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Relevant bibliographies by topics / Brain death

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Academic literature on the topic 'Brain death'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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Journal articles on the topic "Brain death"

1

McMahan, Jeff. "An Alternative to Brain Death." Journal of Law, Medicine & Ethics 34, no. 1 (2006): 44–48. http://dx.doi.org/10.1111/j.1748-720x.2006.00007.x.

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Most contributors to the debate about brain death, including Dr. James Bernat, share certain assumptions. They believe that the concept of death is univocal, that death is a biological phenomenon, that it is necessarily irreversible, that it is paradigmatically something that happens to organisms, that we are human organisms, and therefore that our deaths will be deaths of organisms. These claims are supposed to have moral significance. It is, for example, only when a person dies that it is permissible to extract her organs for transplantation.It is also commonly held that our univocal notion of death is the permanent cessation of integrated functioning in an organism and that the criterion for determining when this has occurred in animals with brains is the death of the brain as a whole – that is, brain death. The reason most commonly given for this is that the brain is the irreplaceable master control of the organism's integration.

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Hills, Teresa E. "Brain death." Nursing 54, no. 8 (July 19, 2024): 17–23. http://dx.doi.org/10.1097/nsg.0000000000000038.

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Abstract: The incidence of brain death/death by neurologic criteria (BD/DNC) among all hospital deaths in the US is approximately 2.06% or 15,000-20,000 cases annually. This article reviews the latest guidelines for adult and pediatric BD/DNC. Although there have not been many changes to the guidelines over the years, BD/DNC guideline updates maintain consistency in determining BD/DNC.

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MORRAY, JEFFREY P., ELLIOT J. KRANE, ANNE M. LYNN, and DONALD C. TYLER. "Brain Death?" Pediatrics 79, no. 6 (June 1, 1987): 1057. http://dx.doi.org/10.1542/peds.79.6.1057.

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To the Editor.— Because we are now able to provide long-term cardio-pulmonary support, the determination of cerebral death in children is a critical issue, both to provide an unambiguous diagnosis of death and, when appropriate, to allow recovery of organs for transplantation. Perhaps this latter issue provided the impetus for Drake et al1 to evaluate their recent experience at Loma Linda and to present a protocol for the determination of brain death in children.

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Pope, Thaddeus Mason. "Brain Death." Chest 148, no. 2 (August 2015): e69. http://dx.doi.org/10.1378/chest.15-0973.

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Kaufman, H. H., and J. Lynn. "Brain death." Neurosurgery 19, no. 5 (November 1986): 850???6. http://dx.doi.org/10.1097/00006123-198611000-00025.

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Evans, D. W. "Brain death." BMJ 325, no. 7364 (September 14, 2002): 598a—598. http://dx.doi.org/10.1136/bmj.325.7364.598/a.

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Hannegan, Lisa. "Brain death." Critical Care Nursing Quarterly 10, no. 3 (December 1987): 83–91. http://dx.doi.org/10.1097/00002727-198712000-00010.

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Elliot, J. "Brain death." Trauma 5, no. 1 (January 1, 2003): 23–42. http://dx.doi.org/10.1191/1460408603ta254oa.

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Dries, David J. "BRAIN DEATH." Shock 30, no. 4 (October 2008): 481. http://dx.doi.org/10.1097/shk.0b013e318189067f.

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Frost, Elizabeth A. M. "Brain Death." Journal of Neurosurgical Anesthesiology 13, no. 4 (October 2001): 340–41. http://dx.doi.org/10.1097/00008506-200110000-00014.

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Dissertations / Theses on the topic "Brain death"

1

Martinez, Bermudez Ana Katherine. "Isoprostanes in brain endothelial cell death." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0025/MQ50832.pdf.

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Martinez, Bermudez Ana Katherine. "Isoprostanes in brain endothelial cell death." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21605.

