Abstracts

Rationale:
We report the case of a 39 year old man with refractory epilepsy who underwent an initial FDG-PET/CT study before intracranial electroencephalography (iEEG) was performed, using subdural electrodes electrodes on the left fronto-temporo-parietal convexity (64-contact subdural grid and strip electrodes). Initial intracranial video EEG monitoring did not localize seizures, and the patient declined further workup. After seizures remained refractory to medical therapy, he proceeded with re-evaluation for epilepsy surgery, which included a repeat FDG-PET/CT study 79 months after iEEG.
Method:
The two PET time points were evaluated using both visual assessment, and the quantitative analysis tool (MIMneuro) for parametric mapping to calculate differences in tracer uptake in the patient’s brain compared to a template of normal subjects (n =43). The results were fused with the most recently acquired brain MR for anatomical localization, and 3D brain cortical surface projections. Parametric mapping analysis of the baseline FDG-PET demonstrated decreased metabolic activity in the left temporal lobe without other abnormalities. The second FDG-PET showed a new large region of greater than 2SD hypometabolism over the left fronto-temporo-parietal convexity limited to superficial cortical regions. Coregistration of images with a volumetric CT of iEEG electrode placement showed that the left fronto-temporo-parietal region of hypometabolism correlated to the anatomic location of grid placement.
Results:
He subsequently underwent placement of bilateral stereotactic depth electrodes. Monitoring was notable for seizures of left basal temporal onset which is outside the region of prior subdural grid placement and area of hypometabolism on PET. He underwent resection of left temporo-occipital epileptogenic focus with good response.
Conclusion:
Our results highlight changes of hypometabolism on FDG-PET/CT after iEEG. This focal area of hypometabolism was confined to the region of intracranial grid placement which is suggestive of a causal relationship between grid placement and FDG hypometabolism. Subsequent iEEG monitoring with sEEG was notable for seizure foci outside of this area of hypometabolism providing further support that these findings were not related to the patient's seizure foci and instead related to subdural grid placement. While definitive etiology of findings are uncertain, past neuroimaging studies document regional cortical edema after placement of iEEG electrodes, and past postoperative neuropathology studies have found inflammatory changes in the region of iEEG placement which suggests that iEEG can cause focal regions of cortical dysfunction (Fong et al., 2012). These findings are important for understanding brain functional changes after intracranial grid placement, and outline a potential avenue for comparison of different modes of intracranial EEG monitoring. Additionally, it highlights the potential for false localization of epileptogenic foci on FDG-PET/CT performed after subdural grid placement.
Funding:
:None