eMedicine - Nerve Entrapment Syndromes of the Lower Extremity : Article by Minoo Hadjari Hollis

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Nerve Entrapment Syndromes of the Lower Extremity

Article Last Updated: Mar 17, 2008

Iliohypogastric nerve

The iliohypogastric nerve arises primarily from the ventral primary rami of L1 and occasionally with a twig from T12. This nerve has a pathway similar to the intercostal nerves in the thoracic region. The iliohypogastric nerve traverses the psoas major muscle to pierce its lateral border anterior to the quadratus lumborum muscle and posterior to the kidney to traverse the lateral abdominal wall. The nerve penetrates the transverse abdominal muscle near the iliac crest, coming between it and the internal oblique musculature. The nerve then supplies the lower fibers of the transverse abdominal muscle and the internal oblique and divides into the lateral and anterior cutaneous branches.

The anterior cutaneous branch continues anteriorly between the internal oblique and transverse abdominal muscle, then pierces the internal oblique 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 iliohypogastric nerve is rarely injured in isolation. The most common causes of injury are surgical procedures. These include transverse lower abdominal incisions, as in hysterectomies, or injuries from procedures such as inguinal herniorrhaphy and appendectomies. The injuries mainly 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 passing a suture around the nerve and incorporating it into the fascial repair, or 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. It may also occur during pregnancy due to the rapidly expanding abdomen in the third trimester. This is called the idiopathic iliohypogastric syndrome and is rare.

Symptoms include burning or lancinating pain immediately following the abdominal operation. The pain extends from the surgical incision laterally into the inguinal region and suprapubic region. Discomfort may occur immediately or up to several years after the procedure and may last for months to years. This discomfort is possibly because of the formation of scar tissue in the region. Occasionally, the pain may extend into the genitalia due to the 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.

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

Three major criteria are used to diagnose this nerve injury. The first is a history of surgical procedure in the lower abdominal area, although 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. Second, a definite area of hypo-esthesia or hyperesthesia should be identified in the region of supply of the iliohypogastric nerve. Third, 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 etiology should be sought for the discomfort. Alternate diagnoses include upper lumbar or lower thoracic nerve root pathology or discogenic etiology of the pain. If the iliohypogastric nerve is clearly identified as the source of pain and a favorable response is not obtained to local anesthetic injection, then surgical exploration and resection of the nerve should be considered. No reliable electrodiagnostic techniques are available to define the integrity of this nerve, although needle electromyography of the lower abdominal musculature may serve as an adjunct in the diagnosis.

Treatment includes the local injection of an anesthetic (as noted above), oral medications, or physical therapy. The oral medications may include antiseizure medications, such as gabapentin (Neurontin), carbamazepine (Tegretol), or lamotrigine (Lamictal), as well as nonsteroidal anti-inflammatory drugs (NSAIDs), tricyclic antidepressant medications (amitriptyline [Elavil], doxepin), capsaicin cream, topical lidocaine (Lidoderm patches), or tramadol (Ultram). With physical therapy, cryotherapy or a transcutaneous electrical nerve stimulation (TENS) unit may be tried. When conservative measures are not successful, surgical excision may result in relief of pain with few potential complications. Potential complications include possible neurolysis of the nerve in refractory cases. Surgical excision is more invasive but has had good outcomes in several reports. Krahenbuhl and colleagues reported an endoscopic approach.¹

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 nerve pierces the transversus abdominis and internal oblique muscles (providing neural branches to these) and sending neural branches to the iliohypogastric nerve. The nerve 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 the male or the mons pubis and labia majora in the female.

Causes of injury 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. Nerve injury can also occur idiopathically. The prevalence of injury with surgery has declined due 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.

Symptoms could include hyperesthesia or hypo-esthesia 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 with the surgical procedure.

Pain and tenderness may be present with application of pressure where the nerve exits the inguinal canal in up to 75% of patients. Sensory impairment is common in the above-noted distribution of the nerve supply. Symptoms usually increase with hip extension (patients walk with a trunk in a forward-flexed posture). Pain may also be reproduced with palpation medial to the anterosuperior iliac spine (ASIS).

The diagnosis can be made on the basis of local infiltration of anesthetic with or without steroid and should result in relief within 10 minutes. Unfortunately, no electrodiagnostic techniques are available to readily test this nerve. Abdominal needle electromyography may be helpful in determining the severity of nerve injury, but electromyography is not sensitive or specific.

Treatment includes local injection of an anesthetic, physical therapy, or oral medications. Types of medications may include antiseizure medications, such as gabapentin (Neurontin), carbamazepine (Tegretol), or lamotrigine (Lamictal), as well as NSAIDs, tricyclic antidepressant medications (amitriptyline [Elavil], doxepin), capsaicin cream, topical lidocaine (Lidoderm patches), or tramadol (Ultram). Ice or possibly a TENS unit may be used with physical therapy. When conservative measures are not successful, surgical excision may result in relief of pain with few potential complications.

