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ARTÍCULO DE REVISIÓN
NEUROINFLAMACIÓN Y EPILEPSIA
Epilepsy and neuroinflammation
Omar Herrera-Vázquez, Andrea Toledo Rojas, Agnès Fleury
Autor para correspondencia
afleury@biomedicas.unam.mx

Autor para correspondencia.
Unidad Periférica para el estudio de la Neuroinflamación en patologías Neurológicas, Instituto de Investigaciones Biomédicas, Facultad de Medicina de la Universidad Nacional Autónoma de México en el Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Insurgentes sur # 3877 Col. La fama, C.P. 14269, México, D.F
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">INTRODUCCI&#211;N</span><p id="par0005" class="elsevierStylePara elsevierViewall">La epilepsia es un trastorno neurol&#243;gico que afecta a 50 millones de personas en el mundo&#59; entre el 75 y 80&#37; de los pacientes afectados se encuentran en pa&#237;ses en v&#237;as de desarrollo&#46; La incidencia de esta enfermedad es de 50&#47;100&#44;000 personas en y 100-190&#47;100&#44;000 personas en pa&#237;ses con un &#237;ndice de crecimiento bajo &#40;Organizaci&#243;n Mundial de la Salud&#44; Nota descriptiva N&#176; 999&#44; Mayo 2015&#59; <a id="intr0005" class="elsevierStyleInterRef" href="http://www.who.int/mediacentre/factsheets/fs999/es/">http&#58;&#47;&#47;www&#46;who&#46;int&#47;mediacentre&#47;factsheets&#47;fs999&#47;es&#47;</a>&#41;&#46; La principal caracter&#237;stica de este trastorno neurol&#243;gico es la presencia de crisis epil&#233;pticas espont&#225;neas resultado de descargas sincr&#243;nicas de una poblaci&#243;n neuronal debido a un dinamismo anormal de las redes neuronales&#46; Las crisis epil&#233;pticas se clasifican en parciales y generalizadas&#59; la principal diferencia entre ellas es que las crisis parciales se originan en una poblaci&#243;n neuronal y no se expanden a todo el sistema nervioso central&#44; mientras que las generalizadas s&#237; lo hacen<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a>&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">Recientemente la Liga Internacional contra la Epilepsia &#40;ILAE&#41; defini&#243; a la epilepsia&#44; f&#225;rmacorresistente y persistente a pesar de haber probado dos reg&#237;menes terap&#233;uticos &#40;apropiados y bien tolerados&#41;&#44; ya sea como monoterapia o en combinaci&#243;n<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a>&#46; En estos casos&#44; la cirug&#237;a de resecci&#243;n del foco epil&#233;ptico es una de las opciones terap&#233;uticas&#44; logrando la ausencia de recidiva de crisis en alrededor del 65&#37; de los pacientes<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a>&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">La epilepsia del l&#243;bulo temporal &#40;ELT&#41; es la forma m&#225;s com&#250;n de epilepsia parcial&#46; Como su nombre lo indica se origina en las estructuras del l&#243;bulo temporal &#40;particularmente en el hipocampo&#44; giro parahipocampal y am&#237;gdala&#41; y es f&#225;rmacorresistente en alrededor del 30&#37; de los pacientes afectados<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4&#44;5</span></a>&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">La epilepsia es un padecimiento con una etiolog&#237;a multifactorial&#46; En particular&#44; en los &#250;ltimos a&#241;os&#44; la relevancia de los procesos inmunol&#243;gicos e inflamatorios en su etiopatogenia ha sido destacada<a class="elsevierStyleCrossRefs" href="#bib0030"><span class="elsevierStyleSup">6&#8211;8</span></a>&#46; Durante d&#233;cadas&#44; se mantuvo la creencia de que las neuronas epil&#233;pticas eran las iniciadoras de las convulsiones&#46; Sin embargo&#44; evidencias recientes han puesto de manifiesto la importancia de la relaci&#243;n entre las c&#233;lulas cerebrales &#40;neuronas pero tambi&#233;n c&#233;lulas gliales&#41; y las c&#233;lulas inmunes perif&#233;ricas<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a>&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">En el presente trabajo revisaremos datos recientes sobre el papel de la inflamaci&#243;n&#47;neuroinflamaci&#243;n en la epilepsia&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">EVIDENCIAS QUE DEMUESTRAN EL V&#205;NCULO EPILEPSIA-INFLAMACI&#211;N&#58; EPILEPSIAS AUTOINMUNES</span><p id="par0030" class="elsevierStylePara elsevierViewall">Diversas observaciones realizadas hace algunas d&#233;cadas han sugerido la implicaci&#243;n de factores inmunoinflamatorios en la epilepsia&#46; La relevancia de la inflamaci&#243;n cerebral en la epilepsia fue inicialmente identificada por estudios patol&#243;gicos realizados en sujetos afectados por encefalitis de Rasmussen&#44; un s&#237;ndrome epil&#233;ptico caracterizado por p&#233;rdida neuronal&#44; inflamaci&#243;n cortical y gliosis confinadas a un hemisferio cerebral<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a>&#46; En estos pacientes se describen en estudios patol&#243;gicos la presencia de autoanticuerpos de linfocitos B y T citot&#243;xicos&#44; activaci&#243;n de