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🎥 Alisha Salsabila (PSKED'23)

• Content Maker

📢 Rifdania Putri Destrinita (PSKED'21)

• Presenter

• A study in the Journal of Clinical Neuroscience (2020) indicates that curcumin can protect nerve cells, potentially lowering stroke risk by lessening brain inflammation.

• Research in Nutrients (2021) shows that natural antioxidants from sources like turmeric and tamarind can shield nerve cells from oxidative injury, thereby decreasing stroke risk.

• A review in the International Journal of Molecular Sciences (2022) examines the protective effect of curcumin, highlighting its potential to lessen brain damage during ischemic strokes.

• Unnithan AKA, Das JM, Mehta P. Hemorrhagic Stroke. [Updated 2023 May 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559173/

• Feigin, V. L., Brainin, M., Norrving, B., Martins, S., Sacco, R. L., Hacke, W., Fisher, M., Pandian, J., & Lindsay, P. (2022). World Stroke Organization (WSO): Global Stroke Fact Sheet 2022. International journal of stroke : official journal of the International Stroke Society, 17(1), 18–29. https://doi.org/10.1177/17474930211065917

• Cook K, Bhatti L, Tursan d’Espaignet E. WHO Tobacco Knowledge Summaries: Tobacco and stroke. WHO, Geneva, 2016.

• Noubiap, J. J., Fitzgerald, J. L., Gallagher, C., Thomas, G., Middeldorp, M. E., & Sanders, P. (2021). Rates, predictors, and impact of smoking cessation after stroke or transient ischemic attack: A systematic review and meta-analysis. Journal of Stroke and Cerebrovascular Diseases, 30(10), 106012. https://doi.org/10.1016/j.jstrokecerebrovasdis.2021.106012

• Kim, B.J., Bae, HJ., Wong, L.K.S. (2016). Pathophysiology and Mechanisms Whereby Hypertension May Cause Stroke. In: Aiyagari, V., Gorelick, P. (eds) Hypertension and Stroke. Clinical Hypertension and Vascular Diseases. Humana Press, Cham. https://doi.org/10.1007/978-3-319-29152-9_6

• Khan, H., Tiwari, C., Kalra, P. et al. Mechanistic correlation of molecular pathways in obesity-mediated stroke pathogenesis. Pharmacol. Rep 76, 463–474 (2024). https://doi.org/10.1007/s43440-024-00590-9

• Rodríguez-Castro, E., Rodríguez-Yáñez, M., Arias-Rivas, S. et al. Obesity Paradox in Ischemic Stroke: Clinical and Molecular Insights. Transl. Stroke Res. 10, 639–649 (2019). https://doi.org/10.1007/s12975-019-00695-x

• Meng, M., Guo, Y., Kuang, Z., Liu, L., Cai, Y., & Ni, X. (2022). Risk of stroke among different metabolic obesity phenotypes: A systematic review and meta-analysis. Frontiers in Cardiovascular Medicine, 9. https://doi.org/10.3389/fcvm.2022.844550

• Dreher, M.L. (2018). Dietary Patterns and Stroke Risk. In: Dietary Patterns and Whole Plant Foods in Aging and Disease. Nutrition and Health. Humana Press, Cham. https://doi.org/10.1007/978-3-319-59180-3_16

• Guo, N., Zhu, Y., Tian, D. et al. Role of diet in stroke incidence: an umbrella review of meta-analyses of prospective observational studies. BMC Med 20, 194 (2022). https://doi.org/10.1186/s12916-022-02381-6

• Hooker, S.P., McDonnell, M.N. (2019). Cardiorespiratory Fitness, Physical Activity, and Stroke. In: Kokkinos, P., Narayan, P. (eds) Cardiorespiratory Fitness in Cardiometabolic Diseases. Springer, Cham. https://doi.org/10.1007/978-3-030-04816-7_19

• Kramer, S.F., Hung, S.H. & Brodtmann, A. The Impact of Physical Activity Before and After Stroke on Stroke Risk and Recovery: a Narrative Review. Curr Neurol Neurosci Rep 19, 28 (2019). https://doi.org/10.1007/s11910-019-0949-4

