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Nerve Entrapment Syndromes of the Lower ExtremityMinoo Hadjari Hollis, MD, Orthopedic Surgeon, Sound Orthopedics and Foot and Ankle CenterDavid E Lemay, MD, Consulting Staff, Pensacola PM&R Group, PA and Gulf Coast Orthopaedic Specialists, PA

Updated: Jul 10, 2009

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 fromT12. This nerve has a pathway similar to that of the intercostal nerves in the thoracic region. The iliohypogastricnerve traverses the psoas major muscle, piercing the lateral border of the muscle anterior to the quadratuslumborum muscle and posterior to the kidney to traverse the lateral abdominal wall. The nerve penetrates thetransverse abdominal muscle near the iliac crest, coming between it and the internal oblique musculature. Thenerve supplies the lower fibers of the transverse abdominal muscle and the internal oblique, and divides into thelateral and anterior cutaneous branches.

The anterior cutaneous branch continues anteriorly between the internal oblique and transverse abdominalmuscle, then pierces the internal oblique and becomes cutaneous through an opening in the fascial aponeurosisof the external oblique muscle, approximately 2-3 cm cephalad to the superficial inguinal ring. The distribution ofthe 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 surgicalprocedures. These include transverse lower abdominal incisions, as in hysterectomies, or injuries fromprocedures such as inguinal herniorrhaphy and appendectomies. The injuries mainly occur if the incisionextends beyond the lateral margin of the inferior rectus abdominis fibers. The damage can result from directsurgical trauma, such as passing a suture around the nerve and incorporating it into the fascial repair, orpostoperative entrapment in scar tissue or neuroma formation. Sports injuries, such as trauma or muscle tearsof the lower abdominal muscles, may also result in injury to the nerve. Injury may also occur duringpregnancy, owing to the rapidly expanding abdomen in the third trimester. This is called the idiopathiciliohypogastric syndrome and is rare.

Clinical

Symptoms include burning or lancinating pain immediately following the abdominal operation. The pain extendsfrom the surgical incision laterally into the inguinal region and suprapubic region. Discomfort may occurimmediately or up to several years after the procedure, and may last for months to years. This discomfort ispossibly because of the formation of scar tissue in the region. Occasionally, the pain may extend into thegenitalia because of significant overlap with other cutaneous nerves. Loss of sensation is usually minimal andnot problematic. Iliohypogastric nerve entrapment causing symptoms similar to trochanteric bursitis refractory toconventional therapy has been reported.

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

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ilioinguinal nerves.

Three major criteria are used to diagnose this nerve injury. The first is a history of a surgical procedure in thelower abdominal area, although spontaneous entrapment can occur. Pain can usually be elicited by palpatinglaterally about the scar margin, and the pain usually radiates inferomedially toward the inguinal region and intothe suprapubic and proximal genital area. Second, a definite area of hypoesthesia or hyperesthesia should beidentified in the region of supply of the iliohypogastric nerve. Third, infiltration of a local anesthetic into the regionwhere the iliohypogastric and ilioinguinal nerves depart the internal oblique muscle and where symptoms can bereproduced 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 diagnosesinclude upper lumbar or lower thoracic nerve root pathology, or discogenic etiology of the pain. If theiliohypogastric nerve is identified clearly as the source of pain, and a favorable response is not obtained withlocal anesthetic injection, then surgical exploration and resection of the nerve should be considered. No reliableelectrodiagnostic techniques are available to define the integrity of this nerve, although needleelectromyography of the lower abdominal musculature may serve as an adjunct in the diagnosis.

Treatment

Treatment includes local injection of an anesthetic (as noted above), oral medications, or physical therapy. Theoral medications may include antiseizure medications, such as gabapentin (Neurontin), carbamazepine(Tegretol), or lamotrigine (Lamictal), as well as nonsteroidal anti-inflammatory drugs (NSAIDs), tricyclicantidepressant medications (amitriptyline [Elavil], doxepin), capsaicin cream, topical lidocaine (Lidodermpatches), or tramadol (Ultram). With physical therapy, cryotherapy or a transcutaneous electrical nervestimulation (TENS) unit may be tried. When conservative measures are not successful, surgical excision mayresult in relief of pain with few potential complications. Potential complications include possible neurolysis of thenerve 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 ofthe 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 internaloblique 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 thefemoral triangle, and either the root of the penis and anterior scrotum in the male or the mons pubis and labiamajora 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. Theprevalence of injury with surgery has declined, owing to the use of laparoscopic procedures. Tearing of thelower external oblique aponeurosis may also cause injury to this nerve. This injury has been reported in hockeyplayers.

Clinical

Symptoms may include hyperesthesia or hypoesthesia of the skin along the inguinal ligament. The sensationmay radiate to the lower abdomen. Pain may be localized to the medial groin, the labia majora or scrotum, and


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the inner thigh. The characteristics of the pain may vary considerably. Patients may be able to associate theirpain 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 upto 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 the trunk in a forward-flexed posture). Painmay 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, which shouldresult in relief within 10 minutes. Unfortunately, no electrodiagnostic techniques are readily available to test thisnerve. Abdominal needle electromyography may be helpful in determining the severity of nerve injury, butelectromyography is not sensitive or specific.

Treatment

Treatment includes local injection of an anesthetic, physical therapy, or oral medications. Types of medicationsmay include antiseizure medications, such as gabapentin (Neurontin), carbamazepine (Tegretol), or lamotrigine(Lamictal), as well as NSAIDs, tricyclic antidepressant medications (amitriptyline [Elavil], doxepin), capsaicincream, topical lidocaine (Lidoderm patches), or tramadol (Ultram). Ice or possibly a TENS unit may be used withphysical therapy. When conservative measures are not successful, surgical excision may result in relief of painwith 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. Thenerve then pierces the anterior surface of the psoas major muscle at the level of L3-4 and descends on thefascial surface of the psoas major muscle past the ureter. It then splits into the genital and femoral branchesnear the inguinal ligament.

The genital branch continues along the psoas major to the deep inguinal ring and enters the inguinal canal. Itsupplies the cremaster muscle, spermatic cord, scrotum, and adjacent thigh in males. In females, it travels withthe round ligament of the uterus and provides cutaneous sensation to the labia majora and adjacent thigh. Thefemoral branch lies lateral to the genital on the psoas major and travels lateral to the femoral artery andposterior to the inguinal ligament to enter the proximal thigh. There, it pierces the sartorius muscle distal to theinguinal ligament and supplies the proximal portion of the thigh about the femoral triangle just lateral to the skinthat is innervated by the ilioinguinal nerve.

Etiology

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

A prospective study was performed to evaluate the genitofemoral nerve electrophysiologically in children withinguinal hernia repair. Latency of the genitofemoral nerve was found to be prolonged after inguinal hernia repairpossibly because of surgical-related injury.[2 ]

Clinical


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Injury to the femoral branch causes hypoesthesia over the anterior thigh below the inguinal ligament, which ishow it is distinguished from the iliohypogastric and ilioinguinal nerve. Groin pain is a common presentation ofneuralgia 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 andgenitofemoral nerves as well as L1-2 radiculopathies. Some anatomic overlap may exist with the supply of theilioinguinal 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. Ohhas discussed a side-to-side sensory comparison study, but this test is technically difficult to perform.[3]Diagnosis typically is made using anesthetic nerve blocks. Injection of the ilioinguinal and iliohypogastric nervesanteriorly should leave the pain or abnormal sensation unchanged. A block of the L1 and L2 roots shouldthen result in relief. This should help to determine the diagnosis and to prevent unnecessary surgical explorationof an uninjured nerve.

Treatment

The above-mentioned blocks are diagnostic and therapeutic. Avoidance of aggravating activities should beemphasized. Treatment may also 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 atransabdominal approach to the nerve (Magee and Lyon) with satisfactory results.[4,5 ]The complications of thisprocedure include hypoesthesia of the scrotum or labium majus and of the skin over the femoral triangle, as wellas loss of the cremasteric reflex. This usually will not result in notable morbidity. According to Harms andcolleagues, an extraperitoneal approach should result in fewer operative complications.[6 ]

Lateral femoral cutaneous nerve

Injury or entrapment of the lateral femoral cutaneous nerve is also known as meralgia paresthetica. It is derivedfrom the Greek word meros, meaning thigh, and algo, meaning pain. It is a syndrome of paresthesia and pain inthe lateral and anterolateral thigh. This syndrome is seen most commonly in individuals aged 20-60 years, but itcan 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 ligamentand 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 in line with the ASIS, and suppliescutaneous sensation to the lateral thigh, including just proximal to the patella. It then communicates withcutaneous branches of the femoral nerve and saphenous nerve to form the patellar plexus. The posteriorbranch pierces the fascia lata posteriorly and laterally, and divides into multiple, small branches that supply theskin from the greater trochanter to the midthigh.[7 ]

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. Theentrapment may be from intrapelvic causes, extrapelvic causes, or mechanical causes. Intrapelvic causesinclude pregnancy, abdominal tumors, uterine fibroids, diverticulitis, or appendicitis. Injury has been described incases of abdominal aortic aneurysm. Examples of extrapelvic causes include trauma to the region of the ASIS


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(eg, from a seatbelt in a motor vehicle accident), tight garments, belts, girdles, or stretch from obesity andascites. 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 butmay be bilateral in rare cases. The symptoms usually improve with sitting unless compressive forces, such astight belts or garments, remain.

Physical examination findings may be completely normal. Findings may include hyperesthesia over the lateralthigh (usually in a smaller area than the symptoms). Pain can be produced by pressure medial to the ASIS. Apositive 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 ligamentor ASIS. Spontaneous recovery usually is expected. Electrodiagnostic testing may be performed for diagnosis.With nerve conduction studies, the technique includes using a bar electrode for recording and reference. Thiscan be performed with either antidromic (conduction against the direction of sensory fiber conduction) ororthodromic (conduction in the direction of nerve conduction) methods. The antidromic study is usually easier toperform, although response may be absent bilaterally on occasion. The response is small and difficult to obtainin obese patients.

