Can microglial iron-driven ferroptosis be the key to post-hemorrhage neuroinflammation?

 Your competent doctor has been working on solving microbleeds  for over two decades, right? And ferroptosis for well over a decade? NO? So, INCOMPETENT THEN? 

• cerebral microbleeds (8 posts to August 2017) And references to a 2005 one!
• Ferroptosis (12 posts to July 2012)

Can microglial iron-driven ferroptosis be the key to post-hemorrhage neuroinflammation?

After a cerebral hemorrhage (CH), heme oxygenase-1 (HO-1) catalyzes the conversion of heme to release Fe²⁺. Microglia are the primary cells responsible for immune function in the brain. Upon the uptake of heme and iron ions, microglia are activated, leading to the subsequent release of inflammatory mediators and reactive oxygen species. Neuroinflammation and oxidative stress are common features of various brain diseases. Cerebral hemorrhage can trigger microglial iron accumulation and ferroptosis, which in turn leads to neuroinflammation and oxidative stress imbalance in the brain. Therefore, inhibiting microglial iron accumulation and ferroptosis alleviates cerebral hemorrhage-mediated neural damage and counteracts various brain diseases induced by it. We propose that the occurrence of many brain diseases is influenced by the location of cerebral microbleeds, suggesting that cerebral microbleeds may be a high-risk factor for inducing these diseases.

REFERENCES

1. Neuroinflammatory diseases triggered by cerebral hemorrhage: microglial iron accumulation and ferroptosis.

   Gao X, Li H, Liang J, Liu S.

   Eur J Pharmacol. 2026 May 14; 1026 178972 [Epub ahead of print]

Cardiovascular Management in Asymptomatic (Silent) Cerebral Microbleeds and Suspected Cerebral Amyloid Angiopathy

 Survivors would DEMAND PROTOCOLS AND RESULTS instead of the crapola of 'suggestions' and 'care'! Do you have any working brain cells at all?

Cardiovascular Management in Asymptomatic (Silent) Cerebral Microbleeds and Suspected Cerebral Amyloid Angiopathy

Andreas Charidimou and

Eric E. Smith

Originally published11 Mar 2024https://doi.org/10.1161/STROKEAHA.123.044167Stroke. 2024;55:1101–1112

Abstract

Cerebral microbleeds (CMBs) detected on blood-sensitive magnetic resonance imaging sequences are usually a sign of an underlying cerebral small vessel disease such as sporadic cerebral amyloid angiopathy or sporadic nonamyloid small vessel pathology (eg, arteriolosclerosis). Much of the enduring interest in CMBs relates to their high prevalence (partly due to the widespread use of magnetic resonance imaging) in the context of stroke, cognitive impairment and in healthy individuals, and the clinical uncertainties created about the safety of antithrombotic medications due to their association with both future hemorrhagic and ischemic stroke. Historically, the research literature overwhelmingly emphasized the future hemorrhagic risk associated with CMBs, potentially leading to unnecessary withholding of treatments proven effective at preventing thrombosis, such as anticoagulants in patients with atrial fibrillation who happened to have some microbleeds. The lack of strong guidelines in this area contributes to wide variation in clinical practice.(The answer is to create protocols, not throw up your hands in the air in defeat!) In this article, we critically review and discuss the implications of silent CMBs and cortical superficial siderosis (ie, without symptomatic intracerebral hemorrhage) in different clinical settings: the general population, patients with ischemic stroke, and the memory clinic. Emerging evidence, albeit not from randomized controlled trials, suggests that in most patients, CMBs alone should not prevent the use of antithrombotics or anticoagulants for stroke prevention, when they are otherwise indicated. Where possible, we provide specific suggestions for clinical care grounded in both the limited available literature and our personal clinical practice.

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Cardiovascular Management in Asymptomatic (Silent) Cerebral Microbleeds and Suspected Cerebral Amyloid Angiopathy

FYI, for your doctor to understand and implement.