• Larsson, S.C., Wallin, A., Wolk, A. et al. Differing association of alcohol consumption with different stroke types: a systematic review and meta-analysis. BMC Med 14, 178 (2016). https://doi.org/10.1186/s12916-016-0721-4

• Benjamin J R Buckley, Stephanie L Harrison, Deirdre A Lane, Andrew Hill, Gregory Y H Lip, Stroke–heart syndrome: mechanisms, risk factors, and adverse cardiovascular events, European Journal of Preventive Cardiology, Volume 31, Issue 5, March 2024, Pages e23–e26, https://doi.org/10.1093/eurjpc/zwad211

• Kato, Y., Tsutsui, K., Nakano, S., Hayashi, T., & Suda, S. (2024). Cardioembolic stroke: Past advancements, current challenges, and Future Directions. International Journal of Molecular Sciences, 25(11), 5777. https://doi.org/10.3390/ijms25115777

• Popa-Wagner, A., Udristoiu, I., Gresita, A., Lledós, M., Cadenas, I.F. (2021). Post-stroke Depression: Genetics, Mechanisms, and Treatment. In: Riederer, P., Laux, G., Nagatsu, T., Le, W., Riederer, C. (eds) NeuroPsychopharmacotherapy. Springer, Cham. https://doi.org/10.1007/978-3-319-56015-1_434-1

• Guo, J., Wang, J., Sun, W. et al. The advances of post-stroke depression: 2021 update. J Neurol 269, 1236–1249 (2022). https://doi.org/10.1007/s00415-021-10597-4

• Liu L, Xu M, Marshall IJ, Wolfe CD, Wang Y, O’Connell MD (2023) Prevalence and natural history of depression after stroke: A systematic review and meta-analysis of observational studies. PLoS Med 20(3): e1004200. doi:10.1371/journal.pmed.1004200

• Cross, James Graham, et al. “A Systematic Review and Evaluation of Post-Stroke Depression Clinical Practice Guidelines.” Journal of Stroke and Cerebrovascular Diseases, vol. 32, no. 9, 1 Sept. 2023, p. 107292, www.sciencedirect.com/science/article/abs/pii/S1052305723003154, https://doi.org/10.1016/j.jstrokecerebrovasdis.2023.107292.

• HEMORRHAGIC STROKE: a stroke that's cause by the occurance of bleeding inside the brain, specifically the bleeding of brain blood vessels

• ISCHEMIC STROKE: a disease that occurs when blood flow to the brain is blocked from its brain blood vessels; preventing the brain from receiving oxygen and nutrients.

Compared to Hemorrhage Stroke, Ischemic Stroke contribute about 87% of the total cases of stroke.

H: Hemiparesis

A: Aphasia

N: Neurological issues

D: Depression

I: Incontinence

C: Cognitive decline

A: Aspiration pneumonia

P: Pressure sores

What are they really?

We'll explain it to you ☺️

Keep reading ⬇️

Ischemic Stroke itself has global prevalence of 68.16 million people in 2020 with the mortality case had reached 3.48 million.

In Indonesia, stroke also considered as concerning in which the prevalence case increases from 7 per 1,000 (2013) to nearly 11 per 1,000 (2018).

1. Biological Changes

   A stroke damages parts of the brain that control mood, emotions, and cognitive function, such as the frontal lobe, basal ganglia, or limbic system via inflammation or blockage. This can disrupt neurotransmitter systems, including serotonin, dopamine, and norepinephrine, which are critical for happy-sad mood regulation; thus contribute to depressive symptoms.

   
   

2. Psychological Impact

   Strokes often cause physical disabilities (e.g., paralysis, speech difficulties) that lead to feelings of helplessness, frustration, and grief over the loss of independence.

3. Social and Environmental Factors

   Stroke survivors may experience reduced social interactions due to mobility issues or communication difficulties, leading to loneliness. Aside from that, the financial burden of treatment and lifestyle changes required after a stroke can contribute to stress and depression.

