The largest database of trusted experimental protocols
> Disorders > Disease or Syndrome > Brain Infarction

Brain Infarction

Brain infarction, also known as cerebral infarction or stroke, is a type of brain injury caused by an interruption of blood supply to a specific area of the brain.
This can result in tissue damage and loss of function in the affected region.
Brain infarction can be caused by a variety of factors, including blood clots, hemorrhage, or other circulatory disturbances.
Symptoms may include sudden onset of weakness, numbness, vision problems, difficulty speaking, and confusion.
Timely diagnosis and appropriate treatment are crucial to minimize long-term damage and improve patient outcomes.
This MeSH term encompasses the clinical presentation, etiology, and management of brain infarction, providing a comprehensive overview for researchers and clinicans.

Most cited protocols related to «Brain Infarction»

Procedures for complete case capture follow international recommendations for capture–recapture and multiple source ascertainment methods.20 (link) Cases are primarily identified through active pursuit of emergency department and directly admitted stroke patients using validated screening terms.21 (link) The abstractors also routinely canvass intensive care units and hospital floors searching for in-house strokes or those not ascertained through the screening logs. The active surveillance is supplemented by review of hospital passive listings of International Classification of Disease, 9th revision discharge codes for stroke (430–438; excluding 433.x0, 434.x0 [x = 1–9]; 437.0, 437.2, 437.3, 437.4, 437.5, 437.7, 437.8, and 438). County coroner records are screened for causes of sudden stroke death not presenting to the hospital. Several minor changes to case ascertainment procedures were made over the course of the project to maintain efficiency. In 2001, the following diagnostic terms were removed from the active surveillance list: dizziness, falling, imbalance, syncope, and trouble walking. These terms were found to be highly inefficient at identifying strokes, with a positive predict value of ≤1%. Starting January 1, 2001, a sample of Nueces County primary care and cardiology offices, as well as 95% of neurologist offices, were contacted frequently and encouraged to report stroke cases to our project. Abstractors reviewed and abstracted cases not previously screened. The sampling of primary care physicians and cardiologists was subsequently discontinued on January 31, 2004, because during the 3 years of the sampling only 13 ischemic stroke patients were identified exclusively from this method of 1,866 ischemic stroke cases identified in BASIC. Because 74 cases from the sample identified came from neurology offices, we did continue to identify these few stroke cases from neurology offices. From January 31, 2004 to July 31, 2008, only 71 strokes were identified via the neurology office of 1,971 ischemic stroke cases identified. In 2008, we therefore stopped screening neurology offices. From January 1, 2000 through December 1, 2007, BASIC identified cases through active surveillance of both the admissions log and emergency department (ED) log. A review of this methodology in 2007 using complete data from calendar year 2004 suggested that frequent passive ED surveillance in combination with active surveillance of admission logs successfully identifies ≥98% of all ischemic strokes. This new methodology was implemented on December 2, 2007. Finally, we were unable to obtain passive listings of stroke from 1 of the hospital systems for 6 months of 2008. In other 6-month periods, this never amounted to >5 cases. A sensitivity analysis was performed to determine the effects of the changes on incidence rate estimates and ethnic comparisons over time.
Cases are validated by neurologists or a stroke fellowship-trained emergency medicine physician, blinded to subjects’ ethnicity and age, using source documentation. Ischemic stroke diagnosis is based on published international clinical criteria20 (link) that require onset of a focal neurologic deficit following a defined vascular distribution without documented resolution within 24 hours (unless treated with recombinant tissue plasminogen activator) and not explainable by a nonvascular etiology. Imaging is used to discriminate ischemic stroke and hemorrhagic stroke. Because the use of brain MRI has increased greatly in the past 10 years, validators are required to use the original clinical criteria for case validation, so that trend data can be assessed without bias. Therefore, subjects having acute infarction on brain MRI without the clinical deficit described above are validated as no stroke.
Publication 2013
Alteplase Blood Vessel Brain Brain Infarction Cardiologists Cardiovascular System Cerebrovascular Accident Coroners Diagnosis Ethnicity Fellowships Hemorrhagic Stroke Hypersensitivity Neurologists Patient Discharge Patients Physicians Primary Care Physicians Primary Health Care Stroke, Ischemic Syncope

