Posttraumatic epilepsy — Disease or comorbidity?

Pitkänen, Asla; Kemppainen, Susanna; Ndode-Ekane, Xavier Ekolle; Huusko, Noora; Huttunen, Jari T.; Gröhn, Olli; Immonen, Riikka; Sierra, Alejandra; Bolkvadze, Tamuna

doi:10.1016/j.yebeh.2014.01.013

Cited by 41 publications

(29 citation statements)

References 50 publications

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“…The second approach involves testing the ability of lead NCEs in suppressing epileptiform activity in the amygdala in an established rat model of moderate brain injury using controlled cortical impact. 50,51 Because stress and anxiety (eg, posttraumatic stress disorder) have been reported to increase the risk of posttraumatic seizures and posttraumatic epilepsy, 52 experiments in the rat controlled cortical impact model have been expanded to include acute application of a nonpainful "stressor" to rats after sufficient recovery from traumatic brain injury. Under these conditions, rats reproducibly exhibit stage 2-3 seizures characterized by electrical activity over a wide range of frequencies up to 500 Hz.…”

Section: Activity In Experimental Models Of Seizures and Epilepsymentioning

confidence: 99%

Progress report on new antiepileptic drugs: A summary of the Fourteenth Eilat Conference on New Antiepileptic Drugs and Devices (EILAT XIV). I. Drugs in preclinical and early clinical development

Bialer

Johannessen

Koepp³

et al. 2018

Epilepsia

115

103

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Summary The Fourteenth Eilat Conference on New Antiepileptic Drugs and Devices (EILAT XIV) took place in Madrid, Spain, on May 13‐16, 2018 and was attended by 168 delegates from 28 countries. The conference provided a forum for professionals involved in basic science, clinical research, regulatory affairs, and clinical care to meet and discuss the latest advances related to discovery and development of drugs and devices aimed at improving the management of people with epilepsy. This progress report provides a summary of findings on investigational compounds for which data from preclinical or early (phase I) clinical studies were presented. The compounds reviewed include adenosine and adenosine kinase inhibitors, BIS‐001 (huperzine A), 2‐deoxy‐d‐glucose, FV‐082, FV‐137, JNJ‐40411813, JNJ‐55511118 and analogs, ketone‐enhanced antiepileptic drugs, oxynytones, OV329, TAK‐935 (OV935), XEN901, and XEN1101. Many innovative approaches to drug development were presented. For example, some compounds are being combined with traditional antiepileptic drugs based on evidence of synergism in seizure models, some act as inhibitors of enzymes involved in modulation of neuronal activity, and some interact in novel ways with excitatory receptors or ion channels. Some of the compounds in development target the etiology of specific epilepsy syndromes (including orphan conditions) through precision medicine, and some offer hope of producing disease‐modifying effects rather than symptomatic seizure suppression. Overall, the results summarized in the report indicate that important advances are being made in the effort to develop compounds with potentially improved efficacy and safety profiles compared with existing agents.

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Section: Activity In Experimental Models Of Seizures and Epilepsymentioning

confidence: 99%

Progress report on new antiepileptic drugs: A summary of the Fourteenth Eilat Conference on New Antiepileptic Drugs and Devices (EILAT XIV). I. Drugs in preclinical and early clinical development

Bialer

Johannessen

Koepp³

et al. 2018

Epilepsia

115

103

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“…It is known that epilepsy or seizure activity is accompanied with enhanced aberrant hippocampal neurogenesis (Parent et al, 1997; Parent, 2008), whereas ablating this seizure –induced aberrant hippocampal neurogenesis can reduce chronic seizure frequency and normalize epilepsy-induced cognitive deficits (Cho et al, 2015). It has been speculated that TBI-induced neurogenesis may contribute to the onset of post-TBI epilepsy (Pitkanen et al, 2014). If so, further augmenting TBI-induced hippocampal neurogenesis may exacerbate this symptom.…”

Section: Enhancement Of Endogenous Neurogenesis As Potential Therapeumentioning

confidence: 99%

Endogenous neurogenic cell response in the mature mammalian brain following traumatic injury

Sun

2016

Experimental Neurology

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In the mature mammalian brain, new neurons are generated throughout life in the neurogenic regions of the subventricular zone (SVZ) and the dentate gyrus (DG) of the hippocampus. Over the past two decades, extensive studies have examined the extent of adult neurogenesis in the SVZ and DG, the role of the adult generated new neurons in normal brain function and the underlying mechanisms regulating the process of adult neurogenesis. The extent and the function of adult neurogenesis under neuropathological conditions have also been explored in varying types of disease models in animals. Increasing evidence has indicated that these endogenous neural stem/progenitor cells may play regenerative and reparative roles in response to CNS injuries or diseases. This review will discuss the potential functions of adult neurogenesis in the injured brain and will describe the recent development of strategies aimed at harnessing this neurogenic capacity in order to repopulate and repair the injured brain following trauma.

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“…Different animal models of focal epilepsy exist (220), such as the kainate- or pilocarpine-models of MTLE (228, 229, 260), posttraumatic epilepsy (261, 262), or electrical kindling (227, 263). Despite an initially focal insult, recent evidence (e.g., 242) shows that remote brain areas become affected by the pathological activity of the epileptic focus.…”

Section: What We Can Learn From Animal Modelsmentioning

confidence: 99%

Mapping Epileptic Activity: Sources or Networks for the Clinicians?

Pittau¹,

Mégevand

Sheybani

et al. 2014

Front. Neurol.

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Epileptic seizures of focal origin are classically considered to arise from a focal epileptogenic zone and then spread to other brain regions. This is a key concept for semiological electro-clinical correlations, localization of relevant structural lesions, and selection of patients for epilepsy surgery. Recent development in neuro-imaging and electro-physiology and combinations, thereof, have been validated as contributory tools for focus localization. In parallel, these techniques have revealed that widespread networks of brain regions, rather than a single epileptogenic region, are implicated in focal epileptic activity. Sophisticated multimodal imaging and analysis strategies of brain connectivity patterns have been developed to characterize the spatio-temporal relationships within these networks by combining the strength of both techniques to optimize spatial and temporal resolution with whole-brain coverage and directional connectivity. In this paper, we review the potential clinical contribution of these functional mapping techniques as well as invasive electrophysiology in human beings and animal models for characterizing network connectivity.

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Posttraumatic epilepsy — Disease or comorbidity?

Cited by 41 publications

References 50 publications

Progress report on new antiepileptic drugs: A summary of the Fourteenth Eilat Conference on New Antiepileptic Drugs and Devices (EILAT XIV). I. Drugs in preclinical and early clinical development

Progress report on new antiepileptic drugs: A summary of the Fourteenth Eilat Conference on New Antiepileptic Drugs and Devices (EILAT XIV). I. Drugs in preclinical and early clinical development

Endogenous neurogenic cell response in the mature mammalian brain following traumatic injury

Mapping Epileptic Activity: Sources or Networks for the Clinicians?

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