F Mancini1, C Comi2, G D Oggioni2, C Pacchetti3, D Calandrella4, M Coletti Moja5, G Riboldazzi6, S Tunesi7, M Dal Fante8, L Manfredi4, M Lacerenza4, R Cantello2, A Antonini9. 1. Parkinson's Disease and Movement Disorders Centre, Neurology Unit, San Pio X Clinic, Fondazione Opera San Camillo, Milan, Italy. Electronic address: francesca.mancini@tin.it. 2. Parkinson's Disease and Movement Disorders Centre, Department of Neurology, University of Eastern Piedmont "Amedeo Avogadro", Novara, Italy. 3. Parkinson's Disease and Movement Disorders Centre, Neurological Institute IRCCS "C. Mondino", Pavia, Italy. 4. Parkinson's Disease and Movement Disorders Centre, Neurology Unit, San Pio X Clinic, Fondazione Opera San Camillo, Milan, Italy. 5. Department of Neurology, Mauriziano Umberto I Hospital, Turin, Italy. 6. Parkinson's Disease and Movement Disorders Centre, University of Insubria, Varese, Italy. 7. Unit of Medical Statistics and Epidemiology, Department Translational Medicine, University of Eastern Piedmont "Amedeo Avogadro", Novara, Italy. 8. Endoscopy Unit San Pio X Clinic, Fondazione Opera San Camillo, Milan, Italy. 9. Department for Parkinson Disease, IRCCS San Camillo, Venice, Italy.
Abstract
BACKGROUND: Recent reports suggest increased frequency of peripheral neuropathy (PN) in Parkinson's disease (PD) patients on levodopa compared with age-matched controls particularly during continuous levodopa delivery by intestinal infusion (CLDII). The aim of this study is to compare frequency, clinical features, and outcome of PN in PD patients undergoing different therapeutic regimens. METHODS: Three groups of consecutive PD patients, 50 on intestinal levodopa (CLDII), 50 on oral levodopa (O-LD) and 50 on other dopaminergic treatment (ODT), were enrolled in this study to assess frequency of PN using clinical and neurophysiological parameters. A biochemical study of all PN patients was performed. RESULTS: Frequency of PN of no evident cause was 28% in CLDII, 20% in O-LD, and 6% in ODT patients. Clinically, 71% of CLDII patients and all O-LD and ODT PN patients displayed a subacute sensory PN. In contrast, 29% of CLDII patients presented acute motor PN. Levodopa daily dose, vitamin B12 (VB12) and homocysteine (hcy) levels differed significantly in patients with PN compared to patients without PN. CONCLUSIONS: Our findings support the relationship between levodopa and PN and confirm that an imbalance in VB12/hcy may be a key pathogenic factor. We suggest two different, possibly overlapping mechanisms of PN in patients on CDLII: axonal degeneration due to vitamin deficiency and inflammatory damage. Whether inflammatory damage is triggered by vitamin deficiency and/or by modifications in the intestinal micro-environment should be further explored. Proper vitamin supplementation may prevent peripheral damage in most cases.
BACKGROUND: Recent reports suggest increased frequency of peripheral neuropathy (PN) in Parkinson's disease (PD) patients on levodopa compared with age-matched controls particularly during continuous levodopa delivery by intestinal infusion (CLDII). The aim of this study is to compare frequency, clinical features, and outcome of PN in PDpatients undergoing different therapeutic regimens. METHODS: Three groups of consecutive PDpatients, 50 on intestinal levodopa (CLDII), 50 on oral levodopa (O-LD) and 50 on other dopaminergic treatment (ODT), were enrolled in this study to assess frequency of PN using clinical and neurophysiological parameters. A biochemical study of all PNpatients was performed. RESULTS: Frequency of PN of no evident cause was 28% in CLDII, 20% in O-LD, and 6% in ODT patients. Clinically, 71% of CLDIIpatients and all O-LD and ODT PNpatients displayed a subacute sensory PN. In contrast, 29% of CLDIIpatients presented acute motor PN. Levodopa daily dose, vitamin B12 (VB12) and homocysteine (hcy) levels differed significantly in patients with PN compared to patients without PN. CONCLUSIONS: Our findings support the relationship between levodopa and PN and confirm that an imbalance in VB12/hcy may be a key pathogenic factor. We suggest two different, possibly overlapping mechanisms of PN in patients on CDLII: axonal degeneration due to vitamin deficiency and inflammatory damage. Whether inflammatory damage is triggered by vitamin deficiency and/or by modifications in the intestinal micro-environment should be further explored. Proper vitamin supplementation may prevent peripheral damage in most cases.
Authors: Elizabeth A Clemmons; Sanjeev Gumber; Elizabeth Strobert; Mollie A Bloomsmith; Sherrie M Jean Journal: Comp Med Date: 2015-06 Impact factor: 0.982
Authors: Alberto Romagnolo; Aristide Merola; Carlo Alberto Artusi; Mario Giorgio Rizzone; Maurizio Zibetti; Leonardo Lopiano Journal: Mov Disord Clin Pract Date: 2018-11-08