Protocol full text hidden due to copyright restrictions

Open the protocol to access the free full text link

Publication 2009
Brain Brain Infarction Cerebellum Cortex, Cerebral Edema Fingers Infarction Mice, Laboratory Olfactory Bulb Reperfusion Sclerosis Striatum, Corpus Tissues
The indirect method for infarct volume of Lin et al.’s algorithm utilizes the area of the contralesional hemisphere, Ci, the area of the non-ischemic (healthy) tissue of the ipsilesional hemisphere, Ni, and the thickness of each brain slice, d. The infarct volume, expressed as a percent of the contralesional hemisphere volume, is [12 (link)] Infarct Volume(%)=(di(CiNi)diCi)100, where (Ci–Ni) is the swelling-corrected infarct area for slice i, (di(CiNi)) is the swelling-corrected infarct volume for the whole ipsilesional hemisphere, and (diCi) is the volume of the contralesional hemisphere. Since the contralesional hemisphere is assumed to be the same size as the ipsilesional hemisphere before injury, the contralesional hemisphere is used to determine the percent of the hemisphere volume that is occupied by the infarction.
Typically, the thickness of each slice is equivalent for a given method, thus Eq. 10 can be reduced to Infarct Volume(%)=(i(CiNi)(iCi))100.
A slight modification of Lin et al. ‘s algorithm was made to compare the infarct volume to the whole brain, (2iCi) , rather than a single hemisphere. This correction results in the version of Lin et al.’s algorithm which is utilized hereafter: Infarct Volume(%)=(i(CiNi)2iCi)100.
Using the photographs of TTC-stained brain slices, the areas of the contralesional, Ci, ipsilesional, Ii, and nonischemic ipsilesional hemispheres, Ni, were traced (ImageJ 1.48, NIH) and the infarct volume from Lin et al.’s algorithm was computed (Eq. 12).
Publication 2015
Brain Brain Infarction Infarction Injuries Tissues
At intervals of 9 to 12 months, an interviewer contacted each participant by telephone to inquire about all interim hospital admissions, cardiovascular outpatient diagnoses, and deaths. To verify self-reported diagnoses, study personnel requested copies of all death certificates and medical records for all hospitalizations and outpatient cardiovascular diagnoses. Next-of-kin interviews were done for out-of-hospital cardiovascular deaths. Hospital records were obtained for an estimated 98% of hospitalized cardiovascular events, and some information was available for 95% of outpatient diagnostic encounters.
Hospital records that suggested possible cardiovascular events were abstracted by study personnel. The MESA coordinating center collated the abstracted or original endpoint records and sent them to 2 paired cardiologists, cardiovascular epidemiologists or neurologists for independent endpoint classification and assignment of incidence dates. If, after review and adjudication, disagreements persisted, a full Mortality and Morbidity Review Committee made the final classification.