A needle stimulation electrode may needed. The sensory response is absent in 71% of patients with meralgiaparesthetica and is prolonged in 24% of patients with this condition. Electromyographic test results with needleare 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 todetermine entrapment. It may be nearly impossible to obtain a response in an obese patient or a patient with alarge abdomen without using a needle for stimulation. Unfortunately, the test may be difficult for the patient totolerate because of the large amount of current (with respect to more peripheral nerves) that is required tostimulate 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 usedto prolong the effects of the local anesthetic and reduce inflammation. Oral medications, such as NSAIDs,antiseizure medications (gabapentin [Neurontin]), tricyclic antidepressants, and tramadol may be used,as may capsaicin cream and topical lidocaine. One must also instruct patients on ways to prevent furtherirritation of the nerve. These may include avoidance of hip extension, prolonged standing, and compressivegarments. The use of ice and a TENS unit may also be helpful. Surgical exploration may be required if theabove treatment options are not helpful. This includes transection of the nerve, or decompression with or withoutneurolysis. Anatomical variations of the nerve and neuromas can occur and lead to recurrence.[8 ]

Femoral nerve

Anatomy

The femoral nerve arises from the posterior divisions of the ventral primary rami of L2, L3, and L4 within thepsoas major muscle. These nerves join to form the largest branch of the lumbar plexus. The nerve emergesfrom the lateral border of the psoas muscle and courses inferiorly in the intermuscular groove between thismuscle 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. In the proximal thigh it divides into sensorybranches that innervate the upper and anterior thigh, and muscular branches that innervate the quadricepsmuscle. One of the major branches is the lateral femoral cutaneous nerve, as discussed previously.[9 ]


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Another branch is the medial femoral cutaneous nerve, which originates just distal to the inguinal ligament,descends on the sartorius muscle, and penetrates the deep fascia about the distal third of the thigh to split into 2terminal nerve branches. One branch innervates the skin covering the medial aspect of the distal thigh and kneejoint region. The second branch supplies the skin superior to the patella and shares several communicatingbranches with the saphenous nerve. The posterior branch of the medial cutaneous nerve travels along themedial border of the sartorius muscle and pierces the deep fascia about the knee to also communicate with thesaphenous nerve in providing cutaneous sensation to the patellar region. The best-known cutaneous nervearising from the femoral nerve is the saphenous nerve (discussed below).

Etiology

The femoral nerve can have several entrapment locations or causes of injury, including intrapelvic injury or injuryin the inguinal region. Diabetic amyotrophy is the most common cause of femoral nerve neuropathy. Openinjuries 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 arteryinjury. 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 tocompression.[10 ]

Conduction of the femoral nerve was measured in diabetic patients without clinical signs of femoral nerveinvolvement, and there was a statistically significant difference between diabetics and healthy individuals interms of both femoral nerve motor latency and amplitude. The authors observed that these abnormalitiesbecame more evident as the polyneuropathy of the patients became more serious.[11 ]

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, thepsoas tendon, the hip, and the joint capsule. The femoral nerve does not have significant protection in this area.

Heat developed by methylmethacrylate during a total hip arthroplasty can injure the femoral nerve. Pelvicprocedures that require the lower extremity to be positioned in an acutely flexed, abducted, and externallyrotated position for long periods can cause compression by angling the femoral nerve beneath the inguinalligament. The nerve may be compromised by pressure from a fetus in a difficult birth. Pelvic fractures and acutehyperextension of the thigh may also cause an isolated femoral nerve injury. Pelvic radiation, appendiceal orrenal abscesses, and tumors can cause femoral nerve injuries as well. The nerve can also be injured by acompartment-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 byflexion and external rotation of the hip, and dysesthesia over the anterior thigh and anteromedial leg. Patientscomplain of difficulty in walking and of knee buckling, depending on the severity of the injury. The nerve givesrise to the saphenous nerve in the thigh; therefore, numbness in this distribution can be present. Anterior kneepain may also be present because the saphenous nerve supplies the patella.

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

Electrodiagnostic testing typically is performed for diagnosis, but is also important to determine the extent of theinjury and the prognosis for recovery. With electrodiagnostic testing, either surface or needle electrodes lateralto the femoral artery in the inguinal region are used for stimulation. The stimulation can be performed above and


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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 femoralnerve over the medial aspect of the leg and ankle). Needle examination should be completed for the paraspinalmuscles as well as for the iliopsoas (also L2-3) and hip adductors supplied by the obturator nerve, to determinethe presence of root or plexus injury versus peripheral nerve injury. Needle electromyography is usually themost revealing portion of the electrodiagnostic test. The examiner must look not only for denervation potentialsbut 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 toprevent instability, and the patient may require an assistive device for walking. Good recovery has been reportedin up to 70% of patients with a femoral neuropathy and may take up to a year. The recovery may even occur inthe 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 apure sensory nerve that is made up of fibers from the L3 and L4 spinal segments. Because of its long course, itcan become entrapped in multiple locations, from the thigh to the leg. It branches from the femoral nerve justdistal to the inguinal ligament and courses with the superficial femoral artery to enter the adductor (Hunter's)canal in the distal third of the thigh. This canal extends proximally from the apex of the femoral triangle tothe inferomedial aspect of the thigh in the adductor magnus tendon, just proximal to the femoral condyle. Thecanal is somewhat triangular and lies between the vastus medialis laterally and the adductor magnus andlongus muscles medially.

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

Etiology

The saphenous nerve can become entrapped where it pierces the roof of the adductor canal.Inflammation results from a sharp angulation of the nerve at its exit and from the dynamic forces of the musclesin this region, which cause contraction and relaxation of the fibrous tissue that impinges on the nerve. The nervecan also be injured as a result of an improperly protected knee or leg support during surgery. It may beinjured by a neurilemoma, entrapment by femoral vessels, direct trauma, pes anserine bursitis, varicose veinoperations, and medial knee arthrotomies and meniscus repairs.[12 ]

Clinical

Symptoms of entrapment may include a deep aching sensation in the thigh, knee pain, and paresthesias in thecutaneous distribution of the nerve in the leg and foot. The infrapatellar branch may also become entrapped onits own. This is because it passes through a separate foramen in the sartorius muscle tendon. It may also beexposed to trauma where courses horizontally across the prominence of the medial femoral epicondyle. Patientsreport paresthesias and numbness about the infrapatellar region that is worse with flexion of the knee orcompression from garments and braces.


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Saphenous nerve entrapment is a frequently overlooked cause of persistent medial knee pain in patients whoexperience trauma or direct blows to the medial aspect of the knee. As this is a purely sensory nerve, weaknessshould not be noted with an isolated injury of this nerve. If weakness is present, look for an injury of the femoralnerve 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. Someweakness may be present because of guarding or disuse atrophy from pain, but no direct weakness will resultfrom the nerve impingement. Sensory loss in the saphenous distribution may be present on examination. Noweakness 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 andproximal to the proposed site of entrapment. Nerve conduction techniques are available to assess neuralconduction in the main branch of the saphenous nerve or in the terminal branches. The routine tests may bedisappointing in persons with subcutaneous adipose tissue or swelling. A side-to-side comparison of the nerveshould be made, and must demonstrate a lesion consistent with the patient's complaints. A somatosensoryevoked potential (SSEP) test can also be performed and the results compared with those of the contralateralside for diagnosis, although this test may be cumbersome and time-consuming.

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

Treatment

Entrapment in the adductor canal usually is treated conservatively with an injection of anesthetic (with or withoutcorticosteroid) at the point of maximal tenderness (usually 10 cm proximal to the medial femoral condyle). Theinjection may need to be repeated periodically. Avoiding aggravating activities and using proper body mechanicswill also be helpful. If this approach fails, surgical decompression may be needed. In patients who have had adirect blow to the medial knee who have persistent medial knee pain despite conservative trials for treatment, aneurectomy or neurolysis of the infrapatellar branch may be helpful.

Obturator Nerve Entrapment

Anatomy

Anterior branches of the anterior primary rami of L2, L3, and L4 fuse to form this nerve. The major contribution isfrom L3, and the least amount of contribution typically is from L2. The rami fuse in the substance of the psoasmuscle and emerge from the medial border of the psoas beneath the common iliac vessels just lateral to thesacrum. The obturator nerve then travels along the lateral wall of the lesser pelvis to enter the obturatorforamen. Just anterior to the internal obturator muscle and prior to entering the thigh, the nerve divides into ananterior and a posterior branch. The anterior branch travels superficial to the internal obturator muscle but deepto 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 bycommunicating with the anterior cutaneous branches of the femoral and saphenous nerves. The nerve thengives off its motor branches to the muscles and extends its articular branches to the hip joint. The motorbranches arise distal to the obturator foramen to supply the adductor brevis, adductor longus, and gracilismuscles. Rarely, a terminal cutaneous branch may emerge from the inferior aspect of the adductor longusmuscle and follow the medial border of the sartorius muscle to the medial knee region, where it supplies the skinof the medial and distal thigh region.

Etiology


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The obturator nerve is rarely injured in isolation. However, injury can occur with pelvic trauma and associatedfractures, during delivery as a result of compression of the nerve between the head of the fetus and the bonystructures of the pelvis, or as a consequence of compression of the nerve between a tumor and the bony pelvis.Entrapment may also occur in the obturator canal during surgery or with total hip arthroplasties. Other potentialcauses include malposition of the lower limb for prolonged periods, entrapment in the adductor magnus inathletes, and abnormal positioning of the lower limb of a newborn during a difficult delivery. Some physiciansbelieve that the anterior branch may be entrapped in the fascia as it passes over the adductor brevis muscle,owing to an inflammatory process.[13 ]

Clinical

The main complaints in obturator entrapment include difficulty with ambulation and the development of anunstable leg. In an anterior branch entrapment, symptoms can consist of exercise-related pain or groinpain. The patient may describe a deep ache in the region of the adductor origin at the pubic bone that increaseswith exercise; the pain may radiate down the medial aspect of the thigh toward the knee. An athlete's ability tojump 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 anexternally rotated foot. Examination reveals wasting of the adductor muscles of the thigh and possiblydiminished 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 cutaneousnerve of the thigh, and inguinal hernia.

