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Cited by 4,649Multiple Sclerosis Research StudiesPeripheral Neuropathies and DisordersOcular Diseases and Behçet’s Syndrome

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International consensus diagnostic criteria for neuromyelitis optica spectrum disorders

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Wingerchuk, Dean M., Banwell, Brenda, Bennett, Jeffrey L., Cabre, Philippe, Carroll, William, Chitnis, Tanuja, de Seze, Jérôme, Fujihara, Kazuo, Greenberg, Benjamin, Jacob, Anu, Jarius, Sven, Lana-Peixoto, Marco, Levy, Michael, Simon, Jack H., Tenembaum, Silvia, Traboulsee, Anthony L., Waters, Patrick, Wellik, Kay E., Weinshenker, Brian G.·2015·Neurology
DOI 10.1212/wnl.0000000000001729PMC PMC4515040
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Abstract

Neuromyelitis optica (NMO) is an inflammatory CNS syndrome distinct from multiple sclerosis (MS) that is associated with serum aquaporin-4 immunoglobulin G antibodies (AQP4-IgG). Prior NMO diagnostic criteria required optic nerve and spinal cord involvement but more restricted or more extensive CNS involvement may occur. The International Panel for NMO Diagnosis (IPND) was convened to develop revised diagnostic criteria using systematic literature reviews and electronic surveys to facilitate consensus. The new nomenclature defines the unifying term NMO spectrum disorders (NMOSD), which is stratified further by serologic testing (NMOSD with or without AQP4-IgG). The core clinical characteristics required for patients with NMOSD with AQP4-IgG include clinical syndromes or MRI findings related to optic nerve, spinal cord, area postrema, other brainstem, diencephalic, or cerebral presentations. More stringent clinical criteria, with additional neuroimaging findings, are required for diagnosis of NMOSD without AQP4-IgG or when serologic testing is unavailable. The IPND also proposed validation strategies and achieved consensus on pediatric NMOSD diagnosis and the concepts of monophasic NMOSD and opticospinal MS.

