eMedicine Specialties > Orthopedic Surgery > Foot & Ankle
Nerve Entrapment Syndromes of the Lower Extremity
Updated: Mar 17, 2008
Proximal Entrapments of the Lower Extremity
Iliohypogastric nerve
Anatomy
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.
Etiology
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.
Clinical
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
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
Anatomy
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.
Etiology
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.
Clinical
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
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.
Anatomy
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.
Etiology
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.
Clinical
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.
Treatment
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.
Anatomy
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.
Etiology
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.
Clinical
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
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
Anatomy
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).
Etiology
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).
Clinical
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
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
Anatomy
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.
Etiology
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.
Clinical
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.
Treatment
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
Obturator Nerve Entrapment
Anatomy
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.
Etiology
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.
Clinical
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.
Treatment
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.
Common Peroneal Nerve Entrapments
Anatomy
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.
Etiology
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.
Clinical
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:
- Sensory conduction studies - A superficial peroneal sensory nerve action potential (SNAP) is important, and an abnormality of the sensory evoked response implies that the lesion is distal to the dorsal root ganglion, although this does not completely rule out the possibility of an L5 radiculopathy. A loss in amplitude of this response implies some axonal loss affecting either the common peroneal nerve or its superficial branch. The particular portion of the nerve that is injured cannot be determined if only a superficial peroneal nerve sensory study is performed. Comparison of the latency and amplitude of the superficial peroneal SNAP with the contralateral limb is required to define an approximate degree of axonal loss.
- Motor conduction studies - The most commonly performed test in determining peroneal conduction in the leg and across the fibular head is performed with the active electrode placed on the EDB muscle. The peroneal nerve is usually stimulated at the ankle, several centimeters below the fibular head and about 10 cm proximal to the fibular head, just medial to the biceps femoris tendon. This allows for calculation of the nerve conduction velocity (NCV) across the fibular head region, with comparison to the distal leg segment.
- Comparison with the contralateral limb is often helpful. When significant EDB atrophy is present (eg, with advanced age or with a polyneuropathy), the active electrode should be placed over the TA. Generally, lower extremity motor NCVs of less than 40 m/s are considered abnormal. Generally, proximal segment NCVs should be greater than distal NCVs, given the presence of greater axonal diameter in the proximal segment of the nerve.
- If the contralateral limb responses are normal, one can estimate the amount of axonal loss by expressing the compound muscle action potential (CMAP) on the affected side as a percentage of the nonaffected side. This method is independent of the location of the active recording electrode and is valid in both circumstances. A change of 20-50%, depending on the source, is believed to represent a conduction block. In addition, one may assess the degree of conduction slowing and temporal dispersion to determine if the lesion is predominantly demyelinating versus axonal.
- Needle electromyography - Needle electromyography helps in confirming axonal loss and in assessing the degree of involvement of the muscles innervated by the superficial peroneal nerve. This portion of the nerve is usually less severely involved than the deep peroneal nerve. It is possible to localize the lesion to either the deep or superficial peroneal nerves, specifically if appropriate abnormalities are detected in the proper distribution for each nerve. The most valuable aspect of the needle EMG examination is that it can be used to define the proximal extent of the lesion. If a lack of amplitude drop occurs across the fibular head but the TA CMAP is lower than that of the unaffected side (suggesting axonal loss), it is difficult to localize the lesion to the fibular head, despite the fact that this is the most common site of peroneal nerve injuries.
- In any peroneal nerve injury, regardless of the suspected site of nerve compromise, examining the short head of the biceps femoris muscle is important. If this muscle demonstrates membrane instability (positive sharp waves and fibrillations), the lesion is proximal to the fibular head.
- Testing muscles innervated by the tibial nerve, particularly the flexor digitorum longus (FDL) and tibialis posterior muscles, is also important, because they contain predominantly L5 neural innervation from the tibial nerve. If a radicular process is present, the muscles innervated by the peroneal and tibial nerves should demonstrate membrane instability.
Treatment
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.
Posterior Tibial Nerve Entrapment: Tarsal Tunnel Syndrome
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
Anatomy
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.
Etiology
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.
Clinical
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
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.
Superficial Peroneal Nerve Entrapment
Anatomy
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.
Etiology
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.
Clinical
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.
An MRI study is rarely necessary to obtain additional information.
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.
