Добірка наукової літератури з теми "Posttraumatic epilepsy"
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Статті в журналах з теми "Posttraumatic epilepsy"
Willmore, L. James. "Posttraumatic Epilepsy." Neurologic Clinics 10, no. 4 (November 1992): 869–78. http://dx.doi.org/10.1016/s0733-8619(18)30184-1.
Повний текст джерелаKharatishvili, Irina, and Asla Pitkänen. "Posttraumatic epilepsy." Current Opinion in Neurology 23, no. 2 (April 2010): 183–88. http://dx.doi.org/10.1097/wco.0b013e32833749e4.
Повний текст джерелаRinaldi, A., and L. Conti. "Posttraumatic epilepsy." Neurological Sciences 24, no. 4 (November 1, 2003): 229–30. http://dx.doi.org/10.1007/s10072-003-0144-9.
Повний текст джерелаMazarati, Andrey. "Is Posttraumatic Epilepsy the Best Model of Posttraumatic Epilepsy?" Epilepsy Currents 6, no. 6 (November 2006): 213–14. http://dx.doi.org/10.1111/j.1535-7511.2006.00149.x.
Повний текст джерелаKennedy, Colin R., and John M. Freeman. "Posttraumatic seizures and posttraumatic epilepsy in children." Journal of Head Trauma Rehabilitation 1, no. 4 (December 1986): 66–73. http://dx.doi.org/10.1097/00001199-198612000-00012.
Повний текст джерелаChen, James W. Y., Robert L. Ruff, Roland Eavey, and Claude G. Wasterlain. "Posttraumatic epilepsy and treatment." Journal of Rehabilitation Research and Development 46, no. 6 (2009): 685. http://dx.doi.org/10.1682/jrrd.2008.09.0130.
Повний текст джерелаSandyk, R., and C. R. Bamford. "Baclofen Responsive Posttraumatic Epilepsy." International Journal of Neuroscience 37, no. 3-4 (January 1987): 183–85. http://dx.doi.org/10.3109/00207458708987146.
Повний текст джерелаHeikkinen, E. R., H. S. Rönty, U. Tolonen, and J. Pyhtinen. "Development of Posttraumatic Epilepsy." Stereotactic and Functional Neurosurgery 54, no. 1-8 (1990): 25–33. http://dx.doi.org/10.1159/000100186.
Повний текст джерелаBrissos, Sofia, Vasco Videira Dias, and Teresa Paiva. "Posttraumatic Parieto-Occipital Epilepsy." Journal of Neuropsychiatry and Clinical Neurosciences 19, no. 2 (April 2007): 200–201. http://dx.doi.org/10.1176/jnp.2007.19.2.200.
Повний текст джерелаSchubert-Bast, S. "Posttraumatic Epilepsy: An Update." Neuropediatrics 48, S 01 (April 26, 2017): S1—S45. http://dx.doi.org/10.1055/s-0037-1602881.
Повний текст джерелаДисертації з теми "Posttraumatic epilepsy"
Avramescu, Sinziana. "Cellular and homeostatic network mechanisms of posttraumatic epilepsy." Thesis, Université Laval, 2008. http://www.theses.ulaval.ca/2008/25580/25580.pdf.
Повний текст джерелаAfter penetrating cortical wounds, the brain becomes gradually hyperexcitable and generates spontaneous paroxysmal activity, but the progressive mechanisms of epileptogenesis remain virtually unknown. The guiding line of our experiments was the hypothesis that the reduced cortical activity following deafferentation triggers homeostatic mechanisms acting at cellular and network levels, leading to an increased neuronal excitability and finally generating paroxysmal activities. We tested this hypothesis either in anesthetized adult cats, or during natural sleep and wake, using the model of partially deafferented suprasylvian gyrus to induce posttraumatic epileptogenesis. We evaluated the effects of acute and chronic cortical deafferentation on the survival of neurons and glial cells and how long-term input deprivation could shape up the properties of neuronal networks and the initiation of spontaneous cortical activity. Following cortical deafferentation of the suprasylvian gyrus, the deeply laying neurons, particularly the inhibitory GABAergic ones, degenerate progressively in parallel with an increased propensity to paroxysmal activity, mainly during slow-wave sleep. The chronic input deprivation and the death of neurons activate homeostatic plasticity mechanisms, which promote a gradual increased neuronal connectivity, higher efficacy of excitatory synaptic connections and changes in intrinsic cellular properties favoring increased excitation. The spontaneous cortical activity quantified by means of firing rate augments also progressively, particularly during slow-wave sleep, characterized by periods of silent states alternating with periods of active states, which supports furthermore our hypothesis regarding the involvement of homeostatic plasticity mechanisms. The degeneration of neurons in the deep cortical layers generates important changes in the laminar distribution of neuronal activity, which is shifted from the deeper layers to the more superficial ones, in the partially deafferented part of the gyrus. This change in the depth profile distribution of firing rates modifies also the initiation of spontaneous cortical activity which, in normal cortex, and in the relatively intact part of the deafferented gyrus, is initiated in the deep cortical layers. Conversely, in late stages of the undercut, both the cortical slow oscillation and the ictal activity are initiated in the more superficial layers and then spread to the deeper ones. Cortical trauma induces also an important reactive gliosis associated with an impaired function of glial cells, responsible for a dysfunctional K+ clearance in the injured cortex, which additionally increases the excitability of neurons, promoting the generation of paroxysmal activity. We conclude, that the homeostatic plasticity mechanisms triggered by the decreased level of activity in the deafferented cortex, generate an uncontrollable cortical hyperexcitability, finally leading to seizures. If this statement is true, augmenting cortical activity rapidly after cortical trauma rather than decreasing it with antiepileptic medication, could prove beneficial in preventing the development of posttraumatic epileptogenesis.
