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Recovery from coma or disordered consciousness is a central issue in patients with acute brain injuries such as stroke, trauma, cardiac arrest, and brain infections. Yet, major gaps remain in the scientific underpinnings of coma and this has led to inaccuracy in prognostication and limited interventions for coma recovery. Even so, recent studies have begun to elucidate mechanisms of consciousness early and prolonged after acute brain injury and some pilot interventions have begun to be tested. The importance and scope of this led in 2019 to the development of the Curing Coma Campaign, an initiative of the Neurocritical Care Society designed to provide a platform for scientific collaboration across the patient care continuum and to empower a community for purposes of research, education, implementation science, and advocacy. Seen as a "grand challenge," the Curing Coma Campaign has developed an infrastructure of scientific working groups and operational modules, along with a 10-year roadmap. [ABSTRACT FROM AUTHOR]

Coma and disordered consciousness are common manifestations of acute neurological conditions and are among the most pervasive and challenging aspects of treatment in neurocritical care. Gaps exist in patient assessment, outcome prognostication, and treatment directed specifically at improving consciousness and cognitive recovery. In 2019, the Neurocritical Care Society (NCS) launched the Curing Coma Campaign in order to address the "grand challenge" of improving the management of patients with coma and decreased consciousness. One of the first steps was to bring together a Scientific Advisory Council including coma scientists, neurointensivists, neurorehabilitationists, and implementation experts in order to address the current scientific landscape and begin to develop a framework on how to move forward. This manuscript describes the proceedings of the first Curing Coma Campaign Scientific Advisory Council meeting which occurred in conjunction with the NCS Annual Meeting in October 2019 in Vancouver. Specifically, three major pillars were identified which should be considered: endotyping of coma and disorders of consciousness, biomarkers, and proof-of-concept clinical trials. Each is summarized with regard to current approach, benefits to the patient, family, and clinicians, and next steps. Integration of these three pillars will be essential to the success of the Curing Coma Campaign as will expanding the "curing coma community" to ensure broad participation of clinicians, scientists, and patient advocates with the goal of identifying and implementing treatments to fundamentally improve the outcome of patients. [ABSTRACT FROM AUTHOR]

Intracerebral hemorrhage (ICH) in patients with oral anticoagulation therapy is an increasingly prevalent problem in large part due to the aging population and the increased use of anticoagulants for patients at high risk of thrombosis. Warfarin has been virtually the only outpatient anticoagulant choice until fairly recently. The development of subcutaneously injected heparinoids, and more recently, of direct thrombin inhibitors, has made the treatment and prognostication of ICH in anticoagulated patients more difficult. In this review, we will review the current state of diagnosis, prognostication, and treatment for patients with this often-devastating type of bleeding. We will focus on warfarin therapy, because the preponderance of evidence comes from studies of warfarin treatment. Where there is evidence, we will contrast warfarin with some of the newer treatment modalities. We review the evidence of the 4 major reversal agents for warfarin, vitamin K, prothrombin complex concentrates, activated factor VII, and fresh frozen plasma as well as rational treatment choices. We offer possible treatments for the newer anticoagulants based on the limited evidence available. Finally, we review recommendations from the major societies and studies that support early and aggressive therapies in intensive care units with dedicated neurological specialists. [ABSTRACT FROM AUTHOR]

Objective: Delayed cerebral ischemia (DCI) is a potentially preventable cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage (aSAH). The authors performed a meta-analysis to assess the effect of antiplatelet therapy (APT) on DCI in patients with aSAH., Methods: A systematic review of the PubMed and MEDLINE databases was performed. Study inclusion criteria were 1) ≥ 5 aSAH patients; 2) direct comparison between aSAH management with APT and without APT; and 3) reporting of DCI, angiographic, or symptomatic vasospasm rates for patients treated with versus without APT. The primary efficacy outcome was DCI. The outcomes of the APT versus no-APT cohorts were compared. Bias was assessed using the Downs and Black checklist., Results: The overall cohort comprised 2039 patients from 15 studies. DCI occurred less commonly in the APT compared with the no-APT cohort (pooled = 15.9% vs 28.6%; OR 0.47, p < 0.01). Angiographic (pooled = 51.6% vs 68.7%; OR 0.46, p < 0.01) and symptomatic (pooled = 23.6% vs 37.7%; OR 0.51, p = 0.01) vasospasm rates were lower in the APT cohort. In-hospital mortality (pooled = 1.7% vs 4.1%; OR 0.53, p = 0.01) and functional dependence (pooled = 21.0% vs 35.7%; OR 0.53, p < 0.01) rates were also lower in the APT cohort. Bleeding event rates were comparable between the two cohorts. Subgroup analysis of cilostazol monotherapy compared with no APT demonstrated a lower DCI rate in the cilostazol cohort (pooled = 10.6% vs 28.1%; OR 0.31, p < 0.01). Subgroup analysis of surgically treated aneurysms demonstrated a lower DCI rate for the APT cohort (pooled = 18.4% vs 33.9%; OR 0.43, p = 0.02)., Conclusions: APT is associated with improved outcomes in aSAH without an increased risk of bleeding events, particularly in patients who underwent surgical aneurysm repair and those treated with cilostazol. Although study heterogeneity is the most significant limitation of the analysis, the findings suggest that APT is worth exploring in patients with aSAH, particularly in a randomized controlled trial setting.

