Spontaneous femoral neuropathy rarely occurs in young, healthy men. Herein, we present the first reported case of bilateral spontaneous femoral neuropathy. A 25-year-old man was admitted to the neuropsychiatric inpatient clinic with drug intoxication and showed bilateral knee extensor weakness. He had taken medication for several years for depression. He took an overdose of medication due to severe stress at the army recruit training center for beginning military service. He had slept for over 24 hours. After waking up, bilateral lower extremity weakness had developed. Magnetic resonance imaging showed a small hematoma between the left psoas and quadratus lumborum muscles, and signal intensity changes in the left femoral nerve–innervated muscles. An electrodiagnostic study demonstrated bilateral femoral neuropathy with axonal injury. Two months later, his weakness had partially recovered, and a follow-up examination revealed partial electrodiagnostic recovery. At a long-term third follow-up visit, both symptoms and electrodiagnostic findings had improved.
Femoral nerve originate from the L2, L3, and L4 nerve roots. It has muscular branches in the psoas, iliacus, quadriceps femoris, sartorius, and pectineus muscles, as well as thigh medial and intermediate cutaneous nerves and saphenous nerves. Isolated femoral neuropathy rarely occurs due to abdomen, hip, or pelvis surgery or stretch stress, compression by hematoma, tumor, abscess. Spontaneously occurring femoral neuropathy in young men is very rare, and bilateral cases have not been reported. We report a case of spontaneous bilateral femoral neuropathy with literature review.
A 25-year-old man suffering from depression was admitted to the Department of Neuropsychiatry for drug intoxication and was accompanied by weakness of bilateral knee extensors. He has been taking depression medications (procyclidine, lamotrigine, lorazepam, quetiapine, sertraline, escitalopram, propranolol) for several years. He enlisted in the army recruit training center for military service ten days before visiting the hospital, and took about ten bags of psychiatric medication for stress and slept for a day. Sleep was done in the supine position, and postures such as the hip extension were not confirmed. After he woke up, he suddenly complained of weakness and pain in both lower extremities and checked out the army recruit training center because he was unable to walk. Afterward, he suffered sleep disorders and suicidal thoughts and was admitted to the Department of Neuropsychiatry. In the blood test, creatine phosphokinase showed a mild elevation of 214 IU/L (normal range, 60-190 IU/L), and other abnormalities were not observed. On physical examination, there was no bruise, swelling, pain, or tenderness on the flank, abdomen, buttocks and thigh that would suspect trauma. Neurological examination showed that measurement of manual strength of right hip with hip flexion 4/5, extension 4/5, right knee with knee flexion 4/5, extension 3/5, left hip with hip flexion 3/5, extension 4/5, and left knee with knee flexion 4/5, extension 2/5. On the 13th days of symptoms, nerve conduction study (NCS) and needle electromyography (EMG) were performed. In the sensory NCS, the bilateral saphenous nerve sensory nerve action potential (SNAP) did not appear, and in the motor NCS, the left femoral nerve compound muscle action potential (CMAP) did not appear. When measured on the extensor digitorum brevis muscle, there was a decrease in the CMAP amplitude of both common peroneal nerves, which was considered to be due to disuse atrophy or focal atrophy (
Follow-up EMG was performed on the 59th day of symptom onset and showed little interval change compared to the previous test. Thoracic and lumbar spine magnetic resonance imaging (MRI) was performed to differentially diagnose radiculopathy on the 10th day. It showed increased signal intensity in T2 weighted image between left psoas and quadratus lumborum muscles, suggesting hematoma. In addition, there was high signal intensity indicating focal muscle fiber tear and strain in both muscles in T2 weighted image. Due to cost problem, tests were selectively performed in the early period. As weakness persisted, hip MRI was performed late for differential diagnosis on the 82nd day of symptom development to check femoral nerve and to identify other lesion that may cause neuropathy. It showed no abnormality of lumbosacral plexus and proximal sciatic nerve, but signal intensity change was observed in the left vastus intermedius, vastus lateralis, psoas, and pectineus muscles (
