Oxaliplatin-induced neurotoxicity and the development of neuropathy
The pathophysiology of oxaliplatin‐induced neurotoxicity remains unclear, although in vitro studies suggest involvement of voltage‐gated Na+ channels. In the present study, clinical assessment was combined with nerve conduction studies (NCS) and nerve excitability studies in 16 patients after comple...
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| Veröffentlicht in: | Muscle & nerve 2005-07, Vol.32 (1), p.51-60 |
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| creator | Krishnan, Arun V. Goldstein, David Friedlander, Michael Kiernan, Matthew C. |
| description | The pathophysiology of oxaliplatin‐induced neurotoxicity remains unclear, although in vitro studies suggest involvement of voltage‐gated Na+ channels. In the present study, clinical assessment was combined with nerve conduction studies (NCS) and nerve excitability studies in 16 patients after completion of oxaliplatin therapy. Chronic neuropathic symptoms persisted in 50% of patients. NCS confirmed abnormalities in symptomatic patients: sensory potentials were significantly low, whereas motor studies remained essentially normal. At 12‐month follow‐up of symptomatic patients, positive sensory symptoms improved but NCS abnormalities persisted. Cumulative oxaliplatin dose was a predictor of neuropathy, and long‐term effects appeared to be minimized by low single‐infusion dosages. Nerve excitability measures in symptomatic patients established that axons were of high threshold. Refractoriness was significantly greater in patients (symptomatic group, 56.3 ± 24.9%; entire patient group, 46.3 ± 12.5%; controls, 27.1 ± 1.9%; P < 0.05). Thus, although positive sensory symptoms of oxaliplatin‐induced neuropathy improved, negative sensory symptoms and abnormalities of sensory nerve conduction persisted. Differences in nerve excitability measures, particularly refractoriness, support in vitro studies indicating involvement of voltage‐gated transient Na+‐channel dysfunction in the development of oxaliplatin‐induced neurotoxicity. Muscle Nerve, 2005 |
| doi_str_mv | 10.1002/mus.20340 |
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In the present study, clinical assessment was combined with nerve conduction studies (NCS) and nerve excitability studies in 16 patients after completion of oxaliplatin therapy. Chronic neuropathic symptoms persisted in 50% of patients. NCS confirmed abnormalities in symptomatic patients: sensory potentials were significantly low, whereas motor studies remained essentially normal. At 12‐month follow‐up of symptomatic patients, positive sensory symptoms improved but NCS abnormalities persisted. Cumulative oxaliplatin dose was a predictor of neuropathy, and long‐term effects appeared to be minimized by low single‐infusion dosages. Nerve excitability measures in symptomatic patients established that axons were of high threshold. Refractoriness was significantly greater in patients (symptomatic group, 56.3 ± 24.9%; entire patient group, 46.3 ± 12.5%; controls, 27.1 ± 1.9%; P < 0.05). Thus, although positive sensory symptoms of oxaliplatin‐induced neuropathy improved, negative sensory symptoms and abnormalities of sensory nerve conduction persisted. Differences in nerve excitability measures, particularly refractoriness, support in vitro studies indicating involvement of voltage‐gated transient Na+‐channel dysfunction in the development of oxaliplatin‐induced neurotoxicity. Muscle Nerve, 2005</description><identifier>ISSN: 0148-639X</identifier><identifier>EISSN: 1097-4598</identifier><identifier>DOI: 10.1002/mus.20340</identifier><identifier>PMID: 15880395</identifier><identifier>CODEN: MUNEDE</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult ; Adult and adolescent clinical studies ; Aged ; Antineoplastic Agents - adverse effects ; Biological and medical sciences ; Chronic Disease ; Colorectal Neoplasms - drug therapy ; Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction ; excitability ; Female ; Follow-Up Studies ; Humans ; Incidence ; Male ; Medical sciences ; Middle Aged ; Motor Neurons - physiology ; Nervous system (semeiology, syndromes) ; Neural Conduction ; Neurology ; Neurons, Afferent - physiology ; neurotoxicity ; Organoplatinum Compounds - adverse effects ; oxaliplatin ; Peripheral Nervous System Diseases - chemically induced ; Peripheral Nervous System Diseases - diagnosis ; Peripheral Nervous System Diseases - epidemiology ; Peripheral Nervous System Diseases - physiopathology ; peripheral neuropathy ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Psychoses ; Referral and Consultation ; Schizophrenia</subject><ispartof>Muscle & nerve, 2005-07, Vol.32 (1), p.51-60</ispartof><rights>Copyright © 2005 Wiley Periodicals, Inc.