Post-Stroke Depression (PSD)

It’s a common complication, affecting about 30–50% of stroke survivors. PSD can hinder rehabilitation, reduce quality of life, and increase the risk of further health issues, including recurrent strokes.

Management

Treatment involves a combination of medication (antidepressants), therapy (e.g., cognitive-behavioral therapy), and social support, as well as addressing any physical and cognitive challenges resulting from the stroke.

1. Dysphagia (Swallowing Difficulties)

   Strokes affecting the brainstem, motor cortex, or cranial nerves can disrupt the coordination of muscles involved in swallowing (dysphagia). This leads to difficulty in properly managing food, liquids, or saliva. When swallowing is impaired, food, liquids, or secretions can enter the airway instead of the esophagus. This is called aspiration, which may lead to pneumonia if the aspirated material contains bacteria or causes inflammation.

2. Impaired Cough Reflex

   Stroke can weaken the cough reflex, which is the body’s natural mechanism to clear aspirated materials from the airway. In some cases, aspiration occurs without triggering noticeable symptoms (e.g., coughing or choking). This is called silent aspiration, which significantly increases the risk of pneumonia.

3. Reduced Mobility and Weakness

   Many stroke patients experience limited mobility or are bedridden, which can impair lung function and clearance of secretions. Weakness in the diaphragm and other respiratory muscles reduces the ability to clear aspirated materials.

   
   

4. Compromised Immune Defense

   Stroke can weaken the immune system, making patients more susceptible to infections like pneumonia. Poor oral hygiene, common in stroke patients, can lead to increased bacterial colonization in the mouth, which may be aspirated into the lungs.

   
   

5. Tube Feeding and Artificial Airway Risks

   If a patient requires a feeding tube due to severe dysphagia, there is a higher risk of aspiration from reflux or improper tube placement. Stroke patients with respiratory support are at increased risk of aspiration-related complications.

Management and Prevention

• Swallowing Assessment: Regular screening for dysphagia using tools like the bedside swallow test.

• Dietary Adjustments: Modifying food texture and liquid consistency to reduce aspiration risk.

• Positioning: Keeping patients upright during and after feeding.

• Speech Therapy: Rehabilitation to improve swallowing function.

• Oral Hygiene: Maintaining proper oral care to reduce bacterial load.

• Antibiotics: Administered if pneumonia develops.

Early identification and management of swallowing difficulties are critical to preventing aspiration pneumonia in stroke patients.

1. Immobility

   Stroke often causes hemiplegia (paralysis on one side of the body) or general muscle weakness, making it difficult for patients to change positions on their own. Lying or sitting in the same position for extended periods compresses the skin and underlying tissues against a surface (e.g., a bed or wheelchair). This pressure reduces blood flow to the area, leading to tissue damage and the formation of pressure sores.

   
   

2. Reduced Sensation

   Strokes affecting sensory pathways can diminish the ability to feel pain or discomfort in certain areas of the body. Patients may not notice the need to shift positions to relieve pressure. Reduced sensation can also mean small injuries, friction, or irritation go unnoticed, making the skin more prone to breakdown.

   
   

3. Poor Blood Circulation

   Stroke can impair blood circulation, especially in areas subjected to prolonged pressure, depriving tissues of oxygen and nutrients. Stroke patients often develop swelling (edema) in the paralyzed limbs, which further reduces blood supply and increases the risk of pressure sores.

   
   

4. Incontinence

   Many stroke patients experience incontinence, leading to prolonged exposure of the skin to moisture (from urine or feces). This weakens the skin's protective barrier, increasing susceptibility to sores.

   
   

5. Nutritional Deficiencies

   Stroke survivors often have difficulty eating (due to dysphagia) or a reduced appetite, leading to malnutrition. A lack of essential nutrients like protein, vitamin C, and zinc impairs wound healing and weakens skin integrity.

   
   

6. Cognitive Impairments

   Strokes that affect cognitive function may reduce a patient’s ability to recognize or communicate discomfort, further delaying necessary position changes.

Common Sites that most at risk, including:

• Back of the head

• Shoulders

• Elbows

• Lower back and sacrum

• Hips

• Knees

• Heels and ankles

Prevention of Pressure Sores

• Frequent Repositioning: Changing the patient’s position every 2 hours to relieve pressure.

