Peroneal neuropathy is either caused by prolonged posture (23.1%), surgical complication (20.3%), weight loss (14.5%), trauma (11.6%), or is idiopathic (16%) [
1]. Although ischemia also has been implicated as one of the causes, this is the first reported case of ischemic common peroneal neuropathy induced by occlusion of the artery supplying nerve. There is currently a lack of research concerning the blood supply of the common peroneal nerve (CPN). It is known that the CPN has fewer supplying arteries and anastomoses than the tibial or sciatic nerves [
5]. This suggests a potentially increased susceptibility of the peroneal nerve to compression, trauma, or other ischemic damage. According to a study by Kadiyala et al. [
6], a single branch from the popliteal artery supplies the CPN in the popliteal fossa and the anterior recurrent tibial artery that branches from the ATA supplies the nerve distal to the fossa. In their study, these arteries anastomose at a point 30 to 60 mm distal to the mid-point of the popliteal fossa (
Fig. 2). However, the distance between these vasa nervorum is 116 mm on average, whereas the distance between vasa nervorum of the tibial nerve is 41 mm on average. Because the distance between the vasa nervorum of the CPN is longer and supply lesser intraneural vessels, CPN has poor vascularization and is vulnerable to ischemic damage. In the study of Ryan et al. [
7], the mean distance of the distal common peroneal nerve from the fibular apex to the deep and superficial peroneal bifurcation point in males was 37.6 mm. Based on this anatomy, and the ischemic susceptibility of the distal common peroneal nerve, tibialis anterior and peroneus longus muscles that are innervated by nerve branches from CPN could be damaged from ischemic injury and show abnormal findings in needle electromyography. We reviewed previous studies concerning ischemic peroneal neuropathy. One case reported femoral bypass surgery as a potential cause of the peroneal and tibial neuropathy [
3]. In another case, peroneal palsy was reported after over 5 hours of leg ischemia due to femoral artery cannulation when performing cardiopulmonary bypass [
2]. Although this case discusses the ischemic vulnerability of peroneal nerve, it deals with the ischemic insult of proximal artery of lower extremity, similar to previous report. Moreover, we could not figure out other ischemic insults of peripheral nerves such as the tibial nerve, because there was no clinical information such as electrodiagnostic findings, symptoms and physical examination. Unlike that case, we report that the common peroneal neuropathy occurred as a result of the specific supplying arterial occlusion. The other report presented a case of sciatic neuropathy that resulted from thromboembolism secondary to a femoral artery aneurysm, with ischemic injury due to nutrient artery obstruction [
8]. McDermott et al. [
9] suggested that peripheral arterial disease impairs peroneal nerve function. In our case, ankle brachial index of affected leg was 90.5, which was in the normal range of ankle brachial index. However, there were no reports of a case of an ischemic peroneal nerve injury from occlusion of single artery supplying peripheral nerve. We report the ischemic common peroneal neuropathy due to occlusion of supplying artery without underlying peripheral arterial disease, which makes our case unique. In 1966, Machacek and Machacek [
10] reported a case of unilateral foot drop, after trauma. Clinical necrosis of the lower leg muscle was found, and surgery was performed. At postoperative angiography, there was an occlusion at the ATA. The foot drop in this case was thought to be due to anterior compartment syndrome which caused insult of lower leg muscles and peripheral nerves. This is dissimilar with our case in that there was no definite clinical evidence of anterior compartment syndrome.
In our case, the patient had no history of direct trauma or compression. However, he had a high risk of thromboembolism because of a history of percutaneous coronary intervention at symptom onset, arrhythmia, and valvular heart disease, with a mitral valve replacement. In addition, there was no radicular pain or symptoms suggestive of lumbosacral radiculopathy. Although a brain MRI could not be performed due to an implanted pacemaker, the presence of a subacute cerebral ischemic lesion suggests that there was a systemic thromboembolic event at the time of symptom onset. Therefore, after ruling out other possibilities, proximal occlusion of the ATA was thought to cause the peroneal neuropathy in this case.
Arterial occlusion-induced CPN palsy is rare and can be easily misdiagnosed. If foot drop occurred in patients with a risk factor of vascular embolism or thrombosis, an ischemic insult to the peroneal nerve should be part of the differential diagnosis. In addition to compression and trauma, nutrient arterial occlusion can be a cause of peroneal neuropathy. Special studies, such as CT angiogram or vascular sonography, could be seriously considered. Furthermore, we can conclude that the ATA has an important role in the blood supply to the CPN.