Markus Hutterer1,2,3, Yvonne Ebner3, Markus J Riemenschneider2,4, Antje Willuweit5, Mark McCoy6, Barbara Egger7, Michael Schröder8, Christina Wendl9, Dirk Hellwig10, Jirka Grosse10, Karin Menhart10, Martin Proescholdt2,11, Brita Fritsch12, Horst Urbach13, Guenther Stockhammer14, Ulrich Roelcke15, Norbert Galldiks5,16, Philipp T Meyer17, Karl-Josef Langen5,18, Peter Hau8,2, Eugen Trinka3. 1. Department of Neurology, University of Regensburg Medical School, Regensburg, Germany markus.hutterer@gmx.at. 2. Wilhelm Sander-Neurooncology Unit, University of Regensburg Medical School, Regensburg, Germany. 3. Department of Neurology and Centre for Cognitive Neuroscience, Christian-Doppler Klinik, Paracelsus Medical University Salzburg, Salzburg, Austria. 4. Department of Neuropathology, University of Regensburg Medical School, Regensburg, Germany. 5. Institute of Neuroscience and Medicine, Forschungszentrum Jülich, Jülich, Germany. 6. Department of Radiology and Division of Neuroradiology, Christian-Doppler Klinik, Paracelsus Medical University Salzburg, Salzburg, Austria. 7. Department of Nuclear Medicine, Landeskrankenhaus Salzburg, Paracelsus Medical University Salzburg, Salzburg, Austria. 8. Department of Neurology, University of Regensburg Medical School, Regensburg, Germany. 9. Department of Radiology and Division of Neuroradiology, University of Regensburg Medical School, Regensburg, Germany. 10. Department of Nuclear Medicine, University of Regensburg Medical School, Regensburg, Germany. 11. Department of Neurosurgery, University of Regensburg Medical School, Regensburg, Germany. 12. Department of Neurology, University Hospital Freiburg, Freiburg, Germany. 13. Department of Neuroradiology, University Hospital Freiburg, Freiburg, Germany. 14. Department of Neurology, Medical University Innsbruck, Innsbruck, Austria. 15. Department of Neurology and Brain Tumor Center, Cantonal Hospital Aarau, Aarau, Switzerland. 16. Department of Neurology, University of Cologne, Cologne, Germany. 17. Department of Nuclear Medicine, University Hospital Freiburg, Freiburg, Germany; and. 18. Department of Nuclear Medicine, University of Aachen, Aachen, Germany.
Abstract
O-(2-18F-fluoroethyl)-l-tyrosine (18F-FET) PET is a well-established method increasingly used for diagnosis, treatment planning, and monitoring in gliomas. Epileptic activity, frequently occurring in glioma patients, can influence MRI findings. Whether seizures also affect 18F-FET PET imaging is currently unknown. The aim of this retrospective analysis was to investigate the brain amino acid metabolism during epileptic seizures by 18F-FET PET and to elucidate the pathophysiologic background. METHODS: Ten patients with 11 episodes of serial seizures or status epilepticus, who underwent MRI and 18F-FET PET, were studied. The main diagnosis was glioma World Health Organization grade II-IV (n = 8); 2 patients suffered from nonneoplastic diseases. Immunohistochemical assessment of LAT1/LAT2/CD98 amino acid transporters was performed in seizure-affected cortex (n = 2) and compared with glioma tissues (n = 3). RESULTS: All patients exhibited increased seizure-associated strict gyral 18F-FET uptake, which was reversible in follow-up studies or negative shortly before and without any histologic or clinical signs of tumor recurrence. 18F-FET uptake corresponded to structural MRI changes, compatible with cortical vasogenic and cytotoxic edema, partial contrast enhancement, and hyperperfusion. Patients with prolonged postictal symptoms lasting up to 8 wk displayed intensive and widespread (≥ 1 lobe) cortical 18F-FET uptake. LAT1/LAT2/CD98 was strongly expressed in neurons and endothelium of seizure-affected brains and less in reactive astrocytosis. CONCLUSION: Seizure activity, in particular status epilepticus, increases cerebral amino acid transport with a strict gyral 18F-FET uptake pattern. Such periictal pseudoprogression represents a potential pitfall of 18F-FET PET and may mimic brain tumor. Our data also indicate a seizure-induced upregulation of neuronal, endothelial, and less astroglial LAT1/LAT2/CD98 amino acid transporter expression.
O-(2-18F-fluoroethyl)-l-tyrosine (18F-FET) PET is a well-established method increasingly used for diagnosis, treatment planning, and monitoring in gliomas. Epileptic activity, frequently occurring in gliomapatients, can influence MRI findings. Whether seizures also affect 18F-FET PET imaging is currently unknown. The aim of this retrospective analysis was to investigate the brain amino acid metabolism during epilepticseizures by 18F-FET PET and to elucidate the pathophysiologic background. METHODS: Ten patients with 11 episodes of serial seizures or status epilepticus, who underwent MRI and 18F-FET PET, were studied. The main diagnosis was glioma World Health Organization grade II-IV (n = 8); 2 patients suffered from nonneoplastic diseases. Immunohistochemical assessment of LAT1/LAT2/CD98 amino acid transporters was performed in seizure-affected cortex (n = 2) and compared with glioma tissues (n = 3). RESULTS: All patients exhibited increased seizure-associated strict gyral 18F-FET uptake, which was reversible in follow-up studies or negative shortly before and without any histologic or clinical signs of tumor recurrence. 18F-FET uptake corresponded to structural MRI changes, compatible with cortical vasogenic and cytotoxic edema, partial contrast enhancement, and hyperperfusion. Patients with prolonged postictal symptoms lasting up to 8 wk displayed intensive and widespread (≥ 1 lobe) cortical 18F-FET uptake. LAT1/LAT2/CD98 was strongly expressed in neurons and endothelium of seizure-affected brains and less in reactive astrocytosis. CONCLUSION:Seizure activity, in particular status epilepticus, increases cerebral amino acid transport with a strict gyral 18F-FET uptake pattern. Such periictal pseudoprogression represents a potential pitfall of 18F-FET PET and may mimic brain tumor. Our data also indicate a seizure-induced upregulation of neuronal, endothelial, and less astroglial LAT1/LAT2/CD98 amino acid transporter expression.
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