Infarction in the brain
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Understanding Brain Infarction: Key Insights and Developments
Biochemical and Molecular Changes in Cerebral Infarction
Cerebral infarction, commonly known as a stroke, involves the occlusion of a cerebral artery, leading to focal ischemia. This condition results in a severely ischemic core where infarction develops rapidly and a surrounding area called the penumbra, where blood flow reduction is moderate and neuronal injury is potentially reversible for several hours. The penumbra can be salvaged through pharmacological agents like glutamate antagonists or prompt reperfusion. Upon reperfusion, brain cells undergo genomic changes, restricting protein synthesis to stress proteins, which help mitigate neuronal injury and confer resistance to subsequent ischemic stress. Additionally, the expansion of infarction may involve apoptotic mechanisms, and ischemia/reperfusion injury is accompanied by inflammatory reactions involving neutrophils and monocytes/macrophages.
Clinical and Topographical Correlations in Brainstem Infarction
Infarctions in the lower brainstem can be categorized into six topographical types: small midlateral, dorsolateral, inferolateral, large inferodorsolateral, dorsal, and paramedian infarcts. These types are associated with specific neurological features and conditions such as Wallenberg's syndrome and cerebellar infarcts. The most common cause of these infarctions is atheromatosis, with vertebral artery dissection and cardioembolism also contributing. MRI and magnetic resonance angiography (MRA) are crucial in identifying these infarcts and understanding their clinical implications.
Diagnostic Advances and Universal Definition of Cerebral Infarction
Recent diagnostic advances have led to a proposed universal definition of cerebral infarction as brain or retinal cell death due to prolonged ischemia. This definition includes both complete and incomplete infarcts and emphasizes the importance of tissue state over time criteria. It aims to harmonize with myocardial ischemia classification and focus diagnostic evaluation on the cause of brain ischemia and the occurrence of end organ injury.
Silent Brain Infarcts: Prevalence and Implications
Silent brain infarcts (SBIs) are increasingly identified with advanced imaging techniques and are found in up to 50% of patients in selected series. These infarcts, often caused by hypertensive small-vessel disease, lack overt stroke-like symptoms but are associated with subtle deficits in physical and cognitive function. SBIs significantly increase the risk of subsequent stroke and dementia, highlighting the need for effective screening and treatment strategies to reduce further infarcts and associated conditions.
Watershed Infarcts: Mechanisms and Clinical Impact
Watershed infarcts occur in the border zones between major cerebral arteries and account for approximately 10% of all brain infarcts. These infarcts can result from systemic hypotension or microembolism and are recognized for their distinct location and potential to cause significant neurological deficits. In the fetal and neonatal brainstem, watershed infarcts can lead to conditions such as central hypoventilation, dysphagia, and Mӧbius syndrome.
Hemorrhagic vs. Pale Infarcts in Cardioembolic Stroke
In cardioembolic stroke, hemorrhagic infarcts can occur even without the reopening of occluded arteries, contradicting the common belief that vessel reopening is necessary for hemorrhage. These hemorrhagic infarcts are associated with surges in arterial blood pressure and the presence of efficient leptomeningeal collaterals. Understanding these mechanisms is crucial for managing and preventing complications in stroke patients.
Conclusion
Cerebral infarction encompasses a range of conditions and mechanisms, from biochemical changes and molecular responses to clinical and topographical variations. Advances in diagnostic techniques and a better understanding of silent and watershed infarcts have significant implications for treatment and prevention strategies. Continued research and a unified definition of cerebral infarction will enhance clinical practice and patient outcomes.
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