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Figure 1 Spinal cord and optic nerve MRI patterns in neuromyelitis optica spectrum disorder Spinal cord imaging in the context of acute myelitis in neuromyelitis optica spectrum disorders (NMOSD) usually reveals a longitudinally extensive transverse myelitis (LETM) lesion extending over 3 or more vertebral segments. Sagittal T2-weighted MRI of the thoracic spinal cord (A) demonstrates a typical LETM lesion involving most of the thoracic spinal cord (arrows). LETM lesions have a predilection for the central cord, as shown by axial T2-weighted (B; arrowhead) and T1-weighted MRI with gadolinium (C; arrowhead). Cervical LETM may extend into the medulla, a characteristic NMOSD pattern demonstrated in D (arrows; sagittal T2-weighted MRI) and E (arrows; sagittal T1-weighted MRI with gadolinium). Acute LETM lesions can be associated with intralesional hypointensity as shown by sagittal T1-weighted MRI (F; arrow); in this example, a rim of gadolinium enhancement surrounds the hypointense region. Chronic sequelae of LETM may include longitudinally extensive segments of spinal cord atrophy as shown by T2-weighted MRI using sagittal (G; the 2 arrowheads indicate the atrophic segment and the top arrow indicates the normal diameter of unaffected cervical spinal cord) and axial planes (H; arrowhead shows an atrophic spinal cord). Fast spin echo fat-suppressed T2-weighted MRI in the axial (I) and coronal (J) planes shows increased signal throughout most the length of the left optic nerve, especially its posterior portion (arrows). Axial T1-weighted MRI with gadolinium shows enhancement of the optic chiasm (K; arrows). These images are from 2 different patients experiencing acute optic neuritis in the setting of NMOSD.
Figure 1 Spinal cord and optic nerve MRI patterns in neuromyelitis optica spectrum disorder Spinal cord imaging in the context of acute myelitis in neuromyelitis optica spectrum disorders (NMOSD) usually reveals a longitudinally extensive transverse myelitis (LETM) lesion extending over 3 or more vertebral segments. Sagittal T2-weighted MRI of the thoracic spinal cord (A) demonstrates a typical LETM lesion involving most of the thoracic spinal cord (arrows). LETM lesions have a predilection for the central cord, as shown by axial T2-weighted (B; arrowhead) and T1-weighted MRI with gadolinium (C; arrowhead). Cervical LETM may extend into the medulla, a characteristic NMOSD pattern demonstrated in D (arrows; sagittal T2-weighted MRI) and E (arrows; sagittal T1-weighted MRI with gadolinium). Acute LETM lesions can be associated with intralesional hypointensity as shown by sagittal T1-weighted MRI (F; arrow); in this example, a rim of gadolinium enhancement surrounds the hypointense region. Chronic sequelae of LETM may include longitudinally extensive segments of spinal cord atrophy as shown by T2-weighted MRI using sagittal (G; the 2 arrowheads indicate the atrophic segment and the top arrow indicates the normal diameter of unaffected cervical spinal cord) and axial planes (H; arrowhead shows an atrophic spinal cord). Fast spin echo fat-suppressed T2-weighted MRI in the axial (I) and coronal (J) planes shows increased signal throughout most the length of the left optic nerve, especially its posterior portion (arrows). Axial T1-weighted MRI with gadolinium shows enhancement of the optic chiasm (K; arrows). These images are from 2 different patients experiencing acute optic neuritis in the setting of NMOSD.CC BY-NC-ND · PubMed Central
Figure 2 Dorsal medulla, area postrema, and other brainstem lesions in neuromyelitis optica spectrum disorder Sagittal T2-weighted fluid-attenuated inversion recovery (FLAIR) MRI shows a lesion in the dorsal medulla (A; arrow). Sagittal T2-weighted (B) and T1-weighted MRI with gadolinium (C) each demonstrate an acute lesion (arrows) associated with area postrema clinical syndrome. Axial T2-weighted FLAIR (D; arrows) and T1-weighted MRI with gadolinium (E; arrowheads) show dorsal medulla involvement in a patient with acute area postrema clinical syndrome. Axial T2-weighted FLAIR MRI shows periependymal lesions involving the pons (F; arrows) and dorsal midbrain (G; arrow). Sagittal T2-weighted FLAIR MRI shows increased signal surrounding the fourth ventricle (H; arrows).
Figure 2 Dorsal medulla, area postrema, and other brainstem lesions in neuromyelitis optica spectrum disorder Sagittal T2-weighted fluid-attenuated inversion recovery (FLAIR) MRI shows a lesion in the dorsal medulla (A; arrow). Sagittal T2-weighted (B) and T1-weighted MRI with gadolinium (C) each demonstrate an acute lesion (arrows) associated with area postrema clinical syndrome. Axial T2-weighted FLAIR (D; arrows) and T1-weighted MRI with gadolinium (E; arrowheads) show dorsal medulla involvement in a patient with acute area postrema clinical syndrome. Axial T2-weighted FLAIR MRI shows periependymal lesions involving the pons (F; arrows) and dorsal midbrain (G; arrow). Sagittal T2-weighted FLAIR MRI shows increased signal surrounding the fourth ventricle (H; arrows).CC BY-NC-ND · PubMed Central
Figure 3 Diencephalic and cerebral lesions in neuromyelitis optica spectrum disorder A variety of brain lesion patterns are associated with neuromyelitis optica spectrum disorder. Axial T2-weighted fluid-attenuated inversion recovery (FLAIR) MRI from 2 patients demonstrates lesions involving the right thalamus (A; arrow) and the hypothalamus (B; arrows). Axial T2-weighted FLAIR MRI shows an extensive subcortical white matter lesion (C; arrow) that enhances after gadolinium administration on T1-weighted sequences (D; arrow). Chronic longitudinally extensive and linear corpus callosum lesions are depicted on sagittal T2-weighted FLAIR MRI (E; arrows). Coronal T2-weighted FLAIR MRI shows longitudinal involvement of the corticospinal tract extending to the cerebral peduncle and pons (F; arrows). Acute periependymal cerebral lesions from one patient are depicted using sagittal (G; arrow) and axial (H; arrows) T2-weighted FLAIR MRI and axial T1-weighted MRI with gadolinium (I; arrows).
Figure 3 Diencephalic and cerebral lesions in neuromyelitis optica spectrum disorder A variety of brain lesion patterns are associated with neuromyelitis optica spectrum disorder. Axial T2-weighted fluid-attenuated inversion recovery (FLAIR) MRI from 2 patients demonstrates lesions involving the right thalamus (A; arrow) and the hypothalamus (B; arrows). Axial T2-weighted FLAIR MRI shows an extensive subcortical white matter lesion (C; arrow) that enhances after gadolinium administration on T1-weighted sequences (D; arrow). Chronic longitudinally extensive and linear corpus callosum lesions are depicted on sagittal T2-weighted FLAIR MRI (E; arrows). Coronal T2-weighted FLAIR MRI shows longitudinal involvement of the corticospinal tract extending to the cerebral peduncle and pons (F; arrows). Acute periependymal cerebral lesions from one patient are depicted using sagittal (G; arrow) and axial (H; arrows) T2-weighted FLAIR MRI and axial T1-weighted MRI with gadolinium (I; arrows).CC BY-NC-ND · PubMed Central