Inscrite au Tableau d'honneur de la Faculté des études supérieures
Hunt, Robert F. III. "LOCAL SYNAPTIC NETWORK INTERACTIONS IN THE DENTATE GYRUS OF A CORTICAL CONTUSION MODEL OF POSTTRAUMATIC EPILEPSY." UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_diss/94.
Повний текст джерела"Cellular and homeostatic network mechanisms of posttraumatic epilepsy." Thesis, Université Laval, 2008. http://www.theses.ulaval.ca/2008/25580/25580.pdf.
Повний текст джерела吳美瑤. "Posttraumatic Growth:A Narrative Research of Women with Epilepsy." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/64967089466857364231.
Повний текст джерела國立臺灣師範大學
社會教育學系
98
Women with traumatic experiences of epilepsy are studied in the life story of recovery and of post-traumatic growth, using longitudinal life history in time sequence and horizontal approaching to the overall narratives. To integrate with the research-based self-narrative of women with epilepsy and the recall narrative of close relatives, the collected information is arranged according to the time table to render a macro epilepsy career. To record patient’s microscopic life story, using qualitative research methods in the "overall-content" approach for data processing and analysis reflects physical experience and stress adaptation. After all, we probe thoroughly into the feminine epilepsy patient and their close relatives with the process of traumatic experience to reveal the strategies of mental adaption and the reacting responses for problems in order to understand the significant change and impact after suffering epilepsy. The results showed: (A) Study of the life history makes a new interpretation of the meaning behind the traumatic events and inspiration to the researcher to re-define herself. (B) Women with epilepsy need to learn trust and share, and explore the positive values of traumatic experiences to become aware of their meaning and growth in the events. (C) "Recognition" from others and “Self-identification" possess decisive and importance meanings, and support from others can encourage the patient to have the positive attitude to generate post-traumatic growth. (D) Trauma patients can be self-identification from the traumatic experience written, and can depend on the positive personality of optimistic philosophy and self-affirmation to get cross over the trauma, resulting in self-transformation.
Wilson, Sarah Marie. "Involvement of Collapsin Response Mediator Protein 2 in Posttraumatic Sprouting in Acquired Epilepsy." Thesis, 2014. http://hdl.handle.net/1805/5604.
Повний текст джерелаPosttraumatic epilepsy, the development of temporal lobe epilepsy (TLE) following traumatic brain injury, accounts for 20% of symptomatic epilepsy. Reorganization of mossy fibers within the hippocampus is a common pathological finding of TLE. Normal mossy fibers project into the CA3 region of the hippocampus where they form synapses with pyramidal cells. During TLE, mossy fibers are observed to innervate the inner molecular layer where they synapse onto the dendrites of other dentate granule cells, leading to the formation of recurrent excitatory circuits. To date, the molecular mechanisms contributing to mossy fiber sprouting are relatively unknown. Recent focus has centered on the involvement of tropomycin-related kinase receptor B (TrkB), which culminates in glycogen synthase kinase 3β (GSK3β) inactivation. As the neurite outgrowth promoting collapsin response mediator protein 2 (CRMP2) is rendered inactive by GSK3β phosphorylation, events leading to inactivation of GSK3β should therefore increase CRMP2 activity. To determine the involvement of CRMP2 in mossy fiber sprouting, I developed a novel tool ((S)-LCM) for selectively targeting the ability of CRMP2 to enhance tubulin polymerization. Using (S)-LCM, it was demonstrated that increased neurite outgrowth following GSK3β inactivation is CRMP2 dependent. Importantly, TBI led to a decrease in GSK3β-phosphorylated CRMP2 within 24 hours which was secondary to the inactivation of GSK3β. The loss of GSK3β-phosphorylated CRMP2 was maintained even at 4 weeks post-injury, despite the transience of GSK3β-inactivation. Based on previous work, it was hypothesized that activity-dependent mechanisms may be responsible for the sustained loss of CRMP2 phosphorylation. Activity-dependent regulation of GSK3β-phosphorylated CRMP2 levels was observed that was attributed to a loss of priming by cyclin dependent kinase 5 (CDK5), which is required for subsequent phosphorylation by GSK3β. It was confirmed that the loss of GSK3β-phosphorylated CRMP2 at 4 weeks post-injury was likely due to decreased phosphorylation by CDK5. As TBI resulted in a sustained increase in CRMP2 activity, I attempted to prevent mossy fiber sprouting by targeting CRMP2 in vivo following TBI. While (S)-LCM treatment dramatically reduced mossy fiber sprouting following TBI, it did not differ significantly from vehicle-treated animals. Therefore, the necessity of CRMP2 in mossy fiber sprouting following TBI remains unknown.