• Pressure-Relieving Devices: Using specialized mattresses, cushions, and pads.

• Skin Care: Keeping the skin clean, dry, and moisturized to prevent breakdown.

• Nutritional Support: Ensuring adequate protein and hydration for skin health and healing.

• Monitoring: Regularly checking the skin for early signs of redness or irritation.

  
  

Pressure sores can significantly impact recovery and quality of life, so proactive management is critical for stroke patients with limited mobility.

1. Endothelial Dysfunction and Atherosclerosis:

   Tobacco smoke contains harmful chemicals: nicotine and carbon monoxide, which damage the endothelium—the inner lining of blood vessels that can promotes atherosclerosis. Atherosclerosis is characterized by the accumulation of plaques within arterial walls, leading to narrowed and less flexible arteries. Such changes impede blood flow to the brain, increasing stroke risk.

   
   

2. Increased Blood Coagulability:

   Smoking enhances platelet aggregation and elevates fibrinogen levels due to its substance called nicotine, making the blood more prone to clotting. This hypercoagulable state heightens the likelihood of thrombus formation, which can obstruct cerebral arteries and result in ischemic stroke.

   
   

3. Elevated Blood Pressure:

   Nicotine stimulates the release of catecholamines, leading to vasoconstriction and increased heart rate, which collectively raise blood pressure in which hypertension is a significant risk factor for both ischemic and hemorrhagic strokes.

   
   

4. Reduction in Oxygen Transport:

   Carbon monoxide in cigarette smoke binds to hemoglobin with high affinity, forming carboxyhemoglobin, which reduces the oxygen-carrying capacity of blood. This diminished oxygen delivery can cause cerebral hypoxia, contributing to neuronal injury and increasing stroke susceptibility.

   
   

5. Development of Aneurysms:

   Smoking weakens arterial walls, predisposing individuals to aneurysm formation. The rupture of a cerebral aneurysm leads to subarachnoid hemorrhage, a severe type of stroke.

Collectively, these mechanisms elucidate how smoking contributes to both ischemic and hemorrhagic strokes. Importantly, smoking cessation can significantly reduce stroke risk, with studies indicating that within 2 to 4 years of quitting, the risk approaches that of non-smokers.

1. Large Artery Atherosclerosis:

   Elevated blood pressure accelerates the development of atherosclerosis in large arteries, leading to plaque formation and arterial stenosis. This can result in ischemic stroke through thrombotic occlusion or artery-to-artery embolism.

   
   

2. Small Vessel Disease:

   Hypertension induces lipohyalinosis and fibrinoid necrosis in small penetrating arterioles, causing lacunar infarctions. These small vessel pathologies are common in hypertensive patients and contribute to ischemic stroke.

   
   

3. Endothelial Dysfunction and Oxidative Stress:

   Chronic high blood pressure leads to endothelial dysfunction and increased oxidative stress, impairing vasodilation and promoting vascular inflammation. These changes facilitate atherosclerosis and thrombosis, increasing stroke risk.

4. Cerebral Blood Flow Autoregulation Impairment:

   Hypertension alters the autoregulatory capacity of cerebral blood vessels, making them less responsive to changes in blood pressure. This can lead to hypoperfusion or hyperperfusion, both of which can precipitate ischemic or hemorrhagic stroke.

   
   

5. Blood-Brain Barrier Disruption:

   Elevated blood pressure can compromise the integrity of the blood-brain barrier, increasing its permeability. This disruption allows neurotoxic substances to enter the brain parenchyma, contributing to neuronal injury and increasing the risk of stroke.

   
   

These pathophysiological processes underscore the critical role of hypertension in stroke development. Effective management of blood pressure is essential in reducing the incidence of both ischemic and hemorrhagic strokes.

1. Atherosclerosis Development:

   Excess adipose tissue in obesity leads to increased levels of low-density lipoprotein (LDL) cholesterol and triglycerides, promoting the formation of atherosclerotic plaques in arterial walls. This process narrows and stiffens arteries, impeding cerebral blood flow and elevating the risk of ischemic stroke.

