Entrapment Neuropathies of the Lower Extremity

The sciatic nerve, the largest nerve in the body, receives contributions from the L4, L5, S1, and S2 nerve roots.¹ When the nerve exits the greater sciatic foramen it is composed of two distinct tibial and peroneal divisions, enclosed by a common nerve sheath (Fig. 6.4). In the pelvis the sciatic nerve descends anterior to the piriformis muscle and courses downward into the thigh successively posterior to the superior gemellus, obturator internus, inferior gemellus, and quadratus femoris muscles (Fig. 6.5). The nerve continues down the thigh posterior to the adductor magnus muscle and the short head of the biceps femoris muscle and anterior to the gluteus maximus and the long head of the biceps femoris. In the distal third of the thigh the tibial and peroneal divisions physically separate into the tibial nerve and the common peroneal nerve.

The sciatic nerve is one of the more important nerves in the lower extremity (Table 6.2). It provides knee flexion via innervation of the posterior thigh muscles and all sensory and motor functions below the knee (with the exception of sensation of the medial leg, which is supplied by the saphenous nerve, a branch of the femoral nerve) (Fig. 6.6). At the level of the hip, the tibial division of the sciatic nerve innervates the hamstring muscles, except for the short head of the biceps femoris muscle (which is innervated by the peroneal division). The tibial nerve provides all motor function to the posterior compartment of the leg and to the plantar muscles of the foot. The common peroneal nerve provides motor function to the anterior and lateral compartment of the leg and to the dorsum of the foot as well as sensation to the dorsum of the foot.

Because it is large and surrounded by fat, the sciatic nerve is easily identified and can be followed as it descends through the pelvis and thigh. On axial MR images it appears as a large (up to 2 cm in diameter) ovoid structure of intermediate signal intensity. The fascicular pattern is clearly appreciated in all planes. The sciatic nerve often displays normally increased signal on all pulse sequences, which should not be mistaken for a fibrolipomatous hamartoma.

The sciatic nerve can be identified on axial, coronal, and sagittal plane images, but size, signal intensity, and relationship to adjacent soft tissue structures are best assessed on axial plane images. Coronal images are often useful in depicting the formation of the sciatic nerve from the L4–S2 nerve roots (Fig. 6.7). Oblique sagittal, axial, and coronal images using either the piriformis muscle^21,44 or the sacrum as reference points have also been recommended for assessment of the sacral plexus and sciatic nerve. The oblique planes provide the advantage of visualizing a long segment of the nerve in a single image.

The following MR characteristics are typical:

Injury to the sciatic nerve is a serious condition that can produce a flail leg and predispose to fractures and infections. Sciatic neuropathy can occur at the hip region or, less commonly, at the thigh. Sciatic neuropathy at the hip is most commonly iatrogenic and is associated with total hip replacements, usually after revision.⁴⁵ The injury to the nerve is related to stretching or direct trauma and usually manifests clinically immediately after surgery. Delayed presentation is less common. The piriformis muscle syndrome (see discussion below) and the obturator internus muscle syndrome are additional causes of sciatic neuropathy.^{46,47,48,49,50,51,52,53} Sciatic neuropathy at the hip may also be secondary to hip fracture, vasculitis, arterial thrombosis, and cardiac surgery. Injury to the sciatic nerve usually spares the hamstring muscles since innervation to these muscles originates quite high.

Sciatic neuropathy more commonly affects the peroneal division of the nerve, with relative sparing of the tibial division. Factors contributing to the greater vulnerability of the peroneal division include:

Not surprisingly, sciatic neuropathy may be difficult to distinguish from the more distal common peroneal neuropathy. Symptoms of sciatic neuropathy vary depending on the level of injury and the relative involvement of the tibial and peroneal divisions. The most prominent feature is foot drop due to loss of innervation of the anterior tibial muscle (peroneal division). Loss of ankle and toe extension and foot eversion (peroneal division) and loss of ankle and toe flexion and foot inversion (tibial division) are other manifestations of sciatic neuropathy. Paresthesias, numbness, and a burning sensation in the lateral leg and dorsum of the foot (peroneal division)

and in the plantar surface of the foot (tibial division) are other manifestations of sciatic neuropathy.

