Entrapment Neuropathies of the Lower Extremity

6 – Entrapment Neuropathies of the Lower Extremity

Chapter 6
Entrapment Neuropathies of the Lower Extremity
Zehava Sadka Rosenberg
Conrado F.A. Cavalcanti
Three major nerves supply the lower extremity: the sciatic nerve, the femoral nerve, and the obturator nerve (Fig. 6.1).1 The distance that these nerves have to travel (Table 6.1) predisposes them to multiple potential entrapment sites and compression neuropathies. Although lower extremity neuro-pathies are a major cause of pain and functional impairment, they are often overlooked or misinterpreted,2 primarily because of the complexity of the clinical picture and the difficulty in distinguishing neuropathies from non-neurologic, more common causes for discomfort in the lower extremity. Other neurologic causes for lower leg symptoms such as disk disease and lumbar plexopathy can mimic peripheral entrapment neuropathies as well as coexist with them, further confounding the clinical diagnosis.
Various imaging modalities can aid in the assessment of nerve entrapments of the lower extremity. Plain radiographs and computed tomography (CT) are useful in assessing osseous abnormalities such as spurs and fracture fragments.3 Ultrasound (US) is a very promising technique for assessing lower entrapment neuropathies because of its accessibility, facility in distinguishing nerves from adjacent vessels, dynamic capabilities, and ability to image long nerve segments.3,4,5,6,7,8,9,10 US, however, requires a high level of operator expertise, and the images are usually difficult for the non-radiologist to interpret.
At present, magnetic resonance (MR) is the imaging modality of choice for directly visualizing nerves, depicting entrapment sites, and mapping denervation patterns.3,11,12 Although the status of MR examination in detecting entrapment neuro-pathies remains to be established, it is evident that, despite some conflicting reports, it can play a significant and complementary role to electrophysiologic studies.13,14,15,16,17,18 West demonstrated increased short tau inversion recovery (STIR) signal compatible with muscle denervation within 4 days after nerve resection, prior to electromyographic (EMG) evidence of disease.16 Fleckenstein, on the other hand, noted that MR imaging was less reliable in


mapping and monitoring subacute and chronic denervation.13 One study correlating quantitative EMG and MR studies of the anterior tibial muscle depicted a high correlation between the two techniques in chronic denervation.15 In this same study MR imaging depicted denervation in additional muscles that were not, however, studied with EMG. In another large study of 90 patients with clinical evidence of peripheral neuropathy, MR examination demonstrated a sensitivity of 84% and a specificity of 100% compared to EMG studies.17 In a small subgroup of patients, however, abnormal EMG activity was noted in more muscles or in the absence of muscle involvement on STIR MR images.17 Comparison of MR studies with EMG in 40 patients with neurogenic foot drop revealed agreement in 92% of the patients.18 In a small percentage of these patients, MR imaging detected more widespread muscle disease than found on the EMG studies. In one patient a follow-up EMG study confirmed the MR finding.18

FIGURE 6.1 ● The origins of the three major nerves supplying the lower extremity: the sciatic nerve, the femoral nerve, and the obturator nerve.
MR imaging may be particularly useful in diagnosing deep entrapment neuropathies, such as the piriformis muscle syndrome, in patients for whom EMG is problematic, such as patients taking anticoagulants, patients with bleeding disorders, patients who require serial studies, and children who have difficulty tolerating the pain associated with EMG.19,20,21 With the advent of recent technologic advances such as T2 neurography, it is likely that MR imaging will play an increasingly important role and may even, in certain settings, replace electrophysiologic studies for the detection of entrapment neuropathies of the lower extremity.
TABLE 6.1 ● Major Motor Innervations of the Lower Extremity
At present, there is relatively little information on the MR features of peripheral entrapment neuropathies of the lower extremity.3,12,22 MR imaging of neuropathies of the foot and ankle is particularly neglected. Even the normal anatomy of the nerves has been only briefly described.11,23 It is important to recognize the clinical and MR imaging features of entrapment neuropathies of the lower extremity, however, since early treatment, while the neurologic changes are still reversible, is crucial for full functional recovery. Knowledge of the detailed anatomy of the peripheral nerves and the muscles they innervate is indispensable.
Pathomechanism of Entrapment Neuropathies
Most entrapment and compression neuropathies in the lower extremity are either mechanical, occurring at fibrous and fibro-osseous tunnels, or dynamic, related to nerve injury during specific limb positioning.24,25 Tumors, osteophytes, fracture fragments, scarring, aberrant muscles, and other mass-occupying lesions can cause local friction, a deviation in the course of the nerve, and subsequent entrapment. In many instances


the symptoms manifest only after a superimposed external force, such as an ill-fitting shoe, aggravates the nerve compression. Trauma, surgery, and ankle inversion injuries are known to cause stretch injuries to many of the nerves of the lower extremity. Hormonal changes, preexisting polyneuropathy, and systemic diseases such as diabetes mellitus and rheumatoid arthritis can also predispose to nerve entrapment.

Nerve entrapment can produce several types of signs and symptoms, including:
  • Motor function impairment, such as weakness, paralysis, and muscle atrophy
  • Sensory deficits, such as pain and paresthesias
  • Autonomic deficits, such as dry skin and ulceration
Treatment varies depending on the site of entrapment, the inciting cause, and the extent and chronicity of the process. Initially treatment is conservative, aimed at removal of the inciting agent by rest, behavior modification, footwear changes, orthotics, anti-inflammatory medications, and local steroid injection. If symptoms persist after 3 to 4 months of conservative management, surgical decompression is required to prevent permanent nerve damage and muscle atrophy. Complete nerve transection may require direct nerve repair or grafting.
Neuropathy is linked to endoneurial edema, increased endoneurial pressure, decreased blood flow to the nerve, and nerve ischemia.26 Demyelinization and neuropathy then follow. Nerve injury can be classified in increasing order of severity into neurapraxia, axonotmesis, and neurotmesis:27
  • Neurapraxia, or first-degree nerve injury, is an early and reversible segmental conduction block without axonal disruption ranging from transient ischemia (such as occurs from crossing the legs) to myelin sheath injury. Neurapraxia usually resolves within hours, days, or months with no residual sequelae.
  • Axonotmesis, or second-degree nerve injury, represents more advanced nerve damage, in which a focal disruption of the axon produces Wallerian degeneration distal to the site of injury. However, the intact investing connective tissues around the nerve allow axonal regeneration at a rate of approximately 1 to 2 mm a day, and the prognosis is still relatively good. Depending on the distance between the site of nerve injury and the muscle affected, axonotmesis can resolve within weeks to months.
  • Neurotmesis, or third-degree nerve injury, is characterized by an irreversible and complete axonal and connective tissue disruption. In addition to significant functional impairment, neurotmesis can produce painful neuromas secondary to unsuccessful attempts at nerve regeneration.
Axonotmesis and neurotmesis can be further subdivided into three categories depending on the number of disrupted surrounding connective tissue layers.28 More than one grade of injury frequently coexists within the same nerve. In general, early and mild nerve compression leads to neurapraxia, whereas chronic or more severe compression can lead to axonotmesis and neurotmesis.
MR Imaging Techniques
Complete visualization of nerves requires imaging in all three planes. Nerves are optimally traced on axial MR images, and high-resolution axial T1-weighted images and fluid-sensitive images, ideally fat-suppressed, are recommended. Sagittal and coronal imaging should also be performed with fluid-sensitive sequences, preferably STIR.
Gadolinium contrast enhancement may be used to detect associated mass lesions that are compressing the nerve. Normal nerves do not enhance after intravenous contrast administration. Changes in the blood–nerve barrier and secondary leakage of gadolinium into the endoneurial space may account for the post-contrast enhancement of compressed nerves.26
A new gadolinium-based agent, Gadofluorine M (Gf), has shown promise in assessing acute nerve degeneration and regeneration in rats.29 Gf binds to degenerated nerves, resulting in nerve enhancement on T1-weighted images. Proximal-to-distal reversal of the enhancement has been noted in regenerating nerves. EMG studies are capable of assessing regeneration only once the nerve reaches the target muscle, and this process may take weeks to months. With Gf it is possible to assess nerve regeneration during the critical time interval in which a decision regarding nerve grafting must be made.
MR T2 neurography is a relatively new and promising technique for high-resolution imaging of peripheral nerves.19,20,21,30,31 The intermediate MR signal of a nerve is a mixture of signal from various nerve tissues, including endoneurial fluid, myelin, fatty interfascicular epineurium, and connective tissue. Neurography selectively highlights only the fluid signal from the imaged nerves using the following parameters:
  • A chemical shift-selective pulse (CHESS), which suppresses fat signal from around and within the nerves
  • High TE values (approximately 90 msec), which suppress signal from adjacent muscle
  • Radiofrequency saturation pulses, which suppress fluid signal from vessels
FIGURE 6.2 ● MR neurography of a young patient with sciatic neuritis. An axial T2-weighted fat-suppressed image (TE 90 msec, 3T) demonstrates increased signal in the sciatic nerve fascicles (arrow). Note suppression of signal from adjacent muscles and vessels.