microglia y astrocitos&#44; c&#233;lulas Natural Killer &#40;NK&#41;&#44; hechos que demuestran la implicaci&#243;n de fen&#243;menos inmunol&#243;gicos en su patogenia<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">11&#8211;17</span></a> &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Tabla I</a>&#41;&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0035" class="elsevierStylePara elsevierViewall">As&#237; mismo la eficacia de la hormona Adrenocorticotr&#243;fica &#40;ACTH&#41; y de los corticosteroides utilizados en diferentes epilepsias pedi&#225;tricas&#44; conocidas ya desde hace d&#233;cadas&#44; hace sugerir tambi&#233;n un v&#237;nculo inflamaci&#243;n&#47;epilepsia&#44; como ha sido demostrado recientemente<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a>&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">La relaci&#243;n entre la activaci&#243;n del sistema inmune y la presencia de crisis fue posteriormente consolidada por la identificaci&#243;n de auto- anticuerpos circulantes en ciertos pacientes con epilepsia &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Tabla I</a>&#41;&#44; as&#237; como por la alta frecuencia de epilepsia en diferentes enfermedades autoinmunes<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13&#44;19&#44;20</span></a>&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">EVIDENCIAS PATOL&#211;GICAS&#58; EXISTE UN FEN&#211;MENO NEUROINFLAMATORIO ASOCIADO A LA EPILEPSIA&#46;</span><p id="par0045" class="elsevierStylePara elsevierViewall">Estudios histol&#243;gicos realizados en el tejido cerebral de pacientes con epilepsia <span class="elsevierStyleItalic">a priori</span> no vinculadas al fen&#243;meno inflamatorio&#44; han demostrado la inducci&#243;n de varias v&#237;as de se&#241;alizaci&#243;n inflamatorias&#44; la sobrexpresi&#243;n de genes de quimiocinas y citocinas pro-inflamatorias&#44; as&#237; como una prominente activaci&#243;n de la microglia y de los astrocitos<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">21&#8211;27</span></a>&#46; La presencia de c&#233;lulas inmunes perif&#233;ricas en el tejido cerebral y la activaci&#243;n de la v&#237;a de se&#241;alizaci&#243;n de receptores tipo Toll &#40;TLR&#41; han sido demostradas recientemente<a class="elsevierStyleCrossRefs" href="#bib0140"><span class="elsevierStyleSup">28&#44;29</span></a>&#46; Estudios de tomograf&#237;a de emisi&#243;n de positrones &#40;PET&#41; con el marcador C-PK11195 &#40;espec&#237;fico de microglia activada&#41;&#44; confirmaron estos hallazgos en pacientes con epilepsia secundaria a encefalitis<a class="elsevierStyleCrossRefs" href="#bib0150"><span class="elsevierStyleSup">30&#44;31</span></a> o con displasia cortical focal<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">32</span></a>&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">Estas observaciones permitieron establecer que el fen&#243;meno inmuno-inflamatorio est&#225; asociado intr&#237;nsecamente a la epilepsia&#44; independientemente de su etiolog&#237;a&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">LAS CRISIS EPIL&#201;PTICAS INDUCEN NEUROINFLAMACI&#211;N Y VICEVERSA</span><p id="par0055" class="elsevierStylePara elsevierViewall">La relaci&#243;n de causalidad entre epilepsia e inflamaci&#243;n se ha podido explorar en condiciones controladas y con mayor profundidad en modelos experimentales&#46; Su uso ha permitido demostrar que las crisis recurrentes inducen neuroinflamaci&#243;n con activaci&#243;n de microglia&#44; de astrocitos&#44; de neuronas&#44; as&#237; como de las c&#233;lulas epiteliales de la barrera hemato-encef&#225;lica<a class="elsevierStyleCrossRefs" href="#bib0030"><span class="elsevierStyleSup">6&#44;7&#44;36</span></a>&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">Sin embargo&#44; a su vez la neuroinflamaci&#243;n favorece la ocurrencia de crisis epil&#233;pticas&#44; ya que se ha demostrado que la neuroinflamaci&#243;n es un factor que favorece la ocurrencia de crisis y agrava su patolog&#237;a&#46; En particular se sabe que las citocinas proinflamatorias liberadas por la gl&#237;a&#44; tienen un papel importante en la hiperexcitabilidad neuronal implicada en la generaci&#243;n de crisis epil&#233;pticas y su recurrencia&#44; as&#237; como en el da&#241;o celular excitot&#243;xico asociado&#46; Esta hiperexcitabilidad es favorecida por alteraciones en la regulaci&#243;n mediada por c&#233;lulas gliales de los neurotransmisores&#44; iones y de agua&#46; El descontrol de la respuesta inmune mediada por las c&#233;lulas gliales puede causar cambios inflamatorios sostenidos los cuales facilitan la epileptog&#233;nesis<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">37</span></a>&#46; Por otro lado&#44; se ha observado que el bloqueo farmacol&#243;gico o la inactivaci&#243;n de diferentes v&#237;as pro-inflamatorias &#40;IL-1&#44; TNF-a&#44; COX-2&#41; o de elementos de las v&#237;as de se&#241;alamiento del receptor tipo Toll-like resulta en potentes efectos anticonvulsivantes<a