Clinical, CSF, and MRI findings in Devic's neuromyelitis optica.

O'Riordan, J I; Gallagher, Helen L.; Thompson, Alan; Howard, RS; Kingsley, D. P. E.; Thompson, E. J.; McDonald, W. I.; Miller, David H.

doi:10.1136/jnnp.60.4.382

Cited by 359 publications

(294 citation statements)

References 26 publications

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“…2J, 2K). Overall, these results suggest that TNFR2 deficiency does not appear to alter the pattern of inflammatory demyelination observed in the 2D2 transgenic mice (7,50), but rather it potentiates a remarkable sex bias increase in disease incidence (23-fold) and severity. Given the similar phenotypes of TNFR2 2/2 2D2 and double-transgenic mice that express MOG-specific receptors on T and B cells (33,47), genetic deficiency of TNFR2 in 2D2 mice appears to be sufficient to overcome the requirement for the MOG-specific BCR transgene for spontaneous autoimmune disease development (33,47).…”

Section: Concentration-and Time-dependent Induction Of Tnfr2 By Foxp3mentioning

confidence: 64%

TNFR2 Deficiency Acts in Concert with Gut Microbiota To Precipitate Spontaneous Sex-Biased Central Nervous System Demyelinating Autoimmune Disease

Miller

Bonn

Franklin

et al. 2015

The Journal of Immunology

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TNF-α antagonists provide benefit to patients with inflammatory autoimmune disorders such as Crohn’s disease, rheumatoid arthritis, and ankylosing spondylitis. However, TNF antagonism unexplainably exacerbates CNS autoimmunity, including multiple sclerosis and neuromyelitis optica. The underlying mechanisms remain enigmatic. We demonstrate that TNFR2 deficiency results in female-biased spontaneous autoimmune CNS demyelination in myelin oligodendrocyte glycoprotein–specific 2D2 TCR transgenic mice. Disease in TNFR2−/− 2D2 mice was associated with CNS infiltration of T and B cells as well as increased production of myelin oligodendrocyte glycoprotein–specific IL-17, IFN-γ, and IgG2b. Attenuated disease in TNF−/− 2D2 mice relative to TNFR2−/− 2D2 mice identified distinctive roles for TNFR1 and TNFR2. Oral antibiotic treatment eliminated spontaneous autoimmunity in TNFR2−/− 2D2 mice to suggest role for gut microbiota. Illumina sequencing of fecal 16S rRNA identified a distinct microbiota profile in male TNFR2−/− 2D2 that was associated with disease protection. Akkermansia muciniphila, Sutterella sp., Oscillospira sp., Bacteroides acidifaciens, and Anaeroplasma sp. were selectively more abundant in male TNFR2−/− 2D2 mice. In contrast, Bacteroides sp., Bacteroides uniformis, and Parabacteroides sp. were more abundant in affected female TNFR2−/− 2D2 mice, suggesting a role in disease causation. Overall, TNFR2 blockade appears to disrupt commensal bacteria–host immune symbiosis to reveal autoimmune demyelination in genetically susceptible mice. Under this paradigm, microbes likely contribute to an individual’s response to anti-TNF therapy. This model provides a foundation for host immune–microbiota-directed measures for the prevention and treatment of CNS-demyelinating autoimmune disorders.

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Section: Concentration-and Time-dependent Induction Of Tnfr2 By Foxp3mentioning

confidence: 64%

TNFR2 Deficiency Acts in Concert with Gut Microbiota To Precipitate Spontaneous Sex-Biased Central Nervous System Demyelinating Autoimmune Disease

Miller

Bonn

Franklin

et al. 2015

The Journal of Immunology

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“…CSF samples of five control patients negative oligoclonal IgG bands, and longitudinally extensive myelitis preferentially involving the central gray matter (Mandler et al 1993;O'Riordan et al 1996;Wingerchuk et al 1999;Misu et al 2002;Nakamura et al 2008).…”

Section: Csf-gfap and Csf-myelin Basic Protein (Mbp) Levels (Fig 2)mentioning

confidence: 99%

A Prominent Elevation of Glial Fibrillary Acidic Protein in the Cerebrospinal Fluid during Relapse in Neuromyelitis Optica

Takano

Misu

Takahashi

et al. 2008

Tohoku J. Exp. Med.

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Neuromyelitis optica (NMO) is a neurologic disease characterized by severe optic neuritis, longitudinally extended, transverse myelitis and serum aquaporin-4 (AQP4) antibody. Our recent neuropathological study revealed the extensive loss of AQP4 and glial fibrillary acidic protein (GFAP), an astrocyte-specific protein, in NMO lesions, but not in MS lesions, suggesting that severe astrocytic damage or dysfunction may be related to the pathogenesis of NMO. Here we report a patient of NMO, in which the cerebrospinal fluid (CSF) levels of GFAP were measured both during relapse of myelitis and after high-dose intravenous methylprednisolone (HIMP). The patient was a 34-year old woman with two previous episodes of optic neuritis. She developed myelitis longitudinally extending from C3 to T12 with contrast enhancement, and was AQP4 antibody-positive. In the acute phase, the GFAP level in the cerebrospinal fluid (CSF) was prominently elevated (18,966.7 ng/ml) as compared with controls (0.6 ± 0.33 ng/ml). However, following HIMP, the clinical and MRI findings improved, and the CSF-GFAP level was near-normal (2.1 ng/ml). The CSF of myelin basic protein was also elevated in relapse (1,016.0 pg/ml), and became lower but still remained high (158.7 pg/ml) after HIMP compared with controls (3.36 ± 3.83 pg/ml). The prominent elevation of the CSF-GFAP level in relapse of NMO, followed by its sharp decline after therapy, suggests severe astrocytic damage with a temporal profile distinct from that of the demyelinating process in NMO. CSF-GFAP may be useful as a biomarker of NMO.glial fibrillary acidic protein (GFAP); neuromyelitis optica; cerebrospinal fluid; myelin basic protein; relapse. Neuromyelitis optica (NMO) is a neurologic disease characterized by severe, often bilateral optic neuritis and transverse myelitis. As well as the unique lesion distribution and severe functional disability in NMO, the clinical and laboratory features of NMO have been reported to be distinct from those of MS, and they include female preponderance, higher onset age, mostly

