Peroneal nerve palsy has been reported in association with traumatic and nontraumatic causes. We encountered a 75-year-old man whose peroneal nerve palsy developed suddenly following varus deformity of the arthritic knee. A review of the literature found 1 other report describing a progressive peroneal nerve palsy associated with a varus deformity of the knee due to arthritis.
Our patient had progressive intractable knee pain; 3-compartment, severe degenerative changes in the knees; varus knee malalignment and laxity; right peroneal nerve palsy; and decreased sensation to light touch and pinprick on the dorsum of the right foot. The preoperative WOMAC score was 36. Nerve conduction studies confirmed acute peroneal neuropathy with conduction block at the fibular neck and secondary axonal degeneration. Magnetic resonance imaging of the knee showed osteophytes and cysts surrounding the fibular neck. Although their compression could be responsible for the nerve palsy, the sudden process made this less possible. Thus, the patient underwent total knee arthroplasty of both knees without exploration of the nerve. At 5-month follow-up, the WOMAC score was 78. The patient walked with a cane with no varus thrust, and his right knee had no varus laxity in full extension. The peroneal nerve did not retain its function. Sensory examination and postoperative nerve conduction studies showed no improvement.
Peroneal nerve palsy is the most common entrapment mononeuropathy in the lower extremity. Most often, peroneal nerve palsy occurs at the fibular neck, where the nerve has a superficial route.1,2
It has been reported in association with traumatic varus injury of the knee,3 traumatic dislocation of the knee,4 high tibial osteotomy,5 knee arthroscopy,6 total knee arthroplasty (TKA),7,8 skin or skeletal traction and casting, and closed or open reduction of lower extremity fractures.1,9,10 Although these traumatic causes account for most peroneal nerve palsies, nontraumatic lesions also trigger it, including intrinsic and extrinsic nerve tumors, extraneural compression by a synovial cyst, ganglion cyst, soft tissue tumor, and osseous mass.1,11-13
A 75-year-old man presented to our institution whose peroneal nerve palsy developed suddenly following varus deformity of the arthritic knee. A review of the literature found just 1 other report describing a progressive peroneal nerve palsy associated with a varus deformity of the knee due to arthritis.14
A 75-year-old man with a 20-year history of knee pain due to osteoarthritis presented with a sudden foot drop in his right foot. He had suffered aggravated knee pain during the past 6 months that was not amenable to medications, and his knees gave way frequently. He had been using a cane for walking and held onto a banister for stair-climbing for the past 5 years. He reported no recent trauma and pain radiating from the back. His foot dorsiflexion was intact until a walk during which he suddenly felt a cramp-like pain in his right leg, and he was unable to dorsiflex his toe and ankle thereafter.
On physical examination, he was 77.5 kg and 161 cm tall. Visual analog scale (VAS) pain score was 5 of 10. He walked with a circumduction gait in his right leg secondary to paralyzed ankle dorsiflexors and had an obvious bilateral varus malalignment and bilateral varus thrust. In the valgus stress test, we observed incomplete correction with a solid endpoint. He had an obvious varus deformity. The knee was in 16° of varus malalignment when he was standing (Figure 1). Palpation of the knees demonstrated patellofemoral crepitus and bony hypertrophy. Range of motion (ROM) was 10° to 100° in both knees.
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Figure 1: Preoperative AP nonweight-bearing (A) and weight-bearing (B) radiographs of the right knee demonstrating 3-compartment, severe degenerative changes with varus deformity, which was aggravated while standing.
Examination of the ligaments with the knee in maximal extension (a 10° flexion contracture) demonstrated 12 mm of varus laxity with a soft endpoint. On the right side, motor examination demonstrated grade 0 of 5 strength of the tibialis anterior and extensor hallucis longus muscles, and ankle and toe dorsiflexion were absent. Plantar flexion was normal, and with passive ankle dorsiflexion, ankle inversion was spared, demonstrating an intact L5 root and sciatic and tibial nerves. There was no muscle weakness in the left side. No neurovascular compromise was detected, except decreased sensation to light touch and pinprick on the dorsum of the right foot.
The preoperative WOMAC score was 36. Examination of the hip and spine was unremarkable. His lumbosacral radiograph revealed degenerative changes. Magnetic resonance imaging (MRI) of the lumbar spine showed no canal stenosis or foraminal narrowing.
Nerve conduction studies showed a severe decrease in compound muscle action potential of the peroneal nerve with conduction block and a decrease in sensory nerve action potential of the superficial peroneal nerve. Other findings were normal. Electromyography showed no spontaneous activity in the tibialis anterior muscle on the right side and a few motor unit action potentials in this muscle. The short head of the biceps femoris was spared. As it is the only muscle supplied by the peroneal division of the sciatic nerve, it implies that the lesion was distal to the sciatic nerve and the neural insult occurred at the level of the knee.