A variety of technologies have been developed to assist decision-making during the management of patients with acute brain injury who require intensive care. A large body of research has been generated describing these various technologies. The Neurocritical Care Society (NCS) in collaboration with the European Society of Intensive Care Medicine (ESICM), the Society for Critical Care Medicine (SCCM), and the Latin America Brain Injury Consortium (LABIC) organized an international, multidisciplinary consensus conference to perform a systematic review of the published literature to help develop evidence-based practice recommendations on bedside physiologic monitoring. This supplement contains a Consensus Summary Statement with recommendations and individual topic reviews on physiologic processes important in the care of acute brain injury. In this article we provide the evidentiary tables for select topics including systemic hemodynamics, intracranial pressure, brain and systemic oxygenation, EEG, brain metabolism, biomarkers, processes of care and monitoring in emerging economies to provide the clinician ready access to evidence that supports recommendations about neuromonitoring.

Delayed deterioration associated with vasospasm (DDAV) after subarachnoid hemorrhage (SAH), (often called vasospasm) continues to be both a difficult entity to treat and a leading cause of morbidity in patients. Until recently, attention was focused on alleviating the vascular spasm. Recent evidence shows that vascular spasm may not account for all the morbidity of DDAV. There is renewed interest in looking for other potential targets for therapy. Inflammation has become a promising area of research for new treatments. This review explores the evidence that inflammation is a driver of DDAV by asking three questions: (1) If inflammation is important in the pathogenesis of the disease, what part or parts of the inflammatory response are involved? (2) When does inflammation occur in SAH? (3) In what compartment of the skull does the inflammation occur, the cerebrospinal fluid and meninges, the cerebral arteries, or the brain itself?

There is increasing evidence that inflammation plays a role in the development of Delayed Deterioration associated with vasospasm (DDAV) after subarachnoid hemorrhage (SAH). Lipopolysaccharide (LPS) is an activator of the innate inflammatory system that causes DDAV in animal models. The effect of low-dose LPS has been shown to be protective in stroke models but has not been investigated in SAH. Two treatments were studied: (1) a single intraperitoneal dose of 0.6 mg/kg injected 24 h prior to SAH and (2) four daily doses administered prior to SAH. DDAV was determined by India ink angiography at day 6; behavioral testing was done in a different cohort of animals, and analysis of brain chemokine levels was accomplished by dot blot. Vessel caliber was improved compared to the SAH group in the single-injection group (ldLPS ×1) (p < 0.05). In the multiple-injection group (ldLPS ×4), the vessel caliber was similar to SAH (p < 0.05). ldLPS ×1 improved performance on the Barnes maze test, whereas the ldLPS ×4 was worse (p < 0.001). Brain levels of the inflammatory chemokine KC (keratinocyte-derived chemokine) were decreased in the ldLPS ×1 and increased in the ldLPS ×4 group. Single-injection low-dose LPS preconditioning was protective for delayed deterioration associated with vasospasm (DDAV), whereas the multiple-injection course exacerbated DDAV. This further supports that inflammation plays an important role in the development of DDAV, and that modulating the inflammatory system may be a potential target for future therapies in SAH.

Aneurysmal subarachnoid hemorrhage is a serious condition with a high morbidity and mortality rate despite advances in neurocritical care. Intraparenchymal monitors providing continuous bedside physiological data have been introduced into the care of the neurocritically ill and are the focus of clinical research. We review the available technology for bedside brain monitoring and the knowledge that has been gathered and its clinical utility by organizing it into 3 main areas: detecting vasospasm early, establishing end points to resuscitation in the management of cerebral vasospasm, and developing insights into the pathophysiology of the disease. Finally, we discuss its implications for the field and future directions.

Subarachnoid hemorrhage (SAH) serves as a good model for the study of heart-brain interactions because it is associated with both a high incidence of arrhythmia and a low prevalence of coronary heart disease. The pathophysiology of cardiac abnormalities in SAH is unsettled. Initial theories focused on sustained stimulation of cardiomyocytes at sympathetic nerve endings, but recent data suggest that dysfunction of the parasympathetic nervous system may contribute as well. We believe that the coupling of catecholamine release with parasympathetic dysfunction may allow unchecked inflammation that leads to myocardial dysfunction and cell death. We have developed a novel murine model of SAH to explore these potential inflammatory underpinnings of cardiac damage in SAH.