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“…La neuromielitis óptica (NMO) y la esclerosis múltiple óptica-espinal asiática presentan características neuroimagenológicas, inmunológicas y serológicas similares, [32,38,39] la idea de que estas dos enfermedades sean la misma entidad está apoyada por la infiltración perivascular de eosinófilos, el depósito de complementos y el patrón en roseta de inmunoglobulinas [33], no obstante en Japón los pacientes con estas particularidades se diagnostican como Esclerosis Múltiple (EM) y en América y Europa tales pacientes reciben el diagnóstico de neuromielitis óptica (NMO) (34,40,41), por lo que el debate continua con respecto a la clasificación clínica (42,61,62).…”

Section: Esclerosis Múltiple óPtica-espinal Asiática Y Neuromielitis unclassified

Neuromielitis Óptica. Patología, diagnóstico y tratamiento en el siglo XXI

Pinzón¹

2015

Rev. Sal. Bosq

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La neuromielitis óptica (NMO) o enfermedad de Devic, pertenece al grupo de las enfermedades desmielinizantes del sistema nervioso central, afecta de manera significativa los nervios ópticos y la médula espinal. Desde el siglo XIX cuando Eugene Devic dio a conocer una serie de casos en los que existía asociación de lesiones en los nervios ópticos y la medula espinal, la relación de la neuromielitis óptica (NMO) y la Esclerosis Múltiple (EM) ha sido controversial, considerándose una variante de esta última; datos recientes muestran que puede ser distinguida de la Esclerosis Múltiple (EM). Los síntomas de la NMO son por lo general más agudos y severos y la presencia de un autoanticuerpo específico en sangre llamado NMO-IgG tipo acuoporina-4 (AQP4) desempeña un rol muy importante en la patogenia de esta enfermedad,asimismo se encuentran varias características entre ellas de tipo clínico, de laboratorio, neuroimágenes y en la anatomía patológica que diferencian la esclerosis múltiple (EM) de esta enfermedad. La proporción entre mujeres y hombres es mayor de 4 a 1.La presentación clínica y el curso de la enfermedad puede ser con recaídas en 80-90% y en un 10-20% curso monofásico. La manifestación distintiva de la entidad NMO es la ocurrencia ya sea consecutiva o simultánea de NO (unilateral o bilateral) y la presencia de mielitis longitudinal extensa (Mle). La terapia con corticosteroides intravenosos normalmente es el tratamiento Andrés Mauricio Álvarez Pinzón. AbstractOptic Neuromyelitis (NMO) or Devic's disease, is a demyelinating disease of central nervous system, affects the optic nerves and spinal cord. Since the nineteenth century when Eugene Devic unveiled a series of cases in which there was an association of lesions in the optic nerves and spinal cord with relation of NMO and Multiple Sclerosis (MS) has been controversial, in some cases described like a variant of the latter but recent data show that can be distinguished from multiple sclerosis (MS). Symptoms of NMO are usually more acute and severe and then we can find a presence of a specific autoantibody called NMO-IgG, it is a blood type acuoporina-4 (AQP4) and plays an important role in the pathogenesis of this disease. Also in the new millennium are various types of clinical, laboratory, neuroimaging and pathological anatomy then differentiates multiple sclerosis (MS) of this disease. In the epidemiology the ratio of women to men is greater than 4 to 1.The clinical presentation and course of the disease can be relapsing by 80-90% and 10-20% monophasic course. The distinctive manifestation is the occurrence NMO entity either consecutively or simultaneously not (unilateral or bilateral) and the presence of extensive longitudinal myelitis. Intravenous corticosteroid therapy is usually the initial therapy for acute attacks of optic neuritis or myelitis. Plasmapheresis therapy is used when the steroids therapy no work during 1. Artículo de revisión.

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Clinical, CSF, and MRI findings in Devic's neuromyelitis optica.

Cited by 359 publications

References 26 publications

TNFR2 Deficiency Acts in Concert with Gut Microbiota To Precipitate Spontaneous Sex-Biased Central Nervous System Demyelinating Autoimmune Disease

TNFR2 Deficiency Acts in Concert with Gut Microbiota To Precipitate Spontaneous Sex-Biased Central Nervous System Demyelinating Autoimmune Disease

A Prominent Elevation of Glial Fibrillary Acidic Protein in the Cerebrospinal Fluid during Relapse in Neuromyelitis Optica

Neuromielitis Óptica. Patología, diagnóstico y tratamiento en el siglo XXI

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