Reviewers assigned a diagnosis of myocardial infarction based on combinations of symptoms, electrocardiographic findings, and cardiac biomarker levels. Death from CHD was classified as definite, probable or absent based on hospital records, death certificates and conversations with families. Definite fatal CHD required a myocardial infarction within 28 days of death, chest pain within 72 hours before death, or history of CHD, and the absence of a known nonatherosclerotic or noncardiac cause of death. If the definite fatal CHD criteria were not met, probable fatal CHD could be assigned with an underlying cause of death consistent with fatal CHD; this required the absence of a known nonatherosclerotic or noncardiac cause of death. Stroke required a focal deficit of >24 hours and was most instances confirmed by neuro-imaging. Stroke included subarachnoid hemorrhages, intraparenchymal hemorrhages, and brain infarctions. The definition of angina was adapted from the Women’s Health Initiative criteria and was classified by reviewers as definite, probable or absent. Definite or probable angina required clinical symptoms to be considered a MESA event, with definite angina requiring objective evidence of coronary atherosclerosis.
Publication 2009
Angina Pectoris Biological Markers Brain Infarction Cardiologists Cardiovascular System Cerebrovascular Accident Chest Pain Coronary Arteriosclerosis Diagnosis Electrocardiography Epidemiologists Heart Hemorrhage Hospitalization Interviewers Myocardial Infarction Neurologists Outpatients Subarachnoid Hemorrhage Woman
Hospitalizations and deaths were ascertained via annual follow-up phone calls, study examinations, and surveillance of hospital discharges in ARIC communities. Hospitalizations meeting one or more of the following criteria were eligible for medical record abstraction: 1) A discharge diagnosis ICD-9-CM code 430 through 438 (1987–1996) or 430 through 436 (since 1997); 2) One or more stroke-related keywords (see Supplemental Methods) in discharge summary; or 3) Diagnostic computed tomography (CT) or magnetic resonance imaging (MRI) scan with cerebrovascular findings or admission to the neurological intensive care unit. A trained nurse abstracted records for each eligible hospitalization, including up to 21 ICD-9-CM discharge codes (see Supplemental Methods).
A computer algorithm and physician reviewer independently classified each event according to criteria adapted from the National Survey of Stroke.22 (link) A second physician reviewer adjudicated in cases where the computer and initial reviewer disagreed.
A definite or probable stroke was defined as a sudden and rapid onset of neurological symptoms lasting >24 hours or leading to death in the absence of evidence for a non-stroke cause (see Supplemental Material). Events that did not meet these criteria were classified as “possible stroke of undetermined type,” “out-of-hospital fatal stroke,” or “no stroke.” Definite and probable strokes were classified further as SAH, ICH, or ischemic stroke (including embolic and thrombotic brain infarction) (Supplemental Table I).23 (link)
Publication 2014
Brain Infarction Cerebrovascular Accident Diagnosis Hospitalization Magnetic Resonance Imaging Neurologic Symptoms Nurses Patient Discharge Physical Examination Physicians Stroke, Ischemic Tomography

