Femoral neuropathy is a lesion of N. femoralis of various etiologies, leading to disruption of nerve impulses along it. Clinical manifestations depend on the topic of the lesion and may represent pain and sensory disorders on the anteromedial surface of the thigh and lower leg, difficulty walking due to impaired extensor movements in the knee, etc. In the diagnosis of neuropathy, N. femoralis relies on nerve ultrasound and EMG data. Therapeutic tactics include the elimination of nerve compression, metabolic, vascular, anti-inflammatory, analgesic and decongestant therapy, physical therapy and electromyostimulation.
General information
For the first time, femoral neuropathy was described under the name “anterior cranial neuritis” in 1822. Today it is one of the most common variants among mononeuropathies of the lower extremities. Despite the almost 200-year history of the study of femoral neuropathy and its sufficient prevalence, it remains in a sense a little-known disease. Insufficient awareness of both general practitioners and some specialists in the field of neurology leads to the fact that femoral neuropathy is often regarded as vertebrogenic pathology (radicular syndrome, myelopathy, etc.) or as manifestations of polyneuropathy. This is facilitated by a wide variability of symptoms, from purely sensory disorders to the predominance of motor dysfunction, depending on the topic of the lesion.
Anatomical features of the femoral nerve
The femoral nerve (n. femoralis) originates from 3 lumbar spinal roots L2, L3 and L4, which, merging, form a single nerve trunk. The latter goes between the iliac and large lumbar muscles, descends to the inguinal ligament, passing under which, it goes to the anterior surface of the thigh, where it divides into cutaneous (sensory) and muscular (motor) branches and subcutaneous nerve. In the ilio-lumbar segment, the femoral nerve innervates the muscles between which it passes. Their function is flexion and supination of the hip, and with a fixed hip — flexion of the lumbar spine, which provides a forward tilt of the trunk.
The muscular branches extending from the femoral nerve after its passage under the inguinal ligament innervate the muscles responsible for hip flexion and knee extension. The cutaneous branches provide sensory sensitivity to the anterior and slightly inner surface of the thigh. The subcutaneous nerve separates from the N. femoralis in the area of the inguinal ligament, goes in front of the thigh, then takes a medial direction and enters the intermuscular Gunther canal (adductor canal), at the exit of which it passes along the medial edge of the knee joint, where it gives the subclavian branch innervating the anterior surface of the patella. Next, the subcutaneous nerve passes along the medial edge of the shin and foot, reaching the base of the thumb. It provides sensitivity to the skin of the lower leg in front and on the medial surface, as well as the skin of the medial edge of the foot.
Causes
Pathology of the femoral nerve at the ilio-lumbar level is often caused by its compression as a result of muscle spasm or hemorrhages in the lumbar muscle that occur when it is overloaded or injured. Less often, femoral neuropathy is caused by retroperitoneal hematomas or tumors (sarcomas, lymphomas). Hematomas can form with hemophilia, thrombocytopathies and thrombocytopenia; as a complication of anticoagulant therapy used for thromboembolism and thrombosis, especially in patients with abdominal aortic aneurysm. Cases of femoral neuropathy caused by nerve damage during appendectomy, operations on the ureters and kidneys, as well as bursitis and abscesses of the ilio-lumbar muscles are described.
The causes of compression of the femoral nerve in the area of the inguinal ligament can be: inguinal lymphogranulomatosis, femoral hernia, compression of the nerve by the inguinal ligament with a long forced hip position (including during surgical interventions). Nerve damage is possible during hip joint operations, surgical treatment of inguinal hernias, etc.
The occurrence of femoral neuropathy at the level of the Hunter channel is observed with professional or sports overstrain of the adductor muscles of the thigh forming this channel. Less often, muscle tension is caused by instability or abnormalities of the knee joint. Iatrogenic neuropathy can develop as a complication of knee joint surgery.
Isolated neuropathy of the subclavian branch of N. femoralis is often idiopathic in nature, but may be associated with thrombophlebitis, varicose veins and recurrent minor knee injuries.
Symptoms
The clinical symptom complex of femoral neuropathy depends on the topic of the process. When pathology occurs at the ilio-lumbar level, a full set of symptoms develops, including sensory, motor and autonomic-trophic disorders throughout the area innervated by the femoral nerve. In rare cases, with a high separation of the nerve, only sensory or only motor disorders can be observed, sometimes a mosaic picture of motor and sensory disorders.
