Infarction of the brain
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Understanding Brain Infarction: Key Insights from Recent Research
Biochemical and Molecular Changes in Cerebral Infarction
Ischemic Core and Penumbra
Cerebral infarction occurs when a cerebral artery is occluded, leading to focal ischemia. This 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 with timely pharmacological interventions such as glutamate antagonists or prompt reperfusion.
Stress Response and Apoptosis
Upon reperfusion, brain cells undergo genomic changes, restricting protein synthesis to stress proteins, which help mitigate neuronal injury and enhance resistance to subsequent ischemic stress. Additionally, the expansion of infarction may involve apoptotic mechanisms, suggesting that targeting apoptosis could be a strategy to prevent ischemic cell death.
Inflammatory Reactions
Ischemia/reperfusion injury is accompanied by inflammatory reactions involving neutrophils and monocytes/macrophages in the ischemic areas. Understanding the role of the inflammatory/immune systems in ischemic brain injury could lead to new therapeutic targets.
Clinical and Imaging Correlations in Brainstem Infarction
Topographical Types and Clinical Features
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. Angiography often reveals embolic occlusions and atheromatosis as common causes.
CT and Angiography Correlation
CT and clinical evidence often show infarction in the brainstem and cerebellum, but the correlation with angiographic findings can be poor due to basal artifacts. Combined infarctions of the brainstem and cerebellum are common, and some cases may develop hydrocephalus, which can be managed with careful medical decompression.
Defining Cerebral Infarction
Universal Definition
A proposed universal definition of cerebral infarction is 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, aligning with myocardial ischemia classification.
Silent Brain Infarcts
Prevalence and Impact
Silent brain infarcts, detected in up to 50% of patients in selected series, are often caused by hypertensive small-vessel disease. Although they lack overt stroke-like symptoms, they are associated with subtle physical and cognitive deficits and significantly increase the risk of subsequent stroke and dementia.
Uncommon Brain Infarctions
Neurovascular Variants and Small Arterial Territories
Uncommon brain infarctions include those associated with neurovascular variants and small arterial territories. These infarctions can lead to various brainstem stroke syndromes, such as Claude and Benedikt syndromes due to midbrain infarction, and Wallenberg syndrome due to lateral medullary infarction.
Watershed Infarcts
Mechanisms and Locations
Watershed infarcts occur in border zones between major arteries and can be caused by systemic hypotension or microembolism. These infarcts account for approximately 10% of all brain infarcts and are more easily recognized in the brain due to the well-defined course of cerebral arteries.
Secondary Neurodegeneration
Diaschisis and Remote Brain Regions
Secondary neurodegeneration, or diaschisis, occurs in brain regions remote from the primary infarct site but connected via synaptic pathways. This degeneration can be detected by neuroimaging and is associated with neurological deficits, potentially predicting motor outcomes after stroke.
Classification and Natural History of Cerebral Infarction Subtypes
Subtypes and Outcomes
Cerebral infarctions can be classified into four subtypes: total anterior circulation infarcts (TACI), partial anterior circulation infarcts (PACI), posterior circulation infarcts (POCI), and lacunar infarcts (LACI). Each subtype has distinct natural histories and outcomes, with TACI having the highest mortality and POCI the best functional outcomes.
Conclusion
Understanding the biochemical, molecular, and clinical aspects of brain infarction is crucial for developing effective treatments and improving patient outcomes. Advances in imaging and a universal definition of cerebral infarction can enhance diagnosis and management, while recognizing the impact of silent infarcts and secondary neurodegeneration can inform future therapeutic strategies.
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