ABSTRACT
INTRODUCCIÓN: las indicaciones de la cirugía endoscópica endonasal en el tratamiento de tumores de base de cráneo continúan expandiéndose, sobre todo para los tumores extradurales, como son los cordomas. A partir de un caso, nuestro objetivo fue revisar la literatura relevante de estos desafiantes tumores operados bajo esta técnica. CASO CLÍNICO: paciente de 59 de edad con antecedentes de depresión mayor, que comenzó con un cuadro de diplopía por compromiso del VI par izquierdo. Los estudios (CT y RM) mostraron un proceso expansivo en la región del ápex petroso. Se realizó un abordaje endoscópico extendido a la región petro-clival con resección tumoral subtotal. Buena evolución postquirúrgica con desaparición de su diplopía. El diagnóstico histológico fue de Cordoma Condroide. Se indicó radioterapia adyuvante. DISCUSIÓN: a partir del conocimiento y la experiencia en el manejo endoscópico de la patología intraselar se desarrollaron abordajes para el tratamiento de patologías que comprometen la fosa anterior, media e inclusive la fosa posterior. Actualmente, los abordajes endoscópicos, se han extendido a otras áreas de la base de cráneo que de otro modo presentan un reto técnico para la exposición a través de los abordajes transcraneales habituales. El abordaje endoscópico endonasal ofrece una ruta quirúrgica adecuada para la resección del tumor que se presenta en este caso. Las vías que pueden ser utilizados para llegar a la región petroclival a través de la acceso endonasal incluyen la medial (con o sin la movilización de ACI) y la infrapetrosa transterigoidea. En este reporte de caso se analizan las indicaciones del abordaje endoscópico endonasal basado en una revisión de la literatura. CONCLUSIÓN: el abordaje endoscópico endonasal extendido se presenta como una alternativa segura para el tratamiento de determinadas lesiones petro-clivales. Se requieren más estudios anatómicos y clínicos para establecer mejor el rol de este tipo de técnicas en el manejo de las lesiones localizadas en esta región
INTRODUCTION: indications for endoscopic endonasal surgery for the treatment of skull base tumors continue to expand, particularly for extradural tumors, such as chordomas. Based on this case report presentation, we aim to review the literature on the endoscopic technique relevant to the management of these challenging tumors. CASE REPORT: a 59 year-old woman who presented with diplopia due to left sixth nerve palsy underwent imaging studies (CT, MRI) that revealed a mainly intra-osseous expansive process of the left petrous apex. An expanded endoscopic endonasal approach to the petroclival region was performed and the tumor was subtotally resected. The patient recovered from surgery with resolved diplopia. Histopathology was compatible with chondroid chordoma. The radiation therapy was indicated after surgery. DISCUSSION: built upon the bulk experience on the treatment of intrasellar pathology, endonasal endoscopic approaches have been developed for the treatment of skull base lesions involving the anterior, middle and even posterior cranial fossae. Nowadays, the use of these techniques has spread to other areas of the skull base, which otherwise present as a formidable technical challenge for exposure through transcranial approaches. The endonasal endoscopic approach provides an adequate surgical corridor for the resection of the tumor presented in this case report. The alternative corridors that can be utilized to reach the petroclival region through the endonasal endoscopic route include the medial corridor (with or without ICA mobilization) and the transpterygoid infrapetrous corridor. In this article, we discuss the indications for the endoscopic endonasal approach for the case presented, and discuss our choice of approach based on our review of the literature. CONCLUSION: the extended endoscopic endonasal approach presents as a safe alternative for the treatment of select petroclival lesions. Further anatomical and clinical studies are required to better establish the role of the endoscopic endonasal approach for lesions located in this region
Subject(s)
Humans , Chordoma , Nose Diseases , EndoscopyABSTRACT
Isquemia cerebral tardia (delayed cerebral ischemia; DCI)é a principal causa potencialmente tratável de mortalidade e incapacidade em pacientes com hemorragia subaracnóide aneurismática (HSA). No entanto, não existe tratamento eficaz para esta condição até o momento. A recente demonstração da falta de resposta clínica à reversão farmacológica do espasmo arterial após HSA estimulou uma reavaliação dos conceitos fisiopatológicos na DCI que segue a HSA,que foram por muito tempo creditados ao espasmo arterial observado em doentes com HSA. Desde a demonstração de resultados eletrocorticográficos de depressão cortical generalizada(cortical spreading depressions, CSD) em pacientes com HSA, um crescente interesse foi despertado sobre opapel destes fenômenos na fisiopatologia da DCI observados em pacientes com HSA. Quando induzida em um cérebro saudável, a CSD está associada com aumento do fluxo sanguíneo cerebral, facilitando a distribuição de substratos de energia necessários para repolarização celular cerebral.Em um cérebro lesado, no entanto, CSDs estão associados a uma redução do fluxo sanguíneo cerebral, que, no contexto de aumento das necessidades da energia, leva à falha de energia e hipóxia, acentuando a gravidade da lesão cerebral. Esta resposta inversa hemodinâmica à CSD foi descoberta pela primeira vez em um modelo animal, replicando as condições de HSA e, posteriormente, demonstrado em pacientes com HSA. A isquemia leva à escassez de substratos energéticos e propagação da hipóxia, resultando em lesões corticais, e podem explicar os padrões de lesão, semelhantemente ao que ocorre em pacientes com HSA. Estas observações sugerem que o déficit de energia produzida por CSD é um fator chave na patogênese dos DCI observados como resultado da HSA.Este artigo detalha as principais características de CSDs e sua potencial relevância na fisiopatologia das complicações isquêmicas da HSA.