One of the best-known entrapment neuropathies of the sciatic nerve is the piriformis muscle syndrome, most often related to spasticity, irritability, or inflammation of the piriformis muscle. The existence of piriformis muscle syndrome, however, remains controversial, and the entity is probably overdiagnosed.⁵³

Related anatomic features include:

There are a number of causes of piriformis muscle syndrome. Piriformis muscle hypertrophy due to overstretching, hip flexion deformities, and lumbar lordosis may compromise the volume of the foramen and compress the sciatic nerve. Any disorders associated with increased spasticity, such as cerebral palsy, may also be associated with piriformis muscle syndrome.⁵¹ Piriformis muscle spasm secondary to sacroiliac disease, bursal distention, and inflammation or degeneration of the muscle/tendon unit are additional causes. Direct or indirect trauma to the sacroiliac or gluteal regions, hematoma, or fibrous adhesions can also decrease the volume of the foramen. Compromise of the vessels traversing the foramen and supplying the nerve can produce local nerve ischemia. Finally, anatomic variations such as a piriformis muscle pierced by the sciatic nerve or by the peroneal division of the sciatic nerve (Fig. 6.9), although present in a significant number of asymptomatic individuals, can also produce nerve compression, especially during contraction of the muscle. Piriformis muscle syndrome may also be caused by compression of the superior gluteal nerve.

The diagnosis of piriformis muscle syndrome should be entertained only after other causes of lower back and ischial pain, sciatic nerve compression elsewhere, and lower extremity pathology are excluded. Sacral or gluteal pain and tenderness over the belly of the piriformis muscle, aggravated by sitting, squatting, or walking and relieved by lying supine, is the most constant finding. In some patients the pain is aggravated when lying down at night or when getting up from a sitting position. Although infrequently seen, neurologic deficits may include a decrease in the ipsilateral ankle reflex, weakness in the knee and hip flexors, and numbness in the sciatic nerve distribution.⁵¹ Buttock pain and gluteal weakness and atrophy are associated with compression of the superior gluteal nerve.

The treatment of piriformis muscle syndrome is initially conservative, with anti-inflammatory medication, physical therapy, and corticosteroid and anesthetic injection into the muscle or bursal area. Surgical release of the superior gluteal and sciatic nerves and sectioning of the piriformis muscle may be attempted in refractory cases.

Direct MR evidence of sciatic neuropathy includes course deviation and increased size and increased signal of the nerve (see Fig. 6.2; Fig. 6.10). Obliteration of the fat planes around the nerve due to tumor, scar, or edema may also be noted (Fig. 6.11). In the thigh, muscle signal alterations consistent with denervation may be seen involving the hamstring muscles as well as the hamstring component of the adductor magnus muscle (Fig. 6.12). More distal signs of denervation may be missed on routine MR studies of the pelvis and hip since most muscles supplied by the sciatic nerve are located in the knee, leg, and foot. The distribution of affected muscles helps to distinguish sciatic neuropathy from more proximal plexopathy (Fig. 6.13). Varicosities, tumors, and inflammation displacing or engulfing the sciatic nerve can easily be detected on MR images (Fig. 6.14).^{44,48,54,55,56,57} Postsurgical complications

affecting the sciatic nerve such as amputation neuromas (Fig. 6.15), can also be evaluated on MR images.

The clinical diagnosis of piriformis muscle syndrome is often missed or delayed due to the rarity of the condition and the nonspecific symptoms.⁵¹ Initially, MR examination is used to assess other potential causes of low back, posterior hip, thigh, or buttock pain such as lumbar disk herniation, lumbar stenosis, and tumors. If MR examination of the lumbar spine is nondiagnostic and EMG for L5–S1 radiculopathy is normal, further MR examinations of the pelvis may be helpful in identifying pathologic changes. MR imaging has also been proposed as a follow-up tool to evaluate denervation in patients treated with botulinum toxin for piriformis muscle syndrome.⁴⁹

MR diagnosis of piriformis muscle syndrome is best made on pelvic images that display both piriformis muscles so that a comparison can be made. Axial and coronal images are both useful for assessing the size of the muscles. Characteristic MR findings include the following:

MR neurography is a promising technique in the diagnosis of sciatic nerve pathology and piriformis muscle syndrome (see Fig. 6.2).^19,21,58 In one study, MR neurography in 239 patients with non-discogenic sciatica demonstrated 93% specificity and 64% sensitivity for diagnosing piriformis muscle syndrome. Diagnosis was based on the concomitant findings of increased nerve signal at the sciatic foramen and asymmetry of the piriformis muscles.⁵⁸ When muscle asymmetry was used as the only criterion, the specificity and sensitivity for piriformis muscle syndrome decreased to 66% and 46% respectively. Hypertrophy and less commonly atrophy of the piriformis muscle on the affected side were also noted.

Open MR-guided anesthetic injections of the piriformis muscle have been used to confirm the diagnosis of piriformis muscle syndrome and to guide treatment.⁵⁸ Long-standing relief was noted in 23% of patients after one or two injections. Open MR-guided injections also proved more reliable than transvaginal blind or fluoroscopically guided injections of the piriformis muscle and have the added benefit of not exposing the patient to the ionizing radiation associated with CT-guided injections.⁵⁸

The femoral nerve originates from the L2, L3, and L4 nerve roots of the lumbar plexus. It supplies motor innervation to all the anterior thigh muscles, with the exception of the tensor fascia lata, and sensation to the anterior and distal medial thigh, anteromedial knee, and medial leg and foot (Fig. 6.18).