No routine conduction studies are available with which to evaluate the integrity of the nerve, and the needleexamination is the mainstay of testing with electrodiagnosis. Membrane instability (positive sharp waves andfibrillation potentials) will occur within 3 weeks of the nerve injury, and needle examination should be performedon patients with groin pain of longer than 3 months in whom this neuropathy is suspected. Complete injuryresults in a lack of active motor unit potentials. Muscles from the quadriceps (femoral nerve), as well as theparaspinal muscles, must be examined and found to be normal before an obturator nerve injury can bediagnosed. In this manner, one must rule out a radiculopathy and a plexus injury as potential causes of theweakness in adduction during the electrodiagnostic examination. A nerve block may be helpful but usually is notnecessary for diagnosis.

Treatment

For anterior nerve entrapment, treatment may consist of electrical stimulation of the adductor and hip flexormuscles, stretching, and massage. These modalities, however, typically have not been successful in resolvingthis condition if it is not recognized early. For athletes, surgery is the preferred treatment when clinical featuresof obturator neuropathy and denervation on electromyography are observed. The surgery involves dividing thefascia over the pectineus and the adductor longus muscles and dissecting the space between the 2 muscles toreveal the anterior branch of the nerve beneath a thick fascia. This fascia is divided along the line of the nerve,and the adductor longus-pectineus junction is closed loosely.

Common Peroneal Nerve Entrapments

Anatomy

The common peroneal nerve arises from the sciatic nerve at approximately the middle to distal third of the thighregion. At this point, it descends to the popliteal fossa, innervating the short head of the biceps femorismuscle.[14 ]It travels along the lateral aspect of the distal thigh beneath the cover of the long and short heads ofthe biceps femoris muscle to the region of the fibular head. Proximal to the fibular head, the common peronealnerve gives off 2 branches: the sural communicating branch, which assists in the formation of the sural nervewith a branch provided by the tibial nerve, and the lateral cutaneous nerve of the calf, which provides cutaneoussensation to the proximal and lateral aspect of the leg. It also supplies the knee joint via its articular branches.


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The common peroneal nerve then courses around the fibular neck and passes through the fibro-osseousopening in the superficial head of the peroneus longus muscle. This opening can be quite tough, and can resultin the nerve angulating through it at an acute angle. Also, significant fibrous connective tissue secures the nerveto this proximal portion of the fibula, potentially compromising the nerve.

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

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) andperoneus tertius muscles. (Please see Superficial Peroneal Nerve Entrapment and Deep Peroneal NerveEntrapment for further anatomic detail on these nerve branches.)

Etiology

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

As Kaminsky reported, the most common form of neural compromise in the region of the fibular head is due tocompression from habitual leg crossing, compression of the nerve against a bed railing or hard mattress indebilitated patients, or prolonged immobility, such as that observed in patients under anesthesia.[15 ]However, ina study of 146 cases, Piton and colleagues noted 55 cases due to idiopathic causes, 16 due to externalcompression, 59 due to various traumatic causes, and 9 due to intraneural and extraneural tumors.[16

]Traumatic causes can include wounds and contusions, direct fractures involving the lateral knee, and directlacerations or postsurgical entrapment in suture hardware.

Common peroneal nerve injuries at the region of the fibular head include ankle sprains with associated proximalfibular 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, fibrolipomatosishamartomas, exostosis, chondromatosis, Baker cysts, and vascular abnormalities.[17 ]

A number of other etiologic factors have been reported in the literature. Compression of the nerve against thefibrous or fascial layers of well-developed muscles of the legs in athletes has also been seen. Patients typicallypresent with exercise-related leg pain with or without associated dermatomal numbness. Coexisting pathologies,such as those in exercise-related compartment syndromes, add to the complexity of this diagnosis. Excessiveweight loss can also be a contributing factor in patients (slimmer's paralysis), as rapid weight loss and anorexiacan 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 peronealnerve compression (strawberry picker's palsy). This is likely the result of compression of the common peronealnerve as it penetrates the fibro-osseous opening in the peroneus longus muscle in persons with a fibrous ortight peroneal tunnel. A rare form of common peroneal nerve injury is that associated with natural childbirth, inwhich the woman compresses both peroneal nerves at the fibular head by pulling back on her knees with wristsresting on the fibular head during birthing. The nerve may also be injured during childbirth in the squatting


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position.

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

Clinical

Peroneal nerve lesions at the region of the knee or distal thigh usually result in patient reports of alteredambulation secondary to paretic or paralyzed ankle dorsiflexors. Loss of sensation in the cutaneous distributionof the superficial and deep peroneal nerves may be noted, but ankle dorsiflexion weakness is often of mostconcern to the patient.[18 ]

Pain is not universal with common peroneal nerve injuries, and, if present, is often related to the specific causeof the nerve compromise. For example, a nerve compromise secondary to traumatic injury from blunt trauma willlikely be accompanied by pain secondary to soft-tissue swelling and inflammation, while chronic compressionsecondary to habitual leg-crossing is often nonpainful. Tapping of the nerve at the fibular head may producepain 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 displaysa steppage gait pattern in which the affected foot is lifted excessively from the ground during the swing phase ofambulation in order to clear the foot. This results in excessive hip and knee flexion, and the appearance is as ifthe patient is stepping over an object in his or her path. In addition, a foot slap may be heard on foot strike, asthe ankle dorsiflexors cannot provide a controlled descent of the foot toward the floor. The patient might alsostumble when walking, secondary to the toes on the affected side dragging or catching on the floor during theswing-through phase of ambulation.

Examination often reveals a variable pattern of weakness, with the extensor digitorum brevis (EDB) musclebeing affected most profoundly. Ankle and toe dorsiflexion can be significantly affected. Dorsiflexion is besttested by having the patient place the ankle in the neutral position and then dorsiflex the foot and invert; thistests the TA muscle optimally. Often, ankle eversion is normal, as patients can have relative sparing of thesemuscles. 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 thefoot. Lateral calf sensation may be spared if the lesion is below the nerve branch to this region. When the neuralinsult occurs at the knee, the short head of the biceps femoris often is spared.

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

Plain radiographs may be helpful in excluding underlying traumatic injuries, such as a proximal fibular headfracture, or osseous tumors, or in assessing the severity of angular deformities about the knee. Computedtomography (CT) scans and magnetic resonance imaging (MRI) are helpful in finding a compressive lesionalong the course of the nerve in cases in which this is suspected. Metabolic and hematologic studies may behelpful 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 isclinically difficult to isolate and test the short head of the biceps muscle, the evaluation of which is critical indetermining whether a lesion is proximal to the knee and whether it involves the sciatic nerve, lumbosacralplexus, or nerve roots. In patients with exercise-induced symptoms, electrodiagnostic tests should be performedbefore and after exercise. Electrodiagnostic studies include the following:

Sensory conduction studies - A superficial peroneal sensory nerve action potential (SNAP) is important,


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and an abnormality of the sensory evoked response implies that the lesion is distal to the dorsal rootganglion, although this does not completely rule out the possibility of an L5 radiculopathy. A loss inamplitude of this response implies some axonal loss affecting either the common peroneal nerve or itssuperficial branch. The particular portion of the nerve that is injured cannot be determined if only asuperficial peroneal nerve sensory study is performed. Comparison of the latency and amplitude of thesuperficial peroneal SNAP with the contralateral limb is required to define an approximate degree ofaxonal loss.

Motor conduction studies - The most commonly performed test in determining peroneal conduction in theleg and across the fibular head is performed with the active electrode placed on the EDB muscle. Theperoneal nerve usually is stimulated at the ankle, several centimeters below the fibular head and about10 cm proximal to the fibular head, just medial to the biceps femoris tendon. This allows for calculation ofthe nerve conduction velocity (NCV) across the fibular head region, with comparison with the distal legsegment.

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 theTA. 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 greater axonaldiameter in the proximal segment of the nerve.

If the contralateral limb responses are normal, one can estimate the amount of axonal loss byexpressing the compound muscle action potential (CMAP) on the affected side as a percentage ofthe nonaffected side. This method is independent of the location of the active recording electrodeand is valid in both circumstances. A change of 20-50%, depending on the source, is believed torepresent a conduction block. In addition, one may assess the degree of conduction slowing andtemporal dispersion to determine whether the lesion is predominantly demyelinating versusaxonal.

Needle electromyography - Needle electromyography helps in confirming axonal loss and in assessingthe degree of involvement of the muscles innervated by the superficial peroneal nerve. This portion of thenerve usually is less severely involved than the deep peroneal nerve. It is possible to localize the lesionto either the deep or superficial peroneal nerves, specifically if appropriate abnormalities are detected inthe proper distribution for each nerve. The most valuable aspect of the needle EMG examination is that itcan be used to define the proximal extent of the lesion. If an amplitude drop is lacking across the fibularhead but the TA CMAP is lower than that of the unaffected side (suggesting axonal loss), it is difficult tolocalize the lesion to the fibular head, despite the fact that this is the most common site of peroneal nerveinjuries.

In any peroneal nerve injury, regardless of the suspected site of nerve compromise, examining theshort head of the biceps femoris muscle is important. If this muscle demonstrates membraneinstability (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) andtibialis posterior muscles, is also important, because they contain predominantly L5 neuralinnervation from the tibial nerve. If a radicular process is present, the muscles innervated by theperoneal and tibial nerves should demonstrate membrane instability.

Treatment

Initial nonoperative treatment should focus on maximizing mobility and function. In addition, the cause of nervecompromise or compression should be corrected to reduce further nerve damage. NSAIDs or oralcorticosteroids may be useful in cases in which an inflammatory process is present. Corticosteroids injected intothe affected region may reduce swelling and pressure on the nerve in some cases. Symptomatic pharmacologictreatment may consist of tricyclic antidepressants (amitriptyline) or neuroleptic medications, such as gabapentinand carbamazepine.


