The first group of patients consisted of 10 surgically treated patients, in the 8 of the patients (80%) epileptogenic lesion was visible on MRI (mesial temporal sclerosis-4, focal cortical displasia-1, subependymal nodular grey matter heterotopia-1, multinodular and vacuolating neuronal tumor-1, arachnoid cyst-1), in 2 patients (20%) structural changes of the brain were not observed on MRI. Area of 18F-FDG hypometabolism was found in all of the patients, its location matched with structural epileptogenic lesion in all 8 patients with structural brain changes. Area of 18F-FDG hypometabolism matched with epilepsy -onset zone found by scalp video-EEG monitoring in 9 patients, 4 of them had other epileptogenic lesions found by EEG. In one patient epileptogenic zone were not found by video-EEG monitoring of the patient had sEEG before surgical resection, in all 4 cases location of the seisure-onset zone matched with the location of the area of 18F-FDG hypometabolism. All of the patients were discharged with improvement, 3 of them did not have seizures, in 7 of the patients decrease of the frequency and intensity of seizures allowed to reduce the dosage of anticonvulsant therapy.

   The second group of the patients consisted from 9 patients who underwent SEEG but did not have surgical resection. 8 of the patients (89%)had structural brain changes found by MRI (unilateral mesial temporal sclerosis-1, bilateral mesial temporal sclerosis-2, hippocampal malrotation-1, bilateral meningoencephalocele-1, developmental venous anomaly, cavernous malformation-1, postsurgical encephalomalatia-1), 1 patient (11%) was MRI-negative. Scalp video-EEG monitoring found one potential epileptogenic zone in 1 patient, multiple epileptogenic zones in 6 of the patients with bilateral localization in 4 of them, EEG refused to find epileptoenic zone in 2 of the patients. SEEG found bilateral seizure-onset zones in all of the patients. In 8 cases area of 18F-FDG hypometabolism matched with epileptogenic zone with a greater part of seizure onsets found by SEEG, after the multidisciplinary team meeting vagus nerve stimulator implantation was recommended for these patients. In one MR-negative patient SEEG found seizure onset zones in the both hippocampi in addition to the diffuse onset, after the multidisciplinary team meeting epilepsy type was categorized as combined focal and generalized,  magnetic resonance-guided focused ultrasound  ablation was recommended for the patient.

   The third group consisted of 10 MR-negative patients who did not have neither invasive EEG nor surgical resection. Scalp video-EEG monitoring found one epileptogenic zone in 5 of the patients, its location was compliant with the location of the areas of the 18F-FDG hypometabolism. 2 patients had two epileptogenic zones found by video-EEG monitoring, localization of one of them corresponded to the 18F-FDG hypometabolism area. One patient had 4 epileptogenic zones found by video-EEG monitoring, two of them were consonant with the areas of 18F-FDG hypometabolism. In one patient scalp video-EEG monitoring refused to find seizure-onset zone, PET/MRI found two areas of 18F-FDG hypometabolism in temporal lobes.

   Quantitative PET parameters (SUVmax, SUVmean, SUVpeak, asymmetry index) were estimated in absolute terms and as a percentage to the contralateral hemisphere. Mean values and standard deviation were calculated for every group of patients (Figure one).  Estimated parameters demonstrate that SUVmean% is associated with the lesser amount of standard deviation  and more homogeneous changes between the groups where suspected localization of the epileptogenic lesion was confirmed by the invasive methods. The largest mean values of all estimated parameters were observed in the first group of patients, which corresponded to the most intense 18F-FDG hypometabolism in the epileptogenic lesion in the group of operated patients.  In the second group of patients we observed decrease of the average percentage of all estimated parameters compared to the group one consistent with lesser intensity of the 18F-FDG hypometabolism in the epileptogenic zone and lesser confidence of the unilateral localization of the lesion.  estimated parameters in the third group may be suggestive for the less intensive 18F-FDG hypobetabolism in the epileptogenic lesion than was not visible on MRI but can be potentially visualized on PET.