Investigation of Cerebral O-(2-[18F]Fluoroethyl)-L-Tyrosine Uptake in Rat Epilepsy Models.

A recent study reported on high, longer lasting and finally reversible cerebral uptake of O-(2-[¹⁸F]fluoroethyl)-L-tyrosine ([¹⁸F]FET) induced by epileptic activity. Therefore, we examined cerebral [¹⁸F]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 [¹⁸F]FET may be a potential marker to localize epileptic foci.

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× [¹⁸F]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. [¹⁸F]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 [¹⁸F]FET PET within 12 days after the last documented seizure.

No abnormalities in [¹⁸F]FET PET or MRI were detected in the kindling model. The SE model showed significantly decreased [¹⁸F]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 T₂-weighted MRI were noted in the amygdala and hippocampus, which recovered 24 days post-SE. No abnormality of cerebral [¹⁸F]FET uptake was noted in the epilepsy patients.

There was no evidence for increased cerebral [¹⁸F]FET uptake after epileptic seizures neither in the rat models nor in patients. The SE model even showed decreased [¹⁸F]FET uptake throughout the brain. We conclude that epileptic seizures per se do not cause a longer lasting increased [¹⁸F]FET accumulation and are unlikely to be a major cause of pitfall for brain tumor diagnostics.