Treatment
Nonoperative options include the use of NSAIDs combined with relative rest, physical therapy for strengthening of muscles in cases of associated weakness or recurrent ankle sprains, and elimination of predisposing or triggering factors. Aids, such as braces, can be used to avoid recurrent ankle sprains. In-shoe orthotic devices may be helpful in certain instances, such as the correction of a biomechanical malalignment in gait for patients with severe flatfoot or cavus foot.
At times, injection of steroids plus lidocaine near the site of involvement in the lower leg can reduce symptoms and serve as a diagnostic tool in confirming the zone of nerve compression. The use of antineuritic medication, such as gabapentin, can also be helpful in reducing or sometimes eliminating symptoms, particularly in cases associated with CRPS. In these cases, combination treatment with medication, physical therapy, and local and sympathetic nerve blocks may be required.
Surgical decompression may be indicated in cases refractory to nonoperative options. This can include release of the superficial peroneal nerve at the lateral leg for surgical decompression with partial or full fasciotomy. Some authors have also advocated fasciectomy in select cases. Neurolysis is generally not indicated, as it has not been shown to improve outcome.
In 1997, Styf and Morberg reported that 80% of their patients were free from symptoms or satisfied with the result after decompression of the superficial peroneal nerve.32 Three of 14 patients had local fasciectomy as well.
In 1989, Styf reported on fasciotomy and neurolysis to treat entrapment of the superficial peroneal nerve in 24 legs (21 patients). Nine patients were satisfied with the result, another 6 had improvement but were not satisfied because of residual limitation of athletic activity, 3 had unchanged conditions, and 1 had a worsened condition. Conduction velocity in the superficial peroneal nerve increased postoperatively, although the change was insignificant. In 5 patients, the nerve had an anomalous course, and in 11 patients, fascial defects were present over the lateral compartment. The author concluded that operative decompression of the superficial peroneal nerve produces cure or improvement in about 75% of cases but that it is less effective in athletes than in others.
Sridhara and Izzo reported complete symptomatic relief after surgical decompression.33 In 1999, Johnston and Howell reported dramatically relieved pain after release and anterior transposition of the nerve in patients who had had neuralgia after inversion ankle sprain.34
The surgical procedure to release the superficial peroneal nerve at the anterolateral leg involves determining the location of maximum tenderness and, if present, a lateral muscle herniation is marked pre-operatively. The procedure is performed using magnifying loupes and a tourniquet. A 5-cm longitudinal incision is made over the anterolateral leg approximately at the junction of the middle and distal third to encompass these 2 points.
A significantly more distal point of tenderness may suggest a more distal piercing of the intermediate dorsal cutaneous nerve through the fascia, in which case 2 separate incisions could be considered. A blunt subcutaneous dissection is made, and the nerve is found where it emerges through the fascia. A local fasciotomy is performed, releasing the nerve proximally and distally until it is completely free. A complete fasciotomy, as advocated by some authors, is considered in cases associated with chronic compartment syndrome. The resultant peroneal muscle weakness, however, may affect athletic performance.
In cases of painful neuromas or clearly abnormal nerves due to direct or indirect trauma to the nerve, surgical excision of the nerve can be performed at the site of neuroma. If several branches are involved, excision of the nerve at the anterolateral leg can be considered. In 1998, Dellon and Aszmann reported excellent results in 9 of 11 patients who underwent resection of the nerve and translocation of the proximal nerve stump into the muscles of the anterolateral compartment, combined with fasciotomy of the anterolateral compartment.35
In cases of superficial peroneal nerve entrapment associated with other conditions, such as ankle instability, treatment of these associated conditions should also be planned.
Vague and diffuse symptoms can create a diagnostic and therapeutic challenge for the treatment of the entrapped superficial peroneal nerve. The use of multiple diagnostic modalities, including repeat examinations, selective injections, and electrodiagnostic studies, is required. Treatment of the underlying cause should be undertaken, as should release of the entrapped nerve and excision of existing neuromas.
Deep Peroneal Nerve Entrapment
Anatomy
The deep peroneal nerve is one of the terminal branches of the common peroneal nerve, originating just distal to the fibular head.36 The deep peroneal nerve enters the anterior compartment in front of the interosseous membrane. It courses lateral to the TA muscle. It travels along with and usually lateral to the anterior tibial artery and vein.
