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Neuro-ophthalmological manifestations as complication of an infection with Mycoplasma pneumoniae and subsequent development of disseminated acute encephalitis
Manifestaciones neuroftalmológicas como complicación de una infección por Mycoplasma pneumoniae y desarrollo posterior de una encefalitis aguda diseminada
M. Molero-Senosiain
, B. Domingo-Gordo, C. Fernández Cabrera, E. Hernández-García, R. Gómez de Liaño
Corresponding author
Departamento de Neuroftalmología, Hospital Clínico San Carlos, Madrid, Spain
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Molero-Senosiain, B. Domingo-Gordo, C. Fernández Cabrera, E. Hernández-García, R. Gómez de Liaño" "autores" => array:5 [ 0 => array:4 [ "nombre" => "M." "apellidos" => "Molero-Senosiain" "email" => array:1 [ 0 => "merce.molero@gmail.com" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:2 [ "nombre" => "B." "apellidos" => "Domingo-Gordo" ] 2 => array:2 [ "nombre" => "C." "apellidos" => "Fernández Cabrera" ] 3 => array:2 [ "nombre" => "E." "apellidos" => "Hernández-García" ] 4 => array:2 [ "nombre" => "R." "apellidos" => "Gómez de Liaño" ] ] "afiliaciones" => array:1 [ 0 => array:2 [ "entidad" => "Departamento de Neuroftalmología, Hospital Clínico San Carlos, Madrid, Spain" "identificador" => "aff0005" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "<span class="elsevierStyleItalic">Corresponding author</span>." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Manifestaciones neuroftalmológicas como complicación de una infección por <span class="elsevierStyleItalic">Mycoplasma pneumoniae</span> y desarrollo posterior de una encefalitis aguda diseminada" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1162 "Ancho" => 1740 "Tamanyo" => 201798 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Supplementary tests of patient 1 (CPG) (A) angio-MRI images without alterations. (B) MRI with gadolinium of cervical spinal column without alterations. (C) axial MRI image in FLAIR sequence with gadolinium showing hyperintense lesions in the capsulo-thalamic region suggesting demyelinizing disease. (D) MRI taken 6 months after the first, showing absence of lesions. (E) Humphrey 24-2 campimetry within normal ranges in both eyes (minimum paracentral defect in LE).</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Acute disseminated encephalomyelitis (ADEM) is one of the most frequent causes of white matter compromise in children in school age and in young adults. It is estimated that the incidence of ADEM is approximately 0.2–0.64 cases/100<span class="elsevierStyleHsp" style=""></span>000 inhabitants/year.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">ADEM is regarded as an immunomediated inflammatory-demyelinizing disease with neurological clinic expressing generally after an infection or vaccination, with acute or subacute onset.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a> Association with an infectious agent is assumed in the majority of cases although its etiology is confirmed in only 25% of cases. The most frequent microorganisms are varicella zoster, measles and rubella,<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> although it is recommended to conduct a large battery of serologies to discard other agents such as human immunodeficiency virus, hepatitis A, B and C virus, Epstein Barr virus, cytomegalovirus, herpes simplex virus 1 and 2, parotitis, coronavirus, Coxsackie B, other nonviral agents such as <span class="elsevierStyleItalic">Mycoplasma pneumoniae</span> (<span class="elsevierStyleItalic">M. pneumoniae</span>), Campylobacter, Chlamydia and beta hemolytic streptococcus.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,2</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">The pathogeny includes selfimmune response to a common antigen present in myelin and in the infectious agent. Participation of lymphocyte B has been described through antiganglioside antibodies (GM1) and lymphocytes T against several myelin antigens such as proteolipid protein, oligodendrocyte myelin glycoprotein or basic myelin protein (BMP), among others.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">In what concerns clinic expressions, the literature describes first a prodromic phase similar to a fever-like condition with high temperature and general discomfort, developing with the triggering agent the predominantly neurological and neuro-ophthalmological clinic symptoms 3–6 weeks after the initial contact. In addition, aseptic meningitis has been described as well as polyradiculitis, hemiparesis, cranial neuropathy, ophthalmoparesis, optic neuritis, seizures, long pathways compromise with spasticity or hyper-reflexia and cerebellar ataxia, among others.