Kaletová, Magdalena. "Člověk s postižením v sourozeneckých konstelacích dvojčat a trojčat." Master's thesis, 2014. http://www.nusl.cz/ntk/nusl-337045.
Повний текст джерелаКниги з теми "Posttraumatic epilepsy"
Peterson, Allison R., Devin K. Binder, and Carrie R. Jonak. Posttraumatic Epilepsy: Basic and Clinical Aspects. Elsevier Science & Technology, 2022.
Знайти повний текст джерелаЧастини книг з теми "Posttraumatic epilepsy"
Martins da Silva, A., A. Rocha Vaz, I. Ribeiro, A. R. Melo, B. Nune, and M. Correia. "Controversies in Posttraumatic Epilepsy." In Neurosurgical Aspects of Epilepsy, 48–51. Vienna: Springer Vienna, 1990. http://dx.doi.org/10.1007/978-3-7091-9104-0_9.
Повний текст джерелаShih, Jerry J. "Head Trauma and Posttraumatic Seizures." In Epilepsy Case Studies, 55–58. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-01366-4_13.
Повний текст джерелаPagni, Carlo A. "Posttraumatic Epilepsy. Incidence and Prophylaxis." In Neurosurgical Aspects of Epilepsy, 38–47. Vienna: Springer Vienna, 1990. http://dx.doi.org/10.1007/978-3-7091-9104-0_8.
Повний текст джерелаSantis, A., E. Sganzerla, D. Spagnoli, L. Bello, and F. Tiberio. "Risk Factors for Late Posttraumatic Epilepsy." In Neurotraumatology: Progress and Perspectives, 64–67. Vienna: Springer Vienna, 1992. http://dx.doi.org/10.1007/978-3-7091-9233-7_17.
Повний текст джерелаGlushakov, Alexander V., Olena Y. Glushakova, Sylvain Doré, Paul R. Carney, and Ronald L. Hayes. "Animal Models of Posttraumatic Seizures and Epilepsy." In Methods in Molecular Biology, 481–519. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3816-2_27.
Повний текст джерелаMori, A., M. Hiramatsu, and I. Yokoi. "Posttraumatic Epilepsy, Free Radicals and Antioxidant Therapy." In Free Radicals in the Brain, 109–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77609-0_9.
Повний текст джерелаSilva, A. Martins, B. Nunes, A. R. Vaz, and D. Mendonça. "Posttraumatic Epilepsy in Civilians: Clinical and Electroencephalographic Studies." In Neurotraumatology: Progress and Perspectives, 56–63. Vienna: Springer Vienna, 1992. http://dx.doi.org/10.1007/978-3-7091-9233-7_16.
Повний текст джерелаPagni, C. A., and F. Zenga. "Posttraumatic epilepsy with special emphasis on prophylaxis and prevention." In Re-Engineering of the Damaged Brain and Spinal Cord, 27–34. Vienna: Springer Vienna, 2005. http://dx.doi.org/10.1007/3-211-27577-0_3.
Повний текст джерелаDa Silva, A. Martins, and L. James Willmore. "Posttraumatic epilepsy." In Handbook of Clinical Neurology, 585–99. Elsevier, 2012. http://dx.doi.org/10.1016/b978-0-444-52899-5.00017-4.
Повний текст джерела"Posttraumatic Epilepsy." In Encyclopedia of Trauma Care, 1281. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-29613-0_101194.
Повний текст джерелаТези доповідей конференцій з теми "Posttraumatic epilepsy"
Akrami, Haleh, Andrei Irimia, Wenhui Cui, Anand Joshi, and Richard Leahy. "Prediction of posttraumatic epilepsy using machine learning." In Biomedical Applications in Molecular, Structural, and Functional Imaging, edited by Barjor S. Gimi and Andrzej Krol. SPIE, 2021. http://dx.doi.org/10.1117/12.2580953.
Повний текст джерелаSorokina, Elena Gennad’evna, Zhanna B. Semenova, Oksana V. Globa, Olga V. Karaseva, Valentin P. Reutov, Galina A. Ignatieva, Sofya A. Afanasieva, et al. "AUTOIMMUNE RESPONSE OF GLUTAMATE RECEPTORS AND NITRIC OXIDE IN EPILEPSY AND TRAUMATIC BRAIN INJURY." In International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.23.
Повний текст джерелаJugl, Sebastian, Aimalohi Okpeku, Brianna Costales, Earl Morris, Golnoosh Alipour-Harris, Juan Hincapie-Castillo, Nichole Stetten, et al. "A Mapping Literature Review of Medical Cannabis Clinical Outcomes and Quality of Evidence in Approved Conditions in the United States, from 2016 to 2019." In 2020 Virtual Scientific Meeting of the Research Society on Marijuana. Research Society on Marijuana, 2021. http://dx.doi.org/10.26828/cannabis.2021.01.000.25.
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