Seminars in Ophthalmology, 2014; 29(1): 18–21 ! Informa Healthcare USA, Inc. ISSN: 0882-0538 print / 1744-5205 online DOI: 10.3109/08820538.2013.835837
Acute Disseminated Encephalomyelitis Without Optic Neuritis Followed by Optic Neuritis in a Child Due to the Sudden Cessation of Steroid Therapy
Department of Ophthalmology, Dong-A University College of Medicine, Busan, Republic of Korea
ABSTRACT Acute disseminated encephalitis (ADEM) is an autoimmune demyelinating disorder of the central nervous system that usually occurs in children after viral infection or vaccination. It is not uncommon for ADEM to be accompanied by optic neuritis. However, ADEM followed by optic neuritis is a rare. We report the case of a 6year-old girl who initially presented with ADEM (without optic neuritis) due to a live measles, mumps, and rubella vaccine and was treated with intravenous high-dose corticosteroids. After steroid therapy, she recovered neurologically and was not prescribed any medication, including an oral steroid taper, for use after discharge. Three weeks later, she developed unilateral optic neuritis and was again treated with steroid therapy. This is a rare case of ADEM without optic neuritis in a child, followed by optic neuritis due to the sudden cessation of steroid therapy. Further studies and follow-ups are needed to determine whether ADEM followed by optic neuritis can be considered a specific clinical form of this disorder. Keywords: Acute disseminated encephalomyelitis, MMR vaccine, pediatric optic neuritis, steroid-dependent relapse, vaccination
Acute disseminated encephalitis (ADEM) is an acute autoimmune demyelinating disorder of the central nervous system that usually occurs in children after viral infection or vaccination.1-3 It is typically considered to be monophasic. Optic neuritis is the most common ocular manifestation in children with ADEM, and ADEM with optic neuritis is not uncommon, with bilateral optic neuritis with optic disc edema being the most common form.4–6 Although ADEM attacks followed by optic neuritis are rare, there has been one reported case of ADEM followed by nine optic neuritis attacks.7 We report the case of six-year-old girl who initially presented with ADEM (without optic neuritis) due to a live measles, mumps, and rubella vaccine (MMR) and then recovered after treatment with intravenous high-dose corticosteroids. After treatment, she
developed optic neuritis due to a sudden cessation of steroid therapy because she was not prescribed any medication after discharge.
CASE REPORT
20 13
Semin Ophthalmol Downloaded from informahealthcare.com by University of Alberta on 10/23/14 For personal use only.
Won Yeol Ryu, MD, Eun Jung Sohn, MD, Yoon Hyung Kwon, MD, Woo Jin Jeung, MD, Hee Bae Ahn, MD, Woo Chan Park, MD, and Sae Heun Rho, MD
A previously healthy six-year-old girl was admitted to the ophthalmic hospital due to headache, ocular pain, and blurred vision in the right eye for several days. At 10 weeks prior to admission for blurred vision, she had been administered a live MMR vaccine and, two weeks later, she had a long-lasting fever. Two weeks after the cessation of the fever, she presented at a children’s hospital with mild right hemiparesis and right facial palsy. Brain magnetic resonance imaging (MRI) revealed ill-defined inhomogenous high signals
Received 8 March 2013; accepted 9 August 2013; published online 18 October 2013 Correspondence: Won Yeol Ryu, M.D., # 3-1 Dongdaeshin-Dong, Seo-gu, Busan, 602-715, Republic of Korea. E-mail: [email protected]
18
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Acute Disseminated Encephalomyelitis Followed by Optic Neuritis
19
FIGURE 1. Magnetic resonance images. Axial fluid-attenuated inversion recovery images for a patient with initial acute disseminated encephalomyelitis (ADEM) showing multiple lesions in both basal ganglia (A), the left thalamus, the left cerebellum (B), and the left temporal area (C). During a later episode of optic neuritis, axial T2-weighted images showed a marked resolution of the previous lesions (D) and slightly thickened and increased signal intensity for the right optic nerve (E). Three months after ADEM treatment, the brain lesion previously observed in the left basal ganglia had decreased in size (F). 144x160mm (300 x 300 DPI).
