A deep learning system for detecting silent brain infarction and predicting stroke risk

 Why the fuck didn't you do research that prevents stroke? This is useless until that occurs! You're all fired!

A deep learning system for detecting silent brain infarction and predicting stroke risk

• Nan Jiang,
• Hongwei Ji,
• Zhouyu Guan,
• Yuesong Pan,
• Chenxin Deng,
• Yuchen Guo,
• Dan Liu,
• Tingli Chen,
• Shiyu Wang,
• Yilan Wu,
• Dawei Yang,
• An Ran Ran,
• Haslina Hamzah,
• Miao Li Chee,
• Changchang Yin,
• Benjamin Sommer Thinggaard,
• Frederik N. Pedersen,
• Qingsheng Peng,
• Ten Cheer Quek,
• Jocelyn Hui Lin Goh,
• Sarkaaj Singh,
• Anis Syazwani Abd Raof,
• Jian Wen Samuel Lee-Boey,
• Yuwei Lu,
• …
• Tien Yin Wong 

Nature Biomedical Engineering (2025)Cite this article

• 71 Altmetric

• Metrics details

Abstract

Current brain imaging to detect silent brain infarctions (SBIs) is not feasible for the general population. Here, to overcome this challenge, we developed a retinal image-based deep learning system, DeepRETStroke, to detect SBI and refine stroke risk. We use 895,640 retinal photographs to pretrain the DeepRETStroke system, which encodes a domain-specific foundation model for representing eye–brain connections. Then, we validated the downstream clinical tasks of DeepRETStroke using 213,762 retinal photographs from diverse datasets across China, Singapore, Malaysia, the USA, the UK and Denmark to detect SBI and predict stroke events. DeepRETStroke performed well in internal validation datasets, with areas under the curve of 0.901 for predicting incident stroke and 0.769 for predicting recurrent stroke. External validations demonstrated consistent performances across diverse datasets. Finally, in a prospective study comprising 218 participants with stroke, we assessed the performance of DeepRETStroke compared with clinical traits in guiding strategies for stroke recurrence prevention. Altogether, the retinal image-based deep learning system, DeepRETStroke, is superior to clinical traits in predicting stroke events, especially by incorporating the detection of SBI, without the need for brain imaging.

ADAPTIVE NEUROPLASTICITY ASSOCIATED WITH ISCHEMIC BRAIN DAMAGE AND ITS ROLE IN STROKE RECOVERY: THEORETICAL PREREQUISITES FOR EFFECTIVE NEUROREHABILITATION

We don't SPECIFICALLY know why a neuron gives up its' current job and takes on a neighbors. Thus, nothing on neuroplasticity is scientifically repeatable on demand. So, DEMAND your doctor give you EXACT PROTOCOLS to use. Don't allow your doctor to give you generalities or guidelines. This person understands that problem because of the word theoretical instead of detailing exactly how to deliver neuroplasticity exactly.

 ADAPTIVE NEUROPLASTICITY ASSOCIATED WITH ISCHEMIC
BRAIN DAMAGE AND ITS ROLE IN STROKE RECOVERY: THEORETICAL PREREQUISITES FOR EFFECTIVE NEUROREHABILITATION

Khairieva Mukhsina Farkhadovna

Bukhoro davlat Tibbet institutes

THESIS

https://orcid.org/0000-0002-0002-0015

xayriyeva.muxsina@bsmi.uz

https://doi.org/10.5281/zenodo.15227136

Ischemic brain damage, like other pathogenic factors, initiates the

reorganization of cortical centers and pathways outside the "nuclear zone" of

acute or chronic ischemia, which limits the spontaneous restoration of functions

in victims. Accordingly, knowledge of the basic patterns of post-ischemic

neuroplastic remodeling(This doesn't exist yet, so your incompetent doctor needs to get that research going! The problem has been known for decades which is why I consider your doctor incompetent for not even attempting to get it solved. It's as if survivor recovery is not in the job description! And that leads directly to board of directors incompetence for not setting correct goals!) is crucial for developing more effective rehabilitation

strategies for stroke patients. The article discusses modern concepts of

neuroplasticity: the main patterns of post-stroke reorganization of the central

nervous system, studied in rodents, as well as clinical markers of compensatory

and regenerative processes in conditions of chronic cerebral ischemia in

cerebrovascular diseases, which allows us to identify the mechanisms

underlying the remodeling of neural networks in the penumbra and

contralateral hemisphere against the background of ischemic damage. At the

same time, the analysis of electrophysiological experimental data demonstrated

the restructuring of functional connections in both hemispheres far beyond the

focus of cerebral infarction, and clinical and biochemical studies on the model of

chronic cerebral ischemia in patients helped to identify key trophic factors

determining compensatory and regenerative processes. The results obtained

make it possible to justify the use of noninvasive brain stimulation methods and

some pharmacological agents to accelerate the recovery of impaired functions in

patients with this profile, and therefore to form rehabilitation protocols using

robotic devices to promote the development of adaptive neuroplasticity and full-

fledged functional recovery.

