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Use of ganglion cell layer analysis for diagnosing anti-glycoprotein neuromyelitis optica of oligodendrocyte myelin
Uso del análisis de la capa de células ganglionares para el diagnóstico en la neuromielitis óptica anti-glucoproteína de la mielina del oligodendrocito
a Departamento de Neurología, Hospital Universitario ‘Marqués de Valdecilla’, Universidad de Cantabria, Instituto de Investigación ‘Marqués de Valdecilla’ (IDIVAL), Santander, Spain
b Departamento de Neurología, Hospital Universitario Marqués de Valdecilla, Universidad de Cantabria, Instituto de Investigación Marqués de Valdecilla (IDIVAL), Santander, Spain
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A-C) Alteraciones producidas durante el primer brote: al inicio, un mes después y a los 2 meses, respectivamente. En el OD se produce deterioro progresivo del cuadrante temporal de CFNR con alteración persistente de sector nasal de la CCG y hemianopsia temporal en el campo visual (B), que se resuelve con el tratamiento (C). En el OI se observa aumento de la CFNR (A) seguida de adelgazamiento de dicha capa (B-C), con alteración progresiva de la CCG y amaurosis completa en el campo visual. D) Afectación del segundo brote, con empeoramiento del sector temporal de la CFNR, leve adelgazamiento de la CCG y sin afectación del campo visual en el OD. E) Alteraciones producidas en el OD por el tercer brote, con empeoramiento de la CFNR, adelgazamiento difuso de la CCG y escotoma altitudinal superior. F) Afectación final del OD, con mantenimiento de la alteración de la CFNR, abolición de la CCG y mejoría del campo visual.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "A. 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A periorbital pain with a specific diagnosis and treatment" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "es" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "150" "paginaFinal" => "152" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Cefalea troclear primaria. Un dolor periorbitario con diagnóstico y tratamiento específicos" ] ] "contieneResumen" => array:2 [ "en" => true "es" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1012 "Ancho" => 1000 "Tamanyo" => 89678 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">trochlea examination maneuver. A) palpation of upper inner angle of the orbit triggers pain. B) said pain intensifies in supraduction gaze position.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "P. Sánchez Ruiz, C. 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RE (A) and LE (B): same section as shown in <a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>C.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "V.M. Asensio-Sánchez, L. Pareja-Aricó, J. Valentín-Bravo" "autores" => array:3 [ 0 => array:2 [ "nombre" => "V.M." "apellidos" => "Asensio-Sánchez" ] 1 => array:2 [ "nombre" => "L." "apellidos" => "Pareja-Aricó" ] 2 => array:2 [ "nombre" => "J." "apellidos" => "Valentín-Bravo" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0365669120300034" "doi" => "10.1016/j.oftal.2019.12.007" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0365669120300034?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2173579420300190?idApp=UINPBA00004N" "url" => "/21735794/0000009500000003/v1_202002280728/S2173579420300190/v1_202002280728/en/main.assets" ] "en" => array:20 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Short communication</span>" "titulo" => "Use of ganglion cell layer analysis for diagnosing anti-glycoprotein neuromyelitis optica of oligodendrocyte myelin" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "146" "paginaFinal" => "149" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "A. Cerveró, M.J. Sedano-Tous, J. Madera, A. López-de-Eguileta, A. Casado" "autores" => array:5 [ 0 => array:3 [ "nombre" => "A." "apellidos" => "Cerveró" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 1 => array:3 [ "nombre" => "M.J." "apellidos" => "Sedano-Tous" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 2 => array:3 [ "nombre" => "J." "apellidos" => "Madera" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 3 => array:3 [ "nombre" => "A." "apellidos" => "López-de-Eguileta" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 4 => array:4 [ "nombre" => "A." "apellidos" => "Casado" "email" => array:1 [ 0 => "casadorojo@hotmail.es" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "*" "identificador" => "cor0005" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Departamento de Neurología, Hospital Universitario ‘Marqués de Valdecilla’, Universidad de Cantabria, Instituto de Investigación ‘Marqués de Valdecilla’ (IDIVAL), Santander, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Departamento de Neurología, Hospital Universitario Marqués de Valdecilla, Universidad de Cantabria, Instituto de Investigación Marqués de Valdecilla (IDIVAL), Santander, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "<span class="elsevierStyleItalic">Corresponding author</span>." