Table 1.
Imaging modality | Animal model | Potential biomarker | Related pathophysiology |
---|---|---|---|
MRI—T2 signal | Post-SE, FPI, kindling, FS | Acute T2 signal increase and T2W hyperintensity | Edema, gliosis, cell loss |
MRI—volumetrics | Post-SE, FPI | Decreased volume of limbic structures (i.e., hippocampus) | Structural atrophy |
MRI—contrast agents | Post-SE | Mn2+- and Gd3+-enhanced signal change | Mossy fibers and BBB breakdown |
DWI | Post-SE, FPI, absence epilepsy, FS | Altered ADC, FA, and tractography | Edema, axonal injury, connectivity |
MRS | Post-SE | Reductions in glutamate, glutamine, GABA, and NAA, and increased myo-inositol and glutathione | Neurotransmitters, neuronal death and dysfunction, glia activation |
PET | Post-SE, FPI | Decreases in [18F]FDG–PET signal, increases in [18F]PBR111–PET signal | Hypometabolism, inflammation |
fMRI | Post-SE, absence epilepsy | Changes in BOLD signal | Neuronal activity and metabolism |
MRI = magnetic resonance imaging; DWI = diffusion-weighted MRI; MRS = magnetic resonance spectroscopy; PET = positron emission tomography; fMRI = functional MRI; SE = status epilepticus; FPI = fluid percussion brain injury; FS = febrile seizure; T2W = T2-weighted; ADC = apparent diffusion coefficient; FA = Fractional anisotropy; GABA = gamma-aminobutyric acid; NAA = N-acetyl aspartate; BOLD = blood oxygen level-dependent; BBB = blood–brain barrier