Genitofemoral nerve

The genitofemoral nerve or its branches (genital or femoral branches) can be entrapped throughout its course. Nerve injury occurs most commonly as a complication of lower abdominal surgeries.

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

The genital branch continues along the psoas major to the deep inguinal ring and enters the inguinal canal. It supplies the cremaster muscle, spermatic cord, scrotum, and adjacent thigh in males. 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 lies lateral to the genital 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 muscle 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.

Nerve injury may result from hernia repair, appendectomy, biopsies, and cesarean delivery. Injury may also occur due to 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.

Injury to the femoral branch causes hypo-esthesia over the anterior thigh below the inguinal ligament, which is how it is distinguished from the iliohypogastric and 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, prolonged walking, or even with light touch. Differential diagnoses include injury to the ilioinguinal and genitofemoral nerves as well as L1-2 radiculopathies. Some anatomic overlap may exist with the supply of the ilioinguinal and genitofemoral nerves, which makes the diagnosis somewhat difficult to establish.

Unfortunately, no reliable electrodiagnostic test exists that can be used for diagnosis of injury to this nerve. Oh has discussed a side-to-side sensory comparison study, but this test is technically difficult to perform.² Diagnosis is typically made using anesthetic nerve blocks. By injecting the ilioinguinal and iliohypogastric nerves anteriorly, the pain or abnormal sensation should remain unchanged. The lumbar roots for L1 and L2 are then blocked, which should result in relief and should also help in determining the diagnosis, aiding in the prevention of unnecessary surgical exploration of an uninjured nerve.

The above-mentioned blocks are diagnostic and therapeutic. Avoidance of aggravating activities should be emphasized. Treatment also may consist of antiseizure medications, such as gabapentin (Neurontin), carbamazepine (Tegretol), or lamotrigine (Lamictal), as well as tricyclic antidepressant medications (amitriptyline [Elavil], doxepin). Other medications include capsaicin cream, topical lidocaine (Lidoderm patches), NSAIDs, or, possibly, tramadol (Ultram). A trial with a TENS unit may also be beneficial.

If conservative treatment fails, surgical excision of the nerve is the treatment of choice. Some authors describe a transabdominal approach to the nerve (Magee and Lyon) with satisfactory results.^{3, 4} The complications of this procedure include hypo-esthesia of the scrotum or labium majus and of the skin over the femoral triangle, as well as loss of the cremasteric reflex. It will usually not result in notable morbidity. According to Harms and colleagues, an extraperitoneal approach should result in fewer operative complications.⁵

Lateral femoral cutaneous nerve

Injury or entrapment of the lateral femoral cutaneous nerve is also known as meralgia paresthetica. It is derived from the Greek word meros, meaning thigh, and algo, meaning pain. It is a syndrome of paresthesia and pain in the lateral and anterolateral thigh. This syndrome is most commonly seen in individuals aged 20-60 years, but it can occur in people of all ages.

This 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 ASIS. The nerve travels posterior to the inguinal ligament and superior to the sartorius muscle at the iliac crest region and divides into anterior and posterior branches. The anterior branch comes off 10 cm distal to the inguinal ligament on line with the ASIS and supplies cutaneous sensation to the lateral thigh, including just proximal to the patella. It then communicates with cutaneous branches of the femoral nerve and saphenous nerve to form the patellar plexus. The posterior branch pierces the fascia lata posterior and lateral and divides into multiple, small branches that supply the skin from the greater trochanter to the midthigh.

Entrapment 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 would include pregnancy, abdominal tumors, uterine fibroids, diverticulitis, or appendicitis. Injury has been described in cases of abdominal aortic aneurism. Examples of extrapelvic causes include trauma to the region of the ASIS (eg, a seatbelt from a motor vehicle accident), tight garments, belts, girdles, or stretch 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 clinical setting of a polyneuropathy.

Symptoms include anterior and lateral thigh burning, tingling, and/or numbness, that increase with standing, walking, or hip extension. Symptoms may also increase with lying prone. Symptoms usually are unilateral but may be bilateral in rare cases. The symptoms usually improve with sitting unless compressive forces, such as tight belts or garments, remain.

Physical examination findings may be completely normal. Findings may include hyperesthesia over the lateral thigh (usually in a smaller area than the symptoms). Pain can be produced by pressure medial to the ASIS. A positive Tinel sign may be present over the ASIS or inguinal ligament.

Diagnosis of this entrapment may again be based on an injection of local anesthetic near the inguinal ligament or ASIS. Spontaneous recovery is usually expected. 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 sensory fibers) or orthodromic (conduction with the direction of the nerves) methods. The antidromic study is usually easier, although it may be absent bilaterally on occasion. The response is small and difficult to obtain in obese patients.