In this regard, it seems relevant to analyze the results of recent

experimental and clinical studies that have studied the processes of

neuroplasticity in ischemic brain lesions in order to develop and implement new

rehabilitation strategies.

The term "brain plasticity" or "neuroplasticity" defines all (morphological

and functional) changes in neural networks and glial complexes that occur in the

central nervous system throughout a person's life [9]. These changes are not

only closely related to the mechanisms of learning, development, aging, and

adaptation to the environment, but also underlie adaptive neuroplasticity –

compensatory and regenerative reactions that occur during the formation of

pathomorphological and/or functional disorders caused by diseases or injuries

of the nervous system [10]. In particular, acute ischemia and chronic ischemia

cause multilevel (in the cerebral cortex, the penumbra zone of the affected

hemisphere and the contralateral hemisphere, subcortical and cerebrospinal

regions) neuroplastic reactions of neural networks with temporal and spatial

organization (Figure) [11, 12], and these changes are sensitive to subsequent

damage regardless of their nature [13, 14].

The degree and range of neuroplastic changes depend on the size and rate

of formation of ischemic brain damage (acute or chronic). In microinfarcts

developing in the cerebral cortex against the background of transient ischemic

attacks or chronic cerebral ischemia caused, for example, by small vessel

disease, periinfarction zones can compensate for lost functions in the shortest

possible time, which explains the existence of "mute" strokes [1, 2]. This is

especially true of the ventral premotor region, which, being in close relationship

with the primary motor cortex, produces and releases vascular endothelial

growth factor, which has angiogenic and neuroprotective properties in the early

period after a heart attack [12]. In rodents, after a stroke, there is a steady

reorganization of the motor map of the rostral zone of representation of the

forelimbs (premotor cortex) [2, 3, 4]. Accordingly, the development of secondary

post-ischemic metabolic disorders in it exacerbates the primary motor deficit

[5].

The mechanisms underlying cortical reorganization and restoration of

impaired functions remain not fully understood [1]. This is especially true of the

gamma-aminobutyric acid (GABA) system and neuroglia, which may play an

important role in the control of neuroplastic reactions. So far, it has been

established that the neuroglial matrix, which consists of condensed chondroitin

sulfate proteoglycans surrounding mainly the bodies of GABAergic neurons,

correlates according to the feedback principle with adaptive neuroplasticity and

repair of the brain due to interneurons containing parvalbumin [6]. The

significance of perineuronal networks has been thoroughly investigated during

the maturation of the visual system. They have been found to have a stabilizing

effect on mature neural networks and a negative effect on neuroplasticity [7, 8].

Thus, inhibition of perineuronal networks by injections of the bacterial enzyme

chondroitinase ABC after damage to the central nervous system accelerated the

restoration of sensorimotor functions [3-4], and a spontaneous decrease in the

number of perineuronal networks in the cortex in the penumbra area indicated

an increase in adaptive neuroplasticity [23]. In turn, increased GABAergic

activity after stroke did not improve recovery rates [2], but rather worsened

motor deficits [4]. Moreover, it has been clinically confirmed that an artificial

decrease in GABAergic activity had a positive effect on functional recovery [4].

A special role in the development of neurological deficits in acute and

chronic ischemia and further functional recovery is played by the hemisphere

contralateral to the actual lesion, since animal studies and clinical practice have

well shown that neuronal connections after acute ischemia change not only in

the damaged hemisphere of the brain, but also on the opposite side.

Due to the improvement of scientific methods, it has become possible to

study changes in remote brain regions with local ischemic damage based on the

concept of connectionism within the framework of microscopic (synapses),

mesoscopic (homotopic brain regions) and macroscopic (thalamo-cortical

connections) neuroplastic reactions.

References at link.

Correlation of silent brain infarcts and leukoaraiosis in middle-aged ischemic stroke patients: a retrospective study

So your competent? doctor is required to have EXACT PROTOCOLS that restore myelin. Is your doctor competent in this regard? Or don't you have a functioning stroke doctor? Does your doctor even know this problem needs to be fixed?