The only remaining signal is from endoneurial fluid, and the nerves stand out as bright signal intensity structures. MR neurography requires the use of phased-array surface coils and careful and constant magnet shimming. It provides excellent fascicular detail, best seen on axial images (Fig. 6.2). Further oblique image reformation and post-processing provide high-resolution selective images of the nerves along their longitudinal axis.
At present MR neurography is particularly useful for imaging large structures such as the lumbar and sacral plexi and the sciatic, femoral, and common peroneal nerves. The high-resolution images allow visualization of selective fascicular disease. Using this technique it is also possible to distinguish intraneural from perineural tumors. Smaller nerves, in the ankle and foot, however, are difficult to distinguish from adjacent bright signal vessels with neurography. Other disadvantages include the length of imaging time and sensitivity to motion artifact.21
Normal MR Anatomy of the Lower Extremity
On T1-weighted images peripheral nerves demonstrate intermediate signal intensity, similar to muscle signal. Mildly increased signal intensity is noted on T2-weighted and other fluid-sensitive sequences, possibly due to the presence of endoneurial fluid within the fascicles of the nerve.3 The following MR characteristics are typical:
  • Nerves are seen as ovoid to round structures on axial MR images.
  • Longer segments of a nerve can occasionally be appreciated on coronal and sagittal images.
  • The fascicular anatomy of larger nerves demonstrates a honeycomb appearance, best appreciated on high-resolution axial MR images. This pattern is difficult to visualize in the smaller nerves.
  • On axial MR images, it is not uncommon to detect major divisions of the larger nerves before they actually branch away from each other. The peroneal and tibial divisions of the sciatic nerve can be visualized as they descend together in the thigh. Similarly, in the distal knee, the common peroneal nerve is subdivided into its two major branches, the superficial and deep peroneal nerves, long before the two divisions physically separate from one another.
Nerves usually travel within intervals between muscles and are typically well highlighted by fat. In young athletic individuals with bulky muscle mass, the nerves may be more difficult to detect because of the paucity of fat between muscle planes. Certain muscles can serve as landmarks for identifying adjacent nerves:
  • The saphenous nerve travels in close proximity to the sartorius muscle throughout most of its course in the thigh and knee.
  • The common peroneal nerve courses along the posteromedial aspect of the biceps femoris muscle.
  • Identifying the medial plantar nerve in the foot is made easy by following the flexor hallucis longus tendon.
Veins and arteries also aid in tracing the course of the nerves since they usually travel in the same fat plane. Conversely, nerves, particularly distally, are frequently difficult to distinguish from their adjacent vessels. On T1-weighted images nerves and vessels are isointense. On fluid-sensitive images both vessels and diseased nerves demonstrate increased signal. Familiarity with the spatial relationships between the nerves and the adjacent vessels, as well as the presence of flow void artifacts and tortuosity of the vessels, may aid in distinguishing between the two structures.
MR of Lower Extremity Nerve Pathology
The MR characteristics of peripheral nerve entrapment can be divided into two major categories:32,33,34
  • Direct evidence of nerve pathology consistent with alterations in the course, morphology, and signal characteristics of the affected nerve
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  • Indirect signs of entrapment evidenced by muscle signal and size alterations compatible with denervation
Direct MR signs of entrapment include:
  • Course deviations. Mechanical deviation of the nerve from its normal course may be related to static conditions associated with mass effect such as bone spurs, scar, soft tissue tumors, ganglia, and aberrant muscles. These processes are easily depicted with MR imaging. Course deviation and entrapment of a nerve, however, can be dynamic and may be appreciated only in certain predisposing limb positions, such as foot pronation in medial plantar nerve entrapment or ankle plantar flexion and dorsiflexion in superficial peroneal nerve entrapment secondary to a muscle hernia.2 These types of entrapments can be missed on routine MR studies and may require additional studies following changes in limb positioning.
  • Morphologic and signal changes. Size and signal alterations also represent direct MR evidence of nerve pathology. Nerve swelling is compatible with edema at the fascicular level and may be a late sign of disease. In the smaller nerves, however, size differences can be difficult to assess. When present, edema may accentuate the honeycomb fascicular appearance of the nerve. Conversely, focal effacement of the normal fascicular pattern may also be encountered.19 The increased nerve signal is believed to reflect endoneurial edema and may also represent a fairly advanced process. Since most normal nerves have mildly increased signal on fluid-sensitive images, assessment of signal alterations can be challenging. The increased signal in asymptomatic individuals is usually mild and also involves the whole course of the nerve, whereas pathologic increased signal is typically focal and is usually found in areas susceptible to entrapment.
Indirect MR signs of entrapment include:
  • Muscle denervation. Motor nerve entrapment can be inferred when there is MR evidence of muscle denervation. Muscle denervation is characterized by signal alterations seen on both T1- and T2-weighted images. These alterations serve to localize the site of entrapment and provide information on the extent of motor damage.18 Bright signal on T2-weighted images is consistent with a fluid shift, due to muscle cell atrophy, from intracellular to extracellular compartments without a significant increase in the total water content of the muscle.35 Increased blood perfusion to the muscle may also contribute to denervation signal alterations. Increased muscle signal on fluid-sensitive images has been labeled as acute denervation edema, although strictly speaking it may be more accurate to refer to it as subacute denervation. Reversal of the muscle signal to normal may be encountered once the entrapment has resolved.16,36
  • Fatty infiltration. In chronic nerve damage there is fatty infiltration and decreased muscle bulk indicative of relatively irreversible muscle atrophy. Chronic denervation is depicted as bright muscle signal on T1-weighted images. Often, ongoing nerve damage manifests as increased signal on T1- and T2-weighted images. This constellation of findings indicates an ongoing partially reversible process. Rarely, muscle pseudohypertrophy related to excessive fatty infiltration and true muscle hypertrophy have also been noted with chronic denervation.37
In general, acute or subacute denervation is easily distinguished from other causes of increased T2 muscle signal such as contusions, musculotendinous injuries, infection, rhabdomyolysis, and compartment syndrome. Denervation edema is usually diffuse and interstitial and involves the whole muscle. It spares the fascial planes between muscles and adheres to a particular nerve distribution.
A few concepts should be kept in mind when assessing peripheral nerve entrapment on MR images: the double crush theory, the Valleix phenomenon, selective muscle involvement, variability in innervations, and the distance between the site of nerve injury and the affected muscle.
  • The double crush syndrome is a phenomenon in which a proximally compromised nerve has a decreased threshold for injury and as a result is more susceptible to entrapment distally.2,25,38,39,40,41 As a result, it is not uncommon to find two sites of entrapment present simultaneously. Spinal stenosis, for example, predisposes to nerve entrapment more distally. Simultaneous entrapment of the medial plantar nerves at both the tarsal tunnel and at the foot may also occur.
  • In the Valleix phenomenon, a distal entrapment affects the more proximal nerve.2,25,42 This process may, in fact, be the same as the double crush syndrome. Both entities can produce an odd distribution of muscle denervation signal, and the concomitant presence of two entrapment sites should be carefully looked for.
  • Selective muscle involvement is a common occurrence that manifests clinically, electrodiagnostically, and on MR examination as selective damage of only a few muscles along a specific nerve distribution. Sciatic nerve injury, for example, typically affects the peroneal division and spares the tibial division, partly because the former is more superficial, has larger fascicles and less connective tissue, and is fixed at two places. Similarly, entrapment of the common peroneal nerve usually affects the deep peroneal nerve more than the superficial peroneal nerve because the former is in closer proximity to the fibular head. This selective fascicular involvement can also occur within a single nerve branch,


    and its etiology is not always known.19 On MR images it is depicted as signal alterations in only a select group of muscles along a single nerve distribution. For example, it is not unusual for only the plantaris and popliteal muscles to depict muscle denervation changes in tibial nerve entrapment. Similarly, denervation signal isolated to the anterior tibial muscle with relative sparing of the extensor digitorum longus muscle is often depicted in common peroneal neuropathy. Neurography may illustrate greater involvement of isolated nerve fascicles.

