CommentaryNeurosurgery has always played an integral role in the management of cerebral trauma but, historically, treatments were limited and mortality and morbidity high. While cerebral trauma remains a leading cause of death worldwide, advancements in basic science injury models, pharmacology, and prevention strategies over the past several decades have resulted in a better understanding of injury mechanisms and have lead to improved outcomes in certain groups. The elucidation of the pathophysiology of secondary brain injury has lead to more targeted therapies; and the establishment of evidence-based guidelines has systematized the management of cerebral trauma, spawning the growth of neurocritical care, multimodal neuromonitoring, and the resurgence of surgical management.Cerebral trauma consists of a heterogeneous group of primary injuries with different causes, presentations, severity, and outcomes, but the final common pathway that leads to the most deleterious effects is that of secondary injury, which involves complex biomechanical and biochemical-triggered cascades that lead to cerebral ischemia, metabolic derangements, inflammation, edema, and cell death. Once cerebral blood flow, and therefore oxygenation, is diminished, neurons depolarize and release excitatory neurotransmitters, such as glutamate, that act at NMDA and AMPA receptors to permit massive influxes of sodium and calcium. The influx of calcium, in particular, activates multiple self-digesting mechanisms that lead to membrane damage, DNA degradation, and ultimately cell death [1]. These processes will often propagate until diffuse ischemia, inflammation, and edema lead to brain herniation and death, unless there is prompt intervention.The goal of neurocritical care is to anticipate the evolution of secondary injury and intervene early. Traditionally, this has been accomplished by measuring intracranial pressure (ICP) with external ventricular drains and parenchymal monitors to derive cerebral perfusion pressure (CPP) by subtracting ICP from mean arterial pressure. The goal has been to keep CPP above an acceptable threshold to ensure adequate cerebral perfusion and oxygenation. While consensus exists for treating ICP greater than 20 mmHg, CPP management has been less straightforward. Some studies have demonstrated improved outcomes with CPP >70 mmHg, whereas several others have not and revealed high rates of pulmonary complications [2]. Currently, the recommended threshold below which CPP should not fall is 50 mmHg, but artificially driving CPP higher than 70 mmHg has fallen out of favor [3]. The difficulty with an ICP and CPP management strategy is that some individuals may benefit from higher or lower CPP values depending upon the nature of their injury. Another complicating factor is that focal injury causing regional metabolic derangements may not be detected by more globally oriented monitoring techniques, such as intracranial pressure monitoring, whereas focal monitoring may not detect the presence of larger areas of injury if the devi...