The femoral nerve initially travels under the psoas muscle and then courses anteriorly between the iliacus and psoas muscles, supplying them with motor innervation.¹ It then enters the leg under the inguinal ligament. As the nerve passes under the inguinal ligament it travels in a relatively rigid tunnel, called the lacuna musculorum, the floor of which is formed by the iliac bone and iliopsoas muscle and the roof of which is formed by the iliopectineal arch (a fascia traversing from the iliopubic or iliopectineal eminence to the inguinal ligament) and the inguinal ligament. The nerve then enters the femoral triangle lateral to the femoral artery and divides into the superficial and deep branches. The superficial branch provides motor innervation to the pectineus and sartorius muscles and carries sensation from the anterior thigh. The deep branch provides motor innervation to the quadriceps muscles and sensation, via the saphenous nerve, to the medial thigh, leg, and foot. The saphenous nerve continues distally in an oblique fashion with the femoral artery and vein deep and parallel to the sartorius muscle (Fig. 6.19).

The femoral nerve is best visualized on axial MR images of the pelvis and hips. It appears as an ovoid, intermediate-intensity structure on all pulse sequences. Compared to the sciatic and obturator nerves, the femoral nerve is more difficult to see on coronal or sagittal images of the pelvis. Depending on the amount of fat present, the nerve may be initially seen deep to the psoas muscle and then anterior to the iliopsoas muscle. The ease with which the nerve can be traced depends on how closely it adheres to the muscle. The nerve is usually easier to identify as it migrates anteriorly into a more superficial position in the lower pelvis, underneath the inguinal ligament. The latter structure may be seen as a fine, low-signal-intensity linear band that migrates medially on sequential axial images. As the femoral nerve approaches the upper thigh it traverses within the femoral triangle, a fat-filled superficial space also occupied by the more medially located femoral vein and artery. Often the nerve is depicted as a poorly defined structure composed of multiple intermediate-signal-intensity fascicles surrounded by fat (Fig. 6.20). The various terminal branches of the nerve can sometimes be seen as they split off from the main femoral nerve.

The largest branch of the femoral nerve, the saphenous nerve, can be followed in the thigh using the sartorius muscle and the femoral vein and artery as landmarks. The saphenous nerve is seen as a small, intermediate-signal-intensity, round structure within a fat plane, first posterior and then lateral to the sartorius muscle (Fig. 6.21). The nerve is accompanied by the femoral vein and artery and is bordered laterally and anteriorly by the vasti muscles. The nerve migrates, along with the sartorius, from a relatively anterior position in the proximal thigh to a posterior location in the knee area. The sartorial branch of the nerve can be followed as it pierces the fascia, between the sartorius and gracilis tendons, to become superficial at the level of the knee joint.⁵⁹ At this location the sartorial branch is usually lateral (in 66% to 70% of cases) to the sartorius muscle but may also be found medial to the muscle. In the medial leg the branches of the saphenous nerve can be visualized within the subcutaneous fat along the great saphenous vein.

Compression of the femoral nerve, known also as the iliacus muscle syndrome, commonly occurs underneath the inguinal ligament within the lacuna musculorum. Injury to the nerve is often iatrogenic,^60,61,62,63 related to gynecologic procedures (e.g., hysterectomy), pelvic surgery, hip surgery/replacement, femoral artery catheterization, and arterial bypass procedures. The relatively superficial course of the nerve in the proximal thigh predisposes it to direct injury. Gunshot wounds, lacerations, and hip and pelvic fractures are additional causes of femoral nerve compression. Since the nerve traverses underneath the inguinal ligament together with the iliacus and psoas muscles, injuries to these muscles can produce femoral nerve injury. The nerve courses deep to the rigid iliac fascia, predisposing it to compressive and ischemic injury^64,65,66 associated with iliacus muscle hematoma.

Clinical indications of femoral neuropathy include:

Entrapment of the saphenous nerve can occur in the adductor canal. The superficial location of the nerve in the leg predisposes it to lacerations and contusions. Saphenous nerve injury is the most common neurovascular injury after knee

arthroscopy and occurs in 7% to 22% of patients undergoing arthroscopic meniscal repair.^{59,67,68,69,70,71} Nerve injury has also been noted in patients with posterolateral instability, possibly related to stretching of the nerve.⁷²

Femoral neuropathy must be differentiated from lumbar plexus and L4 radiculopathy. Conservative treatment of femoral neuropathy should be attempted before surgical intervention, since the complications associated with surgery can have serious consequences.

