Quantitative electrophysiological study of alcoholic neuropathy
Thirty-one chronic alcoholic patients were investigated using quantitative electrophysiological techniques. Estimates of the numbers of functioning motor units in the extensor digitorum brevis muscles and measurements of the parameters of the potentials of these units are presented along with the va...
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| Veröffentlicht in: | Journal of neurology, neurosurgery and psychiatry neurosurgery and psychiatry, 1980-05, Vol.43 (5), p.427-432 |
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| container_title | Journal of neurology, neurosurgery and psychiatry |
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| creator | Ballantyne, J P Hansen, S Weir, A Whitehead, J R Mullin, P J |
| description | Thirty-one chronic alcoholic patients were investigated using quantitative electrophysiological techniques. Estimates of the numbers of functioning motor units in the extensor digitorum brevis muscles and measurements of the parameters of the potentials of these units are presented along with the values for motor nerve conduction velocities in the innervating lateral popliteal nerves. Motor conduction velocities and sensory nerve action potential amplitudes were also measured in the ulnar nerves. The results and their inter-relationships lead us to conclude that the slowing of motor nerve conduction and reduction in sensory nerve action potential amplitudes in alcoholic neuropathy are a consequence of axon loss. We found no evidence of pathological slowing of conduction in surviving axons. Reinnervation by functioning motor axons is poor compared to a number of other neuropathic conditions. In our patients there was no evidence of preferential involvement of sensory axons. The results support a predominant axonal dysfunction in alcoholic neuropathy. |
| doi_str_mv | 10.1136/jnnp.43.5.427 |
| format | Article |
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Estimates of the numbers of functioning motor units in the extensor digitorum brevis muscles and measurements of the parameters of the potentials of these units are presented along with the values for motor nerve conduction velocities in the innervating lateral popliteal nerves. Motor conduction velocities and sensory nerve action potential amplitudes were also measured in the ulnar nerves. The results and their inter-relationships lead us to conclude that the slowing of motor nerve conduction and reduction in sensory nerve action potential amplitudes in alcoholic neuropathy are a consequence of axon loss. We found no evidence of pathological slowing of conduction in surviving axons. Reinnervation by functioning motor axons is poor compared to a number of other neuropathic conditions. In our patients there was no evidence of preferential involvement of sensory axons. The results support a predominant axonal dysfunction in alcoholic neuropathy.</description><identifier>ISSN: 0022-3050</identifier><identifier>EISSN: 1468-330X</identifier><identifier>DOI: 10.1136/jnnp.43.5.427</identifier><identifier>PMID: 7420094</identifier><identifier>CODEN: JNNPAU</identifier><language>eng</language><publisher>England: BMJ Publishing Group Ltd</publisher><subject>Action Potentials ; Alcoholism - complications ; Alcoholism - physiopathology ; Axons - physiology ; Electrophysiology ; Evoked Potentials ; Humans ; Middle Aged ; Motor Neurons - physiology ; Muscles - innervation ; Nerve Regeneration ; Nervous System Diseases - etiology ; Nervous System Diseases - physiopathology ; Neural Conduction ; Reaction Time ; Ulnar Nerve - physiopathology</subject><ispartof>Journal of neurology, neurosurgery and psychiatry, 1980-05, Vol.43 (5), p.427-432</ispartof><rights>Copyright BMJ Publishing Group LTD May 1980</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b3957-75a0fad96172abf0ff93dc5d75cfa4f8e94f32289fe60af499543817b98ac6f23</citedby><cites>FETCH-LOGICAL-b3957-75a0fad96172abf0ff93dc5d75cfa4f8e94f32289fe60af499543817b98ac6f23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC490570/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC490570/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7420094$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ballantyne, J P</creatorcontrib><creatorcontrib>Hansen, S</creatorcontrib><creatorcontrib>Weir, A</creatorcontrib><creatorcontrib>Whitehead, J R</creatorcontrib><creatorcontrib>Mullin, P J</creatorcontrib><title>Quantitative electrophysiological study of alcoholic neuropathy</title><title>Journal of neurology, neurosurgery and psychiatry</title><addtitle>J Neurol Neurosurg Psychiatry</addtitle><description>Thirty-one chronic alcoholic patients were investigated using quantitative electrophysiological techniques. Estimates of the numbers of functioning motor units in the extensor digitorum brevis muscles and measurements of the parameters of the potentials of these units are presented along with the values for motor nerve conduction velocities in the innervating lateral popliteal nerves. Motor conduction velocities and sensory nerve action potential amplitudes were also measured in the ulnar nerves. The results and their inter-relationships lead us to conclude that the slowing of motor nerve conduction and reduction in sensory nerve action potential amplitudes in alcoholic neuropathy are a consequence of axon loss. We found no evidence of pathological slowing of conduction in surviving axons. Reinnervation by functioning motor axons is poor compared to a number of other neuropathic conditions. In our patients there was no evidence of preferential involvement of sensory axons. The results support a predominant axonal dysfunction in alcoholic neuropathy.