Letter to the Editor
An exceptional cause of sudden neurological deterioration and coma
Una causa excepcional de deterioro neurológico repentino y coma
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A) Presencia de hipodensidad difusa de la sustancia blanca predominantemente en los 2 lóbulos frontales y afectación del cuerpo calloso, que indican edema vasogénico. Se aprecia borramiento de los surcos de la convexidad. B) Imagen tomada tras administrar el contraste, que muestra ausencia de realce en las áreas mencionadas. C) Los signos de hipertensión intracraneal son especialmente evidentes en los lóbulos frontales y el cuerpo calloso. D) La herniación cerebral no desaparece a pesar de haber realizado una craniectomía bifrontal. E y F) Se aprecia afectación difusa también a nivel infratentorial.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "A.J. Vargas López, J.M. Garbizu Vidorreta, E. Salinero Paniagua, C. Fernández Carballal" "autores" => array:4 [ 0 => array:2 [ "nombre" => "A.J." "apellidos" => "Vargas López" ] 1 => array:2 [ "nombre" => "J.M." "apellidos" => "Garbizu Vidorreta" ] 2 => array:2 [ "nombre" => "E." 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(B) Contrast brain CT image at 24<span class="elsevierStyleHsp" style=""></span>hours revealing a hyperdense area in the left temporal lobe, infiltrating the ipsilateral Sylvian fissure with no contrast uptake. Brain MRI: (C) Axial T1-weighted sequence. A hyperintense lesion was observed in the left temporal lobe. (D) Coronal contrast T1-weighted sequence. An irregular lesion with a hypointense centre (ring enhancement) was identified. (E) Axial contrast T1-weighted sequence. The scan revealed an irregular area with low contrast with a cyst-like component and central necrosis exerting a mass effect with left temporal horn effacement. F) Axial T2-weighted sequence. A left temporal hyperintense lesion (oedema) was observed. MRI results: glial tumour in the left temporal lobe expanding into the uncus and hippocampus with a cyst-like appearance and central necrosis with an infiltrative/expansive growth pattern.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "F.J. 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"apellidos" => "Cardoso" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0213485316000566" "doi" => "10.1016/j.nrl.2016.02.003" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0213485316000566?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2173580818300063?idApp=UINPBA00004N" "url" => "/21735808/0000003300000003/v1_201804060407/S2173580818300063/v1_201804060407/en/main.assets" ] "itemAnterior" => array:20 [ "pii" => "S217358081830004X" "issn" => "21735808" "doi" => "10.1016/j.nrleng.2015.12.020" "estado" => "S300" "fechaPublicacion" => "2018-04-01" "aid" => "855" "copyright" => "Sociedad Española de Neurología" "documento" => "simple-article" "crossmark" => 1 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "cor" "cita" => "Neurologia. 2018;33:194-6" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 779 "formatos" => array:3 [ "EPUB" => 45 "HTML" => 597 "PDF" => 137 ] ] "en" => array:11 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Letter to the Editor</span>" "titulo" => "Bilateral papilloedema as the initial manifestation of spinal ependymoma" "tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "194" "paginaFinal" => "196" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Papiledema bilateral como forma de debut de un ependimoma espinal" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1500 "Ancho" => 1500 "Tamanyo" => 182831 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">T2-weighted sequence showing the ependymoma.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Y. Miranda Bacallado, A. González Hernández, L. Curutchet Mesner, I. Rúa-Figueroa Fernández de Larrinoa" "autores" => array:4 [ 0 => array:2 [ "nombre" => "Y." "apellidos" => "Miranda Bacallado" ] 1 => array:2 [ "nombre" => "A." "apellidos" => "González Hernández" ] 2 => array:2 [ "nombre" => "L." "apellidos" => "Curutchet Mesner" ] 3 => array:2 [ "nombre" => "I." "apellidos" => "Rúa-Figueroa Fernández de Larrinoa" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0213485316000475" "doi" => "10.1016/j.nrl.2015.12.021" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0213485316000475?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S217358081830004X?idApp=UINPBA00004N" "url" => "/21735808/0000003300000003/v1_201804060407/S217358081830004X/v1_201804060407/en/main.assets" ] "en" => array:16 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Letter to the Editor</span>" "titulo" => "An exceptional cause of sudden neurological deterioration and coma" "tieneTextoCompleto" => true "saludo" => "<span class="elsevierStyleItalic">Dear Editor</span>:" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "196" "paginaFinal" => "199" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "A.J. Vargas López, J.M. Garbizu Vidorreta, E. Salinero Paniagua, C. Fernández Carballal" "autores" => array:4 [ 0 => array:4 [ "nombre" => "A.J." "apellidos" => "Vargas López" "email" => array:2 [ 0 => "ajvargaslopez@hotmail.com" 1 => "is_86@hotmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "J.M." "apellidos" => "Garbizu Vidorreta" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 2 => array:3 [ "nombre" => "E." "apellidos" => "Salinero Paniagua" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 3 => array:3 [ "nombre" => "C." "apellidos" => "Fernández Carballal" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Servicio de Neurocirugía, Hospital Universitario Gregorio Marañón, Madrid, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Servicio de Anatomía Patológica, Hospital Universitario Gregorio Marañón, Madrid, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Una causa excepcional de deterioro neurológico repentino y coma" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1455 "Ancho" => 832 "Tamanyo" => 151992 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Brain CT (A and B) and FLAIR MRI (C–F) images. (A) Predominant presence of diffuse white matter hypodensity in both frontal lobes and involvement of the corpus callosum indicating vasogenic oedema. Convexity sulci effacement is seen. (B) Image was taken after the administration of contrast, showing no focal enhancement. (C) Signs of intracranial hypertension involving both frontal lobes and the corpus callosum are present. (D) Brain herniation persists despite extensive bilateral frontal craniectomy. (E and F) Infratentorial diffuse involvement is also present.