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Oxygen free radicals have been implicated in several diseases including ischemic stroke, and myocardial infarction. They can trigger chain reactions like peroxidation of membrane phospholipids, leading to osmotic imbalance and cell death. Isoprostanes are stable products of lipid peroxidation that have a constrictor effect on the vasculature and bronchii. As isoprostanes are abundantly generated in tissues under oxidant stress, we have hypothesized that they could be related to endothelial dysfunction observed during ischemia/reperfasion by affecting endothelial cell survival. The effects of 8-iso-PGE2 and 8-iso-PGF2alpha, two abundantly produced isoprostanes, were studied on porcine endothelial cultures and isolated brain microvessels. Cell survival was evaluated by MTT reduction, double staining with DNA-binding fluorochromes and in situ DNA fragmentation labeling,
8-Iso-PGF2alpha (1--10 nM) induced 20--25% cell death in endothelial cultures after 24 h coincident with similar increase in the number of cells that become permeable to PI. On the contrary, 8-iso-PGE 2 did not affect endothelial cell survival. Approximately 9% of the cells suffered apoptosis. This percentage remained unchanged regardless the treatment. Several observations indicate a role for thromboxane A2 to mediate 8-iso-PGF2alpha-induced death: (1) the levels of thromboxane A2 increased dramatically in endothelial cultures after 8-iso-PGF2alpha-treatment; (2) inhibitors of thromboxane synthase, CGS12970 and U6355A and Ibuprofen, a non-selective inhibitor of cyclooxygenases, reverted the effect of the isoprostane; (3) analogs of thromboxane A2 U46619 and IBOP, reproduce the effect of 8-iso-PGF 2alpha after 24 h. 8-Iso-PGF2alpha also decreased endothelial viability on isolated brain microvessels. These results suggest, that 8-iso-PGF2alpha, might be a direct contributor to ischemia/reperfusion injury.

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TAKAHASHI, AKIRA, YOSHIO HASHIZUME, and NOBUKO UJIHIRA. "A CLINICO-NEUROPATHOLOGICAL STUDY ON BRAIN DEATH." Nagoya University School of Medicine, 1993. http://hdl.handle.net/2237/15930.

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Atkin, Charlotte J. "Developmental cell death in the rat brain." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393568.

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Michailakis, Dimitris. "Legislating death socio-legal studies of the brain death controversy in Sweden /." Uppsala : Stockholm : [Uppsala University] ; Distributor, Almqvist & Wiksell International, 1995. http://catalog.hathitrust.org/api/volumes/oclc/32780657.html.

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Russell, T. "Philosophical problems with the concepts of death and brain death : a different perspective." Thesis, Swansea University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.638727.

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The criteria and tests for death have changed throughout the history of medicine; these criteria and tests are underpinned by a variety of concepts of death. Recent advances in medicine and especially in the areas of resuscitation, mechanical ventilation and cardiac pacemakers have posed great philosophical and practical problems with the traditional concepts of death and their associated criteria and tests. The concept of brain death has been formulated in an attempt to deal with the practical decisions that have to be made in deciding whether a person is dead or alive. The original concept of brain death has been subdivided into whole-brain death, brainstem death and neocortical death in different geographical areas and by a variety of people. In addition, there are groups of people who do not adhere to any formulation of brain death. In this thesis I put forward reasons for rejecting all the present formulations of brain death. I also put forward a concept of death derived from philosophical argument. This proposed concept of death views death as death of the organism as a whole and, while I argue mainly in terms of human beings, the concept that I propose could be applied equally to other animals. I also present arguments to demonstrate that the proposed concept of death can encompass the traditional criteria and tests for death and does not entail any significant operational changes in the way in which death is diagnosed.

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Ambrose, Natalie Lauren. "Cell Death and Microglia in the Developing Brain." Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/26157.

