The clinical profile of NMOSD in Australia and New Zealand

Bukhari, Wajih; Clarke, Laura; O’Gorman, Cullen; Khalilidehkordi, Elham; Arnett, Simon; Prain, Kerri; Woodhall, Mark; Silvestrini, Roger; Bundell, Christine; Ramanathan, Sudarshini; Abernethy, David; Bhuta, Sandeep; Blum, Stefan; Boggild, Mike; Boundy, Karyn; Brew, Bruce J.; Brownlee, Wallace; Butzkueven, Helmut; Carroll, William M.; Chen, Celia; Coulthard, Alan; Dale, Russell C.; Das, Chandi; Dear, Keith; Fabis-Pedrini, Marzena J.; Fulcher, David A.; Gillis, David; Hawke, Simon; Heard, Robert; Henderson, Andrew; Heshmat, Saman; Hodgkinson, Suzanne; Jimenez-Sanchez, Sofia; Kilpatrick, Trevor J.; King, John; Kneebone, C.; Kornberg, Andrew J.; Lechner‐Scott, Jeannette; Lin, Ming; Lynch, Christopher D.; Macdonnell, Richard; Mason, Deborah; McCombe, Pamela A.; Pereira, Jennifer A.; Pollard, John D.; Reddel, Stephen W.; Shaw, Cameron; Spies, Judith M.; Stankovich, Jim; Sutton, Ian; Vucic, Steve; Walsh, Michael D.; Wong, Richard; Yiu, Eppie M; Barnett, Michael; Kermode, Allan G.; Marriott, Mark; Parratt, John; Slee, Mark; Taylor, Bruce; Willoughby, Ernest; Wilson, Robert J.; Brilot, Fabienne; Vincent, Angela; Waters, Patrick; Broadley, Simon

doi:10.1007/s00415-020-09716-4

Cited by 22 publications

(35 citation statements)

References 32 publications

(29 reference statements)

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“…However, we noted a significantly higher prevalence of the absence of response in at least one eye in patients with NMOSD who were AQP4[+] (44%) vs. AQP4[-] (4%). This has also been reported by others (Watanabe et al, 2009;Bukhari et al, 2020;Vabanesi et al, 2019;Neto et al, 2013). We believe that this disproportion of those lacking VEPs after stimulation imposes a major limitation on the analyses of P100 latencies and amplitudes when assessing the impact of risk predictors, given that omitting patients with absent responses could lead to falsepositive or false-negative results.…”

Section: Discussionsupporting

confidence: 68%

“…Table 5 VEP scores in patients with NMOSD regarding the initial clinical manifestation and anti-AQP4 antibody status. extreme latency delays, while axonopathy is the dominating component in NMOSD as there are more frequent absent responses (Bukhari et al, 2020;Vabanesi et al, 2019;Neto et al, 2013;Ohnari et al, 2016). In contrast to MS, where the prolonged P100 latency may result from the damage at any part of the visual pathway, the abnormal VEP response in NMOSD specifically reflects changes in the optic nerves.…”

Section: Discussionmentioning

confidence: 99%

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The relationship between aquaporin-4 antibody status and visual tract integrity in neuromyelitis optica spectrum disorders: A visual evoked potential study

Barć

Gospodarczyk-Szot

Nojszewska

et al. 2020

Multiple Sclerosis and Related Disorders

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Background: Optic neuritis (ON) is one of the hallmark symptomatic features of neuromyelitis optica spectrum disorders (NMOSD). The majority of patients with NMOSD present highly specific autoantibodies against aquaporin-4 (AQP4). A number of studies have reported poor visual acuity outcomes in individuals with AQP4 seropositive NMOSD, but no such relationship has been found with regard to visual evoked potentials (VEP) parameters such as the amplitude and latency of the P100 component. In this paper, we aimed (i) to describe VEP responses in patients with NMOSD; (ii) to analyze those results based on a scoring system; and (iii) to investigate the association between the VEPs and AQP4 antibody status. Methods: We retrospectively analysed the VEP responses of 40 patients with a diagnosis of NMOSD (according to the 2015 IPND criteria), including 16 with AQP4-postive status (AQP4[+]) and 24 with AQP4-negative status (AQP4[-]). In the first step, we measured the P100 peak latency and P100-N2 peak-to-peak amplitude in each patient. In the second, we converted these measures to the VEP score (0-10) using the scoring proposed by Jung et al. (2008). All recordings were performed using the same VEP device and testing protocol. Results: Abnormal VEPs were recorded in 25 of 40 patients (62.6%). Of these, 17 (42.5%) had prolonged P100 latency, and 8 (20%) had no response detected in at least one eye. The patients with ON as the initial relapse symptom had significantly higher median VEP scores than those who experienced the longitudinally extensive transverse myelitis (LETM) at the disease onset (7.0 [interquartile range (IQR), 2.0-8.0] vs. 0.0 [IQR, 0.0-4.0], p<0.001). A lack of VEP response in at least one eye was detected more frequently in the AQP4[+] group than the AQP4[-] group (7/16 vs. 1/24, p<0.005). Logistic regression model controlling for age, gender, disease duration, and the type of relapse at onset showed an independent impact of AQP4[+] status (OR=35.45, p = 0.018) on the higher rate of absent VEP responses. In the entire group of patients (n = 40), those with AQP4[+] showed a small tendency towards a higher median VEP score (4.0 [IQR, 0.0-7.8] vs. 1.0 [IQR, 0.0-4.0], p = 0.304). Among individuals with abnormal responses (n = 25), the patients with AQP4[+] had significantly higher median VEP scores (7.0 [IQR, 4.0-8.5] vs. 3.0 [IQR, 1.0-7.0], p = 0.034) and more common bilateral involvement of the optic tracts (80% vs. 40%, p = 0.048) than those who were seronegative for anti-AQP4 antibody. A median regression analysis model controlling for age, gender, disease duration, type of onset, and number of relapses in last 12 months showed an independent association between the AQP4-positive status and a higher VEP score in patients with NMOSD (t = 2.882, df=2, p = 0.007). Conclusion: VEP study remains a useful tool in the assessment of NMOSD patients. Due to the high prevalence of absent VEPs in NMOSD patients, the scoring system appears to be more applicable for the precise analysis of VEP recordings. There is a po...