</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4820-cb8c50cbe1244c046be8489b40f3937f3c17221a1e3fdc6d3d2333440fa776953</citedby><cites>FETCH-LOGICAL-c4820-cb8c50cbe1244c046be8489b40f3937f3c17221a1e3fdc6d3d2333440fa776953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmus.20340$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmus.20340$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16888290$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15880395$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Krishnan, Arun V.</creatorcontrib><creatorcontrib>Goldstein, David</creatorcontrib><creatorcontrib>Friedlander, Michael</creatorcontrib><creatorcontrib>Kiernan, Matthew C.</creatorcontrib><title>Oxaliplatin-induced neurotoxicity and the development of neuropathy</title><title>Muscle & nerve</title><addtitle>Muscle Nerve</addtitle><description>The pathophysiology of oxaliplatin‐induced neurotoxicity remains unclear, although in vitro studies suggest involvement of voltage‐gated Na+ channels. In the present study, clinical assessment was combined with nerve conduction studies (NCS) and nerve excitability studies in 16 patients after completion of oxaliplatin therapy. Chronic neuropathic symptoms persisted in 50% of patients. NCS confirmed abnormalities in symptomatic patients: sensory potentials were significantly low, whereas motor studies remained essentially normal. At 12‐month follow‐up of symptomatic patients, positive sensory symptoms improved but NCS abnormalities persisted. Cumulative oxaliplatin dose was a predictor of neuropathy, and long‐term effects appeared to be minimized by low single‐infusion dosages. Nerve excitability measures in symptomatic patients established that axons were of high threshold. Refractoriness was significantly greater in patients (symptomatic group, 56.3 ± 24.9%; entire patient group, 46.3 ± 12.5%; controls, 27.1 ± 1.9%; P < 0.05). Thus, although positive sensory symptoms of oxaliplatin‐induced neuropathy improved, negative sensory symptoms and abnormalities of sensory nerve conduction persisted. Differences in nerve excitability measures, particularly refractoriness, support in vitro studies indicating involvement of voltage‐gated transient Na+‐channel dysfunction in the development of oxaliplatin‐induced neurotoxicity. Muscle Nerve, 2005</description><subject>Adult</subject><subject>Adult and adolescent clinical studies</subject><subject>Aged</subject><subject>Antineoplastic Agents - adverse effects</subject><subject>Biological and medical sciences</subject><subject>Chronic Disease</subject><subject>Colorectal Neoplasms - drug therapy</subject><subject>Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction</subject><subject>excitability</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Humans</subject><subject>Incidence</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Motor Neurons - physiology</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neural Conduction</subject><subject>Neurology</subject><subject>Neurons, Afferent - physiology</subject><subject>neurotoxicity</subject><subject>Organoplatinum Compounds - adverse effects</subject><subject>oxaliplatin</subject><subject>Peripheral Nervous System Diseases - chemically induced</subject><subject>Peripheral Nervous System Diseases - diagnosis</subject><subject>Peripheral Nervous System Diseases - epidemiology</subject><subject>Peripheral Nervous System Diseases - physiopathology</subject><subject>peripheral neuropathy</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Psychoses</subject><subject>Referral and Consultation</subject><subject>Schizophrenia</subject><issn>0148-639X</issn><issn>1097-4598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10DtPwzAQB3ALgWgpDHwBlIWBIa1fSewRIiiPQsWjopvlOI5qyEtxAs23JyUFJqYb7nd3uj8AxwiOEYR4kjV2jCGhcAcMEeSBSz3OdsEQIspcn_DlABxY-wYhRMwP9sEAeYxBwr0hCOdrmZoylbXJXZPHjdKxk-umKupibZSpW0fmsVOvtBPrD50WZabz2imSHpWyXrWHYC-RqdVH2zoCi6vLl_Danc2nN-H5zFWUYeiqiCkPqkgjTKmC1I80o4xHFCaEkyAhCgUYI4k0SWLlxyTGhBDatWUQ-NwjI3DW71VVYW2lE1FWJpNVKxAUmyBEF4T4DqKzJ70tmyjT8Z_cft6B0y2QVsk0qWSujP1zPmMM882iSe8-Tarb_y-K-8Xzz2m3nzC21uvfCVm9Cz8ggSdeH6bi9vEpXF6wOxGSL0fBhD0</recordid><startdate>200507</startdate><enddate>200507</enddate><creator>Krishnan, Arun V.</creator><creator>Goldstein, David</creator><creator>Friedlander, Michael</creator><creator>Kiernan, Matthew C.