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2,4</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">In addition, complications secondary to this clinic condition have been described, including mucocutaneous lesions, arthritis, hemolytic anemia, hemorrhages, pericarditis and severe neurological alterations such as myelitis, meningoencephalitis or even coma.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">The imaging test of choice is nuclear magnetic resonance (MRI) which in T2 emphasizes reversible, well-defined and hyperintense lesions in the white matter, which generally affect the thalamus and basal ganglia. Said lesions could also be found in the gray matter. Even so, images isolated in MRI are not diagnostic for ADEM.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">M. pneumoniae</span> is a free bacteria without cellular walls. It is a causative agent for community acquired pneumonia although it rarely causes central nervous system alterations (0.1%)<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2,3</span></a> (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>).</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0040" class="elsevierStylePara elsevierViewall">The objectives of this paper are to describe 2 neuro-ophthalmological clinic conditions in children due to systemic <span class="elsevierStyleItalic">M. pneumoniae</span> infection and to raise awareness about this etiology and its prognostic importance.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Clinic case reports</span><p id="par0045" class="elsevierStylePara elsevierViewall">Clinic cases of 2 girls aged 14 and 12 years old who visited the Emergency Dept. due to 2 different conditions involving ophthalmological and neurological symptoms. The first exhibited bilateral internuclear ophthalmoplegia with diplopia and left eye (LE) major adduction limitation. Major nystagmus was observed in right eye (RE) abduction in spring fashion with fast phase toward the left, constituting asymmetric internuclear ophthalmoplegia. Visual acuity (VA): 1 in both eyes. Normal convergence with rupture point less than 5<span class="elsevierStyleHsp" style=""></span>cm. neurological examination did not observe dysdiadochokinesia, ataxia or alterations in reflexes or muscular strength, with negative fatigue test. Relevant personal antecedents included idiopathic intracranial hypertension 7 years earlier that was resolved with acetazolamide and corticosteroids.</p><p id="par0050" class="elsevierStylePara elsevierViewall">Multiple imaging tests were conducted (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>), with nuclear magnetic angioresonance being normal, the cervical and dorsolumbar spine did not exhibit demyelinizing lesions. However, T2 of the cerebral MRI (March 2018) showed multiple hyperintense lesions suggesting demyelinizing lesions that were resolved after 5 months.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0055" class="elsevierStylePara elsevierViewall">Among other supplementary tests, spectral domain optical coherence tomography (SD-OCT) was taken, showing a defect in the retina nerve fiber layer in the temporal quadrant as well as an alteration in the ganglion cell layer that could have been a sequel of past intracranial hypertension. Humphrey 24.2 campimetry produce normal results in both eyes. Cerebrospinal fluid (CSF) was analyzed through lumbar puncture, producing negative results for oligoclonal bands. Complete analytics was conducted with normal metabolic profile, negative toxics, normal hemogram, high PCR negative serologies for human immunodeficiency virus, B and C hepatitis, Epstein–Barr virus, cytomegalovirus, herpes simplex virus, varicella zoster virus and rubella. In addition, cultures of blood, urine and sputum were also negative. Serology for M. pneumoniae was positive, both for IgM and IgG, which enabled the identification of the etiological agent of the condition. The PCR results for <span class="elsevierStyleItalic">M. pneumoniae</span> was positive. In the authors hospital, serology is carried out in patients with suspected ADEM in order to discard this etiology due to a number of cases that occurred in 2018 and 2019. Among other supplementary tests, evoked potentials (EP) were carried out with normal speed and amplitude, and normal hearing EP. Electromyogram suggested minimum radiculitis probably in resolution phase, the Ishihara test was normal and the patient did not exhibit afferent pupil defect (AFPD).</p><p id="par0060" class="elsevierStylePara elsevierViewall">The final diagnostic was Wall Eyed Bilateral InterNuclear Ophthalmoplegia [WEBINO]) due to disseminated acute encephalomyelitis caused by <span class="elsevierStyleItalic">M. pneumoniae</span>.