| OCR Text |
Show Parainfectious Optic Neuritis: Manifestations in Children vs Adults Daniel Rappoport, MD, Nitza Goldenberg-Cohen, MD, Judith Luckman, MD, Hana Leiba, MD Background: Parainfectious optic neuritis may appear at any age. The aim of our report was to compare the clinical manifestations and outcomes of this form of optic neuritis between children and adults. Methods: The study sample consisted of all patients diagnosed with parainfectious optic neuritis evaluated by 2 neuro-ophthalmology services between 2005 and 2012. Data were collected retrospectively from the medical files. Findings were compared between patients aged 0-18 years and 19 years or older. Results: Ten children (50% female) and 8 adults (50% female) met the study criteria. Mean duration of follow-up was 29.4 months (range, 2-72 months) in the pediatric group and 14.2 months (range, 5-80 months) in the adult group. Respective rates of bilateral disease were 50% and 38%, and all patients had optic disc swelling. The associ-ated pathogen was identified in 60% of the pediatric group, mainly Mycoplasma pneumoniae, and 75% of the adult group, in which no microorganism predominated. The interval from the febrile illness to symptom onset was 6 days (range, 1-14 days) in the pediatric group and 19.5 days (range, 14-30 days) in the adult group. Acute dis-seminated encephalomyelitis (ADEM) was diagnosed in 40% (4/10) of the children and none of the adults. Final visual outcome was 20/30 or better in all patients. There was a higher frequency of bilateral disease in prepubescent vs postpubescent children. Conclusions: Parainfectious optic neuritis is associated with a favorable visual prognosis regardless of age. Children tend to manifest visual symptoms sooner after the ante-cedent infectious illness and more often bilaterally and in conjunction with ADEM. The causative agent is isolated less frequently in children compared with adults. Journal of Neuro-Ophthalmology 2014;34:122-129 doi: 10.1097/WNO.0000000000000113 © 2014 by North American Neuro-Ophthalmology Society Optic neuritis is a major cause of visual impairment and may be due to demyelinating inflammatory and infec-tious etiologies (1-7). Optic neuritis associated with an infectious etiology may be due to direction invasion by the pathogen or after an infectious disease, presumably on an autoimmune basis (1). This latter setting is designated parainfectious optic neuritis. Optic neuritis may occur at any age. The annual incidence is lower in children (0.33-1.66 per 1,000,000) than in adults (5.1 per 1,000,000) (1). The presentation also differs by age group: children more often have bilateral disease, frequently with optic disc edema (5-9). In children, after a visual illness, optic neuritis has been reported to occur in up to 66% of cases (9). Corresponding data in adults are lacking. The aim of our study was to compare the clinical manifestations, path-ogenic organisms, treatment, and outcome of parainfectious optic neuritis between children and adults. METHODS A retrospective case series design was used. The databases of tertiary pediatric (Schneider Children's Medical Center) and adult (Kaplan Medical Center) medical center neuro-ophthalmology services were searched for all patients diag-nosed with optic neuritis from January 2005 through November 2012. The main criterion for inclusion was acute onset of optic neuritis within 1 month after an infectious disease. Only patients who underwent complete evaluation including neuroimaging were included. The presence of an infectious disease was defined by the clinical history, Department of Ophthalmology (DR, HL), Kaplan Medical Center of Israel, Rehovot, Israel; Hebrew University (DR, HL), Hadassah Medical Center, Jerusalem, Israel; Krieger Eye Research Laboratory (NG-C), Felsenstein Medical Research Center, Petach Tikva, Israel; Pediatric Ophthalmology Unit (NG-C), Schneider Children's Medical Center of Israel, Petach Tikva, Israel; Department of Radiology (JL), Rabin Medical Center; Petach Tikva, Israel; and Sackler Faculty of Medicine (NG-C), Tel Aviv University, Tel