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Brain Infarction

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Description: Brain infarction, commonly known as a cerebral infarction or ischemic stroke, occurs when blood flow to a part of the brain is obstructed, leading to tissue damage due to lack of oxygen and nutrients.
Type: Brain infarction, commonly known as ischemic stroke, is primarily a type of vascular disease. It typically results from an obstruction within a blood vessel supplying blood to the brain, leading to tissue damage.

Regarding genetic transmission, brain infarction is not typically considered a hereditary condition. However, there can be a genetic predisposition to risk factors that increase the likelihood of a stroke, such as hypertension, diabetes, and certain clotting disorders. Therefore, while the stroke itself isn't directly inherited, the tendency to develop conditions that can lead to a stroke can have genetic components.
Signs And Symptoms: Signs and symptoms of brain infarction (ischemic stroke) include:

1. Sudden numbness or weakness in the face, arm, or leg, particularly on one side of the body.
2. Sudden confusion, trouble speaking, or difficulty understanding speech.
3. Sudden trouble seeing in one or both eyes.
4. Sudden trouble walking, dizziness, loss of balance, or lack of coordination.
5. Sudden severe headache with no known cause.

Nan refers to numerical data and is not applicable in this context.
Prognosis: Brain infarction, also known as ischemic stroke, can have varying prognoses depending on factors such as the location and size of the infarct, the patient's age, overall health, pre-existing conditions, and the speed and quality of medical intervention. Early treatment can significantly improve outcomes, but many patients may experience lasting effects such as physical or cognitive impairments. The risk of recurrence and long-term complications like disability also influences the prognosis. Prompt medical attention and comprehensive rehabilitation are crucial for improving recovery prospects.
Onset: Brain infarction, commonly known as an ischemic stroke, typically has a sudden onset. Symptoms can develop quickly and include sudden numbness or weakness in the face, arm, or leg, especially on one side of the body, confusion, trouble speaking or understanding speech, difficulty seeing in one or both eyes, difficulty walking, dizziness, loss of balance, or lack of coordination. Early recognition and immediate medical intervention are crucial.
Prevalence: The prevalence of brain infarction, also known as ischemic stroke, varies widely by demographic factors such as age, gender, and geographic location. In the general population, the incidence ranges from approximately 1-2 cases per 1,000 people per year. The prevalence increases significantly with age, particularly in individuals over 65 years old.
Epidemiology: Brain infarction, also known as cerebral infarction or ischemic stroke, occurs when blood supply to a part of the brain is interrupted, causing tissue death.

Epidemiology:
- Brain infarctions account for approximately 87% of all stroke cases.
- The annual incidence varies globally but is estimated between 100-300 per 100,000 people.
- Risk increases with age, particularly in those over 65 years old.
- Men have a slightly higher incidence compared to women.
- Common risk factors include hypertension, diabetes, smoking, atrial fibrillation, dyslipidemia, and atherosclerosis.
- The burden of brain infarction is higher in low- and middle-income countries due to limited access to preventive healthcare and treatment.
Intractability: Brain infarction, commonly known as a stroke, is not inherently intractable. Its treatability depends on several factors, including the type, severity, and timing of medical intervention. Rapid and appropriate treatment can significantly improve outcomes. However, delayed treatment or severe cases may lead to long-term complications and may be difficult to fully resolve.
Disease Severity: Brain infarction, commonly known as ischemic stroke, varies in severity depending on several factors.

- **Severity**: It can range from mild to severe. Mild cases may involve transient symptoms, while severe cases can lead to significant neurological deficits, disability, or death. The extent of damage largely depends on the location and size of the infarction and how quickly treatment is administered.