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Introduction: Sudden unexpected death in infancy (SUDI) is the leading cause of post-neonatal death in the developed world. SUDI has been sub-categorised into explained causes, such as motor vehicle accidents, drowning and known illness (eSUDI); or unexplained causes, which includes sudden infant death syndrome (SIDS) and undetermined causes of death. SIDS by definition is a diagnosis of exclusion, with the pathogenesis currently elusive with no clear pathological defining features. It has been shown that SIDS infants have multiple abnormalities within brainstem regions crucial to cardio-respiratory control with this proposed to contribute to their premature death, however the linking pathway(s) are yet to be identified. Thus, investigation of the neuropathological changes remains a critical pillar of SIDS research. Notably, increased cell death, beyond that required in normal physiological development, has been implicated in SIDS, with amassing evidence in the literature of apoptotic cell death in regions of the SIDS brain, most notably in the brainstem and hippocampus. To build upon this, this thesis aimed to extend the scope of brain regions examined in the context of cell death in eSUDI and SIDS cases. Furthermore, this thesis also focused on a new cell type of interest in SUDI, being microglia. The role of microglia in the context of central nervous system insult and disease is a rapidly evolving field of neuropathological research, however, to date, literature in the infant brain is limited (reviewed section 2.4.4). Overall, this thesis aimed to: firstly, examine the methods of classifying unexplained SUDI cases to standardise our dataset. Secondly, to investigate cell death marker expression, cell stress and apoptotic pathways, and microglia populations in the developing human brain, specifically to (i) identify variability amongst brain regions, (ii) variability between SUDI sub-groups, and (iii) the effects of intrinsic and extrinsic stimuli. Finally, to investigate the effects of intermittent hypercapnic hypoxia and nicotine exposure (two leading risk factor models of SIDS) in the developing piglet brain. Methods: Both human (Chapters 3-6) and piglet (Chapter 7) brain tissue samples were utilised for this thesis. The primary method used was immunohistochemistry, with the distribution of cell death (active caspase-9, active caspase-3, TUNEL) and microglia (ionised calcium binding adaptor molecule-1 (Iba1), cluster of differentiation factor 68 (CD68) and human leukocyte antigen clone DR-DP-DQ (HLA)) marker expression explored amongst a broad range of brain regions. Human brain tissue was also investigated using a commercially available Cell Stress and Apoptosis Signalling Antibody Array to investigate 18 promoter, executioner, inhibitor and regulator proteins of the cell stress and apoptosis cascade. Results: Of the SUDI cases collected 2008-2012, there was a high level of variation in the diagnostic classification of SIDS and undetermined, thus necessitating the convening of an expert panel to apply a standardised classification of unexplained SUDI, SIDS and its subgroups (Chapter 3). On examining the neurological tissue, regional heterogeneity in all cell death and microglia markers was observed within the developing infant brain. During the first year of life, less than 20% of all neurons are undergoing physiological apoptosis (Chapter 4), and microglia occupy less than 5% of the total area (Chapter 6) in any given brain region. Changes in SIDS brain tissue were region dependent, with the brainstem and amygdala identified as regions of interest in the context of cell death (Chapter 4); the temporal cortex in the context of promoters of cell stress and apoptosis (Chapter 5); and the hippocampus in regards to changes in microglial populations (Chapter 6). Changes predominated in SIDS II suggesting the observations are influenced by confounding risk factors. In the piglet brain, continuous nicotine exposure was not associated with any changes in microglia, however acute/sub-acute IHH mediated region-dependent changes, particularly in the hippocampus (Chapter 7). Conclusion: The neuropathological findings from this work highlight that cell death and microglia markers are heterogeneously expressed in regions of the postnatal developing brain. Region-specific changes in the SIDS brain also have potential links to extrinsic stimuli, based on the findings in the piglet model. The brainstem, amygdala and broader temporal cortex are regions of interest in the context of SIDS and cell death, while the hippocampus is a region of interest in the context of microglia. This thesis provides a comprehensive analysis of microglial and cell death distribution and markers in the SIDS brain, contributing to our understanding of region-unique vulnerabilities. The results suggest new brain regions, and new markers of cell stress and apoptotic pathways, that can be targeted in future studies of the pathogenesis of SIDS.

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Sasaki, Kaori. "Politicised culture, culturalised life and death : the Japanese organ transplantation and brain death debates." Thesis, Lancaster University, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441371.

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Kaul, Aparna. "Mechanisms of Non-Conventional Cell Death in Brain Tumor Cells." University of Toledo Health Science Campus / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=mco1243364096.

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Jarl, Zandra. "The Threshold between Life and Death : An Examination of Near Death Experiences." Thesis, University of Skövde, School of Humanities and Informatics, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-3107.

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In studies on Near Death Experiences (NDE) data has been collected by using the recently developed scaling methods, the scale developed by Ring and the Greyson NDE Scale. In order to illustrate the problems in the empirical study of NDEs, my intention is to compare the Greyson NDE-scale with the most common theories on NDEs. After series of modifications the final scale consisted of a questionnaire consisting of sixteen different questions, that yielded into four different areas, Cognitive components, Emotional components, Paranormal components, and Transcendental components.