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

Many authors have reported spontaneous recovery; therefore, initial nonoperative management for a minimumof 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 nervecompression due to external causes, such as those associated with intraneural or extraneural tumors ormasses. Löwenstein and colleagues recommend early surgical treatment in cases involving intraneural ganglioncysts, in order to minimize neural invasion (which may cause irreversible axonal injury and footdrop).[19 ]Incases 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 andcoauthors reported on 62 patients who were treated with operative decompression of the common peronealnerve.[20 ]The postoperative recovery of motor function was good in 87% of those who had sensory and motorinvolvement preoperatively. All 7 patients who had peroneal nerve entrapment of known etiologyalso demonstrated postoperative improvement. On the basis of their results, the authors recommend opendecompression of the peroneal nerve between the third and fourth months if symptoms persist or recovery isincomplete, even if the patient has only sensory symptoms that have been substantiated by electrophysiologicstudies.

The procedure involves a curved incision about the lateral knee, following the course of the nerve. The nerve isfound initially posteromedial to the biceps femoris. It is tracked distally to where it branches to the deep andsuperficial branches. The nerve is released fully by initially separating the lateral septum between the peroneuslongus and soleus aponeurosis, retracting the peroneus longus muscle medially, and fully dividing the superficialand deep portions of the fibrous arch. Any sites of entrapment or compression along this route should bereleased. Nerve grafting may be warranted in severe cases in which the nerve is structurally damaged orsevered.

Posterior Tibial Nerve Entrapment: Tarsal Tunnel Syndrome

Tarsal tunnel syndrome is the entrapment of the posterior tibial nerve or one of its branches. This entrapmenttypically occurs within or distal to the tarsal canal, resulting in pain and/or sensory disturbance on the plantaraspect of the foot. Kopell and Thompson first reported entrapment of the posterior tibial nerve in 1960.[21 ]In1962, Keck and Lam independently used the term tarsal tunnel.[22,23 ]Historically, tarsal tunnel syndrome wasdefined 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 werenoted 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 differentiatethe location of entrapment, some authors have used the term proximal tarsal tunnel syndrome to defineentrapment of the posterior tibial nerve in the fibro-osseous tunnel behind the medial malleolus, and the termdistal tarsal tunnel syndrome to denote entrapment of the distal branches, that is, the medial and lateral plantarnerves. In addition, others have more specifically identified entrapments involving the first branch of the lateralplantar nerve and the calcaneal nerves. However, the term tarsal tunnel syndrome is often used to define allentrapments of the posterior tibial nerve or its branches starting from posterior to the medial malleolus andextending distally.[24 ]

A slight female predominance has been reported in some studies, and the range of patient ages has beenreported to be 14-80 years. This condition is common in nonathletes, although Baxter initially noted it inlong-distance runners.[25 ]


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Anatomy

The posterior tibial nerve (L4-S3) is a branch of the sciatic nerve. After entering the lower leg between the 2heads of the gastrocnemius, the nerve is deep to the soleus muscle in the deep posterior compartment of theleg. The tibial nerve lies between the posterior tibial muscle and the FDL muscle in the upper leg; in the lowerleg, it is between the FDL and the flexor hallucis longus. It then travels behind the medial malleolus, through theproximal tarsal tunnel, where it divides into its terminal branches, the medial and lateral plantar nerves. Haveland colleagues have shown that in 93% of cases, this bifurcation occurs within 2 cm of an imaginary line drawnbetween the middle of the medial malleolus and the midcalcaneus.[26 ]Calcaneal branches, which have a highlyvariable anatomy, are present.

Most individuals (79%) have a single calcaneal nerve, usually arising from the posterior tibial nerve butsometimes arising from the lateral plantar nerve. About 21% have multiple calcaneal branches originating fromthe posterior tibial nerve, lateral plantar nerve, or medial plantar nerve, or from a combination of these. Thecalcaneal branches travel over the abductor hallucis muscle and supply sensation to the medial heel pad. Themedial calcaneal nerve or nerves penetrate the flexor retinaculum and innervate the skin over the medial andposterior 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, alsocalled the laciniate ligament. The retinaculum is formed by the deep and superficial aponeurosis of the leg andis attached closely 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 themedial fascia of the quadratus plantae and then continues deep to the flexor digitorum brevis muscle. Althoughsomewhat variable, it has several branches. It typically provides a sensory branch to the medial calcanealtuberosity, motor branches to the flexor digitorum brevis muscle, and sometimes a motor branch to thequadratus plantae. It then provides a sensory branch to the lateral heel and a motor branch to the abductor digitiquinti muscle.

Various anomalies have been reported, including the direct origination of all branches of the medial and lateralplantar 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 nerveprovides motor branches to the abductor hallucis, flexor digitorum brevis, and flexor hallucis brevis, as well as tothe first lumbrical.

Etiology

Although tibial nerve entrapment can be seen anywhere along the course of the nerve, the most commonlocation is distal to the ankle. Entrapments above the ankle have been reported in the popliteal fossa, where thenerve can be compressed by the tendinous arch of origin of the soleus muscle, a Baker cyst, or other massesthat may occur in this region.

Compression of the posterior tibial nerve or one of its branches can occur because of intrinsic neuralabnormalities or can result from external compression. External compression etiologies reported in the literaturehave included fibrosis, neurilemomas, ganglion cysts, lipomas, osteochondromas, varicosities, other benign andmalignant tumors, tight tarsal canal, hypertrophic abductor hallucis, anomalous artery, and anomalous extramuscles (eg, the flexor digitorum accessorius longus). Other conditions that have been reported to contribute tothe development of tarsal tunnel syndrome include tenosynovitis of the adjacent tendons, partial or completerupture of the medial tendons, obesity, ankylosing spondylitis, acromegaly, and talocalcaneal coalition.


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Several studies have suggested that compression of the posterior tibial nerve plays a role in the neurologicdeterioration and loss of sensory and motor function in patients with long-standing diabetes mellitus. Wiemanand 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.[27 ]

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

In the original case report and description of the condition in a patient with bilateral symptoms, Keck foundtortuous posterior tibial veins surrounding the nerve, which he describes as resembling a varicocele.[22 ]Sincethen, one of the most commonly encountered and reported causes of tarsal tunnel syndrome has been varicoseveins.

Sammarco and Chang found that the most common surgical findings in 62 tarsal tunnel releases includedarterial vascular leashes and varicosities, which cause indentation and scarring about the nerve.[28 ]Ciminofound 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.[29 ]Gould and Alvarez reporteda case in which surgery revealed varicosities overlying the medial and lateral plantar nerves at their origin.[30

]Turan and colleagues also noted varicose veins more commonly than other compressive etiologies.[31 ]Theenlarged vessels crossing the nerve are theorized to cause direct compression of the posterior tibial nerve andits 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 plantarnerve in the athlete.[25 ]They proposed that entrapment results from the stretching and tethering of the plantarnerves, which are encased in the abductor hallucis deep fascial leashes, and from the hypertrophy of the smallfoot muscles, as well as from the increased forces in the hindfoot in the running athlete that create additionalmicrotrauma 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 factor in chronicstretch injury of the posterior tibial nerve. Budak and coauthors noted prolonged distal latency of the medial andlateral plantar sensory nerves and delayed sensory conduction velocity of the medial plantar sensory nerve inpatients with pes planus.[32 ]Labib and colleagues reported on 14 patients who underwent surgical treatment forwhat they termed the heel pain triad.[33 ]The triad consists of plantar fasciitis, posterior tibial tendon dysfunction,and tarsal tunnel syndrome. They postulated that failure of the static (plantar fascia) and dynamic (posteriortibial tendon) support of the longitudinal arch of the foot results in traction injury to the posterior tibial nerve.Trepman and coauthors reported increased pressure in the tarsal tunnel with the foot and ankle in full eversionor full inversion.[34 ]

Entrapment of the first branch of the lateral plantar nerve beneath the deep fascia of the abductor hallucismuscle and/or beneath the medial edge of the quadratus plantae fascia are the most commonly seen causes oftarsal tunnel syndrome.

Entrapment of the medial plantar nerve typically occurs in the areas of the master knot of Henry. It is seen mostcommonly in athletes; in 1978, Rask called it jogger's foot. It is theorized that excessive valgus or externalrotation of the foot during running puts excessive stretch on the medial plantar nerve, resulting in tarsal tunnelsyndrome. This condition has been seen in runners with flat feet who use corrective orthotics that can compressthe nerve in the medial arch.

Clinical

Patients with proximal tarsal tunnel usually present with diffuse, vague discomfort or pain. They may haveburning, tingling, or frank numbness in the plantar foot. Although occasionally a history of trauma is reported,


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

Patients with distal entrapment of the lateral plantar nerve or its branches usually present with chronic heel painthat has been present for 9-12 months. Many of their symptoms are similar to plantar fasciitis, especially thelocation of their pain and their startup pain. In addition to the mechanical symptoms of plantar fasciitis, theypresent 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, thesymptoms 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 withincreased 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 seen commonly in individuals who are in their fifth and sixth decades of life, and it ismore common in women than in men. Correlation with the patient's weight has not been found consistently.Most investigators have not been able to identify a significant common factor regarding occupation or underlyingfoot structure.

Some patients with tarsal tunnel syndrome have concomitant peripheral neuropathy or radiculopathy. Patientswith 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 vitamindeficiencies, are at increased risk for entrapment neuropathy.

