ReviewFrontiers in neurology2015
Vascular and inflammatory factors in the pathophysiology of blast-induced brain injury.
Review in Frontiers in neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 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.
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Who cites it
72 citing papers in PubMed.
- Primary Blast-Induced Traumatic Brain Injury as a Risk Factor for (Cerebro)vascular Disorder: Clinical Manifestations, Blast Physics, Biomechanics, Pathobiology, and Critical Gaps.International journal of molecular sciences · 2026Review
- Restoring mitochondrial health after blast-induced traumatic brain injury: modifiable factors and therapeutic opportunities.npj metabolic health and disease · 2026Review
- Integrated Blood Biomarker and Neurobehavioural Signatures of Latent Neuroinjury in Experienced Military Breachers Exposed to Repetitive Low-Intensity Blast.International journal of molecular sciences · 2026Article
- Explosive shock wave exposure leads to age-accelerated motor and sensory decline inbioRxiv : the preprint server for biology · 2025Article
- Differential Neuroendocrine Responses and Dysregulation of the Hypothalamic-Pituitary-Adrenal Axis Following Repeated Mild Concussive Impacts and Blast Exposures in a Rat Model.Brain sciences · 2025Article
- Intramural hematomas and astrocytic infiltration precede perivascular inflammation in a rat model of repetitive low-level blast injury.Journal of neuropathology and experimental neurology · 2025Article
- Repetitive Low-Level Blast Exposure Alters Circulating Myeloperoxidase, Matrix Metalloproteinases, and Neurovascular Endothelial Molecules in Experienced Military Breachers.International journal of molecular sciences · 2025Article
- Traumatic brain injury causes early aggregation of beta-amyloid peptides and NOTCH3 reduction in vascular smooth muscle cells of leptomeningeal arteries.Acta neuropathologica · 2025Article
- Minocycline partially reverses established PTSD-related behavioral traits in rats exposed to repetitive low-level blast injury.Frontiers in neurology · 2025Article
- Assessing Mild Traumatic Brain Injury-Associated Blood-Brain Barrier (BBB) Damage and Restoration Using Late-Phase Perfusion Analysis by 3D ASL MRI: Implications for Predicting Progressive Brain Injury in a Focused Review.International journal of molecular sciences · 2024Review
- Spatial Intracranial Pressure Fields Driven by Blast Overpressure in Rats.Annals of biomedical engineering · 2024Article
- Temporal Alterations in Cerebrovascular Glycocalyx and Cerebral Blood Flow after Exposure to a High-Intensity Blast in Rats.International journal of molecular sciences · 2024Article
- The Neurovascular Unit as a Locus of Injury in Low-Level Blast-Induced Neurotrauma.International journal of molecular sciences · 2024Review
- Effects of Low-Level Blast on Neurovascular Health and Cerebral Blood Flow: Current Findings and Future Opportunities in Neuroimaging.International journal of molecular sciences · 2024Review
- Twenty Years of Blast-Induced Neurotrauma: Current State of Knowledge.Neurotrauma reports · 2024Article
- Low-intensity open-field blast exposure effects on neurovascular unit ultrastructure in mice.Acta neuropathologica communications · 2023Article
- Late chronic local inflammation, synaptic alterations, vascular remodeling and arteriovenous malformations in the brains of male rats exposed to repetitive low-level blast overpressures.Acta neuropathologica communications · 2023Article
- Modifications in Macular Perfusion and Neuronal Loss After Acute Traumatic Brain Injury.Investigative ophthalmology & visual science · 2023Observational
- Nanowired Delivery of Cerebrolysin with Mesenchymal Stem Cells Attenuates Heat Stress-Induced Exacerbation of Neuropathology Following Brain Blast Injury.Advances in neurobiology · 2023Article
- Predictors of Treatment Failure in Patients With Pyogenic Brain Abscess.World neurosurgery: X · 2022Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Blast-related traumatic brain injury (TBI) has received much recent attention because of its frequency in the conflicts in Iraq and Afghanistan. This renewed interest has led to a rapid expansion of clinical and animal studies related to blast. In humans, high-level blast exposure is associated with a prominent hemorrhagic component. In animal models, blast exerts a variety of effects on the nervous system including vascular and inflammatory effects that can be seen with even low-level blast exposures which produce minimal or no neuronal pathology. Acutely, blast exposure in animals causes prominent vasospasm and decreased cerebral blood flow along with blood-brain barrier breakdown and increased vascular permeability. Besides direct effects on the central nervous system, evidence supports a role for a thoracically mediated effect of blast; whereby, pressure waves transmitted through the systemic circulation damage the brain. Chronically, a vascular pathology has been observed that is associated with alterations of the vascular extracellular matrix. Sustained microglial and astroglial reactions occur after blast exposure. Markers of a central and peripheral inflammatory response are found for sustained periods after blast injury and include elevation of inflammatory cytokines and other inflammatory mediators. At low levels of blast exposure, a microvascular pathology has been observed in the presence of an otherwise normal brain parenchyma, suggesting that the vasculature may be selectively vulnerable to blast injury. Chronic immune activation in brain following vascular injury may lead to neurobehavioral changes in the absence of direct neuronal pathology. Strategies aimed at preventing or reversing vascular damage or modulating the immune response may improve the chronic neuropsychiatric symptoms associated with blast-related TBI.
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