In the end the theory that has the most likely possibility to explain NDEs in the future must be the Dying Brain theory, but one should not disclose the different features of the Afterlife theory (but without the origin explanation).

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Books on the topic "Brain death"

1

Wijdicks, Eelco F. M., 1954-, ed. Brain death. Philadelphia: Lippincott Williams & Wilkins, 2001.

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2

David, Lamb. Death, brain death, and ethics. Aldershot, Hants, England: Avebury, 1996.

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3

Potts, Michael, Paul A. Byrne, and Richard G. Nilges. Beyond Brain Death. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/0-306-46882-4.

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4

A, Byrne Paul, and Nilges Richard G, eds. Beyond brain death: The case against brain based criteria for human death. Dordrecht: Kluwer Academic Publishers, 2000.

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5

Zaner, Richard M., ed. Death: Beyond Whole-Brain Criteria. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-2707-0.

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M, Zaner Richard, ed. Death: Beyond whole-brain criteria. Dordrecht: Kluwer Academic Publishers, 1988.

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7

International, Symposium on Coma and Death (4th 2004 Havana Cuba). Brain death and disorders of consciousness. New York: Kluwer Academic/Plenum Publishers, 2004.

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8

Machado, Calixto, and D. Alan Shewmon, eds. Brain Death and Disorders of Consciousness. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-0-306-48526-8.

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Calixto, Machado, and Shewmon D. Alan, eds. Brain death and disorders of consciousness. New York: Kluwer Academic/Plenum Publishers, 2004.

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International Symposium on Coma and Death (4th 2004 Havana, Cuba). Brain death and disorders of consciousness. New York: Kluwer Academic/Plenum Publishers, 2004.

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Book chapters on the topic "Brain death"

1

Chaubey, Vikas P., Kevin B. Laupland, Christopher B. Colwell, Gina Soriya, Shelden Magder, Jonathan Ball, Jennifer M. DiCocco, et al. "Brain Death." In Encyclopedia of Intensive Care Medicine, 373–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_372.

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Shemie, Sam D., and Sonny Dhanani. "Brain Death." In Pediatric Critical Care Medicine, 481–95. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6362-6_37.

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Thiex, Ruth, and Sebastian Schulz-Stübner. "Brain Death." In Imaging the ICU Patient, 165–72. London: Springer London, 2014. http://dx.doi.org/10.1007/978-0-85729-781-5_18.

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Mahajan, Charu, Indu Kapoor, and Hemanshu Prabhakar. "Brain Death." In Echography and Doppler of the Brain, 205–11. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-48202-2_18.

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Powell, Tiffany L. "Brain Death." In Encyclopedia of Clinical Neuropsychology, 618–19. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_300.

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Korein, Julius, and Calixto Machado. "Brain Death." In Advances in Experimental Medicine and Biology, 1–14. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-0-306-48526-8_1.

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Ettema, Eric J. "Brain Death." In Encyclopedia of Global Bioethics, 399–408. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-09483-0_66.

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Ettema, Eric J. "Brain Death." In Encyclopedia of Global Bioethics, 1–10. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-05544-2_66-1.

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Gavrilovici, Cristina. "Brain Death." In Encyclopedia of Immigrant Health, 306–9. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-5659-0_95.

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Powell, Tiffany L. "Brain Death." In Encyclopedia of Clinical Neuropsychology, 1–2. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_300-2.

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Conference papers on the topic "Brain death"

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Abdulelah, M., and W. T. McGee. "Diagnostic Ambiguity in Brain Death." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a7048.

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Sutton, J. A., and J. W. Leatherman. "Pseudo Brain Death After Snorting Bupropion." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1700.

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Zrodlowski, T., and M. D. M. Cirino-Marcano. "Brain Death in Posterior Fossa Infarct." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a7033.

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Choi, Ji Yun, Jong Wook Ko, and Mee Ran Park. "Nurses’ Knowledge for Brain Death Organ Donation." In 10th International Workshop on Healthcare and Nursing 2016. Global Vision School Publication, 2016. http://dx.doi.org/10.21742/asehl.2016.7.03.

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Joffe, Ari R., Natalie R. Anton, Jonathan P. Duff, and Allan R. deCaen. "A Survey Of American Neurologists About Brain Death: Understanding Of The Conceptual Basis And Diagnostic Tests For Brain Death." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6218.