Cardiovascular Management in Asymptomatic (Silent) Cerebral Microbleeds and Suspected Cerebral Amyloid Angiopathy

Andreas Charidimou and

Eric E. Smith

Originally published11 Mar 2024https://doi.org/10.1161/STROKEAHA.123.044167Stroke. 2024;0

Abstract

Cerebral microbleeds (CMBs) detected on blood-sensitive magnetic resonance imaging sequences are usually a sign of an underlying cerebral small vessel disease such as sporadic cerebral amyloid angiopathy or sporadic nonamyloid small vessel pathology (eg, arteriolosclerosis). Much of the enduring interest in CMBs relates to their high prevalence (partly due to the widespread use of magnetic resonance imaging) in the context of stroke, cognitive impairment and in healthy individuals, and the clinical uncertainties created about the safety of antithrombotic medications due to their association with both future hemorrhagic and ischemic stroke. Historically, the research literature overwhelmingly emphasized the future hemorrhagic risk associated with CMBs, potentially leading to unnecessary withholding of treatments proven effective at preventing thrombosis, such as anticoagulants in patients with atrial fibrillation who happened to have some microbleeds. The lack of strong guidelines in this area contributes to wide variation in clinical practice. In this article, we critically review and discuss the implications of silent CMBs and cortical superficial siderosis (ie, without symptomatic intracerebral hemorrhage) in different clinical settings: the general population, patients with ischemic stroke, and the memory clinic. Emerging evidence, albeit not from randomized controlled trials, suggests that in most patients, CMBs alone should not prevent the use of antithrombotics or anticoagulants for stroke prevention, when they are otherwise indicated. Where possible, we provide specific suggestions for clinical care grounded in both the limited available literature and our personal clinical practice.

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• Download PowerPoint

First-of-its-kind study reveals a new culprit in the formation of brain hemorrhages

 FYI, hopefully your doctor is fully invested in following this research to prevent your next hemorrhagic stroke.

First-of-its-kind study reveals a new culprit in the formation of brain hemorrhages

Nov 20 2023University of California - Irvine

A first-of-its-kind study led by the University of California, Irvine has revealed a new culprit in the formation of brain hemorrhages that does not involve injury to the blood vessels, as previously believed. Researchers discovered that interactions between aged red blood cells and brain capillaries can lead to cerebral microbleeds, offering deeper insights into how they occur and identifying potential new therapeutic targets for treatment and prevention.

The findings, published online recently in the Journal of Neuroinflammation, describe how the team was able to watch the process by which red blood cells stall in the brain capillaries and then observe how the hemorrhage happens. Cerebral microbleeds are associated with a variety of conditions that occur at higher rates in older adults, including hypertension, Alzheimer's disease and ischemic stroke.

We have previously explored this issue in cell culture systems, but our current study is significant in expanding our understanding of the mechanism by which cerebral microbleeds develop. Our findings may have profound clinical implications, as we identified a link between red blood cell damage and cerebral hemorrhages that occurs at the capillary level."

Dr. Mark Fisher, co-corresponding author, professor of neurology in UCI's School of Medicine

The team exposed red blood cells to a chemical called tert-butyl hydroperoxide that caused oxidative stress; the cells were then marked with a fluorescent label and injected into mice. Using two different methods, the researchers observed the red blood cells getting stuck in the brain capillaries and then being cleared out in a process called endothelial erythrophagocytosis. As they moved out of the capillaries, microglia inflammatory cells engulfed the red blood cells, which led to the formation of a brain hemorrhage.

"It has always been assumed that in order for cerebral hemorrhage to occur, blood vessels need to be injured or disrupted. We found that increased red blood cell interactions with the brain capillaries represent an alternative source of development," said co-corresponding author Xiangmin Xu, UCI professor of anatomy & neurobiology and director of the campus's Center for Neural Circuit Mapping. "We need to examine in detail the regulation of brain capillary clearance and also analyze how that process may be related to insufficient blood supply and ischemic stroke, which is the most common form of stroke, to help advance the development of targeted treatments."

Leveraging the broad, collaborative infrastructure and robust resources of the Center for Neural Circuit Mapping, other team members were Rachita Sumbria, co-first author/co-corresponding author and associate professor in the Chapman University School of Pharmacy; Hai Zhang, co-first author and postdoctoral researcher in UCI's Department of Anatomy & Neurobiology; Rudy Chang, co-first author and Chapman University School of Pharmacy graduate student; Jiahong Sun, postdoctoral researcher at Chapman University; David Cribbs, professor-in-residence at UCI's Institute for Memory Impairments and Neurological Disorders; and Todd Holmes, UCI professor of physiology & biophysics.

This work was supported by the National Institute on Aging under award numbers R01AG062840, R01AG072896, R35127102, RF1 AG065675 and R01NS121246 and by National Institute of Neurological Disorders and Stroke grant R01NS20989.

