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Review
. 2023 Apr 28;22(2):78-86.
doi: 10.1055/s-0043-1764303. eCollection 2023 Jun.

PET/MRI Applications in Pediatric Epilepsy

Christian Pedersen  1 , Mariam Aboian  1 , Steven A Messina  2 , Heike Daldrup-Link  3 , Ana M Franceschi  4
Affiliations
Review

PET/MRI Applications in Pediatric Epilepsy

Christian Pedersen et al. World J Nucl Med. .

Abstract

Epilepsy neuroimaging assessment requires exceptional anatomic detail, physiologic and metabolic information. Magnetic resonance (MR) protocols are often time-consuming necessitating sedation and positron emission tomography (PET)/computed tomography (CT) comes with a significant radiation dose. Hybrid PET/MRI protocols allow for exquisite assessment of brain anatomy and structural abnormalities, in addition to metabolic information in a single, convenient imaging session, which limits radiation dose, sedation time, and sedation events. Brain PET/MRI has proven especially useful for accurate localization of epileptogenic zones in pediatric seizure cases, providing critical additional information and guiding surgical decision making in medically refractory cases. Accurate localization of seizure focus is necessary to limit the extent of the surgical resection, preserve healthy brain tissue, and achieve seizure control. This review provides a systematic overview with illustrative examples demonstrating the applications and diagnostic utility of PET/MRI in pediatric epilepsy.

Keywords: PET/MRI; focal cortical dysplasia; hybrid imaging; malformations of cortical development; mesial temporal sclerosis; pediatric epilepsy; temporal lobe epilepsy; tuberous sclerosis.

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Conflict of interest statement

Conflicts of Interest Heike Daldrup-Link reported below details: Grants or contracts from any entity: R01AR054458 (PI), R01HD081123 (PI), R21AR075863 (PI), R21HD103638 (PI), U24CA264298 (Co-PI), P30CA124435 (Key personnel) Andrew McDonough B+ Foundation ReMission Alliance Sarcoma Foundation of America. Royalties or licenses: US20130344003, WO2015014756, WO2018217943 Monasteria Press LLC Patents: US20130344003, WO2015014756, WO2018217943. Participation on a Data Safety Monitoring Board or Advisory Board: External advisory board member, R24OD019813-01 Advisory board member, Stanford Cancer Imaging T32 Training Program, 5 T T32 Act CA009695 Project 29 Advisory Board, The Lancet Hematology Leadership or fiduciary role in other board, society, committee or advocacy group, paid or unpaid: Member, Editorial Board, Nanotheranostics Member, Editorial Board, Journal of Nuclear Medicine Associate Editor, Radiology: Imaging Cancer Co-Program Director, Mentoring to AdVance womEN in Science (MAVENS) program, Stanford School of Medicine, Associate Chair for Diversity, Department of Radiology, Stanford School of Medicine Co-Director, Cancer Imaging & Early Detection Program, Stanford Cancer Institute, 5P30CA124435-10 Board Member, SPR Research Foundation, Society for Pediatric Radiology (SPR) Member, Noninterpretive Skills and Practice Management Committee, Annual Meeting of the Radiological Society of North America (RSNA) Awards Committee, World Molecular Imaging Society (WMIS) Ana Franceschi reported: Grants or contracts from any entity: Foundation of the ASNR Boerger Grant. Consulting fees: Biogen, Life Molecular Imaging, Genentech. Leadership or fiduciary role in other board: Chair, ACR Neuroradiology Commission Dementia Workgroup. All other authors reported no conflict of interest.