On the 204th day of symptom development, a third follow up EMG was performed, and the SNAP of the bilateral saphenous nerve, which was not previously induced, was observed. In needle EMG, the loss of denervation potential on the right side and some improvement on the left rectus femoris were also observed (
The femoral nerve originates from the L2, L3, and L4 nerve roots and travels between the psoas and iliacus muscles, located under the iliacus fascia in a retroperitoneal space and then under the inguinal ligament. Motor branches innervate to muscles such as iliacus, quadriceps, and sartorius, and sensory branches are responsible for the sense of anterior, medial area of the thigh, and lower leg medial area. Isolated femoral neuropathy is uncommon and rarely occurs bilaterally. Femoral nerve injury can be caused by compression or entrapment, mainly in retroperitoneal space and inguinal ligament [
Femoral neuropathy rarely occurs, and to our knowledge, no spontaneous case has been reported. The reported causes of femoral neuropathy can be classified as traumatic/nontraumatic injury or surgery/non-surgery injury. Surgery-related etiology has been reported such as vaginal hysterectomy, radical retropubic prostatectomy, laparoscopic vaginal surgery, and suggested mechanisms include microvascular injury, compression by retractor, and mechanical stretch due to posture during surgery [
In this case, symptoms occurred after an overdose of the drug. Radiculopathy can also be considered as the cause of knee extensor weakness, but it was excluded from the electrical diagnosis. In a similar case to this case, bilateral femoral neuropathy occurred after massive toxic ingestion in order to commit suicide. It was considered that stretch injury occurred due to improper position [
We report bilateral femoral neuropathy that occurred spontaneously without specific mechanisms after drug intoxication through hip MRI, NCS, and needle EMG [
No potential conflict of interest relevant to this article was reported.
T2-weighted magnetic resonance image showing high signal intensity of a loculated hematoma (arrow) between the psoas and quadratus lumborum muscles, a focal irregular discontinuity with feathery-like high signal intensity of a focal muscle fiber tear, and strain in the left psoas and quadratus lumborum muscles (curved arrows) (A), and a high-signal-intensity lesion (arrowhead) in the left vastus lateralis muscle (B).
Clinical photography showing atrophy of the left quadriceps muscle, especially the vastus medialis muscle (arrows). The case report and patient’s photographs were reviewed and approved by the Institutional Review Board of The Catholic University of Korea, College of Medicine (Registry No. VC14ZISE0072); the requirement for informed consent was waived by the board.
Results of Sensory Nerve Conduction Studies
Nerve | Stimulation | Initial (13 HD) |
Follow-up (204 HD) |
||||
---|---|---|---|---|---|---|---|
Peak latency (ms) | Amplitude (μV) | CV (m/s) | Peak latency (ms) | Amplitude (μV) | CV (m/s) | ||
Rt. sural | Lower leg | 3.8 | 12 | 47.9 | 3.6 | 13.9 | 49.2 |
Lt. sural | Lower leg | 3.7 | 21.6 | 49.6 | 3.6 | 19.9 | 50.3 |
Rt. superficial peroneal | Ankle | 3.9 | 12.4 | 46.6 | 4.1 | 7.9 | 45.1 |
Lt. superficial peroneal | Ankle | 3.3 | 18.4 | 45.4 | 3.9 | 12.1 | 45.1 |
Rt. saphenous | Knee | No response | 2.7 | 6.8 | 70.0 | ||
Lt. saphenous | Knee | No response | 3.0 | 3.7 | 66.6 | ||
Rt. LFCN | Above inguinal ligament | 2.9 | 12.3 | - | 4.4 | 18.0 | - |
Lt. LFCN | Above inguinal ligament | 2.9 | 8.6 |
- | 3.0 | 7.6 |
- |
HD, hospital day; ms, millisecond; μV, microvolt; CV, conduction velocity; m/s, meters per second; Rt., right; Lt., left; LFCN, lateral femoral cutaneous nerve; -, the sensory nerve action potentials of bilateral saphenous nerves were not evoked at the initial test. The amplitude of left LFCN was reduced at initial and follow-up tests.
Decreased amplitude of sensory nerve action potential.
