SUMMARYStatus epilepticus or other brain-damaging insults launch a cascade of events that may lead to the development of epilepsy. MRI techniques available today, including T 2 -and T 1 -weighted imaging, functional MRI, manganese enhanced MRI (MEMRI), arterial spin labeling (ASL), diffusion tensor imaging (DTI), and phase imaging, can detect not only damage caused by status epilepticus but also plastic changes in the brain that occur in response to damage. Optimal balance between damage and recovery processes is a key for planning possible treatments, and noninvasive imaging has the potential to greatly facilitate this process and to make personalized treatment plans possible. KEY WORDS: Arterial spin labeling MRI, Diffusion MRI, Neurodegeneration, Manganese-enhanced MRI, Fractional anisotropy.Status epilepticus or other brain-damaging insults launch a cascade of events that may lead to the development of epilepsy. Noninvasive detection of these often progressive changes would have great value for improving our understanding of the basic pathophysiologic mechanisms of epileptogenesis and for finding novel treatment strategies to prevent epilepsy. Magnetic resonance imaging (MRI) is probably the most versatile noninvasive imaging modality available to study different aspects of these progressive changes in vivo. In addition to structural changes, contemporary MRI techniques are also able to assess, for example, axonal reorganization, brain function, blood flow, and metabolism (Table 1). Our special interest in recent years has been to develop MRI approaches for the detection of plastic recovery processes in the brain. Initial damage not only launches progressive damage but also enhances brain plasticity as a recovery mechanism. Optimal balance between damage and recovery processes is a key for planning possible treatments, and noninvasive imaging has the potential to greatly facilitate this process, and to make personalized treatment plans possible.The time period during (prolonged status epilepticus) and immediately after status epilepticus is associated with cytotoxic edema (disturbance of water balance between intracellular and extracellular compartments), which causes decreased diffusion of the water in the tissue. This can be detected by diffusion MRI and is most often described by using an orientation independent measure of water diffusion (several different abbreviations are used in literature including Trace D, D av , ADC av , mean diffusivity MD; accurately one third of the trace of the diffusion tensor). This is followed by a net accumulation of water during the following days due to vasogenic edema and can typically be assessed using T 2 -or T 1 -weighted MRI in which contrast peaks 24-48 h after the insult begins (Fig. 1A,B). Reabsorption of water decreases the relaxation-based MRI contrast. Consequently, MRI visibility of the lesion can be low during the following weeks. A secondary increase in signal intensity in T 2 -weighted (or decrease in T 1 -weighted) MRI and increased mean diffusivity can be...