Most reports of entrapment neuropathies of the femoral nerve are related to traumatic injury of the iliopsoas compartment. CT and MR images show evidence of mass effect due to iliacus or iliopsoas muscle tears, hematomas (Fig. 6.22), and posttraumatic pseudoaneurysm of the iliac vessels.^64,65,66 Femoral neuropathies secondary to iliopsoas compartment masses and distended iliopsoas bursa have also been described.⁷³ The quadriceps muscles may display signal alterations related to denervation.

There are few descriptions of the imaging characteristics of saphenous nerve injury. Since the nerve is sensory, no muscle denervation changes are noted. In one report a neurilemmoma of the saphenous nerve was detected.⁷⁴ Displacement of the saphenous nerve by a meniscal cyst has also been described on MR and US examinations.⁷⁵ George et al. also reported finding a rare neuritis ossificans (heterotopic ossification) of the saphenous nerve, which presented on MR studies as a soft-tissue mass in the fat planes between the sartorius and vastus medialis muscles.⁷⁶

The obturator nerve supplies the medial thigh muscles. Spinal nerve contributions from L2, L3, and L4 roots fuse to form the obturator nerve within the substance of the psoas major muscle.¹ The coalesced nerve emerges from the medial border of the psoas muscle and descends inferiorly and anteriorly along the iliopectineal line into the lesser pelvis (Fig. 6.23). The nerve exits the pelvis at the superior aspect of the obturator foramen via the obturator canal. Just prior to its exit from the pelvis, the nerve subdivides into its anterior and posterior divisions. Both branches traverse the obturator canal and pierce the obturator externus muscle. The anterior division descends posterior to the pectineus and adductor longus muscles and anterior to the obturator externus and adductor brevis muscles. The nerve supplies the hip joint and sends motor branches to the gracilis, adductor brevis, adductor longus, and occasionally pectineus muscles. It also supplies a patch of skin on the medial side of the thigh. The posterior branch descends posterior to the adductor brevis and anterior to the adductor magnus muscles. It supplies the knee joint, obturator externus muscle, adductor component of the adductor magnus muscle (the hamstring component is supplied by the sciatic nerve), and occasionally adductor brevis muscle. Variability in the obturator nerve and its branches⁷⁷ and the presence of an accessory obturator nerve are common findings.

The obturator nerve is best visualized on pelvic axial MR images, on which it appears as a round, low- to intermediate-signal-intensity

structure (Fig. 6.24). Occasionally, the nerve is seen on anterior coronal images (see Fig. 6.24B). The nerve can be traced as it originates from the lumbar spine and traverses inferiorly and anteriorly surrounded by a large amount of pelvic retroperitoneal fat. The nerve is located anterior to its accompanying vessels and can be followed as it dives under the superior pubic ramus to enter the obturator foramen. The anterior division of the nerve is depicted in the thin fat plane posterior to the pectineus and adductor longus muscles and anterior to the adductor brevis muscle. The posterior branch is identified in a fat stripe between the adductor brevis and adductor magnus muscles.

Obturator neuropathy is uncommon because of the deep location of the nerve in the pelvis and the protection provided by neighboring muscles.⁶² Neuropathy is frequently associated with penetrating and postsurgical trauma to the inguinal area and pelvis.^78,79 Pelvic and acetabular fractures, posttraumatic hematomas, and myositis ossificans can produce damage to the nerve. Compression can occur during total hip replacement surgery secondary to either nerve stretching by retractors or penetration of the medial wall of the acetabulum by cement, screws, or reamers.^{45,79,80,81,82} Additional, albeit rare, causes of obturator neuropathy include genitourologic surgery, pelvic tumors, fibrous bands in the obturator tunnel, fascial thickening,⁷⁷ obturator hernia,⁸³ prolonged lithotomy position,^84,85 and osteitis pubis. Obturator neuropathy is becoming recognized as a cause for groin pain in athletes.^77,86,87,88 The neuropathy is believed to involve the anterior branch of the obturator nerve after it exits the obturator tunnel. Adhesions of the fascia of the adductor brevis muscle, possibly secondary to chronic adductor tendinopathy, entrap the nerve at the level of the obturator foramen.

The clinical presentation of obturator neuropathy includes:

EMG studies and anesthetic injections into the inguinal area may confirm the diagnosis. Postsurgical obturator neuropathy usually resolves spontaneously.⁷⁹ Cases associated with mass lesions may require surgery.

MR evidence of obturator neuropathy includes signal and size alterations of the nerve as well as mass effect related to soft-tissue or bony pelvic tumors (Fig. 6.25).⁷⁹ In addition, signal alterations in the muscles innervated by the obturator nerve indicate denervation. As is the case with saphenous nerve injury, there are few reports of MR evidence of obturator neuropathy. Neuropathy related to an acetabular labral cyst is manifested as increased signal of the gracilis, obturator externus, and adductor muscles on T1-weighted and STIR images consistent with acute or chronic denervation.⁸⁹ Similarly, postpartum obturator neuropathy displayed increased signal and atrophy in the adductor brevis and adductor magnus muscles.⁹⁰ In another report, an obturator hernia⁸³ was noted to obliterate the fat at the entrance of the nerve to the obturator foramen.

