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Benjamin Albright, Roni Dhaher, Helen Wang, Roa Harb, Tih-Shih W Lee, Hitten Zaveri, Tore Eid
Loss of glutamine synthetase (GS) in hippocampal astrocytes has been implicated in the causation of human mesial temporal lobe epilepsy (MTLE).However, the mechanism by which the deficiency in GS leads to epilepsy is incompletely understood. Here we ask how hippocampal GS inhibition affects seizure phenotype and neuronal activation during epilepsy development (epileptogenesis). Epileptogenesis was induced by infusing the irreversible GS blocker methionine sulfoximine (MSO) unilaterally into the hippocampal formation of rats...
October 18, 2016: Experimental Neurology
Guy Bar-Klein, Rebecca Klee, Claudia Brandt, Marion Bankstahl, Pablo Bascuñana, Kathrin Töllner, Hotjensa Dalipaj, Jens P Bankstahl, Alon Friedman, Wolfgang Löscher
OBJECTIVE: Acquired epilepsy is a devastating long-term risk of various brain insults, including trauma, stroke, infections, and status epilepticus (SE). There is no preventive treatment for patients at risk. Due to the complex alterations involved in epileptogenesis, it is likely that multi-targeted approaches are required for epilepsy prevention. We report novel preclinical findings with isoflurane, which exerts various non-anesthetic effects that may be relevant for anti-epileptogenesis...
October 19, 2016: Annals of Neurology
Anna Serafini, Naoum Issa, Sandra Rose, Shasha Wu, Peter Warnke, James X Tao
Electrophysiological studies have suggested that temporal intermittent rhythmic delta activity (TIRDA) has a localizing value similar to interictal spikes in patients with temporal lobe epilepsy, and is associated with a favorable outcome after temporal lobectomyHowever, it remains controversial whether TIRDA is an EEG marker for mesial or lateral temporal epileptogenesis. We simultaneously recorded scalp EEG and stereoencephalography (SEEG) in a patient with mesial temporal lobe epilepsy (mTLE) during epilepsy pre-surgical evaluation...
June 13, 2016: Journal of Clinical Neurophysiology: Official Publication of the American Electroencephalographic Society
Theresa Scholl, Angelika Mühlebner, Gerda Ricken, Victoria Gruber, Anna Fabing, Sharon Samueli, Gudrun Gröppel, Christian Dorfer, Thomas Czech, Johannes A Hainfellner, Avanita S Prabowo, Roy J Reinten, Lisette Hoogendijk, Jasper J Anink, Eleonora Aronica, Martha Feucht
Conventional antiepileptic drugs suppress the excessive firing of neurons during seizures. In drug-resistant patients, treatment failure indicates an alternative important epileptogenic trigger. Two epilepsy-associated pathologies show myelin deficiencies in seizure-related brain regions: Focal Cortical Dysplasia IIB (FCD) and cortical tubers in Tuberous Sclerosis Complex (TSC). Studies uncovering white matter-pathology mechanisms are therefore urgently needed to gain more insight into epileptogenesis, the propensity to maintain seizures, and their associated comorbidities such as cognitive defects...
October 17, 2016: Brain Pathology
Awanish Mishra, Rajesh Kumar Goel
Our previous studies have suggested a strong involvement of serotonergic innervations in epileptogenesis and associated memory impairment. Several studies have suggested that the modulation of 5-HT3 receptors could serve as a promising tool for the management of epilepsy and memory deficit. The present study was envisaged to confirm this hypothesis. In this study, kindling was induced in male Swiss Albino mice by using a subconvulsive dose of pentylenetetrazole (PTZ) (35 mg/kg at 48±2 h). Once the animals were kindled, they were treated with a vehicle, ondansetron (0...
October 13, 2016: Neuroscience
Massimo Rizzi, Itai Weissberg, Dan Z Milikovsky, Alon Friedman
No abstract text is available yet for this article.
October 14, 2016: Scientific Reports
Kenneth I Strauss, Kost V Elisevich
BACKGROUND: Epilepsy patients have distinct immune/inflammatory cell profiles and inflammatory mediator levels in the blood. Although the neural origin of inflammatory cells and mediators has been implied, few studies have measured these inflammatory components in the human brain itself. This study examines the brain levels of chemokines (8), cytokines (14), and vascular injury mediators (3) suspected of being altered in epilepsy. METHODS: Soluble protein extracts of fresh frozen resected hippocampus, entorhinal cortex, and temporal cortex from 58 medically refractory mesial temporal lobe epilepsy subjects and 4 nonepileptic neurosurgical subjects were assayed for 25 inflammation-related mediators using ultrasensitive low-density arrays...
