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Peripheral neuropathies in Parkinson’s disease during levodopa-carbidopa intestinal gel treatment: Results from a long-term prospective follow-up study

A. Romagnolo, A. Merola, M. Zibetti, A. Bernardini, D. Cocito, C.A. Artusi, F. Dematteis, S. Angrisano, M.G. Rizzone, L. Lopiano (Turin, Italy)

Meeting: 2016 International Congress

Abstract Number: 2029

Keywords: Electromyogram(EMG)

Session Information

Date: Thursday, June 23, 2016

Session Title: Parkinson's disease: Clinical trials, pharmacology and treatment

Session Time: 12:00pm-1:30pm

Location: Exhibit Hall located in Hall B, Level 2

Objective: To prospectively evaluate, in a cohort of Parkinson’s disease (PD) patients, the incidence of peripheral neuropathies (PNP) during Levodopa/Carbidopa intestinal gel (LCIG) treatment.

Background: Subacute and chronic PNP have been reported in PD patients treated with LCIG, but several aspects of their incidence and pathogenesis still remain to be clarified. We reported the 3-year extension of a previously published study.

Methods: Thirty-five consecutive PD patients treated with LCIG underwent regular clinical, hematological, nutritional and electrophysiological (EP) assessment. PNP were classified as subacute or chronic according to the temporal progression of symptoms; patients developing only EP alterations were defined as subclinical PNP.

Results: At baseline, 3/35 patients showed symptomatic PNP and 7/35 subclinical PNP. During a follow-up of 35.89±11.31 months, 2/25 patients with normal baseline clinical-EP assessment developed a subacute PNP, 3/25 developed a chronic PNP and 7/25 developed a subclinical PNP. LCIG was immediately halted in the subacute cases, while the infusion was not interrupted in chronic and subclinical forms. All PNP were supplemented with vitamin B1 and B12, showing a clinical improvement and/or stability at the following evaluations. Patients with subacute or subclinical PNP showed no significant differences in B12, folate, homocysteine or levodopa-equivalent daily dose (LEDD) variations over time compared to patients without clinical-EP alterations. Conversely, patients with chronic PNP showed higher LEDD (p:0.029) and homocysteine levels (p:0.035), while no correlations were observed with vitamin B12 or folate. A trend towards BMI reduction was observed in both PNP and normal subjects; patients affected by subclinical PNP at baseline remained substantially stable, except for one case, which developed a symptomatic PNP associated with a relevant weight loss. These 3-year data confirm the results from our previous 2-year follow-up survey.

Conclusions: PNP is a relevant complication among PD patients undergoing LCIG: seriate clinical, hematological and EP evaluations are mandatory. No clear causative factors were recognized in the subacute forms, maybe related to immunological triggers in predisposed subjects, while mechanisms of homocysteine-mediated neurotoxicity seem to be implicated in the pathogenesis of chronic forms.

To cite this abstract in AMA style:

A. Romagnolo, A. Merola, M. Zibetti, A. Bernardini, D. Cocito, C.A. Artusi, F. Dematteis, S. Angrisano, M.G. Rizzone, L. Lopiano. Peripheral neuropathies in Parkinson’s disease during levodopa-carbidopa intestinal gel treatment: Results from a long-term prospective follow-up study [abstract]. Mov Disord. 2016; 31 (suppl 2). https://www.mdsabstracts.org/abstract/peripheral-neuropathies-in-parkinsons-disease-during-levodopa-carbidopa-intestinal-gel-treatment-results-from-a-long-term-prospective-follow-up-study/. Accessed June 14, 2025.
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