Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (461 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Acute and chronic (see also brain injuries, chronic) injuries to the brain, including the cerebral hemispheres, cerebellum, and brain stem. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with diffuse axonal injury or COMA, post-traumatic. Localized injuries may be associated with neurobehavioral manifestations; hemiparesis, or other focal neurologic deficits.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Injuries, Brain; Brain Injury; Injury, Brain; Injuries, Acute Brain; Acute Brain Injuries; Acute Brain Injury; Brain Injury, Acute; Injury, Acute Brain.
Where it fits in the MeSH classification
- Broader topics
- Brain Diseases; Craniocerebral Trauma
- Narrower topics
- Brain Hemorrhage, Traumatic; Brain Injuries, Diffuse; Brain Injuries, Traumatic; Brain Injury, Chronic; Epilepsy, Post-Traumatic; Pneumocephalus; Post-Cardiac Arrest Syndrome; Shaken Baby Syndrome
Related concepts
- Brain Injuries
- Chronic
- Cerebellum
- Brain Stem
- Diffuse Axonal Injury
- Post-Traumatic
- Neurobehavioral Manifestations
- Hemiparesis
Research landscape
PubMed indexes 93,500 records tagged with the MeSH heading “Brain Injuries” (counts retrieved 2026-10-29). 24,184 of them (25.9%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 30,450 records.
Reviews account for 13,733 records (14.7%) and meta-analyses for 957. Randomized controlled trials number 1,908 (2.0%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 23,190 |
| 2000-2009 | 15,676 |
| 2010-2019 | 30,450 |
| 2020 onward | 24,184 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 13,733 | 14.7% |
| Meta-analyses | 957 | 1.0% |
| Randomized controlled trials | 1,908 | 2.0% |
Method: PubMed query "Brain Injuries"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in neuroscience
Neuroscience draws on tools with different strengths: cellular and animal work can manipulate circuits directly, while human imaging and electrophysiology observe the living brain at lower resolution. Small imaging studies are prone to false positives, and findings in animals do not always carry over to people. Clinical neurology and psychiatry rely on trials and cohort studies whose outcomes are often symptom scales. Check the species, the sample size, how the outcome was measured and whether results were replicated.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Disrupted hippocampal theta-gamma coupling and spike-field coherence following experimental traumatic brain injury | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42284087 · DOI · PMC13263039 |
| FcγR- and CD9-dependent synapse-engulfing microglia in the thalamus drive cognitive impairment following cortical brain damage in mice | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42425959 · DOI · PMC13484472 |
| Electroacupuncture Prevents TBI-Induced Synaptic Loss by Inhibiting CaMKII/Drp1-Dependent Mitochondrial Fission | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42650835 · DOI · PMC13511455 |
Disrupted hippocampal theta-gamma coupling and spike-field coherence following experimental traumatic brain injury [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Traumatic brain injury (TBI) often results in persistent learning and memory deficits, likely due to disrupted hippocampal circuitry underlying these processes.
- Closing excerpt
- These results reveal physiological deficits across brain states that may contribute to TBI-associated learning and memory impairments and elucidate potential targets for future neuromodulation therapies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (147 words)
Traumatic brain injury (TBI) often results in persistent learning and memory deficits, likely due to disrupted hippocampal circuitry underlying these processes. Precise temporal control of hippocampal neuronal activity is thought to be important for memory encoding and retrieval and is supported by oscillations that dynamically organize single-unit firing. Using high-density laminar electrophysiology, we found a loss of oscillatory power across CA1 lamina, with a profound, layer-specific reduction in theta-gamma phase-amplitude coupling in injured rats. Interneurons from injured animals were less strongly entrained to theta and gamma oscillations, but both interneurons and pyramidal cells from injured animals became more strongly entrained to theta during periods of high theta power. During quiet immobility, sharp-wave ripple amplitudes were lower in injured animals compared to shams. These results reveal physiological deficits across brain states that may contribute to TBI-associated learning and memory impairments and elucidate potential targets for future neuromodulation therapies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42284087 · DOI · PMC13263039
FcγR- and CD9-dependent synapse-engulfing microglia in the thalamus drive cognitive impairment following cortical brain damage in mice [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Chronic neuroinflammation gives rise to diverse microglial states across the brain, yet how region-specific microglial remodeling contributes to cognitive dysfunction remains unclear.
- Closing excerpt
- These findings demonstrate that the induction of synapse-engulfing CD9hi microglia in the thalamus by IgG/FcγRIII signaling drives recognition memory deficits following cortical damage.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (152 words)
Chronic neuroinflammation gives rise to diverse microglial states across the brain, yet how region-specific microglial remodeling contributes to cognitive dysfunction remains unclear. Here we report that synapse-engulfing microglia in the thalamus drive cognitive impairment after cortical brain damage in mice, primarily studied in females. Region-specific manipulations of microglia during the chronic phase show that reactive microglial changes in the thalamus, but not in the hippocampus, impair recognition memory. Single-cell RNA sequencing reveals an enrichment of synapse-engulfing CD9hi microglia in the thalamus. Antibody-based CD9 blockade in the thalamus, as well as microglia-selective CD9 disruption, rescues thalamic synaptic loss, restores neuronal activity, and improves recognition memory. Further analysis shows that the blood-brain barrier disruption and subsequent γ-immunoglobulin (IgG) extravasation facilitate the generation of CD9hi microglia in an Fcγ receptor III-dependent manner. These findings demonstrate that the induction of synapse-engulfing CD9hi microglia in the thalamus by IgG/FcγRIII signaling drives recognition memory deficits following cortical damage.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42425959 · DOI · PMC13484472
Electroacupuncture Prevents TBI-Induced Synaptic Loss by Inhibiting CaMKII/Drp1-Dependent Mitochondrial Fission [3]
Abstract reading summary — source excerpts
- Opening excerpt
- (1) Background: Traumatic brain injury (TBI) triggers synaptic loss, leading to long-term neurological deficits.