Delayed cerebral ischemia (DCI) is the leading potentially treatable cause of mortality and disability in patients with aneurysmal subarachnoid hemorrhage (SAH). However, to date there is no effective treatment for this entity. The recently demonstrated lack of clinical response to pharmacologic reversal of arterial spasm as a result of SAH has spurred a reassessment of the pathophysiological concepts on DCI that follows SAH.DCI was long believed the consequence of the angiographically visible arterial spasm observed in patients with SAH. Since themeasurement of cortical spreading depolarizations (CSD) inpatients with SAH, increasing evidence has suggested a role for these phenomena in the pathophysiology of DCI. When induced in a healthy brain, CSDs are associated with an increase in regional cerebral blood flow that facilitates the delivery of the necessary energy substrates for cellular repolarization. Ina brain that has been injured, however, CSDs can induce microvascular constriction, or cortical spreading ischemia. This inverse hemodynamic response to CSD was first discovered in an animal model replicating the conditions following SAH, and later demonstrated in patients with SAH. The spreading ischemia leads to energy substrates shortage and hypoxia, resulting in cortical lesions, and may explain similar lesion patterns which occur in SAH patients. This review describes the salient characteristics of CSD and its potential relevance in the pathophysiology, monitoring, and treatment of ischemic complications following SAH.
Subject(s)
Humans , Male , Female , Cortical Spreading Depression , Subarachnoid Hemorrhage , Vasospasm, IntracranialABSTRACT
El vasoespasmo cerebral es la principal causa potencialmente tratable de mortalidad e incapacidad en pacientes que sufren hemorragia subaracnoidea aneurismática (HSA). Sin embargo, a la fecha no existe un tratamiento eficaz para el mismo. La reciente demostración de la falta de respuesta clínica a la reversión farmacológica del espasmo arterial a consecuencia de HSA ha obligado un replanteo de los fundamentos fisiopatológicos de los déficits neurológicos isquémicos tardíos (delayed ischemic neurologic déficit, DIND) a consecuencia de HSA, los cuales se creían en relación al espasmo arterial observado en pacientes con HSA. Desde la demostración de hallazgos electrocorticográficos de depresión cortical propagada (cortical spreading depression, CSD) en pacientes con HSA, un interés creciente se ha despertado respecto del rol de estos fenómenos en la fisiopatología de los DIND observados en pacientes con HSA. Cuando inducidas en un cerebro saludable, las CSD se asocian con un aumento del flujo sanguíneo cerebral, facilitando la entrega del cerebro de los sustratos energéticos necesarios. En un cerebro que ha sido lesionado, sin embargo, la CSD se asocia con una reducción en flujo sanguíneo cerebral, lo cual, en el contexto de un aumento de las necesidades de energía, conduce a la insuficiencia energética y la hipoxia, empeorando así el daño cerebral. Estas observaciones sugieren que el déficit de energía producida por la CSD es un factor clave en la patogénesis de los DIND observados a consecuencia de HSA. Este resumen detalla características sobresalientes de las CSD y su potencial relevancia en la fisiopatología del vasoespasmo.
Cerebral vasospasm is the leading potentially treatable cause of mortality and disability in patients with aneurysmatic subarachnoid hemorrhage (SAH). However, to date there is no effective treatment for this entity. The recently demonstrated lack of clinical response to pharmacologic reversal of arterial spasm as a result of SAH has spurred a reassessment of the pathophysiological concepts on delayed ischemic neurologic deficits (DIND) that follow SAH, which were long believed the effect of the arterial spasm observed in patients with SAH. Since the discovery of electrocorticographic cortical spreading depressions (CSD) in patients with SAH, increasing interest has been shown on the role of these phenomena in the pathophysiology of DIND observed in patients with HSA. When induced in a healthy brain, CSD are associated with an increase in cerebral blood flow by facilitating the delivery of the necessary energy substrates. In a brain that has been injured, however, CSD are associated with a reduction in cerebral blood flow, which, in the context of increased energy requirements leads to energy shortage and hypoxia, thus worsening brain damage. These observations suggest that the energetic deficit produced by the CSD is a key factor in the pathogenesis of DIND observed as a result of HSA. This review details striking characteristics of CSD and their potential relevance in the pathophysiology of vasospasm.