Intracranial pressure (ICP) monitoring and control is a cornerstone of neuroanesthesia and neurocritical care. However, because elevated ICP can be due to multiple pathophysiological processes, its interpretation is not straightforward. We propose a formal taxonomy of intracranial hypertension, which defines ICP elevations into 3 major pathophysiological subsets: increased cerebral blood volume, masses and edema, and hydrocephalus. (1) Increased cerebral blood volume increases ICP and arises secondary to arterial or venous hypervolemia. Arterial hypervolemia is produced by autoregulated or dysregulated vasodilation, both of which are importantly and disparately affected by systemic blood pressure. Dysregulated vasodilation tends to be worsened by arterial hypertension. In contrast, autoregulated vasodilation contributes to intracranial hypertension during decreases in cerebral perfusion pressure that occur within the normal range of cerebral autoregulation. Venous hypervolemia is produced by Starling resistor outflow obstruction, venous occlusion, and very high extracranial venous pressure. Starling resistor outflow obstruction tends to arise when cerebrospinal fluid pressure causes venous compression to thus increase tissue pressure and worsen tissue edema (and ICP elevation), producing a positive feedback ICP cycle. (2) Masses and edema are conditions that increase brain tissue volume and ICP, causing both vascular compression and decrease in cerebral perfusion pressure leading to oligemia. Brain edema is either vasogenic or cytotoxic, each with disparate causes and often linked to cerebral blood flow or blood volume abnormalities. Masses may arise from hematoma or neoplasia. (3) Hydrocephalus can also increase ICP, and is either communicating or noncommunicating. Further research is warranted to ascertain whether ICP therapy should be tailored to these physiological subsets of intracranial hypertension.

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OBJECTIVES: Critically ill patients are at high risk of acute brain injury. Bedside multimodality neuromonitoring techniques can provide a direct assessment of physiologic interactions between systemic derangements and intracranial processes and offer the potential for early detection of neurologic deterioration before clinically manifest signs occur. Neuromonitoring provides measurable parameters of new or evolving brain injury that can be used as a target for investigating various therapeutic interventions, monitoring treatment responses, and testing clinical paradigms that could reduce secondary brain injury and improve clinical outcomes. Further investigations may also reveal neuromonitoring markers that can assist in neuroprognostication. We provide an up-to-date summary of clinical applications, risks, benefits, and challenges of various invasive and noninvasive neuromonitoring modalities. DATA SOURCES: English articles were retrieved using pertinent search terms related to invasive and noninvasive neuromonitoring techniques in PubMed and CINAHL. STUDY SELECTION: Original research, review articles, commentaries, and guidelines. DATA EXTRACTION: Syntheses of data retrieved from relevant publications are summarized into a narrative review. DATA SYNTHESIS: A cascade of cerebral and systemic pathophysiological processes can compound neuronal damage in critically ill patients. Numerous neuromonitoring modalities and their clinical applications have been investigated in critically ill patients that monitor a range of neurologic physiologic processes, including clinical neurologic assessments, electrophysiology tests, cerebral blood flow, substrate delivery, substrate utilization, and cellular metabolism. Most studies in neuromonitoring have focused on traumatic brain injury, with a paucity of data on other clinical types of acute brain injury. We provide a concise summary of the most commonly used invasive and noninvasive neuromonitoring techniques, their associated risks, their bedside clinical application, and the implications of common findings to guide evaluation and management of critically ill patients. CONCLUSIONS: Neuromonitoring techniques provide an essential tool to facilitate early detection and treatment of acute brain injury in critical care. Awareness of the nuances of their use and clinical applications can empower the intensive care team with tools to potentially reduce the burden of neurologic morbidity in critically ill patients.

Wernicke’s encephalopathy (WE) is a neurological emergency that results from thiamine deficiency. It is most commonly associated with chronic alcohol consumption but can result from any cause of impaired thiamine absorption or dietary intake. The classic triad of ophthalmoparesis, ataxia, and altered sensorium is rarely seen in toto, and while certain radiographic findings strongly correlate with the disease, one should have a low threshold to suspect (and promptly treat) patients in order to mitigate the risk of morbidity and mortality. However, atypical presentations can result in delayed or missed diagnoses. In this report, we describe a case of severe non-alcoholic WE associated with atypical brain Magnetic resonance imaging (MRI) manifestations of both cortical diffusion restriction and intracranial hemorrhage, which have previously been associated with poor outcomes. Early treatment with high-dose parenteral thiamine resulted in rapid improvement in ocular motility and reversal of MRI abnormalities, and on long-term follow up, the patient had made a marked functional improvement. This case highlights the importance of recognizing these unusual imaging features of WE in a patient with a compatible clinical syndrome in order to make a timely diagnosis and initiate treatment, as there is potential for a good clinical outcome despite these imaging findings.