal hernia repair, possibly because of surgery-related injury.

Femoral nerve entrapment

The femoral nerve can have several entrapment locations or causes of injury, including intrapelvic injury and injury in the inguinal region. Diabetic amyotrophy is the most common cause of femoral nerve neuropathy. Open injuries can occur from gunshots, knife wounds, glass shards, or needle puncture in some medical procedures.

The most worrisome complication of major trauma to the femoral triangle region is an associated femoral artery injury. The nerve can be injured at the time of the trauma or inadvertently sutured during repair of this injury. Large-blade self-retaining retractors used during pelvic operations can cause injury to the nerve as a consequence of compression. [17]

In a study that measured conduction of the femoral nerve in diabetic patients without clinical signs of femoral nerve involvement, a statistically significant difference was observed between diabetics and healthy individuals in terms of both femoral nerve motor latency and amplitude. [18The authors observed that these abnormalities became more evident as the polyneuropathy of the patients became more serious.

Most entrapment neuropathies occur below the inguinal ligament. After passing beneath the inguinal ligament, the femoral nerve is in close proximity to the femoral head, the tendon insertion of the vastus intermedius, the psoas tendon, the hip, and the joint capsule. The nerve does not have significant protection in this area.

Heat developed by methylmethacrylate during a total hip arthroplasty can injure the femoral nerve. Pelvic procedures that require the lower extremity to be positioned in an acutely flexed, abducted, and externally rotated position for long periods can cause compression by angling the femoral nerve beneath the inguinal ligament. The nerve may be compromised by pressure from a fetus in a difficult birth. Pelvic fractures and acute hyperextension of the thigh may also cause an isolated femoral nerve injury.

Pelvic radiation, appendiceal or renal abscesses, and tumors can cause femoral nerve injuries as well. The nerve can also be injured by a compartmentlike compression from a hemorrhage (caused by a hemorrhagic disorder or by anticoagulant use).

Lateral femoral cutaneous nerve entrapment

Entrapment of the lateral femoral cutaneous nerve usually occurs at the inguinal ligament. The peak incidence for this condition is in middle age. Differential diagnoses include lumbar radiculopathies and discogenic or nerve root problems at L2 and L3. The entrapment may be from intrapelvic causes, extrapelvic causes, or mechanical causes.

Intrapelvic causes include pregnancy, abdominal tumors, uterine fibroids, diverticulitis, or appendicitis. Injury has been described in cases of abdominal aortic aneurysm. Extrapelvic causes include trauma to the region of the ASIS (eg, from a seatbelt in a motor vehicle accident), tight garments, belts, girdles, or stretching from obesity and ascites. Mechanical factors include prolonged sitting or standing and pelvic tilt from leg-length discrepancy. Diabetes can also cause this neuropathy in isolation or in the setting of a polyneuropathy.

Saphenous nerve entrapment

The saphenous nerve can become entrapped where it pierces the roof of the adductor canal. Inflammation results from a sharp angulation of the nerve at its exit and from the dynamic forces of the muscles in this region, which cause contraction and relaxation of the fibrous tissue that impinges on the nerve.

The nerve can also be injured as a result of an improperly protected knee or leg support during surgery. It may be injured by a neurilemoma, entrapment by femoral vessels, direct trauma, pes anserine bursitis, varicose vein operations, and medial knee arthrotomies and meniscus repairs. [19]

Obturator nerve entrapment

The obturator nerve is rarely injured in isolation. However, injury can occur with pelvic trauma and associated fractures, during delivery as a result of compression of the nerve between the head of the fetus and the bony structures of the pelvis, or as a consequence of compression of the nerve between a tumor and the bony pelvis. Entrapment may also occur in the obturator canal during surgery or in conjunction with a total hip arthroplasty.

Other potential causes include malposition of the lower limb for prolonged periods, entrapment in the adductor magnus in athletes, and abnormal positioning of the lower limb of a newborn during a difficult delivery. Some physicians believe that the anterior branch may be entrapped in the fascia as it passes over the adductor brevis, owing to an inflammatory process. [20]

Tibial nerve entrapment

Although tibial nerve entrapment (tarsal tunnel syndrome) can be seen anywhere along the course of the nerve, the most common location is distal to the ankle. Entrapment above the ankle has been reported in the popliteal fossa, where the nerve can be compressed by the tendinous arch of the origin of the soleus, a Baker cyst, or other masses that may occur in this region.

Compression of the tibial nerve or one of its branches can occur as a result either of intrinsic neural abnormalities or of external compression. External-compression etiologies reported in the literature include fibrosis, neurilemomas, ganglion cysts, lipomas, osteochondromas, varicosities, other benign and malignant tumors, a tight tarsal canal, a hypertrophic abductor hallucis, an anomalous artery, and anomalous extra muscles (eg, the flexor digitorum accessorius longus).

Other conditions that have been reported to contribute to the development of tarsal tunnel syndrome include tenosynovitis of the adjacent tendons, partial or complete rupture of the medial tendons, obesity, ankylosing spondylitis, acromegaly, and talocalcaneal coalition.

Several studies have suggested that compression of the tibial nerve plays a role in the neurologic deterioration and loss of sensory and motor function observed in patients with long-standing diabetes mellitus. Wieman and Patel reported on 26 patients with painful diabetic neuropathy who underwent tarsal tunnel decompression; pain improvement or relief was noted in 24 (92%) of these patients within 1 month after surgery. [21]

Proliferative synovitis in conditions such as rheumatoid arthritis, which causes edema and compression of the tibial nerve in the tarsal tunnel, has also been reported. Direct blunt trauma to the nerve and traction injury to the nerve as a result of trauma or heel varus or valgus have been reported as well.

In the original case report and description of tarsal tunnel syndrome in a patient with bilateral symptoms, Keck found tortuous posterior tibial veins surrounding the nerve, which he described as resembling a varicocele. [2Since this initial report, one of the most commonly encountered and reported causes of tarsal tunnel syndrome has been varicose veins.

Sammarco and Chang determined that the most common surgical findings in 62 tarsal tunnel releases included arterial vascular leashes and varicosities, which caused indentation and scarring about the nerve. [22Cimino found that varicosities were the third most common cause of tarsal tunnel syndrome, as reported in the literature, and that idiopathic and traumatic causes were the most common and second most common causes, respectively. [23]

Gould and Alvarez reported a case in which surgery revealed varicosities overlying the medial and lateral plantar nerves at their origin. [24Turan et al also found varicose veins to occur more commonly than other compressive etiologies did. [25The enlarged vessels crossing the nerve are theorized to cause direct compression of the tibial nerve and its branches, particularly when the leg is in a dependent position.

Baxter and Thigpen described a biomechanical basis for entrapment of the first branch of the lateral plantar nerve in athletes. [5They proposed that entrapment results from stretching and tethering of the plantar nerves, which are encased in the abductor hallucis deep fascial leashes, and from hypertrophy of the small foot muscles, as well as from the increased forces in the hindfoot of runners that create additional microtrauma to medial heel structures. Most of their patients with sports-related injuries had a normally arched or cavus-type foot.

Several authors have also found increased valgus deformity of the foot to be a predisposing factor in chronic stretch injury to the tibial nerve. Budak et al noted prolonged distal latency of the medial and lateral plantar sensory nerves and delayed sensory conduction velocity of the medial plantar sensory nerve in patients with pes planus. [26]

Labib et al, reporting on 14 patients who underwent surgical treatment for what they termed the heel pain triad (ie, plantar fasciitis, posterior tibial tendon dysfunction, and tarsal tunnel syndrome), postulated that failure of the static (plantar fascia) and dynamic (posterior tibial tendon) support of the longitudinal arch of the foot results in traction injury to the tibial nerve. [27Trepman et al reported increased pressure in the tarsal tunnel with the foot and ankle in full eversion or full inversion. [28]

Entrapment of the first branch of the lateral plantar nerve beneath the deep fascia of the abductor hallucis muscle or beneath the medial edge of the quadratus plantae fascia is among the most commonly seen causes of tarsal tunnel syndrome.

Entrapment of the medial plantar nerve typically occurs in the areas of the master knot of Henry. It is most frequently observed in athletes; in 1978, Rask called it jogger’s foot. The theory is that excessive valgus or external rotation of the foot during running puts excessive stretch on the medial plantar nerve, resulting in tarsal tunnel syndrome. This condition has been seen in runners with flat feet who use corrective orthotics that can compress the nerve in the medial arch.

Common peroneal nerve entrapment

Peroneal nerve injuries are the most common peripheral nerve injuries of the lower limb to result from multiple traumatic injuries, such as those suffered in motor vehicle accidents. The common peroneal nerve can be injured at any location along the thigh down to the fibular head region in various forms of trauma, such as lacerations, femoral fractures, bullet wounds, and direct injury. However, most peroneal nerve injuries occur at the region of the fibular head.

As Kaminsky reported, the most common form of neural compromise in the region of the fibular head is due to compression from habitual leg crossing, compression of the nerve against a bed railing or hard mattress in debilitated patients, or prolonged immobility, such as that observed in patients under anesthesia. [29]

However, in a study of 146 cases, Piton et al noted 55 cases due to idiopathic causes, 16 due to external compression, 59 due to various traumatic causes, and nine due to intraneural and extraneural tumors. [30Traumatic causes can include wounds and contusions, direct fractures involving the lateral knee, and direct lacerations or postoperative entrapment in suture hardware.

Common peroneal nerve injuries at the region of the fibular head include ankle sprains with associated proximal fibular fractures, knee dislocations, tibial osteotomies, total knee and hip arthroplasties, and arthroscopies. Compression from intraneural or extraneural tumors has been seen, including compression from neurilemomas, intraneural or extraneural ganglia, schwannomas, desmoid tumors, angiomas, neuromas, fibrolipomatosis hamartomas, exostosis, chondromatosis, Baker cysts, and vascular abnormalities. [31]

A number of other etiologic factors have been reported in the literature. Compression of the nerve against the fibrous or fascial layers of well-developed leg muscles in athletes has also been seen. Patients typically present with exercise-related leg pain with or without associated dermatomal numbness. Coexisting pathologies, such as those in exercise-related compartment syndromes, add to the complexity of this diagnosis.

Excessive weight loss can also be a contributing factor in patients (slimmer’s paralysis), in that rapid weight loss and anorexia can result in loss of the fat pad over the fibular head, predisposing the nerve to external compression at this site. Short casts or braces can result in external compression on the fibular neck region.

Individuals who spend long hours in a squatting position can also present with clinical evidence of peroneal nerve compression (strawberry picker’s palsy). This is likely the result of compression of the common peroneal nerve as it penetrates the fibro-osseous opening in the peroneus longus in persons with a fibrous or tight peroneal tunnel.

A rare form of common peroneal nerve injury is that associated with natural childbirth, in which the woman compresses both peroneal nerves at the fibular head by pulling back on her knees with her wrists resting on the fibular head during birthing. The nerve may also be injured during childbirth in the squatting position.