Results of Motor Nerve Conduction Studies
Nerve | Stimulation | Initial (13 HD) |
Follow-up (204 HD) |
||||
---|---|---|---|---|---|---|---|
Onset latency (ms) | Amplitude (mV) | CV (m/s) | Onset latency (ms) | Amplitude (mV) | CV (m/s) | ||
Rt. femoral | Above inguinal ligament | 5.9 | 9.4 | - | 7 | 9.9 | - |
Lt. femoral | Above inguinal ligament | No response | No response | ||||
Rt. peroneal (EDB) | Ankle | 4.2 | 0.5 |
- | 4.6 | 0.4 |
- |
Fibular (head) | 10.8 | 0.8 |
48.4 | 12.5 | 0.4 |
41.1 | |
Lt. peroneal (EDB) | Ankle | 3.7 | 1.4 |
- | 4.5 | - | |
Fibular (head) | 10.1 | 0.9 |
50.0 | 13.3 | 3.6 | 39.7 | |
Rt. peroneal (TA) | Fibular (head) | 2.9 | 4.9 | - | 2.7 | 6.1 | - |
Popliteal fossa | 3.7 | 4.8 | 113.0 | 4.0 | 6.0 | 61.5 | |
Lt. peroneal (TA) | Fibular (head) | 2.2 | 4.6 | - | 3.1 | 5.9 | - |
Popliteal fossa | 3.5 | 4.5 | 53.8 | 4.7 | 5.4 | 65.6 | |
Rt. tibial | Ankle | 5.1 | 28.9 | - | 4.8 | 17.7 | - |
Popliteal fossa | 12.1 | 24.5 | 42.1 | 11.9 | 13.4 | 50.7 | |
Lt. tibial | Ankle | 4.1 | 24.2 | - | 4.1 | 15.1 | - |
Popliteal fossa | 10.9 | 18.8 | 44.1 | 11.4 | 11.2 | 47.2 |
HD, hospital day; ms, millisecond; mV, millivolt; CV, conduction velocity; m/s, meters per second; Rt., right; Lt., left; EDB, extensor digitorum brevis; TA, anterior; -, the compound muscle action potentials (CMAPs) of bilateral femoral nerves were not evoked at initial and follow-up tests. The amplitudes of CMAPs of bilateral EDB muscles on peroneal nerve stimulation were reduced at initial and follow-up tests.
Decreased amplitude of compound muscle action potential.
Results of Needle Electromyography
Muscle | Initial (13 HD) |
Follow-up (204 HD) |
||||||||
---|---|---|---|---|---|---|---|---|---|---|
IA | Fib | PSW | MUAP | Interfer. | IA | Fib | PSW | MUAP | Interfer. | |
Both L2-S1 PSP | NL | None | None | NL | None | None | ||||
Both TFL | NL | None | None | NL | Full | NT | ||||
Both AL | NL | None | None | NL | Full | NL | None | None | NL | Full |
Both TA | NL | None | None | NL | Full | NT | ||||
Both PL | NL | None | None | NL | Full | NT | ||||
Both GCM (medial) | NL | None | None | NL | Full | NT | ||||
Rt. AM | NL | None | 1+ | NL | Full | NL | None | None | NL | Full |
Rt. GMax | NL | None | None | NL | Full | NL | None | None | NL | Full |
Rt. iliopsoas | NL | None | None | NL | Full | NL | None | None | NL | Full |
Rt. RF | NL | 1+ | 2+ | Poly | Discrete | NL | None | None | NL | Discrete |
Rt. VM | NL | None | 1+ | Poly | Discrete | NL | None | None | NL | Discrete |
Rt. BF | NL | None | None | NL | Full | NT | ||||
Lt. AM | NL | None | 1+ | NL | Full | NL | None | 1+ | NL | Full |
Lt. GMax | NL | None | None | NL | Poor volition | NL | None | None | NL | Full |
Lt. iliopsoas | NL | 1+ | 2+ | NL | Reduced | NL | None | None | NL | Full |
Lt. RF | NL | None | 2+ | No MUAP | NL | None | 2+ | Poly | Full | |
Lt. VM | NL | None | 1+ | No MUAP | NL | 1+ | 3+ | No MUAP | ||
Lt. BF | NL | None | None | NL | Poor volition | NT |
HD, hospital day; IA, insertional activity; Fib, fibrillation; PSW, positive sharp wave; MUAP, motor unit action potential; Interfer., interferential pattern; PSP, paraspinalis; NL, normal; TFL: tensor fasciae latae; NT, not tested; AL, adductor longus; TA, tibialis anterior; PL, peroneus longus; GCM, gastrocnemius; Rt., right; Lt., left; AM, adductor magnus; GMax, gluteus maximus; RF, rectus femoris; Poly, polyphasic; VM, vastus medialis; BF, biceps femoris.