Applied Anatomy

The femoral nerve (also called the anterior crural nerve) is formed by the combination of the posterior divisions of the ventral rami of the L2, L3, and L4 spinal roots (the anterior divisions of the same roots form the obturator nerve). It immediately gives branches to the psoas muscle which receives additional branches from the L3 and L4 roots directly. Then, the femoral nerve passes between the psoas and iliacus muscles and is covered by a tight iliac fascia which forms the roof of the iliacus compartment. The iliacus muscle and femoral nerve are the main constituents of this compartment.

The femoral nerve emerges from the iliacus compartment after passing underneath the rigid inguinal ligament in the groin. About 4–5 cm before crossing the inguinal ligament, it innervates the iliacus muscle. Soon after passing under the inguinal ligament (lateral to the femoral vein and artery), the femoral nerve branches widely into (1) terminal motor branches to all four heads of the quadriceps (rectus femoris, vastus lateralis, vastus intermedius, and vastus lateralis) and sartorius muscles, and (2) three terminal sensory branches, the medial and intermediate cutaneous nerve of the thigh which innervate the skin of the anterior thigh, and the saphenous sensory nerve (Figure C4-1).

Figure C4-1 The femoral nerve and its terminal motor and sensory branches including the saphenous nerve.

(From Haymaker W and Woodhall B. Peripheral nerve injuries: principles of diagnosis. Philadelphia, PA: WB Saunders, 1953, with permission.)

The saphenous nerve travels the thigh, lateral to the femoral artery, by passing posteromedially from the femoral triangle through the subsartorial (Hunter or adductor) canal. It gives off the infrapatellar branch that innervates the skin over the anterior surface of the patella. About 10 cm proximal and medial to the knee, the saphenous nerve becomes subcutaneous by piercing the fascia between the sartorius and gracilis muscles. Then, it crosses a bursa at the upper medial end of the tibia (pes anserinus bursa). In the lower third of the leg, it divides into two terminal branches to innervate the skin of the medial surface of the knee, medial leg, medial malleolus, and a small area of the medial arch of the foot.

Clinical Features

The femoral nerve is a relatively short nerve. Its main trunk can be compressed at the inguinal ligament or in the retroperitoneal pelvic space. Most femoral mononeuropathies are iatrogenic, occurring during intra-abdominal, intrapelvic, inguinal, or hip surgical or diagnostic procedures. The nerve injury often results from direct nerve trauma or poor leg positioning during one of these procedures but may be due to a compressive hematoma or rarely due to inadvertent nerve laceration, suturing or stapling. Table C4-1 lists the various causes of femoral mononeuropathy grouped according to the site of injury.

Table C4-1 Common Causes of Femoral Mononeuropathy

By far the most commonly reported causes of femoral mononeuropathies are those related to pelvic surgery. This includes abdominal hysterectomy, radical prostatectomy, renal transplantation, colectomy, proctectomy, inguinal herniorrhaphy, lumbar sympathectomy, appendectomy, tubal ligation, abdominal aortic repair, and a variety of other intra-abdominal vascular, urologic, or gynecologic operations. During these surgical procedures, the femoral nerve becomes compressed between the retractor blade and the pelvic wall. This occurs more often with the use of self-retracting blades than with handheld blades.

Acute hemorrhage within the iliacus compartment in the retroperitoneal space and, less commonly, the psoas muscle can lead to a compartmental syndrome. This usually results in severe femoral nerve injury; however, the hematoma is sometimes large and extends into the retroperitoneal space, leading to extensive injury of either the lumbar plexus or, rarely, the entire lumbosacral plexus. The hematoma may be a complication of anticoagulant therapy (heparin or warfarin), hemophilia or other blood dyscrasias, ruptured abdominal aortic aneurysm, pelvic operations, traumatic rupture of the iliopsoas muscle, or femoral artery (and less commonly femoral vein) catheterization for coronary, cerebral, and aortic angiography. In patients with acute femoral neuropathy and severe pain, particularly in the setting of anticoagulation or coagulopathy, a spontaneous iliacus hematoma should be considered and ruled out urgently by computed tomography (CT) scan or magnetic resonance imaging (MRI) of the pelvis. Controversy continues regarding the indication and timing of surgical evacuation of the hematoma once the femoral nerve lesion is clinically apparent.

Compression of the femoral nerve may follow lithotomy positioning for vaginal delivery, vaginal hysterectomy, prostatectomy, or laparoscopy is not uncommon. The femoral nerve is kinked and becomes compressed underneath the inguinal ligament usually following prolonged lithotomy positioning, particularly with extreme hip flexion and external rotation. This type of femoral nerve injury is frequently reversible, and is likely underestimated. To prevent compression at the inguinal ligament, prolonged lithotomy positioning with extreme hip flexion and external rotation should be avoided.

Femoral nerve injury during surgical procedures of the hip joint occurs mostly after total hip replacement. It is due to misplacement of the anterior acetabular retractors during the procedure, and is highest in revisions and complicated reconstructions.

Although the literature published in the 1950s and 1960s led many to believe that diabetes mellitus is associated with selective “diabetic femoral neuropathy,” it is now clear that this is a misnomer. Diabetic patients actually have more extensive peripheral nerve disease that involves the lumbar plexus and roots, and is better known as diabetic amyotrophy, diabetic proximal neuropathy, or diabetic radiculoplexopathy (see Case 7). Although the brunt of weakness in these patients often falls on the quadriceps muscle, mimicking selective femoral nerve injuries, careful clinical and needle EMG examinations reveal more widespread involvement of thigh adductors and sometimes foot dorsiflexors, muscles not innervated by the femoral nerve.