The lateral femoral cutaneous nerve, a purely sensory nerve, originates from the L2 and L3 nerve roots, travels laterally under the psoas muscle and across the iliacus muscle, and exits the pelvis under the inguinal ligament at the level of the anterior-superior iliac spine (ASIS) (Fig. 6.26).¹ Typically, the nerve divides after it exits the pelvis (below the ASIS) into an anterior branch, which innervates the skin of the anterolateral thigh, and a posterior branch, which innervates the skin of the posterolateral thigh. Both these divisions penetrate the fascia lata a few centimeters below the ASIS. Divisions of the nerve occur proximal to the inguinal ligament as a normal variant in up to 27% of patients.⁹¹

The lateral femoral cutaneous nerve is susceptible to entrapment at two major sites:

There are many reported causes for entrapment of the lateral femoral cutaneous nerve:

Neuropathy of the lateral femoral cutaneous nerve, also called meralgia paresthetica, presents clinically as burning pain, numbness, tingling, and sensory loss along the lateral aspect of the thigh.^98,99 The symptoms can be confused with disk-related low back pain.⁹⁴ Skin sensitivity to even light touch can develop. Hip flexion and sitting usually relieve the symptoms, whereas local pressure at the ASIS aggravates them. Neuropathy can be confirmed by EMG and by relief of pain after local injection of anesthetic. Behavioral modification, anti-inflammatory medication, and local anesthetic and steroid injections are often sufficient to relieve the symptoms.¹⁰⁰ Surgical release of the fascia lata and inguinal ligament, neurolysis, nerve transposition, and, rarely, nerve transection have been attempted with variable success in patients with intractable symptoms.¹⁰⁰

The lateral femoral cutaneous nerve is best seen on axial images of the lower lumbar spine and pelvis. The nerve can be traced as it courses anterior to the iliacus muscle and then as it exits the pelvis just medial to the inguinal ligament. The ASIS can be used as a landmark for identifying the exiting nerve. Increased signal and size of the nerve at its site of entrapment can be expected but have not yet been reported. Since the nerve is purely sensory, no muscle denervation signal alterations are encountered. MR examinations may demonstrate space-occupying lesions displacing or engulfing the nerve.¹⁰¹ A nerve sheath tumor of the lateral femoral cutaneous nerve has been reported.¹⁰²

The common peroneal nerve diverges from the sciatic trunk at the upper popliteal fossa. In the upper popliteal fossa it divides into a lateral cutaneous nerve of the calf, which provides sensation to the proximal third of the lateral leg.¹ It then descends in the posterolateral thigh and knee posteromedial to the biceps femoris muscle. At the knee joint region the nerve migrates into a more superficial, vulnerable location posterior to the lateral gastrocnemius muscle. It then winds around the fibular neck, where it enters the peroneal or fibular tunnel (Fig. 6.27). The nerve pierces the anterior fascia to enter the anterior compartment of the leg between the tendinous origins of the peroneus longus muscle.

MR imaging can also be used for postoperative follow-up depicting the recurrence of a subclinical extraneural ganglion, progressive enlargement of extraneural cysts within or adjacent to an arthritic proximal tibiofibular joint, hematoma, and seroma. If no connection between the tibiofibular joint and intraneural cyst can be appreciated on routine MR images, MR arthrography may be of value. After intra-articular gadolinium injection, Spinner reported that communication between the knee joint, the tibiofibular joint, the articular branch of the deep peroneal nerve, and an intraneural ganglion could be demonstrated in a patient with a recurrent common peroneal intraneural ganglion.¹¹⁴ Intraneural ganglia may involve a large segment of the nerve and mimic a nerve sheath tumor.¹²⁸ The lack of enhancement of a ganglion is a useful distinguishing characteristic.

In the athlete, MR examination can play a crucial role differentiating common peroneal nerve entrapment from other common causes of chronic leg pain, including medial tibial stress syndrome, stress fracture, chronic exertional compartment syndrome, and popliteal artery entrapment syndrome.¹²⁹

The predominantly motor deep peroneal nerve supplies the extensor muscles of the foot and toes (the anterior tibial, extensor hallucis longus, extensor digitorum longus and brevis, and peroneus tertius muscles).¹ It also carries sensation from the dorsal first web space of the foot and may supply a few of the intrinsic muscles in that region.⁴³ The deep peroneal nerve travels in the anterior compartment of the leg along with the tibial artery and vein. Initially it runs deep to the extensor digitorum longus muscle, and more distally deep to the extensor digitorum longus and extensor hallucis longus muscles. In the ankle region the nerve dives under the superior and inferior extensor retinacula to enter the anterior tarsal tunnel (Fig. 6.32). The tarsal tunnel is not a true tunnel, but

rather a flat space between the medial and lateral malleoli defined superiorly by the inferior edge of the extensor retinaculum and inferiorly by the talonavicular joint. Just above the ankle joint the nerve divides into a lateral motor branch, which supplies the extensor digitorum brevis muscle. The medial branch, mostly sensory, continues dorsal to the talonavicular joint and middle cuneiform and between the bases of the first and second metatarsals to provide sensation and occasional motor supply to the first web space.