</p><p id="par0065" class="elsevierStylePara elsevierViewall">The treatment consisted in one cycle of IV methylprednisolone at high dosages of 10<span class="elsevierStyleHsp" style=""></span>mg/kg/day during 3 days and then oral regime of prednisone 1<span class="elsevierStyleHsp" style=""></span>mg/kg/day during 20 days, as well as cotrimoxazole for prophylaxis against <span class="elsevierStyleItalic">Pneumocystis jiroveci</span>. Evolution was positive and the patient did not exhibit new episodes and remains asymptomatic one year after the event.</p><p id="par0070" class="elsevierStylePara elsevierViewall">The second patient visited the Emergency Dept. due to loss of vision with 2<span class="elsevierStyleHsp" style=""></span>h evolution (VA: RE perception of light and finger count in LE at less than 1<span class="elsevierStyleHsp" style=""></span>m) together with oppressive “helmet” holocranial headache with 2<span class="elsevierStyleHsp" style=""></span>h evolution. AFPD RE minor, AFPD LE. Relevant personal history included migraine with atypical visual aura, treated one month earlier with magnesium. MRI with contrast showed hyperintense lesions in T2 suggesting demyelinizing disease (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>).</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0080" class="elsevierStylePara elsevierViewall">Two months after the episode, MRI with contrast showed smaller size and improvement of lesions. OCT of the retinal nerve fiber layer (RNFL) was normal as well as the Humphrey 24-2 campimetry. Metabolic profile and hemogram analyses were normal, toxics analysis negative and, as in the other case, PCR was also high. Serologies were negative for the human immunodeficiency virus, hepatitis B and C virus, Epstein–Barr virus, cytomegalovirus, herpes simplex virus, varicella zoster and rubella virus, and positive (IgM and IgG) for <span class="elsevierStyleItalic">M. pneumoniae</span>. The rest of supplementary tests, including electroencephalogram, one normal (with normal awakened state background activity and without epileptiform activity, or asymmetries or other significant anomalies) and EP without significant alterations throughout the visual pathway. The final diagnostic was ADEM related to <span class="elsevierStyleItalic">M. pneumoniae</span> infection with retrobulbar neuritis.</p><p id="par0085" class="elsevierStylePara elsevierViewall">The patient was treated with IV methylprednisolone during 3 days and oral prednisone at high doses of 1<span class="elsevierStyleHsp" style=""></span>mg/kg/day.</p><p id="par0090" class="elsevierStylePara elsevierViewall">Despite suspecting <span class="elsevierStyleItalic">M. pneumoniae</span> infection with positive IgM, the patient was not treated with antibiotics because this treatment is controversial and immunosuppressant treatment has proven to be more effective.</p><p id="par0100" class="elsevierStylePara elsevierViewall">None of the patients exhibited other neurological foci or macular lesion. After 3 and 6 months of evolution, respectively, the neuro-ophthalmological symptoms resolved in both cases and the control MRI provided surprisingly normal results.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0105" class="elsevierStylePara elsevierViewall">According to some sources, <span class="elsevierStyleItalic">M. pneumoniae</span> causes between 5 and 10% of central nervous system infections, even though it is known in that the main causes of ADEM are measles, rubella and varicella zoster.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,2</span></a></p><p id="par0115" class="elsevierStylePara elsevierViewall">In some cases, exposure to <span class="elsevierStyleItalic">M. pneumoniae</span> produces a situation of asymptomatic carrier. In 75% of cases, ADEM caused by this infection is associated to a slight prodromic condition between 2 and 30 days after the appearance of neurological symptoms.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2,6</span></a></p><p id="par0120" class="elsevierStylePara elsevierViewall">The <span class="elsevierStyleItalic">gold standard</span> method for diagnosing <span class="elsevierStyleItalic">M. pneumoniae</span> is PCR in blood and CSF, although it is generally diagnosed with serology (IgM e IgG) despite poor sensitivity for IgM described in some studies (32–77%).<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a></p><p id="par0125" class="elsevierStylePara elsevierViewall">The main differential diagnostic for ADEM are other infectious causes (human immunodeficiency virus, hepatitis B and C virus, Epstein–Barr virus, cytomegalovirus, herpes simplex virus, varicella zoster and rubella virus, respiratory and gastrointestinal viral infections) as well as demyelinizing diseases.