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">We are writing about an unusual case, to our knowledge not previously reported, of sudden neurological deterioration and coma.</p><p id="par0010" class="elsevierStylePara elsevierViewall">The case is that of a 25-year old woman who had given birth 3 months before after a managed full-term pregnancy without complications. She was treated with oral iron due to postpartum anaemia but had no other relevant medical history. This patient arrived at the ER presenting with a one-month history of headaches, apathy, and bradypsychia. The headaches had worsened in the last 48 hours with incomplete response to conventional analgesic treatment. Nausea and vomiting had appeared in the last few hours. She had no fever. While in the ER she had a sudden deterioration in level of consciousness together with a tonic–clonic seizure. She was intubated. An emergent CT scan showed signs of diffuse cerebral oedema and obliterated subarachnoid cisterns. Leptomeningeal and ependymal enhancement was present (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>A and B). These findings were suggestive of cerebritis accompanied by meningeal involvement and ventriculitis.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">She was admitted to the ICU and 6 hours later suddenly developed non-reactive bilateral mydriasis. A decompressive wide bifrontal craniectomy with bilateral decompression of the frontal and temporal lobes was carried out as a compassionate treatment, and a biopsy of the right frontal lobe was performed. During the intervention, we observed the brain to be congested and of a hard consistency. After the procedure an intracranial pressure sensor was placed which initially recorded pressures below 15<span class="elsevierStyleHsp" style=""></span>mmHg. After intervention mydriasis was reversed and pupillary reflexes were restored. CSF analysis showed no cytochemical abnormalities and the results from the CSF culture were negative for bacteria, viruses, and fungi. The results of blood serology tests for autoimmune diseases were also negative. A brain MRI showed supra and infratentorial diffuse involvement, especially in the frontal lobes and corpus callosum. Small areas of contrast enhancement and signs of intracranial hypertension were also observed (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>C–F).</p><p id="par0020" class="elsevierStylePara elsevierViewall">Clinical and radiological differential diagnosis included infectious entities such as progressive multifocal leukoencephalopathy and other forms of viral encephalitis; autoimmune diseases such as acute disseminated encephalomyelitis, vasculitis or connective tissue diseases; metabolic disorders such as certain forms of leukodystrophy; encephalopathy after radiotherapy; and such tumours as gliomatosis cerebri or primary brain lymphoma.<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">1,2</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Histopathological examination revealed diffuse astrocyte proliferation and low cell density with features of a low-grade glial tumour (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>). These findings added to those from the MRI were consistent with gliomatosis cerebri.</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">Forty eight hours after surgery the patient experienced an increase in intracranial pressure refractory to treatment. After obtaining family consent, a decision was made to limit treatment. The patient died 6 days after surgery.</p><p id="par0035" class="elsevierStylePara elsevierViewall">Gliomatosis cerebri was first described by Nevin in 1938<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">1</span></a> and represents just under 1% of all astrocytomas.<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">3,4</span></a> It is a neoplastic disorder originating from glial cells,<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">3,5,6</span></a> defined by the infiltration of at least 2 lobes.<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">1,3,6</span></a> Despite this fact, gliomatosis cerebri typically preserves the macroscopic structure and cytoarchitecture of the CNS.<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">3,6</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Although this condition has been reported in children,<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">7</span></a> it usually occurs in patients aged between 40 and 50.<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">6</span></a> Its incidence appears to be slightly higher in men.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">3</span></a> It is mainly located in the supratentorial level, but it often spreads to infratentorial structures.<a class="elsevierStyleCrossRefs" href="#bib0115"><span class="elsevierStyleSup">8–10</span></a> The corpus callosum, thalamus, and basal ganglia are frequently involved.<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">6</span></a> In addition, expansion to the entire neuraxis has been reported.<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">8</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">This disease is often overlooked in the early stages, so diagnosis commonly occurs in the advanced stages.<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">7</span></a> Common initial symptoms include the appearance of focal neurological deficits or the presence of less specific signs such as headache, nausea, vomiting, seizures, personality changes, or cognitive impairment.