Fibular nerve neurotmesis after knee dislocation: ultrasonographic findings

Knee dislocation can cause severe fibular nerve damage, as described previously. 1,2 This traumatic event usually produces paralysis or weakness of muscles innervated by the fibular nerve (FN), with denervation and focal enlargement of the injured nerve on ultrasound (US), indicating axonotmesis. Most commonly, the FN is in continuity, and the tibial nerve (TN) is spared. 1 We present a case of traumatic knee dislocation that caused FN neurotmesis and was diagnosed by US. A 35-yearold man came to our attention after experiencing a left knee injury 2 months earlier while playing rugby. He had left foot drop. Objective evaluation revealed paralysis of tibialis anterior, fibularis longus, and extensor hallucis muscles (F50, based on the Medical Research Council scale). Electromyographic evaluation showed absence of voluntary muscle activity and prominent fibrillation potentials in the aforementioned muscles. Magnetic resonance imaging disclosed FN injury with focal enlargement in the proximal segment of the fibular bone, identified as possible amputation neuroma. Moreover, incomplete lesions of anterior cruciate and medial collateral ligaments were found. We performed US assessment of the left sciatic, fibular, and tibial nerves. The sciatic nerve (SN) appeared hypoechoic beginning in the distal third of the thigh with increased size of the fibular component, whereas the tibial division was normal (Fig. 1A). This US-detected alteration was present distally along the course of the SN and after its division into FN and TN in the popliteal fossa. At this point, the FN was hypoechoic and had an increased crosssectional area (CSA) up to 75 mm 2 (Fig. 1C). Even in the popliteal fossa, the TN was normal. In the distal portion of the popliteal fossa, the FN demonstrated further enlargement and then disappeared from view. This US finding suggested an amputation neuroma of the FN. The entire abnormal segment, involving the SN and the FN, was 150 mm in length. To check for discontinuity, we moved the probe to the level of the fibular head, where the FN was evident, and we assessed it proximally from that point. The nerve had increased CSA and was easily followed to just above the fibular head, where its orientation changed unexpectedly. Hence, we needed to rotate the probe about 908 to scan the nerve perpendicularly. The FN continued ventrally toward the patella and terminated in an amputation neuroma with a 40-mm 2 CSA (Fig. 1D). We concluded that the FN distal to the popliteal fossa was completely detached from the proximal stump (with a gap of about 60 mm) and had an abnormal L-shaped course (Fig. 1B). The patient subsequently underwent nerve grafting but had limited benefit, likely secondary to the length of the affected nerve segment (Fig. 1E and F).