Most recents protocols related to «Brain Infarction»

Seven databases (EMbase, PubMed, Cochrane Library, Web of Science, CNKI, VIP, and Wan fang Database) were searched by computer,
The retrieval period was from database construction until August 2022; (III)Pubmed search strategy: (((((acute disease[MeSH Terms])) AND (cerebral infarction[MeSH Terms])) OR (acute cerebral infarction)) OR ((((acute disease[MeSH Terms])) AND (brain infarction[MeSH Terms])) OR (acute brain infarction))) AND (((((3-n-butylphthalide[MeSH Terms])) OR (3-n-butylphthalide[Title/Abstract])) OR (butylphthalide)) OR (NBP)).
Publication 2023
3-n-butylphthalide Acute Cerebrovascular Accidents Acute Disease Brain Infarction cDNA Library Cerebral Infarction
All of the animal experiments mentioned in this article received approval from the Guangdong Medical University Ethics Committee for Animals following the NIH Care Guidelines and usage of experimental animals. Male Sprague Dawley (SD) mice (weight range from 280 to 320 g) were anesthetized with an intraperitoneal dose of ketamine (75 mg/kg) and 3% isoflurane. The transient MCAO model experiment was carried out as reported earlier [20 (link)]. After anesthesia, the remaining internal and external carotid arteries were surgically removed via an endoscopic midline incision. After 24 h, the middle cerebral artery was sealed with a round nylon (4-0 suture) tip, and the junction was detached to allow blood flow restoration. The control rats (sham group) underwent identical operations, but the middle cerebral artery was unblocked. The experimental animals that underwent surgery were treated with heating pads to keep their body temperatures at 37 ± 0.5 °C. The rats were sacrificed 24 h after MCAO modeling. Subsequently, infarcted brain tissue was isolated and cut into 3-mm-thick sections for staining with 2,3,5-triphenyl tetrazolium chloride (TTC) (Sigma, MO, USA).
Full text: Click here
Publication 2023
Anesthesia Animals Animals, Laboratory Blood Circulation Body Temperature Brain Infarction Endoscopy Ethics Committees External Carotid Arteries Isoflurane Ketamine Males Mice, House Middle Cerebral Artery Nylons Operative Surgical Procedures Rattus norvegicus Sutures Tissues Transients triphenyltetrazolium chloride
Our institutional review board approved this retrospective study protocol, and the requirement for informed consent was waived for the review of patient medical records and images. From January 2020 to August 2021, we retrospectively reviewed stroke MR images with 3D BB contrast-enhanced MRI and MRA imaging of patients visiting the emergency room for the evaluation of acute brain infarction. We selected patients with initial or delayed positive DWI findings of the medulla and neurological symptoms. The exclusion criteria were as follows: (a) MR examination 48 hours after symptom onset; (b) evidence of vertebral dissection or vasculitis; (c) slow-flowing artifact or incomplete suppression of the VA lumen on 3D BB contrast-enhanced MRI; (d) any patient who had images of insufficient quality for reliable evaluation on 3D BB contrast-enhanced MRI or MRA; and (e) complete or severe stenosis of the proximal VA (V1–V3 segment) or no visualization of bilateral VA on MRA.
Publication 2023
Brain Infarction Cerebrovascular Accident Dissection Ethics Committees, Research Medulla Oblongata Neurologic Symptoms Patients Stenosis Vasculitis Vertebra
TTC (2,3,5-tripenyltetrazolium chloride) staining was performed for brain infarction size measurement following previous described methods [4 (link)]. Briefly, brain sections (0.2-0.3 cm in thickness) were incubated with 2% TTC solution for half an hour at 25°C in the dark and then imaged. The total infarction size (cm3) of sections was calculated by the equation: total infarction size = infarction area (cm2) of each section section thickness.
Full text: Click here
Publication 2023
Brain Brain Infarction Chlorides CM 2-3 Infarction
The previously
reported protocols31 (link),33 (link) were followed except that the
drugs were injected 3 h after reperfusion and the neurological deficit
score and brain infarct size by TTC staining were evaluated 24 h after
drug treatment.
Publication 2023
Brain Infarction Reperfusion

Top products related to «Brain Infarction»

