Burst-suppression electroencephalography (EEG) patterns of electrical activity, characterized by intermittent high-power broad-spectrum oscillations alternating with isoelectricity, have long been observed in the human brain during general anesthesia, hypothermia, coma and early infantile encephalopathy. Recently, commonalities between conditions associated with burst-suppression patterns have led to new insights into the origin of burst-suppression EEG patterns, their effects on the brain, and their use as a therapeutic tool for protection against deleterious neural states. These insights have been further supported by advances in mechanistic modeling of burst suppression. In this Perspective, we review the origins of burst-suppression patterns and use recent insights to weigh evidence in the controversy regarding the extent to which burst-suppression patterns observed during profound anesthetic-induced brain inactivation are associated with adverse clinical outcomes. Whether the clinical intent is to avoid or maintain the brain in a state producing burst-suppression patterns, monitoring and controlling neural activity presents a technical challenge. We discuss recent advances that enable monitoring and control of burst suppression.

Neurofilament light (NfL) is a scaffolding protein that is located primarily within myelinated axons and that provides increased conduction speed and structural support. In recent years, NfL has been used as a disease biomarker on the basis of the observation that axonal injury results in elevated levels of NfL in cerebrospinal fluid or blood. This review focuses on how cerebrospinal fluid and plasma NfL have been studied in various disorders such as Alzheimer’s disease (AD) and multiple sclerosis (MS) in relation to neuroinflammation and cognitive dysfunction. Focusing on the role of NfL as a biomarker for AD and MS, this review aims to further explore the potential of NfL as a promising biomarker with regard to surgery- and anesthesia-based incidents for postoperative cognitive decline and delirium. A search of the PubMed database yielded 36 articles, 31 of which are from within the last 3 years, that show how NfL has been observed and studied under various types of trials and disease cohorts and potential future directions. Higher levels of NfL have frequently been correlated with disease progression and prognosis of AD and MS, and delirium has been found to share a neuroinflammatory pathophysiology that NfL could help to measure. Focusing on NfL as a biomarker for neurodegenerative decline, these studies indicate that the protein could be further tested and related to postoperative aspects that result in cognitive dysfunction, and it has the potential to be an established delirium biomarker, particularly in the realm of the perioperative course.

No abstract

No abstract