schliessen

Filtern

 

Bibliotheken

Epileptogenesis in Experimental Models

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 (... Full description

Journal Title: Epilepsia Apr 2007, Vol.48(s2), pp.13-20
Main Author: Pitkanen, Asla
Other Authors: Kharatishvili, Irina , Karhunen, Heli , Lukasiuk, Katarzyna , Immonen, Riikka , Nairismagi, Jaak , Grohn, Olli , Nissinen, Jari
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0013-9580 ; E-ISSN: 1528-1167 ; DOI: 10.1111/j.1528-1167.2007.01063.x
Link: http://search.proquest.com/docview/20535715/
Zum Text:
SendSend as email Add to Book BagAdd to Book Bag
Staff View
recordid: proquest20535715
title: Epileptogenesis in Experimental Models
format: Article
creator:
  • Pitkanen, Asla
  • Kharatishvili, Irina
  • Karhunen, Heli
  • Lukasiuk, Katarzyna
  • Immonen, Riikka
  • Nairismagi, Jaak
  • Grohn, Olli
  • Nissinen, Jari
subjects:
  • Molecular Modelling
  • Etiology
  • Brain Injury
  • Epilepsy
  • Seizures
  • Stroke
  • Animal Models
  • Excitability
  • Traumatic Brain Injury
  • Neurology & Neuropathology
  • Endothelin-1
  • Gene Array
  • Lateral Fluid-Percussion Injury
  • Magnetic Resonance Imaging
  • Photothrombotic Stroke
  • Traumatic Brain Injury
  • Video-EEG Monitoring
ispartof: Epilepsia, Apr 2007, Vol.48(s2), pp.13-20
description: 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 andor 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.
language: eng
source:
identifier: ISSN: 0013-9580 ; E-ISSN: 1528-1167 ; DOI: 10.1111/j.1528-1167.2007.01063.x
fulltext: fulltext
issn:
  • 00139580
  • 0013-9580
  • 15281167
  • 1528-1167
url: Link


