 Good evening, I'll be presenting a study on the evaluation of post-ictal MRI changes. The first description of focal peri-ictal hyperpropylution is from the 1930s by Ips and Benfit. In the 1960s, a study utilizing hemocycolograms noted that focal-ictal activity is in one hemisphere could result in ipsilateral cerebral edema with subsequent cerebral atrophy and ventricular dilatation. Seizures are known to occur in 10% of the population during their lifetime. In addition, peri-ictal neurologic deficits and neurological imaging findings of cerebral cortical-teto-hyperintensity and diffusion restriction are well-known mimics of other CNS diseases such as stroke. Also, pre- and post-ictal changes on both anatomic and functional imaging examination have been recognized in many years. Although an exact explanation of these imaging abnormalities is still unclear, seizure-related changes on various imaging studies are believed to be a reflection of the physiologic operation concerning seizure activity. According to the wide range of possible seizure-related lesions on neuro-imaging studies, various disease entities are considered as a differential diagnosis, resulting in a potential risk of misdiagnosis and incorrect clinical management. Hence, there is a necessity to differentiate whether neuro-imaging abnormalities in patients with seizure are caused by seizure itself or other underlying pathological conditions such as stroke. With the wide availability of MRI and PET, a growing range of recognized acute imaging findings can be classified as either local or remote with respect to sight of maximal e.e.g. abnormality. The aim of this study was to evaluate the pattern and distribution of MRI signal changes in patients with immediate post-ictal period. The materials and method, this is a retrospective study carried out in our institution between August 2020 to August 2021. The records of post-ictal signal changes on MRI brain were extracted from radiology department database. The inclusion criteria is all patients with history of seizure who have undergone MRI brain within 24 hours of onset of seizure. Exclusion criteria included the patients with metabolic disorders, tumors, HIE, genital malformations, infections, and genetic abnormalities were excluded. MRI brain performed after 24 hours of the onset of seizure was also excluded. A total of 10 patients were included in the study after the inclusion and exclusion criteria was met. All patients underwent MRI brain at our institution and the imaging was carried out with the Simmons magneton SNSR 1.5 Tesla MRI standard. The sequences included axial T1 weighted, axial coronal and sagittal T2 weighted, axial and coronal flare, axial DWI and EDC maps and SWI sequences. Imaging analysis, evaluation of signal changes, location of the region, and evidence of any diffusion restriction on DWI and EDC maps was done. The population characteristic, the mean age of the patients was about 7.6 years, Imaging from 2 months to 16 years of age showed a male predominance with male to female ratio of 9 to 1. Clinical presentation, seizure, the status epilepticus was seen in 4 cases, a gentler isoclonic-clonic seizure was seen in 3, focal seizures were seen in 3 cases, and fever was seen in about 2 of the 10 patients. The average time from seizure onset to MR imaging was about 10.1 hours. The imaging features in our study is 7 out of 10 patients had cortical and sub-cortical areas of altered signal intensity, which appeared as T2 and flare hypersintensity in 4 cases. The same cases in the 2 cases, 2 cases of which showed the T1 hypointensity, diffusion restriction was seen in 7 cases, unilateral involvement was seen in 20% cases and bilateral involvement was seen in 50% cases. No single low bar cortical region was observed in the study. And the rest of the 3 patients out of 10 patients had hippocampal involvement, wherein T2 flare hypersintensity was seen in 1 case, diffusion restrictions were seen in 1 case and the hippocampus appeared bulky in 1. Followed in imaging was done in 2 cases, after 1 was done after 4 days after initial imaging and the other was done after 10 days. Contest study was done in 2 cases and no abnormal enhancement was seen. MRA was also done in 2 cases, which turned out to be normal. This is the case of a 2-year-old male patient with complaints of generalized cologic seizures. On T2 and flare images, you can see that there are bilateral and symmetrical hyperintensities in the frontal and parietal lobes. This area shows diffusion restriction on DWI and EDC maps. This is another case of a 10-year-old patient with history of repeated seizures. Here, you can see areas of restricted diffusion in the frontal, bilateral, frontal, parietal lobes, which are symmetrical in distribution. This is another case of a 16-year-old male patient with history of status epilepticus. This is the initial imaging which showed areas of hyperintensity in this DWI image. This is a follow-up imaging done 4 days later. You can see that these hyperintensities are disappeared. So therefore, these suggest that these signal changes are only transient. This is another case of a 12-year-old male patient who shows that the hippocampus might be bulky on the right side and there is asymmetry between the hippocampus. So a discussion, MR signal changes in patients with status epilepticus has been reported previously. These signal changes are likely to be caused by vasogenic or cytotoxic edema, increased permeability, loss of auto-regulation, regional ischemia, excitotoxicity, which is seen as areas of hyperintensity on D2 and flare images, a cortical gray matter or a sub-cortical white matter, variable alteration in the DWI and EDC maps, mild mass effect, no contrast enhancement. The findings of this study was consistent with the previous study with seizure-related cortical abnormalities with our study showing seven out of 10 patients with the cortical abnormalities. Hippocampus was a common location of seizure-induced brain abnormality, has been very documented. In our study, there are three out of 10 cases which show hippocampal involvement. Previous studies have also suggested the thalamus to be also involved in various epilepsy syndromes. To conclude, MRI signal changes seen in the immediate post-ticular period are hyper-intense signal on D2 weighted and diffusion weighted images in the cortical gray matter and sub-cortical white matter or the hippocampus. The typical distribution of these lesions can help exclude the epileptogenic structural lesions. Therefore, our awareness of clinical and radiological findings can help to differentiate seizure-related cortical lesions from other CNS disorders and reducing the risk of inappropriate management and chain to practice. These are my references. Thank you.