Nerve entrapment syndromes of the lower extremity can involve the following nerves and branches thereof:
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 posterior 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 posterior tibial nerve in the fibro-osseous tunnel behind the medial malleolus, and it was considered rare.[1, 2, 3] In 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:
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 posterior 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,[6] interdigital neuroma, Morton metatarsalgia, or interdigital nerve compression—results from entrapment of a plantar interdigital nerve as it passes under the transverse metatarsal ligament.[7] It 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 Pain, Bursitis, and Electromyography (EMG).
NextThe 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.
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).
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.
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).[8] Probably 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.
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]
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.
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.
The posterior 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 posterior tibial muscle and the flexor digitorum longus; in the lower leg, it is between the flexor digitorum longus and the flexor hallucis longus.
The posterior 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.[10] Calcaneal branches, which have a highly variable anatomy, are present.
Most individuals (79%) have a single calcaneal nerve, usually arising from the posterior tibial nerve but sometimes arising from the lateral plantar nerve. About 21% have multiple calcaneal branches originating from the posterior 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 posterior 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 posterior 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.
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.[11] It 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).
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]
The deep peroneal nerve, the other branch of the common peroneal nerve, originates just distal to the fibular head,[14] entering 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.
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.
The iliohypogastric nerve is rarely injured in isolation. The most common causes of injury are surgical procedures,[15] including 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.
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.
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.[16] Latency of the genitofemoral nerve was found to be prolonged after inguinal hernia repair, possibly because of surgery-related injury.
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.[18] The 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).
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.
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]
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]
Although posterior 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 posterior 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 posterior 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.[2] Since 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.[22] Cimino 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.[24] Turan et al also found varicose veins to occur more commonly than other compressive etiologies did.[25] The enlarged vessels crossing the nerve are theorized to cause direct compression of the posterior 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.[5] They 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 posterior 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 posterior tibial nerve.[27] Trepman 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.
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.[30] Traumatic 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.
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 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.
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.[33] The 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.[34] These 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.[35] In 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.[36] They 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.
Clinical Presentation
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