Neurocritical care
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While the bioethical principle of beneficence originated in antiquity, the ascension of autonomy, or "self-rule," has redefined the physician-patient relationship to the extent that autonomy often dominates medical decision-making. Philosophical and social movements, medical research atrocities, consumerism, and case law have all had their influence on this paradigm shift. Consequently, the contemporary physician encounters an uncertainty in medical practice on how to resolve conflicts that arise in the pursuit of valuing both autonomy and beneficence. ⋯ This conundrum has been an important subject of the bioethics and social science literature but often this discourse is not disseminated to the clinicians confronting these issues. The purpose of this essay is to present a history of the principles of autonomy and beneficence and then present a shared medical decision-making model, collaborative autonomy, to provide guidance to neurologic critical care providers in how to resolve such dilemmas. Clinical vignettes will help illustrate the model.
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Patients suffering from severe traumatic brain injury (TBI) often develop secondary brain lesions that may worsen outcome. S100B, a biomarker of brain damage, has been shown to increase in response to secondary cerebral deterioration. The aim of this study was to analyze the occurrence of secondary increases in serum levels of S100B and their relation to potential subsequent radiological pathology present on CT/MRI-scans. ⋯ Secondary increases in serum levels of S100B, even as low as ≥0.05 μg/L, beyond 48 h after TBI are strongly correlated to the development of clinically significant secondary radiological findings.
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Brain edema is a serious complication of ischemic stroke that can lead to secondary neurological deterioration and death. Glyburide is reported to prevent brain swelling in preclinical rodent models of ischemic stroke through inhibition of a non-selective channel composed of sulfonylurea receptor 1 and transient receptor potential cation channel subfamily M member 4. However, the relevance of this pathway to the development of cerebral edema in stroke patients is not known. ⋯ Several surrogate markers of vasogenic edema appear to be reduced in the setting of IV glyburide treatment in human stroke. Verification of these potential imaging and blood biomarkers is warranted in the context of a randomized, placebo-controlled trial.
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Chronic traumatic encephalopathy (CTE) formerly known as dementia pugilistica is a long-term neurodegenerative disorder associated with repeated subconcussive head injuries in high-contact sports. We reviewed the existing literature on CTE and examined epidemiological trends, risk factors, and its temporal progression, and proposed the underlying pathophysiological mechanisms that may provide unique insights to clinicians with an in-depth understanding of the disease to aid in the diagnosis and prevention, and provide future perspectives for research via search of Medline and Cochrane databases as well as manual review of bibliographies from selected articles and monographs. The prevalence of CTE in recent years is on the rise and almost exclusively affects men, with pathologic signs characterized by progressive memory loss, behavioral changes, and violent tendencies with some patients demonstrating Parkinsonian-like symptoms and signs. ⋯ Postmortem pathologic analysis is characterized by neurofibrillary tangles and Aβ plaques in 50 % of cases. Currently, there are no ante-mortem diagnostic criteria, but modern imaging techniques such as functional magnetic resonance (MR) imaging, MR spectroscopy, and diffusion tension imaging hold promise for delineating the future diagnostic criteria. Further long-term longitudinal studies are warranted to investigate risk factors that will enhance understanding of the disease progression and its pathogenesis.
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Observational Study
Fluid Responsiveness and Brain Tissue Oxygen Augmentation After Subarachnoid Hemorrhage.
The objective of this study was to investigate the relationship between cardiac index (CI) response to a fluid challenge and changes in brain tissue oxygen pressure (PbtO(2)) in patients with subarachnoid hemorrhage (SAH). ⋯ Bolus fluid resuscitation resulting in augmentation of CI can improve cerebral oxygenation after SAH.