These findings confirmed acute peroneal neuropathy with conduction block at the fibular neck and secondary axonal degeneration.
Total knee arthroplasty of both knees was performed under regional anesthesia with tourniquet. A primary prosthesis (Rotaglide; Corin Medical Technology, London, United Kingdom) with minimum bone resection of the proximal tibia and distal femur was applied. Given the insignificant resection size and establishment of valgus in both knees during surgery, as well as the acceptable ligamentous balance in flexion and extension, there was no need for a more constrained prosthesis. Establishment of valgus during surgery and ligament balancing was particularly important in the right side, where the continuing varus instability could result in ongoing, persistent traction on the peroneal nerve. Inasmuch as we could reach these 2 points, there was no need for constrained TKA. Peroneal nerve exploration and decompression were not performed, since we felt the nerve palsy was due to the traction following varus deformity of the knee and exploration seemed unnecessary at that stage.
As the knee MRI showed osteophytes and cysts surrounding the fibular neck, the nerve palsy could be the result of their compression, but the sudden process made this less possible; thus, the most probable cause of the nerve palsy remained traction due to the varus deformity of the knee (Figures 2, 3).
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Figure 2: T1-weighted sagittal MRI of the right knee demonstrating a large osteophyte posterior to the fibular neck. Figure 3: T2-weighted axial MRI of the right knee showing 2 large osteophytes and cysts surrounding the fibular neck.
Twenty-four hours postoperatively, continuous passive motion of both knees began. The patient walked 48 hours postoperatively with protected weight bearing with the assistance of a walker. Afterward, active and passive ROM was prescribed. A regular physiotherapy program for the right ankle and electrical stimulation of paralyzed muscles were performed. The patient was discharged after achievement of 90° flexion in both knees.
The patient was evaluated at 2 weeks, 2 months, and 5 months postoperatively. His knee pain resolved partially, but the peroneal nerve function did not improve. At 5-month follow-up, the VAS pain score was 2 of 10, he had a circumduction gait on the right side, and he could walk with the cane with no varus thrust and climb stairs using the banister. The right knee had no varus laxity in full extension. Range of knee flexion was 0° to 110°, with no instability but a 10° extensor lack. The neurologic examination demonstrated grade 0 of 5 strength of the extensor hallucis longus muscle and grade 0 of 5 strength of the tibialis anterior muscle. Sensory examination and postoperative nerve conduction studies showed no improvement. The WOMAC score was 78. Radiographs demonstrated a good component alignment and patellar tracking with no radiolucencies (Figure 4).
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Figure 4: Postoperative standing AP (A) and lateral (B) radiographs of the right knee demonstrating a well-fixed total knee prosthesis with good component alignment and patellar tracking with no radiolucencies.
As peroneal nerve improvement did not occur within 5 months, nerve exploration will be considered 6 months postoperatively according to the nerve function and electrodiagnostic assessment results.
Our patient presented with abrupt peroneal nerve palsy and foot drop following a varus arthritic knee. No reports exist in the literature on peroneal nerve palsy due to degenerative varus deformity of the knee, except 1 case reported by Fetzer et al.14 Their patient developed a neurologic deficit progressively over a 4-month period. They performed a constrained TKA along with peroneal nerve decompression. They explored the peroneal nerve and performed a decompression at the level of the fibular head and neck to diagnose and treat any potential compressive lesion or tethering by soft tissue. The absence of a compressive lesion was consistent with a repetitive traction injury of the peroneal nerve. After a medial release and correction of knee alignment, there was a mild residual varus laxity present. Therefore, a constrained tibial insert was used to minimize any residual varus laxity to prevent continued traction on the nerve. At 2-year follow-up, in addition to a complete improvement of the peroneal nerve palsy, the Knee Society clinical and functional scores improved significantly with no remaining symptoms.
As this combination has not been adequately discussed, the optimal treatment strategy was not clear to us. Treatment options include bracing and measures to treat symptoms, nerve exploration and decompression alone, conventional TKA with or without nerve decompression, and constrained TKA with or without nerve decompression. But none of these approaches has been approved as the best strategy.
Regarding the report of Fetzer et al,14 we felt that traction on the common peroneal nerve associated with moderate lateral laxity of the knee must have been the cause of peroneal palsy. Despite the presence of osteophytes surrounding the fibular neck, preoperative electromyography that revealed a common peroneal nerve injury at the level of the knee and acuteness of the nerve palsy support this supposition.