in both basal ganglia and the left thalamus (Figure 1A) and ill-defined high signals in the cerebellum (Figure 1B) and temporal area (Figure 1C). The spine MRI was normal, and cerebrospinal fluid (CSF) analysis did not show evidence of infection. Neither oligoclonal bands (OCB) in the CSF nor serum antiaquaporin-4 antibodies (AQP4-Ab) were detected. These findings indicate signs of optic neuritis, including optic nerve abnormalities on the brain MRI, blurred vision, a relative afferent pupillary defect (RAPD), ocular pain, and reduced color vision, were not observed at this time. Based on the diagnosis of ADEM, the patient was treated with intravenous methylprednisolone 30 mg/kg/day for three days in the children’s hospital, and her neurological manifestations resolved. Thereafter, she was not prescribed any medication, including an oral steroid taper, for use after discharge. Three weeks after the cessation of steroid therapy, she presented at the ophthalmic hospital with !
2014 Informa Healthcare USA, Inc.
headache, ocular pain, and blurred vision in the right eye. Her visual acuity was 10/20 in the right eye and 20/20 in the left eye. There was a RAPD on the right eye. Funduscopy and optical coherence tomography (OCT, Carl Zeiss Meditec Inc., Dublin, CA, USA) revealed a swollen disc on the right. Visual field testing revealed a central scotoma and an enlarged blind spot. There was a delayed latency and a decreased amplitude of pattern visual evoked potentials in the right eye. MRI showed resolution of the multiple brain lesions observed previously, including that in the left basal ganglia (Figure 1D). However, a new lesion was present in the right optic nerve. This nerve was slightly thickened, and the sheath had an increased signal intensity (Figure 1E). A second test for serum AQP4-Ab was negative. There was no serological evidence of infection. The patient had reduced color vision in the right eye. She was diagnosed with optic neuritis of the right eye based on the clinical and MRI findings described
20 W. Y. Ryu et al.
Semin Ophthalmol Downloaded from informahealthcare.com by University of Alberta on 10/23/14 For personal use only.
above, and she received 30 mg of intravenous methylprednisolone every day for three days, followed by oral prednisolone 1 mg/kg/day for 11 days with subsequent tapering for 5.5 weeks. One week after steroid therapy, her visual acuity was 20/20 in the right eye and her visual field had improved. Two months later, the thickness of the retinal nerve fiber layer on OCT was in the normal range. Three months after ADEM treatment, the previously observed lesion in the left ganglia was present on a follow-up MRI; however, it had continuously improved, and we did not find any new lesions (Figure 1F). The patient has been observed for six months without neurological complications or visual relapse.