October 13, 2016: Journal of Neuroinflammation
Kayam Chak, Biswajoy Roy-Chaudhuri, Hak Kyun Kim, Kayla C Kemp, Brenda E Porter, Mark A Kay
MicroRNA-21 (miR-21) is consistently up-regulated in various neurological disorders, including epilepsy. Here, we show that the biogenesis of miR-21 is altered following pilocarpine status epilepticus (SE) with an increase in precursor miR-21 (pre-miR-21) in rats. We demonstrate that pre-miR-21 has an energetically favorable site overlapping with the miR-21 binding site and competes with mature miR-21 for binding in the 3'UTR of TGFBR2 mRNA, but not NT-3 mRNA in vitro. This binding competition influences miR-21-mediated repression in vitro and correlates with the increase in TGFBR2 and decrease in NT-3 following SE...
October 7, 2016: Experimental Neurology
Dariusz Andrzejczak, Agata Woldan-Tambor, Katarzyna Bednarska, Jolanta B Zawilska
A growing body of evidence suggests that inflammatory processes and activation of glial cells could contribute to seizures and epileptogenesis. In various animal studies on epilepsy, proinflammatory cytokines have been demonstrated to exert a proconvulsive activity. On the other hand, it is suggested that antiepileptic drugs could modulate immune system activity. The aim of the present study was to investigate whether topiramate, a new generation antiepileptic drug with a complex mechanism of action, could affect the lipopolysaccharide (LPS)-induced release of TNF-α, IL-1β and IL-6 from primary rat microglial cell cultures...
September 28, 2016: Epilepsy Research
H Yu, G L Qi, J Wang, L Chen, Z Deng, Y S Zhao, S S Lei, X Q Zhu
Epilepsy refers to a clinical syndrome generated by spontaneous seizures in the central nervous system. Epilepsy triggers a complex pathological process including inflammatory response and aquaporin 4 (AQP4) increase. It has been reported that AQP4 helps to enhance the immunological function of the central nervous system in pathological conditions, but the relationship between AQP4 and inflammatory cytokines is poorly understood in chronic epilepsy processes. As an inhibitor of sulfonamide carbonic anhydrase (CA), acetazolamide (AZA) may inhibit water infiltration through AQP4...
September 23, 2016: Genetics and Molecular Research: GMR
Mykaella Andrade de Araújo, Thalita Ewellyn Batista Sales Marques, Shirley Octacílio-Silva, Carmem Lúcia de Arroxelas-Silva, Marília Gabriella Alves Goulart Pereira, José Eduardo Peixoto-Santos, Ludmyla Kandratavicius, João Pereira Leite, Norberto Garcia-Cairasco, Olagide Wagner Castro, Marcelo Duzzioni, Geraldo Aleixo Passos, Maria Luisa Paçó-Larson, Daniel Leite Góes Gitaí
The involvement of miRNA in mesial temporal lobe epilepsy (MTLE) pathogenesis has increasingly become a focus of epigenetic studies. Despite advances, the number of known miRNAs with a consistent expression response during epileptogenesis is still small. Addressing this situation requires additional miRNA profiling studies coupled to detailed individual expression analyses. Here, we perform a miRNA microarray analysis of the hippocampus of Wistar rats 24 hours after intra-hippocampal pilocarpine-induced Status Epilepticus (H-PILO SE)...
2016: PloS One
Manveen Bhardwaj, Anil Kumar
BACKGROUND: Neuroinflammation, oxidative stress and mitochondrial dysfunction play a significant role to explain the pathophysiology of epilepsy. Neuroinflammation through microglia activation has been documented in epileptogenesis. Compounds which inhibit activation of glial cells have been suggested as one of the treatment approaches for the effective treatment of epilepsy. The present study has been designed to investigate the role of coenzyme Q10 and its interaction with minocycline (microglia inhibitor) against pentylenetetrazol induced kindling epilepsy...
July 22, 2016: Pharmacological Reports: PR
Kouichi Itoh, Yasuhiro Ishihara, Rie Komori, Hiromi Nochi, Ruri Taniguchi, Yoichi Chiba, Masaki Ueno, Fuyuko Takata-Tsuji, Shinya Dohgu, Yasufumi Kataoka
Our previous study showed that treatment with levetiracetam (LEV) after status epilepticus (SE) termination by diazepam might prevent the development of spontaneous recurrent seizures via the inhibition of neurotoxicity induced by brain edema events. In the present study, we determined the possible molecular and cellular mechanisms of LEV treatment after termination of SE. To assess the effect of LEV against the brain alterations after SE, we focused on blood-brain barrier (BBB) dysfunction associated with angiogenesis and brain inflammation...