class="elsevierStyleCrossRefs" href="#bib0115"><span class="elsevierStyleSup">23&#44;38&#8211;40</span></a>&#46; Se sabe que en modelos de ratones que sobre-expresan la forma soluble del receptor antagonista de IL1&#946; &#40;IL-1Ra&#41;&#44; en astrocitos son intr&#237;nsecamente resistentes a las crisis epil&#233;pticas<a class="elsevierStyleCrossRefs" href="#bib0205"><span class="elsevierStyleSup">41&#44;42</span></a>&#44; mientras que ratones carentes del gen ICE&#47;Caspasa-1 o del gen IL-1R &#40;los cuales son incapaces de producir y liberar IL-1&#946; o de activar la se&#241;alizaci&#243;n de IL-1&#946;&#44; respectivamente&#41;&#44; muestran un retraso significativo en el inicio de las crisis epil&#233;pticas&#44; presentando resistencia a crisis futuras<a class="elsevierStyleCrossRefs" href="#bib0195"><span class="elsevierStyleSup">39&#44;40</span></a>&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">BARRERA HEMATO-ENCEF&#193;LICA Y EPILEPSIA</span><p id="par0065" class="elsevierStylePara elsevierViewall">Se ha demostrado que las crisis epil&#233;pticas y&#47;o el estatus epil&#233;ptico se asocian con un aumento en la permeabilidad de la barrera hemato-encef&#225;lica&#44; lo cual pudiese participar en la epileptog&#233;nesis y en la progresi&#243;n de la epilepsia<a class="elsevierStyleCrossRefs" href="#bib0215"><span class="elsevierStyleSup">43&#44;44</span></a>&#46; En efecto&#44; las crisis convulsivas prolongadas conllevan una sobre regulaci&#243;n de las mol&#233;culas de adhesi&#243;n ubicadas en las c&#233;lulas endoteliales&#44; facilitando la extravasaci&#243;n de los linfocitos circulantes&#59; en particular&#44; la expresi&#243;n de mol&#233;culas como la E-selectina&#44; P-selectina&#44; ICAM-1 y VCAM-1 se encuentran aumentadas<a class="elsevierStyleCrossRefs" href="#bib0225"><span class="elsevierStyleSup">45&#44;46</span></a>&#46; Los ligandos de estas mol&#233;culas son expresados en los leucocitos circulantes despu&#233;s de las crisis lo que facilita su entrada en el sistema nervioso central<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">47</span></a>&#46; Se ha mostrado en particular que el bloqueo de la &#945;4&#946;1 integrina sobre los leucocitos inhibe su infiltraci&#243;n en el cerebro&#44; y que la inhibici&#243;n terap&#233;utica de la activaci&#243;n de la &#945;4 integrina previene la inducci&#243;n de crisis&#44; as&#237; como el desarrollo de la epilepsia<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">47</span></a>&#46; As&#237;&#44; la infiltraci&#243;n de las c&#233;lulas inmunes perif&#233;ricas parece tener un papel relevante en la inducci&#243;n de las crisis y en el desarrollo de la epilepsia&#44; aunque a&#250;n falta informaci&#243;n suficiente&#44; para entender a cabalidad el alcance que este hecho pudiese tener<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a>&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">INFLAMACI&#211;N PERIF&#201;RICA&#44; NEUROINFLAMACI&#211;N Y EPILEPSIA</span><p id="par0070" class="elsevierStylePara elsevierViewall">Diferentes estudios cl&#237;nicos han demostrado la existencia de un incremento en los niveles de mediadores inflamatorios &#40;IL-6&#44; TNF-&#945;&#44; IL-1&#946;&#44; IL-1&#946; Ra&#44; entre otros&#41; en suero y l&#237;quido cefalorraqu&#237;deo de pacientes con epilepsia<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">48</span></a>&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">Otros estudios apoyan el hecho de que el estado inflamatorio perif&#233;rico puede influenciar la presencia de las crisis epil&#233;pticas&#46; Se ha mostrado que la inflamaci&#243;n sist&#233;mica disminuye el umbral de las crisis epil&#233;pticas en varios modelos experimentales de inflamaci&#243;n perif&#233;rica<a class="elsevierStyleCrossRefs" href="#bib0245"><span class="elsevierStyleSup">49&#8211;52</span></a>&#46; En particular&#44; en un modelo de colitis inflamatoria&#44; la intensidad de las crisis se correlacion&#243; significativamente con la severidad de la inflamaci&#243;n perif&#233;rica y fue revertida con la resoluci&#243;n natural del fen&#243;meno inflamatorio<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a>&#46; As&#237; mismo se demostr&#243; tambi&#233;n la presencia de una respuesta inflamatoria cerebral durante la inflamaci&#243;n perif&#233;rica&#44; ya que fueron detectados niveles altos de TNF-&#945; y de activaci&#243;n microglial en el hipocampo&#44; con lo cual queda de manifiesto que la inflamaci&#243;n perif&#233;rica aumenta la excitabilidad del SNC en las personas con epilepsia&#46;</p><p id="par0080" class="elsevierStylePara elsevierViewall">Debido a la presencia de infiltraci&#243;n de c&#233;lulas inmunes perif&#233;ricas en el SNC durante las crisis epil&#233;pticas&#44; el conocer la composici&#243;n celular perif&#233;rica en pacientes epil&#233;pticos pareciera muy relevante&#46; Comparando el fenotipo de leucocitos perif&#233;ricos entre pacientes con epilepsia en periodo interictal &#40;tiempo trancurrido entre una crisis y otra&#41;&#44; se