The anterior tibial artery and later on the dorsalis pedis artery can serve as landmarks in tracing the course of the deep peroneal nerve. MR depiction of the nerve includes the following:

The deep peroneal nerve is susceptible to multiple sites of entrapment in the leg, ankle, and foot (see Fig. 6.32). The first compression site is under the inferior edge of the superior extensor retinaculum. The most common entrapment syndrome, the anterior tarsal syndrome, occurs more distally, underneath the distal edge of inferior extensor retinaculum or at the talo-navicular joint. Entrapment has been described in athletes, particularly runners. Recurrent ankle sprains and ligamentous laxity produce stretching of the nerve, especially at the talo-navicular joint. Osteophytes exacerbate the compression. Repetitive trauma to the dorsum of the foot, such as occurs in soccer players, may also produce nerve injury. Other causes of entrapment include a hypertrophied extensor hallucis brevis muscle belly and osteophytes or an os intermetatarseum at the base of the first metatarsal. Tight-fitting shoes or ski boots and posttraumatic local fibrosis may produce extrinsic compression of the nerve. Placing keys under the tongues of running shoes has also been described as a cause for compression in runners.² The nerve may also be compressed by performing sit-ups with the feet hooked under a metal bar.² Postpartum edema has been described as a rare case for entrapment at the anterior tarsal tunnel.¹³⁰

The anterior tarsal syndrome produces predominantly sensory deficits since the motor branch of the deep peroneal nerve has branched off above the area of compression. Weakness and wasting of the extensor digitorum brevis muscle may be seen if the compression occurs proximal to the tunnel. A

dull ache on the dorsum of the foot, pain, numbness, and a positive Tinel sign at the first web space may be seen. EMG studies are useful in distinguishing deep peroneal neuropathy from L5 and common peroneal neuropathies.

The initial treatment approach to deep peroneal entrapment neuropathy is conservative management with shoe wear modification, padding, and steroid injection. If conservative management is unsuccessful, surgical release of the extensor retinaculum or excision of the offending spurs at the talonavicular or first tarsometatarsal joint can be attempted.

At present there are only anecdotal reports of MR imaging of the deep peroneal nerve.^11,130,131 Findings include the following:

In the leg the superficial peroneal nerve supplies motor innervation to the peroneus longus and brevis muscles.^1,132 The nerve then becomes predominantly sensory, carrying sensation from the distal two thirds of the lateral leg and from the dorsum of the foot. As the nerve descends down the leg, it migrates from a deep to a more superficial location within the fascial plane between the peroneus longus and extensor digitorum longus muscles. The nerve pierces the deep fascia of the lateral compartment approximately 10 to 15 cm above the ankle joint (Fig. 6.35). It then becomes subcutaneous and divides, approximately 6 cm above the lateral malleolus, into the medial and intermediate dorsal cutaneous nerves.

Axial images are optimal for tracing the course of the superficial peroneal nerve. In the posterior knee the nerve is identified as the more posterior division of the common peroneal nerve. As the two branches of the common peroneal nerve wrap around the fibular neck and move into the anterior leg compartment, the superficial branch is initially posterior and then lateral to the deep peroneal nerve; the nerve, however, may be quite difficult to identify because of paucity of fat along its course. When visualized, the nerve is found within a sliver of fat on the lateral aspect of the neck of the fibula, deep to the peroneus longus muscle. The nerve can be followed along the leg as it migrates more laterally and superficially in the fat plane between the muscles of the anterior and lateral compartment. The amount of surrounding fat increases as the nerve approaches and pierces the fascia of the distal leg and becomes subcutaneous (Fig. 6.36). In the ankle region the nerve and its branches are found within the dorsal subcutaneous fat superficial to the superior and inferior extensor retinacula.