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

Inspection of the patient while the patient is standing and walking allows the examiner to evaluate for alignmentdeformities, 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, includingSemmes-Weinstein monofilament testing of the entire foot, may reveal dermatomal numbness due tocompression neuropathy, or could reveal peripheral neuropathy. The range of motion of the ankle, subtalar, andthe midfoot joints is examined, and any limitations are noted. The patient may report an increase in pain withdorsiflexion and eversion or inversion of the foot; Trepman and colleagues have shown these positions toincrease the tarsal compartment pressure.[34 ]Motor examination should include asking the patient to spread hisor her toes so that an assessment can be made of the abductor digiti minimi or abductor hallucis and abductordigiti 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-occupyinglesions in the tarsal tunnel that may be palpable. They may also have positive Tinel signs along the posteriortibial nerve. Occasionally, nerve percussion causes symptoms and pain to radiate proximally to the nervecourse. This is known as the Valleix phenomenon. Linscheid noted that in most of his patients with proximaltarsal tunnel syndrome, manual compression of the nerve at the tarsal tunnel for 60 seconds reproduced theirsymptoms.[35 ]


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Patients with distal tarsal tunnel syndrome usually have the most severe tenderness over the first branch of thelateral plantar nerve over the plantar medial heel and under the abductor hallucis muscle. Many patients havetenderness along the entire posterior tibial nerve, starting from behind the distal medial malleolus. Additionaltenderness is usually present over the plantar fascia insertion on the medial calcaneal tuberosity and sometimesalong 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 thenavicular tuberosity, but not directly over the plantar fascia. Numbness and/or a Tinel sign over this area may bepresent only after prolonged weightbearing exercise. Stretching of the nerve as a result of eversion of the footor of standing on the toes may also reproduce or exacerbate symptoms.

The diagnosis of tarsal tunnel syndrome (proximal and distal) is based primarily on a detailed history andphysical examination. Plain radiographs should probably be obtained to exclude extrinsic factors, such asexostoses, malunions, or osteochondromas that cause direct nerve compression. In patients with posttraumaticsymptoms, 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. Furtherscreening studies, such as laboratory workup for arthritides, diabetes, alcoholism, and thyroid dysfunction, areindicated 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. Acomplete electromyographic and nerve conduction study of the motor and sensory nerves to the foot, withcomparison to the other foot, is necessary. It is important for the electromyographic examination to includemotor latencies, particularly to the abductor digiti minimi and abductor hallucis muscles, when tarsal tunnelsyndrome is suspected.

Kaplan and Kernahan reported that reduced amplitude and increased duration of the motor response are moresensitive indicators of tarsal tunnel syndrome than is distal motor latency.[36 ]Sensory action potentials may beaffected in earlier stages than are motor fibers; therefore, changes may also be identified prior to any motorabnormalities. This is due to the fact that sensory fibers are more susceptible to injury. In addition, Kaplan andKernahan believed that the lateral plantar branch of the posterior tibial nerve probably is affected earlier than isthe nerve's medial plantar branch. Sensory studies are, therefore, considered to be the most sensitive studiesfor tibial nerve entrapment.

Galardi and colleagues reported that, after stimulation of the plantar nerves, the accuracy of the SNAP andmixed-nerve action potential are almost the same. SNAPs are more sensitive and less specific, andmixed-nerve action potentials are less sensitive and more specific. They concluded that the coexistence ofmixed-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 andNCV studies. However, in the presence of supportive history and physical examination, a normalelectrodiagnostic study does not exclude the diagnosis of tarsal tunnel syndrome. Electrodiagnostic tests,however, can be extremely helpful in diagnosing concomitant polyneuropathy, systemic disorders, andlumbosacral 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 entrapmentsyndromes and signs of proximal nerve damage of the corresponding nerves (partial muscle denervation orabnormalities of the F wave).[37 ]In such cases, simultaneous treatment of both problems may be indicated.

Treatment


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Treatment is directed toward the underlying etiology of neural compression. Nonoperative options can includethe use of NSAIDs (in cases associated with inflammation), aspiration of underlying cystic lesions, and edemaand 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 beenshown to improve symptoms in many patients.

At times, a trial of immobilization with the use of casts or walking boots is indicated. Orthotic management isindicated in patients with proximal entrapment and alignment or postural abnormalities causing chronic tractionor 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 usuallyhelpful. Patients with flatfoot may benefit from semirigid University of California at Berkeley Laboratory(UCBL)–type orthotic devices with a deep heel cup to minimize weightbearing traction on the nerve.

Surgical release is indicated for refractory cases and for most cases with space-occupying lesions. The locationof the release is partially dependent on the location of entrapment. Most cases, however, require a full releaseof the posterior tibial nerve and of the lateral plantar nerve and its branches. The skin is marked for theproposed 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 andplantarly, 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 medialmalleolus and moving distally to include release of the deep fascia of the abductor hallucis muscle. Theneurovascular bundle is posterior to the flexor digitorum brevis. Typically, medial and lateral plantar nervesbranch at the level of the medial malleolus. It is best to identify the posterior tibial nerve proximally and follow itdistally.

All sources of potential impingement are released from the medial and lateral plantar nerves. The medialcalcaneal branches are quite variable and should be watched for closely. A large number of vessels areencountered routinely, and some crossing veins may need to be ligated. Ensuring full release of the lateralplantar nerve and its first branch is important. The superficial and deep fascia of the abductor hallucis isreleased as the nerve is followed distally. Partial release of the plantar fascia is usually necessary for fullvisualization. No consensus exists in the literature about the necessary amount of plantar fascia release.

The extent of the plantar fascia release may be dictated partially by the arch height, and a full release may beindicated 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 lateralplantar nerve and its first branch. The usual course of the lateral plantar nerve is just anterior to the heel pad. Asthe lateral plantar nerve is followed, any compressive fascial bands are cut. The fascia of the quadratus plantaeis also identified and released if it is noted to cause any compression by the medial edge of the quadratusplantae fascia on the first branch of the lateral plantar nerve. In cases of associated space-occupying lesions,the incision is modified as necessary for complete excision of the tumor.

Bipolar electrocautery and surgical loupe magnification are necessary for optimal visualization. It is important tominimize handling of the nerve. Often, large varicosities are present that should be considered as part of theunderlying compressive etiology. Care should be taken to avoid injury to these large vessels, because suchdamage significantly compromises visualization and can cause intraoperative and postoperative bleeding, aswell as postoperative scarring. The medial plantar nerve is fully released. The tourniquet is released prior toclosure to ensure that no major bleeding occurs.

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


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Postoperatively, the patient with a distal release of the nerve and full plantar fascia release is kept onnonweightbearing status for 4-6 weeks. In patients with lesser releases of the plantar fascia, weight bearing isprotected 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 ofthe nerve branches (which usually is associated with intractable heel pain).

If entrapment of the medial plantar nerve is suspected, the incision beyond the medial malleolus curves towardthe 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.[25 ]Theyperformed 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 muscleand at the medial ridge of the calcaneus where the nerve passes over it beneath the tuberosity or origin of theflexor brevis and plantar fascia. They reported that 32 had good results and 2 had poor results. Most patientscould detect improvement during the first or second postoperative day. Anti-inflammatory medication andorthosis use were continued postoperatively.

Watson and colleagues reported good-to-excellent results in 84% of patients who underwent distal tarsal tunnelrelease and partial plantar fasciotomy.[38 ]Bailie and Kelikian reported that 84% of their patients in thenoncompensation group were very or moderately satisfied with the outcome.[39 ]They also reported bettersatisfaction in patients with nontraumatic etiology than in others. Sammarco and Chang subsequently reportedon 108 ankles with tarsal tunnel syndrome.[28 ]They found that patients with symptoms lasting less than 1 yearhad significantly better postoperative scores than did patients who had symptoms for more than 1 year beforesurgery. They did not observe an effect of trauma on the outcome of surgery, and reported that improvementwas predictable even when a space-occupying lesion was not identified at surgery.

Tarsal tunnel syndrome is diagnosed primarily 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 theposterior tibial nerve is a common cause of refractory heel pain, and the most common compression neuropathyseen in the foot and ankle region. Nonoperative management of compression of the posterior tibial nerveinvolves relief of the source of external compression (if any), use of medication, and correction of weightbearingdeformities. Surgical release in patients with proximal or distal entrapment has an 80-90% likelihood ofimproving or resolving the symptoms.

In one study, revision tarsal tunnel surgery was performed on 44 patients (2 bilaterally), including a neurolysis ofthe tibial nerve in the tarsal tunnel; the medial plantar, lateral plantar, and calcaneal nerves in their respectivetunnels; excision of the intertunnel septum; and neuroma resection as indicated. A painful tarsal tunnel scar anda painful heel were treated, respectively, by resection of the distal saphenous nerve and a calcaneal nervebranch. Patient-satisfaction ratings were 54% excellent, 24% good, 13% fair, and 9% poor. Prognostic indicatorsof poor results were coexisting lumbosacral disc disease and/or neuropathy. The authors note that an approachrelated to resecting painful cutaneous nerves and neurolysis of all tibial nerve branches at the ankle offers hopefor relief of pain and recovery of sensation for the majority of patients with failed previous tarsal tunnelsurgery.[40 ]

Superficial Peroneal Nerve Entrapment

Anatomy

The superficial peroneal nerve travels in the lateral compartment and supplies the peroneus longus and brevismuscles. In most individuals, the superficial peroneal nerve pierces the deep fascia and emerges into thesubcutaneous fat at approximately the level of the middle and lower third of the leg and at an average of about10-15 cm above the tip of the lateral malleolus.[41 ]At an average of 4-6 cm proximal to the ankle joint, it dividesinto a large (2.9 mm) medial dorsal cutaneous nerve and a smaller (2 mm), more laterally located intermediate


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dorsal cutaneous nerve.

In 28% of patients, the superficial peroneal nerve branches more proximally. In these cases, the medial dorsalcutaneous branch usually follows the more common track of the superficial peroneal nerve and emerges intothe subcutaneous tissues in the distal lateral leg. The intermediate dorsal cutaneous nerve penetrates the cruralfascia more distally, either anterior or posterior to the fibula and at an average of 4-6 cm proximal to the anklejoint. At the level of the malleoli, in most patients, the medial dorsal cutaneous nerve is located at approximatelyhalf of the distance from the lateral malleolus to the medial malleolus, and the intermediate dorsal cutaneousnerve 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 aspectof the hallux, and the second and third digits (except for the first webspace). The intermediate dorsal cutaneousnerve 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 nervehas also been found to innervate the EDB in some patients.[42 ]

Etiology

Local trauma or compression is the most common underlying cause of entrapment of the superficial peronealnerve. Repeated ankle sprains or the use over many years of certain positions, such as prolonged kneeling andsquatting, can make certain individuals more prone to the development of symptoms. This tendency is thoughtto be due to recurrent stretch injury to the nerve. Perineural fibrosis of the superficial peroneal nerve at the levelof the ankle following an inversion ankle sprain has been reported.[43 ]

This nerve is also at risk for direct injury by any procedure about the anterior ankle, including use of theanterolateral ankle arthroscopy portal. Chronic or exertional lateral compartment syndrome can also causecompression of the superficial peroneal nerve, particularly in athletes.

