This article includes discussion of ulnar neuropathies, Guyon canal neuropathy, ulnar neuropathy at the wrist, and flexor carpi ulnaris exit compression.
Jun. 07, 2021
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This article includes discussion of femoral neuropathy, femoral mononeuropathy, and femoral nerve injury. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
• Femoral neuropathy presents, often acutely, with thigh weakness, numbness, and variable pain. Hip flexion weakness is observed in more proximal lesions.
• Examination typically reveals weakness of knee extension with absent or depressed knee jerk and normal thigh adduction.
• Most femoral neuropathies are caused by iatrogenic compression of the nerve either in the pelvis or beneath the inguinal ligament.
• Isolated femoral neuropathy in diabetics is an extremely rare occurrence.
• Nerve conduction studies and needle EMG are useful for diagnostic and prognostic purposes.
Early published literature led many to believe that diabetes mellitus is associated with selective femoral neuropathy. It is now clear that isolated femoral neuropathy in diabetics is rare, and most reported cases were mislabeled, actually having diabetic amyotrophy or radiculoplexopathy. Diabetic amyotrophy has become more widely recognized and, therefore, both clinically and electrophysiologically, no reliable reports of isolated diabetic femoral neuropathy have been published during the last 3 decades.
Femoral neuropathy presents, often acutely, with thigh weakness and numbness. Patients frequently complain that their leg buckles underneath them. Apart from femoral neuropathy due to iliacus hematoma, groin or thigh pain is usually mild. In the case of femoral neuropathy due to iliacus or retroperitoneal hematoma, pain is severe and often experienced over the anterior thigh in addition to the back, buttock, abdomen, and groin (27). The neurologic examination reveals weakness of knee extension (quadriceps) with absent or depressed knee jerk; however, thigh adduction (thigh adductors innervated by the obturator nerve) is normal. Hip flexion (iliopsoas) is usually weak when the lesion is intrapelvic, but spared when the lesion is at the inguinal region. Hypoesthesia over the anterior thigh and medial calf is common. Sensory symptoms can include pain in the inguinal region, which forces the patient to hold the hip in the antalgic position of flexion and external rotation, as well as pain or dysesthesia at the anterior thigh and anteromedial leg.
In most cases, the femoral neuropathy is unilateral, although bilateral femoral neuropathies may result from the lithotomy position or pelvic surgery. Bono and colleagues presented a unique case of postsurgery bilateral femoral neuropathy after Hartmann surgical procedure in a patient diagnosed with rectosigmoid cancer. The patient was placed in lithotomy position and bilateral self-retaining retractors were used in surgery. The patient complained of hypoesthesia over the anteromedial side of both thighs and proximal weakness in both lower limbs. Diagnosis of bilateral femoral neuropathy was confirmed by electromyography (EMG). It is hypothesized that bilateral nerve damage occurred in this patient because of improper retractor use (09).
The EMG examination is helpful in predicting the prognosis of weakness in acute femoral nerve lesions. The femoral compound muscle action potential, recording rectus femoris, can only be evoked at the groin (because the nerve is not accessible in the pelvis) and, thus, the prognosis is dependent on the pathophysiological process (axonal loss versus demyelination), which is based on the size (amplitude, or area, or both) of the femoral compound muscle action potential (36).
(1) If the femoral compound muscle action potential amplitude, or area, or both is low or absent in the presence of moderate or severe weakness of the quadriceps, the lesion is primarily axonal and the prognosis relatively protracted as it will depend on sprouting and reinnervation. In cases of axonal injury, the femoral compound muscle action potential amplitude is the only independent factor for prognosis (36). If compound muscle action potential amplitude is reduced to less than 50% of the amplitude of the contralateral response, less than 50% of patients recover over the next year. In contrast, if the compound muscle action potential amplitude is more than 50% of the amplitude of the contralateral response, all patients recover in a 1 year period (36).
