ReviewFrontiers in neurology2017
The Role of Substance P in Secondary Pathophysiology after Traumatic Brain Injury.
Review in Frontiers in neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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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.
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Who cites it
29 citing papers in PubMed, 61 citations in OpenAlex.
- The Low Glutamate Diet Effectively Improves Pain and Other Symptoms of Gulf War Illness.Nutrients · 2020Trial
- Article
- The Relationship Between Inflammation and the Development of Cerebral Ischaemia and Hypoxia in Traumatic Brain Injury-A Narrative Review.International journal of molecular sciences · 2025Review
- Abnormal Transcytosis Mechanisms in the Pathogenesis of Hydrocephalus: A Review.International journal of molecular sciences · 2025Review
- Unveiling the inflammatory messengers after intracerebral hemorrhage: the crosstalk between peripheral NETs and microglia.Frontiers in immunology · 2025Review
- Biomarkers and Endophenotypes of Post-traumatic Headaches.Current pain and headache reports · 2024Review
- Current understanding of the link between angiotensin-converting enzyme and pain perception.Drug discovery today · 2024Review
- Role of substance P in cerebral edema and association with an estimated specific gravity of the brain and an outcome prediction in post-traumatic cerebral edema.World neurosurgery: X · 2024Article
- Targeting brain-peripheral immune responses for secondary brain injury after ischemic and hemorrhagic stroke.Journal of neuroinflammation · 2024Review
- Pathophysiology-Based Management of Secondary Injuries and Insults in TBI.Biomedicines · 2024Review
- Magnesium (MgCurrent pharmaceutical design · 2024Review
- Vascular Effects on Cerebrovascular Permeability and Neurodegeneration.Biomolecules · 2023Review
- Magnesium and the Brain: A Focus on Neuroinflammation and Neurodegeneration.International journal of molecular sciences · 2022Review
- A multi-staged neuropeptide response to traumatic brain injury.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022Article
- Immune modulation after traumatic brain injury.Frontiers in medicine · 2022Review
- The Potential Mechanisms of High-Velocity, Low-Amplitude, Controlled Vertebral Thrusts on Neuroimmune Function: A Narrative Review.Medicina (Kaunas, Lithuania) · 2021Review
- Continuous Infusion of Ketamine and Lidocaine Either with or without Maropitant as an Adjuvant Agent for Analgesia in Female Dogs Undergoing Mastectomy.Veterinary medicine international · 2021Article
- Genetic underpinnings of cerebral edema in acute brain injury: an opportunity for pathway discovery.Neuroscience letters · 2020Review
- Protective role ofPharmaceutical biology · 2019Article
- Neuro-Inflammation in Pediatric Traumatic Brain Injury-from Mechanisms to Inflammatory Networks.Brain sciences · 2019Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has recently been shown that substance P (SP) plays a major role in the secondary injury process following traumatic brain injury (TBI), particularly with respect to neuroinflammation, increased blood-brain barrier (BBB) permeability, and edema formation. Edema formation is associated with the development of increased intracranial pressure (ICP) that has been widely associated with increased mortality and morbidity after neurotrauma. However, a pharmacological intervention to specifically reduce ICP is yet to be developed, with current interventions limited to osmotic therapy rather than addressing the cause of increased ICP. Given that previous publications have shown that SP, NK1 receptor antagonists reduce edema after TBI, more recent studies have examined whether these compounds might also reduce ICP and improve brain oxygenation after TBI. We discuss the results of these studies, which demonstrate that NK1 antagonists reduce posttraumatic ICP to near normal levels within 4 h of drug administration, as well as restoring brain oxygenation to near normal levels in the same time frame. The improvements in these parameters occurred in association with an improvement in BBB integrity to serum proteins, suggesting that SP-mediated increases in vascular permeability significantly contribute to the development of increased ICP after acute brain injury. NK1 antagonists may therefore provide a novel, mechanistically targeted approach to the management of increased ICP.
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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.