Aviv, Israel. Supported in part by the Zanvyl and Isabelle Krieger Fund, Balti-more, MD (NG-C). Presented as a poster at the NANOS meeting, Snowbird, UT, Feb-ruary 2013. The authors report no conflicts of interest. Address correspondence to Hana Leiba, MD, Department of Oph-thalmology, Kaplan Medical Center of Israel, POB 1, Rehovot 76100, Israel; E-mail: leiba3@bezeqint.net 122 Rappoport et al: J Neuro-Ophthalmol 2014; 34: 122-129 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. laboratory findings of lymphocytosis or leukocytosis, posi-tive serological testing in blood or cerebrospinal fluid (CSF), and positive blood or CSF culture when performed. The diagnosis of optic neuritis was based on a finding of at least one manifestation of optic nerve disease: reduced visual acuity, abnormal color vision, relative afferent pupillary defect, or visual field defect with or without optic disc edema in one or both eyes. Exclusion criteria were optic neuropathy from causes other than infection, a space-occupying lesion on brain imaging, idiopathic intracranial hypertension, and absence of evidence of infection. The medical files and neuroimaging studies of the eligible patients were reviewed, and demographic, clinical, treatment, and outcome data were recorded. Findings were compared between patients aged 0-18 years and 19 years or older, and between prepubescent and postpubescent chil-dren, alone or combined with the adult group. The study was approved by the institutional review boards of both medical centers. RESULTS Twenty-four patients met the inclusion criteria, of whom 6 were later excluded because of missing hospital or follow-up data. The demographic data of the patients are shown in Tables 1 and 2. There were 10 children aged 7-16 years (mean, 12.7 years), of whom 4 were prepubescent, and 8 adults aged 19-45 years (mean, 31 years). The mean dura-tion of follow-up was 29.4 months (range, 5-72 months) in the pediatric group and 14.2 months (range, 5-40 months) in the adult group. The ophthalmologic findings are shown in Tables 3 and 4. Initial visual acuity was documented in 7 children, of whom 5 (71%) had acuity of 20/150 or worse, and 7 adults, of whom 6 (86%) had visual acuity of 20/40 or better. All patients had either unilateral or bilateral optic disc edema. One adult (patient 3) had a partial macular star. Systemic neurological manifestations (headache, meningitis, enceph-alitis) occurred in 6 children. On magnetic resonance imag-ing (MRI), 4 children (40%) had findings consistent with acute disseminated encephalomyelitis (ADEM) and 1 child (10%) had nonspecific white matter lesions without clinical encephalitis. In the adult group, 2 patients (25%) had non-specific white matter lesions and 1 (12%) had lesions con-sistent with microangiopathic changes. None of the adults had ADEM. Lumbar puncture demonstrated normal opening pressure in all patients. Protein and glucose levels were within normal limits in all the patients, except 2 children with meningitis, although no pathogen was identified in their CSF. An infectious pathogen was identified by serology or culture in 6 children (60%) and 6 adults (75%) (Table 5). The main pathogen in the children's group was Mycoplasma pneumoniae, found in 4 of 6 patients (67%). In the adult group, there was no common pathogen. Four children were prepubescent. Comparison of this subgroup with the postpubescent children alone (6/10) or combined with the adults (total 14 patients) yielded no differences in any of the parameters except for a higher rate of bilateral optic neuritis disease in the prepubescent subgroup (3/4, 75%). Corticosteroid treatment was administered to 7 children and 4 adults (Tables 1 and 2). All treated children received intravenous methylprednisolone (10 mg/kg/day) for at least 3 days. Adults received either oral prednisone (2 mg/kg/day) for 2 weeks or intravenous methylprednisolone (1 g/d) for 3 days followed by oral prednisone 60 mg/d for an additional 11 days. Final visual outcome was 20/30 or better in all patients. There was no correlation between final visual out-come and