Other less common causes of common peroneal nerve entrapment include lower-limb lengthening procedures, anorexia nervosa, and paraneoplastic syndromes. Also, peroneal nerve mononeuropathies can occur in hyperthyroidism, diabetes mellitus, vasculitic disorders, and leprosy. Often, no underlying etiology can be definitively identified, and the condition is termed idiopathic.

Superficial peroneal nerve entrapment

Local trauma or compression is the most common underlying cause of entrapment of the superficial peroneal nerve. Repeated ankle sprains or long-term use of certain positions (eg, prolonged kneeling or squatting) can make certain individuals more prone to the development of symptoms. This tendency is thought to be due to recurrent stretch injury to the nerve. Perineural fibrosis of the superficial peroneal nerve at the level of the ankle after an inversion ankle sprain has been reported. [32]

The superficial peroneal nerve is also at risk for direct injury from any procedure about the anterior ankle, including use of the anterolateral ankle arthroscopy portal. Chronic or exertional lateral compartment syndrome can also cause compression of the superficial peroneal nerve, particularly in athletes.

Nontraumatic causes of superficial peroneal nerve entrapment are commonly due to anatomic variations, such as fascial defects with or without muscle herniation about the lateral lower leg (where the nerve is entrapped as it emerges into the subcutaneous tissue) or a short peroneal tunnel proximally.

Deep peroneal nerve entrapment

Deep peroneal nerve entrapment is most commonly due to compression and repetitive mechanical irritation of the nerve at the ankle beneath the extensor retinaculum. Entrapment of the deep peroneal nerve in this location has also been called the anterior tarsal tunnel syndrome.

The anterior tarsal tunnel contains four tendons, one artery, one vein, and the deep peroneal nerve. Typically, the nerve is trapped beneath the superior edge of the retinaculum. Here, it is compressed by the crossing extensor hallucis longus tendon and under the extensor hallucis brevis, as well as directly over osteophytes, exostosis, or bony prominences of the talotibial, talonavicular, naviculocuneiform, or cuneiform metatarsal joints. An os intermetatarseum between the first and second metatarsal bases has also been associated with symptoms.

Space-occupying lesions (eg, ganglia) also contribute to symptoms in this tight canal. Repeated dorsiflexion and plantarflexion of the ankle contributes to this mechanical condition by pinching the nerve in this tight space, and inversion trauma has been shown to lower the motor conduction velocity of the deep peroneal nerve.

Postural causes, such as wearing high-heeled shoes (in which the nerve is stretched over the midfoot joint) and sitting repeatedly or for prolonged periods on the plantarflexed feet (as is done by Muslims performing salat, or namaz) are other commonly seen etiologies. Other etiologies include anomalies of the extensor hallucis brevis distal to the retinaculum.

Deep peroneal nerve entrapment, however, can occur anywhere along the nerve’s course (eg, just distal to the neck of the fibula, anterior to the ankle joint, or distal to the inferior extensor retinaculum), though such entrapment is not considered anterior tarsal tunnel syndrome. Common causes of proximal entrapment of the deep peroneal nerve include space-occupying lesions about the proximal fibula, surgical procedures about the lateral knee (eg, proximal tibial osteotomy), and chronic anterior exertional compartment syndrome seen in athletes.

Interdigital neuritis

The most direct cause of interdigital nerve entrapment is compression of the nerve as it passes under the transverse intermetatarsal ligament. As weight is transferred to the ball of the foot when the toes are dorsiflexed during the last phase of stance, the interdigital nerve is compressed between the plantar foot and the distal edge of the intermetatarsal ligament. Many theories exist about the pathophysiology of this compression, including ischemia, inflammation, soft-tissue trauma, tumor, muscle imbalance, and fibrous ingrowth.

Edema of the endoneurium, fibrosis beneath the perineurium, axonal degeneration, and necrosis are often seen; their presence suggests that nerve damage occurs secondary to mechanical impingement. Using electron microscopy, Ha’Eri et al saw lesions consisting of a progressive fibrosis that enveloped and disrupted nerves and arteries; they did not see nerve-tissue proliferation or inflammation. [33The authors concluded that repeated trauma leads to reactive overgrowth and scarring that disrupts the nerves and the arteries.

Typically, these changes are evident proximal to the bifurcation of the common digital nerve, immediately distal to the transverse intermetatarsal ligament. In more chronic cases, degeneration of the axons and proliferation of blood vessels may occur about the site of an enlarged nerve. Shereff and Grande described the presence of Renaut bodies, which are densely packed whorls of collagen, in the supraneural space. [34These bodies are characteristically present only in peripheral neural entrapment.

However, Morscher et al, in a histomorphologic study, found only a diameter difference between biopsy results from patients with typical symptoms of interdigital neuritis and nerves examined from autopsies of persons without forefoot problems. [35In addition, some have implicated the inter-MTP bursa as the main cause of interdigital neuritis.

Forefoot deformities (eg, hammertoe) can further aggravate the interdigital nerve because of dorsal subluxation of the proximal phalanx, which stretches the nerve over the intermetatarsal ligament. In addition, several external conditions are known to contribute to the development and aggravation of this compression. High-heeled shoes put the feet in chronic dorsiflexion, forcing one’s weight onto the forefoot; and tight shoes, which compress the foot further, limit the intermetatarsal space.

Multiple investigations have looked into the underlying reason for the common locations in the second and third webspace. Levitsky et al demonstrated that the relative space in the metatarsal head/transverse metatarsal ligament is smaller in the second and third webspaces, where interdigital neuritis is more common, than it is in the other webspaces, a finding that supports mechanical factors as the underlying pathophysiology. [36]

Levitsky et al also dismissed the common theory that the cause of interdigital neuritis is related to the occurrence of a lateral-medial plantar nerve combination and to the anatomic thickness of the nerve. [36They reported third-webspace neuromas in which the plantar nerve did not arise from a combination of medial and lateral plantar nerves. The intermetatarsal head distances in the second and third interspace have been noted to be significantly smaller than those in the first and fourth intermetatarsal spaces.


Iliohypogastric nerve entrapment

Symptoms of iliohypogastric nerve entrapment include burning or lancinating pain immediately following an abdominal operation. The pain extends from the surgical incision laterally into the inguinal and suprapubic regions. Discomfort may occur immediately or as long as several years after the procedure and may last for months to years. This discomfort may derive from the formation of scar tissue in the region. Occasionally, the pain may extend into the genitalia because of significant overlap with other cutaneous nerves.

Loss of sensation is usually minimal and not problematic. Iliohypogastric nerve entrapment causing symptoms similar to trochanteric bursitis refractory to conventional therapy has been reported.

Ilioinguinal nerve entrapment

Symptoms of ilioinguinal nerve entrapment may include hyperesthesia or hypoesthesia of the skin along the inguinal ligament. The sensation may radiate to the lower abdomen. Pain may be localized to the medial groin, the labia majora or scrotum, and the inner thigh. The characteristics of the pain may vary considerably. Patients may be able to associate their pain clearly with a traumatic event or a surgical procedure.

In as many as 75% of patients, pain and tenderness may be present when pressure is applied where the nerve exits the inguinal canal. Sensory impairment is common in the distribution of the nerve supply. Symptoms usually increase with hip extension (patients walk with the trunk in a forward-flexed posture). Pain may also be reproduced with palpation medial to the anterior superior iliac spine (ASIS).

Genitofemoral nerve entrapment

Injury to the femoral branch of the genitofemoral nerve causes hypoesthesia over the anterior thigh below the inguinal ligament; this finding distinguishes entrapment of this nerve from entrapment of the iliohypogastric or ilioinguinal nerve. Groin pain is a common presentation of neuralgia from nerve injury or entrapment. The pain may be worse with internal or external rotation of the hip, with prolonged walking, or even with light touch.

Femoral nerve entrapment

Symptoms of a femoral neuropathy may include pain in the inguinal region that is partially relieved by flexion and external rotation of the hip, as well as dysesthesia over the anterior thigh and anteromedial leg. Patients complain of difficulty in walking and of knee buckling, depending on the severity of the injury. The femoral nerve gives rise to the saphenous nerve in the thigh; therefore, numbness in this distribution can be present. Anterior knee pain may also be present because the saphenous nerve supplies the patella.

Lateral femoral cutaneous nerve entrapment

Symptoms of lateral femoral cutaneous nerve entrapment may include anterior and lateral thigh burning, tingling, and numbness, which increase with standing, walking, or hip extension (and sometimes also with lying prone). Symptoms usually are unilateral but may be bilateral in rare cases. Sitting usually yields improvement, unless compressive forces, such as tight belts or garments, remain.

Saphenous nerve entrapment

Symptoms of saphenous nerve entrapment may include a deep thigh ache, knee pain, and paresthesias in the nerve’s cutaneous distribution in the leg and foot. The infrapatellar branch may become entrapped on its own because it passes through a separate foramen in the sartorius tendon. It may also be exposed to trauma where it runs horizontally across the prominence of the medial femoral epicondyle. Patients report paresthesias and numbness in the infrapatellar region that worsen with knee flexion or compression by garments or braces.

Saphenous nerve entrapment is a frequently overlooked cause of persistent medial knee pain in patients who experience trauma or direct blows to the medial aspect of the knee. Because the saphenous nerve is purely sensory, an isolated injury to this nerve should not result in weakness. If weakness is present, the examiner should look for an injury to the femoral nerve or, possibly, an upper lumbar radiculopathy, particularly if thigh adduction is present (obturator nerve).

Obturator nerve entrapment

The main complaints in obturator nerve entrapment include difficulty with ambulation and the development of an unstable leg. In an anterior branch entrapment, symptoms can consist of exercise-related pain or groin pain. The patient may describe a deep ache in the region of the adductor origin at the pubic bone that increases with exercise; the pain may radiate down the medial aspect of the thigh toward the knee. An athlete’s ability to jump may be reduced. The weakness in these patients usually worsens with exercise.

Tibial nerve entrapment

Patients with proximal tarsal tunnel syndrome usually present with diffuse, vague discomfort or pain. They may have burning, tingling, or frank numbness in the plantar foot. Although occasionally a history of trauma is reported, most patients report an insidious onset of symptoms.

In most instances, symptoms are unilateral. Occasionally, patients may report proximal radiation of pain to the medial leg. Prolonged standing and walking usually exacerbate the symptoms, and rest alleviates them. Many patients also present with night pain that is improved with massage or walking. Patients may note pain secondary to nerve tension when the ankle is placed in extreme dorsiflexion.

Patients with distal entrapment of the lateral plantar nerve or its branches usually present with chronic heel pain that has been present for 9-12 months. Many of their symptoms are similar to plantar fasciitis, especially the location of their pain and their startup pain. In addition to the mechanical symptoms of plantar fasciitis, they present with neuritic pain that is unrelated to weight bearing or loading of the foot.

Most patients report that at first, their symptoms occurred only when they were bearing weight. Over time, the symptoms tended to increase, eventually occurring when the patient was seated and occasionally occurring at night.

