Status epilepticus is associated with significant morbidity and mortality. Neuroimaging is a diagnostic tool used to exclude structural abnormalities as an etiology of status epilepticus. During the early era of computed tomographic scanning, it was recognized that reversible changes can be observed after a prolonged episode of focal status epilepticus. Many case reports in the literature describe structural changes identified by magnetic resonance imaging (MRI) . In status epilepticus, intrinsic neuronal activity results in the release of excessive glutamate in the synaptic cleft, causing cytotoxic edema in neurons and astrocytes. In the initial phase of injury, there is an increase in the water content of glial cells and astrocytes, which is identifiable as hyperintense lesions on conventional T2-weighted images because T2 relaxation time is dependent on local brain water content. Conversely, diffusion is an independent property of intact cell and diffusion-weighted imaging (DWI) remains independent of T2 relaxation times. With further intrinsic cytotoxic injury, there is a reduction in diffusion that manifests on MRI as an increase in signal intensity on DWI and a relative decrease in apparent diffusion coefficient (ADC). In addition, reversible focal gyral effacement, leptomeningeal enhancement, deep gray matter nuclei signal changes, lesions in corpus callosum, and hyperperfusion on magnetic resonance angiography have been described as reversible peri-ictal findings .