DISCUSSION ADEM is a relatively rare demyelinating disorder that usually follows a viral infection or vaccination. ADEM with optic neuritis in particular is a rare complication associated with vaccination.3,8 Among vaccines, the measles, mumps, or rubella vaccine is the most common cause of post-vaccination ADEM, although various other vaccines, including those for hepatitis B, polio, tetanus, Japanese B encephalitis, and influenza, may cause ADEM.2,9,10 Although in ADEM there is typically a latency of one to two weeks between a prolonged febrile illness and neurological manifestations associated with ADEM,2,10 post-vaccination ADEM can have a slightly longer latency.2 Our patient had a continuously febrile illness after vaccination with a live MMR vaccine and, two weeks thereafter, she presented with the onset of neurological symptoms. During that time, she presented with ADEM that was not simutaneouly accompanied by optic neuritis. Therefore, we believe that a detailed vaccination history should be obtained when there is suspicion of ADEM in a child. It is not uncommon for ADEM to be accompanied by optic neuritis, and the frequency of ADEM with optic neuritis has been reported to be 9.1–22.9%.6,10,11 Idiopathic optic neuritis is more commonly the retrobulbar form, whereas optic-neuritis-associated ADEM is commonly associated with optic disk edema.5 In a recent study, Huppke et al.7 suggested that ADEM followed by optic neuritis is rare and should be considered a specific clinical form. All patients in their study had high titers for serum anti-myelin oligodendrocyte glycoprotein (MOG) antibodies. In the case of our patient, although ADEM without optic neuritis developed after the sudden cessation of steroid therapy, the neurological symptoms due to ADEM resolved and, three weeks thereafter, optic neuritis developed with ocular pain, reduced visual acuity, and headache. We do not know whether our case is consistent with the specific clinical
form detailed in Huppke et al.’s study7 because we did not test for serum anti-MOG antibodies. The interval between ADEM and optic neuritis varied from three weeks to two years in their study,7 and the optic neuritis presented three weeks after the ADEM attack in our patient. In addition, other findings for our patient, including the results of OCB AQP4-Ab tests, serological tests, CSF analysis, and MRI, were analogous to the findings for their patients. Although there have been no controlled clinical trials for pediatic ADEM, the recommended treatment is intravenous methylprednisolone (10 to 30 mg/kg/ day) for three to five days, followed by oral prednisolone (1 to 2 mg/kg/day) for 1–2 weeks with subsequent tapering over 4–6 weeks.3,5,10,12,13 The sudden cessation of steroid therapy puts the patient at risk for relapse, and it has been reported that steroid tapers over a period of less three weeks are associated with a greater risk of ADEM relapse.3,6,10,12 In addition, because research has shown that ADEM relapse is a prognostic factor for the development of optic neuritis,11 more attention should be paid to the relationship between time of onset of ADEM and optic neuritis, and additional studies should be conducted. In our case, after treatment with intravenous highdose steroids at a children’s hospital, the patient was not given any oral steroids, and after the cessation of the intravenous steroids, optic neuritis, which was not initially present, developed three weeks later. The optic nerve was slightly thickened, and the sheath showed an increased signal intensity on enhanced MRI scans. However, because the previous brain lesions were improving and because there were no neurological symptoms except headache, it is difficult to attribute these new findings to a relapse of ADEM. Therefore, we believe that this case report provides important about the development of optic neuritis due to the sudden cessation of steroid therapy in a child with ADEM without optic neuritis. In addition, this case may be consistent with a comment7 that ADEM followed by optic neuritis is a specific clinical form of this disease. We think that further studies of this disease are needed. In conclusion, because ADEM in children is often accompanied by optic neuritis and because optic neuritis rarely occurs after an ADEM attack, as in this case, ADEM is a neuro-ophthalmologic disease that general ophthalmologists should pay attention to. In particular, although ADEM responds to intravenous high-dose methylprednisolone, oral steroid with subsequent tapering should be used. In addition, we think that further studies and follow-up are needed to determine whether ADEM followed by optic neuritis can be considered a specific clinical form of this disorder. Seminars in Ophthalmology
Acute Disseminated Encephalomyelitis Followed by Optic Neuritis
DECLARATION OF INTEREST The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
7.
8.
Semin Ophthalmol Downloaded from informahealthcare.com by University of Alberta on 10/23/14 For personal use only.
REFERENCES 1. Garg RK. Acute disseminated encephalomyelitis. Postgrad Med J 2003;79:11–17. 2. Menge T, Hemmer B, Nessler S, et al. Acute disseminated encephalomyelitis: an update. Arch Neurol. 2005;62: 1673–1680. 3. Tenembaum S, Chitnis T, Ness J, Hahn JS; International Pediatric MS Study Group. Acute disseminated encephalomyelitis. Neurology 2007;68(Suppl):S23–S36. 4. Bangsgaard R, Larsen VA, Milea D. Isolated bilateral optic neuritis in acute disseminated encephalomyelitis. Acta Ophthalmol Scand 2006;84:815–817. 5. Kotlus BS, Slavin ML, Guthrie DS, Kodsi SR. Ophthalmologic manifestations in pediatric patients with acute disseminated encephalomyelitis. J AAPOS 2005;9: 179–183. 6. Dale RC, de Sousa C, Chong WK, et al. Acute disseminated encephalomyelitis, multiphasic disseminated
!
