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1 itudinal myelopathy outside of BD, including neuromyelitis optica.
2 the neuroinflammatory demyelinating disease neuromyelitis optica.
3 a postrema may be a first point of attack in neuromyelitis optica.
4 ith multiple sclerosis and optic neuritis in neuromyelitis optica.
5 demyelination, and necrosis that is seen in neuromyelitis optica.
6 s distinguish it from multiple sclerosis and neuromyelitis optica.
7 nostaining is detectable in early lesions of neuromyelitis optica.
8 ncorporated into new diagnostic criteria for neuromyelitis optica.
9 l multiple sclerosis seems to be the same as neuromyelitis optica.
10 cephalomyelitis, Guillain-Barre syndrome and neuromyelitis optica.
11 toimmunity, including multiple sclerosis and neuromyelitis optica.
12 concurrent AQP4 antibodies had conversion to neuromyelitis optica.
13 ents, none of whom had multiple sclerosis or neuromyelitis optica.
14 be recognized as rare presenting features of neuromyelitis optica.
15 of CNS inflammation and astrocytic injury in neuromyelitis optica.
16 le, 207 clinically isolated syndrome and six neuromyelitis optica.
18 many recurrent cases who also have myelitis (neuromyelitis optica) a serum antibody to aquaporin-4 wa
19 oantibodies were discovered in patients with neuromyelitis optica, a demyelinating disease, and are n
21 ous system inflammatory disorders, including neuromyelitis optica, acute disseminated encephalomyelit
22 ary tests, such as diagnostic antibodies for neuromyelitis optica, allows better phenotyping of the h
24 nts with optic neuritis, multiple sclerosis, neuromyelitis optica, Alzheimer disease, and Parkinson d
25 imaging of the retina in multiple sclerosis, neuromyelitis optica, Alzheimer disease, and Parkinson d
27 were 73% (95% CI 60-86) and 91% (79-100) for neuromyelitis optica and 58% (30-86) and 100% (66-100) f
28 all patient groups investigated, those with neuromyelitis optica and a history of optic neuritis exh
29 lassical multiple sclerosis and both Devic's neuromyelitis optica and acute disseminated encephalomye
30 aware of the uncommon presenting features of neuromyelitis optica and associated autoimmune condition
31 NMO-IgG is a specific marker autoantibody of neuromyelitis optica and binds at or near the blood-brai
32 mmunoglobulin G, is strongly associated with neuromyelitis optica and identifies patients with severe
34 ple sclerosis (n = 31) recruited from Oxford neuromyelitis optica and multiple sclerosis clinical ser
36 to be explored further in future prospective neuromyelitis optica and neuromyelitis optica spectrum d
38 rtant implications for interpreting clinical neuromyelitis optica and neuromyelitis optica spectrum d
39 euromyelitis optica (NMO-IgG) to distinguish neuromyelitis optica and related disorders from multiple
40 sion, facilitated the ability to distinguish neuromyelitis optica and related syndromes from typical
41 reproduces the key histological features of neuromyelitis optica and that aquaporin-4 is necessary a
42 7% acute disseminated encephalomyelitis, 7% neuromyelitis optica), and 91% received treatment (85% s
43 ls (30 healthy individuals, 48 patients with neuromyelitis optica, and 64 patients with multiple scle
44 ses such as systemic lupus erythematosus and neuromyelitis optica, and can lead to transient or perma
45 sms of acute disseminated encephalomyelitis, neuromyelitis optica, and classical multiple sclerosis.
46 tion and inflammation in multiple sclerosis, neuromyelitis optica, and in experimental autoimmune enc
47 immunity is prominent in multiple sclerosis, neuromyelitis optica, and the paraneoplastic syndromes w
49 whether patients with multiple sclerosis or neuromyelitis optica develop retinal neuronal layer path
52 ine]) supported the alternative diagnosis of neuromyelitis optica for 2 patients as seropositive by b
53 body marker (NMO-IgG) further differentiates neuromyelitis optica from multiple sclerosis and has hel
56 ologic, and immunologic features distinguish neuromyelitis optica from other severe cases of multiple
59 e-based assays using sera from patients with neuromyelitis optica, immune mouse serum, and Abs raised
60 ecently identified serum antibody biomarker, neuromyelitis optica immunoglobulin G (NMO-IgG), which d
68 The neuroinflammatory demyelinating disease neuromyelitis optica is marked by pathogenic autoantibod
72 ly the disease pattern does not resemble the neuromyelitis optica-like disease observed in mice beari
74 e autoimmune response against aquaporin-4 in neuromyelitis optica may be triggered by infection-induc
77 b was detected in three; two presenting with neuromyelitis optica (NMO) and one with isolated optic n
78 quaporin 4 (AQP4)-specific autoantibodies in neuromyelitis optica (NMO) are immunoglobulin (Ig)G1, a
80 P4) water channel-specific IgG distinguishes neuromyelitis optica (NMO) from multiple sclerosis and c
83 75%) were positive and 12 (25%) negative for neuromyelitis optica (NMO) IgG (per IIF of serial serum
106 rosis is a prominent pathological feature of neuromyelitis optica (NMO) lesions and is clinically rel
108 in-4 (AQP4)-specific T cells are expanded in neuromyelitis optica (NMO) patients and exhibit Th17 pol
111 epeated rituximab treatment in patients with neuromyelitis optica (NMO) revealed significant improvem
112 ceded or followed by independent episodes of neuromyelitis optica (NMO) spectrum disorder (5 cases, 4
113 segments) is considered noncharacteristic of neuromyelitis optica (NMO) spectrum disorders (NMOSDs).
