Pediatric optic neuritis
DOI:
https://doi.org/10.15446/cr.v5n1.76773Palabras clave:
Pediatrics, optic neuritis. (en)pediatría, neuritis óptica. (es)
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https://doi.org/10.15446/cr.v5n1.76773
Pediatric optic neuritis
Editorial
Juan Manuel Pardo-Muñoz
Universidad Nacional de Colombia
- Bogotá Campus - Faculty of Medicine - Department of Surgery
- Bogotá D.C. - Colombia
Corresponding author
Juan Manuel Pardo-Muñoz.
Departamento de Cirugía, Facultad de Medicina,
Universidad Nacional de Colombia.
Bogotá D.C. Colombia.
Email: jmpardom@unal.edu.co.
Received: 13/12/2018 Accepted: 14/01/2019
Optic neuritis in the pediatric population greatly differs from its presentation in the adult population. Firstly, it is usually bilateral in children and mostly unilateral in adults. (1,2,3) Second, it is generally associated with inflammation of the optic disc in pediatrics (1,2,3), whereas the inflammation is often retrobulbar in adults. (2) Finally, pediatric optic neuritis is often considered a post-infectious condition that is not usually associated with the subsequent development of multiple sclerosis (MS) (4,5,2), while in adults, the demyelinating event often precedes the clinical onset of MS. (6)
The neuroimmunological mechanisms involved in several of the demyelinating disorders that affect the optic nerve in children have been elucidated, including the role of B cells and antibody-mediated mechanisms. (7) The diagnosis and management of pediatric optic neuritis is currently based on the search for molecular biomarkers, such as antibodies against aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG), especially in children with recurrent optic neuritis. (7)
The presence of anti-AQP4 antibodies is synonymous with neuromyelitis optica (NMO) (8), while anti-MOG antibodies are mostly found in children with recurrent optic neuritis, acute disseminated encephalomyelitis (ADEM), and some NMO and MS phenotypes. (9,7) Patients with anti-MOG antibodies are usually younger (10) and more likely to develop optic disc inflammation than those without anti-MOG antibodies; these types of optic neuritis tend to be bilateral and more dependent on steroids than in patients with negative MOG antibodies. (9,11) Several recent studies have found that anti-MOG antibodies are generally associated with a course of disease without MS in children. (12,13)
In general terms, in the presence of a more severe initial involvement of the optic nerve, this condition can be associated with NMO, while alterations of the white matter in MRI can be associated with MS. (14) As more biomarkers are identified, it is possible to conclude that infections or immunizations are the triggering stimuli that most frequently activate the cascade of neuroinflammatory events that have historically been diagnosed as post-infectious optic neuritis. (15)
NMO, formerly known as Devic’s disease, is an autoimmune demyelinating disorder that causes recurrent episodes of optic neuritis and transverse myelitis. (16) This disease should be considered as a diagnostic option in any child or adult who develops unilateral or bilateral optic neuritis and myelopathy within a short period of time. (17)
References
1.Kennedy C, Carroll FD. Optic neuritis in children. Arch Ophthalmol. 1960;63:747-55. http://doi.org/bzxh5c.
2.Meadows SP. Doyne memorial lecture (1969).Retrobulbar and optic neuritis in childhood and adolescence. Trans Ophthalmol Soc U K. 1969;89:603-38.
3.Shatriah I, Adlina AR, Alshaarawi S, Wan-Hitam WH. Clinical profile of Malay children with optic neuritis. Pediatr Neurol. 2012;46(5):293-7. http://doi.org/c2tw.
4.Collinge JE, Sprunger DT. Update in pediatric optic neuritis. Curr Opin Ophthalmol. 2013;24(5):448-52. http://doi.org/f5cv5m.
5.El-Dairi MA, Ghasia F, Bhatti MT. Pediatric optic neuritis. Int Ophthalmol Clin. 2012;52(3):29-49. http://doi.org/c2tx.
6.Rizzo JF, Lessell S. Risk of developing multiple sclerosis after uncomplicated optic neuritis. A long-term prospective study. Neurology. 1988;38(2):185-90. http://doi.org/c2tz.
7.Rostasy K, Reindl M. Role of autoantibodies in acquired inflamatory demyelinating diseases of the central nervous system in children. Neuropediatrics. 2013;44(6):297-301. http://doi.org/c2t2.