    FIGURE 6.3 ● Proximal tibial entrapment in a 49-year-old patient with neuropathic foot pain. Symptoms resolved following an intra-articular steroid injection of the knee. This axial T2-weighted fat-suppressed image depicts a loose body in the popliteal muscle bursa (arrow), abutting on the neurovascular structures (arrowheads).
    There are many variations in muscle innervation and many communicating nerve loops in the lower extremity, particularly in the foot region.43 For example, the deep peroneal nerve may, in rare instances, supply muscles such as the adductor hallucis and flexor hallucis brevis, muscles typically innervated by the lateral and medial plantar nerves. This variability can affect the distribution of signal alterations within denervated muscles and may produce puzzling MR patterns. Familiarity with variations in innervation aids in interpreting unexpected muscle denervation signal alterations.
  • Finally, the distance from the site of entrapment to the innervated muscle should be considered when searching for muscle denervation abnormalities. Proximal damage to the peroneal division of the sciatic nerve may depict denervation signal in the leg or foot. This signal alteration may be missed if only the thigh is being imaged. Similarly, MR imaging of a painful foot may overlook a more proximal entrapment in the leg or thigh (Fig. 6.3). It is important to pay careful attention to signal changes on sagittal and coronal planes, where larger portions of the limb are illustrated, to help avoid this pitfall. If the clinical suspicion for entrapment is high and no abnormalities are noted on the initial study, imaging a more distal or proximal section of the limb can also be performed.
Sciatic Nerve
Normal Anatomy
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.
FIGURE 6.4 ● A posterior view of the right lower extremity demonstrating the sciatic nerve and its tibial and peroneal divisions.
TABLE 6.2 ● Motor Distribution of the Sciatic Nerve
FIGURE 6.5 ● A posterior view of the sciatic nerve in the greater sciatic foramen. The nerve descends anterior to the piriformis muscle and successively posterior to the superior gemellus, obturator internus, inferior gemellus, and quadratus femoris muscles.



MR Appearance
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 muscle21,44 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:
  • The sciatic nerve is highlighted by fat as it courses in the greater sciatic foramen anterior to the piriformis muscle and lateral to the internal iliac vessels.
  • The nerve follows the course of the piriformis muscle and can be traced as it curves around the ischial spine into a more posterior and lateral location in the upper thigh. There the nerve is seen within an abundant stripe of fat between the greater trochanter and the ischial tuberosity (Fig. 6.8).
  • In the upper thigh the nerve is anterior to the gluteus maximus muscle and posterior, successively, to the superior gemellus, the obturator internus, the inferior gemellus, and the quadratus femoris muscles. Further down the nerve is anterior to the hamstring muscles and posterior to the adductor magnus muscle.
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  • There is a gradual decrease in the amount of fat surrounding the nerve as it descends down the thigh. Finally, the nerve is flattened between the biceps femoris and the adductor magnus muscles.
  • In the lower thigh and proximal knee, as the adductor magnus muscle mass progressively disappears, the nerve is again highlighted by a significant amount of fat.
  • Not infrequently, the tibial and peroneal divisions of the nerve can be detected as they descend side by side in a common sheath before they diverge from each other in the proximal knee (see Fig. 6.8B).
  • The posterior femoral cutaneous nerve, located posterior to the sciatic nerve, can sometimes be identified as it migrates into a more superficial location in the upper thigh.
FIGURE 6.6 ● Anterior (A) and posterior (B) views of the sensory innervation of the lower extremity.
FIGURE 6.7 ● Coronal T1-weighted image of the sciatic nerve demonstrating the normal fascicular pattern of both sciatic nerves (arrowheads). A slip of the right piriformis muscle is noted (arrow).
FIGURE 6.8 ● Normal sciatic nerve. (A) An axial PD-weighted image at the upper thigh demonstrates a normal ovoid-shaped sciatic nerve (black arrow) anterior to the gluteus maximus muscle (GM), highlighted by the fat. Note the proximity of the nerve to the hamstring tendons (white arrows). (B) An axial PD-weighted image at the middle thigh depicts the tibial (arrowhead) and smaller peroneal (arrow) divisions of the sciatic nerve in a common sheath before they diverge in the proximal knee.
Sciatic Neuropathy
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:
  • The peroneal division is fixed at two points (at the sciatic foramen and at the fibular head), whereas the tibial division is fixed only at the sciatic foramen.
  • The peroneal division has larger fascicles with less protective surrounding connective tissue.
  • The peroneal division is more superficial and lateral than the tibial division.
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.

Piriformis Muscle Syndrome
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:
  • The greater sciatic foramen is bordered superiorly and laterally by the sacrum and the iliac bone and by the sacroischial and sacrotuberous ligaments inferiorly and medially.
  • The piriformis muscle occupies a large part of the foramen as it extends from the sacrum to the greater trochanter (see Fig. 6.5).
  • A bursa is often found between the muscle and the bone.
  • The sciatic nerve traverses the greater sciatic foramen anterior to the piriformis muscle and is susceptible to compression due to loss of sciatic foramen volume, trauma, inflammation, local ischemia, and anatomic variations.
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.
FIGURE 6.9 ● The piriformis muscle pierced by the peroneal division of the sciatic nerve (anatomic variation).
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.
MR Appearance
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.

FIGURE 6.10 ● Sciatic neuropathy associated with rhabdomyolysis. Increased signal in the sciatic nerve (arrows) is shown on this coronal fluid-sensitive fat-suppressed image. Note the increased signal in multiple muscles.
FIGURE 6.11 ● Hamstring tendon tear with secondary edema around the sciatic nerve. Axial T2-weighted (SA) and sagittal T2-weighted fat-suppressed (B) images show partial avulsion of the conjoined tendon of the biceps and semitendinosus muscles (arrowhead) with extensive edema around the sciatic nerve (arrows).
FIGURE 6.12 ● Denervation edema after resection of a sciatic nerve tumor. This axial T2-weighted image demonstrates denervation edema in the hamstring muscles (H) and adductor magnus muscle (A).
FIGURE 6.13 ● Lumbosacral plexopathy with denervation edema in the femoral, obturator, and sciatic nerve distribution. Increased signal in the vasti muscles (V) and adductor magnus (A) and hamstring muscles (arrow) is shown on this axial T2-weighted fat-suppressed image.
FIGURE 6.14 ● Plexiform neurofibromatosis. (A) Coronal T2-weighted fat-suppressed image depicting fusiform enlargement and increased signal of the right (arrows) and left (arrowheads) sciatic nerves. (B) Axial T2-weighted fat-suppressed image demonstrating the “bag of worms” appearance of the right sciatic nerve (black arrow). Note an intramuscular neurofibroma in the rectus femoris muscle (white arrow).
FIGURE 6.15 ● Amputation neuroma. Coronal T1-weighted image demonstrating an amputation neuroma in the right sciatic nerve (arrow). Compare the thickened fascicular pattern of the nerve proximal to the neuroma (black arrowhead) with the normal left sciatic nerve (white arrowheads). (Courtesy of Laercio Rosenberg, MD, Sao Paulo, Brazil)
FIGURE 6.16 ● Surgically proven left piriformis muscle syndrome. (A) Axial T1-weighted image demonstrates a markedly enlarged left piriformis muscle (P) displacing the sciatic nerve (arrow). The normal right piriformis (asterisk) is much smaller. (B) A posterior view during surgery demonstrates indentation on the left sciatic nerve from the piriformis muscle. (Courtesy of Stephen Russel, MD, NY)
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:
  • Significant asymmetry in the piriformis muscles is noted between the symptomatic and asymptomatic sides (Figs. 6.16 and 6.17). Mild asymmetry of the muscles, however, is often present in asymptomatic individuals.
  • Presence of selective atrophy49,50 or hypertrophy of the piriformis muscle and accessory muscle slips47,52
  • Detection of the sciatic nerve or one of its divisions within the substance of the piriformis muscle. An intramuscular location of the sciatic nerve, however, may be a normal variation in up to 10% of individuals.
  • Increased signal in the nerve and in the piriformis muscle may also be seen.49
FIGURE 6.17 ● Piriformis muscle syndrome in a patient kicked by a horse in the left buttock. This axial T2-weighted fat-suppressed image shows engorgement and increased signal in the left piriformis muscle (P), with edema in the region of the sciatic nerve. Compare with a normal right piriformis muscle (white arrows). (Courtesy of Frank Crnkovich, MD, Colorado)


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
Femoral Nerve
Normal Anatomy
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).
MR Appearance
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.
FIGURE 6.18 ● The femoral nerve and its branches.
FIGURE 6.19 ● The saphenous nerve as it descends down the thigh to enter the adductor canal.