114 rosis (MS), anti-aquaporin-4 (AQP4)-negative neuromyelitis optica (NMO), and chronic relapsing inflam
115 emblance the disease shows pathologically to neuromyelitis optica (NMO), including that demyelination
116 ere divided in 5 different groups: controls, neuromyelitis optica (NMO), longitudinally extensive tra
130 sessed the capacity of a putative marker for neuromyelitis optica (NMO-IgG) to distinguish neuromyeli
131 sitive cases identified incidentally, 12 had neuromyelitis optica or a high-risk syndrome for the dis
132 amples from 102 North American patients with neuromyelitis optica or with syndromes that suggest high
133 nction were more likely to meet criteria for neuromyelitis optica (P = 0.04) and were also more likel
134 ly in 98 multiple sclerosis participants, 22 neuromyelitis optica participants and 72 healthy control
135 es, mice injected with immunoglobulin G from neuromyelitis optica patients and human complement into
136 n 12 h of co-injecting immunoglobulin G from neuromyelitis optica patients and human complement, ther
138 In our mouse model, immunoglobulin G from neuromyelitis optica patients does not require pre-exist
139 lin G from aquaporin-4-autoantibody-positive neuromyelitis optica patients has the potential to damag
140 ently been reported that immunoglobulin from neuromyelitis optica patients injected peripherally does
141 utely ill multiple sclerosis patient and two neuromyelitis optica patients revealed instances of infi
143 wever, co-injection of immunoglobulin G from neuromyelitis optica patients with human complement prod
144 e that co-injection of immunoglobulin G from neuromyelitis optica patients with human complement repr
145 mice that received immunoglobulin G from non-neuromyelitis optica patients with human complement, or
146 ull mice that received immunoglobulin G from neuromyelitis optica patients with human complement.
148 gut of patients with multiple sclerosis and neuromyelitis optica provides evidence of communication
149 uropathy, optic neuritis/multiple sclerosis, neuromyelitis optica, pseudotumor cerebri, migraine, opt
150 ng diseases (i.e., multiple sclerosis versus neuromyelitis optica) represents distinct syndromes.
151 t AQP4-IgG is involved in the development of neuromyelitis optica revolutionised our understanding of
152 tity of autoimmune AQP4 myopathy extends the neuromyelitis optica spectrum beyond the central nervous
153 ics of ring-enhancing spinal cord lesions in neuromyelitis optica spectrum disorder (NMOSD) myelitis
154 is a common and debilitating consequence of neuromyelitis optica spectrum disorder (NMOSD) myelitis,
157 ses in which demyelination is a feature (eg, neuromyelitis optica spectrum disorder and acute dissemi
158 e non-Hispanic patients with MS reveals that neuromyelitis optica spectrum disorder is rarely misdiag
159 Previous clinical neuromyelitis optica and neuromyelitis optica spectrum disorder studies have incl
160 terpreting clinical neuromyelitis optica and neuromyelitis optica spectrum disorder studies, since cl
163 -seropositive, aged at least 18 years, had a neuromyelitis optica spectrum disorder, and had at least
165 neuromyelitis optica-IgG, a novel marker of neuromyelitis optica spectrum disorders (including longi
169 We have undertaken a clinic-based survey of neuromyelitis optica spectrum disorders (NMOSDs) in Aust
170 ng atypical multiple sclerosis, seronegative neuromyelitis optica spectrum disorders and relapsing ac
172 ffecting humans, such as multiple sclerosis, neuromyelitis optica spectrum disorders, Parkinson disea
177 ng for this biomarker has suggested that the neuromyelitis optica spectrum is broader than previously
183 exact role of NMO-IgG in the pathogenesis of neuromyelitis optica will provide a foundation for ratio
184 This report highlights the association of neuromyelitis optica with dermatitis herpetiformis, whic
185 ith multiple sclerosis and participants with neuromyelitis optica, with and without a history of opti
186 articipants with multiple sclerosis and with neuromyelitis optica without a history of optic neuritis
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