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 seen in the author's active electrodiagnostic laboratory. (See Treatment and Medication.)
Conditions to consider in the differential diagnosis of femoral mononeuropathy include the following (see Presentation and Workup):
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.
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.
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 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]
Patients with femoral neuropathy complain of difficulty with stairs and frequent falling secondary to "knee buckling." This weakness is typically of acute or subacute onset. On occasion a femoral neuropathy can be associated with an athletic injury.[15] This contrasts with a myopathic process in which the weakness is subacute to chronic in onset and bilateral in nature.
Acute, severe pain in the groin, thigh, and/or lower abdomen may occur if the neuropathy is associated with a retroperitoneal hematoma.[16] Otherwise, the associated pain is usually mild and located near the inguinal ligament.
Patients may complain of medial leg and calf numbness. Sensory symptoms in saphenous nerve distribution are rare with injury to the main trunk of the femoral nerve.
Weakness of the quadriceps muscle and decreased patellar reflex are the most striking examination findings. If the neuropathy is advanced and chronic, wasting of the quadriceps may be noted. If a retroperitoneal hematoma is present, hip extension may cause pain.
In some patients, the iliopsoas muscle is involved. In such cases, the lesion must be above the inguinal ligament, as the motor branch to this muscle comes off before the inguinal ligament.
In isolated femoral neuropathies, the thigh adductors are normal. Although the thigh adductors share common lumbar roots with the muscles innervated by the femoral nerve, they are innervated by the obturator nerve along with the sciatic nerve and therefore are spared. Sensory deficits consist of numbness of the medial thigh and the anteromedial calf.
Evaluation for femoral nerve dysfunction includes nerve conduction studies (NCS) and needle electromyography (EMG). NCS should include sensory studies of the saphenous nerve and motor studies of the femoral nerve. When evaluating femoral NCS, results on the symptomatic side should be compared with those on the asymptomatic side. On EMG, the quadriceps should show neuropathic changes.
In cases of suspected retroperitoneal hematoma, an emergent computed tomography (CT) scan of the pelvis should be performed.
In cases in which the etiology is not apparent, magnetic resonance imaging (MRI) or CT scanning of the pelvis may help in localizing the site of compression and may define the etiology (eg, tumor, abdominal aortic aneurysm, iliac aneurysm).
Treatment is dependent on the etiology of the lesion. As previously stated, most patients with a femoral mononeuropathy can be treated conservatively with physical therapy, avoidance of excessive hip abduction and external rotation, and knee bracing to prevent buckling of the knee. In cases of painful femoral neuropathy, neuropathic pain medications may provide benefit.
In patients with femoral neuropathy associated with positional compression or retraction compression during surgery or delivery, recovery typically occurs over 3-4 months.
When the cause of the neuropathy is a retroperitoneal hematoma, evacuation of the hematoma may be indicated, but this is controversial.[16] In patients on anticoagulation therapy, anticoagulant agents must be stopped until the hematoma has resolved. Outcomes for these patients are worse than for those with a hematoma due to trauma.
If the compression is due to a tumor, then therapy, either surgery or chemotherapy, is directed at the neoplasm. When the neuropathy is due to diabetes or vasculitic causes, immunosuppressive therapy may be warranted.[10]
Surgical decompression of the nerve sometimes is performed for neuropathies resulting from hematomas or mass lesions. Femoral decompression is indicated in cases of intractable pain associated with femoral nerve compression.[1] Occasionally, surgical exploration for other reasons (eg, penetrating wounds, fascia bands) is indicated.
Consultation with an electrodiagnostic laboratory (EMG/nerve conduction velocity [NCV] studies) may help to determine the location, severity, and potential permanency of the lesion.
In cases of painful neuropathy, neuropathic pain medications, used off-label, may be of benefit. These medications are palliative, not curative. In cases in which femoral neuropathic pain is related to a diabetic neuropathy, certain medications are used on-label.
Among the medications used to address neuropathic pain are the anticonvulsants pregabalin and gabapentin, as well as the antidepressants amitriptyline and duloxetine.
As previously stated, in patients on anticoagulation therapy whose neuropathy is caused by a retroperitoneal hematoma, anticoagulant agents must be stopped until the hematoma has resolved.
Clinical Context: Pregabalin is a structural derivative of gamma-aminobutyric acid (GABA). Its mechanism of action is unknown. The drug binds with high affinity to the alpha2-delta site (a calcium channel subunit). In vitro, it reduces the calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function. Pregabalin has been approved by the US Food and Drug Administration (FDA) for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as adjunctive therapy in partial-onset seizures.
Clinical Context: Gabapentin, a membrane stabilizer, is a structural analogue of the inhibitory neurotransmitter GABA, although, paradoxically, it is thought not to exert an effect on GABA receptors. It appears to exert its action via the alpha(2)delta1 and alpha(2)delta2 auxiliary subunits of voltage-gaited calcium channels. Gabapentin is used to manage pain and provide sedation in neuropathic pain.
Some agents in this category have shown benefit in the treatment of neuropathic pain.
Clinical Context: Amitriptyline is an analgesic for certain chronic and neuropathic pain. It blocks the reuptake of norepinephrine and serotonin, which increases their concentration in the central nervous system (CNS). Amitriptyline decreases pain by inhibiting spinal neurons involved in pain perception. This agent is highly anticholinergic. It is often discontinued because of somnolence and dry mouth. Cardiac arrhythmia, especially in overdose, has been described; monitoring the QTc interval after reaching the target level is advised. Up to 1 month may be needed to obtain clinical effects.
Clinical Context: Clomipramine is a dibenzazepine compound belonging to the family of tricyclic antidepressants. The drug inhibits the membrane pump mechanism responsible for the uptake of norepinephrine and serotonin in adrenergic and serotonergic neurons.
Clomipramine affects serotonin uptake while it affects norepinephrine uptake when converted into its metabolite desmethylclomipramine. It is believed that these actions are responsible for its antidepressant activity.
Clinical Context: Doxepin increases the concentration of serotonin and norepinephrine in the CNS by inhibiting their reuptake by the presynaptic neuronal membrane. It inhibits histamine and acetylcholine activity and has proven useful in treatment of various forms of depression associated with chronic pain.
Clinical Context: Nortriptyline has demonstrated effectiveness in the treatment of chronic pain.
Clinical Context: This is the original TCA used for depression. These agents have been suggested to act by inhibiting reuptake of noradrenaline at synapses in central descending pain modulating pathways located in the brainstem and spinal cord.
The analgesic properties of certain agents in this class may improve symptoms associated with neuropathic pain.
Clinical Context: Duloxetine is indicated for diabetic peripheral neuropathic pain. It is a potent inhibitor of neuronal serotonin and norepinephrine reuptake.
The analgesic properties of certain agents in this class may improve symptoms associated with neuropathic pain.