Nontraumatic causes of entrapment are commonly due to anatomical variations, such as fascial defects with orwithout muscle herniation about the lateral lower leg, where the nerve is entrapped as it emerges into thesubcutaneous tissue, or a short peroneal tunnel proximally.

Clinical

Although patients may present with numbness or paresthesia in the distribution of the nerve, and occasionallyhave pain about the lateral leg, the most typical presentation is vague pain over the dorsum of the foot. The paincan be chronic, present for several years, and associated with other foot and ankle symptoms, or the pain canbe acute and associated with recent trauma or surgery about the ankle. Use of the anterolateral arthroscopyportal, specifically, puts this nerve at risk for direct or stretch injury, as do noninvasive traction methods withstraps over the dorsum of the foot. About one quarter of patients have a history of previous or recurrent anklesprains or trauma.

Typically, symptoms increase with activity, such as running, walking, or squatting; rest or the avoidance of aspecific activity often relieves the symptoms. This tendency is particularly pronounced in athletes whosesymptoms 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 fracturesof 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


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bulging mass in the leg.

Examination should include the entire course of the nerve, starting from the lower back and extending throughthe sciatic notch, proximal fibula, and lateral leg, where a muscle bulge due to a fascial defect may be palpatedin some patients. Percussion along the superficial course of the nerve over the proximal fibula, lateral leg, oranterior ankle may result in a positive Tinel sign, with reproduction of radiating pain. Direct palpation withpressure on the site of entrapment may also induce or exacerbate symptoms. Repeating the examination after aparticular 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 3provocative tests for nerve compression at rest and again at rest but after exercise.[44 ]In the first test, pressureis applied over the anterior intermuscular septum while the patient actively dorsiflexes the ankle. In the secondtest, the foot is passively plantarflexed and inverted at the ankle. In the third test, while the patient maintains thepassive 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 maypresent with symptoms of reflex sympathetic dystrophy (RSD)/complex regional pain syndrome (CRPS), whichcreates a diagnostic and therapeutic challenge.

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

Although rare, plain radiographs of the leg may reveal bony abnormalities that may contribute to or be the causeof entrapment. In cases of suspected proximal entrapment, knee radiographs may show abnormalities of theproximal fibula, such as exostoses, osteochondromas, and fracture callus. If necessary, a CT scan can providemore detailed information on the bony anatomy of the area, and an ultrasonogram can help to localize cysticmasses that impinge on 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 atrest after exercise may be helpful.

Injection of the nerve with lidocaine or bupivicaine (Marcaine) just above the site of involvement can be the mostvaluable diagnostic tool. The patient can define the extent of relief obtained from such an injection, which can behelpful 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 fromelectrodiagnostic 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 thenerve and help to better define the zone of compression. They also help in the evaluation of concomitantradiculopathy or peripheral neuropathy.

Treatment

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

At times, injection of steroids plus lidocaine near the site of involvement in the lower leg can reduce symptomsand 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


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associated with CRPS. In these cases, combination treatment with medication, physical therapy, and local andsympathetic nerve blocks may be required.

Surgical decompression may be indicated in cases refractory to nonoperative options. This can include releaseof 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 generally is not indicated, as it hasnot been shown to improve outcome.

Styf and Morberg reported that 80% of their patients were free from symptoms or satisfied with the result afterdecompression of the superficial peroneal nerve.[45 ]Three of 14 patients had local fasciectomy as well.

Styf reported on fasciotomy and neurolysis to treat entrapment of the superficial peroneal nerve in 24 legs (21patients).[44 ]Nine patients were satisfied with the result, another 6 had improvement but were not satisfiedbecause 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 wasinsignificant. In 5 patients, the nerve had an anomalous course, and in 11 patients, fascial defects were presentover the lateral compartment. The author concluded that operative decompression of the superficial peronealnerve 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.[46 ]Johnston and Howellreported dramatically relieved pain after release and anterior transposition of the nerve in patients who had hadneuralgia after inversion ankle sprain.[47 ]

The surgical procedure to release the superficial peroneal nerve at the anterolateral leg involves determiningand marking preoperatively the location of maximum tenderness and, if present, lateral muscle herniation. Theprocedure is performed using magnifying loupes and a tourniquet. A 5-cm longitudinal incision is made over theanterolateral 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 dorsalcutaneous nerve through the fascia, in which case 2 separate incisions could be considered. A bluntsubcutaneous dissection is made, and the nerve is found where it emerges through the fascia. A localfasciotomy is performed, releasing the nerve proximally and distally until it is completely free. A completefasciotomy, as advocated by some authors, is considered in cases associated with chronic compartmentsyndrome. 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, surgicalexcision of the nerve can be performed at the site of neuroma. If several branches are involved, excision of thenerve at the anterolateral leg can be considered. Dellon and Aszmann reported excellent results in 9 of 11patients who underwent resection of the nerve and translocation of the proximal nerve stump into the muscles ofthe anterolateral compartment, combined with fasciotomy of the anterolateral compartment.[48 ]

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

Vague and diffuse symptoms can create a diagnostic and therapeutic challenge for the treatment of theentrapped 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 beundertaken, as should release of the entrapped nerve and excision of existing neuromas.

Deep Peroneal Nerve Entrapment

Anatomy

The deep peroneal nerve is 1 of the terminal branches of the common peroneal nerve, originating just distal to


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the fibular head.[49 ]The deep peroneal nerve enters the anterior compartment in front of the interosseousmembrane. It courses lateral to the TA muscle. It travels along with and usually lateral to the anterior tibial arteryand vein.

It courses between the TA and the EDL in the proximal third, and between the TA and EHL in the middle third ofthe leg and anterior to the anterior tibial vessels. At approximately 3-5 cm proximal to the mortise, the EHLcrosses over the nerve, and the nerve is then seen between the EHL and EDL in the distal part of the leg, at anaverage of 1.25 cm above the ankle joint. Occasionally, the nerve does not enter this interval until just distal tothe ankle mortise. At this level, the nerve is about 3 mm in size and may be under the extensorretinaculum, because the inferior extensor retinaculum can be centered, above, or below the ankle mortise level.

At approximately 1 cm distal to the ankle mortise, the nerve divides into lateral and medial branches. Theterminal lateral branch curves laterally and supplies the EDB, the extensor hallucis brevis (EHB), the adjacenttarsal 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 tarsometatarsaljoint. It travels between EHL tendon and EHB muscle on the dorsum of the foot. At approximately themetatarsophalangeal (MTP) joint level, the EHB crosses over the nerve, and the nerve is then between the EHBand the EDL to the second toe. It then divides into the dorsolateral cutaneous nerve of the great toe and thedorsomedial cutaneous nerve of the second toe. It supplies sensation to the web between the first and secondtoes, the dorsalis pedis artery, the adjacent MTP and interphalangeal joints, and usually the first dorsalinterosseous 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 mechanicalirritation of the nerve at the ankle beneath the extensor retinaculum. Entrapment of the deep peroneal nerve inthis location has also been called the anterior tarsal tunnel syndrome. Within the anterior tarsal tunnel, there are4 tendons, 1 artery, 1 vein, and the deep peroneal nerve. Typically, the nerve is trapped beneath the superioredge of the retinaculum. In this location, it is compressed by the crossing EHL tendon and under the EHBmuscle, 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 andsecond metatarsal base has also been associated with entrapment symptoms.

Space-occupying lesions, such as ganglia, also contribute to symptoms in this tight canal. Repeated dorsiflexionand 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, andprolonged 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, includingjust distal to the neck of the fibula, anterior to the ankle joint, and distal to the inferior extensor retinaculum, butsuch entrapment would not be considered anterior tarsal tunnel syndrome. Common etiologies for proximalentrapment of the deep peroneal nerve include space-occupying lesions about the proximal fibula, surgicalprocedures about the lateral knee (including proximal tibial osteotomy), and chronic anterior exertionalcompartment 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


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associated sensory changes in the first dorsal webspace. Some patients may present with neuritic symptomsalong the course of the nerve, such as unrelenting pain at rest and during sleep. There may be pain in the ankleregion even if only the motor nerve is involved. Symptoms may occur or worsen only with a certain shoe or bootor with certain activities. Although less common, patients with more proximal entrapment may present withfrequent tripping due to foot drop or weakness of the EHL.

With proximal entrapment, motor dysfunction may be demonstrated on regular gait examination, withpresentations such as a dramatic foot drop. However, symptoms are usually more subtle and are noted only onheel walk or a hop test. With long-standing dysfunction, plantarflexion of the ankle with extension of the toes cancompress the nerve as it passes beneath the extensor retinaculum, which can worsen the symptoms. Muscularatrophy 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 anteriorankle or just distal to it, and an underlying bony prominence is usually present. Provocative dorsiflexion andplantarflexion of the ankle may bring on or increase symptoms. A sensory deficit in the first webspace may alsobe detectable. Most patients have a positive Tinel test result over the entrapment site, commonly around thefibular neck or over the anterior ankle.

Incomplete involvement can also occur, affecting isolated sensory or motor branches. Temporary resolution ofneuritic symptoms following an injection of the nerve with plain lidocaine at the site of entrapment is a goodindicator verifying the diagnosis.

Bony impingement can usually be seen on conventional lateral ankle or foot radiographs. Obliqueradiographs taken from different angles are necessary to better define smaller osteophytes, exostosis, or otherbony masses about the anterior ankle or the dorsomedial midfoot. Knee radiographs are needed for suspectedproximal involvement. If necessary, a CT scan will provide more detailed information on the bony anatomy of thearea.