Complete neuropathy of the femoral nerve is accompanied only by a partial disruption of the ilio-lumbar muscles, due to the existence of their alternative innervation. Therefore, hip flexion and supination are practically not violated. Paresis of the quadriceps muscle responsible for the extension of the leg in the knee joint is more pronounced. Due to difficult extension, patients try not to bend the leg at the knee. Running and walking are difficult, especially when it is necessary to climb stairs. The gait changes. The leg is fixed in the flexion position. There is a lack of knee reflex.
Sensory disorders include disorders of tactile and pain perception on the anterior-inner surface of the thigh and lower leg, the medial edge of the foot. Trophic and vegetative changes are observed in the same zone, irritative pains are possible. In the supine position, tension symptoms are revealed — pain on the front surface of the thigh when trying to raise the straight leg as much as possible (Wasserman’s symptom) or bend the leg at the knee joint (Mickiewicz’s symptom).
Neuropathy of the femoral nerve with its lesion in the inguinal ligament is broadly similar to the clinic described above. With a high discharge of the subcutaneous nerve, mainly motor disorders can be observed. Along with the symptoms of tension, soreness is revealed when pressing in the middle of the inguinal ligament.
Compression of the femoral nerve trunk in the Gunther canal is characterized by painful and tactile hypesthesia of the skin of the medial edge of the knee joint, the anterior-inner surface of the lower leg and the inner edge of the foot. In the same area, paresthesia and pain are observed, which increase their intensity when the lower leg is extended. The latter forces the patient to walk and stand with his leg slightly bent at the knee. The knee reflex is not broken. Soreness is determined at the exit point of the subcutaneous nerve from the adductor canal, Tinel’s symptom is the appearance of paresthesia along the nerve when it is tapped with a neurological hammer.
Neuropathy of the femoral nerve with an isolated lesion of the subcutaneous branch is manifested by paresthesia and numbness of the skin above the patella, tenderness of the subcutaneous nerve point and a positive Tinel symptom.
Diagnostics
The diagnosis of femoral neuropathy requires a neurologist to carefully and thoroughly study the topic of the lesion. Spine x-ray is not informative, because often femoral neuropathy occurs in patients who already have changes in the spinal column (spondyloarthrosis, osteochondrosis, etc.) and the pathology of the spine detected radiologically does not exclude the presence of neuropathy. In such cases, the neural, rather than segmental, nature of the disorders detected during neurological examination testifies in favor of neuropathy. The resolution of controversial diagnostic situations is facilitated by EMG. In neuropathy, it reveals a slowdown in the conduction of impulses along the femoral nerve, a decrease in the amplitude of the M-response, signs of denervation in the muscles innervated by the femoral nerve and the absence of such signs in the paravertebral musculature of the L2-L4 segments.
A relatively new, but promising method of studying peripheral nerve trunks is ultrasound, which can be used to assess the integrity of the nerve, identify its tumor changes, edema, scar-adhesive deformation and degenerative processes. Ultrasound diagnostics of the femoral nerve (ultrasound of the nerve) with dynamic tests allows you to determine the degree of its mobility in the adductor canal.
Femoral nerve damage needs to be differentiated from vertebrogenic radiculopathies L2-L4, lumbosacral plexopathy (especially occurring against the background of diabetes mellitus), knee injury or gonarthrosis. To exclude the pathology of the retroperitoneal space, it is necessary to conduct its ultrasound, CT or MRI.
Treatment
Treatment tactics are largely determined by the etiology of femoral neuropathy. With compression of the femoral nerve by retroperitoneal hematoma, urgent surgery is performed. Surgical treatment is also required in cases of traumatic nerve damage with its almost complete interruption. Otherwise, conservative treatment is sufficient. It is based on decongestant therapy, relief of pain, improvement of blood supply and metabolism of the femoral nerve.
Decongestant and anti-inflammatory therapy with glucocorticoids is performed in cases of compression of the femoral nerve in the intermuscular channels or under the inguinal ligament. In this case, solutions of glucocorticoids (hydrocortisone, diprospane) in combination with local anesthetics (lidocaine, novocaine) are injected directly into the compression area in the form of blockades. With the intense nature of pain, NSAIDs and analgesics are combined with the appointment of antidepressants (amitriptyll) or anticonvulsants (topiramate, pregabalin, gabapentin). Vasoactive (pentoxifylline, nicotinic acid) and metabolic (vitamins B6, B1 and their combinations) therapy is of great importance for the functional restoration of the femoral nerve.
With paresis of the quadriceps and lumbosacral muscles, exercise therapy, electromyostimulation and drugs that improve neuromuscular transmission (ipidacrine, neostigmine) are necessary to prevent muscle atrophy and contractures.