- **Nan**: The term "nan" is not applicable in the context of disease severity for brain infarction. Further clarification might be needed.
Healthcare Professionals: Disease Ontology ID - DOID:3454
Pathophysiology: Cerebral infarction is caused by a disruption to blood supply that is severe enough and long enough in duration to result in tissue death. The disruption to blood supply can come from many causes, including:

Thrombosis (obstruction of a blood vessel by a blood clot forming locally)
Embolism (obstruction due to an embolus from elsewhere in the body),
Systemic hypoperfusion (general decrease in blood supply, e.g., in shock)
Cerebral venous sinus thrombosis.
Unusual causes such as gas embolism from rapid ascents in scuba diving.Even in cases where there is a complete blockage to blood flow of a major blood vessel supplying the brain, there is typically some blood flow to the downstream tissue through collateral blood vessels, and the tissue can typically survive for some length of time that is dependent upon the level of remaining blood flow. If blood flow is reduced enough, oxygen delivery can decrease enough to cause the tissue to undergo the ischemic cascade. The ischemic cascade leads to energy failure that prevents neurons from sufficiently moving ions through active transport which leads the neurons to first cease firing, then depolarize leading to ion imbalances that cause fluid inflows and cellular edema, then undergo a complex chain of events that can lead to cell death through one or more pathways.
Carrier Status: Brain infarction, often referred to as a stroke, is not a condition that involves carrier status in the way that genetic disorders do. It results from an interruption of blood supply to a part of the brain, leading to tissue damage. Risk factors include hypertension, diabetes, smoking, and high cholesterol, among others. There is no concept of being a "carrier" for brain infarction.
Mechanism: Brain infarction, commonly known as ischemic stroke, occurs when blood flow to a part of the brain is obstructed, leading to tissue damage.

**Mechanism:**
The primary mechanism of brain infarction involves a blockage within a cerebral artery, resulting in reduced or entirely halted blood flow to the brain tissue. This blockage can be caused by:

1. **Thrombus**: A blood clot that forms in a cerebral artery.
2. **Embolus**: A clot or other debris that travels from another part of the body to the brain.
3. **Atherosclerosis**: The build-up of fatty deposits and plaque within the arterial walls, leading to narrowing and eventual blockage.
4. **Hypoperfusion**: Critically reduced blood flow due to systemic blood pressure drop or other factors, leading to poor perfusion of the brain tissue.

**Molecular Mechanisms:**
At the molecular level, brain infarction involves several key processes, including:

1. **Energy Failure**: The interruption of blood flow leads to a lack of oxygen and glucose, crucial for ATP production. The resulting energy failure disrupts cellular ion homeostasis.
2. **Excitotoxicity**: Reduced energy availability causes the failure of ion pumps, leading to an excessive release of glutamate. This overstimulates NMDA (N-Methyl-D-Aspartate) and AMPA (α-Amino-3-hydroxy-5-Methyl-4-Isoxazole Propionate) receptors, causing an influx of calcium ions (Ca²⁺) into neurons.
3. **Oxidative Stress**: Elevated intracellular Ca²⁺ levels lead to the generation of reactive oxygen species (ROS) and nitrogen species (RNS), resulting in oxidative damage to lipids, proteins, and DNA.
4. **Inflammation**: The ischemic event triggers the activation of microglia and the infiltration of peripheral immune cells, causing the release of proinflammatory cytokines and chemokines. This inflammatory response exacerbates neuronal injury.
5. **Cell Death Pathways**: Both necrotic and apoptotic pathways are activated. Necrosis occurs quickly due to severe ATP depletion, while apoptosis is a programmed cell death pathway induced by prolonged stress signals, mitochondrial dysfunction, and activation of caspases.
6. **Blood-Brain Barrier Disruption**: Loss of endothelial integrity and degradation of extracellular matrix proteins due to proteases like matrix metalloproteinases (MMPs) contribute to the breakdown of the blood-brain barrier, worsening tissue edema and allowing further infiltration by immune cells.

