Fasting has been thought for millennia to be useful for the treatment of many diseases including epilepsy. This notion was confirmed by researchers in the early 20th century. This finding among others gave rise to the ketogenic diet. Ketogenic diets, which can be described as a high fat, adequate protein, and low carbohydrate diet, have had a resurgence in recent decades for the treatment of drug resistant epilepsy in bothg children and adults. More recently there have been more liberal versions of the diet created such as the MCT KD, Modified Atkins Diet (MAD), Low Glycemic Index Treatment (LGIT) and these seem to show similar efficacy to the classical ketogenic diet. Even more recent is the development of exogenous ketone bodies in the form of salts and esters that can be administered without necessarily having to change diet to reach therapeutic blood levels. Research is now showing promising applications to other neurologic diseases. In particular I will focus on the KD and exogenous ketone bodies in the treatment of neurotrauma and ischemic stroke. I will review the pathophysiology of these diseases. I will review the relevant animal data and the limited human data. I will discuss the theoretical and known neuroprotective mechanisms of the ketogenic diet and ketone bodies in the nervous system. Briefly these mechanisms include replenishing neuronal energy stores, lowering reactive oxygen species, increasing antioxidant and anti-inflammatory pathways, and decreasing apoptosis. I will finish by discussing the possible ways they could be implemented clinically and also the limitations and barriers to use.