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Mesi, O., and C. P. Wu. "Absent Brain Stem Reflexes After Cardiac Arrest: Brain Death or Drug Toxicity?" In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3402.

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Herceg-Čavrak, Vesna, Sanja Pek, Ivančica Škarić, and Višnja Tokić Pivac. "183 Children with brain death – findings on echocardiography." In 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.183.

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Sommer, W., M. OJ, B. Pruner, T. Paster, A. Bean, A. Dehnadi, M. Hanekamp, et al. "Donor Brain Death Affects Tolerance Induction in Nonhuman Primates." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678899.

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Abbod, M. F., J. Shieh, J. Yeh, K. Cheng, S. J. Huang, and Y. Y. Han. "Intelligent systems for the prediction of Brain Death Index." In 2008 IEEE Biomedical Circuits and Systems Conference. IEEE, 2008. http://dx.doi.org/10.1109/biocas.2008.4696896.

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Belhaj, Asmae, Laurence Dewachter, Céline Dewachter, Myriam Remmelink, Sandrine Rorive, Robert Naeije, and Benoit Rondelet. "Right ventricular dysfunction in brain death: Effect of corticosteroids." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2453.

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Reports on the topic "Brain death"

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Hayes, Ronald L. Proteolytic Mechanisms of Cell Death Following Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada415983.

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Hayes, Ronald L. Proteolytic Mechanisms of Cell Death Following Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada421034.

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Hayes, Ronald L. Proteolytic Mechanisms of cell Death Following Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, October 2000. http://dx.doi.org/10.21236/ada391291.

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Shujaa, Asaad Suliman, and Qasem Almulihi. Is Hypertonic Saline an Effective Alternative to Mannitol in the Treatment of TBI in Adult and Pediatric Patients? A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0010.

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Review question / Objective: Evaluate and compare the effectiveness of hypertonic saline and mannitol in patients with traumatic brain injury. Rationale: Traumatic brain injury is one of the main reasons for death and disability worldwide. Generally, the frequency of traumatic brain injury in Europe is >2,000 per million yearly; guidelines suggest more conservative interventions, e.g., raising of the upper body, cerebrospinal fluid drainage, and the use of hypertonic saline or mannitol before executing decompressive craniectomy. It is still uncertain whether hypertonic saline is better than mannitol in managing pediatric and adult patients with traumatic brain injury. The present systemic review and meta-analysis aimed to evaluate the effect of hypertonic saline compared to mannitol for managing TBI in traumatic brain injury. Eligibility criteria: Studies were included based on the described eligibility criteria using PICOS: P (Population); I (Intervention); C (Control); O (Outcome); S (Studies); only clinical trials and cohort studies published in English were selected.

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Garsa, Adam, Julie K. Jang, Sangita Baxi, Christine Chen, Olamigoke Akinniranye, Owen Hall, Jody Larkin, Aneesa Motala, Sydne Newberry, and Susanne Hempel. Radiation Therapy for Brain Metasases. Agency for Healthcare Research and Quality (AHRQ), June 2021. http://dx.doi.org/10.23970/ahrqepccer242.