encontr&#243; un elevado porcentaje de monocitos y de c&#233;lulas NK en todos los pacientes incluidos&#44; as&#237; como una disminuci&#243;n de los linfocitos B en los pacientes con epilepsia focal&#44; ambos hallazgos comparando con los controles sanos<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">54</span></a>&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">As&#237; mismo&#44; se encontr&#243; que ni&#241;os con s&#237;ndrome de West &#40;epilepsia caracterizada por espasmos t&#243;nicos breves asociados a un aspecto electroencefalogr&#225;fico particular denominado hipsarritmia y alteraciones en el desarrollo psicomotor&#41;&#44; antes del tratamiento con ACTH presentaban un fenotipo linfocitario perif&#233;rico particular&#44; comparando con sujetos controles&#44; caracterizado por una disminuci&#243;n significativa en los linfocitos CD3<span class="elsevierStyleSup">&#43;</span>CD25<span class="elsevierStyleSup">&#43;</span>&#44; CD19<span class="elsevierStyleSup">&#43;</span> y CD19<span class="elsevierStyleSup">&#43;</span>CD95<span class="elsevierStyleSup">&#43;</span><a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">55</span></a>&#46; De igual forma&#44; comparando ni&#241;os con epilepsia contra controles sanos&#44; se observ&#243; una disminuci&#243;n significativa de los porcentajes de las CD4<span class="elsevierStyleSup">&#43;</span>CD25<span class="elsevierStyleSup">&#43;</span>FoxP3 y CD4<span class="elsevierStyleSup">&#43;</span>&#44; as&#237; como un aumento significativo de las CD8<span class="elsevierStyleSup">&#43;</span>&#44; NK y c&#233;lulas B en los pacientes con epilepsia<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">56</span></a>&#46; Esta observaci&#243;n sugiere la relevancia del estado inmune perif&#233;rico en la fisiopatolog&#237;a de esta enfermedad aunque los mecanismos involucrados quedan todav&#237;a desconocidos&#46;</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">INFLAMACI&#211;N PERIF&#201;RICA&#44; NEUROINFLAMACI&#211;N Y EPILEPSIA F&#193;RMACORRESISTENTE</span><p id="par0090" class="elsevierStylePara elsevierViewall">La epilepsia f&#225;rmacorresistente se asocia a una mortalidad cinco veces m&#225;s alta en comparaci&#243;n con la poblaci&#243;n en general<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">57</span></a>&#46; Se define una epilepsia como f&#225;rmacorresistente cuando se han ensayado uno o dos medicamentos en dosis terap&#233;uticas diarias sin que se logre un control de las crisis convulsivas&#46; Las causas de la epilepsia f&#225;rmacorresistentes son numerosas&#44; muchas de ellas pueden ser debido a anormalidades en la maduraci&#243;n cerebral&#44; a lesiones cerebrales graves con cambios irreversibles respecto a la organizaci&#243;n de la neuroglia cerebral y a una funci&#243;n inhibitoria neuronal&#44; entre otras&#46;</p><p id="par0095" class="elsevierStylePara elsevierViewall">Algunas de las estrategias que se han tomado para tratar esta condici&#243;n&#44; incluyen la resensibilizaci&#243;n de las neuronas hacia cierto tipo de drogas mediante m&#233;todos moleculares&#44; la inhibici&#243;n de la sobreexpresi&#243;n de transportadores de prote&#237;nas mediante la utilizaci&#243;n de bloqueadores de canales de calcio &#40;Verapamil&#41;&#44; que inducen un incremento en la concentraci&#243;n intracelular de las drogas antiepil&#233;pticas<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a>&#44; la utilizaci&#243;n de la atorvastatina que es un inhibidor de la muerte celular hipocampal inducida por un agonista del &#225;cido ka&#237;nico produciendo neuroprotecci&#243;n y acci&#243;n antiepil&#233;ptica<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">58</span></a> y la estimulaci&#243;n el&#233;ctrica del nervio vago &#40;EENV&#41;&#46;</p><p id="par0100" class="elsevierStylePara elsevierViewall">El nervio vago es el d&#233;cimo nervio craneal y es el principal componente del sistema parasimp&#225;tico del sistema nervioso aut&#243;nomo&#46; Su principal neurotransmisor es la acetilcolina&#46; Se ha reportado que la EENV es efectiva en diferentes tipos de crisis epil&#233;pticas parciales y recientemente en crisis epil&#233;pticas generalizadas &#40;reducci&#243;n entre 30 y 85&#37;&#41;&#46; Este efecto ha sido demostrado tanto en la poblaci&#243;n infantil como adulta<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">59</span></a>&#46; En modelos experimentales de epilepsia se ha tambi&#233;n demostrado la efectividad de la EENV&#46; Par&#225;metros como el n&#250;mero de crisis&#44; la severidad de la crisis&#44; la frecuencia de las crisis&#44; la latencia de la primera crisis&#44; etc&#59; han sido disminuidos como consecuencia de la EENV<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">60</span></a>&#46; En un modelo de displasia cortical focal&#44; la cual produce crisis epil&#233;pticas la EENV fue capaz de abolir la actividad epil&#233;ptica<a class="elsevierStyleCrossRef" href="#bib0305"><span class="elsevierStyleSup">61</span></a>&#46; Sin