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Research works printed but not linked: 55

  1. 10.1016/S1474-4422(07)70216-8 · DOI
  2. 10.1212/01.wnl.0000216139.44259.74 · DOI
  3. 10.1186/1742-2094-10-8 · DOI
  4. 10.1212/WNL.53.5.1107 · DOI
  5. 10.1016/S0140-6736(04)17551-X · DOI · Paper page
  6. 10.1084/jem.20050304 · DOI · Paper page
  7. 10.1016/S1474-4422(12)70133-3 · DOI
  8. 10.1212/WNL.0b013e3182190f74 · DOI
  9. 10.1016/j.jns.2007.06.044 · DOI
  10. 10.1007/s00415-009-0009-0 · DOI
  11. 10.1212/WNL.26.6_Part_2.8 · DOI
  12. 10.1111/bpa.12084 · DOI
  13. 10.1212/WNL.0b013e318296ea08 · DOI
  14. 10.1016/j.msard.2012.06.002 · DOI · Paper page
  15. 10.1001/archneurol.2011.216 · DOI
  16. 10.1177/1352458511431973 · DOI
  17. 10.1177/1352458506070732 · DOI
  18. 10.1212/01.wnl.0000303817.82134.da · DOI
  19. 10.1002/ana.20770 · DOI
  20. 10.1136/jnnp-2011-300403 · DOI
  21. 10.1212/01.wnl.0000183151.19351.82 · DOI
  22. 10.1002/ana.22121 · DOI
  23. 10.1177/1352458513507822 · DOI
  24. 10.1191/1352458505ms1200cr · DOI
  25. 10.1212/WNL.48.1.58 · DOI
  26. 10.1177/1352458511404917 · DOI
  27. 10.1212/01.wnl.0000343001.36493.ae · DOI
  28. 10.1001/archneurol.2012.112 · DOI
  29. 10.1212/01.wnl.0000254502.87233.9a · DOI
  30. 10.1001/jamaneurol.2014.2137 · DOI · Paper page
  31. 10.1177/1352458510376640 · DOI
  32. 10.1177/1352458513506953 · DOI
  33. 10.1001/archneurol.2011.949 · DOI
  34. 10.1001/archneur.63.10.1398 · DOI
  35. 10.1186/1742-2094-9-14 · DOI
  36. 10.1001/archneur.63.3.390 · DOI
  37. 10.1001/archneur.63.7.964 · DOI
  38. 10.1177/1352458509103301 · DOI
  39. 10.1001/archneurol.2009.152 · DOI
  40. 10.1016/j.jns.2010.12.001 · DOI
  41. 10.1111/cen3.12107 · DOI
  42. 10.1001/jamaneurol.2014.1581 · DOI · Paper page
  43. 10.1212/WNL.0b013e318296e917 · DOI
  44. 10.1212/WNL.0b013e31826aac4e · DOI · Paper page
  45. 10.1001/jamaneurol.2013.5857 · DOI · Paper page
  46. 10.1093/brain/awn240 · DOI
  47. 10.1212/WNL.0b013e3182a6cb5c · DOI
  48. 10.1212/WNL.0b013e318211c379 · DOI
  49. 10.1016/j.jns.2011.03.038 · DOI · Paper page
  50. 10.1212/WNL.0b013e3181f39a66 · DOI
  51. 10.1212/01.wnl.0000284600.80782.d5 · DOI
  52. 10.1212/01.wnl.0000314832.24682.c6 · DOI
  53. 10.1177/1352458511431077 · DOI
  54. 10.1111/bpa.12099 · DOI
  55. 10.1212/WNL.0000000000001126 · DOI