Patients are usually asymptomatic in the mornings before taking their first step. Symptoms usually worsen with increased activity, as well as toward the end of the day and after long periods of standing, walking, or running. Prolonged standing in one place may be an aggravating factor. Most patients continue to have pain or burning (“afterpain” or “afterburn”) for 30 minutes to several hours after they are off their feet.

Tarsal tunnel syndrome is seen commonly in individuals who are in their fifth and sixth decades of life, and it is more common in women than in men. No consistent correlation with patient body weight has been identified. Most investigators have not been able to identify a significant common factor regarding occupation or underlying foot structure.

Some patients with tarsal tunnel syndrome have concomitant peripheral neuropathy or radiculopathy. Patients with peripheral neuropathy or radiculopathy may have symptoms that mimic tarsal tunnel syndrome.

Patients with certain systemic diseases, such as diabetes mellitus, alcoholism, thyroid disease, and vitamin deficiencies, are at increased risk for entrapment neuropathy.

Common peroneal nerve entrapment

Peroneal nerve lesions at the region of the knee or distal thigh usually result in patient reports of altered ambulation secondary to paretic or paralyzed ankle dorsiflexors. Loss of sensation in the cutaneous distribution of the superficial and deep peroneal nerves may be noted, but ankle dorsiflexion weakness is often of most concern to the patient. [37]

Pain is not universal with common peroneal nerve injuries; if present, it is often related to the specific cause of the nerve compromise. For example, nerve compromise secondary to traumatic injury from blunt trauma will likely be accompanied by pain secondary to soft-tissue swelling and inflammation, whereas chronic compression secondary to habitual leg-crossing is often nonpainful. Tapping of the nerve at the fibular head may produce pain and tingling (Tinel sign) in the sensory distribution of the peroneal nerve.

Superficial peroneal nerve entrapment

With superficial peroneal nerve entrapment, though patients may present with numbness or paresthesia in the distribution of the nerve and occasionally have pain about the lateral leg, the most typical presentation is vague pain over the dorsum of the foot. This pain may be chronic, remaining present for several years, and may be associated with other foot and ankle symptoms; on the other hand, it may be acute and associated with recent trauma or surgery about the ankle.

Specific measure that put the superficial peroneal nerve at risk for direct or stretch injury include the use of the anterolateral arthroscopy portal and the use of noninvasive traction methods with straps over the dorsum of the foot. About one quarter of patients have a history of previous or recurrent ankle sprains or trauma.

Typically, symptoms increase with activity (eg, running, walking, or squatting); they are often relieved by rest or the avoidance of a specific activity. This tendency is particularly pronounced in athletes whose symptoms are suggestive of exertional or chronic anterolateral compartment syndrome.

Bony entrapment of the superficial peroneal nerve in the fracture callus has also been reported when fractures of the fibula heal with abundant callus.

Certain positions (eg, crossing the leg over the opposite thigh) can induce symptoms, as can tight clothing (eg, sock elastic over the lateral leg). Pain may occasionally occur at night. Occasionally, patients report a bulging mass in the leg.

Deep peroneal nerve entrapment

Patients with deep peroneal nerve entrapment commonly complain of vague pain, a burning sensation, or a cramp over the dorsum of the foot, which may or may not involve the first webspace. Associated sensory changes may be noted in the first dorsal webspace. Some patients may present with neuritic symptoms (eg, unrelenting pain at rest and during sleep) along the course of the nerve. There may be pain in the ankle region even if only the motor nerve is involved.

Symptoms may appear or worsen only with a certain shoe or boot or with certain activities. Patients with more proximal entrapment may present with frequent tripping due to foot drop or weakness of the extensor halluces longus, though such a presentation is less common.

Interdigital neuritis

Many patients with interdigital neuritis (also known as Morton neuroma, Morton metatarsalgia, interdigital neuroma, or interdigital nerve compression) present with an intermittent dull ache or cramping sensation on the plantar aspect of either the second or the third interspace. Many patients present with a vague discomfort in the involved toes, and some may feel numbness or burning, with occasional shooting pain. Some patients notice spreading of the involved toes, and others may notice symptoms only with certain shoes.

Symptoms are usually exacerbated by walking, particularly with bare feet on hard surfaces, and sudden sharp pain may result from various activities (eg, sprinting, jumping, squatting, or repeated hopping) or from the wearing of high-heeled or tight shoes. Symptoms improve with rest, and night pain is rare. With progression of the condition, pain may radiate proximally. In chronic cases, patients may sense a mass or a stone bruise in the ball of the foot.

Nearly equal involvement of the second and third interspaces has been reported in the literature; involvement of the first and fourth spaces also has been reported, albeit rarely. Simultaneous tenderness in the second and third interspaces is not rare. Bilateral cases have been reported but are uncommon. Other pathologies of the forefoot (eg, instability of the second metatarsophalangeal [MTP] joint) are frequently present. Coughlin et al reported that 20% of their patients originally had concomitant instability of an adjacent MTP joint.

Clinically, dorsoplantar compression of the second or third intermetatarsal space reproduces pain that may radiate to the toes or proximally along the course of the affected nerve. The patient may display relative paresthesia of the webspace supplied by the injured nerve, though this relative paresthesia is often difficult to ascertain.

Physical Examination

Iliohypogastric nerve entrapment

On examination, pain and tenderness are usually present in the area of scarring or entrapment of the iliohypogastric nerve. Hyperesthesia or hypoesthesia may occur in the area supplied by this nerve. Diagnosis is difficult, owing to the small area of cutaneous supply that this nerve provides. There may be overlap in sensory supply with the genitofemoral and ilioinguinal nerves.

The following three major criteria are used to diagnose iliohypogastric nerve entrapment:

  • History of a surgical procedure in the lower abdominal area (though spontaneous entrapment can occur) - Pain can usually be elicited by palpating laterally about the scar margin, and the pain usually radiates inferomedially toward the inguinal region and into the suprapubic and proximal genital area
  • A definite area of hypoesthesia or hyperesthesia identified in the region of supply of the iliohypogastric nerve
  • Symptoms relieved by local anesthesia - Infiltration of a local anesthetic into the region where the iliohypogastric and ilioinguinal nerves depart the internal oblique muscle and where symptoms can be reproduced on physical examination by palpation should provide symptomatic relief

If no relief is obtained with injection, a different cause of the discomfort should be sought. Alternate diagnoses include upper lumbar or lower thoracic nerve root pathology and pain of discogenic origin. If the iliohypogastric nerve is clearly identified as the source of pain and a favorable response is not obtained with local anesthetic injection, then surgical exploration and resection of the nerve should be considered.

Ilioinguinal nerve entrapment

The diagnosis of ilioinguinal nerve entrapment can be made on the basis of local infiltration of anesthetic with or without steroid, which should result in relief within 10 minutes.

Genitofemoral nerve entrapment

The diagnosis of genitofemoral nerve entrapment is typically made by using anesthetic nerve blocks. Injection of the ilioinguinal and iliohypogastric nerves anteriorly should leave the pain or abnormal sensation unchanged; a block of the L1 and L2 roots should then result in relief. This procedure should help determine the diagnosis and prevent unnecessary surgical exploration of an uninjured nerve.

Femoral nerve entrapment

On examination, patients with femoral nerve entrapment may present with weak hip flexion, weak knee extension, and impaired quadriceps tendon reflex, as well as sensory deficit in the anteromedial aspect of the thigh. Pain may be increased with hip extension and relieved with external rotation of the hip. If compression occurs at the inguinal region, no hip flexion weakness is present. Sensory loss may occur along the medial aspect of the leg below the knee (saphenous distribution).

Lateral femoral cutaneous nerve entrapment

In some cases of lateral femoral cutaneous nerve entrapment, physical examination findings may be completely normal. Hyperesthesia over the lateral thigh (usually in a smaller area than the symptoms) may be noted. Pain can be produced by pressure medial to the ASIS. A positive Tinel sign may be present over the ASIS or the inguinal ligament.

Diagnosis of this entrapment, like that of other lower-extremity nerve entrapments, may be based on an injection of local anesthetic near the inguinal ligament or the ASIS. Spontaneous recovery usually is expected.

Saphenous nerve entrapment

In cases of saphenous nerve entrapment, deep palpation proximal to the medial epicondyle of the femur may reproduce the pain and complaints. Some weakness may be present because of guarding or disuse atrophy from pain, but no direct weakness will result from the nerve impingement. Sensory loss in the saphenous distribution may be present on examination. No weakness should be present in the quadriceps muscles or in the hip adductors.

The diagnosis may be made on the basis of injection of local anesthetic along the course of the nerve and proximal to the proposed site of entrapment. Nerve conduction techniques are available to assess neural conduction in the main branch of the saphenous nerve or in the terminal branches. The routine tests may be disappointing in persons with subcutaneous adipose tissue or swelling.

A side-to-side comparison of the nerve should be made and must demonstrate a lesion consistent with the patient’s complaints. A somatosensory evoked potential (SSEP) test can also be performed and the results compared with those of the contralateral side for diagnosis, though this test may be cumbersome and time-consuming.

Obturator nerve entrapment

With severe injuries to the obturator nerve, loss of adduction and internal rotation occur, and the typical gait pattern is that of an externally rotated foot. Examination reveals wasting of the adductor muscles of the thigh and, possibly, diminished sensation along the medial thigh distally.

The differential diagnosis includes adductor muscle strain, osteitis pubis, stress fracture of the pelvis, inguinal ligament enthesopathy, entrapment of the lateral femoral cutaneous nerve, and inguinal hernia. A nerve block may be helpful but usually is not necessary for diagnosis.

Tibial nerve entrapment

The diagnosis of tibial nerve entrapment, or tarsal tunnel syndrome (proximal and distal), is based primarily on a detailed history and physical examination. Further screening studies (eg, laboratory workup for arthritides, diabetes, alcoholism, and thyroid dysfunction) are indicated in cases of associated inflammation and in patients with symptoms of peripheral neuropathy (see Workup).

Inspection of the patient while he or she is standing and walking allows the examiner to evaluate for alignment deformities, such as hindfoot varus or valgus, swelling, varicosities, or other skin changes.

Palpation of the pulses is used to evaluate the patient’s distal circulation. Sensory examination, including Semmes-Weinstein monofilament testing of the entire foot, may reveal dermatomal numbness due to compression neuropathy, or could reveal peripheral neuropathy.

The range of motion of the ankle, subtalar, and the midfoot joints is examined, and any limitations are noted. Pain may increase with dorsiflexion and eversion or inversion of the foot; these positions increase tarsal compartment pressure. [28Motor examination should include asking the patient to spread the toes to facilitate assessment of the abductor digiti minimi and, if appropriate, the abductor hallucis. Hypertrophy of the abductor hallucis or an accessory muscle may also be present, with fullness in the longitudinal arch.