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2,4,7</span></a> It is important to discard the latter for the prognosis. According to the criteria of the 2013 <span class="elsevierStyleItalic">International Pediatric Multiple Sclerosis Study Group</span> (IPMSSG), the diagnostic of multiple sclerosis (MS) would be defined in MRI like (1) 9 or more lesions in the white matter or enhanced with gadolinium; (2) 3 or more periventricular lesions; (3) a juxtacortical lesion; and (4) an infratentorial lesion. CSF should exhibit oligoclonal bands or increased IgG index. The combination of altered CSF and to lesions in MRI (one of which must be located in the brain) could signify a dissemination criteria in the McDonald classification.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a></p><p id="par0130" class="elsevierStylePara elsevierViewall">In children, two different demyelinizing events, separated in time and space, constitute a criterion for MS, in contrast with an ADEM recurrence in which new lesions do not appear and existing lesions would increase.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a></p><p id="par0135" class="elsevierStylePara elsevierViewall">A study by Dale et al. compared the presentation of clinic conditions of ADEM and MS. They obtained as a demyelinizing infectious disease (74 vs. 38%, <span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>0.05), polysymptomatic presentation (91 vs. 38%, <span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>0.002), pyramid signs (71 vs. 23%, <span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>0.01), encephalopathy (69 vs. 15%, <span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>0.002) and bilateral optic neuritis (23 vs. 8%, not statistically significant) and unilateral only in the MS cases.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a></p><p id="par0140" class="elsevierStylePara elsevierViewall">The importance of anti-MOG antibodies in childhood ADEM, above all in those caused by <span class="elsevierStyleItalic">Mycoplasma</span>, is described in a paper by Mol et al. in the Netherlands. It was observed that in patients with positive anti-MOG, the most frequent presentation phenotype was ADEM (56%) in children, and optic neuritis (44%) in adults. In addition, it was also associated with recurrence: 26% in children and 41% in adults, with a mean follow-up of 27.5 months. Said study also demonstrated that the majority of anti-MOG negative patients did not present relapses (89%).<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a></p><p id="par0145" class="elsevierStylePara elsevierViewall">The role of antibiotics for treating ADEM is controversial. It has not been demonstrated that a specific antibiotic treatment is able to resolve the condition.</p><p id="par0150" class="elsevierStylePara elsevierViewall">The antibiotics utilized for treating <span class="elsevierStyleItalic">M. pneumoniae</span> infections are azithromycin, erythromycin, tetracyclines (doxycycline) and latest generation fluoroquinolones, even though the latter are usually administered to adults.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a></p><p id="par0155" class="elsevierStylePara elsevierViewall">It is a fact that there are no clinic trials shedding light on the treatment of this condition and that management is based on experience and clinic judgment, as well as on clinic cases reported in the literature.</p><p id="par0160" class="elsevierStylePara elsevierViewall">As ADEM is probably an immunomediated disease, immunomodulator drugs are utilized. The first proposed therapeutic step is administering intravenous corticosteroids such as methylprednisolone (20–30<span class="elsevierStyleHsp" style=""></span>mg/kg/day, not more than 1gm/day) during 3–5 days, followed by oral corticosteroids during 4–6 weeks (evidence 2<span class="elsevierStyleHsp" style=""></span>C). If corticoids fail or patient response is insufficient, treatment would begin with IV immunoglobulins (evidence 2<span class="elsevierStyleHsp" style=""></span>C) and, failing this, plasmapheresis would be performed (evidence 2<span class="elsevierStyleHsp" style=""></span>C).<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0165" class="elsevierStylePara elsevierViewall">In what concerns prognosis, some studies have correlated ADEM with possible presentation prior to MS. A recent study by Papetti et al. comprising 91 patients has reported the evolution to MS of 21.2% of patients with ADEM, in a mean follow-up of 5.6<span class="elsevierStyleHsp" style=""></span>±<span class="elsevierStyleHsp" style=""></span>2.3 years. After a multivariate analysis, said study indicates as predictive factors the presence of oligoclonal bands in CSF (<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>0.001), prior infection by the Epstein–Barr virus (<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>0.001), periventricular lesions (<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>0.001), hypointense lesions in T1 (<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>0.001) and lesions in the <span class="elsevierStyleItalic">corpus callosum</span> (<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>0.001). Even so, the IPMSSG has warned that an episode with the clinic characteristics of ADEM cannot be considered as the first MS events unless the course of the clinic disease fulfills the criteria described in the consensus.