It courses between the TA and the EDL in the proximal third, and between the TA and EHL in the middle third of the leg and anterior to the anterior tibial vessels. At approximately 3-5 cm proximal to the mortise, the EHL crosses over the nerve, and the nerve is then seen between the EHL and EDL in the distal part of the leg, an average of 1.25 cm above the ankle joint. Occasionally, the nerve does not enter this interval until just distal to the ankle mortise. At this level, the nerve is about 3 mm in size and may be under the extensor retinaculum, because the inferior extensor retinaculum can be centered, above, or below the ankle mortise level.
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 EDB, the extensor hallucis brevis (EHB), the adjacent tarsal and tarsometatarsal joints (including 2-4 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 EHL tendon and EHB muscle on the dorsum of the foot. At approximately the metatarsophalangeal (MTP) joint level, the EHB crosses over the nerve, and the nerve is then between the EHB and the EDL to the second toe. It then divides into the dorsolateral cutaneous nerve of the great toe and the dorsomedial cutaneous nerve of the second toe. It supplies the sensation to the web between the first and second toes, the dorsalis pedis artery, the adjacent MTP and interphalangeal joints, and usually the first dorsal interosseous muscle. It occasionally supplies the second and third interosseous muscles.
Etiology
This entrapment is most commonly due to compression of the deep peroneal nerve and repetitive mechanical irritation of the nerve at the ankle beneath the extensor retinaculum. The entrapment of the deep peroneal nerve in this location has also been called the anterior tarsal tunnel syndrome. Within the anterior tarsal tunnel, there are 4 tendons, 1 artery, 1 vein, and the deep peroneal nerve. Typically, the nerve is trapped beneath the superior edge of the retinaculum. In this location, it is compressed by the crossing EHL tendon and under the EHB muscle, as well as directly over osteophytes, exostosis, or bony prominences of the talotibial, talonavicular, naviculocuneiform, or cuneiform metatarsal joints. Presence of an os intermetatarseum between the first and second metatarsal base has also been associated with entrapment symptoms.
Space-occupying lesions, such as 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 prolonged or repetitive sitting on the plantarflexed feet, such as is necessary for performing the namaz in Islam, are other commonly seen etiologies. Other etiologies include anomalies of the EHB distal to the retinaculum.
Entrapment of the deep peroneal nerve, however, can occur anywhere along the course of the nerve, including just distal to the neck of the fibula, anterior to the ankle joint, and distal to the inferior extensor retinaculum, but such entrapment would not be considered anterior tarsal tunnel syndrome. Common etiologies for proximal entrapment of the deep peroneal nerve include space-occupying lesions about the proximal fibula, surgical procedures about the lateral knee (including proximal tibial osteotomy), and chronic anterior exertional compartment syndrome, seen in athletes.
Clinical
The usual complaint of patients with deep peroneal nerve entrapment includes vague pain, a burning sensation, or a cramp over the dorsum of the foot, which may or may not involve the first webspace. Patients may have associated sensory changes in the first dorsal webspace. Some patients may present with neuritic symptoms along the course of the nerve, such as unrelenting pain at rest and during sleep. There may be pain in the ankle region even if only the motor nerve is involved. Symptoms may occur or worsen only with a certain shoe or boot or with certain activities. Although less common, patients with more proximal entrapment may present with frequent tripping due to foot drop or weakness of the EHL.
With proximal entrapment, motor dysfunction may be demonstrated on regular gait examination, with presentations such as a dramatic foot drop. However, symptoms are usually more subtle and are noted only on heel walk or a hop test. With long-standing dysfunction, plantarflexion of the ankle with extension of the toes can compress the nerve as it passes beneath the extensor retinaculum, which can worsen the symptoms. Muscular atrophy may also be noted in the anterior compartment of the EDB with distal entrapment of the nerve.
With distal entrapment, tenderness may be elicited along the entrapped segment of the nerve over the anterior ankle or just distal to it, and an underlying bony prominence is usually present. Provocative dorsiflexion and plantarflexion of the ankle may bring on or increase symptoms. A sensory deficit in the first webspace may also be detectable. Most patients have a positive Tinel test result over the entrapment site of the nerve, commonly around the fibular neck or over the anterior ankle.
Incomplete involvement can also occur, affecting isolated sensory or motor branches. Temporary resolution of the neuritic symptoms following an injection of the nerve with plain lidocaine in the site of entrapment is a good indicator verifying the diagnosis.