embargo&#44; hasta el momento&#44; el mecanismo preciso para la efectividad de la estimulaci&#243;n el&#233;ctrica del nervio vago en el control de las crisis&#44; es a&#250;n desconocido&#46;</p><p id="par0105" class="elsevierStylePara elsevierViewall">Hasta el momento lo que se sabe es que la EENV disminuye la inflamaci&#243;n perif&#233;rica&#46; Se ha demostrado en un modelo de inflamaci&#243;n perif&#233;rica inducido por la administraci&#243;n de un lipopolisac&#225;rido&#44; que la EENV disminuye la concentraci&#243;n de TNF-&#945; tanto en suero como en h&#237;gado<a class="elsevierStyleCrossRef" href="#bib0310"><span class="elsevierStyleSup">62</span></a>&#46; En un modelo experimental de golpe de calor el cual genera inflamaci&#243;n sist&#233;mica&#44; tambi&#233;n se ha mostrado el mismo efecto&#59; la EENV permite disminuir la concentraci&#243;n de citocinas pro-inflamatorias como TNF&#945; e IL-6 en el pulm&#243;n a diferentes tiempos<a class="elsevierStyleCrossRef" href="#bib0315"><span class="elsevierStyleSup">63</span></a>&#46;</p><p id="par0110" class="elsevierStylePara elsevierViewall">Como hemos mencionado anteriormente el estado inflamatorio perif&#233;rico es capaz de influenciar el estado inflamatorio del sistema nervioso central&#46; Y se sabe que la EENV es eficaz en el control de crisis epil&#233;pticas&#44; as&#237; como en el control de la inflamaci&#243;n sist&#233;mica&#46; As&#237; podr&#237;a ser factible que uno de los mecanismos que participe en la eficiencia de la EENV en las epilepsias f&#225;rmacorresistentes sea la modulaci&#243;n del estadio inflamatorio perif&#233;rico&#46;</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">TRATAMIENTOS ANTIINFLAMATORIOS&#47;INMUNOMODULADORES Y EPILEPSIA</span><p id="par0115" class="elsevierStylePara elsevierViewall">Como se mencion&#243; anteriormente&#44; los tratamientos anti-inflamatorios y&#47;o inmunomoduladores&#44; han mostrado ser &#250;tiles desde hace tiempo en pacientes con epilepsia con un claro componente inmunol&#243;gico<a class="elsevierStyleCrossRefs" href="#bib0355"><span class="elsevierStyleSup">71&#44;72</span></a>&#46; Considerando estas evidencias&#44; se han explorado en diferentes modelos experimentales el potencial de tratamientos antiinflamatorios sobre la epileptog&#233;nesis y las crisis<a class="elsevierStyleCrossRefs" href="#bib0075"><span class="elsevierStyleSup">15&#44;72&#8211;79</span></a> &#40;ver <a class="elsevierStyleCrossRef" href="#tbl0010">Tabla II</a>&#41;&#46; En particular&#44; se ha mostrado que la inhibici&#243;n de COX-2 tiene efecto antiepileptog&#233;nico<a class="elsevierStyleCrossRefs" href="#bib0335"><span class="elsevierStyleSup">67&#44;80</span></a> y que la minociclina &#40;antibi&#243;tico con potentes efectos antiinflamatorios&#41;&#44; permite reducir la frecuencia&#44; duraci&#243;n y severidad de las crisis epil&#233;pticas en un modelo de epilepsia del l&#243;bulo temporal<a class="elsevierStyleCrossRef" href="#bib0345"><span class="elsevierStyleSup">69</span></a>&#46; Si bien los estudios en pacientes&#44; son hasta el momento escasos se han reportado algunos protocolos que se encuentran actualmente en curso<a class="elsevierStyleCrossRef" href="#bib0360"><span class="elsevierStyleSup">72</span></a> &#40;<a class="elsevierStyleCrossRef" href="#tbl0015">Tabla III</a>&#41;&#46; Uno de los problemas es lograr elegir los pacientes que podr&#237;an beneficiarse de una terapia antiinflamatoria asociada<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">48</span></a>&#46; As&#237;&#44; el contar con biomarcadores perif&#233;ricos de neuroinflamaci&#243;n podr&#237;a&#44; en un futuro&#44; permitir mejorar las indicaciones del tratamiento m&#233;dico de estos pacientes<a class="elsevierStyleCrossRefs" href="#bib0240"><span class="elsevierStyleSup">48&#44;81</span></a>&#46;</p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><elsevierMultimedia ident="tbl0015"></elsevierMultimedia></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">CONCLUSIONES</span><p id="par0120" class="elsevierStylePara elsevierViewall">La epilepsia es uno de los padecimientos neurol&#243;gicos m&#225;s prevalentes&#44; causante de una morbilidad y mortalidad elevadas&#46; Aunque existen varios tratamientos eficientes&#44; las epilepsias f&#225;rmacorresistentes siguen siendo frecuentes&#46; La relevancia de la inflamaci&#243;n central y probablemente perif&#233;rica en su patogenia es un hallazgo muy interesante&#44; ya que la modulaci&#243;n de &#233;stos podr&#237;a permitir mejorar el pron&#243;stico de este padecimiento&#46;</p></span></span>"
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    "fechaRecibido" => "2015-11-27"
    "fechaAceptado" => "2016-01-22"
    "PalabrasClave" => array:2 [
      "es" => array:1 [
        0 => array:4 [
          "clase" => "keyword"
          "titulo" => "Palabras clave"
          "identificador" => "xpalclavsec622557"
          "palabras" => array:3 [
            0 => "epilepsia"
            1 => "inflamaci&#243;n"
