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1 of CNS inflammation and astrocytic injury in neuromyelitis optica.
2 le, 207 clinically isolated syndrome and six neuromyelitis optica.
3 the neuroinflammatory demyelinating disease neuromyelitis optica.
4 a postrema may be a first point of attack in neuromyelitis optica.
5 id antibody syndrome, myasthenia gravis, and neuromyelitis optica.
6 ith multiple sclerosis and optic neuritis in neuromyelitis optica.
7 demyelination, and necrosis that is seen in neuromyelitis optica.
8 s distinguish it from multiple sclerosis and neuromyelitis optica.
9 nostaining is detectable in early lesions of neuromyelitis optica.
10 ncorporated into new diagnostic criteria for neuromyelitis optica.
11 l multiple sclerosis seems to be the same as neuromyelitis optica.
12 cephalomyelitis, Guillain-Barre syndrome and neuromyelitis optica.
13 ple sclerosis, autoimmune encephalitides and neuromyelitis optica.
14 itudinal myelopathy outside of BD, including neuromyelitis optica.
15 toimmunity, including multiple sclerosis and neuromyelitis optica.
16 concurrent AQP4 antibodies had conversion to neuromyelitis optica.
17 ents, none of whom had multiple sclerosis or neuromyelitis optica.
18 be recognized as rare presenting features of neuromyelitis optica.
20 many recurrent cases who also have myelitis (neuromyelitis optica) a serum antibody to aquaporin-4 wa
21 oantibodies were discovered in patients with neuromyelitis optica, a demyelinating disease, and are n
23 , relapsing-remitting multiple sclerosis and neuromyelitis optica, a high proportion of cells express
24 ous system inflammatory disorders, including neuromyelitis optica, acute disseminated encephalomyelit
25 ary tests, such as diagnostic antibodies for neuromyelitis optica, allows better phenotyping of the h
27 nts with optic neuritis, multiple sclerosis, neuromyelitis optica, Alzheimer disease, and Parkinson d
28 imaging of the retina in multiple sclerosis, neuromyelitis optica, Alzheimer disease, and Parkinson d
30 were 73% (95% CI 60-86) and 91% (79-100) for neuromyelitis optica and 58% (30-86) and 100% (66-100) f
31 all patient groups investigated, those with neuromyelitis optica and a history of optic neuritis exh
32 lassical multiple sclerosis and both Devic's neuromyelitis optica and acute disseminated encephalomye
33 aware of the uncommon presenting features of neuromyelitis optica and associated autoimmune condition
34 NMO-IgG is a specific marker autoantibody of neuromyelitis optica and binds at or near the blood-brai
35 mmunoglobulin G, is strongly associated with neuromyelitis optica and identifies patients with severe
37 ple sclerosis (n = 31) recruited from Oxford neuromyelitis optica and multiple sclerosis clinical ser
38 to be explored further in future prospective neuromyelitis optica and neuromyelitis optica spectrum d
40 rtant implications for interpreting clinical neuromyelitis optica and neuromyelitis optica spectrum d
43 euromyelitis optica (NMO-IgG) to distinguish neuromyelitis optica and related disorders from multiple
44 sion, facilitated the ability to distinguish neuromyelitis optica and related syndromes from typical
45 reproduces the key histological features of neuromyelitis optica and that aquaporin-4 is necessary a
46 several other indications, such as uveitis, neuromyelitis optica and, most recently, COVID-19 pneumo
47 7% acute disseminated encephalomyelitis, 7% neuromyelitis optica), and 91% received treatment (85% s
48 ls (30 healthy individuals, 48 patients with neuromyelitis optica, and 64 patients with multiple scle
49 ses such as systemic lupus erythematosus and neuromyelitis optica, and can lead to transient or perma
50 et for such disorders as multiple sclerosis, neuromyelitis optica, and CD4(+) T cell-mediated disorde
51 sms of acute disseminated encephalomyelitis, neuromyelitis optica, and classical multiple sclerosis.