(2) In contrast, if the femoral compound muscle action potential amplitude, or area, or both is normal despite significant reduction of motor unit potentials recruitment, the lesion is primarily demyelinating and the prognosis is good as it is dependent on remyelination.
Of note, obtaining femoral motor responses may be technically challenging, and therefore side-to-side comparison, with comparison to the asymptomatic side, is almost always warranted in these cases.
Two important caveats in determining the pathophysiology and, thus, prognosis, need to be considered:
(1) In evaluating compound muscle action potential for prognosis, special account for the time for Wallerian degeneration needs to be considered. In the hyperacute period, the femoral CMAP is likely to be normal. Several days are required for the CMAP to decrease in amplitude, and it may reach its nadir in 4 to 5 days (16).
(2) Fibrillation potentials are a weak quantitative measure of the extent of this axonal loss as they are identified whenever axonal loss occurs, even if minimal; thus, these potentials identify the presence of axonal loss, but cannot quantitate its extent.
In comparison to other peripheral nerves, femoral neuropathy carries a relatively good prognosis, even when the lesion is due to axonal loss. This is, in part, due to a relatively short distance between common injury sites of the nerve and its target muscles (eg, iliacus and quadriceps), requiring regenerative sprouting to occur over a short distance. Demyelinating lesions may recover in 2 to 3 months by remyelination (02) whereas axonal lesions often require longer.
A 69-year-old woman was admitted to the hospital because of an acute chest pain. She underwent emergency cardiac catheterization and angioplasty through the right femoral artery. She was also placed on intravenous heparin. The next day, she noted severe right leg weakness with numbness in her thigh. She had moderate pain in her groin and anterior thigh. On the third day of admission, her neurologic examination revealed compete paralysis of the right quadriceps and iliopsoas. Thigh adductors and ankle dorsiflexion were normal. The right knee jerk was absent. There was loss of touch and pain sensation over the anterior thigh and medial leg. Urgent CT scan of the pelvis revealed a large right retroperitoneal hematoma involving the iliacus muscle extending to the iliac crest. Surgical evacuation was done that day.
Her neurologic findings did not change. Nerve conduction studies administered on the tenth day revealed absent femoral compound muscle action potential and saphenous sensory nerve action potential on the right, with normal responses on the left. The sural sensory, tibial, and peroneal motor conduction studies were normal. Repeat nerve conduction studies on the third week were unchanged. Needle EMG revealed prominent fibrillation potentials and no voluntary motor units in the right quadriceps and iliacus. The right thigh adductors, tibialis anterior, and paraspinal muscles were normal.
Her recovery of neurologic functions was protracted. She required a knee brace (ankle-knee-foot orthosis) for ambulation. Six months later, the iliacus strength was Medical Research Council grade 4- of 5, and the quadriceps grade 3 of 5. She could not extend her knee actively beyond 160 degrees. Sensory loss was unchanged. EMG revealed nascent (reinnervation) motor unit potentials in the right iliopsoas and quadriceps. At 1.5 years, she did not require a brace, and her iliopsoas and quadriceps strengths were Medical Research Council grade 4 of 5. The right knee jerk was still absent. As a result of painful dysesthesia in the thigh and medial leg, she was placed on a tricyclic. At 3 years, she had an absent right knee jerk, mild weakness of the right iliopsoas and quadriceps (Medical Research Council grade 4+ of 5), and hyperesthesia of the medial leg.
Most femoral neuropathies are caused by iatrogenic compression of the nerve either in the pelvis or beneath the inguinal ligament. Common causes include the following:
(1) Femoral neuropathy during pelvic surgery. Iatrogenic injury to the femoral nerve is well documented. Most femoral neuropathies encountered in clinical practice are those related to various pelvic surgeries utilizing retractor blades, particularly self-retaining retractor blades (37; 28; 26; 11; 43). During these surgical procedures, the femoral nerve becomes compressed between the lateral blade of the retractor and the pelvic wall. Misplaced sutures are also a reported cause of femoral nerve injury in urologic procedures (44). In some series, the incidence of femoral neuropathy after abdominal hysterectomy and after renal transplantation has been reported to be up to 11% and 2%, respectively (37; 21; 59; 52). One study reported that the incidence of femoral neuropathy after abdominal hysterectomies was significantly decreased when retractors were not used (21).