Sourced in United States, Germany, Sao Tome and Principe, Macao, China, Switzerland, Australia, Japan, Spain, Italy, Senegal
The TTC (Triphenyltetrazolium Chloride) is a laboratory reagent used for various analytical and diagnostic applications. It is a colorless compound that is reduced to a red formazan product in the presence of metabolically active cells or tissues. This color change is utilized to assess cell viability, detect active enzymes, and measure cellular respiration in a wide range of biological samples.
Sourced in United States, Japan, Germany, United Kingdom, China, Hungary, Singapore, Canada, Switzerland
Image-Pro Plus 6.0 is a comprehensive image analysis software package designed for scientific and industrial applications. It provides a wide range of tools for image capture, enhancement, measurement, analysis, and reporting.
Sourced in United States, Germany
T8877 is a laboratory equipment product from Merck Group. It is designed for general laboratory applications. The core function of T8877 is to provide a reliable and efficient tool for laboratory tasks.
Sourced in United States, Switzerland, Germany
The TTC solution is a laboratory reagent used for various applications in cell biology and microbiology. It is a colorimetric dye that is used to assess the viability and metabolic activity of cells. The solution is primarily composed of the compound 2,3,5-triphenyltetrazolium chloride (TTC), which is reduced by active cellular enzymes to produce a red formazan dye. The intensity of the color change is proportional to the level of cellular activity, making the TTC solution a useful tool for quantifying cell viability and proliferation.
Sourced in Japan, United States, Germany, China, Macao, United Kingdom
The Digital Camera is a device that captures and records visual images in a digital format. It converts light into electrical signals, which are then processed and stored as digital data. The camera's core function is to enable the user to capture, store, and share visual content.
Sourced in United States, Germany, China, Italy
2,3,5-triphenyltetrazolium chloride is a chemical compound used in various laboratory applications. It is a crystalline solid with a pale yellow color. The compound is soluble in water and organic solvents. 2,3,5-triphenyltetrazolium chloride is utilized as a reagent in various biochemical and analytical procedures, but a detailed description of its core function is not available within the constraints of providing an unbiased and factual approach without interpretation or extrapolation.
Sourced in United States, Germany, United Kingdom, Switzerland, China, Japan, Belgium, Sao Tome and Principe, France, India
Cresyl violet is a histological stain used in microscopy to visualize cellular structures. It is a basic aniline dye that selectively binds to nucleic acids, staining the nuclei of cells. This allows for the identification and differentiation of various cell types in tissue samples.
Sourced in United States, Germany, United Kingdom, China, Italy, France, Macao, Australia, Canada, Sao Tome and Principe, Japan, Switzerland, Spain, India, Poland, Belgium, Israel, Portugal, Singapore, Ireland, Austria, Denmark, Netherlands, Sweden, Czechia, Brazil
Paraformaldehyde is a white, crystalline solid compound that is a polymer of formaldehyde. It is commonly used as a fixative in histology and microscopy applications to preserve biological samples.
Sourced in United States, United Kingdom, Germany, Canada, Denmark, Morocco, Japan, Ireland
NeuN is a protein marker used for the detection and identification of neuronal cell nuclei in various vertebrate species. It is commonly used in immunohistochemistry and other laboratory techniques to study the distribution and properties of neurons in biological samples.
Sourced in Germany, United States, Switzerland, China, United Kingdom, France, Canada, Belgium, Japan, Italy, Spain, Hungary, Australia
The In Situ Cell Death Detection Kit is a laboratory product designed for the detection of programmed cell death, or apoptosis, in cell samples. The kit utilizes a terminal deoxynucleotidyl transferase (TdT) to label DNA strand breaks, allowing for the visualization and quantification of cell death. The core function of this product is to provide researchers with a tool to study and analyze cell death processes.

More about "Brain Infarction"

Brain Infarction, also known as Cerebral Infarction or Stroke, is a serious medical condition caused by an interruption of blood flow to a specific area of the brain.
This disruption in blood supply can lead to tissue damage and loss of function in the affected region.
The underlying causes of brain infarction can vary, including blood clots (thrombosis), bleeding (hemorrhage), or other circulatory disturbances.
Common symptoms often include sudden onset of weakness, numbness, vision problems, difficulty speaking, and confusion.
Timely diagnosis and appropriate treatment are crucial to minimize long-term damage and improve patient outcomes.
Researchers and clinicians utilize a variety of techniques to study and manage brain infarction, such as TTC (2,3,5-triphenyltetrazolium chloride) staining, Image-Pro Plus 6.0 software, and the NeuN (Neuronal Nuclei) marker to assess neuronal damage.
The TUNEL (Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling) assay, part of the In Situ Cell Death Detection Kit, is also employed to detect apoptotic (programmed cell death) cells.
Cresyl violet staining and paraformaldehyde fixation are additional tools used in the investigation of brain infarction.
Improving the understanding of the pathophysiology, early detection, and effective treatment strategies for brain infarction is an ongoing area of research.
By leveraging the latest technologies and research approaches, scientists and healthcare professionals can work towards better outcomes for individuals affected by this devastating condition.