52 tion and inflammation in multiple sclerosis, neuromyelitis optica, and in experimental autoimmune enc
53 immunity is prominent in multiple sclerosis, neuromyelitis optica, and the paraneoplastic syndromes w
54 sition verifies that astrocytic reactions in neuromyelitis optica are not solely dependent on IgG-med
56 whether patients with multiple sclerosis or neuromyelitis optica develop retinal neuronal layer path
57 ed according to 2015 International Panel for Neuromyelitis Optica Diagnosis criteria, who had an Expa
61 ine]) supported the alternative diagnosis of neuromyelitis optica for 2 patients as seropositive by b
62 body marker (NMO-IgG) further differentiates neuromyelitis optica from multiple sclerosis and has hel
66 ologic, and immunologic features distinguish neuromyelitis optica from other severe cases of multiple
69 e-based assays using sera from patients with neuromyelitis optica, immune mouse serum, and Abs raised
70 ecently identified serum antibody biomarker, neuromyelitis optica immunoglobulin G (NMO-IgG), which d
81 The neuroinflammatory demyelinating disease neuromyelitis optica is marked by pathogenic autoantibod
84 nsformation also readily detectable in human neuromyelitis optica lesions, which especially affected
87 ly the disease pattern does not resemble the neuromyelitis optica-like disease observed in mice beari
89 e autoimmune response against aquaporin-4 in neuromyelitis optica may be triggered by infection-induc
92 b was detected in three; two presenting with neuromyelitis optica (NMO) and one with isolated optic n
93 quaporin 4 (AQP4)-specific autoantibodies in neuromyelitis optica (NMO) are immunoglobulin (Ig)G1, a
95 P4) water channel-specific IgG distinguishes neuromyelitis optica (NMO) from multiple sclerosis and c
98 75%) were positive and 12 (25%) negative for neuromyelitis optica (NMO) IgG (per IIF of serial serum
126 rosis is a prominent pathological feature of neuromyelitis optica (NMO) lesions and is clinically rel
129 in-4 (AQP4)-specific T cells are expanded in neuromyelitis optica (NMO) patients and exhibit Th17 pol
132 epeated rituximab treatment in patients with neuromyelitis optica (NMO) revealed significant improvem
133 ceded or followed by independent episodes of neuromyelitis optica (NMO) spectrum disorder (5 cases, 4
134 segments) is considered noncharacteristic of neuromyelitis optica (NMO) spectrum disorders (NMOSDs).
135 rosis (MS), anti-aquaporin-4 (AQP4)-negative neuromyelitis optica (NMO), and chronic relapsing inflam
136 emblance the disease shows pathologically to neuromyelitis optica (NMO), including that demyelination
137 ere divided in 5 different groups: controls, neuromyelitis optica (NMO), longitudinally extensive tra
153 sessed the capacity of a putative marker for neuromyelitis optica (NMO-IgG) to distinguish neuromyeli
156 sitive cases identified incidentally, 12 had neuromyelitis optica or a high-risk syndrome for the dis
157 amples from 102 North American patients with neuromyelitis optica or with syndromes that suggest high
158 nction were more likely to meet criteria for neuromyelitis optica (P = 0.04) and were also more likel
159 ly in 98 multiple sclerosis participants, 22 neuromyelitis optica participants and 72 healthy control
160 Typical brain lesions occurred in 50.9% of neuromyelitis optica patients (18.1% brainstem periventr
161 es, mice injected with immunoglobulin G from neuromyelitis optica patients and human complement into
162 n 12 h of co-injecting immunoglobulin G from neuromyelitis optica patients and human complement, ther
164 In our mouse model, immunoglobulin G from neuromyelitis optica patients does not require pre-exist
166 lin G from aquaporin-4-autoantibody-positive neuromyelitis optica patients has the potential to damag
168 sions along lateral ventricles discriminated neuromyelitis optica patients in both training (sensitiv
169 ently been reported that immunoglobulin from neuromyelitis optica patients injected peripherally does
170 utely ill multiple sclerosis patient and two neuromyelitis optica patients revealed instances of infi
172 wever, co-injection of immunoglobulin G from neuromyelitis optica patients with human complement prod
173 e that co-injection of immunoglobulin G from neuromyelitis optica patients with human complement repr
174 mice that received immunoglobulin G from non-neuromyelitis optica patients with human complement, or
175 ull mice that received immunoglobulin G from neuromyelitis optica patients with human complement.