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Uso del análisis de la capa de células ganglionares para el diagnóstico en la neuromielitis óptica anti-glucoproteína de la mielina del oligodendrocito" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 583 "Ancho" => 1874 "Tamanyo" => 136692 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0010" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">cerebral NMR. A) coronal sequence. B) axial sequence. C) FLAIR and axial reconstruction axial of T1 3D with gadolinium, showing broad anomaly with thickening. T2 hyperintensity and patched highlighting along the left optic nerve (white arrows) and in the optic chiasma and optical pathways (blue arrows).</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Neuromyelitis optica (NMO) disorders comprise a range of central nervous system inflammatory diseases with the involvement of antibodies, clinically characterized by acute recurring episodes of optic neuritis, transversal myelitis and brainstem syndromes.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Within said range 3 groups can be found: seropositive anti-AQP4 NMO, seropositive anti-MOG NMO and seronegative NMO. This classification is based on the target of the antibodies found in each group, i.e. aquaporin-4 (anti-AQP4) and myelin oligodendrocyte glycoprotein (anti- MOG).<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> These differences in antibodies are portrayed in clinic differences within these groups. The seropositive anti-MOG NMO generally exhibit compromise of the longer nerve, in some cases reaching the chiasma, in addition to appearing at earlier ages, with the appearance of transversal myelitis being less frequent.</p><p id="par0010" class="elsevierStylePara elsevierViewall">In said context, a clinic case is presented in which since the first visit and due to ganglion cell analysis it was possible to predict the final diagnostic of seropositive anti-MOG NMO even though the analytic results were initially negative.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Clinic case</span><p id="par0015" class="elsevierStylePara elsevierViewall">Female, age 26, who visited the Emergency Dept. with pain in the left eye (LE) and ocular movements associated to ipsolateral visual loss in the past 48 h. The patient did not refer relevant history and examination showed a best corrected visual acuity (VA) in the right eye (RE) of 0.9 and 0.3 in the LE (Snellen), relative afferent pupil defect in the LE and diffusion of papilla edges in said eye. Optical coherence tomography (OCT) showed increased retina nerve fiber layer (RNFL) in the LE with diffuse alteration of the ganglion cell layer (GCL). The RE exhibited diminished GCL at the nasal level with normal RNFL. The visual field evidenced complete LE amaurosis while the RE showed nonspecific alterations (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>A). With the diagnostic of suspected NMO in the LE due to poor VA, 5 methylprednisolone bolus (500 mg) and 8 plasmapheresis sessions were prescribed but failed to improve VA, which worsened to perception of light. New OCT and visual fields were taken, which evidenced in the LE diminished RNFL and deletion of GCL with persistent visual field alteration. In turn, the RE maintained nasal GCL alteration with diminished RNFL in the temporal quadrant, showing temporal scotoma in the visual field (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>B).</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Cerebral NMR showed extensive highlighting along the left optic nerve as well as thickening and hyperintensity in the optic chiasma and the left optic tract (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>). Even so, etiological study was completed with spinal NMR, microbiological and immunological profile as well as a lumbar puncture with cerebrospinal fluid study (including oligoclonal bands, anti-neuron antibodies, anti-MOG and anti-AQP4) without identifying pathological signs. Visual evoked potentials revealed findings compatible with medium intensity demyelinizing left optic neuropathy.</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0025" class="elsevierStylePara elsevierViewall">After 2 months, a new OCT evidenced persistence of GCL damage at the nasal level in the RE, with increased thinning of the RNFL temporal quadrant. However, clear visual field improvement was observed in said eye. The LE maintained the visual field deletion as well as the GCL and RNFL damages (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>C).</p><p id="par0030" class="elsevierStylePara elsevierViewall">Despite the negativity of anti-AQP4 and anti-MOG antibodies and that the criteria for neuromyelitis diagnostic were not fulfilled<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3,4</span></a> the case was diagnosted as suspected NMO due to the severe visual deficit of the LE which failed to recover after corticoid treatment, associated to the extensive NMR lesion without evidencing typical multiple sclerosis alterations. Immunosuppressant treatment was initiated with azathioprine and oral corticoids.