Patients with proximal tarsal tunnel syndrome often have ganglia, tenosynovitis, or other space-occupying lesions in the tarsal tunnel that may be palpable. They may also have positive Tinel signs along the tibial nerve. Occasionally, nerve percussion causes symptoms and pain to radiate proximal to the nerve course (the so-called Valleix phenomenon). Linscheid noted that in most of his patients with proximal tarsal tunnel syndrome, manual compression of the nerve at the tarsal tunnel for 60 seconds reproduced their symptoms. [38]

Patients with distal tarsal tunnel syndrome usually have the most severe tenderness over the first branch of the lateral plantar nerve over the plantar medial heel and under the abductor hallucis. Many patients have tenderness along the entire tibial nerve, starting from behind the distal medial malleolus. Additional tenderness is usually present over the plantar fascia insertion on the medial calcaneal tuberosity and sometimes along the entire medial edge of the plantar fascia. The Tinel sign is usually absent.

The deep tendon reflexes and straight-leg raise are evaluated with an eye to detecting any isolated or concomitant radiculopathy. Hamstring tightness is evaluated with both legs extended.

Patients with entrapment of the medial plantar nerve have tenderness over the medial arch inferior to the navicular tuberosity, but not directly over the plantar fascia. Pain may radiate to the medial toes and the ankle. Numbness or a Tinel sign over this area may be present only after prolonged weightbearing exercise. Occasionally, orthotic use may be correlated with the onset of the symptoms. Stretching of the nerve as a result of eversion of the foot or of standing on the toes may reproduce or exacerbate symptoms.

Common peroneal nerve entrapment

The history and physical examination are the most helpful initial clinical tools in establishing a high index of suspicion for a common peroneal nerve injury. Nerve biopsy, though largely unnecessary, may confirm the diagnosis.

Observation of the patient’s gait is useful in diagnosing ankle dorsiflexion weakness. A patient with common peroneal nerve entrapment often displays a steppage gait pattern, in which the affected foot is lifted excessively from the ground during the swing phase of ambulation in order to clear the foot. This results in excessive hip and knee flexion, and the appearance is as if the patient is stepping over an object in his or her path.

In addition, a foot slap may be heard on foot strike because of the inability of the ankle dorsiflexors to provide a controlled descent of the foot toward the floor. The patient may also stumble when walking as a consequence of the toes on the affected side dragging or catching on the floor during the swing-through phase of ambulation.

Examination often reveals a variable pattern of weakness, with the extensor digitorum brevis most profoundly affected. Ankle and toe dorsiflexion may be substantially altered. Dorsiflexion is best tested by having the patient place the ankle in the neutral position and then dorsiflex the foot and invert; this tests the anterior tibial muscle optimally. Often, ankle eversion is normal because the relevant muscles are relatively spared.

In a pure common peroneal neuropathy, plantar flexion should be spared. In fibular neck fractures, complete absence of sensation is possible along the anterodistal portion of the leg and the entire dorsum of the foot. Lateral calf sensation may be spared if the lesion is below the nerve branch to this region. When the neural insult occurs at the knee, the short head of the biceps femoris often is spared.

Superficial peroneal nerve entrapment

In the setting of suspected superficial peroneal nerve entrapment, examination should include the entire course of the nerve, starting from the lower back and extending through the sciatic notch, the proximal fibula, and the lateral leg, where a muscle bulge due to a fascial defect may be palpated in some patients.

Percussion along the superficial course of the nerve over the proximal fibula, lateral leg, or anterior ankle may result in a positive Tinel sign, with reproduction of radiating pain. Direct palpation with pressure on the site of entrapment may also induce or exacerbate symptoms. Repeating the examination after a particular activity that exacerbates symptoms may produce findings not present on the initial examination at rest.

Styf described the use of three provocative tests for nerve compression at rest and again at rest after exercise in competitive athletes with symptoms suggestive of exertional compartment syndrome. [39In the first test, pressure is applied over the anterior intermuscular septum while the patient actively dorsiflexes the ankle. In the second, the foot is passively plantarflexed and inverted at the ankle. In the third, while the patient maintains the passive stretch, gentle percussion is applied over the course of the nerve.

In some cases of superficial peroneal nerve entrapment associated with direct or indirect trauma, patients may present with symptoms of reflex sympathetic dystrophy (RSD), or complex regional pain syndrome (CRPS), which creates a diagnostic and therapeutic challenge.

Infrequently, weakness of the dorsiflexors and everters of the foot may be seen with associated foot drop in more proximal entrapments of the superficial peroneal nerve.

Occasionally, in cases of exertional compartment syndrome, measurement of the intramuscular pressure at rest after exercise may be helpful.

Injection of the nerve with lidocaine or bupivacaine just above the site of involvement can be the most valuable diagnostic tool. The patient can define the extent of relief obtained from such an injection, which can be helpful in defining the zone of injury and expected relief from surgical release or excision.

Deep peroneal nerve entrapment

With proximal entrapment of the deep peroneal nerve, motor dysfunction may be demonstrated on regular gait examination, with presentations such as a dramatic foot drop. However, symptoms are usually more subtle and are noted only on heel walk or a hop test.

With long-standing dysfunction, plantarflexion of the ankle with extension of the toes can compress the nerve as it passes beneath the extensor retinaculum, and this can exacerbate the symptoms. Muscular atrophy may also be noted in the anterior compartment of the extensor digitorum brevis with distal entrapment of the nerve.

With distal entrapment, tenderness may be elicited along the entrapped segment of the nerve over the anterior ankle or just distal to it, and an underlying bony prominence is usually present. Provocative dorsiflexion and plantarflexion of the ankle may bring on or increase symptoms. A sensory deficit in the first webspace may also be detectable. Most patients have a positive Tinel test result over the entrapment site, commonly around the fibular neck or over the anterior ankle.

Incomplete involvement can also occur, affecting isolated sensory or motor branches. Temporary resolution of neuritic symptoms following an injection of the nerve with plain lidocaine at the site of entrapment is a good indicator that the diagnosis is correct.

Interdigital neuritis

The Mulder click is a useful diagnostic test for interdigital neuritis. The forefoot is held in one hand, and the metatarsal heads are squeezed while the other hand places direct pressure on the plantar aspect of the interspace. As the metatarsal heads are compressed, the enlarged nerve is pushed plantar and away from the metatarsal heads, and a click is palpated with the digit in the plantar web space just distal to the transverse intermetatarsal ligament.

This test is often uncomfortable for the patients but does not usually reproduce their symptoms. The palpated mass can be pushed up again in the interspace with manual pressure while partial compression is maintained on the metatarsal heads. Many times, one digit is observed to move suddenly.

A range of conditions may mimic interdigital neuritis, including metatarsal stress fracture, MTP joint synovitis, intermetatarsal bursitis, extensor tendon tenosynovitis, tumor, and more proximal nerve injury. Metatarsal stress fracture will present with bony tenderness and pain upon palpation of the metatarsal shaft, rather than the common digital nerve. MTP joint synovitis will often prove painful during active or passive joint motion.

The diagnosis of interdigital neuritis is based primarily on clinical findings. Careful clinical examination usually will reveal other conditions that can mimic or coexist with intermetatarsal neuritis. In complex cases, immediate, temporary resolution in response to a local anesthetic block proximal to the involved area below the intermetatarsal ligament can confirm the diagnosis.

Differential Diagnoses

Electrodiagnostic Testing

Iliohypogastric, ilioinguinal, and genitofemoral nerves

Unfortunately, there are no reliable electrodiagnostic techniques for fully defining the integrity of the iliohypogastric, ilioinguinal, and genitofemoral nerves. Needle electromyography (EMG) of the lower abdominal musculature may serve as an adjunct in the diagnosis of iliohypogastric nerve injury. Although abdominal needle EMG may help determine the severity of ilioinguinal nerve injury, it is neither sensitive nor specific. A side-to-side sensory comparison study has been described for the genitofemoral nerve, but it is technically difficult to perform. [40]

Femoral nerve

Electrodiagnostic testing typically is performed for diagnosis of femoral nerve entrapment, but it is also important for determining the extent of the injury and the prognosis for recovery. With electrodiagnostic testing, either surface or needle electrodes lateral to the femoral artery in the inguinal region are used for stimulation. The stimulation can be performed above and below the inguinal ligament. Disk electrodes from the vastus medialis are used to record stimulation.

A sensory study of the saphenous nerve (continuation of the sensory portion of the femoral nerve over the medial aspect of the leg and ankle) may also be performed. Needle examination should be completed for the paraspinal muscles, as well as for the iliopsoas (also L2-3) and hip adductors supplied by the obturator nerve, to help distinguish root or plexus injury from peripheral nerve injury. Needle EMG is usually the most revealing portion of the test. The examiner must look not only for denervation potentials but also for any active motor units.

Lateral femoral cutaneous nerve

Electrodiagnostic testing may be performed for diagnosis. With nerve conduction studies, the technique includes using a bar electrode for recording and reference. This can be performed with either antidromic (conduction against the direction of sensory fiber conduction) or orthodromic (conduction in the direction of nerve conduction) methods. The antidromic study is usually easier to perform, though on occasion, response may be absent bilaterally. In obese patients, the response is small and difficult to obtain.

A needle stimulation electrode may be needed. The sensory response is absent in 71% of patients with meralgia paresthetica and is prolonged in 24% of patients with this condition. EMG test results with the needle are normal in patients with this diagnosis, which may help to differentiate it from an upper lumbar radiculopathy.

Technically, the sensory test is a difficult study, and a response must be present on the opposite side to determine entrapment. It may be nearly impossible to obtain a response in an obese patient or a patient with a large abdomen without using a needle for stimulation. Unfortunately, the test may be difficult for the patient to tolerate because of the large amount of current (with respect to more peripheral nerves) required to stimulate a nerve that lies under adipose tissue.

Saphenous nerve

No findings should be present on needle examination of the muscle during EMG. Needle examination should include the quadriceps and the adductor longus to assess for femoral and obturator nerve injury. If findings are present in both of these muscles, then paraspinal muscles definitely should be examined to rule out radiculopathy.

Obturator nerve

No routine conduction studies are available with which to evaluate the integrity of the obturator nerve, and the needle examination is the mainstay of testing with electrodiagnosis. Membrane instability (positive sharp waves and fibrillation potentials) will occur within 3 weeks of the nerve injury, and needle examination should be performed on patients with groin pain of longer than 3 months in whom this neuropathy is suspected. Complete injury results in a lack of active motor unit potentials.

Muscles from the quadriceps (femoral nerve), as well as the paraspinal muscles, must be examined and found to be normal before an obturator nerve injury can be diagnosed. In this manner, one must rule out a radiculopathy and a plexus injury as potential causes of the weakness in adduction during the electrodiagnostic examination.

Tibial nerve

Electrodiagnostic tests are indicated in refractory cases or in cases where the diagnosis of tibial nerve injury is uncertain. A complete EMG and nerve conduction study of the motor and sensory nerves to the foot, with comparison to the other foot, is necessary. It is important for EMG examination to include motor latencies, particularly to the abductor digiti minimi and the abductor hallucis, when tarsal tunnel syndrome is suspected.