Bony impingement can usually be seen on conventional lateral ankle or foot radiographs. Oblique radiographs taken from different angles are necessary to better define smaller osteophytes, exostosis, or other bony masses about the anterior ankle or the dorsomedial midfoot. Knee radiographs are needed for suspected proximal involvement. If necessary, a CT scan will provide more detailed information on the bony anatomy of the area.
Ultrasonography has been useful for diagnosis and localization of cystic masses causing an impingement of the nerve. Occasionally, MRI is necessary to obtain additional information about soft-tissue masses, synovial reaction, adjacent bone, and chondral and soft-tissue involvement.
Electrodiagnostic studies are helpful in further defining the zone of compression and in evaluating for concomitant radiculopathy or peripheral neuropathy. In deep peroneal nerve injury or entrapment, the results may show a decrease in the amplitude of the response if axonal involvement is present or conduction block occurs from demyelination. The distal latency may be prolonged if entrapment is present in the anterior tarsal tunnel region, and the NCV is decreased across the leg region if the entrapment or injury is more proximal. An accessory may also be present. The accessory peroneal nerve originates from the superficial peroneal nerve and traverses posterior to the lateral malleolus to provide variable innervation to the EDB. This anomaly is identified when the response is recorded from the EDB that is larger with proximal stimulation (at the fibular head) than with distal stimulation (at the ankle).
Needle examination may reveal the presence of fibrillations and positive sharp waves in the EDB only if present at the anterior tarsal tunnel. If entrapment is present more proximally, the denervation is present in the TA as well as in the EDB.
Denervation may be present, however, with other neurologic conditions. The short head of the biceps femoris, as well as the medial gastrocnemius, tensor fascia lata, and lumbar paraspinal muscles, should be tested if there are findings in the deep peroneal muscles to rule out a more proximal problem, such as a radiculopathy. The absence of findings in these muscles, as well as in the peroneus longus and brevis, confirms the presence of a deep peroneal motor-nerve injury.
Some reports have stated that there may be a high percentage of denervation present in the foot intrinsic muscles in healthy subjects, but subsequent reports have found that the actual percentage of abnormal findings in healthy subjects is low for a well-trained electromyographer. Many times, electrodiagnostic test findings are normal because these dynamic syndromes frequently improve or resolve at rest.
Treatment
Nonsurgical care most importantly involves patient education to eliminate the predisposing factors. For example, padding of the tongue of the shoe, the elimination of shoes with laces, or the use of alternative lacing methods, as well as the avoidance of high heels, may be sufficient to resolve symptoms.
Physical therapy is useful for strengthening the peroneal muscles in cases associated with weakness and in individuals with chronic ankle instability; the use of modalities may also improve symptoms.
In-shoe orthotic devices are helpful in certain instances, such as for correction of a biomechanical malalignment in gait (eg, in patients with severe flatfoot or cavus foot).
The use of NSAIDs and antineuritic medication may be helpful as an adjunct to other treatment modalities. Injection of steroids plus lidocaine near the site of involvement can reduce symptoms in some individuals.
In addition, consideration should be given to a metabolic workup to rule out thyroid dysfunction and diabetes in select individuals. Further workup may be necessary to rule out lumbar radiculopathy.
Surgical options can be considered once symptoms are deemed refractory to nonoperative measures. Options include surgical release of the deep peroneal nerve in primary and idiopathic cases, and excision of the nerve in cases of direct nerve injury due to previous surgery, in cases of direct trauma, or in revision cases. Surgical decompression of the nerve can provide immediate improvement of symptoms.
In 1990, Dellon reported on surgical release of the deep peroneal nerve in 20 patients.37 With a mean follow-up time of more than 2 years, he reported excellent results in 60% of patients, good results in 20% of patients, and no improvement in 20% of patients.
The surgical procedure can include part or all of a longitudinal straight or S -shaped incision on the dorsum of the foot, starting between the bases of the first and second metatarsals and extending proximally to the anterior ankle, depending on the predicted location of entrapment. The deep fascia overlying the deep peroneal nerve and the dorsalis pedis artery is released, as is the inferior part of the extensor retinaculum; the superior part can be preserved to maintain the function of the extensor tendons. The deep peroneal nerve is followed proximally and distally to verify a full release. Nerves that appear to be normal in consistency and size can be released.