            2 => "neuroinflamaci&#243;n&#46;"
          ]
        ]
      ]
      "en" => array:1 [
        0 => array:4 [
          "clase" => "keyword"
          "titulo" => "Keywords"
          "identificador" => "xpalclavsec622558"
          "palabras" => array:3 [
            0 => "epilepsy"
            1 => "inflammation"
            2 => "neuroinflammation&#46;"
          ]
        ]
      ]
    ]
    "tieneResumen" => true
    "resumen" => array:2 [
      "es" => array:2 [
        "titulo" => "RESUMEN"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">La epilepsia es un trastorno neurol&#243;gico que afecta a 50 millones de personas en el mundo&#46; Se define por la presencia de crisis epil&#233;pticas espont&#225;neas resultado de descargas sincr&#243;nicas de una poblaci&#243;n neuronal debido a un dinamismo anormal de las redes neuronales&#46; Diferentes factores han sido implicados en su etiopatogenia&#44; uno de ellos siendo los procesos inmunol&#243;gicos e inflamatorios&#46; En el presente trabajo revisaremos los datos existentes sobre el papel de la inflamaci&#243;n&#47;neuroinflamaci&#243;n en la epilepsia&#46;</p></span>"
      ]
      "en" => array:2 [
        "titulo" => "ABSTRACT"
        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Epilepsy is a neurological disorder affecting 50 million people worldwide&#46; It is defined by the presence of spontaneous seizures result of synchronous discharges of neuronal population due to abnormal dynamics of neural networks&#46; Different factors have been implicated in its pathogenesis&#44; one of them being immune and inflammatory processes&#46; In this paper we review the existing data on the role of inflammation &#47; neuroinflammation in epilepsy&#46;</p></span>"
      ]
    ]
    "multimedia" => array:3 [
      0 => array:7 [
        "identificador" => "tbl0005"
        "etiqueta" => "Tabla I"
        "tipo" => "MULTIMEDIATABLA"
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        "tabla" => array:1 [
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                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="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Tipo de epilepsia&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Auto anticuerpos&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Infiltrado inflamatorio&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Referencias&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Encefalitis deRasmussen&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Ac anti-GluR3Ac anti &#945;7 nACh receptorAc anti-Munc18-1&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Linfocitos T CD8&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Rogers et al&#46;&#44; 1994<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">33</span></a>Watson <span class="elsevierStyleItalic">et al&#46;</span>&#44; 2005<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a>&#193;lvarez Bar&#243;n <span class="elsevierStyleItalic">et al</span>&#46;&#44; 2008<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Encefalitis l&#237;mbica&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Ac-anti AMPARAc-anti GABAbRAc-anti NMDARAc-anti VGKC &#40;LGI1&#44; CASPR2&#44; Contactin-2&#41;Ac-anti GAD&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Linfocitos BLinfocitos T CD4Microglia activada&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Vincent <span class="elsevierStyleItalic">et al&#46;</span>&#44; 2011 a&#44;b<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">14&#44;20</span></a>Quek <span class="elsevierStyleItalic">et al&#46;</span>&#44; 2012<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a>Bien et al&#46;&#44; 2012<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a>Granata <span class="elsevierStyleItalic">et al</span>&#46;&#44; 2011<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Encefalitis paraneopl&#225;sica l&#237;mbica&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Ac antineuronal nuclear tipo 1&#46;Ac-anti CRMP-5Ac-anti HuAc-anti Ma2Ac-anti AbamphiphysinAc anti CV2Ac-anti Sox1&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Linfocitos T CD8&#47;CD3NK CD57&#43;Linfocitos B&#47; C&#233;lulas plasm&#225;ticas &#40;CD138&#43;&#41;Astrocitos activadosMicroglia activada&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Quek et al&#46;&#44; 2012<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a>Bien CG <span class="elsevierStyleItalic">et al</span>&#46;&#44; 2012<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">S&#237;ndrome Landue-Kleffner&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Ac anti-BDNFAc anti-c&#233;lulas endoteliales&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="" valign="top">&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Hirsch et al&#46;&#44; 2006<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">34</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Enfermedad de Batten&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Ac-anti GAD65&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Astrocitos activados&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Granata et al&#46;&#44; 2011<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a>Chattopadhyay <span class="elsevierStyleItalic">et al&#46;</span>&#44; 2002<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">35</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
