Background
Femoral mononeuropathy can occur secondary to direct trauma, compression, stretch injury, or ischemia. The condition causes weakness predominantly of the quadriceps, which results in difficulty with ambulation. Femoral nerve compression may result in debilitating pain, requiring medical therapy and surgical intervention. (See Anatomy, Etiology, Presentation, Treatment, and Medication.) [1]
Most patients with a femoral mononeuropathy, however, can be treated conservatively with physical therapy, avoidance of excessive hip abduction and external rotation, and knee bracing to prevent buckling of the knee. Femoral mononeuropathies account for approximately 1% of all mononeuropathies. (See Treatment and Medication.)
Anatomy
Knowledge of femoral nerve anatomy is essential to understanding the mechanism of its injury and to localizing the lesion.
The femoral nerve is part of the lumbar plexus. It is formed by L2-4 roots and reaches the front of the leg by penetrating the psoas muscle before it exits the pelvis. The femoral nerve leaves the pelvis by passing beneath the medial inguinal ligament to enter the femoral triangle just lateral to the femoral artery and vein. Approximately 4 cm proximal to passing beneath the inguinal ligament, the femoral nerve is covered by a tight fascia, at the iliopsoas groove. The nerve can be compressed anywhere along its course, but it is particularly susceptible within the body of the psoas muscle, at the iliopsoas groove, and at the inguinal ligament.
The main motor component innervates the iliopsoas (a hip flexor) and the quadriceps (a knee extensor). The motor branch to the iliopsoas originates in the pelvis proximal to the inguinal ligament. The sensory branch of the femoral nerve, the saphenous nerve, innervates skin of the medial thigh and the anterior and medial aspects of the calf.
In femoral neuropathy, the iliopsoas is involved if the lesion is in the pelvis (above the inguinal ligament). The adductor magnus and brevis, which share lumbar innervation with the quadriceps and iliopsoas, are spared, since they are innervated primarily by the obturator and sciatic nerves.
Etiology
Compression
The femoral nerve is predisposed to compression within the psoas muscle. This commonly is associated with hemorrhage into this muscle due to hemophilia, anticoagulation therapy, or trauma. [2] Direct trauma to the femoral nerve can occur as a result of penetrating wounds or fractures of the hip or pelvis.
Intrapelvic masses may also cause compression of the femoral nerve. [3] In addition, compression of the femoral nerve can be due to aortic or iliac aneurysms or tumors.
Lithotomy positioning during delivery or in gynecologic/urologic procedures also has been associated with compressive femoral neuropathy. [4, 5, 6] In this position, the sharp flexion of the hip can compress the nerve at the inguinal ligament. Excessive hip abduction and external rotation cause additional stretch on the nerve.
Diabetes
Patients with diabetes have an unusual predilection for femoral and proximal mononeuropathies. Abnormal femoral nerve conduction has been found in patients with diabetes with no clinical femoral nerve involvement. [7] The etiology is suspected to be an inflammatory vasculitis. [8, 9, 10]
Iatrogenic causes
Iatrogenic causes of femoral mononeuropathy include direct pressure or trauma to the nerve during pelvic, abdominal, or spinal surgery [11] or focal damage at the femoral triangle due to a difficult femoral line placement. [11, 12] Rarely, femoral neuropathy may complicate hip arthroplasty. [13, 14]
Prognosis
While the prognosis of incomplete femoral mononeuropathy is good in the majority of cases, [15] it does depend on the degree of axonal compromization. According to one case series of 31 patients measuring outcomes in those with femoral mononeuropathy, excellent, satisfactory, and poor outcomes were observed in 31%, 34%, and 31%, respectively. [16] The estimated degree of axonal loss was the only factor found to influence prognosis.