177 gut of patients with multiple sclerosis and neuromyelitis optica provides evidence of communication
178 uropathy, optic neuritis/multiple sclerosis, neuromyelitis optica, pseudotumor cerebri, migraine, opt
180 ng diseases (i.e., multiple sclerosis versus neuromyelitis optica) represents distinct syndromes.
181 t AQP4-IgG is involved in the development of neuromyelitis optica revolutionised our understanding of
182 scriptions of astrocytic lesions reported in neuromyelitis optica so far have emphasized a characteri
183 tity of autoimmune AQP4 myopathy extends the neuromyelitis optica spectrum beyond the central nervous
184 , 29%), multiple sclerosis (MS) (n = 4,14%), neuromyelitis optica spectrum disease (NMOSD) (n = 3, 11
185 d predicted MOG-antibody disease versus AQP4-neuromyelitis optica spectrum disorder (accuracy: 76%, s
186 sease (MOGAD) (92), aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder (AQP4+NMOSD) (75)
187 s with aquaporin-4 immunoglobulin G-positive neuromyelitis optica spectrum disorder (AQP4-IgG+ NMOSD)
188 ment monitoring; but in aquaporin-4 antibody neuromyelitis optica spectrum disorder (AQP4-NMOSD), the
189 0) before and after treatment, patients with neuromyelitis optica spectrum disorder (n = 87), MOG ant
190 I) and T helper 17 (TH17) drive pathology in neuromyelitis optica spectrum disorder (NMOSD) and in TH
192 -aquaporin-4-antibody (AQP4-Ab)-seronegative neuromyelitis optica spectrum disorder (NMOSD) and relat
193 ittle is known about the association between neuromyelitis optica spectrum disorder (NMOSD) and the r
196 lerosis, and aquaporin-4 antibody-associated neuromyelitis optica spectrum disorder (NMOSD) cumulativ
198 is a pathoanatomical feature differentiating neuromyelitis optica spectrum disorder (NMOSD) from mult
203 ics of ring-enhancing spinal cord lesions in neuromyelitis optica spectrum disorder (NMOSD) myelitis
204 is a common and debilitating consequence of neuromyelitis optica spectrum disorder (NMOSD) myelitis,
207 ive agent (IS) which is widely prescribed in neuromyelitis optica spectrum disorder (NMOSD) patients.
