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 (659 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
Bleeding into one or both cerebral hemispheres including the basal ganglia and the cerebral cortex. It is often associated with hypertension and craniocerebral trauma.
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: Hemorrhage, Cerebral; Cerebral Hemorrhages; Hemorrhages, Cerebral; Intracerebral Hemorrhage; Hemorrhage, Intracerebral; Hemorrhages, Intracerebral; Intracerebral Hemorrhages; Hemorrhage, Cerebrum.
Where it fits in the MeSH classification
- Broader topics
- Intracranial Hemorrhages
- Narrower topics
- Basal Ganglia Hemorrhage; Cerebral Hemorrhage, Traumatic; Cerebral Intraventricular Hemorrhage
Related concepts
- Cerebral Hemispheres
- Basal Ganglia
- Cerebral Cortex
- Hypertension
- Craniocerebral Trauma
Research landscape
PubMed indexes 41,332 records tagged with the MeSH heading “Cerebral Hemorrhage” (counts retrieved 2026-10-29). 7,493 of them (18.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 18,130 records.
Reviews account for 4,380 records (10.6%) and meta-analyses for 673. Randomized controlled trials number 966 (2.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 18,130 |
| 2000-2009 | 6,216 |
| 2010-2019 | 9,493 |
| 2020 onward | 7,493 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 4,380 | 10.6% |
| Meta-analyses | 673 | 1.6% |
| Randomized controlled trials | 966 | 2.3% |
Method: PubMed query "Cerebral Hemorrhage"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
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 |
|---|---|---|---|---|
| Microglial Membranes Wrapped Ultrasmall Medium-Entropy Ru Single-Atom Nanozyme: Enhanced Catalysis for Accelerating Inflammation/Redox Microenvironment Regulation in Intracerebral Hemorrhage | 2026 | Research article Design not recorded in structured metadata | 14 | cc by PMID 41486243 · DOI · PMC13042521 |
| Therapeutic Hypothermia Alleviates Hydrocephalus and Neurological Dysfunction Post Intraventricular Hemorrhage by Enhancing Drainage of Glymphatic-Meningeal Lymphatic-Deep Cervical Lymphatic System | 2026 | Research article Design not recorded in structured metadata | 7 | cc by PMID 41578884 · DOI · PMC12831171 |
| Apelin-13 Attenuates Blood-Brain Barrier Dysfunction Following Intracerebral Hemorrhage via Targeting the Keap1/Nrf2 Signaling | 2025 | Research article Design not recorded in structured metadata | 7 | cc by PMID 41459616 · DOI · PMC12746050 |
Microglial Membranes Wrapped Ultrasmall Medium-Entropy Ru Single-Atom Nanozyme: Enhanced Catalysis for Accelerating Inflammation/Redox Microenvironment Regulation in Intracerebral Hemorrhage [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Intracerebral hemorrhage (ICH) causes severe secondary brain injury (SBI) via excessive inflammation and reactive oxygen species (ROS), and current treatments lack effective dual-target efficacy.
- Closing excerpt
- This study pioneers the integration of SANs with medium-entropy alloys for ICH, offering a dual-target ROS-inflammation regulatory strategy and a generalizable platform for ROS-related degenerative disease 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 (188 words)
Intracerebral hemorrhage (ICH) causes severe secondary brain injury (SBI) via excessive inflammation and reactive oxygen species (ROS), and current treatments lack effective dual-target efficacy. In this study, we designed a microglial membrane-wrapped single-atom nanozyme (PtRhIr/Ru SAN@M) by anchoring a single atom of Ru onto ultrasmall, medium-entropy PtRhIr alloys. This design integrates two underutilized strategies, single-atom nanozymes (SANs) and medium-entropy catalysts, to address critical therapeutic gaps in ICH therapy. PtRhIr/Ru SAN@M exhibited enhanced catalytic activity with superior Hydroxyl radical (•OH) scavenging and superoxide dismutase (SOD)-like and catalase (CAT)-like performances compared to Ru-free PtRhIr@M, enabled by electronically modulated active sites. Fluorescence imaging confirmed its ability to penetrate the blood-brain barrier (BBB) and accumulate in post-ICH neuroinflammatory regions. Both in vitro and in vivo experiments demonstrated that PtRhIr/Ru SAN@M repolarized microglia from the M1 to the M2 phenotype, disrupting the neuroinflammatory cycle and halting neuronal death. Therapeutic intervention with PtRhIr/Ru SAN@M significantly increased survival rates, restored neurological function, and enhanced spatial memory after ICH. This study pioneers the integration of SANs with medium-entropy alloys for ICH, offering a dual-target ROS-inflammation regulatory strategy and a generalizable platform for ROS-related degenerative disease therapies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41486243 · DOI · PMC13042521
Therapeutic Hypothermia Alleviates Hydrocephalus and Neurological Dysfunction Post Intraventricular Hemorrhage by Enhancing Drainage of Glymphatic-Meningeal Lymphatic-Deep Cervical Lymphatic System [2]
Abstract reading summary — source excerpts
- Opening excerpt
- AimsIntraventricular hemorrhage (IVH) has a high mortality and disability rate and poses significant clinical challenges, which often leads to hydrocephalus and neurological dysfunction.
