Axonal Guillain-Barré syndrome
The issue of “axonal” Guillain–Barré syndrome (GBS) remains controversial. Supportive evidence comes from pathological examination of peripheral nerves in 4 extreme cases of GBS 17–29 days after onset which showed severe axonal degeneration without inflammatory‐demyelination. It has been suggested t...
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| Veröffentlicht in: | Muscle & nerve 1994-06, Vol.17 (6), p.678-679 |
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| creator | Feasby, Thomas E. |
| description | The issue of “axonal” Guillain–Barré syndrome (GBS) remains controversial. Supportive evidence comes from pathological examination of peripheral nerves in 4 extreme cases of GBS 17–29 days after onset which showed severe axonal degeneration without inflammatory‐demyelination. It has been suggested that inflammatory‐demyelination may have been missed. This is difficult to disprove but it seems unlikely, given the known correlation between the severity of axonal degeneration and inflammation/demyelination in the experimental model of GBS, experimental allergic neuritis (EAN). Electrically inexcitable nerves in GBS may reflect axonal degeneration, terminal demyelination or both. This finding proved to be a sign of poor prognosis in 19 of 27 (70%) patients, although a good outcome occurred in some cases. © 1994 John Wiley & Sons, Inc. |
| doi_str_mv | 10.1002/mus.880170618 |
| format | Article |
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Supportive evidence comes from pathological examination of peripheral nerves in 4 extreme cases of GBS 17–29 days after onset which showed severe axonal degeneration without inflammatory‐demyelination. It has been suggested that inflammatory‐demyelination may have been missed. This is difficult to disprove but it seems unlikely, given the known correlation between the severity of axonal degeneration and inflammation/demyelination in the experimental model of GBS, experimental allergic neuritis (EAN). Electrically inexcitable nerves in GBS may reflect axonal degeneration, terminal demyelination or both. 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Supportive evidence comes from pathological examination of peripheral nerves in 4 extreme cases of GBS 17–29 days after onset which showed severe axonal degeneration without inflammatory‐demyelination. It has been suggested that inflammatory‐demyelination may have been missed. This is difficult to disprove but it seems unlikely, given the known correlation between the severity of axonal degeneration and inflammation/demyelination in the experimental model of GBS, experimental allergic neuritis (EAN). Electrically inexcitable nerves in GBS may reflect axonal degeneration, terminal demyelination or both. This finding proved to be a sign of poor prognosis in 19 of 27 (70%) patients, although a good outcome occurred in some cases. © 1994 John Wiley & Sons, Inc.</description><subject>axonal degeneration</subject><subject>Axons - ultrastructure</subject><subject>Biological and medical sciences</subject><subject>demyelination</subject><subject>Electrophysiology</subject><subject>Guillain-Barré syndrome</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</subject><subject>Nerve Degeneration</subject><subject>Neurology</subject><subject>Polyradiculoneuropathy - pathology</subject><subject>Polyradiculoneuropathy - physiopathology</subject><subject>Prognosis</subject><issn>0148-639X</issn><issn>1097-4598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kDtPwzAUhS0EKqUwMiIYEFuKX_FjLBUtSKUMtKKb5TiOFMij2I1ofxK_gz-GUaOIiekO57vnnnsAOEdwiCDEt2Xjh0JAxCFD4gD0EZQ8orEUh6APERURI3J1DE68f4MQIsF4D_QEkowj3AeXo21d6eJq2uRFofMqutPOfX9d-V2Vurq0p-Ao04W3Z-0cgOXkfjF-iGbP08fxaBYZSrCIMDGxTFBCWWKRTAUzDHMhLeRSxnGCMLaYGU4FDkLCYaYx0zK2JJNCilSSAbjZ-65d_dFYv1Fl7o0NmSpbN15xFiNEOQ1gtAeNq713NlNrl5fa7RSC6rcQFQpRXSGBv2iNm6S0aUe3DQT9utW1N7rInK5M7juMovACJQHje-wzL-zu_5vqafnyN0AbOPcbu-02tXtXjBMeq9f5VC3oRLD5PFYr8gOttoX_</recordid><startdate>199406</startdate><enddate>199406</enddate><creator>Feasby, Thomas E.</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><scope>7X8</scope></search><sort><creationdate>199406</creationdate><title>Axonal Guillain-Barré syndrome</title><author>Feasby, Thomas E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4328-23c59b1b46be19d86c62789e079955b122e26c7482c62b70fa26a95e3f9898d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>axonal degeneration</topic><topic>Axons - ultrastructure</topic><topic>Biological and medical sciences</topic><topic>demyelination</topic><topic>Electrophysiology</topic><topic>Guillain-Barré syndrome</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</topic><topic>Nerve Degeneration</topic><topic>Neurology</topic><topic>Polyradiculoneuropathy - pathology</topic><topic>Polyradiculoneuropathy - physiopathology</topic><topic>Prognosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Feasby, Thomas E.</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><collection>MEDLINE - Academic</collection><jtitle>Muscle & nerve</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Feasby, Thomas E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Axonal Guillain-Barré syndrome</atitle><jtitle>Muscle & nerve</jtitle><addtitle>Muscle Nerve</addtitle><date>1994-06</date><risdate>1994</risdate><volume>17</volume><issue>6</issue><spage>678</spage><epage>679</epage><pages>678-679</pages><issn>0148-639X</issn><eissn>1097-4598</eissn><coden>MUNEDE</coden><abstract>The issue of “axonal” Guillain–Barré syndrome (GBS) remains controversial. Supportive evidence comes from pathological examination of peripheral nerves in 4 extreme cases of GBS 17–29 days after onset which showed severe axonal degeneration without inflammatory‐demyelination. It has been suggested that inflammatory‐demyelination may have been missed. This is difficult to disprove but it seems unlikely, given the known correlation between the severity of axonal degeneration and inflammation/demyelination in the experimental model of GBS, experimental allergic neuritis (EAN). Electrically inexcitable nerves in GBS may reflect axonal degeneration, terminal demyelination or both. This finding proved to be a sign of poor prognosis in 19 of 27 (70%) patients, although a good outcome occurred in some cases. © 1994 John Wiley & Sons, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>8196712</pmid><doi>10.1002/mus.880170618</doi><tpages>2</tpages></addata></record> |
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| identifier | ISSN: 0148-639X |
| ispartof | Muscle & nerve, 1994-06, Vol.17 (6), p.678-679 |
| issn | 0148-639X 1097-4598 |
| language | eng |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | axonal degeneration Axons - ultrastructure Biological and medical sciences demyelination Electrophysiology Guillain-Barré syndrome Humans Medical sciences Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis Nerve Degeneration Neurology Polyradiculoneuropathy - pathology Polyradiculoneuropathy - physiopathology Prognosis |
| title | Axonal Guillain-Barré syndrome |
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