A needle stimulation electrode may need to be used. The sensory response is absent in 71% of patients with meralgia paresthetica and is prolonged in 24% of patients with this condition. Electromyographic test results with 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) that is required to stimulate a nerve that lies under adipose tissue.

Treatment may include the injection of local anesthetic agents, as previously noted. A steroid can also be used to prolong the effects and reduce the inflammation. Oral medications, such as NSAIDs, antiseizure medications (gabapentin [Neurontin]), tricyclic antidepressants, capsaicin cream, topical lidocaine, and tramadol can be used. One must also instruct patients on ways to prevent 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. Surgical exploration may be required if the above treatment options are not helpful. This includes transection of the nerve or decompression with or without neurolysis. Anatomical variations of the nerve and neuromas can occur and lead to recurrence.

Femoral nerve

The femoral nerve arises from the posterior divisions of the ventral primary rami of L2, L3, and L4 within the psoas major muscle. These nerves join to form the largest branch of the lumbar plexus. The nerve emerges from the lateral border of the psoas muscle and courses inferiorly in the intermuscular groove between this muscle and the iliacus muscle. It then passes under the inguinal ligament lateral to the femoral artery and vein. It then divides into multiple branches within the femoral triangle. It divides into sensory branches in the proximal thigh to innervate the upper and anterior thigh and muscular branches to the quadriceps muscle. One of the major branches is the lateral femoral cutaneous nerve, as previously discussed.

It also divides into the medial femoral cutaneous nerve, which originates just distal to the inguinal ligament to descend on the sartorius muscle, and penetrates the deep fascia about the distal third of the thigh to split into 2 terminal nerve branches. One branch 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 muscle and pierces the deep fascia about the knee to also communicate with the saphenous nerve in providing cutaneous sensation to the patellar region. The best-known cutaneous nerve arising from the femoral nerve is the saphenous nerve (which is discussed below).

The femoral nerve can have several entrapment locations or causes of injury, including intrapelvic injury or 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 due to compression.

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 femoral nerve does not have significant protection in this area.

Heat developed by methylmethacrylate in 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 compartment-like compression from a hemorrhage (caused by a hemorrhagic disorder or by anticoagulant use).

The symptoms of a femoral neuropathy may include pain in the inguinal region that is partially relieved by flexion and external rotation of the hip, and 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 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 due to the saphenous nerve supply to the patella.

On examination, patients may present with weak hip flexion, 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).

Electrodiagnostic testing is typically performed for diagnosis but is also important to determine the extent of the injury and the prognosis of 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 saphenous nerve sensory study may also be performed (continuation of the sensory portion of the femoral nerve over the medial aspect of the leg and ankle). 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 determine the presence of root or plexus injury versus peripheral nerve injury. Needle electromyography is usually the most revealing portion of the electrodiagnostic test. The examiner must look not only for denervation potentials but also for any active motor units.

Treatment may be based on symptoms only, or it may be more invasive and include surgical intervention, depending upon the severity of the injury. 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 has been reported in up to 70% of patients with a femoral neuropathy and may take up to a year. The recovery may even occur in the setting of a fairly severe injury as determined through electrodiagnostic testing and by physical examination. Patients with severe axonal loss have some recovery of function, although it is usually incomplete.

Saphenous nerve

The saphenous nerve, the terminal branch of the femoral nerve, is the femoral nerve's longest branch. 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. It branches from the femoral nerve just distal to the inguinal ligament and courses with the superficial femoral artery to enter Hunter 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 longus muscles medially.

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

The saphenous nerve can become entrapped where it pierces the connective tissue at the roof of the Hunter canal, resulting in inflammation from a sharp angulation of the nerve through the structure and the dynamic forces of the muscles in this region. This results in contraction and relaxation of the fibrous tissue that impinges the nerve. The nerve also can be injured as a result of an improperly protected knee or leg support during surgery. It may be injured due to neurilemoma, entrapment by femoral vessels, direct trauma, pes anserine bursitis, varicose vein operations, and medial knee arthrotomies and meniscus repairs.

Symptoms of entrapment may include a deep aching sensation in the thigh, knee pain, and possibly paresthesias in the cutaneous distribution of the saphenous distribution in the leg and foot. The infrapatellar branch may also become entrapped on its own. This is because it passes through a separate foramen in the sartorius muscle tendon, or it may course horizontally across the prominence of the medial femoral epicondyle, where it may be exposed to trauma. Patients report paresthesias and numbness about the infrapatellar region that is worse with flexion of the knee or compression from garments and braces.

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

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 the 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 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, although this test may be cumbersome and time-consuming.

No findings should be present on needle examination of the muscle during electromyography. Needle examination should include the quadriceps muscle 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.

