Prevalence and features of peripheral neuropathy in Parkinson's disease patients under different therapeutic regimens

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 f...

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Veröffentlicht in:Parkinsonism & related disorders 2014-01, Vol.20 (1), p.27-31
Hauptverfasser: Mancini, F, Comi, C, Oggioni, G.D, Pacchetti, C, Calandrella, D, Coletti Moja, M, Riboldazzi, G, Tunesi, S, Dal Fante, M, Manfredi, L, Lacerenza, M, Cantello, R, Antonini, A
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container_end_page 31
container_issue 1
container_start_page 27
container_title Parkinsonism & related disorders
container_volume 20
creator Mancini, F
Comi, C
Oggioni, G.D
Pacchetti, C
Calandrella, D
Coletti Moja, M
Riboldazzi, G
Tunesi, S
Dal Fante, M
Manfredi, L
Lacerenza, M
Cantello, R
Antonini, A
description 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.
doi_str_mv 10.1016/j.parkreldis.2013.09.007
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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.</description><identifier>ISSN: 1353-8020</identifier><identifier>EISSN: 1873-5126</identifier><identifier>DOI: 10.1016/j.parkreldis.2013.09.007</identifier><identifier>PMID: 24099722</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Aged ; Antiparkinson Agents - adverse effects ; Cross-Sectional Studies ; Electromyography ; Female ; Folic Acid - blood ; Homocysteine - blood ; Humans ; Levodopa - adverse effects ; Levodopa intestinal infusion ; Male ; Middle Aged ; Neurology ; Neuropathy ; Parkinson Disease - blood ; Parkinson Disease - complications ; Parkinson Disease - drug therapy ; Parkinson's disease ; Peripheral Nervous System Diseases - blood ; Peripheral Nervous System Diseases - epidemiology ; Peripheral Nervous System Diseases - etiology ; Prevalence ; Vitamin B 12 - blood</subject><ispartof>Parkinsonism &amp; related disorders, 2014-01, Vol.20 (1), p.27-31</ispartof><rights>Elsevier Ltd</rights><rights>2013 Elsevier Ltd</rights><rights>Copyright © 2013 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c512t-8ac8ed0f675389386ac44d82fe9302a40500065985ebaa9ab0418672ed340adf3</citedby><cites>FETCH-LOGICAL-c512t-8ac8ed0f675389386ac44d82fe9302a40500065985ebaa9ab0418672ed340adf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1353802013003374$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24099722$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mancini, F</creatorcontrib><creatorcontrib>Comi, C</creatorcontrib><creatorcontrib>Oggioni, G.D</creatorcontrib><creatorcontrib>Pacchetti, C</creatorcontrib><creatorcontrib>Calandrella, D</creatorcontrib><creatorcontrib>Coletti Moja, M</creatorcontrib><creatorcontrib>Riboldazzi, G</creatorcontrib><creatorcontrib>Tunesi, S</creatorcontrib><creatorcontrib>Dal Fante, M</creatorcontrib><creatorcontrib>Manfredi, L</creatorcontrib><creatorcontrib>Lacerenza, M</creatorcontrib><creatorcontrib>Cantello, R</creatorcontrib><creatorcontrib>Antonini, A</creatorcontrib><title>Prevalence and features of peripheral neuropathy in Parkinson's disease patients under different therapeutic regimens</title><title>Parkinsonism &amp; related disorders</title><addtitle>Parkinsonism Relat Disord</addtitle><description>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. 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Comi, C ; Oggioni, G.D ; Pacchetti, C ; Calandrella, D ; Coletti Moja, M ; Riboldazzi, G ; Tunesi, S ; Dal Fante, M ; Manfredi, L ; Lacerenza, M ; Cantello, R ; Antonini, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c512t-8ac8ed0f675389386ac44d82fe9302a40500065985ebaa9ab0418672ed340adf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Aged</topic><topic>Antiparkinson Agents - adverse effects</topic><topic>Cross-Sectional Studies</topic><topic>Electromyography</topic><topic>Female</topic><topic>Folic Acid - blood</topic><topic>Homocysteine - blood</topic><topic>Humans</topic><topic>Levodopa - adverse effects</topic><topic>Levodopa intestinal infusion</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Neuropathy</topic><topic>Parkinson Disease - blood</topic><topic>Parkinson Disease - complications</topic><topic>Parkinson Disease - drug therapy</topic><topic>Parkinson's disease</topic><topic>Peripheral Nervous System Diseases - blood</topic><topic>Peripheral Nervous System Diseases - epidemiology</topic><topic>Peripheral Nervous System Diseases - etiology</topic><topic>Prevalence</topic><topic>Vitamin B 12 - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mancini, F</creatorcontrib><creatorcontrib>Comi, C</creatorcontrib><creatorcontrib>Oggioni, G.D</creatorcontrib><creatorcontrib>Pacchetti, C</creatorcontrib><creatorcontrib>Calandrella, D</creatorcontrib><creatorcontrib>Coletti Moja, M</creatorcontrib><creatorcontrib>Riboldazzi, G</creatorcontrib><creatorcontrib>Tunesi, S</creatorcontrib><creatorcontrib>Dal Fante, M</creatorcontrib><creatorcontrib>Manfredi, L</creatorcontrib><creatorcontrib>Lacerenza, M</creatorcontrib><creatorcontrib>Cantello, R</creatorcontrib><creatorcontrib>Antonini, A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Parkinsonism &amp; related disorders</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mancini, F</au><au>Comi, C</au><au>Oggioni, G.D</au><au>Pacchetti, C</au><au>Calandrella, D</au><au>Coletti Moja, M</au><au>Riboldazzi, G</au><au>Tunesi, S</au><au>Dal Fante, M</au><au>Manfredi, L</au><au>Lacerenza, M</au><au>Cantello, R</au><au>Antonini, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prevalence and features of peripheral neuropathy in Parkinson's disease patients under different therapeutic regimens</atitle><jtitle>Parkinsonism &amp; related disorders</jtitle><addtitle>Parkinsonism Relat Disord</addtitle><date>2014-01-01</date><risdate>2014</risdate><volume>20</volume><issue>1</issue><spage>27</spage><epage>31</epage><pages>27-31</pages><issn>1353-8020</issn><eissn>1873-5126</eissn><abstract>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.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>24099722</pmid><doi>10.1016/j.parkreldis.2013.09.007</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record>
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subjects Aged
Antiparkinson Agents - adverse effects
Cross-Sectional Studies
Electromyography
Female
Folic Acid - blood
Homocysteine - blood
Humans
Levodopa - adverse effects
Levodopa intestinal infusion
Male
Middle Aged
Neurology
Neuropathy
Parkinson Disease - blood
Parkinson Disease - complications
Parkinson Disease - drug therapy
Parkinson's disease
Peripheral Nervous System Diseases - blood
Peripheral Nervous System Diseases - epidemiology
Peripheral Nervous System Diseases - etiology
Prevalence
Vitamin B 12 - blood
title Prevalence and features of peripheral neuropathy in Parkinson's disease patients under different therapeutic regimens
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