Posterior femoral cutaneous nerve mononeuropathy: A case report

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Posterior Femoral Cutaneous Nerve Mononeuropathy: A Case Report Henry C. Tong, MD, Andrew Haig, MD ABSTRACT. Tong HC, Haig AJ. Posterior femoral cutaneous nerve mononeuropathy: a case report. Arch Phys Med Rehabil 2000;81:1117-8. Isolated posterior femoral cutaneous nerve (PFCN) lesions are rare, with only six cases reported in the modern literature and one case documented with a nerve conduction study. A 25-year-old woman had sensory loss in the posterolateral thigh after two right gluteal intramuscular injections. Nerve conduction studies using Dumitru’s technique showed a 9µV response on the asymptomatic side, but no response on the symptomatic side, and no abnormalities on needle examination of the back and lower extremities. Although a single case does not prove the validity of a technique, this case provides the rare opportunity to demonstrate the utility of Dumitru’s technique. Key Words: Electromyography; Neural conduction; Femoral nerve; Rehabilitation. r 2000 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

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HE POSTERIOR femoral cutaneous nerve (PFCN) arises from the ventral primary rami of S1, S2, and S3 of the sacral plexus. It exits from the pelvis through the sciatic foramen below the piriformis muscle and posteromedial to the sciatic nerve. Superficially, it gives rise to the perineal and inferior clunial branches, which provide sensory innervation to the inferior posterior buttock. The main nerve trunk then continues distally in the midline along the posterior thigh superficial to and between the long head of the biceps femoris and semitendinosis musculature. Here it provides sensory innervation to the posterior thigh.1 Distally, at the back of the knee, it pierces the deep fascia and its terminal twigs communicate with the sural nerve. It generally supplies the skin over the popliteal fossa and usually a part of the upper posterior leg. Isolated PFCN lesions are rarely reported. A Medline search covering the period 1966 to 1998 found two cases caused by injection,2,3 three by compression,4 and one of unknown etiology.5 Two cases were documented clinically by electrophysiologic testing. Dumitru and Marquis5 reported one case with somatosensory evoked potential (SSEP) findings. Subsequently, Iyer and Shields2 showed a single case with nerve conduction study findings. Dumitru and Nelson6 subsequently described a new technique in 40 asymptomatic persons. The utility of that technique in detecting pathology in the PFCN has

From the Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, MI. Submitted April 30, 1999. Accepted in revised form October 22, 1999. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated. Reprint requests to Henry Tong, MD, Department of PM&R, Spine Program, 325 East Eisenhower, 2nd floor, Ann Arbor, MI 48108. 0003-9993/00/8108-5605$3.00/0 doi:10.1053/apmr.2000.5564

not been demonstrated in a clinical case. We present a case of PFCN mononeuropathy detected by Dumitru’s technique. CASE REPORT A 25-year-old woman was hospitalized for treatment of severe chronic headaches. She received two intramuscular injections in the right buttock for treatment of her headaches, but she did not know what medication was given. On discharge, she noted numbness in the right posterolateral thigh, which persisted more than 5 months, up to the time of referral for electrodiagnostic consultation. She denied having low back pain, bowel and bladder changes, and any focal weakness. She did not report any other associated acute illness or trauma. Her medical history was positive for cervical cancer, status posthysterectomy. She denied having had diabetes mellitus or thyroid disease. There was no family history of nerve or muscle disease. The patient had not experienced fevers, chills, weight change, nausea, or vomiting. Review of systems was otherwise negative. The patient was intelligent, cooperative, well developed, and well nourished, with normal tone, muscle bulk, and passive range of motion. She had normal strength in her legs. Sensation was intact in the L1-S2 dermatomes bilaterally except for decreased sensation in the right buttock and posterior thigh (fig 1). Reflexes were symmetric and 2⫹ at the biceps, triceps, and brachioradialis. They were symmetric and 2⫹ at the knees and ankles. Toes were downgoing bilaterally. METHODS Nerve conduction studies of the right sural sensory, peroneal motor, and tibial motor nerve branches were evaluated with standard techniques.7,8 A 50-mm disposable concentric needle was used to examine the right leg muscles. The MiniPM technique was used to assess the paraspinal muscles.9 Briefly, at four locations across from L3-S1, a 50-mm monopolar needle was inserted in three directions (medial, craniomedial, and caudal-medial) from each of these locations. Nerve conduction study of the PFCN was performed antidromically bilaterally using the technique proposed by Dumitru and Nelson.6 An active electrode is placed at the midline of the posterior thigh 6cm proximal to the popliteal crease and stimulation is performed 12cm proximally. This technique has been shown to reliably detect the PFCN waveform and not a volume conducted sciatic mixed nerve waveform.6 We chose to use a 2-cm circular ‘‘ground’’ electrode as an active electrode. RESULTS Nerve conduction studies of the sural, tibial motor, and peroneal motor branches showed normal distal latencies and amplitudes. Needle examination of the medial gastrocnemus, anterior tibialis, vastus medialis, gluteus medius, external hamstring, and lumbar paraspinal muscles was within normal limits. MiniPM paraspinal evaluation had a total score of 0 (95% of asymptomatic subjects score 0 to 2).9 The left posterior femoral cutaneous nerve sensory evoked response amplitude was 9.2µV, with an onset latency of 2.7msec and a peak latency Arch Phys Med Rehabil Vol 81, August 2000