</description><subject>Action Potentials</subject><subject>Alcoholism - complications</subject><subject>Alcoholism - physiopathology</subject><subject>Axons - physiology</subject><subject>Electrophysiology</subject><subject>Evoked Potentials</subject><subject>Humans</subject><subject>Middle Aged</subject><subject>Motor Neurons - physiology</subject><subject>Muscles - innervation</subject><subject>Nerve Regeneration</subject><subject>Nervous System Diseases - etiology</subject><subject>Nervous System Diseases - physiopathology</subject><subject>Neural Conduction</subject><subject>Reaction Time</subject><subject>Ulnar Nerve - physiopathology</subject><issn>0022-3050</issn><issn>1468-330X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1980</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkEtv1DAUhS1UVKYDS5ZIkbphk-D4EccLhGDaaZFGIJ5iZzmO3Thk4mA7o-bfk9GMBrrq3dzF-e45VweAlznM8hwXb9q-HzKCM5oRxJ6ARU6KMsUY_joDCwgRSjGk8Bm4CKGF-yn5OThnBEHIyQK8-zLKPtooo93pRHdaRe-GZgrWde7OKtklIY71lDiTyE65xnVWJb0eZ0rGZnoOnhrZBf3iuJfgx_r6--o23Xy--bh6v0krzClLGZXQyJoXOUOyMtAYjmtFa0aVkcSUmhODESq50QWUhnBOCS5zVvFSqsIgvARvD77DWG11rXQfvezE4O1W-kk4acVDpbeNuHM7QTikDM73l8d77_6MOkTRutH388siZwyVc1qBZyo9UMq7ELw2p4Acin3bYt-2IFhQMbc986_-_-pEH-v952dD1PcnWfrfomCYUfHp50p8-Hq1Ljbrb4LP_OsDX23bR6L_AtD-me8</recordid><startdate>19800501</startdate><enddate>19800501</enddate><creator>Ballantyne, J P</creator><creator>Hansen, S</creator><creator>Weir, A</creator><creator>Whitehead, J R</creator><creator>Mullin, P J</creator><general>BMJ Publishing Group Ltd</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</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><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>19800501</creationdate><title>Quantitative electrophysiological study of alcoholic neuropathy</title><author>Ballantyne, J P ; Hansen, S ; Weir, A ; Whitehead, J R ; Mullin, P J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b3957-75a0fad96172abf0ff93dc5d75cfa4f8e94f32289fe60af499543817b98ac6f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1980</creationdate><topic>Action Potentials</topic><topic>Alcoholism - complications</topic><topic>Alcoholism - physiopathology</topic><topic>Axons - physiology</topic><topic>Electrophysiology</topic><topic>Evoked Potentials</topic><topic>Humans</topic><topic>Middle Aged</topic><topic>Motor Neurons - physiology</topic><topic>Muscles - innervation</topic><topic>Nerve Regeneration</topic><topic>Nervous System Diseases - etiology</topic><topic>Nervous System Diseases - physiopathology</topic><topic>Neural Conduction</topic><topic>Reaction Time</topic><topic>Ulnar Nerve - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ballantyne, J P</creatorcontrib><creatorcontrib>Hansen, S</creatorcontrib><creatorcontrib>Weir, A</creatorcontrib><creatorcontrib>Whitehead, J R</creatorcontrib><creatorcontrib>Mullin, P J</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neurology, neurosurgery and psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ballantyne, J P</au><au>Hansen, S</au><au>Weir, A</au><au>Whitehead, J R</au><au>Mullin, P J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Quantitative electrophysiological study of alcoholic neuropathy</atitle><jtitle>Journal of neurology, neurosurgery and psychiatry</jtitle><addtitle>J Neurol Neurosurg Psychiatry</addtitle><date>1980-05-01</date><risdate>1980</risdate><volume>43</volume><issue>5</issue><spage>427</spage><epage>432</epage><pages>427-432</pages><issn>0022-3050</issn><eissn>1468-330X</eissn><coden>JNNPAU</coden><abstract>Thirty-one chronic alcoholic patients were investigated using quantitative electrophysiological techniques. 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The results support a predominant axonal dysfunction in alcoholic neuropathy.</abstract><cop>England</cop><pub>BMJ Publishing Group Ltd</pub><pmid>7420094</pmid><doi>10.1136/jnnp.43.5.427</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of neurology, neurosurgery and psychiatry, 1980-05, Vol.43 (5), p.427-432 |
| issn | 0022-3050 1468-330X |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Action Potentials Alcoholism - complications Alcoholism - physiopathology Axons - physiology Electrophysiology Evoked Potentials Humans Middle Aged Motor Neurons - physiology Muscles - innervation Nerve Regeneration Nervous System Diseases - etiology Nervous System Diseases - physiopathology Neural Conduction Reaction Time Ulnar Nerve - physiopathology |
| title | Quantitative electrophysiological study of alcoholic neuropathy |
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