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.
Femoral Neuropathy
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 injury64,65,66 associated with iliacus muscle hematoma.
FIGURE 6.20 ● The normal femoral nerve in the upper thigh. Axial T1-weighted image demonstrating the normal bundles of the femoral nerve (arrowheads) lateral to the femoral vessels (arrows).
FIGURE 6.21 ● Normal saphenous, tibial, and common peroneal nerves in the knee. An axial PD-weighted image depicts the branches of the saphenous nerve (arrow) lateral to the sartorius muscle (S); the tibial nerve (white arrowhead) between the lateral (LG) and medial (MG) heads of the gastrocnemius muscle; and the common peroneal nerve (black arrowhead) between the gastrocnemius muscle and biceps femoris muscle (B). Note that the common peroneal nerve is already split into its deep and superficial branches.
Clinical indications of femoral neuropathy include:
  • Buckling and decreased knee extension (quadriceps weakness)
  • Decreased hip flexion
  • Difficulty arising from a sitting position and climbing up stairs (iliopsoas muscle weakness)
  • Atrophy of the muscles of the anterior compartment
  • Absent knee jerk
  • Sensory deficits in the anterior and medial lower thigh, and medial knee, leg, and foot
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

FIGURE 6.22 ● Femoral neuropathy secondary to sports-related iliacus muscle tear. Axial T1-weighted image demonstrating enlargement of the left iliac (white asterisk) and psoas muscles (black asterisk). The anteriorly displaced femoral nerve is not visualized. Compare with the right normal iliac (I) and psoas (P) muscles.
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.
MR Appearance
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
Obturator Nerve
Normal Anatomy
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.
MR Appearance
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.

FIGURE 6.23 ● The normal obturator nerve. The insert shows the sensory distribution of the nerve along the medial thigh.
FIGURE 6.24 ● Normal obturator nerves in the pelvis. (A) Axial T1-weighted image depicting the nerves (arrows) medial to the acetabula and anterior to the obturator vessels (arrowheads). (B) Coronal T1-weighted image demonstrating the nerves (arrows) surrounded by fat.


Obturator Neuropathy
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:
  • Pain in the groin or medial thigh. Radiation of pain to the medial knee can occur and is related to innervation of the knee joint by the posterior branch of the obturator nerve.
  • Complete sensory loss (uncommon due to overlapping innervation by other cutaneous nerves)
  • Adductor muscle weakness, which may be initially masked since the adductor magnus muscles are also innervated by the sciatic nerve
  • Weak thigh adduction and wide gait due to abducted hip in advanced cases
  • Atrophy of the medial thigh
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.
FIGURE 6.25 ● Acetabular metastasis with obturator neuropathy and denervation edema. (A) An axial PD-weighted image depicts a hyperintense destructive acetabular mass (asterisk) medially displacing the obturator neurovascular structures (arrowheads). (B) This coronal T2-weighted fat-suppressed image of the pelvis demonstrates the acetabular mass (asterisk) medially displacing the pelvic structures. Subacute denervation edema in the obturator externus (arrow) and adductor muscles (arrowheads) is noted.
MR Appearance
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.


Lateral Femoral Cutaneous Nerve
Normal Anatomy
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
FIGURE 6.26 ● The lateral femoral cutaneous nerve as it dives under the inguinal ligament close to the anterior superior iliac spine. The insert shows the sensory distribution of the nerve along the lateral thigh.
Lateral Femoral Cutaneous Neuropathy (Meralgia Paresthetica)
The lateral femoral cutaneous nerve is susceptible to entrapment at two major sites:
  • Under the inguinal ligament, where the nerve makes a 70° to 90° turn as it bends around the anterior superior iliac spine
  • As the nerve perforates the fascia lata
There are many reported causes for entrapment of the lateral femoral cutaneous nerve:
  • Compression due to pelvic and retroperitoneal tumors
  • Trauma such as avulsion fracture of the ASIS
  • Surgical procedures, including spine surgery,92 acetabular fracture fixation, pelvic osteotomy, laparoscopic hernia repair, and iliac crest bone-graft harvesting
  • Posttraumatic neuroma following pelvic injury
  • P.1072

  • Nerve transaction
  • Stretching of the nerve due to prolonged leg and trunk hyperextension
  • Leg length discrepancy
  • Scoliosis
  • Prolonged lithotomy position during surgery
  • Prolonged hip flexion to reduce incisional pain during the postoperative period93
  • Extended periods of standing, with secondary increased tension of the abdominal and fascia lata muscles
  • External compression of the nerve by seat belts, weight gain (obesity, pregnancy), and tight clothing (girdles and military belts94)
  • Anatomic variations predisposing to entrapment91,95,96,97
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
MR Appearance
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
Common Peroneal Nerve
Normal Anatomy
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
FIGURE 6.29 ● Common peroneal neuropathy secondary to a nerve sheath tumor. (A) Coronal T2-weighted fat-suppressed image demonstrating a nerve sheath tumor of the common peroneal nerve (arrow). (B) Sagittal T1-weighted image showing denervation atrophy of the anterior tibial muscle (arrows).
FIGURE 6.30 ● Common peroneal neuropathy with denervation atrophy and edema secondary to varicosities. (A) Axial T1-weighted image demonstrates denervation atrophy of the anterolateral muscles, predominantly the anterior tibial muscle (arrow). (B) Axial T2-weighted image depicts varicosities (arrowheads) next to the peroneal nerves and denervation edema of the anterior tibial muscle (arrow).
FIGURE 6.31 ● Surgically proven common peroneal neuropathy and denervation secondary to a hypertrophied biceps femoris muscle. (A) Axial T1-weighted image showing the common peroneal nerve (arrow) entrapped between a hypertrophied short head of the biceps femoris muscle (white asterisk) and the lateral head of the gastrocnemius muscle (black asterisk). (B) Axial T2-weighted fat-suppressed image displaying denervation edema in the anterolateral compartment muscles (arrows).



Deep Peroneal Nerve
Normal Anatomy
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.

FIGURE 6.32 ● Anterior view of the foot demonstrating the three most common locations for deep peroneal nerve entrapment.
MR Appearance
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:
  • In the very proximal leg the deep peroneal nerve is noted within a small triangle of fat just anterior to the interosseous membrane, coursing first lateral and then anterior to the anterior tibial artery (see Fig. 6.28).
  • More distally, the nerve is again noted lateral to the anterior tibial artery.
  • In the proximal leg the nerve is deep to the anterior tibial and extensor digitorum longus muscles and, more distally, deep to the extensor digitorum and extensor hallucis longus muscles.
  • The deep peroneal nerve is easier to identify in older individuals and in patients with abundant fat; in younger athletic individuals, muscle bulk may obscure the nerve.
  • As the nerve descends down the leg into the ankle, it also migrates anteriorly and medially and becomes more superficial.
  • On axial images in the ankle region, the nerve can be followed within the dorsal fat between the extensor hallucis longus and extensor digitorum longus tendons. Approximately 5 cm above the ankle joint, the deep peroneal nerve is found deep to the superior extensor retinaculum. Approximately 1 cm above the ankle joint, it is seen deep to the superomedial band of the inferior extensor retinaculum. Proximal to the talonavicular joint, the nerve is deep to the inferomedial band of the inferior extensor retinaculum.
  • Distal to the ankle, oblique coronal (short axis) images of the midfoot are optimal for tracing the lateral and medial branches of the deep peroneal nerve (Fig. 6.33).
  • The anterior tarsal tunnel is seen as the space between the inferior edge of the extensor retinaculum and the talonavicular joint.
  • The lateral branch of the deep peroneal nerve can usually be identified as it courses laterally and terminates in the extensor digitorum brevis muscle.
  • The main medial branch is usually medial to the dorsalis pedis artery between the extensor hallucis longus and extensor hallucis brevis tendons. It is found within a small amount of dorsal fat between the first and second cuneiforms and between the first and second metatarsal bases.
  • At the forefoot the deep peroneal nerve can be difficult to distinguish from the adjacent vessels due to its small size, paucity of fat, and proximity to the underlying bones.
FIGURE 6.33 ● The normal deep peroneal nerve at the talonavicular joint. An oblique coronal PD-weighted image demonstrates the medial (white arrow) and lateral (black arrow) branches of the deep peroneal nerve separated by the dorsalis pedis vessels.
Deep Peroneal Neuropathy
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.