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclusion</span><p id="par0170" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">M. pneumoniae</span> exists in the environment and, despite being infrequent, it should be part of the diagnostic approach in acute or subacute neuro-ophthalmological impairments in children. ADEM is within differential diagnostic of demyelinizing diseases and could even be a precursor thereof in some cases.</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Conflict of interest</span><p id="par0175" class="elsevierStylePara elsevierViewall">No conflict of interest was declared by the authors.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:10 [ 0 => array:3 [ "identificador" => "xres1335177" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1229803" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres1335178" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1229804" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Clinic case reports" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Discussion" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Conclusion" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "Conflict of interest" ] 9 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2019-11-28" "fechaAceptado" => "2020-01-21" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1229803" "palabras" => array:5 [ 0 => "<span class="elsevierStyleItalic">Mycoplasma pneumoniae</span>" 1 => "Acute disseminated encephalomyelitis (ADEM)" 2 => "Bilateral internuclear ophthalmoplegia (WEBINO)" 3 => "Neuritis" 4 => "Magnetic resonance imaging" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1229804" "palabras" => array:5 [ 0 => "<span class="elsevierStyleItalic">Mycoplasma pneumoniae</span>" 1 => "Encefalomielitis diseminada aguda (ADEM)" 2 => "Oftalmoplejía internuclear bilateral (WEBINO)" 3 => "Neuritis" 4 => "Resonancia magnética" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">The purpose of this article is to describe two pediatric neuro-ophthalmological clinical cases caused by a systemic infection due to <span class="elsevierStyleItalic">Mycoplasma pneumoniae (M. pneumoniae)</span>. The cases are two girls aged 14 and 12 seen in the Emergency Department: The first one had internuclear ophthalmoplegia and second with loss of vision and headache. They had no other neurological foci. Magnetic resonance imaging showed hyperintense plaques in both, suggestive of a demyelinating disease. One month later, the neuro-ophthalmological symptoms resolved, with normal follow-up magnetic resonance imagings. The diagnosis was acute disseminated encephalitis secondary to <span class="elsevierStyleItalic">M. pneumoniae</span>. The diagnosis was made using PCR (gold standard) and/or IgM in serology. It is important to think about this possible etiology in cases of suggestive demyelinating disease. There is controversy about the role of antibiotics and on whether corticosteroids are contemplated. In conclusion, <span class="elsevierStyleItalic">M. pneumoniae</span> must be a differential diagnosis in acute neuro-ophthalmological disorders in children.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">El objetivo es describir dos cuadros clínicos neuroftalmológicos en niños por infección sistémica por <span class="elsevierStyleItalic">Mycoplasma pneumoniae (M. pneumoniae)</span>. Se presentan los casos de dos niñas de 14 y 12 años que acudieron a urgencias: la primera con oftalmoplejía internuclear y la segunda con pérdida de visión y cefalea. No presentaban otra focalidad neurológica. En la imagen de resonancia magnética se evidenciaron placas hiperintensas en ambas, sugerentes de cuadro desmielinizante. Al mes, los síntomas neuroftalmológicos se resolvieron y las resonancias magnéticas de control fueron normales. El diagnóstico fue encefalitis diseminada aguda secundaria a <span class="elsevierStyleItalic">M. pneumoniae</span>. El diagnóstico se hace por PCR (<span class="elsevierStyleItalic">gold standard</span>) y/o IgM en serología. Es importante pensar en esta posible etiología ante casos sugerentes de enfermedad desmielinizante. Existe controversia sobre el papel de los antibióticos y si se contemplan los corticoides. Como conclusión, <span class="elsevierStyleItalic">M. pneumoniae</span> debe ser diagnóstico diferencial en afectaciones neuroftalmológicas agudas en niños.