2014 Informa Healthcare USA, Inc.
9.
10.
11.
12.
13.
21
encephalomyelitis and multiple sclerosis in children. Brain 2000;123:2407-2422. Huppke P, Rostasy K, Karenfort M, et al. Acute disseminated encephalomyelitis followed by recurrent or monophasic optic neuritis in pediatric patients. Mult Scler 2013;19:941–946. Stevenson VL, Acheson JF, Ball J, Plant GT. Optic neuritis following measles/rubella vaccination in two 13-year-old children. Br J Ophthalmol 1996;80: 1110–1111. Huynh W, Cordato DJ, Kehdi E, et al. Post-vaccination encephalomyelitis: literature review and illustrative case. J Clin Neurosci 2008;15:1315–1322. Tenembaum S, Chamoles N, Fejerman N. Acute disseminated encephalomyelitis: a long-term follow-up study of 84 pediatric patients. Neurology 2002;59:1224–1231. Mikaeloff Y, Caridade G, Husson B, et al.; Neuropediatric KIDSEP Study Group of the French Neuropediatric Society. Acute disseminated encephalomyelitis cohort study: prognostic factors for relapse. Eur J Paediatr Neurol 2007;11: 90–95. Pohl D, Tenembaum S. Treatment of acute disseminated encephalomyelitis. Curr Treat Options Neurol 2012;14: 264–275. Ellis BD, Kosmorsky GS, Cohen BH. Medical and surgical management of acute disseminated encephalitis. J Neuroophthalmol 1994;14:210–213.
Acute Disseminated Encephalomyelitis Without Optic Neuritis Followed by Optic Neuritis in a Child Due to the Sudden Cessation of Steroid Therapy
Department of Ophthalmology, Dong-A University College of Medicine, Busan, Republic of Korea
ABSTRACT Acute disseminated encephalitis (ADEM) is an autoimmune demyelinating disorder of the central nervous system that usually occurs in children after viral infection or vaccination. It is not uncommon for ADEM to be accompanied by optic neuritis. However, ADEM followed by optic neuritis is a rare. We report the case of a 6year-old girl who initially presented with ADEM (without optic neuritis) due to a live measles, mumps, and rubella vaccine and was treated with intravenous high-dose corticosteroids. After steroid therapy, she recovered neurologically and was not prescribed any medication, including an oral steroid taper, for use after discharge. Three weeks later, she developed unilateral optic neuritis and was again treated with steroid therapy. This is a rare case of ADEM without optic neuritis in a child, followed by optic neuritis due to the sudden cessation of steroid therapy. Further studies and follow-ups are needed to determine whether ADEM followed by optic neuritis can be considered a specific clinical form of this disorder. Keywords: Acute disseminated encephalomyelitis, MMR vaccine, pediatric optic neuritis, steroid-dependent relapse, vaccination
Acute disseminated encephalitis (ADEM) is an acute autoimmune demyelinating disorder of the central nervous system that usually occurs in children after viral infection or vaccination.1-3 It is typically considered to be monophasic. Optic neuritis is the most common ocular manifestation in children with ADEM, and ADEM with optic neuritis is not uncommon, with bilateral optic neuritis with optic disc edema being the most common form.4–6 Although ADEM attacks followed by optic neuritis are rare, there has been one reported case of ADEM followed by nine optic neuritis attacks.7 We report the case of six-year-old girl who initially presented with ADEM (without optic neuritis) due to a live measles, mumps, and rubella vaccine (MMR) and then recovered after treatment with intravenous high-dose corticosteroids. After treatment, she
developed optic neuritis due to a sudden cessation of steroid therapy because she was not prescribed any medication after discharge.