   
   

2. Hypertension:

   Obesity is closely associated with hypertension, a major risk factor for stroke. The increased adipose tissue elevates vascular resistance and blood volume, leading to higher arterial pressure. Chronic hypertension can cause damage to blood vessels, increasing the likelihood of both ischemic and hemorrhagic strokes.

   
   

3. Insulin Resistance and Type 2 Diabetes Mellitus:

   Obesity often results in insulin resistance, progressing to type 2 diabetes mellitus. Hyperglycemia and associated metabolic disturbances contribute to endothelial dysfunction and a pro-thrombotic state, heightening the risk of stroke.

4. Pro-inflammatory State:

   Adipose tissue in obesity secretes pro-inflammatory cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α). This chronic low-grade inflammation contributes to endothelial injury and atherosclerosis, facilitating stroke development.

   
   

5. Pro-thrombotic State:

   Elevated levels of plasminogen activator inhibitor-1 (PAI-1) and fibrinogen in obese individuals promote a hypercoagulable state, increasing the risk of thrombus formation and subsequent ischemic stroke.

6. Obstructive Sleep Apnea (OSA):

   Obesity is a leading cause of OSA, characterized by intermittent hypoxia during sleep. OSA contributes to hypertension, atrial fibrillation, and endothelial dysfunction, all of which are risk factors for stroke.

   
   

These interrelated mechanisms illustrate how obesity contributes to both ischemic and hemorrhagic strokes. Addressing obesity through lifestyle modifications and medical interventions is crucial in reducing stroke risk.

1. Atherosclerosis and Endothelial Dysfunction:

   Diets high in saturated fats, trans fats, and cholesterol contribute to the development of atherosclerosis by increasing low-density lipoprotein (LDL) cholesterol levels. This leads to plaque formation within arterial walls, causing narrowing and hardening of the arteries, which impedes cerebral blood flow and increases stroke risk.

   
   

2. Hypertension:

   Excessive sodium intake, often from processed and salty foods, is strongly associated with elevated blood pressure. Hypertension damages blood vessels and is a leading risk factor for both ischemic and hemorrhagic strokes.

   
   

3. Insulin Resistance and Type 2 Diabetes Mellitus:

   Diets high in refined sugars and low in fiber can lead to insulin resistance, a precursor to type 2 diabetes mellitus. Diabetes exacerbates vascular damage and accelerates atherosclerosis, thereby increasing the likelihood of stroke.

   
   

4. Pro-inflammatory State:

   Poor dietary patterns, such as high consumption of red and processed meats and low intake of fruits and vegetables, promote systemic inflammation. Chronic inflammation contributes to endothelial dysfunction and atherogenesis, elevating stroke risk.

5. Oxidative Stress:

   Diets deficient in antioxidants—commonly found in fruits and vegetables—fail to counteract oxidative stress. Oxidative damage to blood vessels fosters atherosclerosis and thrombosis, increasing the potential for stroke.

   
   

6. Thrombosis and Coagulation:

   Unhealthy diets can alter hemostatic factors, leading to a pro-thrombotic state. This increases the likelihood of clot formation, which can obstruct cerebral arteries and cause ischemic stroke.

   
   

7. Gut Microbiota Imbalance:

   Diet influences the composition of gut microbiota. Poor dietary habits can disrupt this balance, leading to the production of metabolites that may adversely affect vascular health and promote stroke.

   
   

These mechanisms illustrate how poor dietary choices can lead to conditions that predispose individuals to stroke. Adopting a balanced diet rich in fruits, vegetables, whole grains, lean proteins, and healthy fats is crucial for stroke prevention.

1. Development of Atherosclerosis:

   Sedentary behavior leads to unfavorable lipid profiles, characterized by elevated low-density lipoprotein (LDL) cholesterol and reduced high-density lipoprotein (HDL) cholesterol levels. These alterations promote the formation of atherosclerotic plaques within arterial walls, narrowing the arteries and impeding cerebral blood flow, thereby increasing the risk of ischemic stroke.

