The clinical profile of NMOSD in Australia and New Zealand
- PMID: 32006158
- DOI: 10.1007/s00415-020-09716-4
The clinical profile of NMOSD in Australia and New Zealand
Abstract
Neuromyelitis optica spectrum disorders (NMOSD) are an inflammation of the central nervous system associated with autoantibodies to aquaporin-4. We have undertaken a clinic-based survey of NMOSD in the Australia and New Zealand populations with the aim of characterising the clinical features and establishing the value of recently revised diagnostic criteria. Cases of possible NMOSD and age and sex-matched controls with multiple sclerosis (MS) were referred from centres across Australia and New Zealand. Cases were classified as NMOSD if they met the 2015 IPND criteria and remained as suspected NMOSD if they did not. Clinical and paraclinical data were compared across the three groups. NMOSD was confirmed in 75 cases and 89 had suspected NMOSD. There were 101 controls with MS. Age at onset, relapse rates and EDSS scores were significantly higher in NMOSD than in MS. Lesions and symptoms referable to the optic nerve were more common in NMOSD whereas brainstem, cerebellar and cerebral lesions were more common in MS. Longitudinally extensive spinal cord lesions were seen in 48/71 (68%) of cases with NMOSD. Elevations of CSF, white cell count and protein were more common in NMOSD. We have confirmed a clinical pattern of NMOSD that has been seen in several geographical regions. We have demonstrated the clinical utility of the current diagnostic criteria. Distinct patterns of disease are evident in NMOSD and MS, but there remains a large number of patients with NMOSD-like features who do not meet the current diagnostic criteria for NMOSD and remain a diagnostic challenge.
Keywords: Aquaporin; Autoimmune disease; Clinical features; Multiple sclerosis; Neuromyelitis optica.
References
-
- Pittock SJ, Lucchinetti CF (2016) Neuromyelitis optica and the evolving spectrum of autoimmune aquaporin-4 channelopathies: a decade later. Ann N Y Acad Sci 1366(1):20–39. https://doi.org/10.1111/nyas.12794 - DOI - PubMed
-
- Trebst C, Jarius S, Berthele A, Paul F, Schippling S, Wildemann B, Borisow N, Kleiter I, Aktas O, Kumpfel T, Neuromyelitis Optica Study G (2014) Update on the diagnosis and treatment of neuromyelitis optica: recommendations of the Neuromyelitis Optica Study Group (NEMOS). J Neurol 261(1):1–16. https://doi.org/10.1007/s00415-013-7169-7 - DOI - PubMed
-
- Palace J, Leite MI, Nairne A, Vincent A (2010) Interferon beta treatment in neuromyelitis optica: increase in relapses and aquaporin 4 antibody titers. Arch Neurol 67(8):1016–1017. https://doi.org/10.1001/archneurol.2010.188 - DOI - PubMed
-
- Jacob A, Hutchinson M, Elsone L, Kelly S, Ali R, Saukans I, Tubridy N, Boggild M (2012) Does natalizumab therapy worsen neuromyelitis optica? Neurology 79(10):1065–1066. https://doi.org/10.1212/WNL.0b013e31826845fe - DOI - PubMed
-
- Kira J, Itoyama Y, Kikuchi S, Hao Q, Kurosawa T, Nagato K, Tsumiyama I, von Rosenstiel P, Zhang-Auberson L, Saida T (2014) Fingolimod (FTY720) therapy in Japanese patients with relapsing multiple sclerosis over 12 months: results of a phase 2 observational extension. BMC Neurol 14:21. https://doi.org/10.1186/1471-2377-14-21 - DOI - PubMed - PMC
MeSH terms
Grants and funding
LinkOut - more resources
Full Text Sources
Medical
Miscellaneous