- Closing excerpt
- TH is expected to become a novel therapeutic strategy for IVH.
- 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 (203 words)
AimsIntraventricular hemorrhage (IVH) has a high mortality and disability rate and poses significant clinical challenges, which often leads to hydrocephalus and neurological dysfunction. Emerging evidence implicates dysfunction of the glymphatic-meningeal lymphatic-deep cervical lymphatic system in the pathogenesis of post-IVH hydrocephalus. Therapeutic hypothermia (TH) holds promise for mitigating these sequelae. This study investigates the potential of TH to ameliorate IVH-induced hydrocephalus and neurological dysfunction, while elucidating its underlying mechanisms.MethodsRat models of IVH are established by intraventricular injection of autologous blood. TH, deep cervical lymph nodes (dCLNs) ligation, and intraperitoneal injection of AMPK inhibitor are used to intervene.ResultsIn rat models of IVH, TH alleviates neurological dysfunction and attenuates hydrocephalus and pathology damage. TH protects physiological function and maintains normal structure of the glymphatic system. TH improves function and structure of the meningeal lymphatic system and promotes drainage of the deep cervical lymphatic system. TH upregulates RTN3, facilitates phosphorylation of AMPK, and suppresses ERS. All the above effects are reversed by ligation of dCLNs and AMPK inhibitor.ConclusionTH alleviates hydrocephalus and neurological dysfunction post IVH by enhancing drainage of the glymphatic-meningeal lymphatic-deep cervical lymphatic system. The RTN3/AMPK/ERS pathway may be the proposed mechanism mediating this effect. TH is expected to become a novel therapeutic strategy for IVH.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41578884 · DOI · PMC12831171
Apelin-13 Attenuates Blood-Brain Barrier Dysfunction Following Intracerebral Hemorrhage via Targeting the Keap1/Nrf2 Signaling [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundBlood-brain barrier (BBB) dysfunction serves as a critical driver of the secondary brain injury following intracerebral hemorrhage (ICH).
- Closing excerpt
- ConclusionsIn conclusion, these findings demonstrate that through its engagement with APJ, Apelin-13 activates the endothelial Keap1/Nrf2 pathway to protect against ICH-induced BBB disruption and facilitate neurological recovery, highlighting its therapeutic promise for ICH.