2. Elevation of Blood Pressure:

   Lack of physical activity is associated with increased arterial stiffness and heightened sympathetic nervous system activity, both of which contribute to elevated blood pressure. Hypertension is a well-established risk factor for both ischemic and hemorrhagic strokes.

   
   

3. Insulin Resistance and Type 2 Diabetes Mellitus:

   Physical inactivity contributes to the development of insulin resistance, a precursor to type 2 diabetes mellitus. Diabetes accelerates atherosclerosis and induces endothelial dysfunction, both of which elevate stroke risk.

   
   

4. Pro-thrombotic State:

   Sedentary lifestyles are linked to increased levels of pro-thrombotic factors, such as fibrinogen and plasminogen activator inhibitor-1 (PAI-1). This pro-thrombotic state enhances the likelihood of clot formation, which can obstruct cerebral arteries and lead to ischemic stroke.

   
   

5. Obesity:

   Physical inactivity is a major contributor to obesity, which is independently associated with increased stroke risk. Obesity exacerbates other risk factors, including hypertension, diabetes, and dyslipidemia, creating a cumulative effect that heightens stroke susceptibility.

   
   

6. Endothelial Dysfunction:

   Regular physical activity enhances endothelial function by increasing nitric oxide bioavailability, which promotes vasodilation and inhibits platelet aggregation. Inactivity impairs these protective mechanisms, facilitating vascular dysfunction and atherogenesis.

Collectively, these mechanisms illustrate how physical inactivity contributes to the pathogenesis of stroke. Engaging in regular physical activity mitigates these risks by improving cardiovascular health, enhancing metabolic function, and reducing pro-thrombotic tendencies. Public health guidelines recommend at least 150 minutes of moderate-intensity aerobic activity per week to confer protective benefits against stroke and other cardiovascular diseases.

1. Hypertension (High Blood Pressure):

   Chronic heavy drinking increases blood pressure, a leading risk factor for stroke. Elevated blood pressure damages blood vessels, making them more susceptible to blockage or rupture.

   
   

2. Atrial Fibrillation (AF):

   Excessive alcohol intake can trigger AF, an irregular heart rhythm that increases stroke risk fivefold. AF can cause blood clots to form in the heart, which may travel to the brain, leading to ischemic stroke.

3. Diabetes Mellitus:

   Alcohol affects insulin sensitivity, potentially leading to type 2 diabetes. Diabetes is a significant risk factor for stroke due to its association with accelerated atherosclerosis and endothelial dysfunction.

   
   

4. Obesity:

   Alcohol is calorie-dense; excessive consumption contributes to weight gain and obesity. Obesity is linked to increased stroke risk through mechanisms like hypertension, diabetes, and dyslipidemia.

   
   

5. Liver Dysfunction:

   Chronic alcohol use can lead to liver damage, impairing the production of clotting factors. This increases the risk of hemorrhagic stroke due to bleeding in the brain.

   
   

6. Pro-thrombotic State:

   Heavy alcohol consumption can alter coagulation pathways, promoting a pro-thrombotic state that increases the likelihood of clot formation, potentially leading to ischemic stroke.

   
   

7. Endothelial Dysfunction:

   Alcohol-induced oxidative stress and inflammation can impair endothelial function, promoting atherosclerosis and increasing stroke risk.

These mechanisms illustrate how excessive alcohol intake contributes to both ischemic and hemorrhagic strokes. Moderation is crucial; while light-to-moderate alcohol consumption may have protective effects against ischemic stroke, heavy drinking significantly increases the risk of all stroke types.

1. Atrial Fibrillation (AF):

   AF causes irregular atrial contractions, leading to blood stasis in the atria, particularly the left atrial appendage. This stasis promotes thrombus formation, which can embolize to cerebral arteries, resulting in ischemic stroke. AF is the most common risk factor for cardioembolic stroke, significantly increasing stroke risk.

   
   

2. Heart Failure (HF):

   HF leads to reduced cardiac output and blood stasis, increasing the risk of intracardiac thrombus formation. Additionally, HF is associated with endothelial dysfunction and a pro-thrombotic state, further elevating stroke risk. HF is associated with up to a three-fold increased risk of ischemic stroke compared to the general population.

