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Investigation of Cerebral O-(2-[(18)F]Fluoroethyl)-L-Tyrosine Uptake in Rat Epilepsy Models
PURPOSE: A recent study reported on high, longer lasting and finally reversible cerebral uptake of O-(2-[(18)F]fluoroethyl)-L-tyrosine ([(18)F]FET) induced by epileptic activity. Therefore, we examined cerebral [(18)F]FET uptake in two chemically induced rat epilepsy models and in patients with foca...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7497431/ https://www.ncbi.nlm.nih.gov/pubmed/32409931 http://dx.doi.org/10.1007/s11307-020-01503-x |
Sumario: | PURPOSE: A recent study reported on high, longer lasting and finally reversible cerebral uptake of O-(2-[(18)F]fluoroethyl)-L-tyrosine ([(18)F]FET) induced by epileptic activity. Therefore, we examined cerebral [(18)F]FET uptake in two chemically induced rat epilepsy models and in patients with focal epilepsy to further investigate whether this phenomenon represents a major pitfall in brain tumor diagnostics and whether [(18)F]FET may be a potential marker to localize epileptic foci. PROCEDURES: Five rats underwent kainic acid titration to exhibit 3 to 3.5 h of class IV–V motor seizures (status epilepticus, SE). Rats underwent 4× [(18)F]FET PET and 4× MRI on the following 25 days. Six rats underwent kindling with pentylenetetrazol (PTZ) 3 to 8×/week over 10 weeks, and hence, seizures increased from class I to class IV. [(18)F]FET PET and MRI were performed regularly on days with and without seizures. Four rats served as healthy controls. Additionally, five patients with focal epilepsy underwent [(18)F]FET PET within 12 days after the last documented seizure. RESULTS: No abnormalities in [(18)F]FET PET or MRI were detected in the kindling model. The SE model showed significantly decreased [(18)F]FET uptake 3 days after SE in all examined brain regions, and especially in the amygdala region, which normalized within 2 weeks. Corresponding signal alterations in T(2)-weighted MRI were noted in the amygdala and hippocampus, which recovered 24 days post-SE. No abnormality of cerebral [(18)F]FET uptake was noted in the epilepsy patients. CONCLUSIONS: There was no evidence for increased cerebral [(18)F]FET uptake after epileptic seizures neither in the rat models nor in patients. The SE model even showed decreased [(18)F]FET uptake throughout the brain. We conclude that epileptic seizures per se do not cause a longer lasting increased [(18)F]FET accumulation and are unlikely to be a major cause of pitfall for brain tumor diagnostics. |
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