 Leukoaraiosis is the rarefaction of the brain white matter caused by loss of axons and myelin due to ischemic injury and appears to be of central importance in the neurocognitive defects associated with HD.

The latest here:

Correlation of silent brain infarcts and leukoaraiosis in middle-aged ischemic stroke patients: a retrospective study

Mohammad Fathi Abdulsalam¹Nour Shaheen^2*†Ahmed Shaheen²Yasmeen Jamal Alabdallat³Abdelraouf Ramadan⁴Mostafa Meshref¹Fathy Mahmoud Mansour¹Elsayed Abed¹Abdel-Ghaffar I. Fayed¹Mohamed Ahmed Zaki¹Ahmad F. El-Adawy¹Oliver Flouty⁵Mohamed Hamed¹

• ¹Department of Neurology, Faculty of Medicine, Al-Azhar University, Cairo, Egypt
• ²Alexandria Faculty of Medicine, Alexandria University, Alexandria, Egypt
• ³Faculty of Medicine, Hashemite University, Zarqa, Jordan
• ⁴Kasr Alainy Faculty of Medicine, Cairo University, Cairo, Egypt
• ⁵Department of Neurosurgery and Brain Repair, University of South Florida, Tampa, FL, United States

Background: Cerebrovascular diseases of the brain are usually defined by transient ischemic attacks and strokes. However, they can also cause brain injuries without neurological events. Silent brain infarcts (SBI) and leukoaraiosis are symptoms of both vascular and neurological abnormalities. This study aims to investigate the association between SBI, leukoaraiosis, and middle-aged patients with ischemic stroke.

Methods: A single-center retrospective study of 50 middle-aged, ischemic stroke patients were studied from November 2022 and May 2023. The patients were divided into two groups based on the presence or absence of leukoaraiosis. History taking, physical examination, brain CT scan, and MRI were all part of the diagnostic process. Metabolic syndrome (MetS) was also assessed through various factors. The statistical analysis included descriptive statistics, logistic regression analysis, and chi-square test.

Results: Out of the cohort comprising 50 patients, characterized by a mean age of 52.26 years (SD 5.29), 32 were male, constituting 64% of the sample. Among these patients, 26 individuals exhibited leukoaraiosis, with 17 of them (65.4%) also presenting with SBI. Moreover, within this cohort, 22 patients were diagnosed with MetS, representing 84.6% of those affected. The Multivariate logistic regression analysis showed a strong and independent association between leukoaraiosis and SBI. Individuals with leukoaraiosis were nearly five times more likely to have SBI compared to those without leukoaraiosis.

Conclusion: The study highlights leukoaraiosis as a significant risk factor for SBI, alongside MetS. Advanced imaging techniques have facilitated their detection, revealing a higher prevalence among stroke patients, particularly associated with age and hypertension. Further research is needed to fully understand their complex relationship and develop better management strategies for cerebrovascular diseases, ultimately improving patient outcomes.

Introduction

Historically, cerebrovascular disease of the brain has been defined by the symptoms and signs of transient ischemic attack or stroke. However, neuropathological studies in highly selected populations have revealed that vascular disease can cause brain injury in the absence of these acute neurological events. The advent of advanced brain-imaging techniques, such as computerized tomography (CT) and Magnetic resonance imaging (MRI), has allowed similar observations to be made in patient groups and healthy individuals, necessitating a reconsideration of the definition of cerebrovascular disease (1, 2). Signs of cerebral small vessel disease on conventional MRI include leukoaraiosis, recent subcortical lacunar infarcts (clinically symptomatic), lacunes (clinically silent), cerebral microbleeds, prominent perivascular spaces, and cerebral atrophy (3). These brain infarcts, while often asymptomatic, demand increased attention to mitigate the deleterious effects of vascular disease in the brain. Silent brain infarctions (SBIs) comprise two subtypes: lacunar and non-lacunar, resulting from small perforating artery occlusion and embolism or athero-sclerotic stenosis, respectively. The advancement of MRI technology enables the distinction between these subtypes (4–6). Therefore, exploring the distinct risk factors between the two subtypes, especially in the case of SBI, could lead to the development of specific prevention strategies, particularly for middle-aged individuals. Hypertension (HTN), apart from age, is the most widely accepted risk factor associated with SBI. Furthermore, the consistent correlation between hypertension and these infarcts suggests a critical role for hypertensive small-vessel disease in their pathogenesis (7). However, further research is necessary to better define the association between hypertension and brain infarcts, particularly in terms of preventing SBI through effective hypertension control. SBI and leukoaraiosis (LA) are intricate cerebral manifestations that have garnered considerable attention due to their association with diverse vascular and metabolic abnormalities. Hence, comprehending the intricate relationship between these cerebral alterations and MetS is of paramount importance for elucidating their underlying mechanisms and devising effective prevention and management strategies. Leukoaraiosis was observed through MRI and manifests as increased signal intensity in the white matter, often attributed to small vessel disease and pathological processes such as demyelination, gliosis, and vessel lipo hyalinosis (8). Conversely, SBIs denote brain tissue damage resulting from inadequate blood supply without acute neurological symptoms. Though often asymptomatic, SBIs pose a substantial risk for future stroke and cognitive decline (9). MetS plays a pivotal role in the development of LA and SBIs, operating through mechanisms such as vascular dysfunction, inflammation, insulin resistance, and dyslipidemia (10). The diagnosis of LA and SBIs primarily relies on MRI techniques, with fluid-attenuated inversion recovery (FLAIR) imaging sequences commonly employed to detect and assess the extent of white matter changes (11). Epidemiological data indicate a higher prevalence of LA and SBIs with advancing age, affecting a significant proportion of individuals over 65 years. This research aims to investigate the association between LA, SBIs, and middle-aged patients with ischemic stroke. The study focuses on middle-aged stroke patients to address the critical period in stroke epidemiology, capture a substantial portion of stroke cases in a relatively younger age group, identify early risk factors and pathophysiological mechanisms, and provide clinically relevant insights for healthcare providers in terms of risk stratification, diagnostics, and treatment strategies.