Understanding these mechanisms helps guide research into therapeutic targets for limiting damage and promoting recovery after brain infarction.
Treatment: In the last decade, similar to myocardial infarction treatment, thrombolytic drugs were introduced in the therapy of cerebral infarction. The use of intravenous rtPA therapy can be advocated in patients who arrive to stroke unit and can be fully evaluated within 3 hours of the onset. The quicker rTPA is started, the better the outcome for the patient.If cerebral infarction is caused by a thrombus occluding blood flow to an artery supplying the brain, definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The more rapidly blood flow is restored to the brain, the fewer brain cells die. In increasing numbers of primary stroke centers, pharmacologic thrombolysis with the drug tissue plasminogen activator (tPA), is used to dissolve the clot and unblock the artery. Giving rTPA lessens the chance of disability after 3 months by 30%. Another intervention for acute cerebral ischemia is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. Mechanical embolectomy devices have been demonstrated effective at restoring blood flow in patients who were unable to receive thrombolytic drugs or for whom the drugs were ineffective, though no differences have been found between newer and older versions of the devices. The devices have only been tested on patients treated with mechanical clot embolectomy within eight hours of the onset of symptoms.
Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute cerebral ischaemia. In a systematic review of six uncontrolled, single-center trials, involving a total of 300 patients, of intra-cranial stenting in symptomatic intracranial arterial stenosis, the rate of technical success (reduction to stenosis of <50%) ranged from 90 to 98%, and the rate of major peri-procedural complications ranged from 4-10%. The rates of restenosis and/or stroke following the treatment were also favorable. This data suggests that a large, randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of this treatment.
If studies show carotid stenosis, and the patient has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after cerebral infarction. Carotid endarterectomy is also indicated to decrease the risk of cerebral infarction for symptomatic carotid stenosis (>70 to 80% reduction in diameter).In tissue losses that are not immediately fatal, the best course of action is to make every effort to restore impairments through physical therapy, cognitive therapy, occupational therapy, speech therapy and exercise.
Permissive hypertension
Compassionate Use Treatment: For brain infarction, also known as an ischemic stroke, compassionate use treatments, off-label, or experimental treatments may include the following:

1. **Thrombectomy Devices**: While standard mechanical thrombectomy is widely accepted, new devices and techniques that are still in experimental stages may be available under compassionate use protocols.

2. **Intra-arterial Thrombolysis**: Administering clot-dissolving drugs directly into the blood clot via catheter can sometimes be employed outside of standard protocols under special circumstances.

3. **Stem Cell Therapy**: Experimental treatments using stem cells aim to repair damaged brain tissue. These are typically in trial phases but may be accessed through compassionate use.

4. **Neuroprotective Agents**: Drugs that aim to protect the brain from damage during a stroke are being studied and may be used experimentally. Examples include certain antioxidants or drugs that modulate glutamate activity.

5. **Hypothermia Treatment**: Inducing mild hypothermia to reduce brain swelling and metabolic demand is an emerging treatment still under investigation.

6. **Advanced Imaging-Guided Thrombolysis**: Utilizing advanced imaging techniques to tailor thrombolytic therapy based on individual patient profiles is another experimental approach.

Patients and physicians considering such treatments should consult clinical trial databases and discuss potential risks and benefits extensively.
Lifestyle Recommendations: ### Brain Infarction: Lifestyle Recommendations

1. **Healthy Diet:**
- Focus on a balanced diet rich in fruits, vegetables, whole grains, lean proteins, and healthy fats.
- Limit intake of salt, sugar, and saturated fats to manage blood pressure and cholesterol levels.

2. **Regular Exercise:**
- Engage in moderate aerobic activities (e.g., walking, cycling, swimming) for at least 150 minutes per week.
- Incorporate strength training exercises at least twice a week.

3. **Avoid Smoking:**
- Quit smoking and avoid exposure to secondhand smoke to reduce the risk of stroke.

4. **Limit Alcohol Consumption:**
- Drink alcohol in moderation—up to one drink per day for women and two drinks per day for men.

5. **Maintain Healthy Weight:**
- Aim for a healthy body weight through a balanced diet and regular physical activity.

