Introduction he overall aims of neuromonitoring are to: 1) identify worsening neurological function and secondary cerebral insults that may benefit from specific treatment(s); 2) improve pathophysiological understanding of cerebral disease in critical illness; 3) provide clear physiological data to guide and individualize therapy; 4) assist with prognostication. In this article, we will outline the neuro- monitoring techniques currently in use in critically ill patients and suggest how they should be best applied to help us care for such patients. We will focus on clinically available techniques and not discuss new approaches that are still largely in the research stage of development. Pathophysiology of acute brain injury he pathophysiology of acute brain injury is complex and can involve several secondary pathological cascades that contribute to aggravate neuronal injury (Figure 1). he clinical rationale for neuromonitoring is to tailor therapy to patient-specific pathophysiology rather than to predefined thresholds or targets. It is thus important to briefly review some basic aspects of brain physiology to help understand the techniques and applications of neuromonitoring. Cerebral metabolism he human brain constitutes 2% of body weight, yet the energy-consuming processes that enable adequate brain function account for about 25% of total body energy expenditure and 20% of the oxygen consumption of the whole organism. Glucose is the main energy substrate of the brain and, given the low glycogen stores in the brain, brain glucose levels are highly dependent on blood glucose. Transport of glucose from the systemic circu- lation to the brain is a tightly regulated process mediated by specialized cell membrane glucose transporters (GLUT). Experimental and human studies show evidence of flow-metabolism uncoupling and increased glucose utilization after acute brain injury (‘cerebral hyper- glycolysis’). Importantly, this occurs in the absence of low cerebral blood flow (CBF) and cerebral ischemia and may lead to a state of reduced availability of the main energy substrate (glucose) with a subsequent risk of cerebral energy dysfunction [1,2]. However, hyperglycolysis also results in increased processing of glucose to pyruvate by astrocytes and conversion to lactate. Endogenous lactate, released in the extracellular space, can in turn be transferred, via specific monocarboxylate transporters, to neurons (a process known as the ‘astrocyte-neuron lactate shuttle’) [3]. Brain lactate may thus be used as an alternative aerobic energy substrate to glucose [4]. Indeed, studies in subarachnoid hemorrhage (SAH) Abstract Critically ill patients are frequently at risk of neurological dysfunction as a result of primary neurological conditions or secondary insults. Determining which aspects of brain function are afected and how best to manage the neurological dysfunction can often be diicult and is complicated by the limited information that can be gained from clinical examination in such patients and the efects of therapies, notably sedation, on neurological function. Methods to measure and monitor brain function have evolved considerably in recent years and now play an important role in the evaluation and management of patients with brain injury. Importantly, no single technique is ideal for all patients and diferent variables will need to be monitored in diferent patients; in many patients, a combination of monitoring techniques will be needed. Although clinical studies support the physiologic feasibility and biologic plausibility of management based on information from various monitors, data supporting this concept from randomized trials are still required. © 2010 BioMed Central Ltd Neuromonitoring: an update {AU query: is this a Clinical review or Bench-to-bedside review?} Nino Stocchetti 1 , Peter Le Roux 2 , Paul Vespa 4 , Mauro Oddo 4 , Giuseppe Citerio 5 , Peter J Andrews 6 , Robert D Stevens 7 , Tarek Sharshar 8 , Fabio S Taccone 9 and Jean-Louis Vincent 9 REVIEW *Correspondence: {AU query: please indicate who is the corresponding author and provide an email address for correspondence} 1 Milan University, Terapia Intensiva Neuroscienze, Fondazione IRCCS Ca’ Granda, Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122 Milano, Italy Stocchetti et al. Critical Care 2012, 16:N http://ccforum.com/content/16/X/N © 2012 BioMed Central Ltd