208 reduced the risk of relapse in patients with neuromyelitis optica spectrum disorder (NMOSD) when adde
210 AQP4-IgG was cloned from a patient with neuromyelitis optica spectrum disorder (NMOSD), an autoi
211 ntation at onset of multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myel
213 ively, in CSF from people with untreated MS, neuromyelitis optica spectrum disorder (NMOSD), other in
218 ears, median EDSS: 2 (0-7.5)], 162 with AQP4-neuromyelitis optica spectrum disorder [132 females, mea
219 ses in which demyelination is a feature (eg, neuromyelitis optica spectrum disorder and acute dissemi
220 ases with an autoantibody component, such as neuromyelitis optica spectrum disorder and autoimmune en
221 nical and MRI features when compared to AQP4-neuromyelitis optica spectrum disorder and multiple scle
222 ere: diagnosis of MOG-antibody disease; AQP4-neuromyelitis optica spectrum disorder and multiple scle
223 tions, such as systemic lupus erythematosus, neuromyelitis optica spectrum disorder and myasthenia gr
225 rial, adults aged 18 years and older with an neuromyelitis optica spectrum disorder diagnosis, Expand
226 ge the therapeutic landscape for people with neuromyelitis optica spectrum disorder in different ways
227 ntibody, demonstrated safety and efficacy in neuromyelitis optica spectrum disorder in the randomised
230 e non-Hispanic patients with MS reveals that neuromyelitis optica spectrum disorder is rarely misdiag
231 nd spinal cord scans were evaluated from 116 neuromyelitis optica spectrum disorder patients (98 sero
232 Previous clinical neuromyelitis optica and neuromyelitis optica spectrum disorder studies have incl
233 terpreting clinical neuromyelitis optica and neuromyelitis optica spectrum disorder studies, since cl
235 lizumab, and inebilizumab) for patients with neuromyelitis optica spectrum disorder that all showed a
236 was identified in 3 of 50 patients (6%) with neuromyelitis optica spectrum disorder, 5 of 228 patient
239 -seropositive, aged at least 18 years, had a neuromyelitis optica spectrum disorder, and had at least
240 e drugs used as DMTs for multiple sclerosis, neuromyelitis optica spectrum disorder, and other immune
241 n drugs used as DMTs for multiple sclerosis, neuromyelitis optica spectrum disorder, and other immune
243 c inflammatory myopathy, systemic sclerosis, neuromyelitis optica spectrum disorder, myasthenia gravi
244 ment of individuals with multiple sclerosis, neuromyelitis optica spectrum disorder, or myelin oligod
245 m inebilizumab treatment in individuals with neuromyelitis optica spectrum disorder, which supports t
251 assify patients as MOG-antibody disease/AQP4-neuromyelitis optica spectrum disorder/multiple sclerosi
252 ing conditions such as multiple sclerosis or neuromyelitis optica spectrum disorder; systemic disease
253 aluated in aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorders (AQP4+NMOSD).
254 to be lower than in aquaporin-4-IgG-positive neuromyelitis optica spectrum disorders (AQP4-IgG+NMOSDs
255 neuromyelitis optica-IgG, a novel marker of neuromyelitis optica spectrum disorders (including longi
260 ppearing white matter (NAWM) is preserved in neuromyelitis optica spectrum disorders (NMOSD) is open
268 quaporin-4 antibody seropositive (AQP4-IgG+) neuromyelitis optica spectrum disorders (NMOSDs) frequen
269 We have undertaken a clinic-based survey of neuromyelitis optica spectrum disorders (NMOSDs) in Aust
273 ic neuritis (20 [17%]), myelitis (13 [11%]), neuromyelitis optica spectrum disorders (six [5%]), and
274 ng atypical multiple sclerosis, seronegative neuromyelitis optica spectrum disorders and relapsing ac
276 e MS n = 9; secondary progressive MS n = 10; neuromyelitis optica spectrum disorders n = 15; and othe
279 ffecting humans, such as multiple sclerosis, neuromyelitis optica spectrum disorders, Parkinson disea
280 he MRI criteria for multiple sclerosis (e.g. neuromyelitis optica spectrum disorders, Susac syndrome)
288 ng for this biomarker has suggested that the neuromyelitis optica spectrum is broader than previously
290 nd differences from aquaporin-4-IgG-positive-neuromyelitis-optica-spectrum-disorder (AQP4+NMOSD), and
292 ct form of immune-mediated axon pathology in neuromyelitis optica that mechanistically differs from k
297 exact role of NMO-IgG in the pathogenesis of neuromyelitis optica will provide a foundation for ratio
298 This report highlights the association of neuromyelitis optica with dermatitis herpetiformis, whic
299 ith multiple sclerosis and participants with neuromyelitis optica, with and without a history of opti
300 articipants with multiple sclerosis and with neuromyelitis optica without a history of optic neuritis