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Epileptic Disorders

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Serial EEG and MRI changes in status epilepticus-induced excitotoxic neuronal necrosis Volume 13, issue 4, December 2011



Figure 1 (A) First day: normal findings on postcontrast T1 (2), T2 (3) and diffusion weighted images (4). There is subtle cortical hyperintensity on FLAIR images (1). (B) Fourth day: diffuse signal increase in FLAIR (1) and T2 weighted image (2) and signal decrease in postcontrast T1 weighted image (3) and diffusion restriction (4) in left cortical areas. Increased left cerebrum volume with shift to the right hemisphere in ADC (5). Left hemispheric vascular signal asymmetry on collapsed 3D TOF image (6). (C) Thirteenth day: pial enhancement on postcontrast T1 (1), signal changes on FLAIR (2), diffusion weighted images (3), hyperperfusion on left cerebrum in rCBF (4) and decreased NAA, mioinositol, increased choline, glutamine-glutamate, lactate on short TE single voxel proton spectroscopy (5). (D) Cortical laminar necrosis plus basal ganglia and thalamus necrosis on T1 weighted image (1), prominent cerebral atrophy on T2 weighted image (2), reversed vascular changes on collapsed 3D TOF image (3), and decrease in all metabolite peaks except choline on short TE proton spectroscopy (4).



Figure 2 (A) Pre-status epilepticus EEG with rare left prominent centrotemporal spikes. (B) First day EEG: generalised slowing with left frontal sharp waves. (C) Third day: left hemispheric PLEDs.



Figure 3 Fourth day EEG: resolution of PLEDs, voltage depression on the left side.



Figure 4 (A) Selective neuronal necrosis, perikaryal vacuoles, perineural satellitosis and cytotoxic/vasogenic oedema, with intact vascular structure (H&E: x200 original magnification). (B) Surviving viable neurons with observable chromogranin reactivity (biotinylated streptavidin complement; chromogranin, x400 original magnification).