                  """
              ]
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                0 => "xTab997007.png"
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        ]
        "descripcion" => array:1 [
          "es" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Epilepsias autoinmunes asociadas a la presencia de autoanticuerpos</p>"
        ]
      ]
      1 => array:7 [
        "identificador" => "tbl0010"
        "etiqueta" => "Tabla II"
        "tipo" => "MULTIMEDIATABLA"
        "mostrarFloat" => true
        "mostrarDisplay" => false
        "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="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Modelo&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">F&#225;rmaco&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Resultado&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Referencia&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Cepa&#58; Sprague-Dawley &#40;rat&#243;n&#41;Agente&#58; &#193;cido kainico&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Rofecoxib &#40;inhibidor de COX-2&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Disminuci&#243;n del 50&#37; de la p&#233;rdida neuronal en hipocampo&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Kunz et al&#46;&#44; 2001<a class="elsevierStyleCrossRef" href="#bib0320"><span class="elsevierStyleSup">64</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Cepas&#58;WAG&#47;Rij &#40;rata&#41;GAERS &#40;rata&#41;Long Evans &#40;rata&#41;Agente&#58; LPS&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Indometacina &#40;inhibidor de COX-2&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Disminuci&#243;n del n&#250;mero deconvulsiones&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Kov&#225;cs et al&#46;&#44; 2014<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">65</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Cepa&#58;C57BL&#47;6Cr &#40;rat&#243;n&#41;Agente&#58; Pilocarpina&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">TG6-10-1 &#40;Antagonista EP2&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Efecto neuroprotector &#40;Suprime mortalidad y d&#233;ficit funcional&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Jiang et al&#46;&#44; 2015<a class="elsevierStyleCrossRef" href="#bib0330"><span class="elsevierStyleSup">66</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Cepa&#58; WAG&#47;Rij &#40;rata&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Etoricoxib &#40;inhibidor de COX-2&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Efecto preventivo y abortivo&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Citraro R et al&#46;&#44; 2015<a class="elsevierStyleCrossRef" href="#bib0335"><span class="elsevierStyleSup">67</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Cepa&#58; Albino &#40;rat&#243;n&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Rofecoxib y Nimesulida &#40;inhibidores COX-2&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Efecto preventivo&#44; abortivo y disminuci&#243;n de mortalidad&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Dhir A et al&#46;&#44; 2006<a class="elsevierStyleCrossRef" href="#bib0340"><span class="elsevierStyleSup">68</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Cepa&#58; Sprague-Dawly &#40;rata&#41;Agente&#58; Pilocarpina&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Minociclina &#40;supresi&#243;n de la activaci&#243;n de microglia&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Efecto preventivo&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Wang et al&#46;&#44; 2015<a class="elsevierStyleCrossRef" href="#bib0345"><span class="elsevierStyleSup">69</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Cepa&#58; Wistar &#40;rata&#41;Agente&#58; Pilocarpina&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Lovastatina &#40;inhibidor de HMG-CoA&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Efecto neuroprotector&#40;Prevenci&#243;n de Excitotoxicidad&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Gouveia et al&#46;&#44; 2014<a class="elsevierStyleCrossRef" href="#bib0350"><span class="elsevierStyleSup">70</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
                  """
              ]
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                0 => "xTab997006.png"
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          ]
        ]
        "descripcion" => array:1 [
          "es" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Tratamientos antiinflamatorios&#47;inmunomoduladores en epilepsia&#58; Evidencias experimentales</p>"
        ]
      ]
