Detection of Hyperexcitability by Functional Magnetic Resonance Imaging after Experimental Traumatic Brain Injury
| Autor: | Carmen Barba, Gabriella Colicchio, Alejandra Sierra Lopez, Joanna K. Huttunen, Olli Gröhn, Asla Pitkänen, Xavier Ekolle Ndode-Ekane, Juha-Pekka Niskanen, Artem Shatillo, Antti M. Airaksinen |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Male Traumatic brain injury Epileptogenesis Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine Seizures Brain Injuries Traumatic medicine Premovement neuronal activity Animals Post-traumatic epilepsy medicine.diagnostic_test business.industry medicine.disease Magnetic Resonance Imaging Rats Functional imaging Electrophysiology 030104 developmental biology Neurology (clinical) business Functional magnetic resonance imaging Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | Journal of neurotrauma. 35(22) |
| ISSN: | 1557-9042 |
| Popis: | Diagnosis 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. |
| Databáze: | OpenAIRE |
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