Kim and colleagues reviewed 119 surgically treated femoral nerve injuries reported over the past 33 years and found that 52 of 89 (58%) traumatic lesions to the femoral nerve were iatrogenic in nature (32). Most frequently implicated were gynecological procedures, with others related to orthopedic operations, femoral nerve blocks, and femoral artery puncture. Hesse and colleagues performed a retrospective case series to highlight the risk of femoral nerve palsy in patients treated for pelvic ring injury with subcutaneous anterior pelvic internal fixation device (INFIX) placement. They reported iatrogenic femoral nerve injury in 6 patients after this procedure. The true incidence of this complication is unknown, but INFIX placement can be associated with femoral neve injury (22). A small case series highlighted the features of femoral neuropathy following kidney transplantation: self-retaining retractors were used in all cases, and patients had good motor recovery anywhere from 3 to 313 days following the onset of symptoms (33).
Although not a specifically intrapelvic procedure, lateral retroperitoneal transpsoas approaches to lumbar spinal surgery have also been highlighted as a cause of femoral neuropathy. One series described that 6 out of 230 patients undergoing this approach to lumbar interbody fusion developed femoral neuropathy – 5 of these were due to direct nerve injury, whereas 1 was due to hematoma. All patients had significant neurologic improvement in a year’s time (01).
(2) Femoral neuropathy due to iliacus or iliopsoas hematoma. Acute retroperitoneal hemorrhage within the iliacus muscle, and less commonly the psoas muscle, can lead to a compartmental syndrome, which may result in femoral nerve injury (77; 51; 74). Rarely, anticoagulant therapy with either warfarin or enoxaparin can lead to bilateral thigh hematomas within the iliopsoas muscle and result in bilateral femoral nerve palsy (23; 71; 39; 73). Low molecular weight heparin infusions may yield similar hematomas with compression (31). Less commonly, the hematoma extends into the retroperitoneal space, leading to a more extensive injury of the lumbar plexus or entire lumbosacral plexus (29). Up to 10% of hemophiliacs may experience iliopsoas bleeding, with 57% of these patients developing femoral neuropathy (07). Iliacus hematomas more commonly occur with anticoagulants and hemophilia, but, rarely, direct trauma can also result in hematoma.
(3) Femoral neuropathy due to surgical positioning. The femoral nerve may become compressed at the inguinal ligament during lithotomy positioning for various procedures such as vaginal delivery, urological and rectal procedures, vaginal hysterectomy, and laparoscopy (70; 02; 24). This type of femoral nerve injury is likely underestimated and is frequently reversible. Femoral neuropathy can also occur after prolonged hyperlordotic positioning. A case is reported in which femoral neuropathy occurred after prolonged dental procedure in which the patient was placed in hyperlordotic position to improve surgical exposure and field of view of surgeon (04). Shorter procedures such as lithotomy may also lead to femoral neuropathy, with a case report of bilateral femoral neuropathies after lithotomy in the lithotomy position described (56).
(4) Femoral neuropathy due to hip replacements or procedures. Approximately 2.3% of total hip replacement patients sustain femoral neuropathy, especially associated with hip revision surgery and reconstructions. A review of the literature reports an incidence rate ranging from 0.1% to 2.4% following primary total hip arthroplasty (mean 0.8%) and 0.3% to 2.3% following revision total hip arthroplasty (mean 1.1%) (20). This is usually due to placement of anterior acetabular retractors over the femoral nerve (72). Femoral nerve injury during total hip replacement is the second most common compressive mononeuropathy after these procedures to sciatic neuropathy (72). They are usually caused by stretch injury, but at times, may be due to encasement and damage by the cementing substance used. In 1 case, acetabular reinforcement rings loosened leading to intrapelvic granuloma formation and subsequent femoral nerve compression (06). A large study reported that peroneal and sciatic nerve palsies are more common after total hip arthroplasty, followed by complete or incomplete femoral nerve palsies (19).