whether or not steroid treatment was given. There were no instances of recurrent optic neuritis during the follow-up period. DISCUSSION In our study of parainfectious optic neuritis, the gender distribution was equal in the adult group and almost equal in the pediatric group. In most previous studies of optic neuritis, a female predominance has been reported and in children, the disease affected male and female patients equally before puberty and female patients more often after puberty (1,7-9). However, in these reports, cases of parainfectious optic neuritis were included in larger patient cohort studies. In our case series, initial visual acuity tended to be worse in children but both groups had equally good visual outcomes. These results are in agreement with previous studies (1,7,10). Nevertheless, the visual field defects were milder than expected, perhaps owing to the early diagnosis due to the acute febrile disease and early and aggressive treatment (antibiotics and steroids). Interestingly, all pa-tients had swollen discs at presentation. This finding was not mentioned in previous reports. Our results highlight additional differences in clinical characteristics of parainfectious optic neuritis between chil-dren and adults. Time elapsed between the febrile illness and the onset of the visual symptoms was shorter in the pediatric group. This finding might be explained by a more fulminant immune response in children, manifested by the presence of bilateral optic nerve involvement and other neurological symptoms, with or without MRI abnormalities, consistent with ADEM. This may also be the reason why more children than adults experienced bilateral optic nerve involvement. This observation has been described in pediatric optic neuritis regardless of etiology (8,10,11). In the adult group, the diagnosis of optic neuritis days to weeks after the presumed systemic infection support the theory that parainfectious optic neuritis is due to an immunologic-inflammatory reaction (1,5-11). The rare occurrence of uveitis in these cases also may be related to this reaction. Rappoport et al: J Neuro-Ophthalmol 2014; 34: 122-129 123 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. TABLE 1. Clinical data of children with parainfectious optic neuritis Patient No. Age, yr Gender Follow-up, mo Side of ON Preceding Infection/ Pathogen Time From Infection to ON (days) MRI/CT Findings at Diagnosis MRI/CT Findings at the End of Follow-up Treatment 1 14 F 72 Bilateral Viral meningitis (no pathogen found) 5 Lesions in thalamus: ADEM; optic nerve enhancement None Steroids IV 2* 11 F 8 Bilateral M. pneumoniae, febrile illness 14 2 nonspecific periventricular lesions Not done Steroids IV 3 14 M 40 LE Pansinusitis 1 MRI: no lesions Not done Steroids IV + oral amoxicillin 4 13 F 7 RE Sinusitis; EBV IgM 5 MRI: diffuse white matter lesions, ADEM None Steroids IV 5* 7 M 9 LE Meningoencephalitis (no pathogen found) 10 MRI: multiple white matter lesions, ADEM Some lesions disappeared or became smaller Steroids IV + oral cefuroxime + doxycycline + acyclovir IV 6 16 F 12 Bilateral Pneumonia, M. pneumoniae 5 MRI: multiple brain lesions, ADEM; optic nerve enhancement None Steroids IV + oral roxithromycin 7 14 M 18 RE Nonspecific viral illness: brother had chicken pox (varicella) 7-10 days before (no pathogen found) Unknown No brain lesions; optic nerve enhancement Not done Steroids IV 8* 12 M 72 Bilateral Nonspecific headaches, throat culture positive for Streptococcus. pyogenes Unknown No brain lesions Not done Oral penicillin 9 13.5 M 16 RE Headaches, gastroenteritis; M. pneumoniae, IgM 5 No brain lesions Not done None 10* 12.5 F 40 RE M. pneumonia, IgM; no febrile illness Unknown No brain lesions Not done Oral azithromycin *Prepubescent children. ADEM, acute disseminated encephalomyelitis; CT, computed tomography; EBV, Epstein-Barr virus; F, female; LE, left eye; M, male; MRI, magnetic resonance imaging; ON, optic neuritis; RE, right eye. 124 Rappoport et al: J Neuro-Ophthalmol 2014; 34: 122-129 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. TABLE 2. Clinical