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>200507</creationdate><title>Oxaliplatin-induced neurotoxicity and the development of neuropathy</title><author>Krishnan, Arun V. ; Goldstein, David ; Friedlander, Michael ; Kiernan, Matthew C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4820-cb8c50cbe1244c046be8489b40f3937f3c17221a1e3fdc6d3d2333440fa776953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adult</topic><topic>Adult and adolescent clinical studies</topic><topic>Aged</topic><topic>Antineoplastic Agents - adverse effects</topic><topic>Biological and medical sciences</topic><topic>Chronic Disease</topic><topic>Colorectal Neoplasms - drug therapy</topic><topic>Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction</topic><topic>excitability</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Humans</topic><topic>Incidence</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Motor Neurons - physiology</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neural Conduction</topic><topic>Neurology</topic><topic>Neurons, Afferent - physiology</topic><topic>neurotoxicity</topic><topic>Organoplatinum Compounds - adverse effects</topic><topic>oxaliplatin</topic><topic>Peripheral Nervous System Diseases - chemically induced</topic><topic>Peripheral Nervous System Diseases - diagnosis</topic><topic>Peripheral Nervous System Diseases - epidemiology</topic><topic>Peripheral Nervous System Diseases - physiopathology</topic><topic>peripheral neuropathy</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Psychoses</topic><topic>Referral and Consultation</topic><topic>Schizophrenia</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Krishnan, Arun V.</creatorcontrib><creatorcontrib>Goldstein, David</creatorcontrib><creatorcontrib>Friedlander, Michael</creatorcontrib><creatorcontrib>Kiernan, Matthew C.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Muscle & nerve</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Krishnan, Arun V.</au><au>Goldstein, David</au><au>Friedlander, Michael</au><au>Kiernan, Matthew C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxaliplatin-induced neurotoxicity and the development of neuropathy</atitle><jtitle>Muscle & nerve</jtitle><addtitle>Muscle Nerve</addtitle><date>2005-07</date><risdate>2005</risdate><volume>32</volume><issue>1</issue><spage>51</spage><epage>60</epage><pages>51-60</pages><issn>0148-639X</issn><eissn>1097-4598</eissn><coden>MUNEDE</coden><abstract>The pathophysiology of oxaliplatin‐induced neurotoxicity remains unclear, although in vitro studies suggest involvement of voltage‐gated Na+ channels. In the present study, clinical assessment was combined with nerve conduction studies (NCS) and nerve excitability studies in 16 patients after completion of oxaliplatin therapy. Chronic neuropathic symptoms persisted in 50% of patients. NCS confirmed abnormalities in symptomatic patients: sensory potentials were significantly low, whereas motor studies remained essentially normal. At 12‐month follow‐up of symptomatic patients, positive sensory symptoms improved but NCS abnormalities persisted. Cumulative oxaliplatin dose was a predictor of neuropathy, and long‐term effects appeared to be minimized by low single‐infusion dosages. Nerve excitability measures in symptomatic patients established that axons were of high threshold. Refractoriness was significantly greater in patients (symptomatic group, 56.3 ± 24.9%; entire patient group, 46.3 ± 12.5%; controls, 27.1 ± 1.9%; P < 0.05). Thus, although positive sensory symptoms of oxaliplatin‐induced neuropathy improved, negative sensory symptoms and abnormalities of sensory nerve conduction persisted. Differences in nerve excitability measures, particularly refractoriness, support in vitro studies indicating involvement of voltage‐gated transient Na+‐channel dysfunction in the development of oxaliplatin‐induced neurotoxicity. Muscle Nerve, 2005</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>15880395</pmid><doi>10.1002/mus.20340</doi><tpages>10</tpages></addata></record> |
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| subjects | Adult Adult and adolescent clinical studies Aged Antineoplastic Agents - adverse effects Biological and medical sciences Chronic Disease Colorectal Neoplasms - drug therapy Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction excitability Female Follow-Up Studies Humans Incidence Male Medical sciences Middle Aged Motor Neurons - physiology Nervous system (semeiology, syndromes) Neural Conduction Neurology Neurons, Afferent - physiology neurotoxicity Organoplatinum Compounds - adverse effects oxaliplatin Peripheral Nervous System Diseases - chemically induced Peripheral Nervous System Diseases - diagnosis Peripheral Nervous System Diseases - epidemiology Peripheral Nervous System Diseases - physiopathology peripheral neuropathy Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychoses Referral and Consultation Schizophrenia |
| title | Oxaliplatin-induced neurotoxicity and the development of neuropathy |
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