@attributes
ID1099212227
RANK0.07
NO1
SEARCH_ENGINEprimo_central_multiple_fe
SEARCH_ENGINE_TYPEPrimo Central Search Engine
LOCALfalse
PrimoNMBib
record
control
sourcerecordid20535715
sourceidproquest
recordidTN_proquest20535715
sourcesystemOther
pqid20535715
galeid164819135
display
typearticle
titleEpileptogenesis in Experimental Models
creatorPitkanen, Asla ; Kharatishvili, Irina ; Karhunen, Heli ; Lukasiuk, Katarzyna ; Immonen, Riikka ; Nairismagi, Jaak ; Grohn, Olli ; Nissinen, Jari
contributorPitkanen, Asla (correspondence author)
ispartofEpilepsia, Apr 2007, Vol.48(s2), pp.13-20
identifier
subjectMolecular Modelling ; Etiology ; Brain Injury ; Epilepsy ; Seizures ; Stroke ; Animal Models ; Excitability ; Traumatic Brain Injury ; Neurology & Neuropathology ; Endothelin-1 ; Gene Array ; Lateral Fluid-Percussion Injury ; Magnetic Resonance Imaging ; Photothrombotic Stroke ; Traumatic Brain Injury ; Video-EEG Monitoring
descriptionEpileptogenesis 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 andor 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.
languageeng
source
version4
lds50peer_reviewed
links
openurl$$Topenurl_article
openurlfulltext$$Topenurlfull_article
backlink$$Uhttp://search.proquest.com/docview/20535715/$$EView_record_in_ProQuest_(subscribers_only)
search
creatorcontrib
0Pitkanen, Asla
1Kharatishvili, Irina
2Karhunen, Heli
3Lukasiuk, Katarzyna
4Immonen, Riikka
5Nairismagi, Jaak
6Grohn, Olli
7Nissinen, Jari
titleEpileptogenesis in Experimental Models
descriptionEpileptogenesis 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 andor 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.
subject
0Molecular Modelling
1Etiology
2Brain Injury
3Epilepsy
4Seizures
5Stroke
6Animal Models
7Excitability
8Traumatic Brain Injury
9Neurology & Neuropathology
10Endothelin-1
11Gene Array
12Lateral Fluid-Percussion Injury
13Magnetic Resonance Imaging
14Photothrombotic Stroke
15Video-EEG Monitoring
16N3 11027
17Gene array
18Lateral fluid-percussion injury
19Magnetic resonance imaging
20Photothrombotic stroke
21Traumatic brain injury
22Video-EEG monitoring
general
0English
110.1111/j.1528-1167.2007.01063.x
2Neurosciences Abstracts
3ProQuest Biological Science Collection
4ProQuest Natural Science Collection
5ProQuest SciTech Collection
6Biological Science Database
7Natural Science Collection
8SciTech Premium Collection
sourceidproquest
recordidproquest20535715
issn
000139580
10013-9580
215281167
31528-1167
rsrctypearticle
creationdate2007
addtitleEpilepsia
searchscope
01007536
11007944
210000004
310000038
410000050
510000120
610000198
710000209
810000217
910000238
1010000253
1110000260
12proquest
scope
01007536
11007944
210000004
310000038
410000050
510000120
610000198
710000209
810000217
910000238
1010000253
1110000260
12proquest
lsr43
01007536false
11007944false
210000004false
310000038false
410000050false
510000120false
610000198false
710000209false
810000217false
910000238false
1010000253false
1110000260false
contributorPitkanen, Asla
startdate20070401
enddate20070401
citationpf 13 pt 20 vol 48 issue s2
lsr30VSR-Enriched:[galeid, pqid]
sort
titleEpileptogenesis in Experimental Models
authorPitkanen, Asla ; Kharatishvili, Irina ; Karhunen, Heli ; Lukasiuk, Katarzyna ; Immonen, Riikka ; Nairismagi, Jaak ; Grohn, Olli ; Nissinen, Jari
creationdate20070401
lso0120070401
facets
frbrgroupid3566628252295355215
frbrtype5
languageeng
creationdate2007
topic
0Molecular Modelling
1Etiology
2Brain Injury
3Epilepsy
4Seizures
5Stroke
6Animal Models
7Excitability
8Traumatic Brain Injury
9Neurology & Neuropathology
10Endothelin-1
11Gene Array
12Lateral Fluid-Percussion Injury
13Magnetic Resonance Imaging
14Photothrombotic Stroke
15Video-EEG Monitoring
collection
0Neurosciences Abstracts
1ProQuest Biological Science Collection
2ProQuest Natural Science Collection
3ProQuest SciTech Collection
4Biological Science Database
5Natural Science Collection
6SciTech Premium Collection
prefilterarticles
rsrctypearticles
creatorcontrib
0Pitkanen, Asla
1Kharatishvili, Irina
2Karhunen, Heli
3Lukasiuk, Katarzyna
4Immonen, Riikka
5Nairismagi, Jaak
6Grohn, Olli
7Nissinen, Jari
jtitleEpilepsia
toplevelpeer_reviewed
delivery
delcategoryRemote Search Resource
fulltextfulltext
addata
aulast
0Pitkanen
1Kharatishvili
2Karhunen
3Lukasiuk
4Immonen
5Nairismagi
6Grohn
7Nissinen
aufirst
0Asla
1Irina
2Heli
3Katarzyna
4Riikka
5Jaak
6Olli
7Jari
au
0Pitkanen, Asla
1Kharatishvili, Irina
2Karhunen, Heli
3Lukasiuk, Katarzyna
4Immonen, Riikka
5Nairismagi, Jaak
6Grohn, Olli
7Nissinen, Jari
addauPitkanen, Asla
atitleEpileptogenesis in Experimental Models
jtitleEpilepsia
risdate20070401
volume48
issues2
spage13
epage20
pages13-20
issn0013-9580
eissn1528-1167
formatjournal
genrearticle
ristypeJOUR
abstractEpileptogenesis 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 andor 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.
doi10.1111/j.1528-1167.2007.01063.x
urlhttp://search.proquest.com/docview/20535715/
date2007-04-01