It is important to remove other underlying etiologies for entrapment or stretch, such as complete excision of underlying osteophytes during surgery. The decision to perform a neurolysis versus an excision, transposition, or both is dependent on the severity of injury to the nerve. Excision of the nerve in cases in which the nerve is abnormal, such as those directly manipulated during surgery or entrapped in scar tissue, is indicated. Neuroma in continuity is best excised and allowed to retract into deep tissues, and transposition of the stump into muscle belly may be possible depending on the level of excision. In 1998, Dellon and Aszmann reported on excision of the superficial and deep peroneal nerves in the lateral leg, with translocation of the nerves into a muscle (with excellent results obtained in 9 of 11 patients).
When entrapment of the nerve is caused by the EHB muscle, the muscle is hypertrophied and has thick fibrous bands that compress the deep peroneal nerve. Decompression of the nerve and excision of the muscle and fibrous band can lead to complete resolution of pain, but numbness in the first webspace may be persistent.
Entrapment of the deep peroneal nerve can occur anywhere throughout its course, from the region just distal to the fibular head to the dorsal first webspace. The most common location of entrapment is just anterior to the ankle, under the extensor retinaculum. Entrapment at this site is also called anterior tarsal tunnel syndrome. The most common etiologies for entrapment include prominent bony or soft-tissue masses, such as exostoses, osteophytes, and ganglion cysts, as well as acute direct trauma and chronic compression or stretch, as with lace-up shoes or high heels.
The most common presenting symptom is a vague pain on the dorsum of the foot, with occasional, associated numbness or weakness. Treatment options are aimed at eliminating underlying etiologies of entrapment. Surgical release or excision is reserved for refractory cases.
Interdigital Neuritis
Interdigital neuritis, which is more commonly known Morton neuroma, is a condition that is the result of entrapment of a plantar interdigital nerve as it passes under the transverse metatarsal ligament.38 This condition was named after Thomas Morton, who reported "a peculiar and painful affection of the fourth metatarso-phalangeal articulation" in 1876.39 This condition has since been defined as a perineural fibrosis of the involved interdigital nerves, and true neuromatous involvement is not seen.
Other terms used for this condition include interdigital neuroma, Morton metatarsalgia, and interdigital nerve compression.
This condition 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. Morton neuromas are more common in women than in men; they can occur in persons of all ages, but they are most common in middle-aged individuals.
Anatomy
The common digital nerves originate from the medial and lateral plantar nerves. The medial plantar nerve divides into 3 common digital nerves, which in turn bifurcate, supplying cutaneous branches to the medial 3.5 digits. The lateral plantar nerve gives rise to 2 common digital nerves, supplying cutaneous branches to the lateral one and a 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 in the plantar aspect of the foot adjacent to the webspace.
Etiology
The most direct cause of entrapment of the interdigital nerve is compression of the nerve as it passes under the transverse intermetatarsal ligament. As weight is transferred to the ball of 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 and colleagues saw lesions consisting of a progressive fibrosis that enveloped and disrupted nerves and arteries.40 They did not see nerve-tissue proliferation or inflammation. 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 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.41 These bodies are characteristically present only in peripheral neural entrapment.
However, Morscher and coauthors, in a histomorphologic study, found only a diameter difference between biopsy results from patients with typical symptoms of Morton neuroma and nerves examined from autopsies of persons without forefoot problems.42 In addition, some have implicated the inter-MTP bursa as the main cause of Morton neuroma.
Forefoot deformities, such as hammertoe, can further aggravate the nerve due to dorsal subluxation of the proximal phalanx, which stretches the interdigital nerve over the intermetatarsal ligament. In addition, there are a number of external conditions that have been noted to contribute to the development and aggravation of this compression. High-heeled shoes put the feet in chronic dorsiflexion and result in forcing one's weight onto the forefoot; 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 and colleagues demonstrated in their study that the relative space in the metatarsal head/transverse metatarsal ligament is smaller in the second and third webspace than it is in the others, where the condition is more common and therefore supports the mechanical factors as the underlying pathophysiology.43 They also dismissed the common theory that the cause relates to the occurrence of a lateral and medial plantar combination and to the anatomical thickness of the nerve. They reported neuromas in third webspaces 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 less than are those in the first and fourth intermetatarsal space.