Entrapment in the Hunter canal is usually treated conservatively with an injection of anesthetic (with or without corticosteroid) at the point of maximal tenderness (usually 10 cm proximal to the medial femoral condyle). The injection may need to be repeated periodically. Avoiding aggravating activities and using proper body mechanics will also be helpful. If this approach fails, surgical decompression may be needed. In patients who have had a direct blow to the medial knee who have persistent medial knee pain despite conservative trials for treatment, a neurectomy or neurolysis of the infrapatellar branch may be helpful.

See also the following related eMedicine topics:
Meralgia Paresthetica [Neurology]
Meralgia Paresthetica [Orthopedic Surgery]
Meralgia Paresthetica [Physical Medicine and Rehabilitation]
Nerve Entrapment Syndromes
Radial Nerve Entrapment
Ulnar Nerve Entrapment

Anterior branches of the anterior primary rami of L2, L3, and L4 fuse to form this nerve. The major contribution is from L3, and the least amount of contribution is typically from L2. The rami fuse in the substance of the psoas muscle 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 prior to entering the thigh, the nerve divides into an anterior and a posterior branch. The anterior branch travels superficial to the internal obturator muscle but deep to the pectineus and adductor longus muscles and then travels superficial to the adductor brevis muscle.

The nerve terminates at the distal aspect of the adductor longus by forming a subsartorial plexus; it forms the 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 muscles. Rarely, a terminal cutaneous branch may emerge from the inferior aspect of the adductor longus muscle and follow the medial border of the sartorius muscle to the medial knee region, where it supplies the skin of the medial and distal thigh region.

The obturator nerve is rarely injured in isolation. However, injury can occur with pelvic trauma and associated fractures, as a result of compression of the nerve between the head of the fetus and the bony structures of the pelvis during delivery, 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 with total hip arthroplasties. 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 muscle, due to an inflammatory process.

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

With severe injuries, 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 cutaneous nerve of the thigh, and inguinal hernias.

No routine conduction studies are available with which to evaluate the integrity of the 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. A nerve block may be helpful but is usually not necessary for diagnosis.

For anterior nerve entrapment, treatment may consist of electrical stimulation of the adductor and hip flexor muscles, stretching, and massage. These modalities, however, have typically not been successful in resolving this condition if it is not recognized early. For athletes with obturator neuropathy, surgery is the preferred treatment when clinical features of obturator neuropathy and denervation on electromyography are observed. The surgery involves dividing the fascia over the pectineus and the adductor longus muscles and dissecting the space between the 2 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 loosely closed.

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 muscle.⁶ It travels along the lateral aspect of the distal thigh beneath the cover of the long and short heads of the biceps femoris muscle to the region of the fibular head. Proximal to the fibular head, the common peroneal nerve gives off 2 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 muscle. This opening can be quite tough and result in the nerve angulating through it at an acute angle. Also, significant fibrous connective tissue secures the nerve to this proximal portion of the fibula, acting to potentially compromise the nerve.

Distal to this fibular tunnel, the common peroneal nerve divides into the superficial and deep peroneal nerves. The superficial peroneal nerve provides innervation to the peroneus longus and brevis muscles and then travels down the leg to pierce an opening in the deep fascia at about the distal third of the anterior leg. This superficial peroneal nerve splits into the medial and lateral terminal sensory branches to pass anterior to the ankle and innervate most of the dorsum of the foot, except for the region that lies between the first and second toes.

The deep peroneal nerve descends along the leg between the tibialis anterior (TA) and extensor hallucis longus (EHL) muscles, innervating those muscles as well as supplying the extensor digitorum longus (EDL) and peroneus tertius muscles. Please see Superficial Peroneal Nerve Entrapment and Deep Peroneal Nerve Entrapment for further anatomic detail regarding these nerve branches.

Peroneal nerve injuries are the most common peripheral nerve injuries of the lower limb to result when multiple traumatic injuries, such as those suffered in motor vehicle accidents, are incurred. 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, femur 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 about 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.⁷ However, in a study of 146 cases, Piton and colleagues noted 55 cases due to idiopathic causes, 16 due to external compression, 59 due to various traumatic causes, and 9 due to intraneural and extraneural tumors.⁸ Traumatic causes can include wounds and contusions, direct fractures involving the lateral knee, and direct lacerations or postsurgical entrapment in suture hardware.

Common peroneal nerve injuries at the region of the fibular head include ankle sprains with associated proximal fibula 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.⁹

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 muscles of the legs of athletes has also been seen. Patients typically present with exercise-related leg pain with or without associated dermatomal numbness. Co-existing 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), as 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 muscle 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 wrists resting on the fibular head during birthing. The nerve may also be injured during childbirth in the squatting position.

Other less common causes include lower-limb lengthening procedures, anorexia nervosa, and paraneoplastic syndromes. Also, peroneal nerve mononeuropathies can occur in hyperthyroidism, diabetes mellitus, vasculitic disorders, and leprosy. Many times, an underlying etiology remains unclear, and the condition is termed idiopathic.