More at link.

Covert Cerebrovascular Changes in People With Heart Disease

Now if we had any brains at all in the stroke medical world this research would trigger more research to find ways to prevent silent brain infarction (SBI) and cerebral small vessel disease (CSVD). But there is NO leadership in stroke.

Covert Cerebrovascular Changes in People With Heart Disease

A Systematic Review and Meta-Analysis

Zien Zhou, MD, PhD https://orcid.org/0000-0001-6543-7113, Shoujiang You, MD, PhD, Yuki Sakamoto, MD, Ying Xu, MD, PhD, Song Ding, MD, PhD, Wenyi Xu, MD, Wenjie Li, MS, … Show All … , and Cheryl Carcel, MD, PhD https://orcid.org/0000-0001-8942-953XAuthors Info & Affiliations

April 23, 2024 issue

102 (8)

https://doi.org/10.1212/WNL.0000000000209204

• 
  

• Abstract
• Study Funding
• Disclosure
• Publication History
• Supplementary Material
• References

• Information & Authors
• Metrics & Citations
• Get Access
• References
• 
  

• • Share

Abstract

Background and Objectives

To determine the prevalence of silent brain infarction (SBI) and cerebral small vessel disease (CSVD) in adults with atrial fibrillation (AF), coronary artery disease, heart failure or cardiomyopathy, heart valve disease, and patent foramen ovale (PFO), with comparisons between those with and without recent stroke and an exploration of associations between heart disease and SBI/CSVD.

Methods

Medline, Embase, and Cochrane Library were systematically searched for hospital-based or community-based studies reporting SBI/CSVD in people with heart disease. Data were extracted from eligible studies. Outcomes were SBI (primary) and individual CSVD subtypes. Summary prevalence (95% confidence intervals [CIs]) were obtained using random-effects meta-analysis. Pooled prevalence ratios (PRs) (95% CI) were calculated to compare those with heart disease with available control participants without heart disease from studies.

Results

A total of 221 observational studies were included. In those with AF, the prevalence was 36% (31%–41%) for SBI (70 studies, N = 13,589), 25% (19%–31%) for lacune (26 studies, N = 7,172), 62% (49%–74%) for white matter hyperintensity/hypoattenuation (WMH) (34 studies, N = 7,229), and 27% (24%–30%) for microbleed (44 studies, N = 13,654). Stratification by studies where participants with recent stroke were recruited identified no differences in the prevalence of SBI across subgroups (p_homogeneity = 0.495). Results were comparable across participants with different heart diseases except for those with PFO, in whom there was a lower prevalence of SBI [21% (13%–30%), 11 studies, N = 1,053] and CSVD. Meta-regressions after pooling those with any heart disease identified associations of increased (study level) age and hypertensives with more SBIs and WMH (p_regression <0.05). There was no evidence of a difference in the prevalence of microbleed between those with and without heart disease (PR [95% CI] 1.1 [0.7–1.7]), but a difference was seen in the prevalence of SBI and WMH (PR [95% CI] 2.3 [1.6–3.1] and 1.7 [1.1–2.6], respectively).