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 99%

The relationship between aquaporin-4 antibody status and visual tract integrity in neuromyelitis optica spectrum disorders: A visual evoked potential study

Barć

Gospodarczyk-Szot

Nojszewska

et al. 2020

Multiple Sclerosis and Related Disorders

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“…Testing for MOG antibodies was conducted on 42/75 (56%) of NMOSD cases, including all of the seronegative cases and 52/101 (51%) of MS controls, and all were negative (5). The demographic and clinical features of the NMOSD cases and MS controls have been previously reported (6) and show that they were well matched for age and sex, but differ in a number of predictable clinical features as summarized in Table 1. Age of onset in MS cases was younger and consequently disease duration was longer.…”

Section: Nmosd Cases and Ms Controlsmentioning

confidence: 95%

“…This was a retrospective case-control study of NMOSD cases and MS controls. Cases of suspected NMOSD and MS were referred by a network of 23 clinical centres in Australia and New Zealand specializing in the assessment of patients with inflammatory diseases of the central nervous system in both adult and pediatric populations as previously described (4,6). Cases of NMOSD were defined according to the 2015 IPND criteria (1).…”

Section: Case Ascertainmentmentioning

confidence: 99%

“…Age-and sex-matched MS cases were identified from each centre with the diagnosis of MS being confirmed according to the 2010 McDonald criteria (7) with the added requirements of having no clinical features suspicious for NMOSD and being negative for AQP4 antibodies. Basic demographic and clinical features were recorded for all cases and controls as per a standardized data collection questionnaire as previously described (6). All participants provided written informed consent and the study was approved by the human research ethics committee of all participating institutions.…”

Section: Case Ascertainmentmentioning

confidence: 99%

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Relapse Patterns in NMOSD: Evidence for Earlier Occurrence of Optic Neuritis and Possible Seasonal Variation

et al. 2020

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Pathogenesis of autoimmune demyelination: from multiple sclerosis to neuromyelitis optica spectrum disorders and myelin oligodendrocyte glycoprotein antibody‐associated disease

et al. 2021

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Autoimmunity plays a significant role in the pathogenesis of demyelination. Multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are now recognised as separate disease entities under the amalgam of human central nervous system demyelinating disorders. While these disorders share inherent similarities, investigations into their distinct clinical presentations and lesion pathologies have aided in differential diagnoses and understanding of disease pathogenesis. An interplay of various genetic and environmental factors contributes to each disease, many of which implicate an autoimmune response. The pivotal role of the adaptive immune system has been highlighted by the diagnostic autoantibodies in NMOSD and MOGAD, and the presence of autoreactive lymphocytes in MS lesions. While a number of autoantigens have been proposed in MS, recent emphasis on the contribution of B cells has shed new light on the well-established understanding of T cell involvement in pathogenesis. This review aims to synthesise the clinical characteristics and pathological findings, discuss existing and emerging hypotheses regarding the aetiology of demyelination and evaluate recent pathogenicity studies involving T cells, B cells, and autoantibodies and their implications in human demyelination.

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The clinical profile of NMOSD in Australia and New Zealand

Cited by 22 publications

References 32 publications

The relationship between aquaporin-4 antibody status and visual tract integrity in neuromyelitis optica spectrum disorders: A visual evoked potential study

The relationship between aquaporin-4 antibody status and visual tract integrity in neuromyelitis optica spectrum disorders: A visual evoked potential study

Relapse Patterns in NMOSD: Evidence for Earlier Occurrence of Optic Neuritis and Possible Seasonal Variation

Pathogenesis of autoimmune demyelination: from multiple sclerosis to neuromyelitis optica spectrum disorders and myelin oligodendrocyte glycoprotein antibody‐associated disease

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