Source:

University of California - Irvine

Journal reference:

Zhang, H., et al. (2023). Erythrocyte–brain endothelial interactions induce microglial responses and cerebral microhemorrhages in vivo. Journal of Neuroinflammation. doi.org/10.1186/s12974-023-02932-5.

EXPRESS: Cerebral microbleeds development after stroke thrombolysis: A secondary analysis of the THAWS randomized clinical trial

 You described a problem of cerebral microbleeds but gave us nothing on how to prevent them or treat them after they've occurred. Useless.

EXPRESS: Cerebral microbleeds development after stroke thrombolysis: A secondary analysis of the THAWS randomized clinical trial

Show all authors

Kaori Miwa, Masatoshi Koga, Manabu Inoue, , , , , , , , , , , , , , , , ...

First Published July 20, 2021 Research Article 

https://doi.org/10.1177/17474930211035023

Article information

Abstract

Background and aim: 

 We determined to investigate the incidence and clinical impact of new cerebral microbleeds (CMBs) after intravenous thrombolysis (IVT) in patients with acute stroke.

Methods: 

The THAWS was a multicenter, randomized trial to study the efficacy and safety of IVT with alteplase in patients with wake-up stroke or unknown onset stroke. Prescheduled T2*-weighted imaging assessed CMBs at 3-time points: baseline, 22–36 hours, and 7–14 days. Outcomes included new CMBs development, modified Rankin Scale [mRS] ≥3 at 90 days, and change in the National Institutes of Health Stroke Scale [NIHSS] score from 24 h to 7 days.

Results:  

Of all 131 patients randomized in the THAWS trial, 113 patients (mean 74.3±12.6 years, 50 female, 62 allocated to IVT) were available for analysis. Overall, 46 (41%) had baseline CMBs (15 strictly lobar CMBs, 14 mixed CMBs, and 17 deep CMBs). New CMBs only emerged in the IVT group (7 patients, 11%) within a median of 28.3 h, and did not additionally increase within a median of 7.35 days. In adjusted models, number of CMBs (relative risk [RR]1.30, 95%confidence interval [CI]: 1.17–1.44), mixed distribution (RR 19.2, 95%CI: 3.94–93.7), and CMBs burden ≥5 (RR 44.9, 95%CI: 5.78–349.8) were associated with new CMBs. New CMBs was associated with an increase in NIHSS score (p=0.023). Treatment with alteplase in patients with baseline ≥5 CMBs resulted in a numerical shift toward worse outcomes on ordinal mRS (median [IQR]; 4 [3–4] vs. 0 [0–3]), compared with those with <5 CMBs (common odds ratio 17.1, 95% CI: 0.76 –382.8). The association of baseline ≥5 CMBs with ordinal mRS score differed according to the treatment group (P interaction=0.042).

Conclusion: 

New CMBs developed within 36 h in 11% of the patients after IVT, and they were significantly associated with mixed-distribution and ≥5 CMBs. New CMBs development might impede neurological improvement. Furthermore, CMBs burden might affect the effect of alteplase.

Keywords

Brain microbleeds, Intracerebral hemorrahage, Ischaemic stroke, Stroke, Thrombolysis, rtPA

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Cerebral Microbleeds Should Not Deter Antithrombotics in Stroke

Do you prefer your hospital incompetence to be: Not knowing? OR not doing? Or maybe you prefer stroke survivors running a stroke hospital, they can't do any worse than stroke medical professionals.  This should prompt a change in the next week, test your hospital on that responsibility.

Cerebral Microbleeds Should Not Deter Antithrombotics in Stroke

Sue Hughes

May 23, 2019

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The presence of cerebral microbleeds should not deter the use of antithrombotic treatment in patients with recent ischemic stroke or transient ischemic attack (TIA), new data from a pooled analysis of cohort studies suggest.
The presence of microbleeds was linked to a greater risk for both future ischemic stroke and intracranial hemorrhage (ICH) in the analysis. Although the number of microbleeds was associated with a greater relative risk for subsequent ICH than for ischemic stroke, the absolute risk for ischemic stroke was consistently higher than the absolute risk for ICH regardless of microbleed burden or anatomic distribution.
The analysis was presented today at the 5th European Stroke Organisation Conference (ESOC) 2019 and was simultaneously published online May 23 in the Lancet Neurology.
"We found that the relative risk of ICH goes up more dramatically with increasing microbleed burden than the relative risk for ischemic stroke," senior author David J. Werring, PhD, UCL Queen Square Institute of Neurology, London, United Kingdom, told Medscape Medical News.