Risk factors for the occurrence of motor nerve palsy after hip arthroplasty may include developmental dysplasia of the hip, posttraumatic arthritis, surgical lengthening of a leg, cement-less femoral fixation, and a posterior surgical approach (19). Neurologists should also be mindful of the surgical approach used when evaluating cases of suspected femoral mononeuropathy. The direct anterior approach to hip replacement is muscle-sparing and typically offers faster recovery and less postoperative pain. A series of 1756 patients undergoing a direct anterior approach total hip arthroplasty had a low femoral neuropathy incidence of 0.34% (50).
Singh and associates presented a rare case of femoral neuropathy in a 57-year-old male who developed significant iliopsoas bursitis 10 years after successful total hip arthroplasty. Symptomatic iliopsoas bursitis after total hip arthroplasty is a rare condition and may be associated with femoral neuropathy even after a long interval between procedure and development of the cystic lesion (62).
A case of femoral neuropathy stemming from hematoma and pseudoaneurysm formation 3 months after hip arthroplasty is described (35).
(5) Femoral neuropathy due to other local compression. Inguinal lymphadenopathies, femoral vessel catheterization, and localized hematomas rarely can cause femoral neuropathy. Rheumatoid arthritis has been described to cause iliopsoas bursitis and iliopectineal synovitis, with this inflammation leading to femoral nerve entrapment (41; 66; 67; 46). Large renal cysts, as can occur in polycystic kidney disease, may rarely affect femoral nerve function (76). Infection from taenia echinococcus leading to hydatid cyst formation in the psoas muscle with femoral nerve compression has also been reported (25).
Stretch, radiation (42), and laceration, misplaced injection and tourniquet application (34) are extremely rare causes of femoral nerve injury. Patellar dislocation has been rarely identified as a cause of femoral nerve injury more proximally at the level of the inguinal ligament (68). Women of thin habitus and smokers are at higher risk of lithotomy-induced femoral neuropathy (63).
Over time, neuroendovascular procedures utilizing the femoral vessels for access are becoming more common. Qureshi and colleagues reviewed 270 neuroendovascular procedures and found that 4 of their patients reported symptoms of femoral neuropathy that were typically transient and sensory predominant (53).
Compression in pelvis
• During pelvic surgery by retractor blade
- abdominal hysterectomy
• By iliacus or psoas retroperitoneal hematoma
• By pelvic mass
• By iliopsoas inflammation
- rheumatoid arthritis causing iliopsoas bursitis (41)
Compression at the inguinal ligament
• During lithotomy position by inguinal ligament
- vaginal delivery
• By inguinal hematoma
- femoral artery catheterization (05)
• During total hip replacement (72)
• Stretch injury, radiation, misplaced injection, laceration
In order to understand the pathophysiology of femoral neuropathy, it is essential to review the anatomy of the femoral nerve, which is also called the anterior crural nerve. The nerve is formed when the posterior divisions of the ventral rami of L2, L3, and L4 spinal roots combine. Note that the anterior divisions of the same roots form the obturator nerve. Once formed, the femoral nerve immediately gives branches to the psoas muscle before it enters its substance. Then, covered by a tight iliac fascia, the femoral nerve passes between the psoas and iliacus muscles where it innervates the latter. After passing underneath the rigid inguinal ligament, the femoral nerve branches widen into its terminal motor branches (to the quadriceps and sartorius) and sensory branches (to the anterior thigh), including the saphenous sensory nerve, which innervates the skin over the medial half of the leg to the ankle.