FIGURE 6.34 ● Deep peroneal neuropathy secondary to a dorsal ganglion. (A) Oblique coronal T2-weighted fat-suppressed image depicts a ganglion (arrow) dorsal to the second cuneiform (asterisk). (B) A more distal oblique coronal T1-weighted image demonstrates denervation atrophy of the first dorsal interosseous muscle (arrow).
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.
MR Appearance
At present there are only anecdotal reports of MR imaging of the deep peroneal nerve.11,130,131 Findings include the following:
  • Due to the small size of the nerve, signal alterations and increased girth of the nerve may be difficult to appreciate.
  • Acute and subacute muscle denervation secondary to isolated entrapment of the nerve in the leg manifests as increased signal on fluid-sensitive images in the anterior compartment muscles, including the anterior tibial, extensor hallucis longus, extensor digitorum longus, and peroneus tertius muscle.
  • Increased T1 signal due to fatty infiltration and atrophy of the muscles is noted with more advanced entrapment.
  • Sparing of the lateral compartment muscles (the peroneus longus and peroneus brevis) is noted since the latter are supplied by the superficial peroneal nerve.
  • Tibial or fibular fractures with displaced fragments may be seen impinging on the nerve.
  • A mass effect due to tumors or ganglia, soft-tissue edema due to anterior compartment syndrome, muscle contusions, and infarcts may all be indirect MR features of deep peroneal entrapment neuropathy.
  • At the ankle and dorsal foot, injury to the deep peroneal nerve can be surmised when obliteration of the fat along the course of the nerve and its branches is identified. Mass effect by ganglia or tumors may also be depicted (Fig. 6.34).
  • Entrapment of the medial branch of the deep peroneal nerve produces bony and soft-tissue abnormalities such as talonavicular osteophytes, first metatarsal and first cuneiform osteoarthritis and spurs, a prominent os intermetatarseum, edema, and exuberant periostitis associated with stress fracture of the base of the second metatarsal, and first and second cuneiform fracture fragments.
  • Isolated muscle denervation of the extensor digitorum brevis is indicative of entrapment neuropathy of the lateral branch of the deep peroneal nerve. Because of the variability in innervation of the intrinsic muscles of the first web space, entrapment of the deep peroneal nerve may also demonstrate signal alterations in the first dorsal interosseous muscles (see Fig. 6.34B) and, less commonly, in the lateral head of the flexor hallucis brevis and oblique head of the adductor hallucis muscle.
FIGURE 6.35 ● The superficial peroneal nerve as it pierces the deep fascia of the lateral compartment. Inversion injury can cause stretching of the nerve against the fascia.


Superficial Peroneal Nerve
Normal Anatomy
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.
MR Appearance
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 Neuropathy
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.

FIGURE 6.36 ● The normal superficial peroneal nerve. Axial PD-weighted image of the distal leg illustrating the nerve (arrow) in the subcutaneous fat, after it has pierced the fascia.
MR Appearance
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
FIGURE 6.37 ● Superficial peroneal neuropathy secondary to muscle herniation. Axial T1-weighted image shows fascial herniation of the peroneus longus muscle (arrowheads) abutting on the superficial peroneal nerve (arrow).
Tibial Nerve
The tibial nerve, also called the posterior tibial nerve, is the largest division of the sciatic nerve (see Fig. 6.4).1 There are six distinct tibial neuropathies:135
  • Proximal tibial neuropathy (in the leg)
  • Tarsal tunnel syndrome
  • Medial plantar neuropathy
  • Lateral plantar neuropathy
  • Interdigital neuropathy (Morton's neuroma)
  • Medial plantar proper digital neuropathy (Joplin's neuroma)
Proximal tibial neuropathy in the leg is quite uncommon and is usually related to space-occupying masses in the popliteal fossa such as tumors, popliteal cysts, popliteal artery aneurysm, and ganglia. External compression is quite rare because of the deep location of the nerve. Clinical manifestations include weakness of the plantar and invertor muscles, as well as the intrinsic muscles of the foot. Sensory loss is noted in the heel and occasionally along the sural nerve distribution. MR imaging is quite useful for diagnosing mass lesions in the popliteal fossa and can play a crucial role in the assessment of tibial neuropathy (see Fig. 6.3; Figs. 6.38 and 6.39). The distribution of muscle signal alterations can aid in distinguishing tibial neuropathy from the more proximal sciatic or lumbosacral plexus neuropathies (Fig. 6.40).
Normal Anatomy
Tibial Nerve in Thigh, Leg, and Foot
The tibial nerve branches off from the sciatic nerve at the popliteal fossa. It then continues within the posterior compartment


of the leg between the two heads of the gastrocnemius muscle before proceeding anteriorly to the soleus muscle. The tibial nerve descends in an oblique fashion becoming more superficial approximately 15 cm above the ankle joint, at which point it travels medial to the Achilles tendon. It then proceeds deep to the flexor retinaculum (the lancinate ligament) within the tarsal tunnel. In the calf the tibial nerve provides motor innervation to the deep and superficial posterior compartment muscles, including the plantaris, popliteus, gastrocnemius, soleus, posterior tibial, flexor digitorum longus, and flexor hallucis longus muscles. Most of the sensory and motor innervation of the foot is supplied by the tibial nerve.

FIGURE 6.38 ● Proximal tibial neuropathy and muscle denervation in the leg secondary to a nerve sheath tumor. Axial T2-weighted fat-suppressed image demonstrates a hyperintense nerve sheath tumor (arrow) in the soleus muscle, in the region of a tibial nerve ramus, with secondary denervation edema in the medial (black arrowheads) and lateral (white arrowheads) heads of the gastrocnemius muscle.
FIGURE 6.39 ● Proximal tibial neuropathy with denervation edema. Axial T2-weighted fat-suppressed image demonstrates denervation edema of the popliteus (black arrow) and medial head of the gastrocnemius muscles (white arrow).
MR Appearance
The tibial nerve, like all other nerves in the lower extremity, is best appreciated on axial MR images. The larger tibial division of the sciatic nerve is noted in the distal thigh as it descends medial to the peroneal division. In the popliteal fossa, the tibial nerve diverges from the common peroneal nerve and is seen surrounded by fat between the biceps femoris and semimembranosus muscles. The nerve is relatively large, oval, and of intermediate signal on T1-weighted sequences and of mildly brighter signal on fluid-sensitive sequences. Fascicles of the nerve can be appreciated on high-resolution axial images and MR T2 neurography. The nerve continues its downward descent, first between and then anterior to the lateral and medial heads of the gastrocnemius muscle


in the knee (see Fig. 6.21) and finally anterior to the soleus muscle in the calf. A gradual and significant decrease in the surrounding fat in the calf may make it difficult to separate the nerve from the adjacent muscles and vascular bundle. The nerve continues its downward medial course until it becomes superficial in the distal calf, posterior to the posterior tibial muscle and medial to the flexor hallucis longus muscle. At this level it is again highlighted by abundant fat.