Whereas the traction was considered as the most probable cause of the peroneal nerve palsy, we did not explore the nerve during the operation. Furthermore, since we could establish knee valgus alignment with no residual varus laxity during surgery, there was no need for constrained TKA. The patient was evaluated at 2 weeks, 2 months, and 5 months postoperatively, over which time the knee pain resolved partially and knee ROM improved, but the peroneal nerve function did not improve.
It seems that, although uncommon, peroneal nerve palsy can develop following varus deformity of the arthritic knee, and when it develops, a patients condition will deteriorate and his walking disability associated with degenerative knee disorders will be aggravated.
In our patient, traction on the common peroneal nerve at the level of the fibular neck is likely the cause of peroneal nerve palsy. The efficacy of the recommended strategies is not yet known, but it seems that TKA establishing accurate knee alignment with no residual varus laxity and elimination of the nerve traction are the best choices, and peroneal nerve exploration can be considered if nerve function improvement has not been achieved within 6 months.
- Aprile I, Caliandro P, La Torre G, et al. Multicenter study of peroneal mononeuropathy: clinical, neurophysiologic, and quality of life assessment. J Peripher Nerv Syst. 2005; 10(3):259-268.
- Kim DH, Murovic JA, Tiel RL, Kline DG. Management and outcomes in 318 operative common peroneal nerve lesions at the Louisiana State University Health Sciences Center. Neurosurgery. 2004; 54(6):1421-1428.
- Bowman AJ Jr, Kilfoyle RM, Broom JS. Varus injury of the knee with common peroneal nerve palsy. J Natl Med Assoc. 1984; 76(2):157-161.
- Almekinders LC, Logan TC. Results following treatment of traumatic dislocations of the knee joint. Clin Orthop Relat Res. 1992; (284):203-207.
- Coventry MB. Upper tibial osteotomy for osteoarthritis. J Bone Joint Surg Am. 1985; 67(7):1136-1140.
- Johnson DS, Sharma DP, Bangash IH. Common peroneal nerve palsy following knee arthroscopy. Arthroscopy. 1999; 15(7):773-774.
- Idusuyi OB, Morrey BF. Peroneal nerve palsy after total knee arthroplasty. Assessment of predisposing and prognostic factors. J Bone Joint Surg Am. 1996; 78(2):177-184.
- Rose HA, Hood RW, Otis JC, Ranawat CS, Insall JN. Peroneal-nerve palsy following total knee arthroplasty. A review of The Hospital for Special Surgery experience. J Bone Joint Surg Am. 1982; 64(3):347-351.
- Weiss AP, Schenck RC Jr, Sponseller PD, Thompson JD. Peroneal nerve palsy after early cast application for femoral fractures in children. J Pediatr Orthop. 1992; 12(1):25-28.
- Butcher CC, Hoffman EB. Supracondylar fractures of the femur in children: closed reduction and percutaneous pinning of displaced fractures. J Pediatr Orthop. 2005; 25(2):145-148.
- Kim JY, Ihn YK, Kim JS, Chun KA, Sung MS, Cho KH. Non-traumatic peroneal nerve palsy: MRI findings. Clin Radiol. 2007; 62(1):58-64.
- Ozturk K, Akman S, Erturer E, Ayanoglu S, Aksoy B. A case of an intraneural ganglion cyst in the peroneal nerve resulting in drop foot [in Turkish]. Acta Orthop Traumatol Turc. 2000; (34):426-429.
- Loredo R, Hodler J, Pedowitz R, Yeh LR, Trudell D, Resnick D. MRI of the common peroneal nerve: normal anatomy and evaluation of masses associated with nerve entrapment. J Comput Assist Tomogr. 1998; 22(6):925-931.
- Fetzer GB, Prather H, Gelberman RH, Clohisy JC. Progressive peroneal nerve palsy in a varus arthritic knee. A case report. J Bone Joint Surg Am. 2004; 86(7):1538-1540.
Drs Seyyed Hosseinzadeh, Eajazi, Kazemi, Daftari Besheli, Hassas Yeganeh, and Aydanloo are from Akhtar Orthopaedic Hospital, and Drs Seyyed Hosseinzadeh, Kazemi, Hassas Yeganeh, and Aydanloo are also from Shahid Beheshti University of Medical Science, and Drs Eajazi and Daftari Besheli are also from Tehran University of Medical Sciences, Tehran, Iran.
Drs Seyyed Hosseinzadeh, Eajazi, Kazemi, Daftari Besheli, Hassas Yeganeh, and Aydanloo have no relevant financial relationships to disclose.
Correspondence should be addressed to: ALireza Eajazi, MD, Akhtar Orthopaedic Hospital Research Center, Elahieh, Tehran, Iran (firstname.lastname@example.org).