CASE REPORT
20 13
Semin Ophthalmol Downloaded from informahealthcare.com by University of Alberta on 10/23/14 For personal use only.
Won Yeol Ryu, MD, Eun Jung Sohn, MD, Yoon Hyung Kwon, MD, Woo Jin Jeung, MD, Hee Bae Ahn, MD, Woo Chan Park, MD, and Sae Heun Rho, MD
A previously healthy six-year-old girl was admitted to the ophthalmic hospital due to headache, ocular pain, and blurred vision in the right eye for several days. At 10 weeks prior to admission for blurred vision, she had been administered a live MMR vaccine and, two weeks later, she had a long-lasting fever. Two weeks after the cessation of the fever, she presented at a children’s hospital with mild right hemiparesis and right facial palsy. Brain magnetic resonance imaging (MRI) revealed ill-defined inhomogenous high signals
Received 8 March 2013; accepted 9 August 2013; published online 18 October 2013 Correspondence: Won Yeol Ryu, M.D., # 3-1 Dongdaeshin-Dong, Seo-gu, Busan, 602-715, Republic of Korea. E-mail: [email protected]
18
Semin Ophthalmol Downloaded from informahealthcare.com by University of Alberta on 10/23/14 For personal use only.
Acute Disseminated Encephalomyelitis Followed by Optic Neuritis
19
FIGURE 1. Magnetic resonance images. Axial fluid-attenuated inversion recovery images for a patient with initial acute disseminated encephalomyelitis (ADEM) showing multiple lesions in both basal ganglia (A), the left thalamus, the left cerebellum (B), and the left temporal area (C). During a later episode of optic neuritis, axial T2-weighted images showed a marked resolution of the previous lesions (D) and slightly thickened and increased signal intensity for the right optic nerve (E). Three months after ADEM treatment, the brain lesion previously observed in the left basal ganglia had decreased in size (F). 144x160mm (300 x 300 DPI).
in both basal ganglia and the left thalamus (Figure 1A) and ill-defined high signals in the cerebellum (Figure 1B) and temporal area (Figure 1C). The spine MRI was normal, and cerebrospinal fluid (CSF) analysis did not show evidence of infection. Neither oligoclonal bands (OCB) in the CSF nor serum antiaquaporin-4 antibodies (AQP4-Ab) were detected. These findings indicate signs of optic neuritis, including optic nerve abnormalities on the brain MRI, blurred vision, a relative afferent pupillary defect (RAPD), ocular pain, and reduced color vision, were not observed at this time. Based on the diagnosis of ADEM, the patient was treated with intravenous methylprednisolone 30 mg/kg/day for three days in the children’s hospital, and her neurological manifestations resolved. Thereafter, she was not prescribed any medication, including an oral steroid taper, for use after discharge. Three weeks after the cessation of steroid therapy, she presented at the ophthalmic hospital with !
2014 Informa Healthcare USA, Inc.
headache, ocular pain, and blurred vision in the right eye. Her visual acuity was 10/20 in the right eye and 20/20 in the left eye. There was a RAPD on the right eye. Funduscopy and optical coherence tomography (OCT, Carl Zeiss Meditec Inc., Dublin, CA, USA) revealed a swollen disc on the right. Visual field testing revealed a central scotoma and an enlarged blind spot. There was a delayed latency and a decreased amplitude of pattern visual evoked potentials in the right eye. MRI showed resolution of the multiple brain lesions observed previously, including that in the left basal ganglia (Figure 1D). However, a new lesion was present in the right optic nerve. This nerve was slightly thickened, and the sheath had an increased signal intensity (Figure 1E). A second test for serum AQP4-Ab was negative. There was no serological evidence of infection. The patient had reduced color vision in the right eye. She was diagnosed with optic neuritis of the right eye based on the clinical and MRI findings described
20 W. Y. Ryu et al.
Semin Ophthalmol Downloaded from informahealthcare.com by University of Alberta on 10/23/14 For personal use only.
