EL CEREBRO Y EL COVID-19 Un mundo desconocido en peligro

En los primeros meses de la pandemia de COVID-19, los médicos han luchado por mantener la respiración de los pacientes y se han concentrado principalmente en tratar los daños en los pulmones y el sistema circulatorio.Sin embargo, se está acumulando evidencias de efectos neurológicos por este virus, cuyos científicos están luchando por saber por qué aparecen estos síntomas en particular. Se han descrito algunos cuadros clínicos de personashospitalizadas con COVID-19 experimentando delirio: estaban confundidas, desorientadas y agitadas La lista ahora incluye accidente cerebrovascular,hemorragia cerebral y pérdida de memoria

COVID-19: ICU delirium management during SARS-CoV-2 pandemic

The novel coronavirus, SARS-CoV-2-causing Coronavirus Disease 19 (COVID-19), emerged as a public health threat in December 2019 and was declared a pandemic by the World Health Organization in March 2020. Delirium, a dangerous untoward prognostic development, serves as a barometer of systemic injury in critical illness. The early reports of 25% encephalopathy from China are likely a gross underestimation, which we know occurs whenever delirium is not monitored with a valid tool. Indeed, patients with COVID-19 are at accelerated risk for delirium due to at least seven factors including (1) direct central nervous system (CNS) invasion, (2) induction of CNS inflammatory mediators, (3) secondary effect of other organ system failure, (4) effect of sedative strategies, (5) prolonged mechanical ventilation time, (6) immobilization, and (7) other needed but unfortunate environmental factors including social isolation and quarantine without family. Given early insights into the pathobiology of the virus, as well as the emerging interventions utilized to treat the critically ill patients, delirium prevention and management will prove exceedingly challenging, especially in the intensive care unit (ICU). The main focus during the COVID-19 pandemic lies within organizational issues, i.e., lack of ventilators, shortage of personal protection equipment, resource allocation, prioritization of limited mechanical ventilation options, and end-of-life care. However, the standard of care for ICU patients, including delirium management, must remain the highest quality possible with an eye towards long-term survival and minimization of issues related to post-intensive care syndrome (PICS). This article discusses how ICU professionals (e.g., physicians, nurses, physiotherapists, pharmacologists) can use our knowledge and resources to limit the burden of delirium on patients by reducing modifiable risk factors despite the imposed heavy workload and difficult clinical challenges posed by the pandemic

Covert Consciousness and Traumatic Brain Injury Prognostication: The Acute Care Perspective

Traumatic brain injury (TBI) remains a major cause of death and disability in the United States and beyond. Loss of consciousness is common after TBI but is usually transient. Assessment of level of consciousness is of paramount clinical relevance in the acute setting after TBI, as it influences important decisions about approaches to care and is a key factor in determining prognosis. The bedside neurologic examination is currently the gold standard for consciousness assessment in acute TBI. While this provides a window into the extent of brain injury, it relies on the capability of a patient to demonstrate overt clinical responses that are identified by the examiner. Reliance on overt behaviors to determine level of consciousness is problematic because a variety of factors (e.g., sedation, intoxication, polytrauma) may confound the assessment, leading to misdiagnosing a conscious patient as being unconscious. The term covert consciousness refers to a state of awareness not detectable using traditional bedside neurobehavioral tests but that is detectable via task-based functional magnetic resonance imaging (fMRI) or electroencephalography (EEG). In this narrative review, we will describe techniques to detect both overt and covert consciousness after TBI. In particular, we will address use of the behavioral exam, EEG, fMRI, and other tools to identify consciousness and/or predict its recovery after severe TBI starting in the acute setting

Pathomechanisms of Non-Traumatic Acute Brain Injury in Critically Ill Patients

Delirium, an acute alteration in mental status characterized by confusion, inattention and a fluctuating level of arousal, is a common problem in critically ill patients. Delirium prolongs hospital stay and is associated with higher mortality. The pathophysiology of delirium has not been fully elucidated. Neuroinflammation and neurotransmitter imbalance seem to be the most important factors for delirium development. In this review, we present the most important pathomechanisms of delirium in critically ill patients, such as neuroinflammation, neurotransmitter imbalance, hypoxia and hyperoxia, tryptophan pathway disorders, and gut microbiota imbalance. A thorough understanding of delirium pathomechanisms is essential for effective prevention and treatment of this underestimated pathology in critically ill patients

Brain-wide human oscillatory local field potential activity during visual working memory

Summary: Oscillatory activity in the local field potential (LFP) is thought to be a marker of cognitive processes. To understand how it differentiates tasks and brain areas in humans, we recorded LFPs in 15 adults with intracranial depth electrodes, as they performed visual-spatial and shape working memory tasks. Stimulus appearance produced widespread, broad-band activation, including in occipital, parietal, temporal, insular, and prefrontal cortex, and the amygdala and hippocampus. Occipital cortex was characterized by most elevated power in the high-gamma (100–150 Hz) range during the visual stimulus presentation. The most consistent feature of the delay period was a systematic pattern of modulation in the beta frequency (16–40 Hz), which included a decrease in power of variable timing across areas, and rebound during the delay period. These results reveal the widespread nature of oscillatory activity across a broad brain network and region-specific signatures of oscillatory processes associated with visual working memory

Effect of propranolol and clonidine after severe traumatic brain injury: a pilot randomized clinical trial

Abstract Objective To evaluate the safety, feasibility, and efficacy of combined adrenergic blockade with propranolol and clonidine in patients with severe traumatic brain injury (TBI). Background Administration of adrenergic blockade after severe TBI is common. To date, no prospective trial has rigorously evaluated this common therapy for benefit. Methods This phase II, single-center, double-blinded, pilot randomized placebo-controlled trial included patients aged 16–64 years with severe TBI (intracranial hemorrhage and Glasgow Coma Scale score ≤ 8) within 24 h of ICU admission. Patients received propranolol and clonidine or double placebo for 7 days. The primary outcome was ventilator-free days (VFDs) at 28 days. Secondary outcomes included catecholamine levels, hospital length of stay, mortality, and long-term functional status. A planned futility assessment was performed mid-study. Results Dose compliance was 99%, blinding was intact, and no open-label agents were used. No treatment patient experienced dysrhythmia, myocardial infarction, or cardiac arrest. The study was stopped for futility after enrolling 47 patients (26 placebo, 21 treatment), per a priori stopping rules. There was no significant difference in VFDs between treatment and control groups [0.3 days, 95% CI (− 5.4, 5.8), p = 1.0]. Other than improvement of features related to sympathetic hyperactivity (mean difference in Clinical Features Scale (CFS) 1.7 points, CI (0.4, 2.9), p = 0.012), there were no between-group differences in the secondary outcomes. Conclusion Despite the safety and feasibility of adrenergic blockade with propranolol and clonidine after severe TBI, the intervention did not alter the VFD outcome. Given the widespread use of these agents in TBI care, a multi-center investigation is warranted to determine whether adrenergic blockade is of therapeutic benefit in patients with severe TBI. Trial Registration Number NCT01322048