Superficial peroneal nerve entrapment usually occurs as the nerve pierces the deep fascia of the lower leg. Thickening of the fascia, tenting of the nerve associated with a fascial defect, and secondary muscle herniation are common causes. The injury is frequently seen in athletes such as runners, dancers, and soccer, hockey, tennis, and racquetball players.² Symptoms include numbness and tingling along the lateral aspect

of the lower leg and dorsum of the foot with sparing of the first web space (innervated by the deep peroneal nerve). The pain is worsened with activity. Focal swelling, point tenderness, and exacerbation of symptoms with pressure occur approximately 10 to 12 cm above the ankle joint, where the nerve exits the deep fascia. When muscle herniation is the causative agent, a focal mass accentuated by resisted dorsiflexion may be seen.²⁴ Prior trauma, particularly chronic ankle sprain, has been noted in approximately 25% of patients with superficial peroneal neuropathy. The neuropathy is most likely related to traction and stretching of the nerve.² Impingement on the nerve following prior anterior compartment fasciotomy has also been described.

Most entrapment neuropathies of the superficial peroneal nerve occur where the nerve pierces the fascia of the leg to become subcutaneous.¹³³ A fascial defect or fascial thickening, best appreciated on axial MR images, can be detected.¹³³ Peroneus longus muscle hernias (Fig. 6.37), occasionally requiring imaging in plantarflexion and dorsiflexion of the foot, can be identified as small masses of muscle signal intensity extending beyond the fascia of the leg. Occasionally, focal increased signal of the muscle at or close to the site of hernia can be detected.¹³⁴

The three major causes of tarsal tunnel syndrome are trauma, space-occupying lesions, and foot deformities. The etiology of the syndrome remains unknown in 20% to 40% of patients.^140,141 Trauma (primarily scarring after a sprain, following a fracture, and after surgery¹⁴²) accounts for one third of cases.¹³⁵ Entrapment of the tibial nerve and its branches may be due to extrinsic compression by varicosities, ganglia, anomalous muscles,^143,144 and other space-occupying masses within the tunnel. Fracture fragments, posttraumatic scar, and synovial proliferation associated with rheumatologic disorders may directly entrap the nerve or cause decreased tunnel volume. In cases of mass-occupying lesions, a concomitant more proximal nerve entrapment (double crush syndrome) may be present.¹⁴⁵ Congenital foot deformities (such as varus heel with forefoot pronation or valgus heel [less likely], pes planus, and tarsal coalition) and posttraumatic foot deformities may cause stretching of the nerve and its branches. Dynamic foot deformities, which sometimes occur with excessive pronation of the foot during activities such as jogging or aerobic exercises, may also predispose to tarsal tunnel syndrome. Increased pressure within the tunnel associated with foot and ankle position is also a predisposing factor for nerve compression.¹⁴⁶ A variety of systemic diseases, including diabetes mellitus and peripheral vascular disease, have also been implicated as causes for tarsal tunnel syndrome.

Symptoms of tarsal tunnel syndrome vary depending on the location of entrapment and the number of involved nerve branches. They include:

Proximal migration of symptoms may be related to the Valleix phenomenon or the double crush syndrome. In one study, intractable chronic heel pain, refractory to conservative treatment, was the major complaint in 51 patients with tarsal tunnel syndrome.¹⁴⁷ Sensory loss along the plantar aspect of the foot and a positive Tinel sign at the tarsal tunnel are the most helpful diagnostic signs. A positive Phalen's sign (reproduction of symptoms during inversion and plantarflexion of the foot) is also indicative of compression of the tibial nerve and its branches. Because the medial calcaneal nerve is usually not involved, there is no sensory loss along the medial aspect of the heel. Motor loss in tarsal tunnel syndrome is less frequently described, possibly because intrinsic muscle weakness may be masked by the normal activity of the extrinsic muscles and may be detected only with EMG. It has been postulated that isolated sensory loss may be related to vascular compromise of the nerve, whereas concomitant motor and sensory loss is more likely related to direct compression of the nerve.

Electrophysiologic tests are helpful in diagnosing tarsal tunnel syndrome and in excluding more proximal causes for tibial nerve disease, such as sacral radiculopathy. However, EMG studies should be interpreted with caution since false-positive and false-negative results have been reported. It is important to consider the results in light of the clinical history, the character of the pain, and findings on physical examination.³⁸

Treatment of tarsal tunnel syndrome is initially conservative and includes behavioral modification, physical therapy, immobilization, and anti-inflammatory medication. This approach is more successful in athletes.^148,149 Surgical release of the flexor retinaculum and removal of the offending mechanism is attempted in refractory cases or in cases with mass effect, but results vary depending on the etiology and duration of symptoms and the age of the patient.¹⁵⁰ Patients with space-occupying lesions tend to do better than those with an idiopathic or traumatic etiology. Also, the longer the duration of symptoms and the older the patient, the worse the prognosis.

