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Post-Traumatic Epilepsy

Jennifer A Kim, Emily Boyle, Alexander C Wu, Andrew J Cole, Kevin J Staley, Sahar Zafar, Sydney S Cash, M Brandon Westover
We hypothesize that epileptiform abnormalities (EA) in the electroencephalopgram (EEG) during the acute period following traumatic brain injury (TBI) independently predict first-year post-traumatic epilepsy (PTE1 ). We analyzed PTE1 risk factors in two cohorts matched for TBI severity and age (n=50). EA independently predict risk for PTE1 (OR 3.16[0.99 11.68]); subdural hematoma is another independent risk factor (OR 4.13 [1.18 39.33]). Differences in EA rates are apparent within 5 days following TBI. Our results suggest increased EA prevalence identifies patients at increased risk for PTE1 , and that EA acutely post-TBI can identify patients most likely to benefit from anti-epileptogenesis drug trials...
March 14, 2018: Annals of Neurology
Seon-Ah Chong, Silvia Balosso, Catherine Vandenplas, Gregory Szczesny, Etienne Hanon, Kasper Claes, Xavier Van Damme, Bénédicte Danis, Jonathan Van Eyll, Christian Wolff, Annamaria Vezzani, Rafal M Kaminski, Isabelle Niespodziany
Understanding the mechanisms of epileptogenesis is essential to develop novel drugs that could prevent or modify the disease. Neuroinflammation has been proposed as a promising target for therapeutic interventions to inhibit the epileptogenic process that evolves from traumatic brain injury. However, it remains unclear whether cytokine-related pathways, particularly TNFα signaling, have a critical role in the development of epilepsy. In this study, we investigated the role of innate inflammation in an in vitro model of post-traumatic epileptogenesis...
February 20, 2018: Neurotherapeutics: the Journal of the American Society for Experimental NeuroTherapeutics
Feng Gu, Isabel Parada, Tao Yang, Frank M Longo, David A Prince
Post-traumatic epilepsy is one of the most common and difficult to treat forms of acquired epilepsy worldwide. Currently, there is no effective way to prevent post-traumatic epileptogenesis. It is known that abnormalities of interneurons, particularly parvalbumin-containing interneurons, play a critical role in epileptogenesis following traumatic brain injury. Thus, enhancing the function of existing parvalbumin interneurons might provide a logical therapeutic approach to prevention of post-traumatic epilepsy...
February 2, 2018: Neurobiology of Disease
Mirjam Brackhan, Pablo Bascuñana, Tobias L Ross, Frank M Bengel, Jens P Bankstahl, Marion Bankstahl
OBJECTIVE: Accumulating evidence suggests that brain inflammation, elicited by epileptogenic insults, is involved in epilepsy development. Noninvasive nuclear imaging of brain inflammation in animal models of epileptogenesis represents a diagnostic in vivo approach with potential for direct translation into the clinic. Here, we investigated up-regulation of the translocator protein (TSPO) indicative of microglial activation by serial [18 F]GE180 positron emission tomographic (PET) imaging in a mouse model of temporal lobe epilepsy...
March 2018: Epilepsia
G Ntsambi-Eba, A Beltchika Kalubye, J P Kalala Okito
Surgery is a treatment to consider in epilepsy when the condition is refractory or epileptic events are related to a clearly identified brain abnormality. The tropical climate of the DRC explains the high risk of epilepsy and the potentially large number of refractory cases. The number of patients with epilepsy in Kinshasa is estimated to be at least 120 000, and almost one third may be refractory. Hence, the need to integrate the use of surgery in the treatment of this disease. Most neurosurgical techniques used for treating epilepsy are practiced with a neurosurgical microscope and neuronavigation...
November 1, 2017: Médecine et Santé Tropicales
X Y Tai, B Bernhardt, M Thom, P Thompson, S Baxendale, M Koepp, N Bernasconi
Cognitive decline is increasingly described as a co-morbidity of temporal lobe epilepsy (TLE). Mechanisms underlying cognitive impairment are not fully understood despite examining clinical factors, such as seizure frequency, and cellular mechanisms of excitotoxicity. We review the neuropsychometry evidence for progressive cognitive decline and examine the pathology and neuroimaging evidence supporting a neurodegenerative process in hippocampal sclerosis (HS)-related TLE. Accelerated cognitive decline is described in groups of adult HS-related TLE patients...
December 30, 2017: Neuropathology and Applied Neurobiology
Nicholas O Kuhl, Aaron M Yengo-Kahn, Hannah Burnette, Gary S Solomon, Scott L Zuckerman
OBJECTIVES: The incidence of sport-related concussion (SRC) continues to rise. Presentations of concussed athletes vary from subtle symptoms to notable signs. Between the 4th and 5th iterations of the Concussion in Sport Group (CISG) guidelines, concussive convulsions were removed as a modifying factor, but little evidence or discussion supported this change. While considerable research exists regarding post-traumatic epilepsy in moderate to severe traumatic brain injury, convulsions following SRC are relatively understudied...