</p><p id="par0035" class="elsevierStylePara elsevierViewall">The follow-up with OCT and visual field showed stabilization of the condition. Five months later the patient began to exhibit blurred vision in the RE (RE VA of 0.5) associated to pain with ocular movements. This improved with corticoids bolus and 5 plasmapheresis sessions (RE VA: 0.9). Ocular fundus examination did not evidence alterations in the right optic nerve. The RE OCT showed worsening of the RNFL temporal sector and slight worsening of GCL without compromising the visual field (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>D). Due to recurrence despite azathioprine treatments, it was decided to add rituximab.</p><p id="par0040" class="elsevierStylePara elsevierViewall">Two months later, after diminishing the oral corticoids dosage, the patient presented with a new episode of right retrobulbar optic neuritis (RE VA: 0.5, pain with ocular movements and dyschromatopsia). RE OCT showed diffused GCL alteration as well as RNFL temporal sector alteration and upper altitudinal scotoma (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>E). Treatment was initiated with corticoids bolus and 5 plasmapheresis sessions with improvement of VA (RE VA: 0.8) and visual field, with persistence of RNFL and GCL alteration (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>F). During this hospital stay, brainstem NMR was repeated, with persistence of signal alteration in the optic chiasma, left optic nerve and stem of posterior optic tract, with normal spinal cord. Anti-AQP4 and anti-MOG tests were repeated and this time the anti-MOG antibodies were positive, fulfilling the criteria for diagnosing recurrent optic neuritis associated to positive anti-MOG antibodies.</p><p id="par0045" class="elsevierStylePara elsevierViewall">Clinical stability was maintained during 7 months, at which time a new episode of right optic neuritis took place, which remitted with methylprednisolone bolus and 5 plasmapheresis sessions. An additional relapse of right optic neuritis occurred 6 months later and was treated with methylprednisolone bolus and 3 plasmapheresis sessions. Despite said treatment, the following month a new relapse occurred and it was decided to withdraw rituximab and initiate treatment with cyclophosphamide.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0050" class="elsevierStylePara elsevierViewall">NMO with MOG and AQP4 antibodies exhibit some differences: the former are more frequent in Caucasian and younger patients with generally better clinic outcomes. Seropositive anti-MOG cases frequently associate optic neuritis episodes and exhibit less transversal myelitis as well as higher association with bilateral optic neuritis when compared to seropositive anti-AQP4 cases. In addition, the seropositive anti-MOG NMO is characterized by the presence of extensive longitudinal lesions along the optic nerve or the spinal cord.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,2,5</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">The present case evidenced thickening and extensive hyperintensity in the left optic nerve compromising the optic chiasma in the cerebral NMR. It is worthy pointing out that the message in the present case is that the initial compromise of the nasal RE GCL sector during the first optic neuritis episodes of the LE (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>A) without having the NMR or visual field compromise at the time, could be a sign of extensive left optic nerve compromise, involving the optic chiasma and thus causing damages to the RE nasal GCL. This finding enables the suspicion of seropositive anti-MOG NMO prior to the involvement of the NMR and the visual field.</p><p id="par0060" class="elsevierStylePara elsevierViewall">It is important to emphasize the need to maintain diagnostic suspicion of NMO disorder in the presence of recurring optic neuritis with significant VA compromise despite the initial absence of myelitis in spinal cord NMR and negative antibodies. If clinic suspicion is high, said tests must be repeated.</p><p id="par0065" class="elsevierStylePara elsevierViewall">In what concerns treatment of NMO range disorders, methylprednisolone bolus constitutes the first line of treatment, with plasmapheresis and human immunoglobulin regarded as second choice. The combination of plasmapheresis and methylprednisolone bolus has demonstrated to be more effective as it improves prognosis in optic neuromyelitis relapses. It has been observed that said combination produces better visual results than corticoid monotherapy. Maintenance treatment is based on immunosuppressant therapy in order to prevent relapses. It has also been proposed to maintain prophylactic immunotherapy after first episode during at least 5 years, with azathioprine, rituximab and mycophenolate mofetil being the first choice, while methotrexate, mitoxantrone and cyclophosphamide are the second choice.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclusions</span><p id="par0070" class="elsevierStylePara elsevierViewall">Demyelinizing inflammatory syndromes associated to anti-MOG antibodies, specifically optic neuritis, constitute a recurring disease associated to the presence of lesions in the optic nerve that are more extensive than those associated to anti-AQP4 antibodies or to optic neuritis in other contexts. OCT could enable the suspicion of seropositive anti-MOG NMO due to the compromise of the contralateral GCL in extensive compromises reaching the optic chiasma.