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

Electrodiagnostic studies are helpful in further defining the zone of compression and in evaluating forconcomitant radiculopathy or peripheral neuropathy. In deep peroneal nerve injury or entrapment, the resultsmay show a decrease in the amplitude of the response if axonal involvement is present or conduction blockoccurs from demyelination. The distal latency may be prolonged if entrapment is present in the anterior tarsaltunnel region, and the NCV is decreased across the leg region if the entrapment or injury is more proximal. Anaccessory nerve may also be present. The accessory peroneal nerve originates from the superficial peronealnerve and traverses posterior to the lateral malleolus to provide variable innervation to the EDB. This anomaly isidentified when the response is recorded from the EDB that is larger with proximal stimulation (at the fibularhead) than with distal stimulation (at the ankle).

Needle examination may reveal the presence of fibrillations and positive sharp waves in the EDB only if presentat the anterior tarsal tunnel. If entrapment is present more proximally, the denervation is present in the TA aswell 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 iffindings in the deep peroneal muscles rule out a more proximal problem, such as a radiculopathy. The absenceof findings in these muscles, as well as in the peroneus longus and brevis, confirms the presence of a deepperoneal motor-nerve injury.

Some reports have stated that there may be a high percentage of denervation in the foot intrinsic muscles inhealthy subjects, but subsequent reports have found that the actual percentage of abnormal findings in healthy


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subjects is low for a well-trained electromyographer. Many times, electrodiagnostic test findings are normalbecause these dynamic syndromes frequently improve or resolve at rest.

Treatment

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

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

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

NSAIDs and antineuritic medication may be helpful as an adjunct to other treatment modalities. Injection ofsteroids 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 inselect 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 thenerve in cases of direct nerve injury due to previous surgery, in cases of direct trauma, or in revision cases.Surgical decompression of the nerve can provide immediate improvement of symptoms.

Dellon reported on surgical release of the deep peroneal nerve in 20 patients.[50 ]With a mean follow-up time ofmore than 2 years, he reported excellent results in 60% of patients, good results in 20% of patients, and noimprovement in 20% of patients.

The surgical procedure can include part or all of a longitudinal straight or S -shaped incision on the dorsum ofthe foot, starting between the bases of the first and second metatarsals and extending proximally to the anteriorankle, depending on the predicted location of entrapment. The deep fascia overlying the deep peroneal nerveand the dorsalis pedis artery is released, as is the inferior part of the extensor retinaculum; the superior part canbe preserved to maintain the function of the extensor tendons. The deep peroneal nerve is followed proximallyand distally to verify a full release. Nerves that appear to be normal in consistency and size can be released.[51 ]

It is important to treat other underlying etiologies for entrapment or stretch, such as complete excision ofunderlying 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 isabnormal, such as those directly manipulated during surgery or entrapped in scar tissue, is indicated. Neuromain continuity is best excised and allowed to retract into deep tissues, and transposition of the stump into musclebelly may be possible, depending on the level of excision. Dellon and Aszmann reported on excision of thesuperficial and deep peroneal nerves in the lateral leg, with translocation of the nerves into a muscle (withexcellent results obtained in 9 of 11 patients).[48 ]

When entrapment of the nerve is caused by the EHB muscle, the muscle is hypertrophied and has thick fibrousbands that compress the deep peroneal nerve. Decompression of the nerve and excision of the muscle andfibrous 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 tothe fibular head to the dorsal first webspace. The most common location of entrapment is just anterior to theankle, under the extensor retinaculum. Entrapment at this site is also called anterior tarsal tunnel syndrome. Themost common etiologies for entrapment include prominent bony or soft-tissue masses, such as exostoses,


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osteophytes, and ganglion cysts, as well as acute direct trauma and chronic compression or stretch, as withlace-up shoes or high heels.

The most common presenting symptom is a vague pain on the dorsum of the foot, with occasional, associatednumbness 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 known more commonly as Morton neuroma, is a condition that results fromentrapment of a plantar interdigital nerve as it passes under the transverse metatarsal ligament.[52 ]Thiscondition was named after Thomas Morton, who reported "a peculiar and painful affection of the fourthmetatarso-phalangeal articulation" in 1876.[53 ]The condition has since been defined as a perineural fibrosis ofthe involved interdigital nerves, and true neuromatous involvement is not seen.

Other terms used for this condition include interdigital neuroma, Morton metatarsalgia, and interdigital nervecompression.

This condition is most common in the second or third interspace, but occurrences in the first and fourthinterspace have been reported. Double neuromas occurring in the second and third interspace are notuncommon. 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 nervedivides into 3 common digital nerves, which in turn bifurcate, supplying cutaneous branches to the medial 3.5digits. The lateral plantar nerve gives rise to 2 common digital nerves, supplying cutaneous branches to thelateral one and a half digits. As the common digital nerves travel distally, they pass plantar to the transverseintermetatarsal ligament.

Substantial variability has been noted in the cutaneous innervation of the webspace and in the plantar aspect ofthe 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 thetransverse intermetatarsal ligament. As weight is transferred to the ball of foot when the toes are dorsiflexedduring the last phase of stance, the interdigital nerve is compressed between the plantar foot and the distaledge 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 often areseen; their presence suggests that nerve damage occurs secondary to mechanical impingement. Using electronmicroscopy, Ha'Eri and colleagues saw lesions consisting of a progressive fibrosis that enveloped and disruptednerves and arteries.[54 ]They did not see nerve-tissue proliferation or inflammation. The authors concluded thatrepeated 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 tothe transverse intermetatarsal ligament. In more chronic cases, degeneration of the axons and proliferation ofblood vessels may occur about the site of an enlarged nerve. Shereff and Grande described the presence ofRenaut bodies, which are densely packed whorls of collagen, in the supraneural space.[55 ]These bodies arecharacteristically present only in peripheral neural entrapment.


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However, Morscher and coauthors, in a histomorphologic study, found only a diameter difference betweenbiopsy results from patients with typical symptoms of Morton neuroma and nerves examined from autopsies ofpersons without forefoot problems.[56 ]In addition, some have implicated the inter-MTP bursa as the main causeof Morton neuroma.

Forefoot deformities, such as hammertoe, can further aggravate the nerve because of dorsal subluxation of theproximal phalanx, which stretches the interdigital nerve over the intermetatarsal ligament. In addition, there area number of external conditions that have been noted to contribute to the development and aggravation of thiscompression. High-heeled shoes put the feet in chronic dorsiflexion, forcing one's weight onto the forefoot; andtight 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 thirdwebspace. Levitsky and colleagues demonstrated that the relative space in the metatarsal head/transversemetatarsal ligament is smaller in the second and third webspaces, where the condition is more common, than itis in the other webspaces, therefore supporting mechanical factors as the underlying pathophysiology.[57 ]Theyalso dismissed the common theory that the cause relates to the occurrence of a lateral and medial plantarnerve combination and to the anatomical thickness of the nerve. They reported neuromas in third webspaces inwhich the plantar nerve did not arise from a combination of medial and lateral plantar nerves. Theintermetatarsal head distances in the second and third interspace have been noted to be significantly less thanare those in the first and fourth intermetatarsal space.

Clinical

Many patients with Morton metatarsalgia present with an intermittent dull ache or cramping sensation on theplantar aspect of either the second or third interspace. Many patients present with a vague discomfort in theinvolved toes, and some may feel numbness or burning, with occasional shooting pain. Some patients noticespreading of the involved toes, and others may notice symptoms only with certain shoes. Symptoms usuallyworsen with walking, particularly with bare feet on hard surfaces, and sudden, sharp pain may result fromvarious activities, such as such as sprinting, jumping, squatting, or repeated hopping, as well as with wearinghigh-heeled or tight shoes. Symptoms improve with rest, and night pain is rare. With progression of thecondition, pain may radiate proximally. In chronic cases, patients may sense a mass or a stone bruise in the ballof the foot.

Nearly equal involvement of the second and third interspace has been reported in the literature. Involvement ofthe 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 butare uncommon. Coexistence of other pathologies of the forefoot, such as instability of the second MTP joint, isnot uncommon. Coughlin and colleagues reported that 20% of their patients originally had concomitantinstability of an adjacent MTP joint.

Clinically, dorsoplantar compression of the second or third intermetatarsal space reproduces pain that mayradiate to the toes or proximally along the course of the affected nerve. The patient may display relativeparesthesia 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 aresqueezed while the other hand places direct pressure on the plantar aspect of the interspace. As the metatarsalheads are compressed, the enlarged nerve is pushed plantar and away from the metatarsal heads, and a clickis palpated with the digit in the plantar web space just distal to the transverse intermetatarsal ligament. This isoften uncomfortable for the patients but does not usually reproduce their symptoms. This palpated mass can bepushed up again in the interspace with manual pressure, while partial compression is maintained on themetatarsal 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,


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intermetatarsal bursitis, extensor tendon tenosynovitis, tumor, and more proximal nerve injury. Metatarsal stressfracture will present with bony tenderness and pain upon palpation of the metatarsal shaft, rather than thecommon digital nerve. MTP joint synovitis will often prove painful during active or passive joint motion.

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

Ultrasonography and MRI are helpful in rare, complex situations.[58 ]The accuracy of these studies, however,varies significantly and depends on multiple factors, including the MRI machine, the technician and thetechnique, and the interpreting radiologist or orthopedic surgeon.

Ultrasonography reveals a hypoechoic, ovoid mass parallel to the long axis of the metatarsal. Ultrasonographycan 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 Mortonneuroma could not be distinguished clearly from an associated mass, such as mucoid degeneration in theadjacent loose connective tissue.

Quinn and coauthors found that ultrasonography revealed the diagnosis in 85% of cases in which it wassuspected.[59 ]They reported limitation in detecting neuromas shorter than 5 mm. Terk and colleagues reportedon MRI with T1- and T2-weighted sequences, along with a combination of fat suppression and theadministration of gadopentetate dimeglumine.[60 ]Williams and colleagues showed that T1-weighted axial andcoronal images obtained with an axial, fast spin-echo (FSE), T2-weighted sequence depict neuromata moreconsistently than do other methods.

