Peripheral neuropathy in Parkinson's disease: levodopa exposure and implications for duodenal delivery.

Autor(es): Müller Thomas; van Laar Teus.; Cornblath David R.; Odin Per; Klostermann Fabian.; Grandas Francisco J.; Ebersbach Georg; Urban Peter P.; Valldeoriola Francesc; Antonini Angelo

Resumo: In advanced Parkinson's disease (PD) patients, continuous intra-duodenal infusion of levodopa/carbidopa intestinal gel (LCIG) is an established approach in the management of motor complications that cannot be further improved by conventional oral therapy. In general, tolerability of LCIG has resembled that of oral dopaminergic therapy; however, cases of symptomatic peripheral neuropathy (PN), sometimes severe, have been reported in patients receiving LCIG. Cases are generally a sensorimotor polyneuropathy with both subacute and chronic onsets, often associated with vitamin B12 and/or B6 deficiency. Rare cases clinically resemble Guillain-Barré syndrome. In the absence of prospectively collected data on possible associations between LCIG and PN, it is prudent to explore potential mechanisms that may explain a possible relationship. The PN may be linked to use of high-dose levodopa, promoting high levels of homocysteine and methylmalonic acid or reduced absorption of vitamins essential for homocysteine metabolism. Cases of LCIG-associated PN often have responded to vitamin suplementation without need for LCIG cessation, although LCIG cessation is sometimes necessary. It may be advisable to monitor vitamin B12/B6 status before and after patients start LCIG and be vigilant for signs of PN. Prospective, large-scale, long-term studies are needed to clarify whether vitamin suplementation and routine use of a catechol-O-methyltransferase inhibitor may help prevent PN in LCIG recipients and whether these measures should be routine practice in patients with PD on high-dose oral levodopa.

Imprenta: Parkinsonism & Related Disorders, v. 19, n. 5, p. 501-507, 2013

Identificador do objeto digital: 10.1016/j.parkreldis.2013.02.006

Descritores: Guillain-Barre Syndrome - Biosynthesis ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Public health

Data de publicação: 2013