Review ArticleContinuing Education

The Role of Radionuclide Imaging in Epilepsy, Part 1: Sporadic Temporal and Extratemporal Lobe Epilepsy

Ajay Kumar and Harry T. Chugani
Journal of Nuclear Medicine October 2013, 54 (10) 1775-1781; DOI: https://doi.org/10.2967/jnumed.112.114397

Article Figures & Data

Figures

  • FIGURE 1.
    FIGURE 1.

    Axial 18F-FDG PET scan in patient with intractable epilepsy, showing hypometabolism in left frontotemporal cortex (solid arrows). Also seen is hypometabolism in ipsilateral thalamus (broken arrow) and contralateral cerebellum (arrowhead), likely representing thalamic and cerebellar diaschisis, respectively.

  • FIGURE 2.
    FIGURE 2.

    SPM analysis of 18F-FDG PET scan in child with intractable epilepsy, normal findings on MR imaging, and generalized electroencephalogram changes. Initial reading showed normal findings on 18F-FDG PET; however, SPM analysis revealed area of hypometabolism in left medial frontal/cingulate cortex (left image), which appeared to be suggestive/hypometabolic in rereview of 18F-FDG PET scan (arrow; right image). Child underwent 2-stage epilepsy surgery with intracranial subdural interhemispheric electrode placement, which showed ictal discharges from this region. These medial discharges perhaps resulted in generalized (nonlateralized) electroencephalogram changes. Area was resected and child is seizure-free after surgery.

  • FIGURE 3.
    FIGURE 3.

    11C-flumazenil PET (left image) showing focal abnormality (decreased tracer binding) involving right hippocampus (solid arrow) in patient with medial temporal lobe epilepsy. In comparison, 18F-FDG PET (right image) shows widespread 18F-FDG hypometabolism in right temporal lobe, including neocortex (broken arrows).

  • FIGURE 4.
    FIGURE 4.

    Interictal 99mTc-ethyl cysteinate dimer SPECT (left image) showing the usual hypoperfusion in presumed epileptogenic focus (arrow) in left frontal cortex region, which becomes hyperperfused during ictal SPECT (right image).

  • FIGURE 5.
    FIGURE 5.

    Axial 18F-FDG PET scan showing subcortical band heterotopia (arrows) in right temporal–occipital white matter in child with intractable epilepsy and normal MR imaging findings. Heterotopic band has higher glucose uptake than adjacent white matter but lower uptake than cortex.

  • FIGURE 6.
    FIGURE 6.

    11C-α-methyl-l-tryptophan PET scan (middle image) showing increased tracer uptake in left parietal lobe (arrow) in child with intractable epilepsy and normal findings on MR imaging (left image). Postsurgical histopathology (right image) revealed type IIB cortical dysplasia with balloon cells (×40, hematoxylin and eosin). Child remains seizure-free after epilepsy surgery.

  • FIGURE 7.
    FIGURE 7.

    SISCOM may result in better delineation of epileptogenic focus, which may sometimes be missed even on ictal SPECT. In child with intractable complex partial epilepsy with normal findings on MR imaging and nonlocalizing scalp electroencephalography, SISCOM revealed focus of hyperperfusion in left inferior frontal cortex (red cross), likely representing seizure focus.

Tables

  • TABLE 1

    Targeted Pathways, Used Radiotracers, and Their Usual Uptake Pattern in Epileptogenic Region

    TargetUsed radiotracersUptake pattern in epileptogenic region
    Blood perfusion15O-H2O, 99mTc-ethyl cysteinate dimer, 99mTc-hexamethyl propyleneamine oximeInterictal decrease; ictal increase
    Metabolic pathways
     Glucose metabolism18F-FDGInterictal decrease*; ictal increase
     Serotonin/kynurenine metabolism11C-α-methyl-l-tryptophanInterictal increase
     Dopamine synthesis18F-l-DOPA†Interictal decrease
     Monoamine oxidase11C-deuterium-deprenyl‡Interictal increase
    Receptors
     Benzodiazepine11C-flumazenil§
     Opiate11C-carfentanil∥, 18F-cyclofoxy, 11C-diprenorphine#, 11C-methylnaltrindole**Interictal increase; interictal decrease
     5-hydroxytryptamine18F-FCWAY††, 11C-WAY††, 18F-MPPF††Interictal decrease
     Dopamine18F-fallypride‡‡, 11C-SCH23390§§Interictal decrease
     Peripheral benzodiazepine or translocator protein11C-PK11195∥∥, 11C-PBR28∥∥Interictal increase
     Histamine11C-doxepin¶¶Interictal increase
     N-methyl-d-aspartic acid11C-ketamine##Interictal decrease
     Acetylcholine18F-FA85380***Interictal decrease

    • FCWAY = trans-4-fluoro-N-2-[4-(2-methoxyphenyl) piperazin-1-yl] ethyl-N-(2-pyridyl) cyclohexanecarboxamide; MPPF = 4-18F-fluoro-N-(2-[4-(2-methoxyphenyl)-l-piperazinyl]ethyl)-N-(2-pyridinyl)benzamide; l-DOPA = l-3,4-dihydroxyphenylalanine (levodopa); PK11195 = 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinoline carboxamide; PBR28 = N-acetyl-N-(2-[11C-methoxybenzyl)-2-phenoxy-5-pyridinamine.

    • ↵* Can show increased uptake if continuous spiking (interictal) or epileptiform discharges (ictal).

    • ↵† Acts on dopamine receptors.

    • ↵‡ Monoamine oxidase-B inhibitor.

    • ↵§ γ-aminobutyric acid A benzodiazepine receptor.

    • ↵∥ μ-receptor agonist.

    • ↵ μ and κ antagonist.

    • ↵# μ-, δ- and κ-receptor antagonist.

    • ↵** δ-receptor antagonist.

    • ↵†† 5HT1A antagonist.

    • ↵‡‡ D2/D3 antagonist.

    • ↵§§ D1 antagonist.

    • ↵∥∥ Peripheral benzodiazepine receptor or translocator protein antagonist.

    • ↵¶¶ 1H receptor antagonist.

    • #NMDA antagonist.

    • ↵*** α4/β2 nAChR agonist.

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