Discussion

People with heart disease have a high prevalence of SBI (and CSVD), which is similar in those with vs without recent stroke. More research is required to assess causal links and implications for management.

Trial Registration Information

PROSPERO CRD42022378272 (crd.york.ac.uk/PROSPERO/).

Get full access to this article

Silent brain changes precede Alzheimer's. Researchers have new clues about which come first

Well isn't your competent? doctor already testing you for Alzheimer's biomarkers?

Alzheimer's Biomarkers Show Specific Changes 20 Years Before Diagnosis February 2024 

Blood Profile at Age 35 Linked to Subsequent Alzheimer's Dementia March 2022 

Simple Tool Predicts Individual Alzheimer's Risk 2-6 years in advance June 2021 

Two Memory Tests Accurately Predict Brain Atrophy, Alzheimer’s Disease  3 years in advance December 2018 

A Deep Learning Model to Predict a Diagnosis of Alzheimer Disease by Using 18F-FDG PET of the Brain 75.8 months prior to the final diagnosis November 2018

 

Your risk of dementia, has your doctor told you of this?  Your doctor is responsible for preventing this!

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

 

Silent brain changes precede Alzheimer's. Researchers have new clues about which come first

WASHINGTON (AP) — Alzheimer’s quietly ravages the brain long before symptoms appear and now scientists have new clues about the dominolike sequence of those changes — a potential window to one day intervene.

A large study in China tracked middle-aged and older adults for 20 years, using regular brain scans, spinal taps and other tests.

Compared to those who remained cognitively healthy, people who eventually developed the mind-robbing disease had higher levels of an Alzheimer's-linked protein in their spinal fluid 18 years prior to diagnosis, researchers reported Wednesday. Then every few years afterward, the study detected another so-called biomarker of brewing trouble.

Scientists don’t know exactly how Alzheimer’s forms. One early hallmark is that sticky protein called beta-amyloid, which over time builds up into brain-clogging plaques. Amyloid alone isn’t enough to damage memory — plenty of healthy people’s brains harbor a lot of plaque. An abnormal tau protein that forms neuron-killing tangles is one of several co-conspirators.

The new research, published in the New England Journal of Medicine, offers a timeline for how those abnormalities pile up.

The study’s importance “cannot be overstated,” said Dr. Richard Mayeux, an Alzheimer’s specialist at Columbia University who wasn’t involved in the research.

• 
  
• 
  
• 
  

Related video

Loaded: 73.47%

Current Time 0:13

/

Duration 0:49

New York Post

Doctors said she had anxiety — but it was actually a severe form of brain inflammation

0

View on Watch

New York Post

Doctors said she had anxiety — but it was actually a severe form of brain inflammation

“Knowledge of the timing of these physiological events is critical” for testing new ways of treating and maybe eventually even preventing Alzheimer’s, he wrote in an accompanying editorial.

The findings have no practical implications yet.

More than 6 million Americans, and millions more worldwide, have Alzheimer’s, the most common form of dementia. There’s no cure. But last year a drug named Leqembi became the first approved with clear evidence that it could slow the worsening of early Alzheimer’s — albeit for a few months.

It works by clearing away some of that gunky amyloid protein. The approach also is being tested to see if it's possible to delay Alzheimer's onset if high-risk people are treated before symptoms appear. Still other drugs are being developed to target tau.

Tracking silent brain changes is key for such research. Scientists already knew that in rare, inherited forms of Alzheimer’s that strike younger people, a toxic form of amyloid starts accumulating about two decades ahead of symptoms and at some point later tau kicks in.

www.akoyabh.com/abatherapyHome-Based ABA Therapy - Potential Ready to Shine

Ad

The new findings show the order in which such biomarker changes occurred with more common old-age Alzheimer’s.

Researchers with Beijing’s Innovation Center for Neurological Disorders compared 648 people eventually diagnosed with Alzheimer’s and an equal number who remained healthy. The amyloid finding in future Alzheimer's patients was the first, 18 years or 14 years prior to diagnosis depending on the test used.

Differences in tau were detected next, followed by a marker of trouble in how neurons communicate. A few years after that, differences in brain shrinkage and cognitive test scores between the two groups became apparent, the study found.

“The more we know about viable Alzheimer’s treatment targets and when to address them, the better and faster we will be able to develop new therapies and preventions,” said Claire Sexton, the Alzheimer's Association's senior director of scientific programs. She noted that blood tests are coming soon that promise to also help by making it easier to track amyloid and tau.