8.Petzold A, Pittock S, Lennon V, Maggiore C, Weinshenker BG, Plant GT. Neuromyelitis optica-IgG (aquaporin-4) autoantibodies in immune mediated optic neuritis. J Neurol Neurosurg Psychiatry. 2010;81(1):109-11. http://doi.org/fgkmzz.
9.Ramanathan S, Reddel SW, Henderson A, Parratt JD, Barnett M, Gatt PN, et al. Antibodies to myelin oligodendrocyte glycoprotein in bilateral and recurrent optic neuritis. Neurol Neuroimmunol Neuroinflam. 2014;1(4):e40. http://doi.org/c2t3.
10.Fernández-Carbonell C, Vargas-Lowy D, Musallam A, Healy B, McLaughlin K, Wucherpfennig KW, et al. Clinical and MRI phenotype of children with MOG antibodies. Mult Scler. 2016;22(2):174-84. http://doi.org/f8bbsk.
11.Ramanathan S, Prelog K, Barnes EH, Tantsis EM, Reddel SW, Henderson AP, et al. Radiological differentiation of optic neuritis with myelin oligodendrocyte glycoprotein antibodies, aquaporin-4 antibodies, and multiple sclerosis. Mult Scler. 2016;22(4):470-82. http://doi.org/f8f6xs.
12.Hochohen Y, Absoud M, Deiva K, Hemingway C, Nytrova P, Woodhall M, et al. Myelin oligodendrocyte glycoprotein antibodies are associated with a non-MS course in children. Neurol Neuroimmunol Neuroinflamm. 2015;2(2):e81. http://doi.org/c2t4.
13.Ketelslegers IA, Van Pelt DE, Bryde S, Neuteboom RF, Catsman-Berrevoets CE, Hamann D, et al. Anti-MOG antibodies plead against MS diagnosis in an acquired demyelinating cohort. Mult Scler. 2015;21(12):1513-20. http://doi.org/f7txz7.
14.Lim YM, Pyun SY, Lim HT, Jeong IH, Kim KK. First-ever optic neuritis: distinguishing subsequent euromyelitis optica from multiple sclerosis. Neurol Sci. 2014;35(5):781-3. http://doi.org/f54wgw.
15.Tardieu M, Deiva K. Rare inflammatory diseases of the white matter and mimics of multiple sclerosis and related disorders. Neuropediatrics. 2013;44(6):302-8. http://doi.org/f5p3fq.
16.Levin MH, Bennett JL, Verkman AS. Optic neuritis in neuromielitis optica. Prog Retin Eye Res. 2013;36:159-71. http://doi.org/f498zz.
17.Weinschenker BG, Winderchuk DM. The two faces of neuromielitis optica. Neurology. 2014;82(6):466-7. http://doi.org/c2t5.
Recibido: 13 de diciembre de 2018; Aceptado: 14 de enero de 2019
Optic neuritis in the pediatric population greatly differs from its presentation in the adult population. Firstly, it is usually bilateral in children and mostly unilateral in adults. 1,2,3 Second, it is generally associated with inflammation of the optic disc in pediatrics 1,2,3, whereas the inflammation is often retrobulbar in adults. 2 Finally, pediatric optic neuritis is often considered a post-infectious condition that is not usually associated with the subsequent development of multiple sclerosis (MS) 4,5,2, while in adults, the demyelinating event often precedes the clinical onset of MS. 6
The neuroimmunological mechanisms involved in several of the demyelinating disorders that affect the optic nerve in children have been elucidated, including the role of B cells and antibody-mediated mechanisms. 7 The diagnosis and management of pediatric optic neuritis is currently based on the search for molecular biomarkers, such as antibodies against aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG), especially in children with recurrent optic neuritis. 7
The presence of anti-AQP4 antibodies is synonymous with neuromyelitis optica (NMO) 8, while anti-MOG antibodies are mostly found in children with recurrent optic neuritis, acute disseminated encephalomyelitis (ADEM), and some NMO and MS phenotypes. 9,7 Patients with anti-MOG antibodies are usually younger 10 and more likely to develop optic disc inflammation than those without anti-MOG antibodies; these types of optic neuritis tend to be bilateral and more dependent on steroids than in patients with negative MOG antibodies. 9,11 Several recent studies have found that anti-MOG antibodies are generally associated with a course of disease without MS in children. 12,13
In general terms, in the presence of a more severe initial involvement of the optic nerve, this condition can be associated with NMO, while alterations of the white matter in MRI can be associated with MS. 14 As more biomarkers are identified, it is possible to conclude that infections or immunizations are the triggering stimuli that most frequently activate the cascade of neuroinflammatory events that have historically been diagnosed as post-infectious optic neuritis. 15
NMO, formerly known as Devic's disease, is an autoimmune demyelinating disorder that causes recurrent episodes of optic neuritis and transverse myelitis. 16 This disease should be considered as a diagnostic option in any child or adult who develops unilateral or bilateral optic neuritis and myelopathy within a short period of time. 17
REFERENCES
Referencias
Kennedy C, Carroll FD. Optic neuritis in children. Arch Ophthalmol. 1960;63:747-55. http://doi.org/bzxh5c.