FIGURE 6.40 ● Tibial and common peroneal neuropathy secondary to a traumatic spinal root avulsion. Axial T2-weighted fat-suppressed image shows muscle denervation edema in the popliteus muscle (black arrow) (innervated by the tibial nerve) and in the anterolateral compartment muscles (asterisk) (innervated by the common peroneal nerve). Note postsurgical metallic susceptibility artifacts (white arrows) in the tibia and fibula.
The course of the tibial nerve can be traced by following the posterior tibial artery and vein. In general, the nerve is lateral to the accompanying vessels throughout its course, with only minimal variation. Occasionally the nerve is seen to travel lateral to the popliteal artery in the distal thigh, posterolateral to the artery in the knee, medial to the artery in the upper calf, and again lateral to the artery in the distal calf. The popliteal vein is always located between the artery and nerve.
Tibial Nerve in Tarsal Tunnel and Foot
In the ankle the tibial nerve courses behind and below the medial malleolus within two tunnels:
  • The upper tibiotalar tunnel, at the ankle region, is bordered by the distal tibia and medial malleolus laterally and the deep aponeurosis of the leg medially.
  • The lower talocalcaneal tunnel, in the hindfoot (in strict anatomic terms the true tarsal tunnel), is bordered by the talus and calcaneus laterally and the flexor retinaculum medially (Fig. 6.41).
The flexor retinaculum is a thin fibrous band that arises from the medial malleolus and inserts onto the medial tuberosity of the calcaneus.1 The term tarsal tunnel is frequently used to refer to both the upper and lower tunnels, since the causes and clinical manifestations of tibial nerve entrapment at both sites are quite similar.
The tarsal tunnel is traversed by the tendons of the posterior tibial, flexor digitorum longus, and flexor hallucis longus muscles; the tibial nerve and its branches; and the tibial artery and veins. Thin fibrous septa between the tendons and the neurovascular bundle divide the tunnel into multiple compartments. The tibial nerve has three terminal branches: the medial calcaneal nerve, the medial plantar nerve, and the lateral plantar nerve.
FIGURE 6.41 ● The tarsal tunnel. The tibial nerve and its branches descend, deep to the flexor retinaculum, along with the flexor tendons and vascular structures.
The medial calcaneal nerve arises proximal to the tarsal tunnel in up to 40% of individuals135,136,137 and thus may be superficial to the flexor retinaculum. It provides sensory innervation to the medial plantar heel.
In over 90% of patients the tibial nerve bifurcates into the medial and lateral plantar nerves within the tarsal tunnel; in the rest the nerve divides proximal to the tunnel. The medial and lateral plantar nerves exit the tunnel and dive deeply within the plantar aspect of the foot deep to the abductor hallucis and flexor digitorum brevis muscles (Fig. 6.42). The more anterior medial plantar nerve travels forward within the foot in a fat plane between the abductor hallucis and flexor digitorum brevis muscles. The nerve is located lateral to the medial plantar artery. It carries sensation from the medial two thirds of the plantar surface of the foot (the medial sole of forefoot and midfoot; the plantar side of first, second, and third toes; and the medial side of the fourth toe), but its motor supply is to only four medially located muscles: the flexor digitorum brevis, the abductor hallucis, the flexor hallucis brevis, and the first lumbrical.
The lateral plantar nerve travels in the foot between the muscle bellies of the flexor digitorum brevis and abductor digiti minimi. The nerve provides motor innervation to most of the muscles of the foot, including the abductor digiti minimi, quadratus plantae, flexor digiti minimi brevis, adductor hallucis, all the interossei, and the second, third, and fourth lumbricals. It carries sensation from the lateral sole of the forefoot and midfoot and from the lateral one and a half to two toes. The terminal branches of the medial and lateral plantar nerves form the interdigital nerves.
The nerve to the abductor digiti minimi, also called the inferior calcaneal nerve or Baxter's nerve, is the first branch of the lateral plantar nerve.138 It takes a sharp, almost 90° turn from a vertical to a horizontal position as it courses from the medial aspect of the foot toward the abductor digiti quinti muscle (Fig. 6.43). The nerve then divides into three major



branches, one to the periosteum of the medial calcaneal tuberosity, one to the abductor digiti minimi, and one to the flexor digitorum brevis muscle. The long plantar ligament and the quadratus plantae may also be innervated by the inferior calcaneal nerve.11

FIGURE 6.42 ● Posterior view of the foot depicts the tibial nerve and its medial and lateral plantar nerve branches.
FIGURE 6.43 ● Posterior view of the foot demonstrates the inferior calcaneal nerve (Baxter's nerve) making a sharp, almost 90°, turn from a vertical to a horizontal position as it courses toward the calcaneus.
MR Appearance
The upper tarsal tunnel, at the level of the ankle, is bordered by the low-signal aponeurosis of the leg medially and by the tibia laterally. The medial border of the lower tarsal tunnel is formed by the flexor retinaculum, best seen on axial and coronal images of the ankle and depicted as a low-signal linear structure extending from the medial malleolus toward the calcaneus (Fig. 6.44). The talus, the calcaneus, and the quadratus plantae muscle form the lateral border of the lower tunnel. The inferomedial border of the tunnel is defined by the abductor hallucis muscle. The proximal and distal borders of the retinaculum are difficult to identify because they blend imperceptibly with the deep fascia of the leg proximally and envelop the abductor hallucis muscle distally.
MR imaging findings in the tarsal tunnel include the following:
  • The thin septa separating the tunnel into multiple compartments are seen as delicate, linear low-signal structures extending from the flexor retinaculum toward the calcaneus. The most common of these is the transverse interfascicular septum, which subdivides the tunnel into lower and upper chambers and is seen on axial or coronal images of the ankle as a low-signal-intensity fine line extending from the abductor hallucis muscle toward the calcaneus and quadratus plantae muscle.
  • The tibial nerve and its branches can be traced on axial and coronal images of the ankle and then on oblique coronal images of the foot. Thin-section sagittal images can sometimes demonstrate long portions of the nerves in a single slice.
  • In the upper tunnel, the tibial nerve is depicted as an oval structure of intermediate signal intensity deep to the aponeurosis of the leg, in close proximity to the tibia and medial to the flexor hallucis longus tendon.139 The nerve can be distinguished from its accompanying posterior tibial artery and vein since it maintains its position lateral to the vessels (see Fig. 6.44A). The vessels, therefore, are found more superficially, closer to the retinaculum.
  • Occasionally, the medial calcaneal nerve is seen on either axial or sagittal images as it branches off the tibial nerve proximal to the flexor retinaculum.
  • The division of the tibial nerve into the medial and lateral plantar nerves is usually noted within the tunnel but may be seen proximal to it.
  • The medial plantar nerve, found within the upper chamber, can be seen on all image planes, maintaining close proximity to the flexor hallucis longus tendon.


    It is posteromedial to the tendon in the hindfoot and plantar to the tendon in the foot.

  • The lateral plantar nerve is found more posterior and lateral to the medial plantar nerve, in the lower chamber, between the muscle bellies of the abductor hallucis and quadratus plantae muscles (see Fig. 6.44B). Not infrequently, the first branch of the lateral plantar nerve, the inferior calcaneal or Baxter's nerve, can be followed as it takes off from the lateral plantar nerve and dives toward the abductor digiti minimi muscle (Fig. 6.45).
  • The nerve is usually seen in close proximity to the quadratus plantae muscle on axial or coronal images of the ankle.
  • Distal to the tunnel, the medial and lateral plantar nerves are easiest to identify on oblique coronal images of the foot (Fig. 6.46). Accompanied by the more medially located medial plantar artery, the medial plantar nerve and its branches are noted at the talonavicular joint within a fat plane between the abductor hallucis medially and the quadratus plantae muscle laterally. The nerve is plantar to the flexor hallucis longus and flexor digitorum longus tendons as they cross each other at Henry's knot (Fig. 6.47). At the bases of the


    metatarsals the nerve is bordered by the abductor hallucis muscle medially and the flexor digitorum brevis laterally. The lateral plantar nerve and its branches are seen more laterally within the fat planes between the abductor digiti minimi and the flexor digitorum brevis muscles. The nerve is accompanied by the more laterally located lateral plantar artery.

