000			03171naaaa2200313uu 4500
001			https://directory.doabooks.org/handle/20.500.12854/54517
005			20220219194523.0
020			_a978-2-88919-382-0
020			_a9782889193820
024	7		_a10.3389/978-2-88919-382-0 _cdoi
041	0		_aEnglish
042			_adc
100	1		_aRoberto Di Maio _4auth
245	1	0	_aNeuronal mechanisms of epileptogenesis
260			_bFrontiers Media SA _c2015
300			_a1 electronic resource (223 p.)
506	0		_aOpen Access _2star _fUnrestricted online access
520			_aSeveral types of brain injuries are causes of acquired temporal lobe epilepsy (TLE). The seizure-free "latent period" that often follows the brain injury is of unknown mechanistic significance but is commonly considered as the "epileptogenic" period characterized by gradual pathogenic processes leading to the onset of clinically detectable epilepsy. Acute convulsive status epilepticus (SE) is often associated with an adverse developmental outcome characterized by learning disabilities related to the cumulative effects of seizures and development of TLE. The symptomatic manifestations of TLE appear only after a widespread irreversible damage of entorhinal cortex, and hippocampus, the brain area most affected by this disease. These pathological features of TLE reduce the possibility of successful therapeutic approaches, often rendering the disease refractory. The difficult clinical management of chronic TLE and the limited success rate of surgical approaches, increase the incapacitating nature of this specific epileptic disorder. Prevention of TLE with an appropriate intervention after a known inciting event (in the case of acquired epilepsy) might represent the most ambitious goal in the clinical treatment of this epileptic disorder, but has been largely unsuccessful to this point. Clinical trials aimed at prevention of chronic epilepsy have often produced negative, disappointing results. However, in most cases, these studies ultimately evaluated the downstream clinical manifestations, failing to monitor early, specific molecular epileptogenic events. Therefore, elucidation of the underlying mechanisms of epileptogenesis, and their time course(s) are essential. The primary purpose of this topic is to collect scientific contributions providing novel insights in the cellular and molecular mechanisms of epileptogenesis as potential targets for innovative therapeutic approaches aimed at preventing the chronic epileptic disorder.
540			_aCreative Commons _fhttps://creativecommons.org/licenses/by/4.0/ _2cc _4https://creativecommons.org/licenses/by/4.0/
546			_aEnglish
653			_aEpileptogenesis
653			_aTLE prevention
653			_aEpilepsy
653			_aHippocampal damage
653			_aNeuronal epileptic damage
653			_aTemporal Lobe Epilepsy (TLE)
856	4	0	_awww.oapen.org _uhttp://journal.frontiersin.org/researchtopic/1097/neuronal-mechanisms-of-epileptogenesis _70 _zDOAB: download the publication
856	4	0	_awww.oapen.org _uhttps://directory.doabooks.org/handle/20.500.12854/54517 _70 _zDOAB: description of the publication
999			_c39483 _d39483