Clinical
Many patients with Morton metatarsalgia present with an intermittent dull ache or cramping sensation on the plantar aspect of either the second or third interspace. Many patients present with a vague discomfort in the involved toes and some may feel numbness or burning, with occasional shooting pain. Some patients notice spreading of the involved toes, and others may notice symptoms only with certain shoes. Symptoms usually worsen with walking, particularly with bare feet on hard surfaces, and sudden, sharp pain may result from various activities, such as such as sprinting, jumping, squatting, or repeated hopping, as well as with wearing high-heeled or tight shoes. They improve with rest, and night pain is rare. With progression of the condition, pain may radiate proximally. In chronic cases, patients may sense a mass or a stone bruise in the ball of the foot.
Nearly equal involvement of the second and third interspace has been reported in the literature. Involvement of the first and fourth space also has been reported, albeit rarely.
Simultaneous tenderness in the second and third interspace is not rare. Bilateral cases have been reported but are uncommon. Co-existence of other pathologies of the forefoot, such as instability of the second MTP joint, is not uncommon. Coughlin and colleagues reported that 20% of their patients originally had concomitant instability of an adjacent MTP joint.
Clinically, dorsoplantar compression of the second or third intermetatarsal space reproduces pain that may radiate to the toes or proximally along the course of the affected nerve. The patient may display relative paresthesia of the webspace supplied by the injured nerve, although this is often difficult to ascertain.
The Mulder click is a useful diagnostic test. The forefoot is held in one hand, and the metatarsal heads are squeezed while the other hand places direct pressure on the plantar aspect of the interspace. As the metatarsal heads are compressed, the enlarged nerve is pushed plantar and away from the metatarsal heads, and a click is palpated with the digit in the plantar web space just distal to the transverse intermetatarsal ligament. This is often uncomfortable for the patients but does not usually reproduce their symptoms. This palpated mass can be again pushed up in the interspace with manual pressure, while partial compression is maintained on the metatarsal heads. Many times, 1 digit is noted to move suddenly.
A range of conditions may mimic Morton neuroma, including metatarsal stress fracture, MTP joint synovitis, intermetatarsal bursitis, extensor tendon tenosynovitis, tumor, and more proximal nerve injury. Metatarsal stress fracture will present with bony tenderness and pain upon palpation of the metatarsal shaft, rather than the common digital nerve. MTP joint synovitis will often prove painful during active or passive joint motion.
The diagnosis of Morton neuroma is primarily based on clinical findings. Careful clinical examination will usually reveal other conditions that can mimic or co-exist with intermetatarsal neuritis. In complex cases, immediate temporary resolution in response to a local anesthetic block proximal to the involved area below the intermetatarsal ligament can confirm the diagnosis.
Ultrasonography and MRI are helpful in rare, complex situations.44 The accuracy of these studies, however, varies significantly and depends on multiple factors, including the MRI machine, the technician and the technique, and the interpreting radiologist or orthopedic surgeon.
Ultrasonography reveals a hypoechoic, ovoid mass parallel to the long axis of the metatarsal. Ultrasonography can also be used to diagnose other pathologic conditions in the forefoot, such as bursitis and MTP joint effusion. Reed and colleagues reported this study to be 95% sensitive in detection of webspace abnormality, but Morton neuroma could not be clearly distinguished from an associated mass, such as mucoid degeneration in the adjacent loose connective tissue.
Quinn and co-authors found that ultrasonography revealed the diagnosis in 85% of cases in which it was suspected.45 They reported limitation in detecting neuromas shorter than 5 mm. Terk and colleagues reported on MRI with T1- and T2-weighted sequences, along with a combination of fat suppression and the administration of gadopentetate dimeglumine.46 Williams and colleagues showed that T1-weighted axial and coronal images obtained with an axial, fast spin-echo (FSE), T2-weighted sequence depict neuromata more consistently than do other methods.
Zanetti and co-authors studied 54 feet in which Morton neuroma was suspected in order to determine the effect of MRI results on diagnostic thinking and the therapeutic decisions made by orthopedic surgeons.47 The authors noted considerable change in the diagnosis, location, and number of neuromas, as well as in the treatment plans, after MRI.