FIGURE 6.44 ● The normal tarsal tunnel. (A) Axial T1-weighted image of the upper tunnel demonstrates the tibial nerve (arrow) deep to the flexor retinaculum (small arrows) and anteromedial to the tibial vessels (arrowheads). (B) Axial T1-weighted image in the lower tunnel demonstrates the medial (white arrow) and lateral (black arrow) plantar nerves deep to the tibial vessels (arrowheads).
FIGURE 6.45 ● The inferior calcaneal nerve. The inferior calcaneal nerve (arrow) is shown in close proximity to the quadratus plantae muscle (asterisk) and posterior to the lateral plantar nerve (arrowhead) on this axial T1-weighted image.
FIGURE 6.46 ● The normal medial (black arrow) and lateral (white arrow) plantar nerves in the midfoot as noted on an oblique coronal PD-weighted image.
FIGURE 6.47 ● The medial plantar nerve at Henry's knot. The close proximity of the nerve (arrow) to the flexor hallucis longus and flexor digitorum longus tendons as they cross each other at Henry's knot is shown on an oblique coronal PD-weighted image.
Tarsal Tunnel Syndrome
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:
  • Sharp, radiating or shooting pain, worsened with activity
  • Paresthesia, dysesthesia, and numbness along the distribution of the nerve and its branches
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.
MR Appearance
The clinical diagnosis of tarsal tunnel syndrome can be challenging. The pain may be nonspecific and intrinsic muscle motor loss can be difficult to assess. Also, normal electro-diagnostic tests do not exclude the diagnosis, since they are positive in only 90% of cases.24,151,152 In patients with prominent fatty tissue around the ankle, the tibial nerve and its branches may be difficult to stimulate with cutaneous electrodes.153,154


Thus, imaging can play a contributory role in the diagnosis of tarsal tunnel syndrome.

FIGURE 6.48 ● Tarsal tunnel nerve sheath tumor. Axial T1-weighted fat-suppressed post-gadolinium image demonstrating a hyperintense nodule (black arrow) with a hypo-intense center (“target sign”) in the tarsal tunnel. Note incidental finding of peroneal tendon tenosynovitis (white arrow).
FIGURE 6.49 ● Tarsal tunnel syndrome and medial plantar nerve denervation edema due to proliferative synovitis. (A) Axial T2-weighted image demonstrates a synovial mass (asterisk) in the tarsal tunnel. (B) Sagittal T2-weighted fat-suppressed image illustrates denervation edema in the flexor digitorum brevis muscle (asterisk). Note associated osteoarthritic changes in the anterior tibiotalar joint (arrow).
Plain films and CT are best for depicting fracture fragments or other osseous pathology that may compromise the tarsal tunnel, but MR imaging is the optimal modality for direct visualization of the nerves, retinaculum, and tunnel contents. MR identification of the cause and location of entrapment is also used in preoperative assessment to determine the extent of required release and for determining causes for a failed tarsal tunnel surgery.155,156 MR studies are also helpful in excluding other entrapment neuropathies that may mimic the tarsal tunnel syndrome.157,158 At present the role of MR imaging in the diagnosis of tarsal tunnel syndrome has not been fully explored and its accuracy is yet to be determined.153,154,155,159
MR studies are particularly well suited to the identification of space-occupying lesions, such as varicosities, soft-tissue and intraneural ganglia,160 and tumors within the tarsal tunnel (Figs. 6.48 and 6.49).11,153,156,161,162 Accessory muscles within the tunnel (such as the accessory flexor digitorum longus muscle) and outside the tunnel (such as the accessory soleus muscle) (Fig. 6.50) may demonstrate obliteration of the fat planes and anterior displacement of the tibial nerve and its branches against the tibia or calcaneus.143,144,163,164,165,166 In most instances displacement of the nerves by the accessory soleus muscle occurs in the upper tunnel or more proximally in the distal leg. Other lesions producing mass effect within the tarsal tunnel include tenosynovitis, displaced calcaneal


fracture fragments, pigmented villonodular tenosynovitis, and low-signal scar tissue.11,153,162,165

FIGURE 6.50 ● Accessory soleus muscle. Axial T1-weighted image illustrates an accessory soleus muscle (arrow) anteriorly displacing the tibial nerve (arrowhead) in the distal leg.
Although it is difficult to detect increased signal and size of the tibial nerve and its branches associated with the tarsal tunnel syndrome due to the small size of the nerves, occasionally these changes are noted.167 Denervation signal changes within the muscles are less frequently detected since tarsal tunnel entrapment often manifests with sensory deficits only. The involved muscles vary depending on the branch of the tibial nerve affected. In addition, muscle denervation signal may occur in the distal foot and thus may be overlooked if only the ankle is imaged. Since many of the muscles of the foot are at least partially seen at the level of ankle and hindfoot, however, muscle signal alterations should be carefully sought on ankle MR studies.
Distal Foot Entrapment Neuropathies
Medial Calcaneal Nerve Entrapment
Entrapment of the medial calcaneal nerve occurs after it branches off the tibial nerve and descends within a fibromuscular tunnel between the anterior medial calcaneus and the deep fascia of the proximal abductor hallucis muscle. Patients, often athletes, present with chronic heel pain, exacerbated by standing, and tenderness and decreased sensation along the medial heel pad.25,168 Treatment is initially conservative and includes rest, shoe modification, anti-inflammatory medication, steroid injection, and night splints. Surgical decompression of the nerve with release of the deep fascia of the abductor hallucis muscle is reserved for refractory cases.
Medial Plantar Nerve Entrapment
Midfoot entrapment of the medial plantar nerve, distal to the tarsal tunnel, can occur in the region of Henry's knot, between the navicular tuberosity superiorly and the abductor hallucis muscle belly inferiorly (Fig. 6.51). Repetitive trauma to the nerve, particularly in joggers who run with increased heel valgus and foot pronation, has been termed jogger's foot. Heel and arch pain, tenderness, a positive Tinel sign behind the navicular tuberosity, and numbness along the medial plantar aspect of the foot may be present. Local anesthetic injection at the site of tenderness can confirm the diagnosis. A secondary hallux rigidus is believed to be related to increased stress on the first metatarsophalangeal joint in patients with medial plantar nerve denervation.25 Surgical release of the nerve, if conservative treatment is unsuccessful, is recommended.
Lateral Plantar and Inferior Calcaneal (Baxter's) Neuropathy
The lateral plantar nerve can be compressed along its course distal to the tarsal tunnel. Sensory loss confined to the lateral third of the sole of the foot is a common finding. Weakness of the abductor digiti minimi may also be present but is difficult to detect clinically.
Entrapment of the inferior calcaneal nerve (first branch of the lateral plantar nerve), also called Baxter's neuropathy, may be associated with ordinary activities of daily living, but


almost half of the cases are secondary to athletic activity, particularly distance running, with secondary hypertrophy of the abductor hallucis muscle. It is believed that up to 15% of athletes with chronic unresolving heel pain suffer from entrapment of the inferior calcaneal nerve.2 A hypermobile, pronated foot predisposes to stretching of the nerve.

