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Objective: Due to supply shortage, amobarbital, the traditional anesthetic agent in Wada testing, was replaced by methohexital in many epilepsy centers. This study aimed to compare the two barbiturates to identify possible advantages or disadvantages of methohexital as compared to amobarbital with regard to the adequacy of language and memory testing during the Wada test., Methods: Data from 75 patients with temporal lobe epilepsy who underwent bilateral Wada tests using either amobarbital (n = 53) or methohexital (n = 22) as part of presurgical work-up were analyzed retrospectively. The two subgroups were compared regarding hemispheric language and memory lateralization results and Wada testing characteristics, and the adequacy of language and memory testing was assessed., Results: We observed shorter durations of motor-, speech-, and EEG recovery after each injection in patients receiving methohexital compared to amobarbital. In addition, significantly more items could be presented during effective hemispheric inactivation in the methohexital group. Moreover, significant correlations of Wada memory scores with standard neuropsychological memory test scores could be found in the methohexital group., Significance: Our findings confirm that methohexital is not only equally suitable for Wada testing but has several advantages over amobarbital. Wada testing can be performed more efficiently and under more constant hemispheric inactivation using methohexital. Furthermore, the adequacy of language and memory testing during the Wada test might be affected by the anesthetic agent used., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Since its introduction, functional transcranial Doppler sonography (fTCD) has been extensively applied in research and clinical settings and has now become part of the routine presurgical work-up of patients with epilepsy. Because of its importance in planning neurosurgical interventions and predicting possible cognitive risks, the reproducibility of fTCD in determining hemispheric language lateralization (HLL) has to be ensured. In the present study, fTCD was performed twice in 33 initially lateralized patients with temporal lobe epilepsy (TLE) as part of their presurgical work-up, using a standard word generation paradigm. Initially, the standard analysis, including only the statistical examination of fTCD data, was applied, and a rather poor retest reliability of r = 0.41 was obtained (p = 0.017). Because of doubts concerning appropriate task performance in some patients, subsequently, a two-step data analysis was introduced, including an additional qualitative evaluation of fTCD data regarding (1) instruction-compliant task performance, (2) sufficient quality of the baseline phase, and (3) adequate increase in cerebral blood flow velocity (CBFV) during the activation phase. Attributable to a more valid interpretation of fTCD data after the application of the qualitative step, the reproducibility of HLL significantly improved (p = 0.007) to a high retest reliability of r = 0.84 (p < 0.000). In clinical settings, psychological and situational factors seem to strongly influence the reproducibility of fTCD determining HLL. Accordingly, we highly recommend the complementation of the standard statistical examination of fTCD data by an additional qualitative evaluation (two-step data analysis), as this extra security is particularly desirable because of its direct implications for the further evaluation of neurosurgical interventions. This article is part of the Special Issue "Individualized Epilepsy Management: Medicines, Surgery and Beyond"., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Objective: Juvenile myoclonic epilepsy (JME) is the most common idiopathic generalized epilepsy syndrome. Neuropsychological, electrophysiological, and neuroimaging studies have led to the hypothesis that JME is related to dysfunction of frontal brain regions and mainly frontal thalamocortical networks., Methods: We investigated possible microstructural white matter abnormalities of 20 patients with JME as compared with 20 healthy control subjects using diffusion tensor imaging (DTI). We analyzed whole-head DTI scans without an a-priori hypothesis using Tract-Based Spatial Statistics (TBSS). To analyze associated gray matter changes, we applied voxel-based morphometry (VBM) to a 3D T1 magnetization prepared rapid gradient echo (MPRAGE) sequence. Neuropsychological testing and personality trait tests were performed to bridge the gap between structure and function., Results: In patients, DTI revealed microstructural white matter changes in anterior parts of the Corpus callosum, anterior parts of the cingulate gyrus, and widespread frontal white matter bilaterally as well as in anterior parts of the right thalamus, which were not accompanied by gray matter changes in VBM. Microstructural changes in the cingulum correlated with personality traits. Neuropsychological test results showed impaired attention and executive functions and reduced short-term memory in the patient group. Also, there was a tendency toward alexithymia and significantly higher scores on depression., Significance: The present study results showed neuropsychological deficits including frontal lobe cognitive performance and a tendency