Purpose

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.

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× [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.

Results

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.

Conclusions

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.

中文翻译：

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大鼠癫痫模型中脑 O-(2-[18F] 氟乙基)-L-酪氨酸摄取的研究。

目的

最近的一项研究报告了由癫痫活动诱导的 O-(2-[ ¹⁸ F] 氟乙基)-L-酪氨酸 ([ ¹⁸ F] FET) 的高、持久和最终可逆的大脑摄取。因此，我们在两种化学诱导的大鼠癫痫模型和局灶性癫痫患者中检查了脑 [ ¹⁸ F] FET 的摄取，以进一步研究这种现象是否代表脑肿瘤诊断的主要缺陷，以及 [ ¹⁸ F]FET是否可能是一个潜在的标志物定位癫痫病灶。

程序

五只大鼠接受红藻氨酸滴定以表现出 3 至 3.5 小时的 IV-V 级运动性癫痫发作（癫痫持续状态，SE）。在接下来的 25 天，大鼠接受了 4×[ ¹⁸ F]FET PET 和 4× MRI。6 只大鼠在 10 周内接受了 3 至 8 次/周的戊四唑 (PTZ) 点燃，因此，癫痫发作从 I 级增加到 IV 级。[ ¹⁸ F]FET PET 和 MRI 在有和没有癫痫发作的日子里定期进行。四只大鼠作为健康对照。此外，5 名局灶性癫痫患者在最后一次记录癫痫发作后的 12 天内接受了 [ ¹⁸ F] FET PET。

结果

在点燃模型中未检测到[ ¹⁸ F]FET PET 或MRI异常。SE 模型在所有检查的大脑区域，特别是杏仁核区域，在 SE 后 3 天显示 [ ¹⁸ F]FET 摄取显着降低，在 2 周内恢复正常。在杏仁核和海马体中注意到T ₂加权 MRI 中的相应信号改变，其在 SE 后 24 天恢复。在癫痫患者中未发现脑[ ¹⁸ F]FET 摄取异常。

结论

在大鼠模型和患者中，没有证据表明癫痫发作后脑 [ ¹⁸ F] FET 摄取增加。SE 模型甚至显示整个大脑的[ ¹⁸ F] FET 摄取减少。我们得出结论，癫痫发作本身不会导致 [ ¹⁸ F] FET 积累的持续增加，并且不太可能成为导致脑肿瘤诊断失败的主要原因。