Objective: (1) To make an inventory of the current strategies used to treat or prevent the occurrence of chronic polyneuropathy (CPN) in patients with Parkinson’s disease (PD) treated by levodopa-carbidopa intestinal gel infusion (LCIG), (2) to evaluate if there could be other strategies to prevent the risk of occurrence or of worsening of a CPN, based on the patho physiology of the CPN observed in PD and more particularly when patients are treated by LCIG.

Background: Many cases of CPN have been described in PD, and more particularly with LCIG treatment . The physio pathological mechanisms responsible, its frequency and its management remained unclear.

Methods: A systematic computer-based literature search was conducted on PubMed database, concerning the cases of CPN in the context of the PD, with or without any oral antiparkinsonian drugs and for patients PD treated by LCIG. We reported all the strategies commonly used the monitoring and the management protocols.We proposed base on the patho physiology of the CPN some perspectives of monitoring and of treatment.

Results: 14 studies were selected, involving 173 patients under LCIG. CPN was found in 19% to 73% of patients according to the studies. Most often, the neuropathy was axonal and sensitive, more severe than in patients receiving oral levodopa. There was no consensus in the management of neuropathies, resulting in a wide variability of the preventive or curative strategies. Treatment with LCIG was usually carried on, with LCIG dose reduction in 2 studies, and a definitive discontinuation in 2 others. Vitamin B12 supplementation was initiated alone in 6 studies, associated with folic acid in 4 others. Patients were systematically supplemented before the initiation of LCIG in 2 studies, slowing the onset of neuropathy. There was no standardized protocol for the monitoring. There was little evidence to support a direct link between levodopa treatment and the development of these CPN in PD. In the majority of the cases, CPN had been linked to abnormalities in vitamin B12, methylmalonic acid or homocysteine levels. The mechanisms causing a higher frequency of neuropathies under LCIG were unclear, but probably resulted from a higher dose of levodopa and a decrease in vitamin absorption due to intestinal diffusion.

Conclusions: Harmonization of practices is needed for patients with CPN under LCIG. This frequent and debilitating symptoms associated with LCIG, justifies a standardized and regular follow-up. Systematic vitamin B12 and folic acid supplementation could slow down the onset of polyneuropathy, but it is essential to better understand the pathophysiology in order to better support patients in order to elaborate more efficient strategies.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/management-of-chronic-polyneuropathy-associated-with-levodopa-carbidopa-intestinal-gel-infusion-in-parkinsons-disease-review-of-the-strategies-and-perspectives/