Experimental evidence shows that nerve injury occurs if the nerve is elongated by more than 6% of its original length; hence, females with shorter nerves are more prone to injuries with the use of retractors (20).
The primary pathological process in femoral neuropathy is either demyelinating or axonal. This determines the prognosis for recovery.
Epidemiological studies exist on the incidence or prevalence of femoral neuropathies. Estimated frequencies of iatrogenic femoral nerve injury following certain procedures are as follows:
• 7% to 11% following abdominal hysterectomy (21).
• 2% following total hip replacement (72; 61).
• 2.5% following Pavlik harness treatment for developmental dysplasia of the hip (45).
• 0.14% to 2.2% following renal transplantation (59; 69).
• 0.1% following femoral artery cannulation for cardiac catheterization that results in retroperitoneal hemorrhage (29). The prevalence of retroperitoneal hemorrhage is about 0.5%, and about one-third of these hemorrhages result in femoral nerve injury or a lumbar plexopathy.
• 2.8 of 100,000 deliveries during lithotomy positioning for vaginal delivery. This is likely underestimated, representing only patients with severe femoral nerve lesions necessitating neurologic consultations (70). Prospective studies suggest the incidence is closer to 1% (75).
Femoral nerve injury may be prevented during pelvic surgery by careful retraction against the iliopsoas and pelvic wall where the nerve is usually compressed. Avoiding the use of retractors cut the incidence of femoral nerve lesions after abdominal hysterectomy by more than 90% (21). If necessary, the use of handheld retractors should be encouraged, as a trend for more femoral lesions with the application of self retractors exists (11). Additional preventive measures relating to renal artery transplantation include monitoring hemostasis parameters, short clamping time, and limiting iliac artery manipulation (69).
To prevent compression of the femoral nerve at the inguinal ligament during lithotomy, it is recommended that extreme hip flexion (not hyper flexed more than 80 or 90 degrees) and external rotation be avoided and prolonged lithotomy positioning discouraged (02; 10). Intraoperative neural monitoring for high-risk cases is 1 proposed method to assess nerve injury, but the ability of this method to prevent nerve injury remains unestablished.
A history of acute quadriceps weakness, anterior thigh numbness, and depressed-absent knee jerk following pelvic surgery or lithotomy positioning is highly suggestive of a femoral neuropathy. In patients with suspected acute femoral neuropathy and severe thigh or pelvic pain, particularly in the setting of anticoagulation or coagulopathy, a retroperitoneal hematoma should be considered and excluded by urgent CT scan or MRI of the pelvis. The next step in the diagnosis of femoral neuropathy is to differentiate it from upper lumbar (L2, L3, and L4) compressive radiculopathy, and lumbar plexopathy (including diabetic amyotrophy).
Three important clinical features are useful:
(1) Weakness of thigh adductors, innervated by the obturator nerve, excludes a selective femoral lesion.
(2) A positive reversed straight leg test may not be especially useful – it is common in lumbar radiculopathy; however, it may occur with lumbar plexopathy and femoral nerve lesion, particularly when due to retroperitoneal hematoma.
(3) In plexopathy or radiculopathy, weakness of ankle dorsiflexion is common and does not occur in femoral nerve lesions.
A good neurologic examination will detect weakness separable from pain-induced false weakness. Knee extension weakness will be associated with knee reflex depression whereas hip flexion will be normal if the lesion is beyond the inguinal ligament. Sensory examination may detect a deficit over the anteromedial thigh and medial leg.
Apart from urgent CT or MRI of the pelvis in patients with suspected retroperitoneal hemorrhage, EMG examination, including detailed nerve conduction studies and needle EMG, is frequently employed for diagnostic and prognostic purposes.