toward alexithymia as well as accompanying microstructural neuroimaging changes in patients with JME, which all point to alterations in frontal brain regions and frontal thalamocortical networks in these patients., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Despite the availability of more than 15 new "antiepileptic drugs", the proportion of patients with pharmacoresistant epilepsy has remained constant at about 20-30%. Furthermore, no disease-modifying treatments shown to prevent the development of epilepsy following an initial precipitating brain injury or to reverse established epilepsy have been identified to date. This is likely in part due to the polyetiologic nature of epilepsy, which in turn requires personalized medicine approaches. Recent advances in imaging, pathology, genetics and epigenetics have led to new pathophysiological concepts and the identification of monogenic causes of epilepsy. In the context of these advances, the First International Symposium on Personalized Translational Epilepsy Research (1st ISymPTER) was held in Frankfurt on September 8, 2016, to discuss novel approaches and future perspectives for personalized translational research. These included new developments and ideas in a range of experimental and clinical areas such as deep phenotyping, quantitative brain imaging, EEG/MEG-based analysis of network dysfunction, tissue-based translational studies, innate immunity mechanisms, microRNA as treatment targets, functional characterization of genetic variants in human cell models and rodent organotypic slice cultures, personalized treatment approaches for monogenic epilepsies, blood-brain barrier dysfunction, therapeutic focal tissue modification, computational modeling for target and biomarker identification, and cost analysis in (monogenic) disease and its treatment. This report on the meeting proceedings is aimed at stimulating much needed investments of time and resources in personalized translational epilepsy research. Part I includes the clinical phenotyping and diagnostic methods, EEG network-analysis, biomarkers, and personalized treatment approaches. In Part II, experimental and translational approaches will be discussed (Bauer et al., 2017) [1]., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Despite the availability of more than 15 new "antiepileptic drugs", the proportion of patients with pharmacoresistant epilepsy has remained constant at about 20-30%. Furthermore, no disease-modifying treatments shown to prevent the development of epilepsy following an initial precipitating brain injury or to reverse established epilepsy have been identified to date. This is likely in part due to the polyetiologic nature of epilepsy, which in turn requires personalized medicine approaches. Recent advances in imaging, pathology, genetics, and epigenetics have led to new pathophysiological concepts and the identification of monogenic causes of epilepsy. In the context of these advances, the First International Symposium on Personalized Translational Epilepsy Research (1st ISymPTER) was held in Frankfurt on September 8, 2016, to discuss novel approaches and future perspectives for personalized translational research. These included new developments and ideas in a range of experimental and clinical areas such as deep phenotyping, quantitative brain imaging, EEG/MEG-based analysis of network dysfunction, tissue-based translational studies, innate immunity mechanisms, microRNA as treatment targets, functional characterization of genetic variants in human cell models and rodent organotypic slice cultures, personalized treatment approaches for monogenic epilepsies, blood-brain barrier dysfunction, therapeutic focal tissue modification, computational modeling for target and biomarker identification, and cost analysis in (monogenic) disease and its treatment. This report on the meeting proceedings is aimed at stimulating much needed investments of time and resources in personalized translational epilepsy research. This Part II includes the experimental and translational approaches and a discussion of the future perspectives, while the diagnostic methods, EEG network analysis, biomarkers, and personalized treatment approaches were addressed in Part I [1]., (Copyright © 2017. Published by Elsevier Inc.)

Memory for public events (PEs) was assessed as a marker of remote declarative memory in 36 patients with temporal lobe epilepsy (TLE) and compared with that of 19 patients with extra-TLE (ETLE), 17 patients with idiopathic generalized epilepsy (IGE), and 23 healthy volunteers. Verbal IQ, inventory-based evidence of depression, handedness, onset of illness, disease duration, and medication were obtained. Memory for PEs was reduced in all patient groups (TLE, P<0.0001; ETLE, P=0.009; IGE, P=0.008). The TLE group showed reduced memory for PEs compared with the other patients with epilepsy (P=0.001). A time gradient was observed, with worse memory for PEs of the 1990 s and for PEs that occurred after onset of illness. Our data support the key role of the temporal lobe in remote declarative memory. With patients with TLE remembering fewer PEs from the period after onset of epilepsy, the deficits can be partly attributed to unsuccessful consolidation rather than retrieval difficulties alone., ((c) 2009 Elsevier Inc. All rights reserved.)