Kaplan and Kernahan reported that reduced amplitude and increased duration of the motor response are more sensitive indicators of tarsal tunnel syndrome than distal motor latency is. [41Sensory action potentials may be affected in earlier stages than motor fibers are; therefore, changes may also be identified before any motor abnormalities. This is because sensory fibers are more susceptible to injury.

In addition, Kaplan and Kernahan believed that the lateral plantar branch of the tibial nerve probably is affected earlier than the nerve’s medial plantar branch is. Sensory studies are, therefore, considered to be the most sensitive studies for tibial nerve entrapment.

Galardi et al reported that after stimulation of the plantar nerves, the accuracy of the sensory-nerve action potential (SNAP) and the mixed-nerve action potential (MNAP) are almost the same. SNAPs are more sensitive and less specific, whereas MNAPs are less sensitive and more specific. Galardi et al concluded that the coexistence of MNAP and SNAP abnormalities, especially if asymmetric, is highly indicative of tarsal tunnel syndrome. The mixed-response test is technically much easier to perform and is better tolerated by many patients.

Approximately 90% of patients with tarsal tunnel syndrome have abnormal findings on EMG and nerve conduction velocity (NCV) studies. However, in the presence of supportive history and physical examination, a normal electrodiagnostic study does not exclude the diagnosis of tarsal tunnel syndrome. Electrodiagnostic tests, however, can be extremely helpful in diagnosing concomitant polyneuropathy, systemic disorders, and lumbosacral radiculopathy.

Positive results on electrodiagnostic tests are an affirmation of the diagnosis of tarsal tunnel syndrome. Golovchinsky reported a high incidence of double crush syndrome with overlapping of peripheral entrapment syndromes and signs of proximal nerve damage of the corresponding nerves (partial muscle denervation or abnormalities of the F wave). [42In such cases, simultaneous treatment of the two problems may be indicated.

Common peroneal nerve

Electrodiagnostic evaluation is arguably the best method for assessing a potential peroneal nerve insult. It is clinically difficult to isolate and test the short head of the biceps, the evaluation of which is critical in determining whether a lesion is proximal to the knee and whether it involves the sciatic nerve, the lumbosacral plexus, or nerve roots. In patients with exercise-induced symptoms, electrodiagnostic tests should be performed before and after exercise. Such tests include sensory and motor conduction studies, as well as needle EMG.

Sensory conduction studies

A superficial peroneal SNAP is important, and an abnormality of the sensory evoked response implies that the lesion is distal to the dorsal root ganglion, though it does not completely rule out an L5 radiculopathy. A loss in amplitude of this response implies some axonal loss affecting either the common peroneal nerve or its superficial branch.

The particular portion of the nerve that is injured cannot be determined if only a superficial peroneal nerve sensory study is performed. Comparison of the latency and amplitude of the superficial peroneal SNAP with the contralateral limb is required to define an approximate degree of axonal loss.

Motor conduction studies

The most commonly performed test in determining peroneal conduction in the leg and across the fibular head is performed with the active electrode placed on the extensor digitorum brevis. The peroneal nerve usually is stimulated at the ankle, several centimeters below the fibular head and about 10 cm proximal to the fibular head, just medial to the biceps femoris tendon. This allows calculation of the NCV across the fibular head region, with comparison with the distal leg segment.

Comparison with the contralateral limb is often helpful. When significant extensor digitorum brevis atrophy is present (eg, with advanced age or with a polyneuropathy), the active electrode should be placed over the anterior tibial muscle. Generally, lower-extremity motor NCVs less than 40 m/sec are considered abnormal. Generally, proximal-segment NCVs should be greater than distal NCVs, given the greater axonal diameter in the proximal segment of the nerve.

If contralateral limb responses are normal, axonal loss can be estimated by expressing the compound muscle action potential (CMAP) on the affected side as a percentage of that on the unaffected side. This method is independent of the location of the active recording electrode and is valid in both circumstances. A 20-50% change (depending on the source) indicates a conduction block. The degree of conduction slowing and temporal dispersion may also be assessed to determine whether the lesion is mainly demyelinating or axonal.

Needle EMG

Needle EMG helps in confirming axonal loss and in assessing the degree of involvement of the muscles innervated by the superficial peroneal nerve. This portion of the nerve usually is less severely involved than the deep peroneal nerve. It is possible to localize the lesion to either the deep or the superficial peroneal nerve, specifically if appropriate abnormalities are detected in the proper distribution for each nerve.

The most valuable aspect of the needle EMG examination is that it can be used to define the proximal extent of the lesion. If an amplitude drop is lacking across the fibular head but the CMAP for the anterior tibial muscle is lower than that of the unaffected side (suggesting axonal loss), it is difficult to localize the lesion to the fibular head, even though this is the most common site of peroneal nerve injuries.

In any peroneal nerve injury, regardless of the suspected site of nerve compromise, examining the short head of the biceps femoris is important. If this muscle demonstrates membrane instability (positive sharp waves and fibrillations), the lesion is proximal to the fibular head.

Testing muscles innervated by the tibial nerve, particularly the flexor digitorum longus and the posterior tibial muscle, is also important because these muscles contain predominantly L5 neural innervation from the tibial nerve. If a radicular process is present, the muscles innervated by the peroneal and tibial nerves should demonstrate membrane instability.

Superficial peroneal nerve

The value of electrodiagnostic studies for superficial peroneal nerve injury varies in the literature. In many cases, findings from electrodiagnostic tests are normal because these dynamic syndromes frequently improve or resolve at rest; however, in some instances, these tests may reveal an unrecordable evoked response or a prolonged distal latency of a segment of the nerve and thus help better define the zone of compression. Such tests also help in the evaluation of concomitant radiculopathy or peripheral neuropathy.

Deep peroneal nerve

Electrodiagnostic studies of the deep peroneal nerve are helpful in further defining the zone of compression and in evaluating for concomitant radiculopathy or peripheral neuropathy. In deep peroneal nerve injury or entrapment, the results may show a decrease in the amplitude of the response if axonal involvement is present or conduction block occurs from demyelination. The distal latency may be prolonged if entrapment is present in the anterior tarsal tunnel region, and the NCV is decreased across the leg region if the entrapment or injury is more proximal.

An accessory nerve may also be present. The accessory peroneal nerve originates from the superficial peroneal nerve and travels posterior to the lateral malleolus to provide variable innervation to the extensor digitorum brevis. This anomaly is identified when a response is recorded from the extensor digitorum brevis that is larger with proximal stimulation (at the fibular head) than with distal stimulation (at the ankle).

Needle examination may reveal the presence of fibrillations and positive sharp waves in the extensor digitorum brevis only if entrapment is present at the anterior tarsal tunnel. If entrapment is present more proximally, the denervation is present in the anterior tibial muscle as well as in the extensor digitorum brevis.

Denervation may, however, be present with other neurologic conditions. The short head of the biceps femoris, as well as the medial gastrocnemius, the tensor fasciae latae, and the lumbar paraspinal muscles, should be tested if findings in the deep peroneal muscles rule out a more proximal problem (eg, a radiculopathy). The absence of findings in these muscles, as well as in the peroneus longus and peroneus brevis, confirms the presence of a deep peroneal motor-nerve injury.

Some reports stated that there may be a high percentage of denervation in the foot intrinsic muscles in healthy subjects, but subsequent reports found that the actual percentage of abnormal findings in healthy subjects is low for a well-trained electromyographer. In many cases, electrodiagnostic test findings are normal because these dynamic syndromes frequently improve or resolve at rest.

Radiography, CT, MRI, and Ultrasonography

Tibial nerve

Plain radiographs should probably be obtained to exclude extrinsic factors (eg, exostoses, malunions, or osteochondromas) that cause direct compression of the tibial nerve. In patients with posttraumatic symptoms, further investigation (eg, with computed tomography [CT] or magnetic resonance imaging [MRI]) can help identify occult sources of pain, such as medial talar process fractures, medial malleolus stress fractures, and space-occupying lesions.

Common peroneal nerve

Plain radiographs may be helpful in excluding underlying traumatic injuries (eg, proximal fibular head fracture) or osseous tumors or in assessing the severity of angular deformities about the knee. CT and MRI are helpful in finding a compressive lesion along the course of the common peroneal nerve in cases in which this is suspected. Metabolic and hematologic studies may be helpful in conditions such as diabetic peripheral polyneuropathy, alcoholic polyneuropathy, polyarteritis nodosa, and hyperthyroidism.

Superficial peroneal nerve

In rare cases, plain radiographs of the leg can reveal bony abnormalities that may contribute to or constitute the cause of superficial peroneal nerve entrapment. In cases of suspected proximal entrapment, knee radiographs may show abnormalities of the proximal fibula (eg, exostoses, osteochondromas, or fracture callus). If necessary, CT can provide more detailed information on the bony anatomy of the area, and ultrasonography can help localize cystic masses that impinge on the nerve. MRI is rarely necessary to obtain additional information.

Deep peroneal nerve

Bony impingement can usually be seen on conventional lateral ankle or foot radiographs. Oblique radiographs taken from different angles are necessary for better definition of smaller osteophytes, exostosis, or other bony masses about the anterior ankle or the dorsomedial midfoot. Knee radiographs are needed for suspected proximal involvement. If necessary, a CT scan will provide more detailed information on the bony anatomy of the area.

Ultrasonography has been useful for diagnosis and localization of cystic masses impinging on the nerve. Occasionally, MRI is necessary to obtain additional information about soft-tissue masses, synovial reaction, adjacent bone, and chondral and soft-tissue involvement.

Plantar and digital nerves

In rare, complex situations, ultrasonography and MRI may be helpful for defining interdigital neuritis (also known as Morton neuroma, Morton metatarsalgia, interdigital neuroma, or interdigital nerve compression). [43The accuracy of these studies, however, varies significantly and depends on multiple factors, including the MRI machine, the technician and the technique, and the interpreting radiologist or orthopedic surgeon.

Ultrasonography reveals a hypoechoic, ovoid mass parallel to the long axis of the metatarsal. Ultrasonography can also be used to diagnose other pathologic conditions in the forefoot, such as bursitis and metatarsophalangeal (MTP) joint effusion. Redd et al reported that this study was 95% sensitive in the detection of webspace abnormality but could not clearly distinguish interdigital neuritis from an associated mass (eg, mucoid degeneration in the adjacent loose connective tissue). [44]

In a study by Quinn et al, ultrasonography revealed the diagnosis in 85% of cases in which it was suspected, [45though the ability to detect neuromas shorter than 5 mm was limited. Terk et al reported on MRI with T1- and T2-weighted sequences, along with a combination of fat suppression and the administration of gadopentetate dimeglumine. [46Williams et al showed that T1-weighted axial and coronal images obtained with an axial, fast spin-echo (FSE), T2-weighted sequence depict neuromata more consistently than other methods do.

