ArticleCritical care (London, England)2010
Pathophysiology of septic encephalopathy--an unsolved puzzle.
Article in Critical care (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- Loss of C3 and CD14 reduces region-specific neuroinflammation in a murine polytrauma model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Article
- Extracellular Histones Associate with Blood-Brain Barrier Disruption and Astrocyte-Mediated Neuroinflammation During Polymicrobial Sepsis.International journal of molecular sciences · 2026Article
- Biomarkers of sepsis associated encephalopathy: a bibliometric and visualized analysis.Frontiers in neurology · 2025Article
- Elevated brain derived neurotrophic factor in plasma and interleukin-6 levels in cerebrospinal fluid in meningitis compared to cerebral malaria.Journal of the neurological sciences · 2023Article
- Paediatric sepsis-associated encephalopathy (SAE): a comprehensive review.Molecular medicine (Cambridge, Mass.) · 2023Review
- Integrated transcriptomics and metabolomics analysis of the hippocampus reveals altered neuroinflammation, downregulated metabolism and synapse in sepsis-associated encephalopathy.Frontiers in pharmacology · 2022Article
- Acoustocerebrography in septic patients: A randomized and controlled pilot study.Frontiers in medical technology · 2022Article
- Xenon attenuated neonatal lipopolysaccharide exposure induced neuronal necroptosis and subsequently improved cognition in juvenile rats.Frontiers in pharmacology · 2022Article
- Association Among the Gut Microbiome, the Serum Metabolomic Profile and RNA mFrontiers in genetics · 2022Article
- Clinical values of cerebral oxygen saturation monitoring in patients with septic shock.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021Article
- Role of microRNAs As Biomarkers in Sepsis-Associated Encephalopathy.Molecular neurobiology · 2021Review
- Observational
- Delirium in medical intensive care units: Incidence, subtypes, risk factors, and outcome.Indian journal of psychiatry · 2019Article
- Immunosenescence in neurocritical care.Journal of intensive care · 2018Review
- Translational evidence for two distinct patterns of neuroaxonal injury in sepsis: a longitudinal, prospective translational study.Critical care (London, England) · 2017Article
- Article
- Mechanisms of long-term cognitive dysfunction of sepsis: from blood-borne leukocytes to glial cells.Intensive care medicine experimental · 2015Article
- CD40-CD40 Ligand Pathway is a Major Component of Acute Neuroinflammation and Contributes to Long-term Cognitive Dysfunction after Sepsis.Molecular medicine (Cambridge, Mass.) · 2015Article
- Hunting mimics and chameleons: diagnostic difficulties in atypical acute ischaemic stroke.BMJ case reports · 2014Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The exact cellular and molecular mechanisms of sepsis-induced encephalopathy remain elusive. The breakdown of the blood-brain barrier (BBB) is considered a focal point in the development of sepsis-induced brain damage. Contributing factors for the compromise of the BBB include cytokines and chemokines, activation of the complement cascade, phagocyte-derived toxic mediators, and bacterial products. To date, we are far from fully understanding the neuropathology that develops as a secondary remote organ injury as a consequence of sepsis. However, recent studies suggest that bacterial proteins may readily cross the functional BBB and trigger an inflammatory response in the subarachnoid space, in absence of a bacterial invasion. A better understanding of the pathophysiological events leading to septic encephalopathy appears crucial to advance the clinical care for this vulnerable patient population.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.