February 2018: Physician and Sportsmedicine
Pavel Klein, Raymond Dingledine, Eleonora Aronica, Christophe Bernard, Ingmar Blümcke, Detlev Boison, Martin J Brodie, Amy R Brooks-Kayal, Jerome Engel, Patrick A Forcelli, Lawrence J Hirsch, Rafal M Kaminski, Henrik Klitgaard, Katja Kobow, Daniel H Lowenstein, Phillip L Pearl, Asla Pitkänen, Noora Puhakka, Michael A Rogawski, Dieter Schmidt, Matti Sillanpää, Robert S Sloviter, Christian Steinhäuser, Annamaria Vezzani, Matthew C Walker, Wolfgang Löscher
The most common forms of acquired epilepsies arise following acute brain insults such as traumatic brain injury, stroke, or central nervous system infections. Treatment is effective for only 60%-70% of patients and remains symptomatic despite decades of effort to develop epilepsy prevention therapies. Recent preclinical efforts are focused on likely primary drivers of epileptogenesis, namely inflammation, neuron loss, plasticity, and circuit reorganization. This review suggests a path to identify neuronal and molecular targets for clinical testing of specific hypotheses about epileptogenesis and its prevention or modification...
December 15, 2017: Epilepsia
Christopher D Wilson, Josh D Burks, Richard B Rodgers, Robert M Evans, Adewale A Bakare, Sam Safavi-Abbasi
BACKGROUND: Moderate to severe traumatic brain injury confers increased risk of posttraumatic seizures (PTSs). Early PTSs are diagnosed when seizures develop within 7 days after injury, whereas seizures diagnosed as late PTSs occur later. Patients have been treated with phenytoin (PHT) to prevent early PTSs and more recently with levetiracetam (LEV). Various regimens have been tried in patients to prevent late PTSs with variable success. We assessed and compared effectiveness of these drugs on early and late PTS prevention...
February 2018: World Neurosurgery
Arko Sen, Katherine Gurdziel, Jenney Liu, Wen Qu, Oluwademi O Nuga, Rayanne B Burl, Maik Hüttemann, Roger Pique-Regi, Douglas M Ruden
Traumatic brain injury (TBI) can cause persistent pathological alteration of neurons. This may lead to cognitive dysfunction, depression and increased susceptibility to life threatening diseases, such as epilepsy and Alzheimer's disease. To investigate the underlying genetic and molecular basis of TBI, we subjected w 1118 Drosophila melanogaster to mild closed head trauma and found that mitochondrial activity is reduced in the brains of these flies 24 h after inflicting trauma. To determine the transcriptomic changes after mild TBI, we collected fly heads 24 h after inflicting trauma, and performed RNA-seq analyses...
2017: Frontiers in Genetics
Simone Bittencourt, Enéas Ferrazoli, Maria Fernanda Valente, Simone Romariz, Nilma R L L Janisset, Carlos Eduardo Macedo, Bruno de Brito Antonio, Vanessa Barros, Mayara Mundim, Marimélia Porcionatto, Mayra Consuelo Aarão, Maísa Ferreira Miranda, Antônio Márcio Rodrigues, Antônio-Carlos Guimarães de Almeida, Beatriz M Longo, Luiz E Mello
Brain injuries are often associated with the later development of epilepsy. Evidence suggests that morphological and functional changes occur in the remaining neural tissue during a silent (or latent) period in which no seizures are expressed. It is believed that this silent (reorganization) period may provide a therapeutic window for modifying the natural history of disease progression. Here we provide evidence that biperiden, a muscarinic anticholinergic agent, is able to alter disease progression in an animal model of epilepsy...
October 29, 2017: Epilepsy Research
Kenneth R Kaufman, Melissa Coluccio, Kartik Sivaraaman, Miriam Campeas
BACKGROUND: Optimal anti-epileptic drug (AED) treatment maximises therapeutic response and minimises adverse effects (AEs). Key to therapeutic AED treatment is adherence. Non-adherence is often related to severity of AEs. Frequently, patients do not spontaneously report, and clinicians do not specifically query, critical AEs that lead to non-adherence, including sexual dysfunction. Sexual dysfunction prevalence in patients with epilepsy ranges from 40 to 70%, often related to AEDs, epilepsy or mood states...
September 2017: BJPsych Open
D K Takahashi, Sha Jin, D A Prince
Neocortical injury initiates a cascade of events, some of which result in maladaptive epileptogenic reorganization of surviving neural circuits. Research focused on molecular and organizational changes that occur following trauma may reveal processes that underlie human post-traumatic epilepsy (PTE), a common and unfortunate consequence of traumatic brain injury. The latency between injury and development of PTE provides an opportunity for prophylactic intervention, once the key underlying mechanisms are understood...