Zanetti et al studied 54 feet in which interdigital neuritis was suspected in order to determine the effect of MRI results on diagnostic thinking and the therapeutic decisions made by orthopedic surgeons. [47The authors noted considerable change in the diagnosis, location, and number of neuromas, as well as in the treatment plans, after MRI.

In another report, Zanetti et al suggested that diagnosis of interdigital neuritis on the basis of MRI results is relevant only when the transverse diameter of the fluid collection in the bursa is 5 mm or more and when the MRI results are correlated with the clinical findings. [48Fluid collections in the first three metatarsal bursae with a transverse diameter of 3 mm or less are probably physiologic.

In a histomorphologic study of patients and autopsies, Morscher et al concluded that diagnostic MRI or ultrasonography is unnecessary for making decisions about operative treatment. [35In addition, Resch et al found that MRI modalities had little or no value in the diagnosis of interdigital neuritis, because of the high rate of false-negative results. 

Pharmacologic and Physical Therapy

Iliohypogastric or ilioinguinal nerve entrapment

Treatment of iliohypogastric or ilioinguinal nerve entrapment may include local injection of an anesthetic, oral or topical medications, or physical therapy.

Among the oral agents that may be considered are antiseizure medications (eg, gabapentin, carbamazepine, and lamotrigine), nonsteroidal anti-inflammatory drugs (NSAIDs), tricyclic antidepressants (TCAs; eg, amitriptyline and doxepin), and tramadol; capsaicin cream or topical lidocaine may also be useful. With physical therapy, cryotherapy or a transcutaneous electrical nerve stimulation (TENS) unit may be tried.

Genitofemoral nerve entrapment

Anesthetic nerve blocks are diagnostic and therapeutic for genitofemoral nerve entrapment. Avoidance of aggravating activities should be emphasized. Treatment may also consist of antiseizure medications (eg, gabapentin, carbamazepine, or lamotrigine), as well as TCAs (eg, amitriptyline and doxepin). Other medications include capsaicin cream, topical lidocaine, NSAIDs, and, possibly, tramadol. A trial with a TENS unit may also be beneficial.

Femoral nerve entrapment

In less severe cases, treatment of femoral nerve entrapment may be purely symptomatic. Quadriceps weakness may be treated with a locking knee brace to prevent instability, and the patient may require an assistive device for walking. Good recovery is achieved in as many as 70% of patients and may take as long as 1 year. Recovery may occur even when the injury is fairly severe, as determined by electrodiagnostic testing and physical examination. Patients with severe axonal loss have some recovery of function, though it is usually incomplete.

Lateral femoral cutaneous nerve entrapment

Treatment of lateral femoral cutaneous nerve entrapment may include injection of local anesthetic agents. A steroid can also be used to prolong the effects of the local anesthetic and reduce inflammation. Oral medications, such as NSAIDs, antiseizure medications (eg, gabapentin), TCAs, and tramadol, may be used, as may capsaicin cream and topical lidocaine.

It is also important to instruct patients regarding ways of preventing further irritation of the nerve. These may include avoidance of hip extension, prolonged standing, and compressive garments. The use of ice and a TENS unit may also be helpful.

Saphenous nerve entrapment

Saphenous nerve entrapment in the adductor canal usually is treated conservatively by injecting an anesthetic (with or without a corticosteroid) at the point of maximal tenderness (usually 10 cm proximal to the medial femoral condyle). The injection may have to be repeated periodically. Avoiding aggravating activities and using proper body mechanics will also be helpful. If this approach fails, surgical intervention may be needed.

Obturator nerve entrapment

For anterior obturator nerve entrapment, treatment may consist of electrical stimulation of the adductor and hip flexor muscles, stretching, and massage. These modalities, however, typically have not been successful in resolving this condition if it is not recognized early.

Tibial nerve entrapment

Compression of the branches of the tibial nerve is a common cause of refractory heel pain and is the most common compression neuropathy seen in the foot and ankle region. Nonoperative management of compression of the tibial nerve involves relief of the source of external compression (if any), use of medication, and correction of weightbearing deformities.

Treatment of tibial nerve entrapment (tarsal tunnel syndrome) is directed toward the underlying etiology of neural compression. Nonoperative options can include the use of NSAIDs (in cases associated with inflammation), aspiration of underlying cystic lesions, and control of edema and varicosity. Medical treatment of underlying systemic conditions is helpful in the indicated situation. The use of antineuritic medications (eg, gabapentin and, occasionally, TCAs) has also been shown to alleviate symptoms in many patients.

At times, a trial of immobilization with the use of casts or walking boots is indicated. Orthotic management is indicated in patients with proximal entrapment and alignment or postural abnormalities causing chronic traction or compression trauma to the nerve. In patients with distal entrapment and associated heel pain, the use of accommodative orthotics with a relief area in the anterior heel pad (ie, under the tibial nerve) is usually helpful.

Patients with flatfoot may benefit from semirigid University of California at Berkeley Laboratory (UCBL)-type orthotic devices with a deep heel cup to minimize weightbearing traction on the nerve.

Common peroneal nerve entrapment

Initial nonoperative treatment of common peroneal nerve entrapment should focus on maximizing mobility and function. In addition, the cause of nerve compromise or compression should be corrected to reduce further nerve damage.

NSAIDs or oral corticosteroids may be useful in cases where an inflammatory process is present. Corticosteroids injected into the affected region may reduce swelling and pressure on the nerve in some cases. Symptomatic pharmacologic treatment may consist of TCAs (eg, amitriptyline) or neuroleptic medications (eg, gabapentin and carbamazepine).

A brace (ankle-foot orthosis [AFO]), splints, or orthopedic shoes may control the abnormal dynamics at the ankle and provide dorsiflexion assistance for a more ideal gait pattern during nerve recovery. In-shoe orthotics may be helpful in certain instances, as in the correction of a biomechanical malalignment in gait (eg, in patients with severe flatfoot or cavus foot).

Many authors have reported spontaneous recovery; therefore, initial nonoperative management for a minimum of 3-4 months is recommended for idiopathic cases and for those suggestive of neurapraxia.

Superficial peroneal nerve entrapment

Vague and diffuse symptoms can create a diagnostic and therapeutic challenge for the treatment of superficial peroneal nerve entrapment. The use of multiple diagnostic modalities, including repeat examinations, selective injections, and electrodiagnostic studies, is required. Treatment of the underlying cause should be undertaken, as should release of the entrapped nerve and excision of existing neuromas.

Nonoperative options include the use of NSAIDs combined with relative rest, physical therapy for strengthening of muscles in cases of associated weakness or recurrent ankle sprains, and elimination of predisposing or triggering factors. Aids, such as braces, can be used to avoid recurrent ankle sprains. In-shoe orthotic devices may be helpful in certain instances, such as the correction of a biomechanical malalignment in gait for patients with severe flatfoot or cavus foot.

At times, injection of steroids plus lidocaine near the site of involvement in the lower leg can reduce symptoms and serve as a diagnostic tool in confirming the zone of nerve compression. The use of antineuritic medication (eg, gabapentin) can also be helpful in reducing or sometimes eliminating symptoms, particularly in cases associated with complex regional pain syndrome (CRPS). In these cases, combination treatment with medication, physical therapy, and local and sympathetic nerve blocks may be required.

Deep peroneal nerve entrapment

Nonsurgical care of patients with deep peroneal nerve entrapment most importantly involves patient education to eliminate predisposing factors. For example, padding of the tongue of the shoe, the elimination of shoes with laces, or the use of alternative lacing methods, as well as the avoidance of high heels, may be sufficient to resolve symptoms.

Physical therapy is useful for strengthening the peroneal muscles in cases associated with weakness and in individuals with chronic ankle instability; physical therapy may also improve symptoms.

In-shoe orthotic devices are helpful for certain applications, such as for correction of a biomechanical malalignment in gait (eg, in patients with severe flatfoot or cavus foot).

NSAIDs and antineuritic medication may be helpful as adjuncts to other treatment modalities. Injection of steroids plus lidocaine near the site of involvement can reduce symptoms in some individuals.

In addition, consideration should be given to a metabolic workup to rule out thyroid dysfunction and diabetes in select individuals. Further workup may be necessary to rule out lumbar radiculopathy.

Interdigital neuritis

If interdigital neuritis (also referred to as Morton neuroma, Morton metatarsalgia, interdigital neuroma, or interdigital nerve compression) is detected early, conservative measures may be reasonably successful. About 20-30% of patients achieve adequate relief with nonoperative management. This may be accomplished by eliminating or minimizing the external sources of compression or stretch on the interdigital nerve.

Extra-wide shoes and low heels, as well as the placement of a small metatarsal pad just proximal to the heads of the central three metatarsals, may reduce symptoms by increasing the intermetatarsal space, elevating the metatarsals and the intermetatarsal ligament, and reducing the likelihood of neural irritation. Accommodative orthotic devices with built-in metatarsal pads may at times be helpful, especially in patients with alignment abnormalities. Stiffer, rocker-soled shoes may be useful.

NSAIDs may relieve acute pain and inflammation. If NSAIDs provide insufficient relief, a local anesthetic injection can also relieve pain and may help to confirm the diagnosis of interdigital neuritis.

Mann et al did not find corticosteroid injections to result in predictable or lasting relief. [50Rasmussen et al reported initial pain relief in 80% of patients who received a single corticosteroid injection [51; however, 47% of the 41 feet studied ultimately required surgical excision, and most of the remaining 53% had residual symptoms.

In addition, corticosteroid injection for intermetatarsal neuroma has been associated with a number of complications, including plantar fat-pad atrophy, skin depigmentation, hyperpigmentation, and telangiectasias. Fat-pad atrophy can result in metatarsalgia and gait impairment.

Surgical Intervention

Iliohypogastric or ilioinguinal nerve entrapment

When conservative measures are not successful in treating entrapment of the iliohypogastric or ilioinguinal nerve, surgical excision may result in relief of pain with few potential complications (eg, possible neurolysis of the nerve in refractory cases). Surgical excision is more invasive but has had good outcomes in several reports. Krahenbuhl et al reported an endoscopic approach. [52]

Genitofemoral nerve entrapment

If conservative treatment of genitofemoral nerve entrapment fails, surgical excision of the nerve is the treatment of choice. A transabdominal approach to the nerve has been described as having satisfactory results. [5354Complications of this procedure include hypoesthesia of the scrotum or labium majus and of the skin over the femoral triangle, as well as loss of the cremasteric reflex; this usually does not result in notable morbidity. According to Harms et al, an extraperitoneal approach should result in fewer operative complications. [55]

Femoral nerve entrapment

In many cases, as noted (see above), treatment of femoral nerve entrapment may be based on symptoms only. In some instances, it may be more invasive and include surgical intervention, depending on the severity of the injury.

