Catálogo de publicaciones - revistas

<jats:title>Summary</jats:title><jats:sec><jats:title>Purpose</jats:title><jats:p>The 2005 diagnostic criteria for <jats:styled-content style="fixed-case">R</jats:styled-content>asmussen encephalitis (<jats:styled-content style="fixed-case">RE</jats:styled-content>) are based on seizures, clinical deficits, electroencephalography (<jats:styled-content style="fixed-case">EEG</jats:styled-content>), neuroimaging, and pathology (<jats:italic>Brain</jats:italic>, 128, 2005, 451). We applied these criteria to patients evaluated for <jats:styled-content style="fixed-case">RE</jats:styled-content> and epilepsy surgery controls to determine the sensitivity, specificity, and positive and negative predictive values (<jats:styled-content style="fixed-case">PPV</jats:styled-content>s, <jats:styled-content style="fixed-case">NPV</jats:styled-content>s) using pathology as the gold standard.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>We identified patients evaluated for <jats:styled-content style="fixed-case">RE</jats:styled-content> based on medical records from 1993 to 2011. Fifty‐two control patients with refractory epilepsy, unilateral magnetic resonance imaging (<jats:styled-content style="fixed-case">MRI</jats:styled-content>) changes, and biopsies were selected from an epilepsy surgery database from matching years. Patients meeting all three of group A and/or two of three group B criteria were classified as meeting full criteria (positive). Patients not meeting full criteria were classified as negative. When available, pathology findings were re‐reviewed with neuropathologists, and <jats:styled-content style="fixed-case">MRI</jats:styled-content> imaging was re‐reviewed with a neuroradiologist.</jats:p></jats:sec><jats:sec><jats:title>Key Findings</jats:title><jats:p><jats:styled-content style="fixed-case">RE</jats:styled-content> was considered in the differential diagnosis for 82 patients, of whom 35 had biopsies. Twenty patients met full criteria (positive) without another explanation, including seven for whom biopsy was required to meet criteria and one in whom another etiology was identified. Two patients met full criteria but had another explanation. Thirty‐five met partial criteria (negative), of whom 14 had another etiology identified. Twenty‐five met no criteria (negative). The diagnostic criteria had a sensitivity of 81% with four false negatives (criteria‐negative, biopsy‐positive) when compared to pathology as a gold standard. Five false positives (criteria positive, biopsy negative) had identifiable alternate diagnoses.</jats:p></jats:sec><jats:sec><jats:title>Significance</jats:title><jats:p>The 2005 <jats:styled-content style="fixed-case">B</jats:styled-content>ien clinical diagnostic criteria for <jats:styled-content style="fixed-case">RE</jats:styled-content> have reasonably high sensitivity and specificity and good clinical‐pathologic correlation in most cases. We suggest modification of the criteria to allow inclusion of cases with well‐described but less common features. Specifically we suggest making the diagnosis in the absence of epilepsia partialis continua (<jats:styled-content style="fixed-case">EPC</jats:styled-content>) or clear progression of focal cortical deficits or <jats:styled-content style="fixed-case">MRI</jats:styled-content> findings if biopsy is positive and two of the <jats:styled-content style="fixed-case">A</jats:styled-content> criteria are met (B3 plus two of three <jats:styled-content style="fixed-case">A</jats:styled-content> criteria). This would improve the sensitivity of the criteria.</jats:p></jats:sec>

<jats:title>Abstract</jats:title><jats:p>Epilepsy is a common neurological disorder that increases the risk of morbidity and mortality. Autoimmune epilepsy is a subset of epilepsy that occurs in the setting of autoimmunity, such as in autoimmune encephalitis (AIE). AIE is an autoimmune disorder characterized by immune‐mediated neuroinflammation resulting in a variety of neurological symptoms, including psychiatric disturbance, cognitive dysfunction, and seizures. Seizures in AIE are thought to be a result of antibodies directed against neuronal cell‐surface proteins involved in synaptic transmission. The role of blood‐brain barrier dysfunction, myeloid cell infiltration, and the initiation of proinflammatory cascades in epileptogenesis has been shown to be important in animal models and human patients with epilepsy. Epileptogenesis in AIE is likely to arise from the synergistic effect of both innately driven neuroinflammation and antibody‐induced hyperexcitability. Together, these processes produce persistent drug‐resistant seizures that contribute to the morbidity seen in AIE. Understanding the proinflammatory pathways involved in this process may improve diagnostics and provide alternative treatment targets in AIE.</jats:p>

<jats:title>Abstract</jats:title><jats:p>Presurgical evaluation and surgery in the pediatric age group are unique in challenges related to caring for the very young, range of etiologies, choice of appropriate investigations, and surgical procedures. Accepted standards that define the criteria for levels of presurgical evaluation and epilepsy surgery care do not exist. Through a modified Delphi process involving 61 centers with experience in pediatric epilepsy surgery across 20 countries, including low–middle‐ to high‐income countries, we established consensus for two levels of care. Levels were based on age, etiology, complexity of presurgical evaluation, and surgical procedure. Competencies were assigned to the levels of care relating to personnel, technology, and facilities. Criteria were established when consensus was reached (≥75% agreement). Level 1 care consists of children age 9 years and older, with discrete lesions including hippocampal sclerosis, undergoing lobectomy or lesionectomy, preferably on the cerebral convexity and not close to eloquent cortex, by a team including a pediatric epileptologist, pediatric neurosurgeon, and pediatric neuroradiologist with access to video‐electroencephalography and 1.5‐T magnetic resonance imaging (MRI). Level 2 care, also encompassing Level 1 care, occurs across the age span and range of etiologies (including tuberous sclerosis complex, Sturge‐Weber syndrome, hypothalamic hamartoma) associated with MRI lesions that may be ill‐defined, multilobar, hemispheric, or multifocal, and includes children with normal MRI or foci in/abutting eloquent cortex. Available Level 2 technologies includes 3‐T MRI, other advanced magnetic resonance technology including functional MRI and diffusion tensor imaging (tractography), positron emission tomography and/or single photon emission computed tomography, source localization with electroencephalography or magnetoencephalography, and the ability to perform intra‐ or extraoperative invasive monitoring and functional mapping, by a large multidisciplinary team with pediatric expertise in epilepsy, neurophysiology, neuroradiology, epilepsy neurosurgery, neuropsychology, anesthesia, neurocritical care, psychiatry, and nursing. Levels of care will improve safety and outcomes for pediatric epilepsy surgery and provide standards for personnel and technology to achieve these levels.</jats:p>