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==Other Diagnostic Studies== | ==Other Diagnostic Studies== | ||
Other diagnostic studies for Multiple sclerosis disease include: | |||
Delay in response after stimulation of [[retina]] with light is an indicator of a problem in visual tracts due to [[Axonal|axona]]<nowiki/>l [[demyelination]].<ref name="pmid18825673">{{cite journal |vauthors=Klistorner A, Arvind H, Nguyen T, Garrick R, Paine M, Graham S, O'Day J, Grigg J, Billson F, Yiannikas C |title=Axonal loss and myelin in early ON loss in postacute optic neuritis |journal=Ann. Neurol. |volume=64 |issue=3 |pages=325–31 |date=September 2008 |pmid=18825673 |doi=10.1002/ana.21474 |url=}}</ref> The indication of this test is when patient is not fulfilling MS criteria and is a probable MS case.<ref name="pmid3070342">{{cite journal |vauthors=Chiappa KH |title=Use of evoked potentials for diagnosis of multiple sclerosis |journal=Neurol Clin |volume=6 |issue=4 |pages=861–80 |date=November 1988 |pmid=3070342 |doi= |url=}}</ref><ref name="pmid7077339">{{cite journal |vauthors=Matthews WB, Wattam-Bell JR, Pountney E |title=Evoked potentials in the diagnosis of multiple sclerosis: a follow up study |journal=J. Neurol. Neurosurg. Psychiatry |volume=45 |issue=4 |pages=303–7 |date=April 1982 |pmid=7077339 |pmc=491364 |doi= |url=}}</ref> | * Visual evoked potential studies | ||
Delay in response after stimulation of [[retina]] with light is an indicator of a problem in visual tracts due to [[Axonal|axona]]<nowiki/>l [[demyelination]].<ref name="pmid18825673">{{cite journal |vauthors=Klistorner A, Arvind H, Nguyen T, Garrick R, Paine M, Graham S, O'Day J, Grigg J, Billson F, Yiannikas C |title=Axonal loss and myelin in early ON loss in postacute optic neuritis |journal=Ann. Neurol. |volume=64 |issue=3 |pages=325–31 |date=September 2008 |pmid=18825673 |doi=10.1002/ana.21474 |url=}}</ref> The indication of this test is when patient is not fulfilling MS criteria and is a probable MS case.<ref name="pmid3070342">{{cite journal |vauthors=Chiappa KH |title=Use of evoked potentials for diagnosis of multiple sclerosis |journal=Neurol Clin |volume=6 |issue=4 |pages=861–80 |date=November 1988 |pmid=3070342 |doi= |url=}}</ref><ref name="pmid7077339">{{cite journal |vauthors=Matthews WB, Wattam-Bell JR, Pountney E |title=Evoked potentials in the diagnosis of multiple sclerosis: a follow up study |journal=J. Neurol. Neurosurg. Psychiatry |volume=45 |issue=4 |pages=303–7 |date=April 1982 |pmid=7077339 |pmc=491364 |doi= |url=}}</ref> | |||
* Antimyelin antibodies | |||
[[myelin oligodendrocyte glycoprotein]] ([[Myelin oligodendrocyte glycoprotein|MOG]]) and [[myelin basic protein]] ([[Myelin basic protein|MBP]]), thought to be a predictor of [[disease]] progression, but some studies denied any relationship between these auto [[antibodies]] and [[disease]] severity or progression.<ref name="pmid12853586">{{cite journal |vauthors=Berger T, Rubner P, Schautzer F, Egg R, Ulmer H, Mayringer I, Dilitz E, Deisenhammer F, Reindl M |title=Antimyelin antibodies as a predictor of clinically definite multiple sclerosis after a first demyelinating event |journal=N. Engl. J. Med. |volume=349 |issue=2 |pages=139–45 |date=July 2003 |pmid=12853586 |doi=10.1056/NEJMoa022328 |url=}}</ref><ref name="pmid15623705">{{cite journal |vauthors=Gaertner S, de Graaf KL, Greve B, Weissert R |title=Antibodies against glycosylated native MOG are elevated in patients with multiple sclerosis |journal=Neurology |volume=63 |issue=12 |pages=2381–3 |date=December 2004 |pmid=15623705 |doi= |url=}}</ref><ref name="pmid17251533">{{cite journal |vauthors=Kuhle J, Pohl C, Mehling M, Edan G, Freedman MS, Hartung HP, Polman CH, Miller DH, Montalban X, Barkhof F, Bauer L, Dahms S, Lindberg R, Kappos L, Sandbrink R |title=Lack of association between antimyelin antibodies and progression to multiple sclerosis |journal=N. Engl. J. Med. |volume=356 |issue=4 |pages=371–8 |date=January 2007 |pmid=17251533 |doi=10.1056/NEJMoa063602 |url=}}</ref><ref name="pmid15184621">{{cite journal |vauthors=Lampasona V, Franciotta D, Furlan R, Zanaboni S, Fazio R, Bonifacio E, Comi G, Martino G |title=Similar low frequency of anti-MOG IgG and IgM in MS patients and healthy subjects |journal=Neurology |volume=62 |issue=11 |pages=2092–4 |date=June 2004 |pmid=15184621 |doi= |url=}}</ref> | [[myelin oligodendrocyte glycoprotein]] ([[Myelin oligodendrocyte glycoprotein|MOG]]) and [[myelin basic protein]] ([[Myelin basic protein|MBP]]), thought to be a predictor of [[disease]] progression, but some studies denied any relationship between these auto [[antibodies]] and [[disease]] severity or progression.<ref name="pmid12853586">{{cite journal |vauthors=Berger T, Rubner P, Schautzer F, Egg R, Ulmer H, Mayringer I, Dilitz E, Deisenhammer F, Reindl M |title=Antimyelin antibodies as a predictor of clinically definite multiple sclerosis after a first demyelinating event |journal=N. Engl. J. Med. |volume=349 |issue=2 |pages=139–45 |date=July 2003 |pmid=12853586 |doi=10.1056/NEJMoa022328 |url=}}</ref><ref name="pmid15623705">{{cite journal |vauthors=Gaertner S, de Graaf KL, Greve B, Weissert R |title=Antibodies against glycosylated native MOG are elevated in patients with multiple sclerosis |journal=Neurology |volume=63 |issue=12 |pages=2381–3 |date=December 2004 |pmid=15623705 |doi= |url=}}</ref><ref name="pmid17251533">{{cite journal |vauthors=Kuhle J, Pohl C, Mehling M, Edan G, Freedman MS, Hartung HP, Polman CH, Miller DH, Montalban X, Barkhof F, Bauer L, Dahms S, Lindberg R, Kappos L, Sandbrink R |title=Lack of association between antimyelin antibodies and progression to multiple sclerosis |journal=N. Engl. J. Med. |volume=356 |issue=4 |pages=371–8 |date=January 2007 |pmid=17251533 |doi=10.1056/NEJMoa063602 |url=}}</ref><ref name="pmid15184621">{{cite journal |vauthors=Lampasona V, Franciotta D, Furlan R, Zanaboni S, Fazio R, Bonifacio E, Comi G, Martino G |title=Similar low frequency of anti-MOG IgG and IgM in MS patients and healthy subjects |journal=Neurology |volume=62 |issue=11 |pages=2092–4 |date=June 2004 |pmid=15184621 |doi= |url=}}</ref> | ||
* Optimal coherence tomography | |||
Optimal coherence tomography of the retina can be helpful in [[diagnosis]] of multiple sclerosis.<ref name="pmid17987252">{{cite journal |vauthors=Albrecht P, Fröhlich R, Hartung HP, Kieseier BC, Methner A |title=Optical coherence tomography measures axonal loss in multiple sclerosis independently of optic neuritis |journal=J. Neurol. |volume=254 |issue=11 |pages=1595–6 |date=November 2007 |pmid=17987252 |doi=10.1007/s00415-007-0538-3 |url=}}</ref> | Optimal coherence tomography of the retina can be helpful in [[diagnosis]] of multiple sclerosis.<ref name="pmid17987252">{{cite journal |vauthors=Albrecht P, Fröhlich R, Hartung HP, Kieseier BC, Methner A |title=Optical coherence tomography measures axonal loss in multiple sclerosis independently of optic neuritis |journal=J. Neurol. |volume=254 |issue=11 |pages=1595–6 |date=November 2007 |pmid=17987252 |doi=10.1007/s00415-007-0538-3 |url=}}</ref> | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Irfan Dotani
Overview
visual evoked potential studies and antimyelin antibodies may be helpful in the diagnosis of multiple sclerosis.