Meadows SP. Doyne memorial lecture (1969).Retrobulbar and optic neuritis in childhood and adolescence. Trans Ophthalmol Soc U K. 1969;89:603-38.
Shatriah I, Adlina AR, Alshaarawi S, Wan-Hitam WH. Clinical profile of Malay children with optic neuritis. Pediatr Neurol. 2012;46(5):293-7. http://doi.org/c2tw.
Collinge JE, Sprunger DT. Update in pediatric optic neuritis. Curr Opin Ophthalmol. 2013;24(5):448-52. http://doi.org/f5cv5m.
El-Dairi MA, Ghasia F, Bhatti MT. Pediatric optic neuritis. Int Ophthalmol Clin. 2012;52(3):29-49. http://doi.org/c2tx.
Rizzo JF, Lessell S. Risk of developing multiple sclerosis after uncomplicated optic neuritis. A long-term prospective study. Neurology. 1988;38(2):185-90. http://doi.org/c2tz.
Rostasy K, Reindl M. Role of autoantibodies in acquired inflamatory demyelinating diseases of the central nervous system in children. Neuropediatrics. 2013;44(6):297-301. http://doi.org/c2t2.
Petzold A, Pittock S, Lennon V, Maggiore C, Weinshenker BG, Plant GT. Neuromyelitis optica-IgG (aquaporin-4) autoantibodies in immune mediated optic neuritis. J Neurol Neurosurg Psychiatry. 2010;81(1):109-11. http://doi.org/fgkmzz.
Ramanathan S, Reddel SW, Henderson A, Parratt JD, Barnett M, Gatt PN, et al. Antibodies to myelin oligodendrocyte glycoprotein in bilateral and recurrent optic neuritis. Neurol Neuroimmunol Neuroinflam. 2014;1(4):e40. http://doi.org/c2t3.
Fernández-Carbonell C, Vargas-Lowy D, Musallam A, Healy B, McLaughlin K, Wucherpfennig KW, et al. Clinical and MRI phenotype of children with MOG antibodies. Mult Scler. 2016;22(2):174-84. http://doi.org/f8bbsk.
Ramanathan S, Prelog K, Barnes EH, Tantsis EM, Reddel SW, Henderson AP, et al. Radiological differentiation of optic neuritis with myelin oligodendrocyte glycoprotein antibodies, aquaporin-4 antibodies, and multiple sclerosis. Mult Scler. 2016;22(4):470-82. http://doi.org/f8f6xs.
Hochohen Y, Absoud M, Deiva K, Hemingway C, Nytrova P, Woodhall M, et al. Myelin oligodendrocyte glycoprotein antibodies are associated with a non-MS course in children. Neurol Neuroimmunol Neuroinflamm. 2015;2(2):e81. http://doi.org/c2t4.
Ketelslegers IA, Van Pelt DE, Bryde S, Neuteboom RF, Catsman-Berrevoets CE, Hamann D, et al. Anti-MOG antibodies plead against MS diagnosis in an acquired demyelinating cohort. Mult Scler. 2015;21(12):1513-20. http://doi.org/f7txz7.
Lim YM, Pyun SY, Lim HT, Jeong IH, Kim KK. First-ever optic neuritis: distinguishing subsequent euromyelitis optica from multiple sclerosis. Neurol Sci. 2014;35(5):781-3. http://doi.org/f54wgw.
Tardieu M, Deiva K. Rare inflammatory diseases of the white matter and mimics of multiple sclerosis and related disorders. Neuropediatrics. 2013;44(6):302-8. http://doi.org/f5p3fq.
Levin MH, Bennett JL, Verkman AS. Optic neuritis in neuromielitis optica. Prog Retin Eye Res. 2013;36:159-71. http://doi.org/f498zz.
Weinschenker BG, Winderchuk DM. The two faces of neuromielitis optica. Neurology. 2014;82(6):466-7. http://doi.org/c2t5.
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