The PET Sandwich: Using Serial FDG-PET Scans with Interval Burst Suppression to Assess Ictal Components of Disease.

BACKGROUND

Determining the cause of refractory seizures and/or interictal continuum (IIC) findings in the critically ill patient remains a challenge. These electrographic abnormalities may represent primary ictal pathology or may instead be driven by an underlying infectious, inflammatory, or neoplastic pathology that requires targeted therapy. In these cases, it is unclear whether escalating antiepileptic therapy will be helpful or harmful. Herein, we report the use of serial [F-18] fluorodeoxyglucose positron emission tomography (FDG-PET) coupled with induced electrographic burst suppression to distinguish between primary and secondary ictal pathologies. We propose that anesthetic suppression of hypermetabolic foci suggests clinical responsiveness to escalating antiepileptic therapy, whereas non-suppressible hypermetabolic foci are suggestive of non-ictal pathologies that likely require multimodal therapy.

METHODS

We describe 6 patients who presented with electrographic findings of seizure or IIC abnormalities, severe neurologic injury, and clinical concern for confounding pathologies. All patients were continuously monitored on video electroencephalography (cvEEG). Five patients underwent at least two sequential FDG-PET scans of the brain: one in a baseline state and the second while under electrographic burst suppression. FDG-avid loci and EEG tracings were compared pre- and post-burst suppression. One patient underwent a single FDG-PET scan while burst-suppressed.

RESULTS

Four patients had initially FDG-avid foci that subsequently resolved with burst suppression. Escalation of antiepileptic therapy in these patients resulted in clinical improvement, suggesting that the foci were related to primary ictal pathology. These included clinical diagnoses of electroclinical status epilepticus, new-onset refractory status epilepticus, stroke-like migraine attacks after radiotherapy, and epilepsy secondary to inflammatory cerebral amyloid angiopathy. Conversely, two patients with high-grade EEG abnormalities had FDG-avid foci that persisted despite burst suppression. The first presented with a poor examination, fever, and concern for encephalitis. Postmortem pathology confirmed suspicion of herpes simplex virus encephalitis. The second patient presented with concern for checkpoint inhibitor-induced autoimmune encephalitis. The persistence of the FDG-avid focus, despite electrographic burst suppression, guided successful treatment through escalation of immunosuppressive therapy.

CONCLUSIONS

In appropriately selected patients, FDG-PET scans while in burst suppression may help dissect the underlying pathophysiologic cause of IIC findings observed on EEG and guide tailored therapy.