Delayed presentation of post-traumatic lumbar plexopathy

A 34-year-old male underwent MRI due to ongoing right lower limb motor and sensory symptoms following a fall down a flight of stairs approximately 8 weeks previously. On examination patient had reduced flexion at right hip with a right sided foot drop. Extension at right hip was maintained.

At the time of initial presentation, a CT of the abdomen and pelvis performed. This demonstrated marked asymmetric swelling of the visualised right thigh with oedema of the muscles in both the posterior and medial compartments. No focal haematoma or fracture was identified. [Figure1a-c]

Subsequent MRI of the pelvis was performed 8 weeks following initial injury which showed extensive STIR hyperintense signal, predominantly centred in the gluteal and adductor muscles [Figure 2a-d]. Axial T2 weighted imaging demonstrated marked asymmetric thickening of the right sciatic nerve along its course. [Figure3]

Due to persisting lower limb neurological symptoms as described above, patient also underwent nerve conduction studies. These demonstrated impaired conduction in the distribution of the lumbar plexus in keeping with a post-traumatic lumbar plexopathy.

Muscular denervation can occur secondary to a wide variety of pathology including trauma, demyelination, and infectious/inflammatory processes. While the pathophysiology can vary significantly, the resultant signs and symptoms are relatively consistent with pain, weakness and muscular atrophy widely described in the literature. Lumbosacral plexopathy is a particular subtype of neural injury involving the lumbosacral (LS) plexus[1]. 

Post-traumatic LS plexopathy most often occurs secondary to direct trauma such as in cases of posterior hip dislocation and sacral fractures. Traction on the plexus can also result in a plexopathy. These cases of traction plexopathy can be particularly challenging due to a lack of clear causative abnormality on either clinical examination or imaging. In patients who present with ongoing neurological symptoms in the distribution of the LS plexus, both cross-sectional imaging and nerve conduction studies have a role to play. Imaging is particularly useful in not only assessing for a potential underlying cause of the plexopathy but also outlining the extent of muscular involvement.

The classic finding associated with denervated muscle is hyperintense signal on fluid-sensitive sequences such as T2 and STIR. These signal abnormalities can become apparent as early as 4 days after injury and have been seen to progress in intensity, peaking after approximately 4 months[2]. The duration over which this signal abnormality persists varies significantly based on underlying injury; however, in severe cases of irreparable neural injury, these changes may be irreversible. With regard to outcomes, significant variations also exist depending on underlying aetiology. Traumatic LS plexopathies have generally been considered to have poorer outcomes compared to other aetiologies. Despite this, however, a previous case series of 72 patients demonstrated spontaneous recovery in approximately 70% after 18 months[3]. In attempting to optimise outcomes in these patients, imaging can play an important role in assessing the extent and distribution of muscular involvement. This can allow for targeted treatments such as physiotherapy.

In summary, it is important that all radiologists understand both the appearances of muscular denervation and the role cross-sectional imaging has in diagnosis and management of this patient cohort. While the majority of post-traumatic muscular signal abnormality will likely reflect oedema, in those patients with signal abnormality which is seen to persist and indeed progress over time, consideration should be given to denervation as an underlying diagnosis.