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. The loss of sensation in the cutaneous distribution of the superficial and deep peroneal nerves may be noted, but the ankle dorsiflexion weakness is often of most concern to the patient.

Pain is not universal with common peroneal nerve injuries, and if present, it is often related to the specific cause of the common peroneal nerve compromise. For example, a nerve compromise secondary to traumatic injury from blunt trauma will likely result in pain secondary to soft-tissue swelling and inflammation, while 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.

Observation of the patient's gait is useful in diagnosing ankle dorsiflexion weakness. The patient 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, as the ankle dorsiflexors cannot provide a controlled descent of the foot toward the floor. The patient might also stumble when walking, secondary to 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 (EDB) muscle being most profoundly affected. Ankle and toe dorsiflexion can be significantly affected. Dorsiflexion is best tested by having the patient place the ankle in the neutral position and then dorsiflex the foot and invert it to optimally test the TA muscle. Often, ankle eversion is normal, as patients can have relative sparing of these muscles. 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 is often spared.

The history and physical examination are the most helpful initial clinical tools in determining a high suspicion for a common peroneal nerve injury.

Plain radiographs may be helpful in excluding underlying traumatic injuries, such as a proximal fibular head fracture or osseous tumors, or in assessing the severity of angular deformities about the knee. Computed tomography (CT) scans and magnetic resonance imaging (MRI) are helpful in finding a compressive lesion along the course of the 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. Nerve biopsy, although largely unnecessary, may confirm the disorder.

The 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 muscle, the evaluation of which is critical in determining whether a lesion is proximal to the knee and whether it involves the sciatic nerve, lumbosacral plexus, or nerve roots. In patients with exercise-induced symptoms, electrodiagnostic tests should be performed before and after exercise. Electrodiagnostic studies include the following:

Initial nonoperative treatment 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 in which 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 tricyclic antidepressants (amitriptyline) or neuroleptic medications, such as gabapentin and carbamazepine.

The use of 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, such 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 neuropraxia.

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 and colleagues recommend early surgical treatment in cases involving intraneural ganglion cysts, in order to minimize neural invasion (which may cause irreversible axonal injury and footdrop).¹⁰ In 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 and co-authors reported on 62 patients who were treated with operative decompression of the common peroneal nerve.¹¹ The postoperative recovery of motor function was good in 87% of those who had sensory and motor involvement preoperatively. All 7 patients who had peroneal nerve entrapment of known etiology also demonstrated postoperative improvement. On the basis of their results, the authors recommend 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.

The procedure involves a curved incision about the lateral knee, following the course of the nerve. The nerve is initially found posteromedial to the biceps femoris. It is tracked distally to where it branches to the deep and superficial branches. The nerve is fully released by initially separating the lateral septum between the peroneus longus and soleus aponeurosis, retracting the peroneus longus muscle 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.

Tarsal tunnel syndrome is the entrapment of the posterior tibial nerve or one of its branches. This entrapment typically occurs within or distal to the tarsal canal, resulting in pain and/or sensory disturbance on the plantar aspect of the foot. Kopell and Thompson first reported entrapment of the posterior tibial nerve in 1960.¹² In 1962, Keck and Lam independently used the term tarsal tunnel.^{13, 14} Historically, tarsal tunnel syndrome was defined as the entrapment of the posterior tibial nerve in the fibro-osseous tunnel behind the medial malleolus, and the condition was considered to be rare. In time, however, the lateral plantar nerve and its branches were noted to be a more common site of entrapment. Patients typically present with intractable heel pain.

Tarsal tunnel syndrome is the most common entrapment neuropathy in the foot and ankle area. To differentiate the location of entrapment, some authors have used the term proximal tarsal tunnel syndrome to define entrapment of the posterior tibial nerve in the fibro-osseous tunnel behind the medial malleolus, and the term distal tarsal tunnel syndrome to denote entrapment of the distal branches, that is, 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. However, the term tarsal tunnel syndrome is often used to define all entrapments of the posterior tibial nerve or its branches starting from posterior to the medial malleolus and extending distally.

A slight female predominance has been reported in some studies, and the range of patients' ages has been reported to be 14-80 years. This condition is common in nonathletes, although Baxter initially noted it in long-distance runners.¹⁵

The posterior tibial nerve (L4-S3) is a branch of the sciatic nerve. After entering the lower leg between the 2 heads of the gastrocnemius, the nerve is deep to the soleus muscle in the deep posterior compartment of the leg. The tibial nerve lies between the posterior tibial muscle and the FDL muscle in the upper leg; in the lower leg, it is between the FDL and the flexor hallucis longus. It then travels behind the medial malleolus, the proximal tarsal tunnel, where it divides to its terminal branches, the medial and lateral plantar nerves, behind the medial malleolus. Havel and colleagues 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 midcalcaneus.¹⁶ 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, lateral plantar nerve, or medial plantar nerve, or from a combination of these. The calcaneal branches travel over the abductor hallucis muscle 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 closely attached to the sheaths of the posterior tibial, FDL, and flexor hallucis tendons.

