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

27th May 2020

Carina Stegmayr, Rainer Surges, Chang-Hoon Choi, Nicole Burda, Gabriele Stoffels, Christian Filß, Antje Willuweit, Bernd Neumaier, Alexander Heinzel, N. Jon Shah, Felix M. Mottaghy, Karl-Josef Langen

Epileptic seizure is a frequent onset symptom of brain tumours with between 20–40 % of patients experiencing seizures prior to diagnosis and another 20– 40 % of patients experiencing seizures during the course of the disease. In low-grade tumours, the incidence of seizures can be over 80 %.

Control of these seizures is dependent on the nature of the brain tumour treatment and patient response to anti-epileptic drugs.

The use of positron emission tomography (PET) in the diagnosis of brain tumours and treatment planning is long-established and enables the measurement of metabolic and pathological processes in the brain. In a recent PET study on brain tumour patients by Hutterer et al., it was thought that high, longer-lasting and finally reversible cerebral uptake of the amino acid PET tracer O-(2-[18F]fluoroethyl)-L-tyrosine ([18F]FET) was indicative of tumour recurrence. However, following histological confirmation and follow-up, it was found that this accumulation was caused by previous epileptic seizures.

In response to this finding, this research paper examined cerebral [18F]FET uptake in two chemically induced rat epilepsy models and patients with focal epilepsy to further investigate whether this phenomenon represents a major pitfall in brain tumour diagnostics and whether [18F]FET may be a potential marker to localize epileptic foci.

Based on the data gathered, no evidence was found for increased cerebral [18F]FET uptake after epileptic seizures in either the rat models or in the patient cohort. The research concludes 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 tumour diagnostics.

Reference:
Hutterer M, Ebner Y, Riemenschneider MJ, Willuweit A, McCoy M, Egger B, Schroder M, Wendl C, Hellwig D, Grosse J, Menhart K, Proescholdt M, Fritsch B, Urbach H, Stockhammer G, Roelcke U, Galldiks N, Meyer PT, Langen KJ, Hau P, Trinka E (2017) Epileptic activity increases cerebral amino acid transport assessed by 18F- fluoroethyl-l-tyrosine amino acid PET: a potential brain tumor mimic. J Nucl Med 58:129–137

Original publication:

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


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