Figures

Fig. 1
Fig. 1
18 F-FDG-PET ( A, B ) and automated voxel by voxel z-score database map (Cortex ID, GE Healthcare) ( C ) shows focal areas of hypometabolism in the parietal and occipital lobes, more pronounced on the left side, which resulted in focused review of corresponding MRI. Focal hypometabolism corresponds to gray matter bands adjacent to the occipital horns of the lateral ventricles on the MPRAGE and DIR sequences ( D–F ), which were isointense to cortex on all sequences, and compatible with band heterotopia.
Fig. 2
Fig. 2
Focal hypometabolism along the medial right frontal lobe ( A ) corresponds to underlying cortical and subcortical irregularity on fused FLAIR PET/MRI sequence ( B ) with gray–white junction blurring, hyperintense T2 signal and positive transmantle sign, best defined on FLAIR sequence ( C ).
Fig. 3
Fig. 3
Brain MRI in patient with focal cortical dysplasia visualized as abnormal cortical thickening and effacement of white matter in the right temporal pole, best visualized on thin coronal T2-weighted MRI ( arrows , A ). On 18 F-FDG-PET ( arrows and arrowheads , B–D ) and fused axial 18 F-FDG PET/CT ( arrowheads , E ), there is corresponding hypometabolism in the right anterior temporal lobe.
Fig. 4
Fig. 4
A 11-year-old male patient with medically refractory epilepsy. EEG demonstrated left temporal lobe seizure focus. Fused 18 F-FDG PET/MRI ( A, B ), coronal T2 and FLAIR ( C, D ) views demonstrate focal hypometabolism in the left temporal pole involving the left hippocampal formation, entorhinal cortex, and amygdala. There is decreased volume of the left hippocampal formation ( open arrow ) with abnormal morphology and subtle T2/FLAIR hyperintensity, and with associated decreased caliber of the left fornix ( black arrow ) and smaller size of the left mamillary body (not shown). Semiquantitative analysis using Z scores calculated in comparison to age-matched normal controls ( E ) reveals significantly decreased values in the left temporal lobe including in the left temporal pole, hippocampus, parahippocampal gyrus, and amygdala.
Fig. 5
Fig. 5
Brain MRI in a patient with tuberous sclerosis demonstrates multiple FLAIR hyperintense cortical tubers ( arrowheads , A ). The regions of the tubers appear to be hypometabolic on corresponding 18 F-FDG-PET ( arrowheads , B ). There are small enhancing subependymal nodules ( arrows ) along the left lateral ventricle, which are consistent with diagnosis of TS ( C ).
Fig. 6
Fig. 6
A 3-year-old child with refractory status epilepticus. MRI brain demonstrates parenchymal volume loss and white matter FLAIR hyperintense foci ( A, B ). Extensive laboratory testing was negative for arbovirus, AQP4 antibody, myelin oligodendrocyte glycoprotein, and SARS CoV-2. N-methyl-D-Aspartate IgG antibodies were detected. Subsequent 18 F-FDG-PET was performed to identify primary malignancy, which was negative ( C ).
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References

    1. Aaberg K M, Gunnes N, Bakken I J. Incidence and prevalence of childhood epilepsy: a nationwide cohort study. Pediatrics. 2017;139(05):e20163908. doi: 10.1542/peds.2016-3908. - DOI - PubMed
    1. Fine A, Wirrell E C. Seizures in children. Pediatr Rev. 2020;41(07):321–347. doi: 10.1542/pir.2019-0134. - DOI - PubMed
    1. Sultana B, Panzini M A, Veilleux Carpentier A. Incidence and prevalence of drug-resistant epilepsy: a systematic review and meta-analysis. Neurology. 2021;96(17):805–817. doi: 10.1212/WNL.0000000000011839. - DOI - PubMed
    1. Engel J., Jr The current place of epilepsy surgery. Curr Opin Neurol. 2018;31(02):192–197. doi: 10.1097/WCO.0000000000000528. - DOI - PMC - PubMed
    1. Dwivedi R, Ramanujam B, Chandra P S. Surgery for drug-resistant epilepsy in children. N Engl J Med. 2017;377(17):1639–1647. doi: 10.1056/NEJMoa1615335. - DOI - PubMed