Nerve conduction studies can be performed to examine the compound motor action potential amplitude of the femoral nerve stimulation with recording over rectus femoris, with stimulation placed at the groin. Latency of the femoral compound motor action potential response is of little clinical use. The presence of conduction block in the femoral nerve above the inguinal ligament cannot be detected with conventional nerve conduction studies, but evidence of impaired firing rates and reduced recruitment within the quadriceps during needle EMG may suggest this is present. The sensory nerve action potential amplitude of the saphenous nerve can be useful. This will be of low amplitude or absent in femoral neuropathy and lumbar plexopathies but normal in L4 radiculopathy and in conduction block of the femoral nerve. However, saphenous studies can be technically difficult to obtain and absent in normal individuals.
Another role of EMG in femoral neuropathy is to localize the femoral nerve lesion, which is dependent on whether the hip flexors are denervated. Denervation in these muscles suggests a more proximal lesion.
MR neurography (MRN) for femoral neuropathy may be useful if electrophysiologic studies are equivocal or if an etiology for femoral neuropathy is not obvious from prior workup. Advantages to MRN are that benign and malignant peripheral nerve sheath tumors can be delineated and characterized further by MR imaging (14) and potentially lead to a site-directed biopsy to determine pathological diagnosis.
The utility of ultrasound in assessment of traumatic peripheral nerve lesions is increasing. High resolution ultrasound can be used for anatomic understanding and surgical planning of femoral neuropathy. Zeidenberg and colleagues presented a case of femoral neuropathy in a patient developing pseudoaneurysm after undergoing a procedure for cardiac ablation via percutaneous femoral artery approach (78). Ultrasound was performed the same day to evaluate the patient and it showed a pseudoaneurysm dissecting and displacing the left femoral nerve. Surgery for vascular repair and neurolysis of the left femoral nerve with sural nerve grafting was performed.
Controversy exists regarding the indication and timing of surgical evacuation of hematoma if a compressive femoral nerve lesion is clinically apparent. In theory, surgical evacuation should occur as soon as possible, even before signs of severe femoral nerve injury and axonal degeneration occur (49). Practically, limited data on natural history of hematomas are available; therefore, decisions regarding surgical management are often made on a case-by-case basis. Good outcomes have been reported with both conservative and early surgical management. Therefore, factors for consideration include severity of femoral neuropathy, surgical risk, size of hematoma, hemodynamic stability, degree of axonal loss on electrophysiology (based on side-to-side comparison of femoral motor CMAP) and etiology (51).
In patients without a compressive lesion, watchful waiting for spontaneous remyelination or reinnervation by regenerative or collateral sprouting is indicated. The majority of femoral neuropathies after pelvic surgery may resolve with conservative management (08). One study proposes serial electrodiagnostic testing at 6 weeks and 3 months and MRI if no improvement is observed within 3 months (20). Complete recovery is common in incomplete iatrogenic nerve injuries, particularly with regard to motor deficits, although residual sensory symptoms occur (43). In a small case series, femoral nerve palsy due to traumatic or other cause may benefit from femoral neurolysis (18). This method is unproven. A knee-ankle-foot orthosis is helpful for patients with severe weakness of the quadriceps so as to prevent falls. A case report indicates that percutaneous femoral nerve stimulation can ameliorate intractable causalgic pain (47).
Salminger and colleagues published a paper to explain the utility of tensor fasciae latae-tendon transfer to restore active extension in the knee joint in a patient with a 1-year history of femoral nerve palsy following hip replacement revision. This patient was able to achieve an independent and fully functional gait 2 months following their surgery (57).
In a retrospective series of acute femoral neuropathy postrenal transplant, 78 of 83 patients had full recovery within 12 months (38). Of the remaining cases, 1 patient had atrophy of the quadriceps. The other 4 cases had only persistent mild numbness in the anterior and medial thigh.
Ryan Jacobson MD
Dr. Jacobson of Rush University has no relevant financial relationships to disclose.See Profile
Randolph W Evans MD
Dr. Evans of Baylor College of Medicine received honorariums from Allergan, Amgen and Novartis, Biohaven, Lilly, and Teva for speaking engagements.See Profile
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