Other Diagnostic Studies
Other diagnostic studies for Multiple sclerosis disease include:
- Visual evoked potential studies
Delay in response after stimulation of retina with light is an indicator of a problem in visual tracts due to axonal demyelination.[1] The indication of this test is when patient is not fulfilling MS criteria and is a probable MS case.[2][3]
- Antimyelin antibodies
myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP), thought to be a predictor of disease progression, but some studies denied any relationship between these auto antibodies and disease severity or progression.[4][5][6][7]
- Optimal coherence tomography
Optimal coherence tomography of the retina can be helpful in diagnosis of multiple sclerosis.[8]
References
- ↑ Klistorner A, Arvind H, Nguyen T, Garrick R, Paine M, Graham S, O'Day J, Grigg J, Billson F, Yiannikas C (September 2008). "Axonal loss and myelin in early ON loss in postacute optic neuritis". Ann. Neurol. 64 (3): 325–31. doi:10.1002/ana.21474. PMID 18825673.
- ↑ Chiappa KH (November 1988). "Use of evoked potentials for diagnosis of multiple sclerosis". Neurol Clin. 6 (4): 861–80. PMID 3070342.
- ↑ Matthews WB, Wattam-Bell JR, Pountney E (April 1982). "Evoked potentials in the diagnosis of multiple sclerosis: a follow up study". J. Neurol. Neurosurg. Psychiatry. 45 (4): 303–7. PMC 491364. PMID 7077339.
- ↑ Berger T, Rubner P, Schautzer F, Egg R, Ulmer H, Mayringer I, Dilitz E, Deisenhammer F, Reindl M (July 2003). "Antimyelin antibodies as a predictor of clinically definite multiple sclerosis after a first demyelinating event". N. Engl. J. Med. 349 (2): 139–45. doi:10.1056/NEJMoa022328. PMID 12853586.
- ↑ Gaertner S, de Graaf KL, Greve B, Weissert R (December 2004). "Antibodies against glycosylated native MOG are elevated in patients with multiple sclerosis". Neurology. 63 (12): 2381–3. PMID 15623705.
- ↑ Kuhle J, Pohl C, Mehling M, Edan G, Freedman MS, Hartung HP, Polman CH, Miller DH, Montalban X, Barkhof F, Bauer L, Dahms S, Lindberg R, Kappos L, Sandbrink R (January 2007). "Lack of association between antimyelin antibodies and progression to multiple sclerosis". N. Engl. J. Med. 356 (4): 371–8. doi:10.1056/NEJMoa063602. PMID 17251533.
- ↑ Lampasona V, Franciotta D, Furlan R, Zanaboni S, Fazio R, Bonifacio E, Comi G, Martino G (June 2004). "Similar low frequency of anti-MOG IgG and IgM in MS patients and healthy subjects". Neurology. 62 (11): 2092–4. PMID 15184621.
- ↑ Albrecht P, Fröhlich R, Hartung HP, Kieseier BC, Methner A (November 2007). "Optical coherence tomography measures axonal loss in multiple sclerosis independently of optic neuritis". J. Neurol. 254 (11): 1595–6. doi:10.1007/s00415-007-0538-3. PMID 17987252.