Lateral femoral cutaneous nerve entrapment

If conservative or pharmacologic treatment of lateral femoral cutaneous nerve entrapment is not helpful, surgical exploration may be required. This may include transection of the nerve or decompression with or without neurolysis. [5657Anatomic variations of the nerve and neuromas can occur and may lead to recurrence. [58]

Saphenous nerve entrapment

If nonoperative therapy for saphenous nerve entrapment fails, surgical decompression may be needed. In patients who have sustained a direct blow to the medial knee and are experiencing persistent medial knee pain despite conservative trials for treatment, a neurectomy or neurolysis of the infrapatellar branch may be helpful.

Obturator nerve entrapment

For athletes, surgery is the preferred treatment when clinical features of obturator neuropathy and denervation on electromyography (EMG) are observed. The surgical procedure involves dividing the fascia over the pectineus and the adductor longus and dissecting the space between the two muscles to reveal the anterior branch of the nerve beneath a thick fascia. This fascia is divided along the line of the nerve, and the adductor longus−pectineus junction is closed loosely.

Tibial nerve entrapment

Surgical release is indicated for refractory cases of tibial nerve entrapment (tarsal tunnel syndrome) and for most cases with space-occupying lesions. In patients with proximal or distal tibial nerve entrapment, this has an 80-90% likelihood of improving or resolving the symptoms.

The location of the release is partially dependent on the location of entrapment. Most cases, however, call for a full release of the tibial nerve and of the lateral plantar nerve and its branches. The skin is marked for the proposed skin incision. For proximal entrapment, the incision is started 2 cm proximal to the medial malleolus, approximately halfway between the medial malleolus and the Achilles tendon. It is extended distally and plantarly, directly superficial to the course of the tibial nerve.

A full release includes release of the flexor retinaculum overlying the nerve, starting proximal to the medial malleolus and moving distally to include release of the deep fascia of the abductor hallucis. The neurovascular bundle is posterior to the flexor digitorum brevis. Typically, medial and lateral plantar nerves branch at the level of the medial malleolus. It is best to identify the tibial nerve proximally and follow it distally.

All sources of potential impingement are released from the medial and lateral plantar nerves. The medial calcaneal branches are quite variable and should be watched for closely. A large number of vessels are encountered routinely, and some crossing veins may need to be ligated.

It is important to ensure full release of the lateral plantar nerve and its first branch. The superficial and deep fascia of the abductor hallucis is released as the nerve is followed distally. Partial release of the plantar fascia is usually necessary for full visualization. No consensus exists in the literature about the necessary amount of plantar fascia release.

The extent of the plantar fascia release may be dictated partially by the arch height, and a full release may be indicated in patients with a cavus foot, whereas a minimal release could be considered in patients with flatfoot. Retraction of the abductor hallucis and the flexor digitorum brevis allows good visualization of the lateral plantar nerve and its first branch. The usual course of the lateral plantar nerve is just anterior to the heel pad.

As the lateral plantar nerve is followed, any compressive fascial bands are cut. The fascia of the quadratus plantae is also identified and released if it is noted to cause any compression by the medial edge of the quadratus plantae fascia on the first branch of the lateral plantar nerve. In cases of associated space-occupying lesions, the incision is modified as necessary for complete excision of the tumor.

Bipolar electrocautery and surgical loupe magnification are necessary for optimal visualization. Handling of the nerve should be minimized. Often, large varicosities are present that should be considered part of the underlying compressive etiology. Care must be taken to avoid injury to these large vessels, which can compromise visualization and can cause intraoperative and postoperative bleeding and postoperative scarring. The medial plantar nerve is fully released. The tourniquet is released before closure to ensure that no major bleeding occurs.

The plantar skin incision is reapproximated without the use of subcutaneous sutures. Reapproximating the subcutaneous tissues and the skin closes the medial segment of the incision. A bulky soft-tissue dressing is then applied, and range-of-motion exercises are encouraged.

Postoperatively, the patient with a distal release of the nerve and full plantar fascia release is kept on nonweightbearing status for 4-6 weeks. In patients with lesser releases of the plantar fascia, weightbearing is protected until pain and swelling are improved and the wound is closed, which takes approximately 2-3 weeks. Complete release is indicated in most cases of tibial nerve entrapment, including those with distal entrapment of the nerve branches (usually associated with intractable heel pain).

If entrapment of the medial plantar nerve is suspected, the incision beyond the medial malleolus curves toward the plantar aspect of the medial navicular, and full release is performed to the knot of Henry.

In a report of operative results from patients with recalcitrant heel pain, Baxter and Thigpen performed a full release of the lateral plantar nerve and its branches with minimal or no plantar fascia release. [5The two most common areas of compression were noted at the sharp fascial edge of the abductor hallucis and at the medial ridge of the calcaneus where the nerve passes over it beneath the tuberosity or origin of the flexor brevis and plantar fascia.

Of the 34 heels that were operated on in this study, 32 had good results and two had poor results. [5Most patients could detect improvement during the first or second postoperative day. Anti-inflammatory medication and orthosis use were continued postoperatively.

Watson et al reported good-to-excellent results in 84% of patients who underwent distal tarsal tunnel release and partial plantar fasciotomy. [59Bailie and Kelikian reported that 84% of their patients in the noncompensation group were very satisfied or moderately satisfied with the outcome. [60They also reported better satisfaction in patients with nontraumatic etiology than in others.

Sammarco and Chang, reporting on 108 ankles with tibial nerve entrapment, found that patients with symptoms lasting less than 1 year had significantly better postoperative scores than did patients who had symptoms for more than 1 year before surgery. [22They did not observe an effect of trauma on the outcome of surgery, and they noted that improvement was predictable even when a space-occupying lesion was not identified at surgery.

In one study, revision tarsal tunnel surgery was performed on 44 patients (two bilaterally), including the following components [61:

  • Neurolysis of the tibial nerve in the tarsal tunnel and of the medial plantar, lateral plantar, and calcaneal nerves in their respective tunnels
  • Excision of the intertunnel septum
  • Neuroma resection as indicated

A painful tarsal tunnel scar and a painful heel were treated by resection of the distal saphenous nerve and resection of a calcaneal nerve branch, respectively.

Patient-satisfaction ratings in this study were 54% excellent, 24% good, 13% fair, and 9% poor. [61Prognostic indicators of poor results were coexisting lumbosacral disc disease and neuropathy. The authors noted that an approach related to resecting painful cutaneous nerves and neurolysis of all tibial nerve branches at the ankle may offer hope for relief of pain and recovery of sensation for the majority of patients in whom previous tarsal tunnel surgery has failed.

Common peroneal nerve entrapment

Surgical decompression of the nerve and excision of the offending lesion are indicated in cases of nerve compression due to external causes, such as those associated with intraneural or extraneural tumors or masses.

Löwenstein et al recommend early surgical treatment in cases involving intraneural ganglion cysts, in order to minimize neural invasion (which may cause irreversible axonal injury and foot drop). [62In cases in which severe paresis and muscle atrophy are present, surgical exploration may also be warranted, especially if electrodiagnostic evidence of active motor axonal degeneration is present.

In one of the largest studies of patients with idiopathic peroneal nerve entrapment, Fabre et al reported on 62 patients who were treated with operative decompression of the common peroneal nerve. [63The postoperative recovery of motor function was good in 87% of those who had sensory and motor involvement preoperatively. All seven patients who had peroneal nerve entrapment of known etiology also demonstrated postoperative improvement.

On the basis of these results, the authors recommended open decompression of the peroneal nerve between the third and fourth months if symptoms persist or recovery is incomplete, even if the patient has only sensory symptoms that have been substantiated by electrophysiologic studies. [63]

The procedure involves a curved incision about the lateral knee, following the course of the nerve. The nerve is found initially posteromedial to the biceps femoris. It is tracked distally to where it branches to the deep and superficial branches. The nerve is released fully by initially separating the lateral septum between the peroneus longus and soleus aponeurosis, retracting the peroneus longus medially, and fully dividing the superficial and deep portions of the fibrous arch. Any sites of entrapment or compression along this route should be released.

Nerve grafting may be warranted in severe cases in which the nerve is structurally damaged or severed.

Superficial peroneal nerve entrapment

Surgical decompression may be indicated in cases of superficial peroneal nerve entrapment that is refractory to nonoperative options. This can include release of the nerve at the lateral leg for surgical decompression with partial or full fasciotomy. Some authors have also advocated fasciectomy in select cases. Neurolysis generally is not indicated, because it has not been shown to improve outcome.

Styf and Morberg reported that 80% of their patients were free from symptoms or satisfied with the result after decompression of the superficial peroneal nerve. [64Three of 14 patients underwent local fasciectomy as well.

Styf reported on the use of fasciotomy and neurolysis to treat entrapment of the superficial peroneal nerve in 24 legs (21 patients). [39Nine patients were satisfied with the result, another six had improvement but were not satisfied because of residual limitation of athletic activity, three had unchanged conditions, and one had a worsened condition. Conduction velocity in the superficial peroneal nerve increased postoperatively, though the change was insignificant.

In five of the patients, the nerve had an anomalous course, and in 11, fascial defects were present over the lateral compartment. [39The author concluded that operative decompression of the superficial peroneal nerve produces cure or improvement in about 75% of cases but that it is less effective in athletes than in others.

Sridhara and Izzo reported complete symptomatic relief after surgical decompression. [65Johnston and Howell reported dramatically relieved pain after release and anterior transposition of the nerve in patients who had had neuralgia after inversion ankle sprain. [66]

The surgical procedure to release the superficial peroneal nerve at the anterolateral leg involves preoperative determination and marking of the location of maximum tenderness and, if present, lateral muscle herniation. The procedure is performed with magnifying loupes and a tourniquet. A 5-cm longitudinal incision is made over the anterolateral leg approximately at the junction of the middle third and the distal third to encompass the two points.

A significantly more distal point of tenderness suggests a more distal piercing of the intermediate dorsal cutaneous nerve through the fascia, in which case two separate incisions may be made. Blunt subcutaneous dissection is done, and the nerve is found emerging through the fascia. A local fasciotomy is performed, releasing the nerve proximally and distally until it is completely free. In the setting of chronic compartment syndrome, a complete fasciotomy may be considered; however, the ensuing peroneal muscle weakness may affect athletic performance.

In cases of painful neuromas or clearly abnormal nerves due to direct or indirect trauma to the nerve, surgical excision of the nerve can be performed at the site of neuroma. If several branches are involved, excision of the nerve at the anterolateral leg can be considered. Dellon and Aszmann reported excellent results in nine of 11 patients who underwent resection of the nerve and translocation of the proximal nerve stump into the muscles of the anterolateral compartment, combined with fasciotomy of the anterolateral compartment. [67]

In cases of superficial peroneal nerve entrapment associated with other conditions, such as ankle instability, treatment of the associated conditions should also be planned.

Deep peroneal nerve entrapment

Once symptoms of deep peroneal nerve entrapment are deemed refractory to nonoperative measures, surgical options may be considered. Such options include the following:

  • Surgical release of the deep peroneal nerve in primary and idiopathic cases
  • Excision of the nerve in cases of direct nerve injury due to previous surgery, in cases of direct trauma, or in revision cases

Surgical decompression of the nerve can provide immediate improvement of symptoms.