</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Conflict of interests</span><p id="par0075" class="elsevierStylePara elsevierViewall">No conflict of interests was declared by the authors.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:10 [ 0 => array:3 [ "identificador" => "xres1312674" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1211553" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres1312673" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1211552" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Clinic case" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Discussion" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Conclusions" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "Conflict of interests" ] 9 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2019-07-31" "fechaAceptado" => "2019-11-24" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1211553" "palabras" => array:3 [ 0 => "Neuromyelitis optica" 1 => "Anti-myelin oligodendrocyte glycoprotein antibodies" 2 => "Ganglion cells" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1211552" "palabras" => array:3 [ 0 => "Neuromielitis óptica" 1 => "Anticuerpos anti-glucoproteína de la mielina del oligodendrocito" 2 => "Células ganglionares" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">The case concerns a 26-year-old patient with bilateral recurrent optic neuritis episodes in the context of suspected neuromyelitis optica (NMO). In the first outbreak, she had greatly impaired visual acuity of the left eye, as well as seeing ganglion cell layer (GCL) damage in both eyes in the optic coherence tomography, with evidence of a possible extensive lesion in the optic chiasma. Likewise, MRI with contrast showed a great involvement of the left optic nerve that compromises the chiasma increasing the suspicion of a neuromyelitis origin. Althogh the anti- myelin oligodendrocyte glycoprotein (MOG) and anti-AQP4 (aquaporin-4) antibodies were negative at first, bilateral involvement of the ganglion cells suggested an extensive lesion that is more characteristic of seropositive anti-MOG neuromyelitis.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Paciente de 26 años con episodios de neuritis óptica recurrentes en contexto de diagnóstico de sospecha de neuromielitis óptica. En el primer brote la paciente presenta gran afectación de la agudeza visual del ojo izquierdo, objetivándose en la tomografía de coherencia óptica afectación de la capa de células ganglionares en ambos ojos, evidenciando posible lesión extensa del nervio que llega hasta el quiasma óptico. Así mismo, en la RMN con contraste se objetiva afectación del nervio óptico izquierdo de gran longitud que compromete el quiasma permitiendo la sospecha etiológica de neuromielitis. A pesar de que los anticuerpos anti-MOG y anti-AQP4 fueron negativos en un primer momento, la afectación bilateral de las células ganglionares, hace sospechar una lesión extensa que es más característica de las neuromielitis anti-MOG seropositivas.</p></span>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Cerveró A, Sedano-Tous MJ, Madera J, López-de-Eguileta A, Casado A. Uso del análisis de la capa de células ganglionares para el diagnóstico en la neuromielitis óptica anti-glucoproteína de la mielina del oligodendrocito. Arch Soc Esp Oftalmol. 2020;95:146–149.</p>" ] ] "multimedia" => array:2 [ 0 => array:8 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1869 "Ancho" => 2175 "Tamanyo" => 496152 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">RNFL, GCL and visual field of right eye and left eye, respectively. A–C) alterations during the first episode: at onset, after 1 and 2 months, respectively. RE exhibits progressive deterioration of RNFL temporal quadrant with persistent alteration in GCL nasal sector and temporal hemianopsia in the visual field (B), which is resolved with treatment (C). The LE shows increased RNFL (A) followed by thinning of said layer (B–C), with progressive GCL alteration and complete amaurosis in the visual field. D) compromise of second episode, with worsening of RNFL temporal sector, slight GCL thinning without compromising RE visual field. E) alterations in RE caused by the third episode, with worsening of RNFL, diffuse GCL thinning and upper altitudinal scotoma. F) final RE compromise maintaining RNFL alteration, GCL deletion and visual field improvement.</p>" ] ] 1 => array:8 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 583 "Ancho" => 1874 "Tamanyo" => 136692 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0010" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">cerebral NMR. A) coronal sequence. B) axial sequence. C) FLAIR and axial reconstruction axial of T1 3D with gadolinium, showing broad anomaly with thickening. T2 hyperintensity and patched highlighting along the left optic nerve (white arrows) and in the optic chiasma and optical pathways (blue arrows).</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:6 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Neuromyelitis optica" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "S.L. Patterson" 1 => "S.E. 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