"But — and this is the really key finding — it doesn't matter how many microbleeds there were. The absolute risk of ischemic stroke is always higher than the absolute risk of ICH," Werring said.
"This evidence therefore does not support withholding antithrombotic treatment in patients with a history of stroke/TIA in patients with a high microbleed burden," he said.
Werring explained that new, sophisticated scanning methods that are often used in assessing stroke patients can detect the presence of microbleeds in the cerebral circulation. In radiologic examinations, these microbleeds appear as small, hypointense, ovoid or rounded regions.
"The question we are addressing in this analysis is whether the presence of microbleeds in patients who have had an ischemic stroke or TIA is a signal of an increased risk of ICH, which could have implications for the use of antithrombotic medications," he said. "This is something that has been challenging stroke doctors for several years now and generating considerable anxiety about whether to continue antithrombotic medication.

"Our results show that regardless of the type of antithrombotics/anticoagulants/antiplatelets used and however many microbleeds were present, the risk of ischemic stroke is always higher than the risk of ICH," he added. "This provides reassurance for clinicians and patients that in patients with a previous ischemic stroke or TIA, we do not need to worry too much about the presence of microbleeds on the scan — they should be treated with antithrombotic regardless."
In the Lancet Neurology article, Werring and colleagues note that in previous studies of this issue, the sample sizes were small and there were few ICH outcome events. Thus, these studies could not reliably answer the important clinical question of whether many cerebral microbleeds or patterns of cerebral microbleeds indicate a higher risk for ICH than for recurrent ischemic stroke.
The authors therefore conducted the current pooled analysis. The analysis included data regarding individual patients with ischemic stroke or TIA from 38 cohort studies in which microbleeds and future stroke/ICH events were documented. The analysis included a total of 20,322 patients; the median follow-up was 1.34 years.
During follow-up, 189 ICH events and 1113 ischemic strokes occurred.
Results showed that patients with cerebral microbleeds were at increased risk for ischemic stroke (hazard ratio [HR], 1.23) and ICH (HR, 2.45) in comparison with patients who did not have microbleeds.
Although the HR for ICH increased more with increasing microbleed burden than the HR for ischemic stroke, the rate of ischemic stroke always exceeded that of ICH.
Table. Rate of ICH and Ischemic Stroke With Increasing Microbleed Burden

Number of Microbleeds	Symptomatic ICH (Rate/1000 Patient-Years)	Symptomatic Ischemic Stroke (Rate/1000 Patient-Years)
0	4	30
1	8	37
2 – 4	9	48
≥5	23	64
≥10	27	64
≥20	39	73

"These microbleeds appear to be a marker of small vessel disease," Werring commented. "The vessels can either get blocked or bleed. The dots on the scan might not all be actual bleeds — they could be red cells that have not been cleared properly or previous ischemic lesions than have transformed into hemorrhage."
Commenting on the study for Medscape Medical News, Alistair Webb, BMBCh, MRCP(Neurol), DPhil FESO, University of Oxford, United Kingdom, said the results were "very interesting."
"This is observational data, so it is not the most reliable data we can have, but it does provide reassurance," Webb said. "It has been a concern that these imaging changes are a risk of future bleeding which we haven't quantified, but this new information shows patients with numerous microbleeds are still much more likely to have an ischemic stroke than an ICH, so antithrombotic treatment is still likely to have more benefit than harm."

Complements RESTART

Webb noted that this study fits in well with the RESTART study, which was also presented at ESOC 2019. That study showed that restarting antithrombotic therapy for patients after an ICH was safe.
"With these two new studies, we have a lot more security that in a patient who has an increased risk of ischemic stroke, we can give antithrombotic therapy and not be deterred by whether they've had an ICH (as in RESTART) or their scan shows the presence of these microbleeds (as in this study)," Webb said.
Werring agreed. "There is a common theme in these two studies — that antithrombotics appear to be safer than we thought."
In a comment that accompanied the article in the Lancet Neurology, Georgios Tsivgoulis, MD, and Aristeidis Katsanos, MD, University of Athens, Greece, point out that the main strengths of the new microbleed analysis are the large sample size, the prospective study design with strict inclusion and exclusion criteria, and the comprehensive, prespecified, robust statistical analysis. They add that the observational study design is prone to confounding and selection and indication biases.
They agree that the findings "suggest that cerebral microbleed presence, burden, and pattern on neuroimaging should not influence the decision to select appropriate antithrombotic therapy for secondary stroke prevention."
But they add that additional research is required to establish whether cerebral microbleeds should be incorporated as a neuroimaging marker in clinical risk prediction scores of recurrent ischemic stroke or ICH in patients with recent cerebral ischemia treated with oral anticoagulants or antiplatelet drugs.
The study was supported by the British Heart Foundation and UK Stroke Association. Werring has received personal fees from Bayer outside the submitted work. Disclosures of relevant financial relationships of the study's coauthors appear in the original article. The editorialists have disclosed no relevant financial relationships.
Lancet Neurol. Published online May 23, 2019. Full text, Comment
5th European Stroke Organisation Conference (ESOC) 2019: Presented May 23, 2019.