FIGURE 6.51 ● Compression of the medial plantar nerve at the knot of Henry.
Three entrapment sites of the inferior calcaneal nerve have been described:
  • Deep to or by the fascial edge of a hypertrophied abductor hallucis muscle
  • At the medial edge of the quadratus plantae muscle, where the nerve changes from a vertical to a horizontal course
  • Near the medial calcaneal tuberosity (see Fig. 6.43)
When entrapment occurs near the medial calcaneal tuberosity, it is usually related to adjacent inflammation secondary to a heel spur or to plantar fasciitis.
Clinically, entrapment of the inferior calcaneal nerve often presents with intractable heel pain.147,168,169 A burning sensation has also been described. The entity may be difficult to diagnose clinically, since sensory loss is not present unless there is also more proximal entrapment of the lateral plantar nerve. Additionally, it may not be possible to distinguish lateral plantar nerve entrapment at the tunnel from inferior calcaneal nerve entrapment with electrodiagnostic tests. Therefore, it is difficult to differentiate this entity from other causes of heel pain, such as plantar fasciitis or more proximal entrapment of the lateral plantar nerve. The coexistence of plantar fasciitis with entrapment of the inferior calcaneal nerve further confounds the diagnosis.
Rest, orthosis, anti-inflammatory medication, cortico-steroid injections, and night splints are all part of the first course of treatment. Surgical release of the nerve is attempted if the pain is persistent.
MR Appearance of Medial and Lateral Plantar Neuropathy
There is little information in the literature on the MR manifestations of entrapment neuropathies of the medial and lateral plantar nerves distal to the tarsal tunnel. Space-occupying masses such as tumors and ganglia can be identified at the fat intervals between the abductor hallucis and flexor digitorum brevis muscle (medial plantar nerve entrapment) and between the flexor digitorum brevis and abductor digiti minimi (lateral plantar nerve entrapment). The following MR findings have been reported:
  • Tenosynovitis with tendon sheath distention at the intersection of the flexor digitorum longus and flexor hallucis longus tendons in the talonavicular region may occur in entrapment of the medial plantar nerve.
  • Muscle denervation edema or atrophy of the abductor hallucis and flexor digitorum brevis muscles, seen on MR images of the ankle, is compatible with medial plantar nerve entrapment (Fig. 6.52).
  • Denervation of the first lumbrical and of the flexor hallucis brevis muscle, also consistent with medial plantar nerve entrapment, is better seen on MR images of the foot (Figs. 6.53 and 6.54).
  • Abductor hallucis muscle hypertrophy and plantar fasciitis with medial calcaneal spur formation and adjacent soft-tissue edema are suggestive of entrapment of the first branch of the lateral plantar nerve.
  • In our experience, incidental MR detection of denervation edema and atrophy of the abductor digiti quinti muscle is not uncommon and most likely reflects a clinically missed entrapment of the first branch of the lateral plantar nerve (Figs. 6.55 and 6.56).
  • Decreased bulk, fatty atrophy, and increased signal on fluid-sensitive images of the intrinsic muscles of the foot in a diabetic patient are commonly secondary to peripheral neuropathy (Fig. 6.57).170,171,172
FIGURE 6.52 ● Medial plantar neuropathy. Denervation edema of the flexor digitorum brevis (asterisk) and abductor hallucis muscles (arrow) is shown on this coronal T2-weighted fat-suppressed image of the ankle.
FIGURE 6.53 ● Medial plantar neuropathy. Oblique coronal (A) and axial (B) fluid-sensitive fat-suppressed images of the foot show denervation edema in the flexor digitorum brevis (arrow) and abductor hallucis (asterisk) muscles.
FIGURE 6.54 ● Medial plantar neuropathy. Oblique coronal T1-weighted image of the foot shows denervation atrophy of the flexor digitorum brevis muscle (arrow).
FIGURE 6.55 ● Neuropathy of the inferior calcaneal nerve (Baxter's neuropathy). Coronal T1-weighted image of the ankle demonstrating denervation atrophy of the abductor digiti quinti (arrow). Note metallic susceptibility artifact secondary to a distal fibular fixation plate and screws.
FIGURE 6.56 ● Neuropathy of the inferior calcaneal nerve (Baxter's neuropathy) in a 66-year-old patient with tarsal tunnel varicosities. Sagittal (A) and axial (B) T1-weighted images of the ankle demonstrate denervation atrophy of the abductor digiti quinti muscle (asterisk). (C and D). Normal abductor digiti quinti muscle (asterisk) in an asymptomatic patient for comparison.
FIGURE 6.57 ● Lateral plantar neuropathy. Oblique coronal fluid-sensitive fat-suppressed sequential images show denervation edema in the first, second, and third interosseous muscles (arrows).




Morton's Neuroma
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
FIGURE 6.58 ● A third interdigital Morton's neuroma at the confluence of the terminal branches of the medial and lateral plantar nerves.
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.
MR Appearance
MR imaging has been shown to be accurate in the diagnosis of Morton's neuroma, with sensitivity and specificity of 87% and 100% respectively.183,193,194 MR examination is useful in narrowing the broad differential diagnosis of forefoot pain. It also permits preoperative determination of the size and location of the Morton's neuroma, as well as the presence of coexisting neuromas.183,184,185 MR detection of a Morton's neuroma, however, does not necessarily imply symptomatology, since the entity can be found in up to 33% of asymptomatic patients.179,183 Careful correlation of clinical and MR imaging fndings is mandatory, therefore, before the neuroma is considered clinically relevant.
Typically, MR findings in Morton's neuroma include the following:
  • An oval or dumbbell-shaped mass of intermediate to low signal on both T1- and T2-weighted MR images located in the intermetatarsal space. The mass frequently extends into the plantar subcutaneous fat and may be associated with intermetatarsal bursitis (Fig. 6.59).
  • The low signal of the lesion reflects its predominant histologic composition of dense fibrous tissue.
  • T1-weighted images are optimal for detecting the neuroma since they provide good contrast between the lesion and the adjacent fat.
  • T2-weighted images serve to confirm the diagnosis as well as to exclude other diagnostic possibilities, such as true neuromas, intermetatarsal bursitis, ganglion cysts, and synovial cysts.178,193,194,195
  • The usefulness of STIR and contrast-enhanced fat-saturated T1-weighted images is controversial due to variable signal intensity of the neuroma on these sequences.193
  • Intravenous gadolinium injection does not provide sufficient additional information to warrant its routine use.177,184
Zanetti et al.193 suggested three MR imaging criteria for the diagnosis of Morton's neuroma:
  • The lesion is centered in the neurovascular bundle, within the intermetatarsal space and on the plantar side of the transverse metatarsal ligament.
  • The lesion is well demarcated.
  • The signal intensity of the lesion is similar to that of skeletal muscle on TI-weighted images and less than that of fat on T2-weighted images (see Fig. 6.59).
Several studies have demonstrated the importance of measuring the size of Morton's neuroma on transverse MR images since larger lesions (.5 mm in diameter) are more commonly symptomatic.183,192,193 Moreover, the size of the lesion may have implications for the outcome of surgical treatment. Biasca et al.196 reported a good outcome following surgical excision in 77% of patients with neuromas 5 mm or larger in transverse diameter. Only 17% of patients with smaller Morton's neuromas (.5 mm in transverse diameter) had a good postoperative outcome.
Care must be taken in determining the size of a Morton's neuroma, since the transverse diameter has been shown to depend on the patient's body position during the MR examination.197 Statistically significant differences in the diameter of the neuroma were noted in the prone versus the supine position and in the prone versus a weight-bearing position. Differences


in the shape of the neuroma and in its location relative to the metatarsal heads were also reported. Optimal visualization of Morton's neuroma is obtained in the prone position.

FIGURE 6.59 ● Third intermetatarsal Morton's neuroma. Dumbbell mass (arrows) of intermediate to low signal on both T1-weighted (A) and T2-weighted (B) images extends from the intermetatarsal space to the plantar aspect of the foot. (C) The mass enhances after gadolinium administration.
Joplin's Neuroma
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.
Sural Nerve
The sural nerve, a pure sensory nerve, is formed by the merger of the medial sural nerve (a branch of the tibial nerve) and the smaller lateral sural cutaneous nerve (a branch of the common peroneal nerve) (Fig. 6.60).1 In a minority of cases the nerve originates from only the tibial nerve or only the common peroneal nerve. The sural nerve courses downward along the midline of the calf, lateral to the Achilles tendon, and then superficial and posterior to the peroneal tendons behind the medial malleolus (Fig. 6.61).203,204 The nerve supplies sensation to the lateral aspect of the ankle and foot up to the base of the fifth toe.
Entrapment of the sural nerve is usually related to trauma (Fig. 6.62) and may occur following a direct contusion or secondary to calcaneal, talar, or fifth metatarsal fractures (Fig. 6.63). Traction injury with secondary fibrosis of the nerve has been noted in athletes following severe ankle sprains.22,205 Peroneal or Achilles tendinosis, space-occupying lesions,



ganglia, entrapment secondary to gastrocnemius injury,206 and fibrous bands are additional causes of sural nerve entrapment.

FIGURE 6.60 ● The posterior leg, showing the formation of the sural nerve from the tibial and peroneal contributions.
FIGURE 6.61 ● The normal sural nerve. Axial T1-weighted image demonstrates the sural nerve (arrow) deep to subcutaneous vessels (arrowheads).
FIGURE 6.62 ● Sural nerve laceration in a 20-year-old male patient. Axial T1-weighted image demonstrates edema and obliteration of fat planes in the region of the sural nerve (asterisk). Note concomitant lacerations of the soleus and peroneal muscles.
FIGURE 6.63 ● Sural nerve entrapment secondary to a fracture of the base of the fifth metatarsal.
Pain (worse at night), paresthesias, and tenderness along the lateral aspect of the foot are common. Chronic calf pain exacerbated during physical exertion may also occur.205 Symptoms can be provoked with plantarflexion and inversion of the foot. Electrodiagnostic tests usually confirm the diagnosis of sural nerve entrapment.
Imaging studies such as plain films and CT can depict osseous causes for sural nerve entrapment such as fractures, myositis ossificans, or osteochondromas. MR imaging may better depict the location of the nerve and compromising soft-tissue masses. Surgical release of the nerve is indicated after failure of conservative measures.
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