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        "etiqueta" => "Tabla III"
        "tipo" => "MULTIMEDIATABLA"
        "mostrarFloat" => true
        "mostrarDisplay" => false
        "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="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Tipo de Epilepsia&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">N &#40;pacientes&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">F&#225;rmaco&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Resultado&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Referencia&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Epilepsia refractaria a tratamiento&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">61&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Placebo &#40;n&#61;18&#41;Inmunoglobulina IV &#40;n&#61;43&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">19 respondedores &#40;grupo Ig&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Van Rijckevorsel et al&#46;&#44; 1994<a class="elsevierStyleCrossRef" href="#bib0365"><span class="elsevierStyleSup">73</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Epilepsia resistente a f&#225;rmacos&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">35 &#40;ni&#241;os&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">a&#41; Hidrocortisona &#40;n&#61;16&#41;b&#41; Deflazacort &#40;n&#61;19&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Mejor&#237;a en 44&#37; &#40;a&#41; y 47&#37; &#40;b&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Grosso et al&#46;&#44; 2008<a class="elsevierStyleCrossRef" href="#bib0370"><span class="elsevierStyleSup">74</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">S&#237;ndromes convulsivos continuos de pico-onda durante sue&#241;o-ondas lentas&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">44 &#40;ni&#241;os&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Hidrocortisona&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">77&#46;2&#37; normalizaci&#243;n de EEG45&#46;4&#37; respondedores a largo plazo&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Buzatu et al&#46;&#44; 2009<a class="elsevierStyleCrossRef" href="#bib0375"><span class="elsevierStyleSup">75</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Epilepsia intratableS&#237;ndrome de WestS&#237;ndrome de Lennox-Gastaut&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">37&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Inmunoglobulina IV&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">43&#37; con mejor&#237;a&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Mikati et al&#46;&#44; 2010<a class="elsevierStyleCrossRef" href="#bib0380"><span class="elsevierStyleSup">76</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Epilepsias con componente inmunol&#243;gico&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">368&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Inmunoglobulina&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">52&#37; con reducci&#243;n de convulsiones23&#37; con remisi&#243;n completa&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">&#214;zkara et al&#46;&#44; 2011<a class="elsevierStyleCrossRef" href="#bib0360"><span class="elsevierStyleSup">72</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Epilepsias autoinmunes&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">32&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Metilprednisolona IVInmunoglobulina IVCombinaci&#243;n de metilprednisolona&#44; inmunoglobulina&#44; plasmaf&#233;resis o ciclofosfamida&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">81&#37; con mejoramiento postinmunoterapia&#46;66&#37; libres de convulsiones&#46;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Quek et al&#46;&#44; 2012<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">S&#237;ndrome de West&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">916&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">PrednisolonaTetracosactide depot&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Mejor&#237;a&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">Hancock et al&#46;&#44; 2013<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">78</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Epilepsia f&#225;rmacorresistente&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">29&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">MetilprednisolonaInmunoglobulinaPlasmaf&#233;resisAzatioprinaMicofenolato&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">50&#37; respondieron al primer tratamiento45&#37; no respondedores mejoraron luego de la administraci&#243;n de un segundo agente&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="left" valign="top">R&#252;egg &#38; Panzer et al&#46;&#44; 2014<a class="elsevierStyleCrossRef" href="#bib0395"><span class="elsevierStyleSup">79</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
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ISSN: 1405888X
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