Dellon reported on surgical release of the deep peroneal nerve in 20 patients. [68At a mean follow-up of more than 2 years, excellent results were reported in 60% of patients, good results in 20% of patients, and no improvement in 20% of patients.

The surgical procedure can include part or all of a longitudinal straight or S-shaped incision on the dorsum of the foot, starting between the bases of the first and second metatarsals and extending proximally to the anterior ankle, depending on the predicted location of entrapment.

The deep fascia overlying the deep peroneal nerve and the dorsalis pedis artery is released, as is the inferior part of the extensor retinaculum; the superior part can be preserved to maintain the function of the extensor tendons. The deep peroneal nerve is followed proximally and distally to verify a full release. Nerves that appear to be normal in consistency and size can be released. [69]

It is important to treat other underlying causes of entrapment or stretch (eg, complete excision of underlying osteophytes during surgery). The decision to perform neurolysis as opposed to excision, transposition, or both is dependent on the severity of injury to the nerve.

Excision of the nerve is indicated in cases where the nerve is abnormal, as when it is directly manipulated during surgery or entrapped in scar tissue. Neuroma in continuity is best excised and allowed to retract into deep tissues, and transposition of the stump into muscle belly may be possible, depending on the level of excision. In a report describing excision of the superficial and deep peroneal nerves in the lateral leg, with translocation of the nerves into a muscle, Dellon and Aszmann obtained excellent results in nine of 11 patients. [67]

When entrapment of the deep peroneal nerve is caused by the extensor hallucis brevis, the muscle is hypertrophied and has thick fibrous bands that compress the nerve. Decompression of the nerve and excision of the muscle and fibrous band can lead to complete resolution of pain, but numbness may persist in the first webspace.

Interdigital neuritis

Surgical excision of the interdigital nerve and release of the intermetatarsal ligament with a dorsal or plantar approach results in a high percentage of successful results. The dorsal approach is recommended because of fewer potential complications and because it allows early weight bearing. Patients should be counseled preoperatively that varying degrees of postoperative numbness are commonly associated with resection of a Morton neuroma. Other surgical options include isolated intermetatarsal ligament release.

Most surgeons in the United States perform a primary surgical procedure via a dorsal approach. An incision approximately 3 cm long is centered in the relevant interspace, starting from the metatarsal head level and extending distally into the webspace. Blunt dissection into the webspace and placement of a lamina-style spreader reveals the intermetatarsal ligament. The proximal and distal aspects of the ligament are identified and released sharply.

An enlarged nerve may be identified readily beyond the ligament. Smaller nerves are more difficult to identify. In most cases, intertwining vessels require careful dissection and protection. The digital branches are identified and are sharply amputated distally. The nerve is then followed proximally, gently pulled distally, sharply amputated as far proximally as is visible, and allowed to retract into the deep soft tissues.

Mann and Reynolds reported retrospectively on a surgical excision of 76 Morton neuromas. [50Although 65% of patients still noted some local plantar tenderness to touch, 80% showed subjective improvement. Coughlin and Pinsonneault noted residual pain in either the involved interspace or the adjacent one, which is not uncommon. [70They also reported 85% good-to-excellent results and noted mild or major footwear restrictions in 70% of patients.

Dereymaeker et al reported on 32 feet treated with excision of a Morton neuroma via a dorsal incision. [71Of the 32, 25 had a macroscopically visible neuroma, and two had no evidence of a neuroma on histologic examination. After resection, 81% had a good or excellent result, and 6.5% had no improvement. After the operation, 60% of the patients benefited from the long-term use of adapted shoes or inner soles. At the final follow-up, only 30% of the patients were found to be unrestricted in their choice of shoes.

The plantar approach to primary resection of an intermetatarsal neuroma, advocated by some, provides more direct access to the nerve and is technically simpler; however, painful plantar scars, intractable plantar keratosis beneath an adjacent lesser metatarsal head, and wound drainage have been reported. Consequently, most surgeons reserve this approach for revision cases. In a study of 57 plantar procedures done via a plantar incision, 23% of subjects had indurated plantar keratosis after surgery, and only 7% had poor results. [63]

Potential complications of interdigital nerve excision, including development of a stump neuroma and digital numbness, have led some authors to recommend release of the transverse metatarsal ligament with or without epineurolysis. Gauthier, reporting on the release of 304 intermetatarsal ligaments with epineural neurolysis, stated that 83% of patients had rapid and stable improvement and that 15% showed improvement but nonetheless experienced some persistent pain. [72]

Others, such as Weinfeld and Myerson, have advocated this procedure without neurolysis and have reported good preliminary results. [73Mann and Reynolds cautioned against the use of this procedure except in the case of interdigital neuritis, noting reconstitution of the ligament in revision cases. [50]

Adjacent neuromas in the second and third interspace are not uncommon and should be investigated. Published reports of double neuromas are sparse. Benedetti et al reported simultaneous excision of two primary Morton neuromas in adjacent webspaces and noted significant pain relief in 84% of patients, but substantial numbness involving the third toe resulted. [74Thompson and Deland described 89 adjacent neurectomies and reported results similar to those achieved with single neurectomies. [75]

Hort and DeOrio described 23 patients with adjacent intermetatarsal nerve irritation who underwent excision of the more enlarged nerve in one space and release of the intermetatarsal ligament in the other space, [76an approach that allowed preservation of protective sensation. They reported 95% complete satisfaction, with no or only minimal activity limitation. Approximately 11% of patients had persistent pain with compression of the interspace where the nerve was released; none had pain in the interspace where the nerve was excised.

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Local Anesthetics

Class Summary

Treatment of iliohypogastric or ilioinguinal nerve entrapment may include local injection of an anesthetic.

Lidocaine (Xylocaine)

Lidocaine is an amide local anesthetic used in a 0.5-1% concentration in combination with bupivacaine (50:50 mixture). This agent inhibits depolarization of type C sensory neurons by blocking sodium channels.

Bupivacaine (Marcaine, Sensorcaine)

Bupivacaine 0.25% may be used in combination with lidocaine plus epinephrine (50:50 mixture). It decreases permeability to sodium ions in neuronal membranes. This results in the inhibition of depolarization, blocking the transmission of nerve impulses.

Anticonvulsants, Other

Class Summary

Some agents in this category have shown benefit in the treatment of neuropathic pain.

Pregabalin (Lyrica)

Pregabalin is a structural derivative of gamma-aminobutyric acid (GABA). Its mechanism of action is unknown. The drug binds with high affinity to the alpha2-delta site (a calcium channel subunit). In vitro, it reduces the calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function.

Gabapentin (Neurontin)

Gabapentin, a membrane stabilizer, is a structural analogue of the inhibitory neurotransmitter GABA, although, paradoxically, it is thought not to exert an effect on GABA receptors. It appears to exert its action via the alpha2delta1 and alpha2delta2 auxiliary subunits of voltage-gaited calcium channels.

Carbamazepine (Tegretol, Carbatrol, Epitol)

Carbamazepine has antineuralgic effects. It may depress the activity of the nucleus ventralis of the thalamus or may decrease synaptic transmission or summation of temporal stimulation, thus leading to neural discharge by limiting the influx of sodium ions across the cell membrane or through other unknown mechanisms. The target blood serum concentration range is 4-12 mg/L.

Antidepressants, TCAs

Class Summary

The analgesic properties of certain agents in this class may improve symptoms associated with neuropathic pain.


Amitriptyline is an analgesic for certain chronic and neuropathic pain. It blocks the reuptake of norepinephrine and serotonin, which increases their concentration in the central nervous system (CNS). Amitriptyline decreases pain by inhibiting spinal neurons involved in pain perception. This agent is highly anticholinergic. It is often discontinued because of somnolence and dry mouth. Cardiac arrhythmia, especially in overdose, has been described; monitoring the QTc interval after reaching the target level is advised. Up to 1 month may be needed to obtain clinical effects.

Clomipramine (Anafranil)

Clomipramine is a dibenzazepine compound belonging to the family of tricyclic antidepressants. The drug inhibits the membrane pump mechanism responsible for the uptake of norepinephrine and serotonin in adrenergic and serotonergic neurons.

Clomipramine affects serotonin uptake while it affects norepinephrine uptake when converted into its metabolite desmethylclomipramine. It is believed that these actions are responsible for its antidepressant activity.

Doxepin (Silenor)

Doxepin increases the concentration of serotonin and norepinephrine in the CNS by inhibiting their reuptake by the presynaptic neuronal membrane. It inhibits histamine and acetylcholine activity and has proven useful in the treatment of various forms of depression associated with chronic pain.

Nortriptyline (Pamelor)

Nortriptyline has demonstrated effectiveness in the treatment of chronic pain.

Desipramine (Norpramin)

This is the original TCA used for depression. These agents have been suggested to act by inhibiting reuptake of noradrenaline at synapses in central descending pain modulating pathways located in the brainstem and spinal cord.

Nonsteroidal Anti-Inflammatory Drugs

Class Summary

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase (COX) activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Ibuprofen (Motrin, Advil, Addaprin, Caldolor)

Ibuprofen is the drug of choice for patients with mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Naproxen sodium (Anaprox, Naprelan, Naprosyn, Anaprox)

This agent is used for the relief of mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease in prostaglandin synthesis.

Diclofenac (Voltaren, Cataflam XR, Zipsor, Cambia)

Diclofenac inhibits prostaglandin synthesis by decreasing COX activity, which, in turn, decreases formation of prostaglandin precursors.

Indomethacin (Indocin)

Indomethacin is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.


Ketoprofen is used for relief of mild to moderate pain and inflammation. Small dosages are indicated initially in small patients, elderly patients, and patients with renal or liver disease. Doses higher than 75 mg do not increase the therapeutic effects. Administer high doses with caution, and closely observe the patient's response.

Opioid Analgesics

Class Summary

Tramadol is a weak opioid and an inhibitor of serotonin and norepinephrine reuptake in the dorsal horn.

Tramadol (Ultram, Conzip)

Tramadol is an analgesic that probably acts over monoaminergic and opioid mechanisms. Its monoaminergic effect is shared with tricyclic antidepressants. Tolerance and dependence appear to be uncommon.

Analgesics, Topical

Class Summary

Analgesics may aid in decreasing the severity of pain.

Lidocaine anesthetic (Topicaine, Lido Patch, Lidoderm 5% patch)

Several studies support topical administration of lidocaine as treatment of postherpetic neuralgia. In a placebo-controlled study, lidocaine gel (5%) yielded significant relief in 23 patients studied. Lidocaine tape also decreases the severity of pain.

Capsaicin topical (Capzasin-P, Trixaicin, Zostrix)

Capsaicin is a natural chemical derived from plants of the Solanaceae family. By depleting and preventing reaccumulation of substance P in peripheral sensory neurons, capsaicin may render treated areas insensitive to pain. Substance P is thought to be a chemomediator of pain transmission from the periphery to the CNS.