data of adults with parainfectious optic neuritis Patient No. Age, yr Gender Follow-up (months) Side of ON Preceding Infection/ Pathogen Time From Infection to ON (days) MRI/CT Findings at Diagnosis MRI/CT Findings at End of Follow-up Treatment 1 27 M 6 Bilateral Febrile illness, CMV IgM 28 Enlarged lateral ventricles None Vitamin B12 (because of deficiency) 2 23 F 5 LE Gastroenteritis, CMV IgM 21 No abnormalities Not done Steroids IV and then oral 3 24 M 7.5 RE Headache, Coxiella burnetii/Q fever, IgM 14 One nonspecific white matter lesion Not done Oral doxycycline 4 19 F 5 Bilateral Nonspecific febrile illness (no pathogen found) 14 Optic nerve thickening, no enhancement, no brain lesions Not done Oral steroids 5 34 M 6 LE Nonspecific febrile illness (no pathogen found) 28 Nonspecific white matter lesions Not done None 6 45 M 30 RE Uveitis: posterior; HBV: HBcAg, HBeAb At same time of uveitis White matter lesions: periventricular and supraventricular (microangiopathic changes) Not done Oral steroids + lamivudine + steroid eye drops 7 32 F 40 RE Fever, Toxoplasma IgM 28 No abnormalities Not done Oral clindamycin + pyrimethamine + sulfadiazine + leucovorin CMV, cytomegalovirus; F, female; HBcAg, hepatitis B core antigen; HBcAb, hepatits B E antibody; HBV, hepatitis B virus; LE, left eye; M, male; ON, optic neuritis; RE, right eye. Rappoport et al: J Neuro-Ophthalmol 2014; 34: 122-129 125 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. TABLE 3. Ophthalmologic findings in children with parainfectious optic neuritis Patient No. At Onset Optic Disc Edema Visual Acuity RE LE Dyschromatopsia RAPD VF 1 Bilateral NA NA NA NA NA 2 Bilateral 20/150 20/50 Bilateral RE Binasal constriction 3 LE 20/20 FC NA LE LE superior field defect 4 RE NA = diminished NA NA NA NA 5 LE NA NA = diminished NA LE NA 6 Bilateral LP 20/480 Bilateral severe RE RE: central scotoma + superonasal constriction; LE: inferonasal constriction 7 RE HM 20/22 Bilateral RE Bilateral nasal step 8 Bilateral 20/30 20/30 NA No Bilateral enlarged blind spot 9 RE 20/20 20/20 No NA RE: cecocentral scotoma 10 RE FC 20/20 NA RE RE: enlarged blind spot Patient No. At end of Follow-up Optic Disc Visual Acuity RE LE Dyschromatopsia RAPD VF 1 Bilateral temporal pallor 20/20 20/25 No No Generalized depression 2 Normal 20/25 20/20 No RE mild Normal 3 Normal 20/20 20/20 No No Normal 4 Normal 20/20 20/20 No No Normal 5 LE: mild pallor 20/20 20/30 No No Normal 6 Bilateral temporal pallor 20/20 20/20 No No Bilateral mild nasal constriction 7 Normal 20/25 20/22 No RE: mild RE constriction 8 Normal 20/20 20/20 No No Normal 9 RE: mild pallor; LE: drusen 20/20 20/20 No No RE: mild cecocentral scotoma 10 Normal 20/20 20/20 No RE: trace Normal FC, finger counting; HM, hand motion; LE, left eye; LP, light perception; NA, not available/not checked at onset due to peer condition; RAPD, relative afferent pupillary defect; RE, right eye; VF, visual fields. 126 Rappoport et al: J Neuro-Ophthalmol 2014; 34: 122-129 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. TABLE 4. Ophthalmologic findings in adults with parainfectious optic neuritis Patient No. At Onset Optic Disc Edema BCVA RE LE Dyschromatopsia RAPD VF 1 Bilateral 20/40 20/25 No No Normal 2 LE 20/20 20/30 LE LE LE: concentric constriction 3 RE 20/20 20/20 RE RE RE: enlarged blind spot 4 Bilateral 20/200 20/60 Bilateral RE Bilateral inferior deficit 5 LE 20/40 20/40 Bilateral LE LE: enlarged blind spot 6 RE 20/40 20/20 RE RE RE: enlarged blind spot + inferior arcuate scotoma 7 RE 20/40 20/20 RE RE RE: enlarged blind spot Patient No. At End of Follow-up Optic disc BCVA RE LE Dyschromatopsia RAPD VF 1 RE mild elevation 20/25 20/20 No No Normal 2 Normal 20/20 20/20 No No LE: generalized depression 3 Normal 20/20 20/20 No No Normal 4 Normal 20/20 20/20 No RE RE: enlarged blind spot 5 Normal 20/15 20/15 No No Bilateral inferior field loss 6 RE: disc pallor 20/30 20/20 No No RE: generalized depression 7 Normal 20/20 20/20 No No Normal BCVA, best corrected visual acuity; LE, left eye; NA, not available/not checked due to general deteriorated condition; RAPD, relative