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">5</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">Neuroimaging findings of gliomatosis cerebri are characteristic but rarely specific.<a class="elsevierStyleCrossRefs" href="#bib0120"><span class="elsevierStyleSup">9,10</span></a> This implies the need for a broad differential diagnosis. T2 and FLAIR MRI sequences usually reveal hyperintense areas with asymmetric and/or heterogeneous distribution.<a class="elsevierStyleCrossRefs" href="#bib0120"><span class="elsevierStyleSup">9,10</span></a> The corpus callosum is usually involved and appears thickened.<a class="elsevierStyleCrossRefs" href="#bib0120"><span class="elsevierStyleSup">9,10</span></a> Loss of differentiation between grey and white matter is also characteristic.<a class="elsevierStyleCrossRefs" href="#bib0120"><span class="elsevierStyleSup">9,10</span></a> In type I gliomatosis cerebri there is usually no contrast enhancement, while type II commonly displays areas with contrast enhancement that correlate with anaplastic transformation.<a class="elsevierStyleCrossRefs" href="#bib0120"><span class="elsevierStyleSup">9,10</span></a> Spectroscopy and sequences of relative cerebral blood volume can help in recognising the glial origin of this tumour.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">3</span></a> These sequences can also be useful to more accurately determine areas for biopsy.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">3</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">Histopathological features often correspond to low-grade glial tumours,<a class="elsevierStyleCrossRefs" href="#bib0100"><span class="elsevierStyleSup">5,6</span></a> although tumour progression showing high grade features can take place.<a class="elsevierStyleCrossRefs" href="#bib0100"><span class="elsevierStyleSup">5,6</span></a> The most common cellular phenotype is astrocytic, but it may also present oligoastrocytic or oligodendrocytic phenotype.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">5</span></a> Despite its histological appearance the clinical behaviour of this tumour correlates to at least grade III in the WHO classification.<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">6</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">A definitive diagnosis is made with neuroimaging and histopathological features.<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">3,6</span></a> Nevertheless heterogeneity in histological findings may hamper the diagnosis.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">3</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">Because glioma are highly infiltrative and diffuse, the role of surgery is limited to biopsy for diagnostic purposes.<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">3,4</span></a> The mainstays of treatment are radiotherapy<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">11,12</span></a> and chemotherapy.<a class="elsevierStyleCrossRefs" href="#bib0140"><span class="elsevierStyleSup">13,14</span></a> Even so, median survival time is estimated at around 14.5–18 months.<a class="elsevierStyleCrossRefs" href="#bib0145"><span class="elsevierStyleSup">14,15</span></a> Prognostic factors are similar to those of other gliomas.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">3</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">A dismal clinical presentation of gliomatosis cerebri is featured in the current case. To our knowledge, intracranial hypertension syndrome with coma refractory to treatment resulting in fatality had not previously been reported as a presentation of gliomatosis cerebri.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0075" class="elsevierStylePara elsevierViewall">The authors report no conflicts of interest concerning the materials or methods used in this study or the findings described in this paper.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Conflicts of interest" ] 1 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Vargas López AJ, Garbizu Vidorreta JM, Salinero Paniagua E, Fernández Carballal C. Una causa excepcional de deterioro neurológico repentino y coma. Neurología. 2018;33:196–199.</p>" ] ] "multimedia" => array:2 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1455 "Ancho" => 832 "Tamanyo" => 151992 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Brain CT (A and B) and FLAIR MRI (C–F) images. (A) Predominant presence of diffuse white matter hypodensity in both frontal lobes and involvement of the corpus callosum indicating vasogenic oedema. Convexity sulci effacement is seen. (B) Image was taken after the administration of contrast, showing no focal enhancement. (C) Signs of intracranial hypertension involving both frontal lobes and the corpus callosum are present. (D) Brain herniation persists despite extensive bilateral frontal craniectomy. (E and F) Infratentorial diffuse involvement is also present.</p>" ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1218 "Ancho" => 1605 "Tamanyo" => 430568 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Photomicrographs showing frozen and permanent sections. (A) Haematoxylin–eosin stain. Proliferation of moderate cellularity characterised by the presence of naked nuclei (arrows) can be observed. (B) Haematoxylin–eosin stain. Oligodendroglial lineage cells are abundant. Glial elements composed of bare spindle-shaped moderately atypical nuclei can be seen (arrows). (C) Immunohistochemical GFAP (glial fibrillary acidic protein) staining showing atypical astrocytic elements with short irregular coarse extensions (arrows). (D) Ki67 staining showing proliferative activity around 2%. A, B, and D: original magnification 10×; C: original magnification 40×.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:15 [ 0 => array:3 [ "identificador" => "bib0080" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Gliomatosis cerebri" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:1 [ 0 => "S. 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