September 27, 2016: Brain Research
Feyza Alyu, Miriş Dikmen
OBJECTIVE: Epilepsy is a chronic neurological disease characterised with seizures. The aetiology of the most generalised epilepsies cannot be explicitly determined and the seizures are pronounced to be genetically determined by disturbances of receptors in central nervous system. Besides, neurotransmitter distributions or other metabolic problems are supposed to involve in epileptogenesis. Lack of adequate data about pharmacological agents that have antiepileptogenic effects point to need of research on this field...
October 3, 2016: Acta Neuropsychiatrica
Emilio Russo, Rita Citraro, Andrew Constanti, Antonio Leo, Annika Lüttjohann, Gilles van Luijtelaar, Giovambattista De Sarro
The WAG/Rij rat model has recently gathered attention as a suitable animal model of absence epileptogenesis. This latter term has a broad definition encompassing any possible cause that determines the development of spontaneous seizures; however, most of, if not all, preclinical knowledge on epileptogenesis is confined to the study of post-brain insult models such as traumatic brain injury or post-status epilepticus models. WAG/Rij rats, but also synapsin 2 knockout, Kv7 current-deficient mice represent the first examples of genetic models where an efficacious antiepileptogenic treatment (ethosuximide) was started before seizure onset...
September 26, 2016: Neuroscience and Biobehavioral Reviews
Ling-Lin Chen, Mei-Ling Wu, Feng Zhu, Jie-Jing Kai, Jing-Yin Dong, Xi-Mei Wu, Ling-Hui Zeng
AIMS: Previous study suggests that mTOR signaling pathway may play an important role in epileptogenesis. The present work was designed to explore the contribution of raptor protein to the development of epilepsy and comorbidities. METHODS: Mice with conditional knockout of raptor protein were generated by cross-bred Rptor(flox/flox) mice with nestin-CRE mice. The expression of raptor protein was analyzed by Western blotting in brain tissue samples. Neuronal death and mossy fiber sprouting were detected by FJB staining and Timm staining, respectively...
September 28, 2016: CNS Neuroscience & Therapeutics
S Tang, E Hughes, K Lascelles, M A Simpson, D K Pal
We report a de novo SMARCA2 missense mutation discovered on exome sequencing in a patient with myoclonic astatic epilepsy, leading to reassessment and identification of Nicolaides-Baraitser syndrome. This de novo SMARCA2 missense mutation c.3721C>G, p.Gln1241Glu is the only reported mutation on exon 26 outside the ATPase domain of SMARCA2 to be associated with Nicolaides-Baraitser syndrome and adds to chromatin remodeling as a pathway for epileptogenesis. © 2016 The Authors. American Journal of Medical Genetics Part A published by Wiley Periodicals, Inc...
September 26, 2016: American Journal of Medical Genetics. Part A
Joanna Bednarczyk, Konrad J Dębski, Anna M Bot, Katarzyna Lukasiuk
The aim of the present study was to examine involvement of MBD3 (methyl-CpG-binding domain protein 3), a protein involved in reading DNA methylation patterns, in epileptogenesis and epilepsy. We used a well-characterized rat model of temporal lobe epilepsy that is triggered by status epilepticus, evoked by electrical stimulation of the amygdala. Stimulated and sham-operated animals were sacrificed 14 days after stimulation. We found that MBD3 transcript was present in neurons, oligodendrocytes, and astrocytes in both control and epileptic animals...
2016: Scientific Reports
Lia Tsverava, Tamar Lordkipanidze, Eka Lepsveridze, Maia Nozadze, Marina Kikvidze, Revaz Solomonia
Identification of compounds preventing or modifying the biochemical changes that underlie the epileptogenesis process and understanding the mechanism of their action are of great importance. We have previously shown that myoinositol (MI) daily treatment for 28 days prevents certain biochemical changes that are triggered by kainic acid (KA) induced status epilepticus (SE). However in these studies we have not detected any effects of MI on the first day after SE. In the present study we broadened our research and focused on other molecular and morphological changes at the early stages of SE induced by KA and effects of MI treatment on these changes...
2016: BioMed Research International
Martin J Brodie
The outpatient services at the Epilepsy Unit in the Western Infirmary, Glasgow, Scotland was set up in September 1982. From the outset patient data were collected prospectively. A focused approach to patients with newly diagnosed epilepsy was developed and a series of 4 analyses have been undertaken over the intervening years, with results from the latest still being written up for publication. A total of 16 published papers have described patient outcomes over the years, focusing on response to different drug schedules...
September 3, 2016: Seizure: the Journal of the British Epilepsy Association
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