June 26, 2017: Cerebral Cortex
Maeike Zijlmans, Jolien S van Campen, Al de Weerd
No abstract text is available yet for this article.
September 18, 2017: Seizure: the Journal of the British Epilepsy Association
Lindsay Wilson, William Stewart, Kristen Dams-O'Connor, Ramon Diaz-Arrastia, Lindsay Horton, David K Menon, Suzanne Polinder
Traumatic brain injury (TBI) can have lifelong and dynamic effects on health and wellbeing. Research on the long-term consequences emphasises that, for many patients, TBI should be conceptualised as a chronic health condition. Evidence suggests that functional outcomes after TBI can show improvement or deterioration up to two decades after injury, and rates of all-cause mortality remain elevated for many years. Furthermore, TBI represents a risk factor for a variety of neurological illnesses, including epilepsy, stroke, and neurodegenerative disease...
October 2017: Lancet Neurology
Wei Chen, Ming-De Li, Gui-Fang Wang, Xia-Feng Yang, Lin Liu, Fan-Gang Meng
BACKGROUND: To explore the incidence and risk factors, including type of seizures for post-traumatic epilepsy (PTE) after severe traumatic brain injury (TBI). SUBJECTS AND METHODS: This was a retrospective follow-up study of patients discharged from Liaocheng People's Hospital between March 2011 and June 2015 with a diagnosis of post-traumatic seizures. Risk factors for PTE were evaluated in 68 inpatients by using Kaplan-Meier curves and the Cox model. RESULTS: Complete clinical information was available for 68 patients...
2017: Neuropsychiatric Disease and Treatment
Ilaria Cuomo, Georgios D Kotzalidis, Sergio De Filippis
BACKGROUND AND AIM OF THE WORK: Mood disorders are often complicated by comorbidity with epilepsy. Anxiety and personality disorders may worsen prognosis and treatment outcome. Lacosamide has been recently introduced as adjunctive treatment for partial epilepsy. Its mechanism consists of selective slow inactivation of voltage-gated sodium channels, thus promoting an extended stabilisation of cell membranes. Antiepileptic drugs have been largely used since the 1950s in psychiatry as mood stabilisers due to their membrane stabilising and anti-kindling effects...
August 23, 2017: Acta Bio-medica: Atenei Parmensis
Eric J Neuberger, Bogumila Swietek, Lucas Corrubia, Anagha Prasanna, Vijayalakshmi Santhakumar
Hippocampal dentate gyrus is a focus of enhanced neurogenesis and excitability after traumatic brain injury. Increased neurogenesis has been proposed to aid repair of the injured network. Our data show that an early increase in neurogenesis after fluid percussion concussive brain injury is transient and is followed by a persistent decrease compared with age-matched controls. Post-injury changes in neurogenesis paralleled changes in neural precursor cell proliferation and resulted in a long-term decline in neurogenic capacity...
September 12, 2017: Stem Cell Reports
Soo Young Kim, Vladimir V Senatorov, Christapher S Morrissey, Kristina Lippmann, Oscar Vazquez, Dan Z Milikovsky, Feng Gu, Isabel Parada, David A Prince, Albert J Becker, Uwe Heinemann, Alon Friedman, Daniela Kaufer
Brain damage due to stroke or traumatic brain injury (TBI), both leading causes of serious long-term disability, often leads to the development of epilepsy. Patients who develop post-injury epilepsy tend to have poor functional outcomes. Emerging evidence highlights a potential role for blood-brain barrier (BBB) dysfunction in the development of post-injury epilepsy. However, common mechanisms underlying the pathological hyperexcitability are largely unknown. Here, we show that comparative transcriptome analyses predict remodeling of extracellular matrix (ECM) as a common response to different types of injuries...
August 9, 2017: Scientific Reports
Jari Nissinen, Pedro Andrade, Teemu Natunen, Mikko Hiltunen, Tarja Malm, Katja Kanninen, Joana I Soares, Olena Shatillo, Jukka Sallinen, Xavier Ekolle Ndode-Ekane, Asla Pitkänen
Treatment of TBI remains a major unmet medical need, with 2.5 million new cases of traumatic brain injury (TBI) each year in Europe and 1.5 million in the USA. This single-center proof-of-concept preclinical study tested the hypothesis that pharmacologic neurostimulation with proconvulsants, either atipamezole, a selective α2-adrenoceptor antagonist, or the cannabinoid receptor 1 antagonist SR141716A, as monotherapy would improve functional recovery after TBI. A total of 404 adult Sprague-Dawley male rats were randomized into two groups: sham-injured or lateral fluid-percussion-induced TBI...
July 12, 2017: Epilepsy Research
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