Brain infarction
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Brain Infarction: Insights from Recent Research
Types and Clinical Correlations of Brainstem Infarctions
Brainstem infarctions can be categorized into several types based on MRI patterns, including small midlateral, dorsolateral, inferolateral, large inferodorsolateral, dorsal, and paramedian infarcts. These types are associated with distinct clinical syndromes. For instance, Wallenberg's syndrome is commonly linked with small midlateral, dorsolateral, inferolateral, and inferodorsolateral infarcts, each presenting specific clusters and severity of neurological features. Dorsal infarcts often coincide with cerebellar infarcts in the posterior inferior cerebellar artery (PICA) territory, while paramedian infarcts can lead to crossed tongue and sensorimotor hemiplegia. The study highlights that atheromatosis is the predominant cause of these infarctions, with vertebral artery dissection and cardioembolism also contributing.
Biochemical and Molecular Changes in Cerebral Infarction
Cerebral infarction involves complex biochemical and molecular changes. The occlusion of a cerebral artery results in focal ischemia, creating a severely ischemic core and a surrounding penumbra where blood flow reduction is moderate. Neuronal injury in the penumbra is reversible for a limited time, making it a target for pharmacological interventions like glutamate antagonists or reperfusion. 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, ischemia/reperfusion injury triggers inflammatory reactions involving neutrophils and monocytes/macrophages, suggesting potential therapeutic targets in the inflammatory/immune response.
Silent Brain Infarcts: Prevalence and Implications
Silent brain infarcts (SBIs) are increasingly detected due to advancements in imaging techniques. These infarcts, often lacunes caused by hypertensive small-vessel disease, are found in 20% of healthy elderly individuals and up to 50% of patients in specific series. Despite the absence of overt stroke-like symptoms, SBIs are associated with subtle physical and cognitive deficits and significantly increase the risk of subsequent stroke and dementia. Studies suggest that screening and treating high-risk patients could potentially reduce the risk of further infarcts, stroke, and dementia.
Cognitive Outcomes and Risk Factors Post-TAVI
SBIs are frequently identified after transcatheter aortic valve implantation (TAVI), with a significant proportion of patients showing new SBIs on diffusion-weighted MRI post-procedure. Risk factors for SBIs post-TAVI include diabetes, chronic renal disease, and pre-dilation. These infarcts are linked to early post-procedural cognitive dysfunction, with the prevalence of cognitive deficits increasing over time. The use of cerebral embolic protection devices (CEPDs) has been shown to reduce the volume of SBIs but not their overall incidence.
Imaging and Diagnosis of Brain Infarctions
Imaging plays a crucial role in diagnosing brain infarctions, especially in uncommon cases involving neurovascular variants and small arterial territories. Conditions like Claude and Benedikt syndromes (midbrain infarction) and Wallenberg syndrome (lateral medullary infarction) are identified through specific imaging features. Accurate imaging is essential for proper diagnosis and management of these conditions.
Aging and Brain Infarction
Aging exacerbates brain infarction, primarily due to increased acrolein production and decreased glutathione (GSH) levels. In older mice, the volume of brain infarction is significantly larger, attributed to higher spermine oxidase activity and reduced GSH, a key acrolein-detoxifying compound. This suggests that interventions targeting acrolein production and GSH levels could mitigate age-related aggravation of brain infarction.
Secondary Neurodegeneration Post-Infarction
Secondary neurodegeneration occurs in brain regions remote from the primary infarct site but connected via synaptic pathways. This phenomenon, known as diaschisis, involves neuronal death, gliosis, and axonal degeneration in areas like the ipsilateral thalamus and substantia nigra following middle cerebral artery infarction. Understanding secondary neurodegeneration is crucial for developing strategies to improve stroke recovery and manage long-term neurological deficits.
Conclusion
Recent research provides valuable insights into the types, biochemical changes, and clinical implications of brain infarctions. Understanding the diverse presentations and underlying mechanisms of brain infarctions, including silent brain infarcts and secondary neurodegeneration, is essential for improving diagnosis, treatment, and patient outcomes. Continued research and advancements in imaging and molecular biology will further enhance our ability to manage and mitigate the effects of brain infarctions.
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