   
   

3. Sinus Node Dysfunction (SND):

   SND can lead to bradyarrhythmias and atrial fibrillation, both of which increase the risk of thrombus formation and subsequent embolic stroke. SND is associated with an increased risk of stroke, with hazard ratios indicating a significant association.

   
   

4. Valvular Heart Diseases:

   Diseases such as mitral stenosis or prosthetic heart valves can cause turbulent blood flow and stasis, leading to thrombus formation and potential embolization to the brain. Valvular heart diseases are recognized risk factors for cardioembolic stroke.

   
   

5. Coronary Artery Disease (CAD):

   Atherosclerosis in coronary arteries reflects systemic atherosclerosis, including in cerebral arteries, increasing the risk of ischemic stroke. Additionally, myocardial infarction can lead to left ventricular thrombus formation, which can embolize to cerebral circulation. CAD increases the risk for stroke due to shared risk factors and pathophysiological mechanisms.

These cardiac conditions contribute to stroke risk through mechanisms such as thrombus formation, embolization, and systemic atherosclerosis. Management of these conditions is crucial in reducing stroke incidence.

If stands singularly:

• High blood pressure contributing to 55.5% of the total stroke

• High BMI / Obesity accounted for 24.4%

• High fasting plasma glucose --> 20.2%

• Pollution --> 20.1%

• Smoking --> 17.7%

(Hewlings & Kalman, 2017).

• Turmeric (Kunyit):

  Fresh or powdered turmeric is the base ingredient, providing its bright yellow color and health benefits.

• Tamarind (Asam Jawa):

  Tamarind pulp gives the drink its sour flavor and is rich in antioxidants.

• Palm Sugar (Gula Jawa):

  Used as a sweetener to balance the sourness of tamarind.

• Water:

  Acts as the base for the herbal drink.

Key Points:
>Causes: Frequently triggered by a stroke, Bell's palsy, or various neurological disorders.
>Symptoms: The appearance of a sagging face on one side, along with challenges in smiling or fully shutting the eye on that side.
>Treatment: Varies based on the root cause and can involve medications, therapy, or additional medical treatments.

Key points:
>Origins: Frequently the result of a stroke, nerve impairment, muscle trauma, or brain-related issues.
>Signs: Trouble or inability to raise the arm, lack of strength, loss of sensation, or a prickling feeling.
>Care: Relies on the root issue and could include physical rehabilitation, drugs, or operative procedures.

A. Receptors and Molecular Target

1. Nrf2 (Nuclear Factor Erythroid 2–Related Factor 2):

   Curcumin activates Nrf2, which regulates the expression of antioxidant genes such as heme oxygenase-1 (HO-1) and glutathione peroxidase, protecting cells from oxidative stress.

   
   

2. NF-κB (Nuclear Factor Kappa-Light-Chain-Enhancer of Activated B Cells):

   Curcumin inhibits NF-κB activation, a key factor in inflammation. By suppressing NF-κB, curcumin reduces the production of pro-inflammatory cytokines like TNF-α and IL-6.

3. Akt/mTOR Pathway:

   Curcumin modulates the Akt/mTOR pathway, promoting neuronal survival and reducing cell damage during ischemia.

4. Peroxisome Proliferator-Activated Receptor Gamma (PPAR-γ):

   Curcumin interacts with PPAR-γ, which is involved in regulating lipid metabolism and inflammation, making it relevant for stroke prevention

• Antioxidant Activity:

  Tartaric acid scavenges free radicals, reducing oxidative stress, which is a significant factor in atherosclerosis and vascular damage leading to strokes.

• Improving Lipid Profiles:

  Tartaric acid may modulate lipid metabolism by enhancing the degradation of low-density lipoprotein (LDL) and preventing its oxidation. Oxidized LDL is a key factor in atherosclerosis.

• Anti-inflammatory Effects:

  Tartaric acid indirectly modulates inflammation by reducing oxidative stress, decreasing endothelial dysfunction, and lowering the risk of plaque formation.

