Submit to Brain Sciences Review for Brain Sciences Propose a Special Issue

Journal Browser

► Journal Browser

The Immune System, Neuroinflammation and Epilepsy

Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Systems Neuroscience".

Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 9884

Share This Special Issue

Special Issue Editor

Dr. Pedro Jesus Serrano-Castro

E-Mail Website
Guest Editor

1. Biomedical Research Institute of Málaga (IBIMA), University of Málaga, 29010 Málaga, Spain
2. Neurosciences Clinical Unit, University Regional Hospital of Málaga, 29010 Málaga, Spain
3. Andalusian Network for Clinical and Translational Research in Neurology (Neuro-RECA), 29010 Málaga, Spain
Interests: epilepsy; neuroinflammatory bases of epilepsy; neuromodulation in epilepsy; antiepileptogenic medications; biomarkers of epilepsy; personalized medicine in epilepsy

Special Issue Information

Dear Colleagues,

Epilepsy is one of the most prevalent chronic neurological diseases, as it is estimated that approximately 50 million people suffer from it worldwide. The prevalence of active epilepsy in developed countries is between 5 and 7 cases per 1000 inhabitants, this figure being considerably higher in developing countries. Traditionally, a considerable group of patients have been considered as epilepsies of cryptogenic or “non-lesional” origin. However, it is becoming increasingly clear that a significant part of this heterogeneous group of patients may respond to causes mediated by the immune system or even inflammatory causes. The emergence of recently recognized autoimmune encephalopathies, among which epileptic seizures are a major manifestation, has increased the possibility that chronic epileptic syndromes may also have an immune-mediated cause even in the absence of an initial encephalitic event. Thus, the International League Against Epilepsy (ILAE), in its latest review, recognized for the first time the existence of an epilepsy of autoimmune origin. The possibility of the existence of a relationship between epileptogenesis and neuroinflammatory mechanisms is also being extensively studied by various research groups.

Dr. Pedro Jesus Serrano-Castro
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

Epilepsy
Seizures
Autoimmune epilepsy
Neuroinflammation
Cytokines
Interleukines
Cheomokines
Autoantibodies
Limbic encephalitis

Published Papers (3 papers)

Download All Papers

Research

Jump to: Review

11 pages, 5748 KiB

Open AccessArticle

Risk of Developing Epilepsy after Autoimmune Encephalitis

by Ariadna Gifreu, Mercè Falip, Jacint Sala-Padró, Neus Mongay, Francisco Morandeira, Ángels Camins, Pablo Naval-Baudin, Misericordia Veciana, Montserrat Fernández, Jordi Pedro, Belia Garcia, Pablo Arroyo and Marta Simó

Brain Sci. 2021, 11(9), 1182; https://doi.org/10.3390/brainsci11091182 - 8 Sep 2021

Cited by 12 | Viewed by 2274

Abstract

Background: Acute symptomatic seizures (ASS) are a common manifestation of autoimmune encephalitis (AE), but the risk of developing epilepsy as a sequela of AE remains unknown, and factors predisposing the development of epilepsy have not been fully identified. Objective: To assess the risk of developing epilepsy in AE and study related risk factors. Materials and methods: This was a retrospective single centre study including patients diagnosed with AE according to criteria described by Graus et al., with a minimum follow-up of 12 months after AE resolution. The sample was divided according to whether patients developed epilepsy or not. Results: A total of 19 patients were included; 3 (15.8%) had AE with intracellular antibodies, 9 (47.4%) with extracellular antibodies, and 7 (36.8%) were seronegative. During follow-up, 3 patients (15.8%) died, 4 (21.1%) presented relapses of AE, and 11 (57.89%) developed epilepsy. There was a significant association between the development of epilepsy and the presence of hippocampal atrophy in control brain magnetic resonance imaging (MRI) (p = 0.037), interictal epileptiform discharges (IED) on control electroencephalogram (EEG) (p = 0.045), and immunotherapy delay (p = 0.016). Conclusions: Hippocampal atrophy in neuroimaging, IED on EEG during follow-up, and immunotherapy delay could be predictors of the development of epilepsy in patients with AE. Full article

(This article belongs to the Special Issue The Immune System, Neuroinflammation and Epilepsy)