The clinical presentation of femoral mononeuropathy often is acute, with thigh weakness and numbness. Patients frequently complain that their legs buckle underneath them, leading to many falls. Except with iliacus hematoma, groin or thigh pain is usually mild. Neurologic examination reveals weakness of the quadriceps muscle (knee extension), with absent or depressed knee jerk. Thigh adduction is, however, normal. The iliopsoas muscle (hip flexion) usually is weak when the lesion is intrapelvic (such as during pelvic surgery), but is spared when the lesion is at the inguinal region (such as during lithotomy positioning). Hypesthesia over the anterior thigh and medial calf is common.

Femoral mononeuropathy should be differentiated from L2, L3, and L4 radiculopathy, and from lumbar plexopathy. Weakness of the thigh adductors, which are innervated by the obturator nerve, excludes a selective femoral lesion. Positive reversed straight leg test is common in lumbar radiculopathy, but it may occur with plexopathy and femoral nerve lesion caused by iliacus hematoma. In plexopathy or L4 radiculopathy, weakness of ankle dorsiflexion (tibialis anterior) is common.

Except for iliacus or retroperitoneal hematoma, which might require surgical intervention, most other patients with femoral mononeuropathy are treated conservatively, allowing for spontaneous remyelination or reinnervation. A knee brace is helpful in preventing falls for patients with severe weakness of the quadriceps.

Electrodiagnosis

The role of electrodiagnostic testing in femoral mononeuropathy is threefold.

The first role is to confirm the presence of a selective femoral nerve injury. This is particularly important when the neurologic examination is difficult to perform because of pain, recent pelvic surgery, or vaginal delivery. A femoral mononeuropathy may mimic a lumbar plexopathy and upper lumbar (L2, L3, or L4) radiculopathy (Table C4-2). The saphenous SNAP, which evaluates the postganglionic L4 sensory fibers, is often absent in femoral mononeuropathy and lumbar plexopathy but normal in L4 radiculopathy since the root lesion is intraspinal, i.e., proximal to the dorsal root ganglion. Rarely, the saphenous SNAP is normal in “purely” demyelinating femoral mononeuropathies where there is no wallerian degeneration which is usually complete in 10–11 days in sensory fibers. The saphenous SNAPs should be studied bilaterally for comparison, since these potentials may be difficult to obtain in the elderly and obese patients and in patients with leg edema. On needle EMG, fibrillation potentials and decreased recruitment of large and polyphasic MUAPs are seen in the quadriceps in all three entities (femoral mononeuropathy, lumbar plexopathy, or radiculopathy). However, these changes are also present in the thigh adductors (L2/L3/L4 obturator nerve) in patients with upper lumbar radiculopathy or plexopathy. Also, in L4 radiculopathy, similar changes may be present in the tibialis anterior (L4/L5 common peroneal nerve).

The second role of EDX study is to localize the site of the femoral nerve lesion. Since the branch to the iliacus muscle originates 4–5 cm above the inguinal ligament, needle EMG of this muscle is crucial to help determining whether the femoral nerve lesion is distal (i.e., around the inguinal ligament) or proximal (i.e., intrapelvic). When the iliacus is denervated, the lesion is in the pelvis and when spared, the lesion is distal, such as at the inguinal ligament. This is particularly important when clinical examination of the iliopsoas (hip flexion) is difficult because of groin pain, recent pelvic surgery, or vaginal delivery. Also, weakness of hip flexion could be attributed falsely to involvement of the iliopsoas muscle when the quadriceps is flaccid because the latter assists in hip flexion.

A third and important role of the EDX study is to prognosticate the recovery of motor function in acute femoral nerve lesions. A femoral CMAP amplitude and/or area is the most useful semiquantitative measure of the extent of femoral motor axonal loss. The femoral nerve could only be stimulated at the groin and, hence, lesions at the inguinal ligament or pelvis cannot be bracketed by two stimulation sites as done in many other peripheral nerve motor conduction studies. Femoral nerve stimulation at the groin is usually distal to the site of the lesion, and allows evaluation of a distal CMAP only. Care should be taken in accounting for the time for wallerian degeneration: the CMAP amplitude reaches its nadir in 4 to 5 days while the decrease in SNAP amplitudes lags behind and is completed in 8 to 11 days (Figure C4-2). Hence, the femoral CMAP must be obtained bilaterally for comparison at least after 4 to 5 days from injury before any conclusion could be made regarding the primary pathophysiologic process or prognosis. In contrast to the CMAP, fibrillation potentials are a poor quantitative measure of the extent of axonal loss since they are identified whenever axonal loss occurs, even if minimal. In other words, fibrillation potentials are extremely sensitive for the presence of any recent axonal loss, but do quantitate its degree, and are therefore, by themselves, poor indicators of the extent of peripheral nerve injury. Based on the above, the primary pathophysiologic process and prognosis of a unilateral femoral nerve lesion are assessed according to the following:

Figure C4-2 A diagrammatic representation of the decline of distal compound motor action potential (CMAP) and sensory nerve action potential (SNAP) amplitudes, due to wallerian degeneration.