- 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 (268 words)
BackgroundBlood-brain barrier (BBB) dysfunction serves as a critical driver of the secondary brain injury following intracerebral hemorrhage (ICH). Previous research has indicated that Apelin-13 demonstrates the potential to alleviate BBB dysfunction in various cerebrovascular disorders. However, the precise mechanisms through which Apelin-13 preserves BBB integrity remain elusive. This study investigated whether Apelin-13 exerted neuroprotective effects by targeting the Keap1/Nrf2 signaling.MethodsAn in vivo ICH model was established using collagenase. Neurological function, brain edema, tight junction protein levels, and Evans blue leakage were assessed. In vitro, bEnd.3 monolayers were induced by hemin to simulate ICH conditions. To assess the role of Apelin-13 in the Keap1/Nrf2 signaling, we employed specific shRNAs targeting Nrf2 and apelin receptor (APJ). The neuroprotective effects of Apelin-13 in hemin-stimulated bEnd.3 cells were assessed through transendothelial electrical resistance assay, western blotting, and immunofluorescence analysis.ResultsApelin-13 treatment significantly mitigated brain damage, reduced cerebral edema, and promoted neurological recovery in ICH mice. These effects were accompanied by a significant decrease in matrix metalloproteinase-9 expression and an increase in tight junction protein levels. Similar protective effects were observed in hemin-induced bEnd.3 cells, where Apelin-13 additionally promoted Nrf2 expression and suppressed Keap1 expression, suggesting the involvement of the Keap1/Nrf2 signaling. Critically, APJ silencing blocked the effects of Apelin-13 on the Keap1/Nrf2 pathway. Furthermore, Nrf2 knockdown eliminated the protective effects of Apelin-13, reversing its attenuation of apoptosis, preservation of tight junction integrity, and reduction of oxidative stress in hemin-stimulated bEnd.3 cells.ConclusionsIn conclusion, these findings demonstrate that through its engagement with APJ, Apelin-13 activates the endothelial Keap1/Nrf2 pathway to protect against ICH-induced BBB disruption and facilitate neurological recovery, highlighting its therapeutic promise for ICH.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41459616 · DOI · PMC12746050
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 Incidence, case fatality, and functional outcome of intracerebral haemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis [4]
- Research article Clinical Significance of Magnetic Resonance Imaging Markers of Vascular Brain Injury: A Systematic Review and Meta-analysis [5]
- Research article Risk factors for intracerebral hemorrhage in the general population: a systematic review [6]
- Research article Long-term prognosis after intracerebral haemorrhage: systematic review and meta-analysis [7]
- Research article Absolute risk and predictors of the growth of acute spontaneous intracerebral haemorrhage: a systematic review and meta-analysis of individual patient data [8]
- Research article Thrombectomy for anterior circulation stroke beyond 6 h from time last known well (AURORA): a systematic review and individual patient data meta-analysis [9]
References
- Li J, Wei P, Pan Y, Zheng H, Hu J, Chen Q, et al.. Microglial Membranes Wrapped Ultrasmall Medium-Entropy Ru Single-Atom Nanozyme: Enhanced Catalysis for Accelerating Inflammation/Redox Microenvironment Regulation in Intracerebral Hemorrhage. . 2026. PMID 41486243 · DOI · PMC13042521
- Yang Y, Ouyang Q, Sun Y, Liang A, Wang J, Wang K, et al.. Therapeutic Hypothermia Alleviates Hydrocephalus and Neurological Dysfunction Post Intraventricular Hemorrhage by Enhancing Drainage of Glymphatic-Meningeal Lymphatic-Deep Cervical Lymphatic System. . 2026. PMID 41578884 · DOI · PMC12831171
- Guo P, Siddique R, Qian J, Qi L, Yong VW, Xue M. Apelin-13 Attenuates Blood-Brain Barrier Dysfunction Following Intracerebral Hemorrhage via Targeting the Keap1/Nrf2 Signaling. . 2025. PMID 41459616 · DOI · PMC12746050
- van Asch CJ, Luitse MJ, Rinkel GJ, van der Tweel I, Algra A, Klijn CJ. Incidence, case fatality, and functional outcome of intracerebral haemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol. 2010. PMID 20056489 · DOI
- Debette S, Schilling S, Duperron MG, Larsson SC, Markus HS. Clinical Significance of Magnetic Resonance Imaging Markers of Vascular Brain Injury: A Systematic Review and Meta-analysis. JAMA Neurol. 2019. PMID 30422209 · DOI · PMC6439887
- Ariesen MJ, Claus SP, Rinkel GJ, Algra A. Risk factors for intracerebral hemorrhage in the general population: a systematic review. Stroke. 2003. PMID 12843354 · DOI
- Poon MT, Fonville AF, Al-Shahi Salman R. Long-term prognosis after intracerebral haemorrhage: systematic review and meta-analysis. J Neurol Neurosurg Psychiatry. 2014. PMID 24262916 · DOI
- Al-Shahi Salman R, Frantzias J, Lee RJ, Lyden PD, Battey TWK, Ayres AM, et al.. Absolute risk and predictors of the growth of acute spontaneous intracerebral haemorrhage: a systematic review and meta-analysis of individual patient data. Lancet Neurol. 2018. PMID 30120039 · DOI · PMC6143589
- Jovin TG, Nogueira RG, Lansberg MG, Demchuk AM, Martins SO, Mocco J, et al.. Thrombectomy for anterior circulation stroke beyond 6 h from time last known well (AURORA): a systematic review and individual patient data meta-analysis. Lancet. 2022. PMID 34774198 · DOI
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.