</p></span>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Molero-Senosiain M, Domingo-Gordo B, Fernández Cabrera C, Hernández-García E, Gómez de Liaño R. Manifestaciones neuroftalmológicas como complicación de una infección por <span class="elsevierStyleItalic">Mycoplasma pneumoniae</span> y desarrollo posterior de una encefalitis aguda diseminada. Arch Soc Esp Oftalmol. 2020;95:254–258.</p>" ] ] "multimedia" => array:3 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1162 "Ancho" => 1740 "Tamanyo" => 201798 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Supplementary tests of patient 1 (CPG) (A) angio-MRI images without alterations. (B) MRI with gadolinium of cervical spinal column without alterations. (C) axial MRI image in FLAIR sequence with gadolinium showing hyperintense lesions in the capsulo-thalamic region suggesting demyelinizing disease. (D) MRI taken 6 months after the first, showing absence of lesions. (E) Humphrey 24-2 campimetry within normal ranges in both eyes (minimum paracentral defect in LE).</p>" ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1426 "Ancho" => 2175 "Tamanyo" => 299862 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Supplementary tests of patient 2 (AOJ) (A) MRI sagittal and axial images with FLAIR sequence with gadolinium showing hyperintense lesions in juxtacortical white matter suggesting demyelinizing disease. (B) MRI gadolinium in T2 showing production and/or disappearance of some of the hyperintense lesions at month 3. (C) Angio-MRI images without alterations. (D) OCT-SD of the retina nerve fiber layer without alterations.</p>" ] ] 2 => array:8 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at1" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black"> \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Case 1 \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Case 2 \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Age (years) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">14 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">12 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Sex \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " colspan="2" align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Female</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Baseline symptomatology \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">DiplopiaInternuclear ophthalmoplegia \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Oppressive headacheDiminished visual acuity \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleItalic">M. pneumoniae</span> serology \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " colspan="2" align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Ig M positive</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Magnetic resonance (MRI) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Hyperintense lesions in capsulo-thalamic region \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Hyperintense lesions in juxtacortical white matter \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Diagnostic \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " colspan="2" align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Acute disseminated encephalomyelitis (ADEM) secondary to <span class="elsevierStyleItalic">M. pneumoniae</span> infection</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Prognosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Resolution of lesions in MRI in 6 monthsNo other sequelsNo recurrences \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Resolution of lesions in MRI in 3 monthsNo other sequelsNo recurrences \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab2288561.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Comparative summary of clinic cases.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:10 [ 0 => array:3 [ "identificador" => "bib0055" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Acute disseminated encephalomyelitis in childhood: epidemiologic, clinical and laboratory features" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "J.A. Leake" 1 => "S. Albani" 2 => "A.S. Kao" 3 => "M.O. Senac" 4 => "G.F. Billman" 5 => "M.P. Nespeca" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1097/01.inf.0000133048.75452.dd" "Revista" => array:5 [ "tituloSerie" => "Pediatr Infect Dis J" "fecha" => "2004" "volumen" => "23" "paginaInicial" => "756" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/15295226" "web" => "Medline" ] ] ] ] ] ] ] ] 1 => array:3 [ "identificador" => "bib0060" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Asymptomatic mycoplasma infection causing acute demyelinating encephalitis: case report and review of literature" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "E. Dawson" 1 => "D. Singh" 2 => "C. Armstrong" 3 => "O. Maatouk" 4 => "O. Akingbola" 5 => "S. 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