ReviewSeminars in neurology2015
Pathophysiology and clinical management of moderate and severe traumatic brain injury in the ICU.
Review in Seminars in neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05095857 (S-ketamine for Cortical Spreading Depolarisation in Patients With Severe Acute Brain Injury), which is not on this map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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.
S-ketamine for Cortical Spreading Depolarisation in Patients With Severe Acute Brain Injury
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Ketamine for Critically Ill Patients with Severe Acute Brain Injury: A Systematic Review with Meta-analysis and Trial Sequential Analysis of Randomized Clinical Trials.Neurocritical care · 2025Pooled it
- Adverse events registration in clinical trial participants with severe acute brain injury: a Delphi consensus study.Acta neurochirurgica · 2025Article
- Article
- Recovery Potential in Patients Who Died After Withdrawal of Life-Sustaining Treatment: A TRACK-TBI Propensity Score Analysis.Journal of neurotrauma · 2024Article
- Hippocampal Expression of Cytochrome P450 1B1 in Penetrating Traumatic Brain Injury.International journal of molecular sciences · 2022Article
- Dexmedetomidine inhibits the PSD95-NMDA receptor interaction to promote functional recovery following traumatic brain injury.Experimental and therapeutic medicine · 2021Article
- Article
- The Therapeutic Potential and Limitations of Ketones in Traumatic Brain Injury.Frontiers in neurology · 2021Review
- Neuroprognostication of Consciousness Recovery in a Patient with COVID-19 Related Encephalitis: Preliminary Findings from a Multimodal Approach.Brain sciences · 2020Article
- The delayed detection of an acute neurological worsening increases traumatic brain injury lethalityBiomedica : revista del Instituto Nacional de Salud · 2020Article
- Allosteric GABAMolecules (Basel, Switzerland) · 2020Review
- Simultaneous electrophysiological and morphological assessment of functional damage to neural networks in vitro after 30-300 g impacts.Scientific reports · 2019Article
- Cerebral Blood Flow Autoregulation in Sepsis for the Intensivist: Why Its Monitoring May Be the Future of Individualized Care.Journal of intensive care medicine · 2018Review
- Growth Differentiation Factor 5 Improves Neurogenesis and Functional Recovery in Adult Mouse Hippocampus Following Traumatic Brain Injury.Frontiers in neurology · 2018Article
- Nursing Management of Adults with Severe Traumatic Brain Injury: A Narrative Review.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2017Review
- Neurotrauma: The Crosstalk between Neurotrophins and Inflammation in the Acutely Injured Brain.International journal of molecular sciences · 2017Review
- Endoplasmic reticulum stress-induced apoptosis in the penumbra aggravates secondary damage in rats with traumatic brain injury.Neural regeneration research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Moderate and severe traumatic brain injury (TBI) is the leading cause of morbidity and mortality among young individuals in high-income countries. Its pathophysiology is divided into two major phases: the initial neuronal injury (or primary injury) followed by secondary insults (secondary injury). Multimodality monitoring now offers neurointensivists the ability to monitor multiple physiologic parameters that act as surrogates of brain ischemia and hypoxia, the major driving forces behind secondary brain injury. The heterogeneity of the pathophysiology of TBI makes it necessary to take into consideration these interacting physiologic factors when recommending for or against any therapies; it may also account for the failure of all the neuroprotective therapies studied so far. In this review, the authors focus on neuroclinicians and neurointensivists, and discuss the developments in therapeutic strategies aimed at optimizing intracranial pressure and cerebral perfusion pressure, and minimizing cerebral hypoxia. The management of moderate to severe TBI in the intensive care unit is moving away from a pure "threshold-based" treatment approach toward consideration of patient-specific characteristics, including the state of cerebral autoregulation. The authors also include a concise discussion on the management of medical and neurologic complications peculiar to TBI as well as an overview of prognostication.
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.