Impact of Microbleeds on Outcome Following Recanalization in Patients With Acute Ischemic Stroke

Just why the hell are we using the Rankin scale for measuring anything in stroke? It has no discriminatory power and nothing objective except for 6 - death.

Impact of Microbleeds on Outcome Following Recanalization in Patients With Acute Ischemic Stroke

Kang-Ho Choi

,

Ja-Hae Kim

,

Kyung-Wook Kang

,

Joon-Tae Kim

,

Seong-Min Choi

,

Seung-Han Lee

,

Man-Seok Park

,

Byeong-Chae Kim

,

Myeong-Kyu Kim

,

Ki-Hyun Cho

Originally published7 Dec 2018Stroke. 2018;0:STROKEAHA.118.023084

Abstract

Background and Purpose—

We analyzed the association between cerebral microbleeds (CMBs) and clinical outcome in acute ischemic stroke patients and especially in a subgroup of patients with successful recanalization.(Your definition of success is obviously not what it should be. 100% recovery, not the lazy, 'Hey we got the artery open')

Methods—

A total of 1532 acute ischemic stroke patients treated with intravenous thrombolysis or mechanical thrombectomy were enrolled in this prospective cohort study. The primary outcome was measured using the modified Rankin Scale at 3 months, according to the CMB status based on magnetic resonance imaging at admission. Favorable outcome was defined as functional independence with modified Rankin Scale scores of 0 to 2. Secondary outcomes included the occurrence of symptomatic intracranial hemorrhage.

Results—

There was no statistically significant association between the presence of CMB and favorable outcome at 3 months when considering all patients (44.3% versus 37.6%; P=0.121). In patients with recanalization, the number of patients with favorable outcomes was significantly higher in the CMB-negative than in the CMB-positive group (57.0% versus 36.0%; P<0.001). In the final multivariate analysis, the presence of CMB, and in particular high CMB burden (≥5), and lobar location, were significantly associated with less favorable 3-month outcomes (odds ratio=0.57; 95% CI, 0.33−0.97; P=0.038) and symptomatic intracranial hemorrhage (odds ratio=3.21; 95% CI, 1.37−7.49; P=0.007) in patients with recanalization. In the analysis of subgroups, a statistically significant interaction was found between CMB presence and recanalization in predicting functional outcomes at 3 months.

Conclusions—

These results indicate that the presence of CMBs, and especially high burden and lobar location, are independent predictors of poor 3-month clinical outcomes and may increase symptomatic intracranial hemorrhage risk in acute ischemic stroke patients with recanalization. Our findings suggest that CMBs lead to more unfavorable effects in patients with recanalization after large vessel occlusion than in those without recanalization.

Diverse Inflammatory Response After Cerebral Microbleeds Includes Coordinated Microglial Migration and Proliferation

You'll have to ask your doctors what they are doing to control this inflammatory response. Your doctor has had 12.5 years to come up with a solution and I bet NOTHING was done. INCOMPETENCE AT ITS FINEST.

Cerebral microbleeds are common in ischemic stroke but rare in TIA December 2005

 

Diverse Inflammatory Response After Cerebral Microbleeds Includes Coordinated Microglial Migration and Proliferation

Sung Ji Ahn, Josef Anrather, Nozomi Nishimura, Chris B. Schaffer

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https://doi.org/10.1161/STROKEAHA.117.020461

Stroke. STROKEAHA.117.020461

Originally published May 29, 2018

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Abstract

Background and Purpose—Cerebral microbleeds are linked to cognitive decline, but it remains unclear how they impair neuronal function. Infarction is not typically observed near microbleeds, suggesting more subtle mechanisms, such as inflammation, may play a role. Because of their small size and largely asymptomatic nature, real-time detection and study of spontaneous cerebral microbleeds in humans and animal models are difficult.