above, and she received 30 mg of intravenous methylprednisolone every day for three days, followed by oral prednisolone 1 mg/kg/day for 11 days with subsequent tapering for 5.5 weeks. One week after steroid therapy, her visual acuity was 20/20 in the right eye and her visual field had improved. Two months later, the thickness of the retinal nerve fiber layer on OCT was in the normal range. Three months after ADEM treatment, the previously observed lesion in the left ganglia was present on a follow-up MRI; however, it had continuously improved, and we did not find any new lesions (Figure 1F). The patient has been observed for six months without neurological complications or visual relapse.
DISCUSSION ADEM is a relatively rare demyelinating disorder that usually follows a viral infection or vaccination. ADEM with optic neuritis in particular is a rare complication associated with vaccination.3,8 Among vaccines, the measles, mumps, or rubella vaccine is the most common cause of post-vaccination ADEM, although various other vaccines, including those for hepatitis B, polio, tetanus, Japanese B encephalitis, and influenza, may cause ADEM.2,9,10 Although in ADEM there is typically a latency of one to two weeks between a prolonged febrile illness and neurological manifestations associated with ADEM,2,10 post-vaccination ADEM can have a slightly longer latency.2 Our patient had a continuously febrile illness after vaccination with a live MMR vaccine and, two weeks thereafter, she presented with the onset of neurological symptoms. During that time, she presented with ADEM that was not simutaneouly accompanied by optic neuritis. Therefore, we believe that a detailed vaccination history should be obtained when there is suspicion of ADEM in a child. It is not uncommon for ADEM to be accompanied by optic neuritis, and the frequency of ADEM with optic neuritis has been reported to be 9.1–22.9%.6,10,11 Idiopathic optic neuritis is more commonly the retrobulbar form, whereas optic-neuritis-associated ADEM is commonly associated with optic disk edema.5 In a recent study, Huppke et al.7 suggested that ADEM followed by optic neuritis is rare and should be considered a specific clinical form. All patients in their study had high titers for serum anti-myelin oligodendrocyte glycoprotein (MOG) antibodies. In the case of our patient, although ADEM without optic neuritis developed after the sudden cessation of steroid therapy, the neurological symptoms due to ADEM resolved and, three weeks thereafter, optic neuritis developed with ocular pain, reduced visual acuity, and headache. We do not know whether our case is consistent with the specific clinical
form detailed in Huppke et al.’s study7 because we did not test for serum anti-MOG antibodies. The interval between ADEM and optic neuritis varied from three weeks to two years in their study,7 and the optic neuritis presented three weeks after the ADEM attack in our patient. In addition, other findings for our patient, including the results of OCB AQP4-Ab tests, serological tests, CSF analysis, and MRI, were analogous to the findings for their patients. Although there have been no controlled clinical trials for pediatic ADEM, the recommended treatment is intravenous methylprednisolone (10 to 30 mg/kg/ day) for three to five days, followed by oral prednisolone (1 to 2 mg/kg/day) for 1–2 weeks with subsequent tapering over 4–6 weeks.3,5,10,12,13 The sudden cessation of steroid therapy puts the patient at risk for relapse, and it has been reported that steroid tapers over a period of less three weeks are associated with a greater risk of ADEM relapse.3,6,10,12 In addition, because research has shown that ADEM relapse is a prognostic factor for the development of optic neuritis,11 more attention should be paid to the relationship between time of onset of ADEM and optic neuritis, and additional studies should be