Cerebral ischemia causes
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These studies suggest that cerebral ischemia is caused by factors such as abnormal intracellular ion homeostasis, oxidative stress, inflammation, and various pathomechanisms including cerebral vasospasm and thrombin influence.
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Causes of Cerebral Ischemia: An Overview
Cerebral ischemia, a condition characterized by insufficient blood flow to the brain, leads to significant brain damage due to the lack of oxygen and essential nutrients. This article synthesizes the key causes and mechanisms underlying cerebral ischemia, drawing from multiple research studies.
Insufficient Blood Flow and Thrombosis
Critical Reduction in Cerebral Blood Flow
The primary cause of cerebral ischemia is a critical reduction in cerebral blood flow, which can result from various factors such as thrombosis and arterial hemorrhage. Thrombosis, the formation of a blood clot within a blood vessel, is responsible for about 60% of cerebral ischemia cases. The clot formation involves the transformation of liquid fibrinogen into insoluble fibrin, leading to increased permeability of the blood-brain barrier and subsequent brain damage .
Arterial Hemorrhage
Arterial hemorrhage, another significant cause, involves the rupture of blood vessels, leading to bleeding within the brain. This bleeding disrupts normal blood flow and contributes to ischemic conditions.
Metabolic and Cellular Pathologies
Metabolic Disturbances
Cerebral ischemia triggers complex metabolic and cellular pathologies, including neuronal cell death and cerebral infarction. These metabolic disturbances are often analyzed through metabolome-based techniques, which provide insights into the cellular pathologic status and help identify potential biomarkers for ischemic stroke.
Cellular Acidosis and Ion Homeostasis
Cellular acidosis and biochemical disturbances due to abnormal intracellular ion homeostasis are critical factors in determining the survival of nerve cells during ischemia. These biochemical events are initiated by the ischemic condition and play a significant role in the extent of brain damage.
Oxidative Stress and Inflammation
Oxidative Stress
Oxidative stress, caused by reactive oxygen species (ROS) during cerebral ischemia, is a major contributor to cell death and brain damage. The production of free radicals such as superoxide anion, hydroxyl radicals, and nitric oxide during reperfusion exacerbates the damage through lipid peroxidation, inflammation, and apoptosis .
Inflammatory Response
Inflammation is another critical factor, where the balance between pro-inflammatory and anti-inflammatory factors is disrupted, leading to aggravated ischemic injury. The interaction between oxidative stress and inflammation further complicates the pathological processes involved in cerebral ischemia.
Neurovascular Unit and Blood-Brain Barrier
Blood-Brain Barrier Breakdown
The breakdown of the blood-brain barrier (BBB) is a significant event in cerebral ischemia, leading to the extravasation of blood components into the brain and altering the brain microenvironment. This change affects the neurovascular unit (NVU), which is crucial for maintaining brain function .
Role of Coagulation Factors
Coagulation factors, particularly thrombin, interact with the NVU and its components, influencing the extent of brain injury during ischemia. Understanding these interactions is essential for exploring new therapeutic approaches to reduce the risk of coagulation and subsequent brain damage.
Conclusion
Cerebral ischemia is a multifaceted condition caused by insufficient blood flow, thrombosis, arterial hemorrhage, metabolic disturbances, oxidative stress, and inflammation. The breakdown of the blood-brain barrier and the role of coagulation factors further complicate the pathology. Understanding these mechanisms is crucial for developing effective therapeutic strategies to prevent and treat cerebral ischemia.
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