POLYNEUROPATHY SPECTRUM IN LEVODOPA/CARBIDOPA INTESTINAL GEL THERAPY: REPORT OF TWO CASES AND REVIEW OF THE LITERATURE

Abstract

Background: Peripheral neuropathy is increasingly recognized in Parkinson’s disease (PD), particularly in patients receiving levodopa–carbidopa intestinal gel (LCIG). While most cases are chronic and slowly progressive, acute and subacute neuropathies with variable pathophysiology have also been reported. Objective: To describe two cases of advanced PD complicated by severe polyneuropathy during LCIG therapy, and to contextualize their clinical and electrophysiological findings within current literature. Methods: We conducted a detailed clinical assessment, laboratory evaluation, nerve conduction studies (NCS), and electromyography (EMG) in two male patients with advanced PD treated with LCIG. Relevant laboratory and nutritional factors were also examined. Results: Both patients developed severe sensorimotor axonal polyneuropathy. Case 1, a 67-year-old man, exhibited chronic axonal damage with reinnervation in the context of folate deficiency, systemic illness, and renal impairment. Case 2, a 70-year-old man, presented with active denervation and sensory ataxia, associated with mild vitamin B12 deficiency, weight loss, and renal dysfunction. Both received intravenous immunoglobulin (IVIG) with partial clinical improvement. Conclusion: LCIG-associated neuropathy is heterogeneous, encompassing both chronic compensated forms and more aggressive phenotypes with ongoing denervation. Multiple mechanisms—including high levodopa exposure, vitamin depletion, malnutrition, renal impairment, and possible immune factors—may converge in its pathogenesis. These cases emphasize the importance of early prophylactic vitamin supplementation, regular metabolic and neurophysiological monitoring, and timely recognition of both acute and chronic forms to optimize outcomes in LCIG-treated patients.