conducted. In our case, after treatment with intravenous highdose steroids at a children’s hospital, the patient was not given any oral steroids, and after the cessation of the intravenous steroids, optic neuritis, which was not initially present, developed three weeks later. The optic nerve was slightly thickened, and the sheath showed an increased signal intensity on enhanced MRI scans. However, because the previous brain lesions were improving and because there were no neurological symptoms except headache, it is difficult to attribute these new findings to a relapse of ADEM. Therefore, we believe that this case report provides important about the development of optic neuritis due to the sudden cessation of steroid therapy in a child with ADEM without optic neuritis. In addition, this case may be consistent with a comment7 that ADEM followed by optic neuritis is a specific clinical form of this disease. We think that further studies of this disease are needed. In conclusion, because ADEM in children is often accompanied by optic neuritis and because optic neuritis rarely occurs after an ADEM attack, as in this case, ADEM is a neuro-ophthalmologic disease that general ophthalmologists should pay attention to. In particular, although ADEM responds to intravenous high-dose methylprednisolone, oral steroid with subsequent tapering should be used. In addition, we think that further studies and follow-up are needed to determine whether ADEM followed by optic neuritis can be considered a specific clinical form of this disorder. Seminars in Ophthalmology
Acute Disseminated Encephalomyelitis Followed by Optic Neuritis
DECLARATION OF INTEREST The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
7.
8.
Semin Ophthalmol Downloaded from informahealthcare.com by University of Alberta on 10/23/14 For personal use only.
REFERENCES 1. Garg RK. Acute disseminated encephalomyelitis. Postgrad Med J 2003;79:11–17. 2. Menge T, Hemmer B, Nessler S, et al. Acute disseminated encephalomyelitis: an update. Arch Neurol. 2005;62: 1673–1680. 3. Tenembaum S, Chitnis T, Ness J, Hahn JS; International Pediatric MS Study Group. Acute disseminated encephalomyelitis. Neurology 2007;68(Suppl):S23–S36. 4. Bangsgaard R, Larsen VA, Milea D. Isolated bilateral optic neuritis in acute disseminated encephalomyelitis. Acta Ophthalmol Scand 2006;84:815–817. 5. Kotlus BS, Slavin ML, Guthrie DS, Kodsi SR. Ophthalmologic manifestations in pediatric patients with acute disseminated encephalomyelitis. J AAPOS 2005;9: 179–183. 6. Dale RC, de Sousa C, Chong WK, et al. Acute disseminated encephalomyelitis, multiphasic disseminated
!
2014 Informa Healthcare USA, Inc.
9.
10.
11.
12.
13.
21
encephalomyelitis and multiple sclerosis in children. Brain 2000;123:2407-2422. Huppke P, Rostasy K, Karenfort M, et al. Acute disseminated encephalomyelitis followed by recurrent or monophasic optic neuritis in pediatric patients. Mult Scler 2013;19:941–946. Stevenson VL, Acheson JF, Ball J, Plant GT. Optic neuritis following measles/rubella vaccination in two 13-year-old children. Br J Ophthalmol 1996;80: 1110–1111. Huynh W, Cordato DJ, Kehdi E, et al. Post-vaccination encephalomyelitis: literature review and illustrative case. J Clin Neurosci 2008;15:1315–1322. Tenembaum S, Chamoles N, Fejerman N. Acute disseminated encephalomyelitis: a long-term follow-up study of 84 pediatric patients. Neurology 2002;59:1224–1231. Mikaeloff Y, Caridade G, Husson B, et al.; Neuropediatric KIDSEP Study Group of the French Neuropediatric Society. Acute disseminated encephalomyelitis cohort study: prognostic factors for relapse. Eur J Paediatr Neurol 2007;11: 90–95. Pohl D, Tenembaum S. Treatment of acute disseminated encephalomyelitis. Curr Treat Options Neurol 2012;14: 264–275. Ellis BD, Kosmorsky GS, Cohen BH. Medical and surgical management of acute disseminated encephalitis. J Neuroophthalmol 1994;14:210–213.
