Epileptogenesis in experimental models

Pitkänen, Asla, Kharatishvili, Irina, Karhunen, Heli, Lukasiuk, Katarzyna, Immonen, Riikka, Nairismägi, Jaak, Gröhn, Olli and Nissinen, Jari (2007) Epileptogenesis in experimental models. Epilepsia, 48 s2: 13-20.


Author Pitkänen, Asla
Kharatishvili, Irina
Karhunen, Heli
Lukasiuk, Katarzyna
Immonen, Riikka
Nairismägi, Jaak
Gröhn, Olli
Nissinen, Jari
Title Epileptogenesis in experimental models
Journal name Epilepsia   Check publisher's open access policy
ISSN 0013-9580
1528-1167
Publication date 2007-04
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1111/j.1528-1167.2007.01063.x
Volume 48
Issue s2
Start page 13
End page 20
Total pages 8
Place of publication Hoboken, NJ, United States
Publisher Wiley-Blackwell Publishing
Language eng
Abstract Epileptogenesis refers to a phenomenon in which the brain undergoes molecular and cellular alterations after a brain-damaging insult, which increase its excitability and eventually lead to the occurrence of recurrent spontaneous seizures. Common epileptogenic factors include traumatic brain injury (TBI), stroke, and cerebral infections. Only a subpopulation of patients with any of these brain insults, however, will develop epilepsy. Thus, there are two great challenges: (1) identifying patients at risk, and (2) preventing and/or modifying the epileptogenic process. Target identification for antiepileptogenic treatments is difficult in humans because patients undergoing epileptogenesis cannot currently be identified. Animal models of epileptogenesis are therefore necessary for scientific progress. Recent advances in the development of experimental models of epileptogenesis have provided tools to investigate the molecular and cellular alterations and their temporal appearance, as well as the epilepsy phenotype after various clinically relevant epileptogenic etiologies, including TBI and stroke. Studying these models will lead to answers to critical questions such as: Do the molecular mechanisms of epileptogenesis depend on the etiology? Is the spectrum of network alterations during epileptogenesis the same after various clinically relevant etiologies? Is the temporal progression of epileptogenesis similar? Work is ongoing, and answers to these questions will facilitate the identification of molecular targets for antiepileptogenic treatments, the design of treatment paradigms, and the determination of whether data from one etiology can be extrapolated to another. © International League Against Epilepsy.
Keyword Endothelin-1
Gene array
Lateral fluid-percussion injury
Magnetic resonance imaging
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collection: Centre for Advanced Imaging Publications
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 71 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 74 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Access Statistics: 24 Abstract Views  -  Detailed Statistics
Created: Wed, 30 Mar 2011, 16:02:24 EST by Sandrine Ducrot on behalf of Centre for Advanced Imaging