Observational studyNeurocritical care2019
Neuroimaging Findings in Sepsis-Induced Brain Dysfunction: Association with Clinical and Laboratory Findings.
Observational study in Neurocritical care, 2019. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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, 41 citations in OpenAlex.
- Neuroimmune Mechanisms Transforming Acute Injury to Long-Term Brain Dysfunction After Sepsis.Clinics in chest medicine · 2026Review
- Pathophysiology-driven neuroimaging: decoding brain injury in sepsis.Frontiers in molecular neuroscience · 2026Review
- Management of severe acute encephalopathy in the ICU: an expert consensus statement from the french society of intensive care medicine.Annals of intensive care · 2025Review
- Modulation of brain immune microenvironment and cellular dynamics in systemic inflammation.Theranostics · 2025Article
- Sepsis-Associated Brain Dysfunction: Mechanisms, Clinical Insights, and Therapeutic Strategies.Current drug targets · 2025Review
- Delirium in the ICU: how much do we know? A narrative review.Annals of medicine · 2024Review
- The Thalamus in Perioperative Neurocognitive Disorders.Neuropsychology review · 2024Review
- Acute Encephalopathies in SARS-CoV-2 Infection: A Clinical and Neuroimaging Perspective.Advances in experimental medicine and biology · 2024Review
- Brain morphometry and chronic inflammation in Bangladeshi children growing up in extreme poverty.Imaging neuroscience (Cambridge, Mass.) · 2024Article
- The spectrum of sepsis-associated encephalopathy: a clinical perspective.Critical care (London, England) · 2023Review
- Recent advances in the study of sepsis-induced depression.Journal of intensive medicine · 2023Review
- Paediatric sepsis-associated encephalopathy (SAE): a comprehensive review.Molecular medicine (Cambridge, Mass.) · 2023Review
- Observational
- Sepsis-associated brain injury: underlying mechanisms and potential therapeutic strategies for acute and long-term cognitive impairments.Journal of neuroinflammation · 2022Review
- Posterior Reversible Encephalopathy in Sepsis-Associated Encephalopathy: Experience from a Single Center.Neurocritical care · 2022Observational
- Sepsis-Related Brain MRI Abnormalities Are Associated With Mortality and Poor Neurological Outcome in Pediatric Sepsis.Pediatric neurology · 2022Article
- Current Understanding of Long-Term Cognitive Impairment After Sepsis.Frontiers in immunology · 2022Review
- Complement as driver of systemic inflammation and organ failure in trauma, burn, and sepsis.Seminars in immunopathology · 2021Review
- Basic research and clinical progress of sepsis-associated encephalopathy.Journal of intensive medicine · 2021Review
- Sleep Disorder and Long-Term Mortality Among Sepsis Survivors: A Nationwide Cohort Study in South Korea.Nature and science of sleep · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIncidence and patterns of brain lesions of sepsis-induced brain dysfunction (SIBD) have been well defined. Our objective was to investigate the associations between neuroimaging features of SIBD patients and well-known neuroinflammation and neurodegeneration factors.
methodsIn this prospective observational study, 93 SIBD patients (45 men, 48 women; 50.6 ± 12.7 years old) were enrolled. Patients underwent a neurological examination and brain magnetic resonance imaging (MRI). Severity-of-disease scoring systems (APACHE II, SOFA, and SAPS II) and neurological outcome scoring system (GOSE) were used. Also, serum levels of a panel of mediators [IL-1β, IL-6, IL-8, IL-10, IL-12, IL-17, IFN-γ, TNF-α, complement factor Bb, C4d, C5a, iC3b, amyloid-β peptides, total tau, phosphorylated tau (p-tau), S100b, neuron-specific enolase] were measured by ELISA. Voxel-based morphometry (VBM) was employed to available patients for assessment of neuronal loss pattern in SIBD.
resultsMRI of SIBD patients were normal (n = 27, 29%) or showed brain lesions (n = 51, 54.9%) or brain atrophy (n = 15, 16.1%). VBM analysis showed neuronal loss in the insula, cingulate cortex, frontal lobe, precuneus, and thalamus. Patients with abnormal MRI findings had worse APACHE II, SOFA, GOSE scores, increased prevalence of delirium and mortality. Presence of MRI lesions was associated with reduced C5a and iC3b levels and brain atrophy was associated with increased p-tau levels. Regression analysis identified an association between C5a levels and presence of lesion on MRI and p-tau levels and the presence of atrophy on MRI.
conclusionsNeuronal loss predominantly occurs in limbic and visceral pain perception regions of SIBD patients. Complement breakdown products and p-tau stand out as adverse neuroimaging outcome markers for SIBD.
Indexed as
Identifiers
What OpenQuestion holds
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.