Typically, a fibrous septum courses between the calcaneus and the deep fascia of the abductor hallucis muscle 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 and then continues deep to the flexor digitorum brevis muscle. Although somewhat variable, it has several branches. It typically provides a sensory branch to the medial calcaneal tuberosity, motor branches to the flexor digitorum brevis muscle, 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 muscle.

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 3.5 digits. The nerve provides motor branches to the abductor hallucis, flexor digitorum brevis, and flexor hallucis brevis, as well as to the first lumbrical.

Although tibial nerve entrapment can be seen anywhere along the course of the nerve, the most common location is distal to the ankle. Entrapments above the ankle have been reported in the popliteal fossa, where the nerve can be compressed by the tendinous arch of origin of the soleus muscle, 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 because of intrinsic neural abnormalities or can result from external compression. External compression etiologies reported in the literature have included fibrosis, neurilemomas, ganglion cysts, lipomas, osteochondromas, varicosities, other benign and malignant tumors, tight tarsal canal, hypertrophic abductor hallucis, 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 in patients with long-standing diabetes mellitus. Wieman and Patel reported on 26 patients with painful diabetic neuropathy who underwent tarsal tunnel decompression, with pain improvement or relief in 24 (92%) of these patients within 1 month after surgery.¹⁷

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 are reported as well.

In the original case report and description of the condition in a patient with bilateral symptoms, Keck found tortuous posterior tibial veins surrounding the nerve, which he describes as resembling a varicocele.¹³ Since then, one of the most commonly encountered and reported causes of tarsal tunnel syndrome has been varicose veins.

Sammarco and Chang found that the most common surgical findings in 62 tarsal tunnel releases included arterial vascular leashes and varicosities, which cause indentation and scarring about the nerve.¹⁸ Cimino found that varicosities are the third most common cause of tarsal tunnel syndrome, as reported in the literature, and that idiopathic and traumatic causes are the first and second most common.¹⁹ Gould and Alvarez reported a case in which surgery revealed varicosities overlying the medial and lateral plantar nerves at their origin.²⁰ Turan and colleagues also noted varicose veins more commonly than other compressive etiologies.²¹ 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 the entrapment of the first branch of the lateral plantar nerve in the athlete.¹⁵ They proposed that entrapment results from the stretching and tethering of the plantar nerves, which are encased in the abductor hallucis deep fascial leashes, and from the hypertrophy of the small foot muscles, as well as from the increased forces in the hindfoot in the running athlete that create additional microtrauma to the runner's medial heel structures. They also noted that most of their patients with sports-related injuries had a normally arched or cavus-type foot.

Several authors have also reported increased valgus deformity of the foot to be a predisposing cause of chronic stretch injury to the posterior tibial nerve. Budak and co-authors 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.²² Labib and colleagues reported on 14 patients who underwent surgical treatment for what they termed the heel pain triad.²³ The triad is combination of plantar fasciitis, posterior tibial tendon dysfunction, and tarsal tunnel syndrome. They 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. Trepman and co-authors reported increased pressure in the tarsal tunnel with the foot and ankle in full eversion or full inversion.²⁴

Entrapment of the first branch of the lateral plantar nerve beneath the deep fascia of the abductor hallucis muscle and/or beneath the medial edge of the quadratus plantae fascia are 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 has been most commonly seen in athletes; in 1978, Rask called it jogger's foot. It is theorized 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.

Patients with proximal tarsal tunnel 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 present with insidious onset. Most patients have unilateral symptoms. Occasionally, patients may report proximal radiation of pain to the medial leg. Prolonged standing and walking usually exacerbate the symptoms, and rest improves symptoms. Many patients also present with night pain that is improved with massage or walking. Patients may note pain when the ankle is placed in extreme dorsiflexion secondary to nerve tension.

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 their symptoms started exclusively when they were bearing weight. With time, the symptoms usually increase and eventually occur when the patient is seated; occasionally, they occur 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 1 place may be an aggravating factor. Most patients continue to have pain or burning ("after pain" or "after burn") for 30 minutes to several hours after they are off their feet.

Tarsal tunnel syndrome is commonly seen in individuals who are in their fifth and sixth decades of life, and it is more common in women than in men. Correlation with the patient's weight has not been consistently found. 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.

Patients with medial plantar nerve entrapment usually present with pain in the medial aspect of the arch. They may have radiation of their pain to the medial toes and to the ankle. As with entrapment of the lateral plantar pain, it is worse with weight bearing. Occasionally, orthotics use may be correlated with the onset of the symptoms.