In a second report, Zanetti and colleagues suggested that the diagnosis of Morton neuroma based on MRI results are relevant only when the transverse diameter of the fluid collection in the bursa is 5 mm or more and when it was correlated with the clinical findings. Fluid collections in the first 3 metatarsal bursae with a transverse diameter of 3 mm or less are probably physiologic.
In a histomorphologic study of patients and autopsies, Morscher and co-authors concluded that diagnostic MRI or ultrasonography is unnecessary for making decisions about operative treatment.42 In addition, Resch and co-authors found that MRI modalities had little or no value in the diagnosis of Morton neuroma because of the high rate of false-negative results.48
Treatment
If Morton neuroma is detected early, conservative measures may be reasonably successful. About 20-30% of patients achieve adequate relief with nonoperative management. This may be accomplished by eliminating or minimizing the external sources of compression or stretch on the interdigital nerve.
Extra-wide shoes and low heels, as well as the placement of a small metatarsal pad just proximal to the heads of the central 3 metatarsals, may reduce symptoms by increasing the intermetatarsal space, elevating the metatarsals and the intermetatarsal ligament, and reducing the likelihood of neural irritation. Accommodative orthotic devices with built in metatarsal pads may at times be helpful, especially in patients with alignment abnormalities.
NSAIDs may relieve acute pain and inflammation. If NSAIDs provide insufficient relief, a local anesthetic injection can also relieve pain and may help to confirm the diagnosis of Morton neuroma.
Corticosteroid injections have not been shown to result in predictable or lasting relief, as reported by Mann and colleagues. Rasmussen and co-authors reported initial pain relief in 80% of patients who received a single corticosteroid injection.49 However, 47% of the 41 feet in the study ultimately required surgical excision; the majority of the remaining 53% caused residual symptoms in patients. In addition, corticosteroid injection for intermetatarsal neuroma has been associated with a number of complications, including plantar fat-pad atrophy depigmentation, hyperpigmentation, and telangiectasias. Fat-pad atrophy can result in metatarsalgia and gait impairment.
A number of different surgical procedures have been used. Excision of the interdigital nerve and release of the intermetatarsal ligament is the most commonly performed procedure. A variable degree of subjective numbness occurs in the 2 toes served by that nerve, which is symptomatic in fewer than 10% of cases. Dorsal or plantar incisions have been reported in the literature.
Most surgeons in the United States perform a primary surgery through a dorsal approach. The incision is approximately 3 cm in length and is centered in the respective interspace, starting from the metatarsal head level and extending distally into the respective webspace. Blunt dissection into the webspace and placement of a lamina-style spreader reveals the intermetatarsal ligament. The proximal and distal aspects of the ligament are identified and released sharply. An enlarged nerve may be readily identified beyond the ligament. Smaller nerves are more difficult to identify. In most cases, intertwining vessels require careful dissection and protection. The digital branches are identified and are sharply amputated distally. The nerve is then followed proximally, gently pulled distally, sharply amputated as far proximally as is visible, and allowed to retract into the deep soft tissues.
Mann and Reynolds reported retrospectively on a surgical excision of 76 Morton neuromas.50 Although 65% of patients still noted some local plantar tenderness to touch, 80% were subjectively improved. Coughlin and Pinsonneault noted residual pain in either the involved or adjacent interspace, which is not uncommon.51 They also reported 85% good or excellent results. They noted mild or major footwear restrictions in 70% of patients.
Dereymaeker and colleagues reported on 32 feet that were treated with excision of the Morton neuroma by using a dorsal incision.52 Twenty-five of 32 patients had a macroscopically visible neuroma, and 2 patients had no evidence of a neuroma on histologic examination. After resection, 81% had a good or excellent result, and 6.5% had no improvement after their operation. The authors noted that, following the operation, 60% of their patients benefited from the use, over a long period of time, of adapted shoes or inner soles. At the final follow-up, only 30% of the patients were found to be unrestricted in their choice of shoes.
Some authors advocate the plantar approach for primary resection of an intermetatarsal neuroma, as it provides more direct access to the nerve and is technically simpler. However, painful plantar scars, intractable plantar keratosis beneath an adjacent lesser metatarsal head, and wound drainage have been reported. Because of these potential complications, most surgeons reserve the plantar approach in revision cases. Karges reported on 57 plantar surgeries performed using a plantar incision.26 He reported 23% indurated plantar keratosis (IPK) after surgery, and only 7% had poor results.