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Objective. This evidence report synthesizes the available evidence on radiation therapy for brain metastases. Data sources. We searched PubMed®, Embase®, Web of Science, Scopus, CINAHL®, clinicaltrials.gov, and published guidelines in July 2020; assessed independently submitted data; consulted with experts; and contacted authors. Review methods. The protocol was informed by Key Informants. The systematic review was supported by a Technical Expert Panel and is registered in PROSPERO (CRD42020168260). Two reviewers independently screened citations; data were abstracted by one reviewer and checked by an experienced reviewer. We included randomized controlled trials (RCTs) and large observational studies (for safety assessments), evaluating whole brain radiation therapy (WBRT) and stereotactic radiosurgery (SRS) alone or in combination, as initial or postoperative treatment, with or without systemic therapy for adults with brain metastases due to non-small cell lung cancer, breast cancer, or melanoma. Results. In total, 97 studies, reported in 190 publications, were identified, but the number of analyses was limited due to different intervention and comparator combinations as well as insufficient reporting of outcome data. Risk of bias varied; 25 trials were terminated early, predominantly due to poor accrual. Most studies evaluated WBRT, alone or in combination with SRS, as initial treatment; 10 RCTs reported on post-surgical interventions. The combination treatment SRS plus WBRT compared to SRS alone or WBRT alone showed no statistically significant difference in overall survival (hazard ratio [HR], 1.09; confidence interval [CI], 0.69 to 1.73; 4 RCTs; low strength of evidence [SoE]) or death due to brain metastases (relative risk [RR], 0.93; CI, 0.48 to 1.81; 3 RCTs; low SoE). Radiation therapy after surgery did not improve overall survival compared with surgery alone (HR, 0.98; CI, 0.76 to 1.26; 5 RCTs; moderate SoE). Data for quality of life, functional status, and cognitive effects were insufficient to determine effects of WBRT, SRS, or post-surgical interventions. We did not find systematic differences across interventions in serious adverse events radiation necrosis, fatigue, or seizures (all low or moderate SoE). WBRT plus systemic therapy (RR, 1.44; CI, 1.03 to 2.00; 14 studies; moderate SoE) was associated with increased risks for vomiting compared to WBRT alone. Conclusion. Despite the substantial research literature on radiation therapy, comparative effectiveness information is limited. There is a need for more data on patient-relevant outcomes such as quality of life, functional status, and cognitive effects.

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liu, qing, peng Wang, shufan Li, xiaojing Zhou, xing Wang, and zhichao Cao. A meta-analysis of the effects of MOTOmed intelligent exercise training on balance function and neurological function in patients with hemiplegia with stroke. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2023. http://dx.doi.org/10.37766/inplasy2023.3.0045.

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Review question / Objective: This study aimed to systematically evaluate the effects of MOTOmed intelligent exercise training on balance function, neurological function and activities of daily living ability in patients with hemiplegia after stroke. Condition being studied: Stroke is a neurological disease caused by abnormal blood supply to the brain and is the third leading cause of death and disability in humans. Stroke-related disability-adjusted life-years are lost in 5.7 percent of the total, and 25 million new patients are expected each year by 2050. Hemiplegia is one of the most common sequelae of stroke ，and its clinical symptoms are often accompanied by neurological deficits in addition to common motor dysfunction, and due to damage to the central nervous system, proprioceptive and motor function is weakened, resulting in imbalance and increasing the risk of falls, seriously affecting the quality of daily life of patients .

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Faul, Mark, Marlena M. Wald, Likang Wu, and Victor G. Coronado. Traumatic brain injury in the United States : emergency department visits, hospitalizations, and deaths, 2002-2006. Centers for Disease Control and Prevention, March 2010. http://dx.doi.org/10.15620/cdc.5571.

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Newman-Toker, David E., Susan M. Peterson, Shervin Badihian, Ahmed Hassoon, Najlla Nassery, Donna Parizadeh, Lisa M. Wilson, et al. Diagnostic Errors in the Emergency Department: A Systematic Review. Agency for Healthcare Research and Quality (AHRQ), December 2022. http://dx.doi.org/10.23970/ahrqepccer258.