6. **Manage Chronic Conditions:**
- Keep chronic conditions like diabetes, hypertension, and high cholesterol under control with appropriate medications and lifestyle changes.

7. **Stress Management:**
- Practice stress-reducing techniques such as meditation, yoga, or deep-breathing exercises.

8. **Regular Health Check-ups:**
- Schedule regular check-ups with your healthcare provider to monitor and manage risk factors.

Adhering to these lifestyle recommendations can significantly contribute to reducing the risk of brain infarction and improving overall brain health.
Medication: For brain infarction (ischemic stroke), common medications include:

1. **Anticoagulants**: Such as warfarin or newer agents like dabigatran to prevent further clot formation.
2. **Antiplatelets**: Including aspirin, clopidogrel, or a combination therapy to prevent platelets from clumping together.
3. **Thrombolytics**: Tissue plasminogen activator (tPA) to dissolve clots, typically used within a few hours of stroke onset.
4. **Statins**: Like atorvastatin or simvastatin to manage cholesterol levels.
5. **Antihypertensives**: Such as ACE inhibitors, beta-blockers, or diuretics to control blood pressure.
6. **Glycemic Control Medications**: For patients with diabetes, medications like metformin to maintain blood glucose levels.

It’s essential that these medications are prescribed and managed by healthcare professionals according to the individual patient's needs.
Repurposable Drugs: For brain infarction, also known as ischemic stroke, several drugs originally developed for other conditions have shown potential for repurposing. Some of these include:

1. Statins (e.g., Atorvastatin) - primarily used for lowering cholesterol, they have been found to have neuroprotective properties.
2. ACE Inhibitors and Angiotensin II Receptor Blockers (e.g., Candesartan) - typically prescribed for hypertension, they may help in improving cerebral blood flow and reducing the risk of stroke.
3. Minocycline - an antibiotic that has demonstrated anti-inflammatory and neuroprotective effects in stroke models.
4. Metformin - primarily used for type 2 diabetes, it has shown promise in reducing brain injury severity.

These drugs are still under investigation for stroke treatment and are not yet part of standard care specifically for brain infarctions. Clinical trials and further research are necessary to confirm their efficacy and safety for this condition.
Metabolites: Brain infarction involves several metabolic changes in the brain tissue. Here are key metabolites associated with brain infarction:

1. **Lactate:** Increased levels due to anaerobic glycolysis.
2. **N-acetylaspartate (NAA):** Decreased levels indicating neuronal injury.
3. **Choline-containing compounds:** Increased levels associated with cell membrane breakdown.
4. **Creatine:** Typically unchanged or slightly altered, marking energy metabolism stability.
5. **Glutamate:** Increased levels contributing to excitotoxicity.

These metabolic changes can be detected using magnetic resonance spectroscopy and provide insights into the extent of brain damage and the metabolic state of brain tissue following an infarction.
Nutraceuticals: There is currently no strong evidence to support the use of specific nutraceuticals (nutritional supplements or functional foods) in the treatment or prevention of brain infarction, also known as ischemic stroke. The management of brain infarction typically involves medical therapies such as antiplatelet drugs, anticoagulants, thrombolytics, and lifestyle changes such as a healthy diet, regular exercise, and controlling risk factors like hypertension, diabetes, and hyperlipidemia. Always consult healthcare professionals for personalized advice and treatment plans.
Peptides: Brain infarction, commonly known as a stroke, can be influenced by peptides in several ways. Peptides are short chains of amino acids that can play various roles in cell signaling, inflammation, and tissue repair. Some peptides, such as those derived from the breakdown of proteins like fibrin or amyloid, may contribute to inflammation or vascular problems associated with stroke.

Research is ongoing into therapeutic peptides that may help reduce damage from strokes, promote neuroprotection, or aid in recovery. These peptides can potentially mitigate ischemic damage, reduce oxidative stress, and enhance angiogenesis, thereby improving outcomes for individuals experiencing brain infarction.