Zanetti and coauthors studied 54 feet in which Morton neuroma was suspected in order to determine the effectof MRI results on diagnostic thinking and the therapeutic decisions made by orthopedic surgeons.[61 ]Theauthors noted considerable change in the diagnosis, location, and number of neuromas, as well as in thetreatment plans, after MRI.

In a second report, Zanetti and colleagues suggested that the diagnosis of Morton neuroma based on MRIresults are relevant only when the transverse diameter of the fluid collection in the bursa is 5 mm or more andwhen it was correlated with the clinical findings. Fluid collections in the first 3 metatarsal bursae with atransverse diameter of 3 mm or less are probably physiologic.

In a histomorphologic study of patients and autopsies, Morscher and coauthors concluded that diagnostic MRIor ultrasonography is unnecessary for making decisions about operative treatment.[56 ]In addition, Resch andcoauthors found that MRI modalities had little or no value in the diagnosis of Morton neuroma because of thehigh rate of false-negative results.[62 ]

Treatment

If Morton neuroma is detected early, conservative measures may be reasonably successful. About 20-30% ofpatients achieve adequate relief with nonoperative management. This may be accomplished by eliminating orminimizing 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 headsof the central 3 metatarsals, may reduce symptoms by increasing the intermetatarsal space, elevating themetatarsals and the intermetatarsal ligament, and reducing the likelihood of neural irritation. Accommodativeorthotic devices with built-in metatarsal pads may at times be helpful, especially in patients with alignmentabnormalities.

NSAIDs may relieve acute pain and inflammation. If NSAIDs provide insufficient relief, a local anesthetic


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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 andcolleagues. Rasmussen and coauthors reported initial pain relief in 80% of patients who received a singlecorticosteroid injection.[63 ]However, 47% of the 41 feet in the study ultimately required surgical excision; themajority of the remaining 53% had residual symptoms. In addition, corticosteroid injection for intermetatarsalneuroma has been associated with a number of complications, including plantar fat-pad atrophy,skin depigmentation, hyperpigmentation, and telangiectasias. Fat-pad atrophy can result in metatarsalgia andgait impairment.

A number of different surgical procedures have been used. Excision of the interdigital nerve and release of theintermetatarsal ligament is the most commonly performed procedure. A variable degree of subjective numbnessoccurs in the 2 toes served by that nerve, which is symptomatic in fewer than 10% of cases. Dorsal and plantarincisions have been reported in the literature.

Most surgeons in the United States perform a primary surgery through a dorsal approach. The incision isapproximately 3 cm in length and is centered in the respective interspace, starting from the metatarsal headlevel and extending distally into the respective webspace. Blunt dissection into the webspace and placement ofa lamina-style spreader reveals the intermetatarsal ligament. The proximal and distal aspects of theligament are identified and released sharply. An enlarged nerve may be identified readily beyond the ligament.Smaller nerves are more difficult to identify. In most cases, intertwining vessels require careful dissection andprotection. The digital branches are identified and are sharply amputated distally. The nerve is then followedproximally, gently pulled distally, sharply amputated as far proximally as is visible, and allowed to retract into thedeep soft tissues.

Mann and Reynolds reported retrospectively on a surgical excision of 76 Morton neuromas.[64 ]Although 65% ofpatients still noted some local plantar tenderness to touch, 80% were subjectively improved. Coughlin andPinsonneault noted residual pain in either the involved or adjacent interspace, which is not uncommon.[65 ]Theyalso reported 85% good-to-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 byusing a dorsal incision.[66 ]Twenty-five of 32 patients had a macroscopically visible neuroma, and 2 patients hadno evidence of a neuroma on histologic examination. After resection, 81% had a good or excellent result, and6.5% had no improvement. The authors noted that, following the operation, 60% of their patients benefitedfrom the use, over a long period of time, of adapted shoes or inner soles. At the final follow-up, only 30% of thepatients 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 providesmore direct access to the nerve and is technically simpler. However, painful plantar scars, intractable plantarkeratosis beneath an adjacent lesser metatarsal head, and wound drainage have been reported. Because ofthese potential complications, most surgeons reserve the plantar approach for revision cases. Karges reportedon 57 plantar surgeries performed using a plantar incision.[36 ]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 digitalnumbness, have led some authors to recommend release of the transverse metatarsal ligament with or withoutepineurolysis. Gauthier reported on the release of 304 intermetatarsal ligaments and epineural neurolysis.[67

]He stated that 83% had rapid and stable improvement, and that 15% were improved but nonethelesssuffered some persistent pain. Others, such as Weinfeld and Myerson, have advocated this procedure withoutneurolysis and have reported good preliminary results.[68 ]Mann and Reynolds cautioned against the use of thisprocedure except for Morton neuroma, as they noted reconstitution of the ligament in revision cases.[64 ]

Adjacent neuromas in the second and third interspace should be investigated. Reports of double neuromas inthe literature are sparse. Benedetti and colleagues reported simultaneous excision of 2 primary Morton


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neuromas in adjacent webspaces and noted significant pain relief in 84% of patients, but substantial numbnessinvolving the third toe resulted.[69 ]Thompson and Deland described 89 adjacent neurectomies and reportedsimilar results to those achieved with single neurectomies.[70 ]

Hort and DeOrio reported on 23 patients with adjacent intermetatarsal nerve irritation who underwent excision ofthe more enlarged nerve in 1 space and the release of the intermetatarsal ligament in the other.[71 ]This allowedpreservation of protective sensation. They reported 95% complete satisfaction, with no or only minimal activitylimitation. Approximately 11% had persistent pain with compression of the interspace where the nerve wasreleased. None had pain in the interspace where the nerve was excised. The investigators performed thisprocedure through 1 incision centered over the third metatarsal.

In summary, Morton neuroma is the result of chronic compression of the interdigital nerve as it passes under thetransverse intermetatarsal ligament. It is seen most commonly 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 withcompression 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 theavoidance of high-heeled and tight shoes, as well as the use of a small metatarsal pad and stiffer, rocker-soledshoes. Surgical excision of the nerve and release of the intermetatarsal ligament with a dorsal or plantarapproach results in a high percentage of successful results. The dorsal approach is recommended because offewer potential complications, and also because it allows early weight bearing. Patients should be counseledpreoperatively that varying degrees of postoperative numbness are commonly associated with resection of aMorton 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 nerveand release of the intermetatarsal ligament in the less-involved nerve lead to good relief of symptoms withoutsignificant neurologic deficit.

Patient Education

For excellent patient education resources, visit eMedicine's Foot, Ankle, Knee, and Hip Center and ProceduresCenter. Also, see eMedicine's patient education articles Knee Pain Overview, Bursitis, and Electromyography(EMG).

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Keywords

nerve entrapment, nerve entrapment of lower extremity, iliohypogastric nerve entrapment, ilioinguinal nerveentrapment, genitofemoral nerve entrapment, lateral femoral cutaneous nerve entrapment, femoral nerveentrapment, saphenous nerve entrapment, obturator nerve entrapment, peroneal nerve entrapment, posteriortibial nerve entrapment, tarsal tunnel syndrome, superficial peroneal nerve entrapment, deep peroneal nerveentrapment, interdigital neuritis, Morton metatarsalgia, meralgia paresthetica, Morton neuroma, slimmer'sparalysis, strawberry picker's palsy, Tinel sign, heel pain triad

Contributor Information and Disclosures

Author

Minoo Hadjari Hollis, MD, Orthopedic Surgeon, Sound Orthopedics and Foot and Ankle CenterMinoo Hadjari Hollis, MD is a member of the following medical societies: American Academy of OrthopaedicSurgeons, American Orthopaedic Foot and Ankle Society, and Florida Orthopaedic SocietyDisclosure: Nothing to disclose.

Coauthor(s)

David E Lemay, MD, Consulting Staff, Pensacola PM&R Group, PA and Gulf Coast Orthopaedic Specialists, PADisclosure: Nothing to disclose.

Medical Editor

John S Early, MD, Foot/Ankle Specialist, Texas Orthopaedic Associates, LLP; Co-Director, North Texas Footand Ankle Fellowship Baylor University Medical CenterJohn S Early, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons,American Medical Association, American Orthopaedic Foot and Ankle Society, Orthopaedic TraumaAssociation, and Texas Medical AssociationDisclosure: Zimmer Inc Consulting fee Consulting; Smith Nephew Consulting fee Consulting; AO NorthAmerica Honoraria Speaking and teaching; Osteotech Consulting fee Consulting; Stryker Consultingfee Consulting

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicineDisclosure: eMedicine Salary Employment

Managing Editor

Shepard R Hurwitz, MD, Executive Director, American Board of Orthopaedic SurgeryShepard R Hurwitz, MD is a member of the following medical societies: American Academy of OrthopaedicSurgeons, American Association for the Advancement of Science, American College of Rheumatology,American College of Sports Medicine, American College of Surgeons, American Diabetes Association,American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, Association for theAdvancement of Automotive Medicine, Eastern Orthopaedic Association, Orthopaedic Research Society,Orthopaedic Trauma Association, and Southern Orthopaedic AssociationDisclosure: Nothing to disclose.

CME Editor

Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief ofArthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital


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Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of OrthopaedicSurgeons, American Association of Physicians of Indian Origin, American College of International Physicians,and American College of SurgeonsDisclosure: Nothing to disclose.

Chief Editor

Jason H Calhoun, MD, FAAOS, Chairman, J Vernon Luck Distinguished Professor, Department of OrthopedicSurgery, University of MissouriJason H Calhoun, MD, FAAOS is a member of the following medical societies: American Academy ofOrthopaedic Surgeons, American College of Surgeons, and American Orthopaedic Foot and Ankle SocietyDisclosure: Nothing to disclose.

Acknowledgments

Robert P Jensen, MD, is gratefully acknowledged for contributions made to this topic.

Further Reading

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

Clinical guidelines

Guideline for management of wounds in patients with lower-extremity neuropathic disease. Wound, Ostomy, and ContinenceNurses Society - Professional Association. 2004. 57 pages. NGC:003898

Clinical trials

Study on the Role of Decompression of Lower Extremity Nerves for the Treatment of Patients With Symptomatic DiabeticNeuropathy With Chronic Nerve Compression

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