Inspection of the patient while the patient 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. The patient may report an increase in pain with dorsiflexion and eversion or inversion of the foot; Trepman and colleagues have shown these positions to increase the tarsal compartment pressure.²⁴ Motor examination should include asking the patient to spread his or her toes so that an assessment can be made of the abductor digiti minimi or abductor hallucis and abductor digiti minimi muscles. Hypertrophy of the abductor hallucis muscle or an accessory muscle may also present, with fullness in the longitudinal arch.

Patients with proximal tarsal tunnel syndrome may 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 posterior tibial nerve. Occasionally, nerve percussion causes symptoms and pain to radiate proximally to the nerve course. This is known as the 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.²⁵

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 muscle. Many patients have tenderness along the entire posterior 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 to look for 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. Numbness and/or a Tinel sign over this area may only be present after prolonged weight-bearing exercise. Stretching of the nerve as a result of eversion of the foot or of standing on the toes may also reproduce or exacerbate symptoms.

The diagnosis of tarsal tunnel syndrome (proximal and distal) is primarily made based on a detailed history and physical examination. Plain radiographs should probably be obtained to exclude extrinsic factors, such as exostoses, malunions, or osteochondromas that cause direct nerve compression. In patients with posttraumatic symptoms, further investigation (eg, with CT scanning or MRI) are helpful in identifying occult sources of pain, such as medial talar process fractures, medial malleolus stress fractures, and space-occupying lesions. Further screening studies, such as hematologic workup for arthritides, diabetes, alcoholism, and thyroid dysfunction, are indicated in cases of associated inflammation and in patients with symptoms of peripheral neuropathy.

Electrodiagnostic tests are indicated in refractory cases or in cases in which the diagnosis is uncertain. A complete electromyography 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 the electromyography examination to include motor latencies, particularly to the abductor digiti minimi and abductor hallucis muscles, when tarsal tunnel syndrome is suspected.

Kaplan and Kernahan reported that reduced amplitude and increased duration of the motor response were more sensitive indicators of the presence of tarsal tunnel syndrome than is the distal motor latency.²⁶ Sensory action potentials may be affected in earlier stages than are motor fibers; therefore, changes may also be identified prior to any motor abnormalities. This is due to the fact that sensory fibers are more susceptible to injury. In addition, Kaplan and Kernahan believed that the lateral plantar branch of the posterior tibial nerve is probably affected earlier than is the nerve's medial plantar branch. The sensory studies are therefore considered to be the most sensitive studies for tibial nerve entrapment.

Galardi and colleagues reported that, after stimulation of the plantar nerves, the accuracy of the SNAP and mixed-nerve action potential are almost the same. SNAPs were more sensitive and less specific, and mixed-nerve action potentials were less sensitive and more specific. They concluded that the co-existence of mixed-nerve and SNAP abnormalities, especially if asymmetric, is highly indicative of tarsal tunnel syndrome. The mixed-response test is technically much easier to perform and better tolerated by many patients.

Approximately 90% of patients with tarsal tunnel syndrome have abnormal findings on electromyography and 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).²⁷ In such cases, simultaneous treatment of both problems may be indicated.

Treatment 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 edema and varicosity control. Medical treatment of underlying systemic conditions is helpful in the indicated situation. The use of antineuritic medication, such as gabapentin and occasionally tricyclic antidepressants, has also been shown to improve 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, accommodative orthotics with a relief area in the anterior heel pad (ie, under the posterior 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 weight-bearing traction on the nerve.

Surgical release is indicated for refractory cases and for most cases with space-occupying lesions. The location of the release is partially dependent on the location of entrapment. Most cases, however, require a full release of the posterior 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 posterior 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 muscle. 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 posterior 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 closely watched for. A large number of vessels are routinely encountered, and some crossing veins may need to be ligated. Ensuring full release of the lateral plantar nerve and its first branch is important. 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 partially dictated by the arch height, and a full release may be indicated in patients with a cavus foot, while minimal release could be considered in patients with flatfoot. Retraction of the abductor hallucis and the flexor digitorum brevis muscle 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 is necessary for optimum visualization. It is important to minimize handling of the nerve. Often, large varicosities are present that should be considered as part of the underlying compressive etiology. Care should be taken to avoid injury to these large vessels, because such damage significantly compromises visualization and can cause intra-operative and postoperative bleeding, as well as postoperative scarring. The medial plantar nerve is fully released. The tourniquet is released prior to closure to ensure that no major bleeding occurs.

The plantar skin incision is re-approximated without the use of subcutaneous sutures. Re-approximating 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 non–weight-bearing status for 4-6 weeks. In patients with lesser releases of the plantar fascia, weight bearing 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 tarsal tunnel syndrome, including those with distal entrapment of the nerve branches (which is 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.

Baxter and Thigpen reported on 34 heels that underwent surgery in patients with recalcitrant heel pain.¹⁵ They performed a full release of the lateral plantar nerve and its branches with minimal or no plantar fascia release. The 2 most common areas of compression were noted at the sharp fascial edge of the abductor hallucis muscle 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. They reported that 32 had good results and 2 had poor results. Most patients could detect improvement during the first or second postoperative day. Anti-inflammatory medication and orthosis use were continued postoperatively.