► Show Figures

Figure 1

Review

Jump to: Research

11 pages, 621 KiB

Open AccessReview

Neuropsychological Evaluations in Limbic Encephalitis

by Juri-Alexander Witt and Christoph Helmstaedter

Brain Sci. 2021, 11(5), 576; https://doi.org/10.3390/brainsci11050576 - 29 Apr 2021

Cited by 14 | Viewed by 4047

Abstract

Limbic encephalitis (LE) can cause dynamic and permanent impairment of cognition and behavior. In clinical practice, the question arises as to which cognitive and behavioral domains are affected by LE and which assessment is suited to monitor the disease progress and the success of treatment. Current findings on cognition and behavior in LE are reviewed and discussed based on current guidelines and consensus papers. In addition, we outline approaches for the neuropsychological monitoring of LE and its treatment. Dependent on disease acuity and severity, LE leads to episodic long-term memory dysfunction in different variants (e.g., anterograde memory impairment, accelerated long-term forgetting, and affection of autobiographical memory) and executive deficits. In addition, affective disorders are very common. More severe psychiatric symptoms may occur as well. In the course of the disease, dynamic phases with functional recovery must be differentiated from residual defect states. Evidence-based neuropsychological diagnostics should be conducted ideally before treatment initiation and reassessments are indicated when any progress is suggested, and when decisive anti-seizure or immunomodulatory treatment changes are made. Cognition and behavior may but must not run in synchrony with seizures, MRI pathology, or immune parameters. Cognitive and behavioral problems are integral aspects of LE and represent important biomarkers of disease acuity, progress, and therapy response beyond and in addition to parameters of immunology, neurological symptoms, and brain imaging. Thus, evidence-based neuropsychological assessments are essential for the diagnostic workup of patients with suspected or diagnosed limbic encephalitis, for treatment decisions, and disease and treatment monitoring. Full article

(This article belongs to the Special Issue The Immune System, Neuroinflammation and Epilepsy)

► Show Figures

Figure 1

12 pages, 1306 KiB

Open AccessReview

Prevalence of Neural Autoantibodies in Epilepsy of Unknown Etiology: Systematic Review and Meta-Analysis

by Pablo Cabezudo-García, Natalia Mena-Vázquez, Nicolás L. Ciano-Petersen, Guillermina García-Martín, Guillermo Estivill-Torrús and Pedro J. Serrano-Castro

Brain Sci. 2021, 11(3), 392; https://doi.org/10.3390/brainsci11030392 - 19 Mar 2021

Cited by 7 | Viewed by 2917

Abstract

Background: The prevalence of neural autoantibodies in epilepsy of unknown etiology varies among studies. We aimed to conduct a systematic review and meta-analysis to determine the pooled global prevalence and the prevalence for each antibody. Methods: A systematic search was conducted for studies that included prospectively patients ≥16 years old with epilepsy of unknown etiology and systematically determined neural autoantibodies. A meta-analysis was undertaken to estimate pooled prevalence in total patients with a positive result for at least one neural autoantibody in serum and/or cerebrospinal fluid (CSF) and for each autoantibody. Results: Ten of the eleven studies that met the inclusion criteria and a total of 1302 patients with epilepsy of unknown etiology were included in themeta-analysis. The global pooled prevalence (IC95%) was 7.6% (4.6–11.2) in a total of 82 patients with a positive result for any neural autoantibody. None of the controls available in the studies had a positive result. Individual pooled prevalence for each autoantibody was: glycine receptor (GlyR) (3.2%), glutamic acid decarboxylase (GAD) (1.9%), N-methyl-d-aspartate receptor (NMDAR) (1.8%), leucine-rich glioma inactivated-1 protein (LGI1) (1.1%), contactin-2-associated protein (CASPR2) (0.6%) and onconeuronal (0.2%). Conclusions: The pooled prevalence of neural autoantibodies in patients with epilepsy of unknown etiology is small but not irrelevant. None of the controls had a positive result. There was high heterogeneity among studies. In the future, a homogeneous protocol for testing neural autoantibodies is recommended. Full article

(This article belongs to the Special Issue The Immune System, Neuroinflammation and Epilepsy)

► Show Figures