Methods—We used in vivo 2-photon microscopy through a chronic cranial window in adult mice to follow the inflammatory response after a cortical microhemorrhage of ≈100 µm diameter, induced by rupturing a targeted cortical arteriole with a laser.

Results—The inflammatory response included the invasion of blood-borne leukocytes, the migration and proliferation of brain-resident microglia, and the activation of astrocytes. Nearly all inflammatory cells responding to the microhemorrhage were brain-resident microglia, but a small number of CX3CR1⁺ and CCR2⁺ macrophages, ultimately originating from the invasion of blood-borne monocytes, were also found near the lesion. We found a coordinated pattern of microglia migration and proliferation, where microglia within 200 µm of the microhemorrhage migrated toward the lesion over hours to days. In contrast, microglia proliferation was not observed until ≈40 hours after the lesion and occurred primarily in a shell-shaped region where the migration of microglia decreased their local density. These data suggest that local microglia density changes may trigger proliferation. Astrocytes activated in a similar region as microglia but delayed by a few days. By 2 weeks, this inflammatory response had largely resolved.

Conclusions—Although microhemorrhages are small in size, the brain responds to a single bleed with an inflammatory response that involves brain-resident and blood-derived cells, persists for weeks, and may impact the adjacent brain microenvironment.

Relationship of cerebral microbleeds to inflammatory marker levels

I got nothing out of this article. What problems does this cause? What solutions there are to prevent them? What interventions are needed to resolve the problems caused?
http://nnjournal.net/article/view/1904

Qiao-Li Lu¹, Chen Li¹, Ying Song¹, Liang Wang², Zhi-Rong Jia³

¹Department of Neurology, Tianjin 5th Center Hospital, Tianjin 300450, China.

²Department of Neurosurgery, Tianjin 5th Center Hospital, Tianjin 300450, China.

³Department of Neurology, Peking University First Hospital, Beijing 100034, China.

Correspondence Address: Dr. Chen Li, Department of Neurology, Tianjin 5th Center Hospital, 41 Zhejiang Road, Tanggu, Tianjin 300450, China. 
E-mail: lichenokk@163.com

Dr. Chen Li works in Department of Neurology, Tianjin 5th Center Hospital. She graduated from Tianjin Medical University and got her Master of Medicine in July 2011, and she is skilled in the diagnosis and treatment of cerebrovascular diseases, neuroimmune diseases and anxiety-depression diseases. She enjoys reading and writing as well as looking after her daughter.
Click here to view

Date of Submission           24-02-2017

Date of Acceptance           10-05-2017

Date of Web Publication    08-08-2017

DOI:10.20517/2347-8659.2017.05

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License (http://creativecommons.org/licenses/by-nc-sa/3.0/), which allows others to remix, tweak and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article:

Lu QL, Li C, Song Y, Wang L, Jia ZR. Relation of cerebral microbleeds to inflammatory marker levels. Neuroimmunol Neuroinflammation 2017;4:145-51.

Abstract

Aim: The purpose of this study is to investigate the incidence, distribution and risk factors of cerebral microbleeds (CMBs) and the relation between CMBs and inflammation in ischemic cerebrovascular disease.  
Methods: Two hundred and one patients without acute infarction or transient ischemic attack were enrolled. The presence and number of CMB were assessed on susceptibility-weighted imaging. The traditional risk factors of CMB were recorded. Levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and matrix metalloproteinase-9 (MMP-9) were tested. Logistic regression analyses were used for multiple-factor analysis of risk factors of CMB.  
Results: Of the 201 patients, 49 (24.38%) had CMB. Multivariate logistic regression analyses showed that the age, the prevalence of hypertension, silent lacunar infarction, white matter lesion, Montreal Cognitive Assessment Score, the using rate of antithrombotic drugs and levels of hs-CRP, IL-6, MMP-9 were the risk factors for CMB. After adjustments for traditional risk factors, inflammatory marker levels remained to be associated with CMBs. The adjusted odd ratios of hs-CRP, IL-6 and MMP-9 were 1.745 (1.342-2.270), 1.223 (1.018-1.533) and 1.284 (1.082-1.423), respectively. Furthermore, inflammatory marker levels were the risk factor for deep or infratentorial CMBs and lobar CMBs.  
Conclusion: The age, prevalence of hypertension, silent lacunar infarction, white matter lesion, MoCA Score, the using rate of antithrombotic drugs and serum hs-CRP, IL-6, and MMP-9 levels were the independent risk factors for CMBs.