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Objectives. Diagnostic errors are a known patient safety concern across all clinical settings, including the emergency department (ED). We conducted a systematic review to determine the most frequent diseases and clinical presentations associated with diagnostic errors (and resulting harms) in the ED, measure error and harm frequency, as well as assess causal factors. Methods. We searched PubMed®, Cumulative Index to Nursing and Allied Health Literature (CINAHL®), and Embase® from January 2000 through September 2021. We included research studies and targeted grey literature reporting diagnostic errors or misdiagnosis-related harms in EDs in the United States or other developed countries with ED care deemed comparable by a technical expert panel. We applied standard definitions for diagnostic errors, misdiagnosis-related harms (adverse events), and serious harms (permanent disability or death). Preventability was determined by original study authors or differences in harms across groups. Two reviewers independently screened search results for eligibility; serially extracted data regarding common diseases, error/harm rates, and causes/risk factors; and independently assessed risk of bias of included studies. We synthesized results for each question and extrapolated U.S. estimates. We present 95 percent confidence intervals (CIs) or plausible range (PR) bounds, as appropriate. Results. We identified 19,127 citations and included 279 studies. The top 15 clinical conditions associated with serious misdiagnosis-related harms (accounting for 68% [95% CI 66 to 71] of serious harms) were (1) stroke, (2) myocardial infarction, (3) aortic aneurysm and dissection, (4) spinal cord compression and injury, (5) venous thromboembolism, (6/7 – tie) meningitis and encephalitis, (6/7 – tie) sepsis, (8) lung cancer, (9) traumatic brain injury and traumatic intracranial hemorrhage, (10) arterial thromboembolism, (11) spinal and intracranial abscess, (12) cardiac arrhythmia, (13) pneumonia, (14) gastrointestinal perforation and rupture, and (15) intestinal obstruction. Average disease-specific error rates ranged from 1.5 percent (myocardial infarction) to 56 percent (spinal abscess), with additional variation by clinical presentation (e.g., missed stroke average 17%, but 4% for weakness and 40% for dizziness/vertigo). There was also wide, superimposed variation by hospital (e.g., missed myocardial infarction 0% to 29% across hospitals within a single study). An estimated 5.7 percent (95% CI 4.4 to 7.1) of all ED visits had at least one diagnostic error. Estimated preventable adverse event rates were as follows: any harm severity (2.0%, 95% CI 1.0 to 3.6), any serious harms (0.3%, PR 0.1 to 0.7), and deaths (0.2%, PR 0.1 to 0.4). While most disease-specific error rates derived from mainly U.S.-based studies, overall error and harm rates were derived from three prospective studies conducted outside the United States (in Canada, Spain, and Switzerland, with combined n=1,758). If overall rates are generalizable to all U.S. ED visits (130 million, 95% CI 116 to 144), this would translate to 7.4 million (PR 5.1 to 10.2) ED diagnostic errors annually; 2.6 million (PR 1.1 to 5.2) diagnostic adverse events with preventable harms; and 371,000 (PR 142,000 to 909,000) serious misdiagnosis-related harms, including more than 100,000 permanent, high-severity disabilities and 250,000 deaths. Although errors were often multifactorial, 89 percent (95% CI 88 to 90) of diagnostic error malpractice claims involved failures of clinical decision-making or judgment, regardless of the underlying disease present. Key process failures were errors in diagnostic assessment, test ordering, and test interpretation. Most often these were attributed to inadequate knowledge, skills, or reasoning, particularly in “atypical” or otherwise subtle case presentations. Limitations included use of malpractice claims and incident reports for distribution of diseases leading to serious harms, reliance on a small number of non-U.S. studies for overall (disease-agnostic) diagnostic error and harm rates, and methodologic variability across studies in measuring disease-specific rates, determining preventability, and assessing causal factors. Conclusions. Although estimated ED error rates are low (and comparable to those found in other clinical settings), the number of patients potentially impacted is large. Not all diagnostic errors or harms are preventable, but wide variability in diagnostic error rates across diseases, symptoms, and hospitals suggests improvement is possible. With 130 million U.S. ED visits, estimated rates for diagnostic error (5.7%), misdiagnosis-related harms (2.0%), and serious misdiagnosis-related harms (0.3%) could translate to more than 7 million errors, 2.5 million harms, and 350,000 patients suffering potentially preventable permanent disability or death. Over two-thirds of serious harms are attributable to just 15 diseases and linked to cognitive errors, particularly in cases with “atypical” manifestations. Scalable solutions to enhance bedside diagnostic processes are needed, and these should target the most commonly misdiagnosed clinical presentations of key diseases causing serious harms. New studies should confirm overall rates are representative of current U.S.-based ED practice and focus on identified evidence gaps (errors among common diseases with lower-severity harms, pediatric ED errors and harms, dynamic systems factors such as overcrowding, and false positives). Policy changes to consider based on this review include: (1) standardizing measurement and research results reporting to maximize comparability of measures of diagnostic error and misdiagnosis-related harms; (2) creating a National Diagnostic Performance Dashboard to track performance; and (3) using multiple policy levers (e.g., research funding, public accountability, payment reforms) to facilitate the rapid development and deployment of solutions to address this critically important patient safety concern.

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Tranexamic acid is safe to use following mild-to-moderate traumatic brain injury and reduces deaths. National Institute for Health Research, January 2020. http://dx.doi.org/10.3310/signal-000870.

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