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Fig 1. Sensory loss on physical examination. Pinprick testing from sensate toward insensate areas, and from insensate toward sensate areas corresponded to within 1cm.

of 3.7msec from a distance of 12cm (conduction velocity 44m/sec). Exact location of the nerve’s course was confirmed by decreased response on movement of either the stimulating or active electrode across the thigh. The right PFCN showed no response despite high amperage stimulation attempted at 5-mm intervals from medial to lateral across the posterior thigh and movement of the active electrode methodically across the distal thigh in similar 5-mm intervals. A diagnosis of an isolated right PFCN neuropathy was made, based on the clinical findings substantiated by the results of electrophysiologic testing. DISCUSSION Standard electrodiagnostic techniques using nerve conduction studies and needle electromyography are often adequate for identifying pathology involving most peripheral nerves.5 Until recently, however, there was no described formal method to evaluate the PFCN.6 In this case, the method described by Dumitru and Nelson6 was used for several reasons. The method is described in detail; it uses easily identifiable landmarks (ie, the midline of the thigh and the midpopliteal region), and there are exact measurements for the location of the recording and stimulating electrodes. In the technique described by Iyer and Shields,2 the PFCN was stimulated at the gluteal fold with recording electrodes placed over the upper angle of the popliteal fossa. This is not as rigorous a technique since the distance between the stimulating cathode and active electrode will vary, depending on the femur lengths being equal, the rotation of the pelvis on the sacrum, the anatomic variation of the location of the popliteal fossa, and the ability to locate the same spot of the gluteal crease bilaterally. Also, the technique described by Dumitru has been tested in 40 healthy subjects (20 men, 20 women) and a response was obtained in all 80 nerves tested. The technique used by Iyer was only used in the one case and has not been tested in healthy subjects. This is the first case to be described that uses the surface electrode nerve conduction study method described by Dumitru6 to diagnose a PFCN mononeuropathy. Although a single case does not prove the validity of a technique, this case does demonstrate the utility of Dumitru’s technique.

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The previous case verified by SSEP was a 40-year-old patient who had a nonspecific connective tissue disease with a positive rheumatoid factor and antinuclear antibody. Her symptoms began after a left putamen hemorrhage 4 years earlier. No cause of her mononeuropathy was found. The three cases of compressive neuropathy were diagnosed clinically; in two of the cases the symptoms were provoked by sitting and alleviated by standing or lying prone.4 Our case is probably related to a gluteal intramuscular injection, which was also reported to be the cause in two of the four reports we found.2,3 Isolated PFCN injury caused by injections is rare since usually the sciatic nerve is involved. In two reviews of 137 and 247 cases of nerve injuries resulting from injections in the legs, isolated injuries of the sciatic nerve accounted for about 95% of the injuries, while isolated PFCN injuries accounted for about 1%.2,3 In our case, the loss of sensation in the posterior thigh is consistent with a PFCN lesion. There was also, however, sensory loss in the inferior medial buttock region that is consistent with an inferior medial clunial nerve lesion. This is explained by the fact that as the PFCN leaves the sciatic foramen, it gives rise to inferior medial clunial branches that provide sensory innervation to the inferior posterior buttock. This means that the intramuscular injection must have injured the PFCN as it left the sciatic foramen before it gave rise to the inferior cluneal branches. This is rare, since the sciatic nerve is in close proximity to the PFCN at this level and is more commonly injured due to the large size of the nerve.2 In the case report section of the six cases reported, one did not mention the physical examination3 and two only mentioned that there was numbness in the region of the PFCN.4,5 Two cases had decreased sensation in the posterior thigh and lower buttock, which is similar to our patient.4 This suggests that in a significant number of posterior femoral cutaneous neuropathies, the inferior clunial nerve is also affected. In none of the other cases was outcome discussed. Our case was never retested with nerve conduction studies. Before she was lost to follow-up, however, she was seen in clinic 6 months later and had continued numbness in her right posterior thigh. References 1. Hollinshead WH. Anatomy for surgeons: the back and limbs, Vol. 3. 3rd ed. Philadelphia: Harper & Row; 1982. 2. Iyer VG, Shields CB. Isolated injection injury to the posterior femoral cutaneous nerve. Neurosurgery 1989;25:835-8. 3. Obach J, Aragones JM, Ruano D. The infrapiriformis foramen syndrome resulting from intragluteal injection. J Neurol Sci 1983;58: 135-42. 4. Arnoldussen WJ, Korten JJ. Pressure neuropathy of the posterior femoral cutaneous nerve. Clin Neurol Neurosurg 1980;82:57-60. 5. Dumitru D, Marquis S. Posterior femoral cutaneous nerve neuropathy and somatosensory evoked potentials. Arch Phys Med Rehabil 1988;69:44-5. 6. Dumitru D, Nelson MR. Posterior femoral cutaneous nerve conduction. Arch Phys Med Rehabil 1990;71:979-82. 7. Dumitru D. Electrodiagnostic medicine. Philadelphia: Hanley & Belfus; 1995. 8. Kimura J. Electromyography in diseases of nerve and muscle: principles and practice. Philadelphia: FA Davis; 1983. 9. Haig AJ. Clinical experience with paraspinal mapping II: a simplified technique that eliminates three-fourths of needle insertions. Arch Phys Med Rehabil 1997;78:1185-90.