- Closing excerpt
- (4) Conclusions: Thus, EA limits TBI deficits by restraining CaMKII/Drp1-driven mitochondrial fission and subsequent synaptic loss.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (162 words)
(1) Background: Traumatic brain injury (TBI) triggers synaptic loss, leading to long-term neurological deficits. Electroacupuncture (EA) benefits neurological conditions, but its mechanisms after TBI remain unclear. (2) Methods: We used a controlled cortical impact (CCI) mouse model. Behavioral outcomes were assessed using the modified neurological severity score (mNSS), rotarod, Y-maze, and novel object recognition test (NORT). Synaptic morphology was examined by transmission electron microscopy (TEM). Energy metabolism was assessed using biochemical assays, and mitochondrial function was assessed using flow cytometry. Quantitative real-time PCR (qPCR) and Western blotting (WB) were used to examine the underlying molecular mechanisms. (3) Results: We found that EA ameliorates TBI-induced motor and cognitive impairments by preserving synaptic and mitochondrial integrity. EA-treated mice showed improvements in mNSS, rotarod, NORT, and Y-maze performance, along with preserved synaptic ultrastructure and mitochondrial function. CaMKII overexpression abolished EA-induced neuroprotection, identifying the CaMKII/Drp1 axis as a key mediator. (4) Conclusions: Thus, EA limits TBI deficits by restraining CaMKII/Drp1-driven mitochondrial fission and subsequent synaptic loss.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42650835 · DOI · PMC13511455
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Post-Concussion Symptoms and Disability in Adults With Mild Traumatic Brain Injury: A Systematic Review and Meta-Analysis [4]
- Research article Rest and exercise early after sport-related concussion: a systematic review and meta-analysis [5]
- Research article Preterm Brain Injury and Neurodevelopmental Outcomes: A Meta-analysis [6]
- Research article Clinical recovery from concussion-return to school and sport: a systematic review and meta-analysis [7]
- Research article Prevention strategies and modifiable risk factors for sport-related concussions and head impacts: a systematic review and meta-analysis [8]
- Research article Neurologic Prognostication After Cardiac Arrest Using Brain Biomarkers: A Systematic Review and Meta-analysis [9]
References
- Adam CD, Mirzakhalili E, Gagnon KG, Cottone C, Arena JD, Ulyanova A, et al.. Disrupted hippocampal theta-gamma coupling and spike-field coherence following experimental traumatic brain injury. . 2026. PMID 42284087 · DOI · PMC13263039
- Matoba K, Kochi T, Fatoba O, Parvez MSA, Berkiks I, Mreyoud YR, et al.. FcγR- and CD9-dependent synapse-engulfing microglia in the thalamus drive cognitive impairment following cortical brain damage in mice. . 2026. PMID 42425959 · DOI · PMC13484472
- Zhao S, Cao L, Deng F, Liao Z, Li X, Li G, et al.. Electroacupuncture Prevents TBI-Induced Synaptic Loss by Inhibiting CaMKII/Drp1-Dependent Mitochondrial Fission. . 2026. PMID 42650835 · DOI · PMC13511455
- Cancelliere C, Verville L, Stubbs JL, Yu H, Hincapié CA, Cassidy JD, et al.. Post-Concussion Symptoms and Disability in Adults With Mild Traumatic Brain Injury: A Systematic Review and Meta-Analysis. J Neurotrauma. 2023. PMID 36472218 · DOI
- Leddy JJ, Burma JS, Toomey CM, Hayden A, Davis GA, Babl FE, et al.. Rest and exercise early after sport-related concussion: a systematic review and meta-analysis. Br J Sports Med. 2023. PMID 37316185 · DOI
- Rees P, Callan C, Chadda KR, Vaal M, Diviney J, Sabti S, et al.. Preterm Brain Injury and Neurodevelopmental Outcomes: A Meta-analysis. Pediatrics. 2022. PMID 36330752 · DOI · PMC9724175
- Putukian M, Purcell L, Schneider KJ, Black AM, Burma JS, Chandran A, et al.. Clinical recovery from concussion-return to school and sport: a systematic review and meta-analysis. Br J Sports Med. 2023. PMID 37316183 · DOI
- Eliason PH, Galarneau JM, Kolstad AT, Pankow MP, West SW, Bailey S, et al.. Prevention strategies and modifiable risk factors for sport-related concussions and head impacts: a systematic review and meta-analysis. Br J Sports Med. 2023. PMID 37316182 · DOI
- Hoiland RL, Rikhraj KJK, Thiara S, Fordyce C, Kramer AH, Skrifvars MB, et al.. Neurologic Prognostication After Cardiac Arrest Using Brain Biomarkers: A Systematic Review and Meta-analysis. JAMA Neurol. 2022. PMID 35226054 · DOI · PMC8886448
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.