Relevance to Stroke and Cholesterol:

By mitigating oxidative stress and improving lipid profiles, tartaric acid reduces the risk of atherosclerosis and cardiovascular events, thereby lowering stroke risk.

• Antioxidant Effects:

  Curcumin directly neutralizes reactive oxygen species (ROS) due to its phenolic structure. It also enhances antioxidant enzyme production by activating Nrf2.

  
  

• Anti-inflammatory Effects:

  Curcumin inhibits pro-inflammatory pathways such as NF-κB and COX-2, reducing inflammation—a major risk factor for both ischemic and hemorrhagic strokes.

• Neuroprotective Effects:

  A. Curcumin reduces amyloid plaque accumulation and prevents oxidative stress in the brain, supporting cognitive function and protecting brain tissue.

  
  

  B. Its modulation of NMDA (N-Methyl-D-Aspartate) receptors prevents excitotoxicity, a primary cause of neuronal damage during stroke.

• Anti-apoptotic Effects:

  Curcumin prevents neuronal apoptosis by modulating mitochondrial pathways and proteins like Bcl-2 and caspase-3.

• Improvement of Cerebral Blood Flow

  Curcumin enhances endothelial function by increasing nitric oxide (NO) availability, promoting vasodilation and better cerebral circulation.

A. Receptors and Molecular Targets:

• PPAR-γ (Peroxisome Proliferator-Activated Receptor Gamma):

  Flavonoids activate PPAR-γ, improving lipid metabolism and reducing the expression of inflammatory cytokines.

• Scavenger Receptors (SRs):

  Flavonoids inhibit scavenger receptors like SR-A and CD36, which mediate the uptake of oxidized LDL by macrophages, preventing foam cell formation and atherosclerosis.

• Nrf2 (Nuclear Factor Erythroid 2–Related Factor 2):

  Flavonoids activate Nrf2, leading to the production of antioxidant enzymes such as glutathione peroxidase and superoxide dismutase, protecting endothelial cells from oxidative stress.

• eNOS (Endothelial Nitric Oxide Synthase):

  Flavonoids enhance eNOS activity, increasing nitric oxide (NO) production. NO promotes vasodilation, improving blood flow and preventing hypertension, a major stroke risk factor.

• Inhibition of LOX-1 (Lectin-Like Oxidized LDL Receptor-1):

  Flavonoids block LOX-1, reducing the uptake of oxidized LDL by endothelial cells and macrophages.

B. Mechanisms:

• Antioxidant Effects:

  Flavonoids neutralize reactive oxygen species (ROS) and enhance endogenous antioxidant systems, protecting against LDL oxidation and endothelial dysfunction.

  
  

• Anti-inflammatory Effects:

  Flavonoids suppress NF-κB signaling, reducing the production of inflammatory mediators like TNF-α, IL-6, and CRP, which contribute to vascular inflammation and atherosclerosis.

• Improved Lipid Profiles:

  Flavonoids decrease total cholesterol, LDL cholesterol, and triglycerides while increasing high-density lipoprotein (HDL) cholesterol by modulating PPAR-γ and hepatic cholesterol metabolism.

• Platelet Aggregation Inhibition:

  Flavonoids inhibit platelet aggregation and thrombus formation by modulating thromboxane and prostacyclin pathways, reducing the risk of ischemic stroke.

1. Prevention of Atherosclerosis:

   Flavonoids reduce LDL oxidation, foam cell formation, and plaque development, which are central to atherosclerosis.

2. Improved Vascular Function:

   By increasing NO availability and reducing vascular inflammation, flavonoids enhance endothelial health and lower stroke risk.

3. Cholesterol Reduction:

   Flavonoids improve lipid metabolism, decreasing cholesterol levels and reducing cardiovascular risk factors.

Summary

Tartaric Acid: Acts as an antioxidant and supports lipid metabolism, indirectly reducing oxidative stress, atherosclerosis, and stroke risk.

Flavonoids: Target specific receptors like PPAR-γ, Nrf2, and eNOS, and act through antioxidant, anti-inflammatory, and lipid-lowering mechanisms to prevent atherosclerosis, reduce cholesterol, and lower the risk of stroke.