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Metadata

Authors
Wingerchuk, D. M., Banwell, B., Bennett, J. L., Cabre, P., Carroll, W., Chitnis, T., de Seze, J., Fujihara, K., Greenberg, B., Jacob, A., Jarius, S., Lana-Peixoto, M., Levy, M., Simon, J. H., Tenembaum, S., Traboulsee, A. L., Waters, P., Wellik, K. E., & Weinshenker, B. G.
Affiliations
  • Mayo Clinic (US)
  • From the Departments of Neurology (D.M.W.) and Library Services (K.E.W.), Mayo Clinic, Scottsdale, AZ; the Children's Hospital of Philadelphia (B.B.), PA; the Departments of Neurology and Ophthalmology (J.L.B.), University of Colorado Denver, Aurora; the Service de Neurologie (P.C.), Centre Hospitalier Universitaire de Fort de France, Fort-de-France, Martinique; Department of Neurology (W.C.), Sir Charles Gairdner Hospital, Perth, Australia; the Department of Neurology (T.C.), Massachusetts General...
Corresponding author
  • Wingerchuk, Dean M.
  • Weinshenker, Brian G.
ORCID
Venue
Neurology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2015-07-14
Volume
85
Issue
2
Pages
177-189
ISSN
  • 0028-3878 (ISSN-L)
  • 1526-632X
DOI
10.1212/wnl.0000000000001729
PMC
PMC4515040
OpenAlex
W2129229339
Cited by
4,649
References
5
Citations by year
2026: 434 · 2025: 457 · 2024: 496 · 2023: 432 · 2022: 476 · 2021: 524 · 2020: 477 · 2019: 388 · 2018: 353 · 2017: 308 · 2016: 241 · 2015: 56
FWCI
253.64
Type
journal article
Language
en
Open access
Licence
cc-by-nc-nd
Locations
  • Neurology (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • eScholarship (California Digital Library) (submittedVersion, cc-by-nc-nd)
  • HAL (submittedVersion, cc-by-nc-nd)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
  • GlaxoSmithKline
  • Sanofi
  • Biogen
  • Viropharma
  • Teva Pharmaceutical Industries
  • Alexion Pharmaceuticals
  • Guthy-Jackson Charitable Foundation
  • European Committee for Treatment and Research in Multiple Sclerosis
  • Acorda Therapeutics
  • Multiple Sclerosis Society of Canada
  • Eisai
  • Ministry of Education, Science and Technology
  • Astellas Pharma
  • Teijin Pharma
  • Mitsubishi Tanabe Pharma Corporation
  • Ono Pharmaceutical
  • National Institutes of Health
  • Novartis Pharma
  • Chugai Pharmaceutical
  • National Eye Institute (R01EY022936)
  • National Institute of Neurological Disorders and Stroke (K08NS078555)
  • Daiichi Sankyo Europe
Topics
  • Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
  • Health Sciences › Medicine › Clinical Neurology › Peripheral Neuropathies and Disorders
  • Health Sciences › Medicine › Ophthalmology › Ocular Diseases and Behçet’s Syndrome
Keywords
neuromyelitis optica spectrum disorder, neuromyelitis optica, diagnostic criteria, aquaporin-4 antibodies, opticospinal multiple sclerosis, neuroimaging findings, area postrema, brainstem involvement, serologic testing
MeSH terms
Humans, Neuromyelitis Optica

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