Habitual peroneal nerve palsy

Clinical History

A 15-year-old male patient was referred because of right lower limb atrophy, dysesthesia in the proximal third of the right lateral leg, mild ipsilateral pain and weak right foot eversion lasting for 9 months. He was regularly squatting while studying (Fig. 1). Tinel sign was possitive.

Imaging Findings

MR imaging was performed with a 1.5T scanner using standard sequences. The axial and coronal T1-w images showed increased signal intensity at the lateral compartment muscles in keeping with fatty infiltration (Fig. 2). Neither mass nor oedema was shown on STIR images (Fig. 3). The muscles were atrophic, in keeping with chronic denervation of the common peroneal nerve (CPN).

Discussion

Peroneal neuropathy is the most common mononeuropathy of the lower extremity [1, 2, 3, 4]. It results commonly from direct trauma, traction injuries, and surgery. Rarely, vascular lesions, diabetes, external compression (casts, immobilization) and space occupying lesions including aberrant muscle, scar, schwannoma, neurofibroma, osteochondroma, ganglion cyst, osteophytes, and fracture fragments.
Entrapment neuropathies (compression of a short segment of a nerve) may result from mechanical pressure due to mass occupying lesions or dynamically due to limb positioning [1-4].The most common site of CPN entrapment is the fibular neck, as at this site, the nerve is covered only by skin and could be easily compressed [5]. The second site of entrapment is at the fibrous channel underneath the peroneus longus muscle (drawing).
Limb positioning associated to CPN palsy includes habitual cross legging as in this case, with direct pressure on the peroneus longus muscle and/or the fibular neck (Fig.1, drawing), and prolonged immobilization [6, 7] . Prolonged squatting and extended lithotomy position due to childbirth or obstetric surgery usually produce bilateral CPN entrapment [2].
Until recently the diagnosis was based on clinical (foot drop, positive Tinnel sign, loss of sensation at the distribution of CPN) and neurophysiological studies [7]. Early diagnosis is related to the degree of functional recovery as treatment depends on the cause and the site of entrapment.
Imaging strategy includes plain x-ray to exclude osseous abnormalities, and ultrasonography and MR imaging for direct assessment of the nerve and the causative pathology [3]. Muscle denervation at the acute stage is demonstrated with high signal intensity of the affected muscles on fluid sensitive sequences and normal signal and morphology on T1-w images [4-6]. In the chronic stage, there is muscle atrophy with fatty infiltration and loss of volume of the affected muscles which is depicted as high signal intensity on T1-w MR images and lack of any abnormal signal on fluid sensitive sequences.
The treatment depends upon the underlying cause of CPN paresis. It includes conservative therapy (NSAIDS, rest, physiotherapy), local injections of steroids and if symptoms persist, surgical decompression. Mass lesions are also treated surgically. In our patient the treatment was conservative as the injury to the CPN was chronic with non-reversible denervation muscle atrophy.

Differential Diagnosis List

Final Diagnosis

Peroneal nerve entrapment neuropathy due to habitual leg crossing

URL:	https://www.eurorad.org/case/10762
DOI:	10.1594/EURORAD/CASE.10762
ISSN:	1563-4086