Abstract
BACKGROUND: O-(2-[F-18]fluoroethyl)-L-tyrosine (18F-FET) PET has become an important diagnostic tool in addition to standard MRI to delineate cerebral gliomas. However, 18F-FET uptake has also been observed in non-tumoral lesions. METHODS AND RESULTS: We report on abnormal non-tumoral 18F-FET uptake in 6 patients with epileptic disorders: Patients A-C with clinically stable anaplastic astrocytoma over years, Patient D with anaplastic oligodendroglioma with stable residual tumor, Patient E with initial diagnosis of glioblastoma, Patient F with subacute cerebral ischemia. All patients presented initially with repeated epileptic seizures or status epilepticus and typical clinical and EEG findings. Standard MRI (T1 + /-contrast, T2/FLAIR) showed cortical and subcortical contrast enhancement and/or T2/FLAIR signal alterations and 18F-FET PET demonstrated a significantly increased cortical amino acid uptake. 18F-FET uptake and contrast enhancement on MRI resolved completely after cessation of epileptic activity. Patient C suffered from a prolonged postictal state. In that patient, EEG monitoring demonstrated a left hemispheric deceleration without signs of epileptic discharges; additionally, 18F-FDG PET and HMPAO SPECT showed cortical glucose hypometabolism and hypoperfusion, not consistent with a status epilepticus. After 14 weeks, clinical symptoms and the cortical 18F-FET uptake resolved completely. CONCLUSION: Abnormal 18F-FET uptake may occur in patients with epileptic disorders in brain areas not infiltrated by tumor. The reason for this phenomenon is yet unknown.
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