Watson and colleagues reported good-to-excellent results in 84% of patients who undergo distal tarsal tunnel release and partial plantar fasciotomy.²⁸ Bailie and Kelikian reported that 84% of their patients in the noncompensation group were very or moderately satisfied with the outcome.²⁹ They also reported better satisfaction in patients with nontraumatic etiology than in others. Sammarco and Chang subsequently reported on 108 ankles with tarsal tunnel syndrome.¹⁸ They 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. They did not observe an effect of trauma on the outcome of surgery and reported that improvement was predictable even when a space-occupying lesion was not identified at surgery.

Tarsal tunnel syndrome is primarily diagnosed on the basis of the patient's history and physical examination. Electrodiagnostic studies support the diagnosis in about 80% of cases. Compression of the branches of the posterior tibial nerve is a common cause of refractory heel pain and the most common compression neuropathy seen in the foot and ankle region. Nonoperative management of compression of the posterior tibial nerve involves relief of the source of external compression (if any), the use of medication, and the correction of weight-bearing deformities. Surgical release in patients with proximal or distal entrapment has an 80-90% likelihood of improving or resolving the symptoms.

The superficial peroneal nerve travels in the lateral compartment and supplies the peroneus longus and brevis muscles. In most individuals 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, the superficial peroneal nerve pierces the deep fascia and emerges into the subcutaneous fat.³⁰ An average of 4-6 cm proximal to the ankle joint, it 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 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 at approximately one third of the 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 EDB in some patients.

Local trauma or compression is the most common underlying cause of entrapment of the superficial peroneal nerve. Repetitive ankle sprains or the use over many years of certain positions, such as prolonged kneeling and 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 following an inversion ankle sprain has been reported.

This nerve is also at risk for direct injury by any procedure about the anterior ankle, including 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 entrapment are commonly due to anatomical 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.

Although 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. The pain can be chronic, present for several years, and be associated with other foot and ankle symptoms, or the pain can be acute and be associated with recent trauma or with surgery about the ankle. The anterolateral arthroscopy portal, specifically, puts this nerve at risk for direct or stretch injury, as do noninvasive traction methods with straps over the dorsum of the foot. About one quarter of patients have a history of previous or recurrent ankle sprain or trauma.

Typically, symptoms increase with activity, such as running, walking, or squatting; rest or the avoidance of a specific activity often relieves the symptoms. 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, such as crossing the leg over the opposite thigh, can induce symptoms, as can tight clothing, such as sock elastic over the lateral leg. Pain may occasionally occur at night. Occasionally, patients report a bulging mass in the leg.

Examination should include the entire course of the nerve, starting from the lower back and extending through the sciatic notch, proximal fibula, and lateral leg, where a muscle bulge due to a facial 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 cause a positive result on the Tinel test, 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.

In competitive athletes who have symptoms suggestive of exertional compartment syndrome, Styf describes 3 provocative tests for nerve compression at rest and again at rest but after exercise.³¹ In the first test, pressure is applied over the anterior intermuscular septum while the patient actively dorsiflexes the ankle. In the second test, the foot is passively plantarflexed and inverted at the ankle. In the third test, 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)/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.

Although rare, plain radiographs of the leg may reveal bony abnormalities that may contribute or be the cause of entrapment. In cases of suspected proximal entrapment, knee radiographs may show abnormalities of the proximal fibula, such as exostoses, osteochondromas, and fracture callus. If necessary, a CT scan can provide more detailed information on the bony anatomy of the area, and an ultrasonogram can help to localize cystic masses that cause impingement of the nerve.

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

Injection of the nerve with lidocaine or Marcaine 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.

The value of electrodiagnostic studies varies in the literature. Although in many cases findings from electrodiagnostic tests are normal because these dynamic syndromes frequently improve or resolve at rest, these tests may reveal an unrecordable evoked response or a prolonged distal latency of a segment of the nerve and help to better define the zone of compression. They also help in the evaluation of concomitant radiculopathy or peripheral neuropathy.

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

Nerve Entrapment Syndromes of the Lower Extremity

AUTHOR AND EDITOR INFORMATION

PROXIMAL ENTRAPMENTS OF THE LOWER EXTREMITY

Iliohypogastric nerve

Ilioinguinal nerve

Genitofemoral nerve

Lateral femoral cutaneous nerve

Femoral nerve

Saphenous nerve

OBTURATOR NERVE ENTRAPMENT

COMMON PERONEAL NERVE ENTRAPMENTS

POSTERIOR TIBIAL NERVE ENTRAPMENT: TARSAL TUNNEL SYNDROME

SUPERFICIAL PERONEAL NERVE ENTRAPMENT