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dc.contributor.authorHuttunen, JK
dc.contributor.authorAiraksinen, AM
dc.contributor.authorBarba, C
dc.contributor.authorColicchio, G
dc.contributor.authorNiskanen, JP
dc.contributor.authorShatillo, A
dc.contributor.authorSierra Lopez, A
dc.contributor.authorNdode-Ekane, XE
dc.contributor.authorPitkanen, A
dc.contributor.authorGröhn, O
dc.date.accessioned2018-10-16T07:57:25Z
dc.date.available2018-10-16T07:57:25Z
dc.date.issued2018
dc.identifier.urihttps://erepo.uef.fi/handle/123456789/7051
dc.description.abstractDiagnosis of ongoing epileptogenesis and associated hyperexcitability after brain injury is a major challenge. Given that increased neuronal activity in the brain triggers a blood oxygenation level–dependent (BOLD) response in functional magnetic resonance imaging (fMRI), we hypothesized that fMRI could be used to identify the brain area(s) with hyperexcitability during post-injury epileptogenesis. We applied fMRI to detect onset and spread of BOLD activation after pentylenetetrazol (PTZ)-induced seizures (PTZ, 30 mg/kg, intraperitoneally) in 16 adult male rats at 2 months after lateral fluid percussion (FPI)-induced traumatic brain injury (TBI). In sham-operated controls, onset of the PTZ-induced BOLD response was bilateral and first appeared in the cortex. After TBI, 5 of 9 (56%) rats exhibited ipsilateral perilesional cortical BOLD activation, followed by activation of the contralateral cortex. In 4 of 9 (44%) rats, onset of BOLD response was bilateral. Interestingly, latency from the PTZ injection to onset of the BOLD response increased in the following order: sham-operated controls (ipsilateral 132 ± 57 sec, contralateral 132 ± 57 sec; p > 0.05) < TBI with bilateral BOLD onset (ipsilateral 176 ± 54 sec, contralateral 178 ± 52 sec; p > 0.05) < TBI with ipsilateral BOLD onset (ipsilateral 406 ± 178 sec, contralateral 509 ± 140 sec; p < 0.05). Cortical lesion area did not differ between rats with ipsilateral versus bilateral BOLD onset (p > 0.05). In the group of rats with ipsilateral onset of PTZ-induced BOLD activation, none of the rats showed a robust bilateral thalamic BOLD response, only 1 of 5 rats had robust ipsilateral thalamic calcifications, and 4 of 5 rats had perilesional astrocytosis. These findings suggest the evolution of the epileptogenic zone in the perilesional cortex after TBI, which is sensitive to PTZ-induced hyperexcitability. Further studies are warranted to explore the evolution of thalamo-cortical pathology as a driver of epileptogenesis after lateral FPI.
dc.language.isoenglanti
dc.publisherMary Ann Liebert Inc
dc.relation.ispartofseriesJOURNAL OF NEUROTRAUMA (NEW YORK NY)
dc.relation.urihttp://dx.doi.org/10.1089/neu.2017.5308
dc.rightsAll rights reserved
dc.subjectepileptogenesis
dc.subjectfunctional imaging
dc.subjectlateral fluid-percussion injury
dc.subjectpost-traumatic epilepsy
dc.titleDetection of Hyperexcitability by fMRI After Experimental Traumatic Brain Injury
dc.description.versionfinal draft
dc.contributor.departmentA.I. Virtanen -instituutti
uef.solecris.id56018319en
dc.type.publicationTieteelliset aikakauslehtiartikkelit
dc.rights.accessrights© Mary Ann Liebert, Inc.
dc.relation.doi10.1089/neu.2017.5308
dc.description.reviewstatuspeerReviewed
dc.relation.issn0897-7151
dc.relation.volume[Epub ahead of print 27 Sept 2018]
dc.rights.accesslevelopenAccess
dc.type.okmA1
uef.solecris.openaccessEi


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