Delayed radiation-induced lumbosacral radiculoplexus neuropathy – a diagnostic dilemma

Abstract

The delayed effects of neurotoxicity related to radiation therapy present a diagnostic challenge. It is essential for clinicians to recognize radiation-induced radiculoplexus neuropathy, which should also be discussed with patients as a potential iatrogenic complication of cancer treatment. CaseA 70-year-old gentleman presented to our EMG laboratory in early 2015 for recurrent episodes of right lower extremity "buckling" and falls. His symptoms were gradual in onset and had been worsening over several weeks. His past medical history included ankylosing spondylitis, a decade-long history of poorly controlled diabetes mellitus (most recent HbA1c at that time 8.2%), and remote prostate adenocarcinoma (T1c with perineural invasion, Gleason 3+4, PSA 4.36), for which he had received definitive radiotherapy in early 2008 (45 Gy whole pelvis, followed by serial coned-down boosts to the prostate and seminal vesicles; total dose 75.6 Gy). Radiotherapy was complicated by recurrent prostatitis, radiation-induced enteritis, and an associated partial small bowel obstruction in 2014.He was found to have severe proximal right lower extremity weakness, with near-inability to flex at the hip or extend at the knee. There was moderate weakness in hip abduction and adduction noted, while knee flexion, ankle dorsiflexion, and ankle plantar flexion were preserved and unaffected. There was an area of hypesthesia along the right upper anterior thigh, as well as length-dependent bilateral lower extremity sensory loss and hyporeflexia. The distal lower extremities were edematous. The remainder of his neurological and general medical examinations at that time were unremarkable. An EMG was performed (Tables 1 and 2), with abnormalities taken within clinical context concerning for a severe proximal right lumbosacral radiculoplexopathy and underlying sensorimotor axon loss-predominant peripheral polyneuropathy.He was admitted for additional workup and treatment. A pelvic MRI was notable for a T2/STIR hyperintense signal abnormality and enhancement involving the right pectineus, adductor magnus, iliacus, and psoas muscles, and faint enhancement of the right femoral and obturator nerves (Figure 1). For a presumed diagnosis of diabetic amyotrophy, he received 12 weeks of intravenous methylprednisolone and inpatient rehabilitation.He was lost to follow-up until early 2016, when he presented with progressively worsening painless right leg weakness. He reported no subjective improvement either during or following his earlier treatment course with corticosteroids. His interim glycemic control had remained suboptimal (average HbA1c 8.5%). He otherwise denied any significant change in his weight or general medical wellbeing. On reevaluation, he was found to have pronounced atrophy of the right quadriceps, continued proximal right leg weakness graded similarly to the year before, and the interim development of a nearcomplete right foot drop of uncertain chronicity. Sensory deficits were unchanged. The lower extremities were areflexic. A follow...