afferent pupillary defect; RE, right eye; VF, visual fields. Rappoport et al: J Neuro-Ophthalmol 2014; 34: 122-129 127 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. We were able to identify an infectious pathogen in 6 children (55%) and 6 adults (75%). The majority of the culture studies in the pediatric group (67%) grew M. pneumoniae; 2 of these cases were associated with ADEM. Among the adults with a positive culture, we did not find a common pathogen, which is consistent with the previous reports (3,4,7,11,12). Neurological complications of M. pneumoniae infection in children include encephalitis and ADEM (12-21). Mycoplasma also has been associated with optic neuritis in children and adults (17-20). In our study, half of the children infected with Mycoplasma had bilateral disease, an observation described previously, especially in patients with other neurological involvement such as encephalomy-elitis (16-20). One child in our study (Table 1, patient 4) had Epstein- Barr virus-related sinusitis 5 days preceding the develop-ment of unilateral optic neuritis and ADEM. Our search of the literature yielded only one previous case report of a child with bilateral parainfectious optic neuritis related to Epstein-Barr virus infection (22). There are also reports of 4 adults, 3 of whom had concomitant systemic neuro-logical disease (23-26). There is no consensus regarding treatment of parainfec-tions optic neuritis (1-8,11). In our study, children were given antibiotics and/or systemic corticosteroids more often because they had concurrent systemic disease. However, treat-ment was not associated with improved outcome in terms of visual acuity, visual fields, or residual optic nerve damage. In this case series, parainfectious optic neuritis presented with optic disc swelling in 100% of the cases in both children and adults. However, we found several differences in the clinical presentation between these 2 age groups. The disease in children tends to be diagnosed earlier, presents more often bilaterally, and may be associated with ADEM. Although the causative agent was isolated less frequently in children, it tended to be consistent (usually M. pneumoniae). Even in the presence of negative serology and blood and CSF cultures, patients with a history and clinical presentation suggesting a preceding infection should be treated appropri-ately. In general, the visual prognosis is good. We are aware of the limitations of our study. Our sample size was small, particularly the prepubescent subgroup. We attempted to exclude patients with multiple sclerosis, and none developed clinical or neuroimaging evidence of demyelinating disease. However, the follow-up period was short and brain MRI was repeated in only 5 cases. Finally, ours was a retrospective study that included potential patient selection bias and nonstandardized approaches to patient evaluation and treatment. REFERENCES 1. El-Dairi MA, Ghasia F, Bhatti MT. Pediatric optic neuritis. Int Ophthalmol Clin. 2012;52:29-49. 2. Shams PN, Plant GT. Optic neuritis: a review. Int MS J. 2009;16: 82-89. TABLE 5. Comparison of children and adults with parainfectious optic neuritis in which a pathogenetic organism was identified Characteristics Children Adults Initial VA 71%: ,20/40; 57%: ,20/200 25%: ,20; 40%: ,20/200 Gender 55% female 43% female Laterality 55% bilateral 43% bilateral Mean age (range), yr 13 (7-17) 29 (19-45) Site of inflammation 100% papillitis 100% papillitis Etiology 55% positive specific serology; 4: Mycoplasma (36%); 1: EBV (9%); 1: Streptococcus A (9%) 70% positive specific serology; 2: CMV (25%); 1: Q fever (13%); 1: HBV (13%); 1: Toxoplasma (13%) Associated encephalitis/ADEM 45% None MRI white matter lesions 54% (5: ADEM1 nonspecific lesions) 42% (1: microangiopathic lesions; 2: nonspecific lesions) Time from systemic illness to ON (range), d 6 (1-14) 19 (14-30) Treatment Systemic steroids 72% (all IV) 47% (IV; PO) Systemic antibiotics 55% 29% Vision recovery ,20/40 None None At least 1 eye with #20/25 36% 42% ADEM, acute disseminated encephalomyelitis; CMV-cytomegalovirus; EBV, Epstein-Barr virus; HBV, hepatitis B virus; MRI, magnetic resonance imaging; ON, optic neuritis; VA, visual acuity. 