Potential complications of interdigital nerve excision, including development of a stump neuroma and digital numbness, have led some authors to recommend release of the transverse metatarsal ligament with or without epineurolysis. Gauthier reported on the release of 304 intermetatarsal ligaments and epineural neurolysis.53 He stated that 83% had rapid and stable improvement, and that 15% were improved but nonetheless suffered some persistent pain. Others, such as Weinfeld and Myerson, have advocated this procedure without neurolysis and have reported good preliminary results.54 Mann and Reynolds cautioned against the use of this procedure except for Morton neuroma, as they noted reconstitution of the ligament in revision cases.50
Adjacent neuromas in the second and third interspace should be investigated. Reports of double neuromas in the literature are sparse. Benedetti and colleagues reported simultaneous excision of 2 primary Morton neuromas in adjacent webspaces and noted significant pain relief in 84% of patients, but substantial numbness involving the third toe resulted.55 Thompson and Deland described 89 adjacent neurectomies and reported similar results to those achieved with single neurectomies.56
Hort and DeOrio reported on 23 patients with adjacent intermetatarsal nerve irritation who underwent excision of the more enlarged nerve in one space and the release of the intermetatarsal ligament in the other.57 This allowed preservation of protective sensation. They reported 95% complete satisfaction, with no or only minimal activity limitation. Approximately 11% had persistent pain with compression of the interspace where the nerve was released. None had pain in the interspace where the nerve was excised. The investigators performed this procedure through 1 incision centered over the third metatarsal.
Morton neuroma is the result of chronic compression of the interdigital nerve as it passes under the transverse intermetatarsal ligament. It is most commonly seen in the second and third intermetatarsal space, and it causes pain that may radiate to the toes or proximally along the course of the affected nerve. Pain with compression of the intermetatarsal space and the presence of a Mulder click confirm the diagnosis.
Nonoperative management is successful in about 20-30% of all cases. Nonoperative management includes the avoidance of high-heeled and tight shoes, as well as the use of a small metatarsal pad and stiffer, rocker-soled shoes. Surgical excision of the nerve and release of the intermetatarsal ligament with a dorsal or plantar approach results in a high percentage of successful results. The dorsal approach is recommended because of fewer potential complications, and also because it allows early weight bearing. Patients should be counseled pre-operatively that varying degrees of postoperative numbness are commonly associated with resection of a Morton neuroma. Other surgical options include isolated intermetatarsal ligament release.
Adjacent neuromas in the second and third interspace are not uncommon. Excision of the most involved nerve and release of the intermetatarsal ligament in the less involved nerve lead to good relief of symptoms without significant neurologic deficit.
See also the following related eMedicine topics:
Morton Neuroma [Orthopedic Surgery]
Morton Neuroma [Physical Medicine and Rehabilitation]
Morton Neuroma [Radiology]
Patient Education
For excellent patient education resources, visit eMedicine's Foot, Ankle, Knee, and Hip Center and Procedures Center. Also, see eMedicine's patient education articles Knee Pain Overview, Bursitis, and Electromyography (EMG).
Keywords
iliohypogastric nerve entrapment, ilioinguinal nerve entrapment, genitofemoral nerve entrapment, lateral femoral cutaneous nerve entrapment, femoral nerve entrapment, saphenous nerve entrapment, obturator nerve entrapment, peroneal nerve entrapment, posterior tibial nerve entrapment, tarsal tunnel syndrome, superficial peroneal nerve entrapment, deep peroneal nerve entrapment, interdigital neuritis, Morton metatarsalgia, meralgia paresthetica, Morton neuroma, slimmer's paralysis, strawberry picker's palsy, Tinel sign, heel pain triad
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References
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Further Reading
Keywords
iliohypogastric nerve entrapment, ilioinguinal nerve entrapment, genitofemoral nerve entrapment, lateral femoral cutaneous nerve entrapment, femoral nerve entrapment, saphenous nerve entrapment, obturator nerve entrapment, peroneal nerve entrapment, posterior tibial nerve entrapment, tarsal tunnel syndrome, superficial peroneal nerve entrapment, deep peroneal nerve entrapment, interdigital neuritis, Morton metatarsalgia, meralgia paresthetica, Morton neuroma, slimmer's paralysis, strawberry picker's palsy, Tinel sign, heel pain triad