As mentioned, the terminal branches of the medial and lateral plantar nerves join to form the interdigital nerves (Fig. 6.58).¹ These nerves pass distally alongside the metatarsal bones and cross the deep transverse metatarsal ligaments. An intermetatarsal (Morton's) neuroma is a fibrotic nodule caused by damage to the interdigital nerve, either by entrapment of the nerve against the transverse metatarsal ligament or by nerve ischemia. It is not a true tumor but rather a degenerative process of the nerve with epineurial and perineurial fibrosis and demyelinization. Histologic findings include neural degeneration, epineural and endoneural vascular hyalinization, and perineural fibrosis surrounding the intermetatarsal nerve.^173,174

Intermetatarsal neuroma is one of the most common causes of metatarsalgia and was first reported by Durlacher in 1845. The term Morton's neuroma was popularized after the

description of this condition by Thomas G. Morton in 1876.^175,176 Initially the lesion was thought to affect the third intermetatarsal space exclusively. However, later studies revealed that although the second and third intermetatarsal spaces are the most common locations for Morton's neuroma, other intermetatarsal spaces can also be affected.^177,178,179

Morton's neuroma is most commonly seen in middle-aged women and may be related to the propensity for wearing high-heeled, tight-boxed shoes.¹⁷⁶ Clinically it is characterized by intermetatarsal pain, numbness, and sensory disturbances that radiate to the toes and are exacerbated by standing and walking. The symptoms can be relieved by rest and shoe removal. In up to 80% of patients, intermetatarsal neuromas may be associated with forefoot deformities such as hallux valgus, hammertoe, or pes planus.^180,181 On physical examination a mass can be palpated in up to one third of patients. This fnding is often accompanied by a characteristic click or Mulder's sign.¹⁸²

The clinical diagnosis of Morton's neuromas is usually straightforward. Occasionally, however, the diagnosis is equivocal and other causes of metatarsalgia (e.g., intermetatarsal bursitis, synovitis, inflammatory arthritis, stress fracture, Freiberg's infraction, pigmented villonodular synovitis, osteomyelitis, foreign body granuloma, true neuroma, and metatarsophalangeal joint dislocation) are encountered. In these instances imaging studies such as sonography, CT, and MR have proven valuable in establishing the underlying cause of intermetatarsal pain.^183,184,185

The treatment of Morton's neuroma is initially conservative and includes shoe wear modification, metatarsal padding, orthoses, and steroid injections. In about 30% of cases the symptoms do not respond to conservative measures and operative treatments, such as surgical excision of the neuroma (neurectomy), division of the transverse metatarsal ligament, and neurolysis are performed.¹⁸⁶ Recurrent symptoms develop in up to 20% to 30% of patients.^187,188 Treatment failures have been attributed to inadequate resection, recurrent neuroma and scar tissue, referred symptoms from adjacent neuromas, as well as other overlooked or coexisting causes of metatarsalgia.

Sonography has been used successfully for the diagnosis of Morton's neuroma, with reported sensitivity of 85% to 98%.^{189,190,191,192} The sonographic appearance of Morton's neuroma is described as a hypoechoic intermetatarsal mass.¹⁹² Missed neuromas are attributed to variability in the sonographer's experience and technique and to the small size of the lesion. At the level of the intermetatarsal heads, the diameter of the normal plantar digital nerve is only 1 to 2 mm, and it is not readily identifiable on sonograms.^191,192 Most symptomatic neuromas are larger than 5 mm, and this diameter has been proposed as a threshold for symptomatology.^191,192,193 However, size and symptomatology are not absolutely related, as shown by Pollack et al.,¹⁸⁹ and it is possible that some symptomatic lesions are too small to be revealed on sonography.

Joplin's neuroma, a rare condition first described by Joplin in 1971, is consistent with entrapment or compression neuropathy of the plantar proper digital nerve (PPD).¹⁹⁸ The plantar proper digital nerve is a terminal sensory branch arising from the medial plantar nerve. It pierces the plantar aponeurosis posterior to the tarsometatarsal joint and in its course gives off a muscular branch to the flexor hallucis brevis muscle.^199,200 The nerve is subject to pressure as it crosses to the first metatarsophalangeal joint and along the plantar aspect of the hallux. Moreover, due to its superficial location, the nerve is susceptible to repetitive trauma or chronic compression.

Chronic compression, which may be caused by tight shoes or by sports activities that require repetitive pivoting or produce impact and motion at the first metatarsophalangeal joint (such as soccer, ballet, and skiing), predispose the nerve to entrapment.^2,200,201 Joplin's neuroma is also encountered after surgery for hallux valgus repair. The most common symptoms are pain, tingling, numbness, and paresthesias along the medial and plantar aspects of the first metatarsal bone and the first metatarsophalangeal joint. Tinel's sign can often be elicited on percussion of the plantar proper digital nerve along the medial aspect of the first metatarsophalangeal joint.¹⁹⁸,¹⁹⁹,²⁰⁰,²⁰² The differential diagnosis includes bursitis, capsulitis, arthritis, tibial sesamoiditis, and avascular necrosis of the tibial sesamoid.