128 Rappoport et al: J Neuro-Ophthalmol 2014; 34: 122-129 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. 3. Bhatti MT. Optic neuropathy from viruses and spirochetes. Int Ophthalmol Clin. 2007;47:37-66. 4. Vaphiades M, Golnik KC. Optic neuropathy from bacteria. Int Ophthalmol Clin. 2007;47:25-36. 5. Absoud M, Cummins C, Desai N, Gika A, McSweeney N, Munot P, Hemingway C, Lim M, Nischal KK, Wassmer E. Childhood optic neuritis clinical features and outcome. Arch Dis Child. 2011;96:860-862. 6. Brady KM, Brar AS, Lee AG, Coats DK, Paysse EA, Steinkuller PG. Optic neuritis in children: clinical features and visual outcome. J AAPOS. 1999;3:98-103. 7. Boomer JA, Siatkowski RM. Optic neuritis in adults and children. Semin Ophthalmol. 2003;18:174-180. 8. Koraszewska-Matuszewska B, Samochowiec-Donocik E, Rynkiewicz E. Optic neuritis in children and adolescents [in Polish]. Klin Oczna. 1995;97:207-210. 9. Morale DS, Siatkowski RM, Howard CW, Warman R. Optic neuritis in children. J Pediatr Ophthalmol Strabismus. 2000;37:254-259. 10. Mihai C, Jubelt B. Post-infectious encephalomyelitis. Curr Neurol Neurosci Rep. 2005;5:440-445. 11. Pau D, Al Zubidi N, Yalamanchili S, Plant GT, Lee AG. Optic neuritis. Eye (Lond). 2011;2:833-842. 12. Daxboeck F. Mycoplasma pneumoniae central nervous system infections. Curr Opin Neurol. 2006;19:374-378. 13. Fisher RS, Clark AW, Wolinsky JS, Parhad IM, Moses H, Mardiney MR. Postinfectious leukoencephalitis complicating Mycoplasma pneumoniae infection. Arch Neurol. 1983;40:109-113. 14. Koskiniemi M. CNS manifestations associated with Mycoplasma pneumoniae infections: summary of cases at the University of Helsinki and review. Clin Infect Dis. 1993;17:S52-S57. 15. Ponka A. Central nervous system manifestations associated with serologically verified Mycoplasma pneumoniae infection. Scand J Infect Dis. 1980;12:175-184. 16. Ginestal RC, Plaza JF, Callejo JM, Rodríguez-Espinosa N, Fernández-Ruiz LC, Masjuán J. Bilateral optic neuritis and Guillain-Barré syndrome following an acute Mycoplasma pneumoniae infection. J Neurol. 2004;251:767-768. 17. Guo ZN, Zhang HL, Bai J, Wu J, Yang Y. Meningitis associated with bilateral optic papillitis following Mycoplasma pneumoniae infection. Neurol Sci. 2012;33:355-358. 18. Milla E, Zografos L, Piguet B. Bilateral optic papillitis following mycoplasma pneumoniae pneumonia. Ophthalmologica. 1998;212:344-346. 19. Nadkarni N, Lisak RP. Guillain-Barre syndrome (GBS) with bilateral optic neuritis and central white matter disease. Neurology. 1993;43:842-843. 20. Pfausler B, Engelhardt K, Kampfl A, Spiss H, Taferner E, Schmutzhard E. Post-infectious central and peripheral nervous system diseases complicating Mycoplasma pneumoniae infection. Report of three cases and review of the literature. Eur J Neurol. 2002;9:93-96. 21. Bae JW, Kim HJ, Chang GY, Kim EJ. Combined striatum, brain stem, and optic nerve involvement due to Mycoplasma pneumoniae in an ambulatory child. Case Rep Neurol. 2011;3:109-112. 22. Pahor D. Bilateral optic neuritis in a child following Epstein-Barr virus infection. Coll Antropol. 2005;29:129-132. 23. An JY, Yoon B, Kim JS, Song IU, Lee KS, Kim YI. Guillain-Barre syndrome with optic neuritis and a focal lesion in the central white matter following Epstein-Barr virus infection. Intern Med. 2008;47:1539-1542. 24. Corssmit EP, Leverstein-van Hall MA, Portegies P, Bakker P. Severe neurological complications in association with Epstein- Barr virus infection. J Neurovirol. 1997;3:460-464. 25. Phowthongkum P, Phantumchinda K, Jutivorakool K, Suankratay C. Basal ganglia and brainstem encephalitis, optic neuritis, and radiculomyelitis in Epstein-Barr virus infection. J Infect. 2007;54:e141-e144. 26. Anderson MD, Kennedy CA, Lewis AW, Christensen GR. Retrobulbar neuritis complicating acute Epstein-Barr virus infection. Clin Infect Dis. 1994;18:799-801. Rappoport et al: J Neuro-Ophthalmol 2014; 34: 122-129 129 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
