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(99m)Tc-HMPAO SPECT imaging reveals brain hypoperfusion during status epilepticus

Status epilepticus (SE) is a clinical emergency with high mortality. SE can trigger neuronal death or injury and alteration of neuronal networks resulting in long-term cognitive decline or epilepsy. Among the multiple factors contributing to this damage, imbalance between oxygen and glucose requirem...

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Detalles Bibliográficos
Autores principales: Bascuñana, Pablo, Wolf, Bettina J., Jahreis, Ina, Brackhan, Mirjam, García-García, Luis, Ross, Tobias L., Bengel, Frank M., Bankstahl, Marion, Bankstahl, Jens P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8580894/
https://www.ncbi.nlm.nih.gov/pubmed/34570340
http://dx.doi.org/10.1007/s11011-021-00843-z
Descripción
Sumario:Status epilepticus (SE) is a clinical emergency with high mortality. SE can trigger neuronal death or injury and alteration of neuronal networks resulting in long-term cognitive decline or epilepsy. Among the multiple factors contributing to this damage, imbalance between oxygen and glucose requirements and brain perfusion during SE has been proposed. Herein, we aimed to quantify by neuroimaging the spatiotemporal course of brain perfusion during and after lithium-pilocarpine-induced SE in rats. To this purpose, animals underwent (99m)Tc-HMPAO SPECT imaging at different time points during and after SE using a small animal SPECT/CT system. (99m)Tc-HMPAO regional uptake was normalized to the injected dose. In addition, voxel-based statistical parametric mapping was performed. SPECT imaging showed an increase of cortical perfusion before clinical seizure activity onset followed by regional hypo-perfusion starting with the first convulsive seizure and during SE. Twenty-four hours after SE, brain (99m)Tc-HMPAO uptake was widely decreased. Finally, chronic epileptic animals showed regionally decreased perfusion affecting hippocampus and cortical sub-regions. Despite elevated energy and oxygen requirements, brain hypo-perfusion is present during SE. Our results suggest that insufficient compensation of required blood flow might contribute to neuronal damage and neuroinflammation, and ultimately to chronic epilepsy generated by SE.