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These studies suggest that brain infarcts can result from various causes such as atheromatosis, hypotension, and microembolism, and are associated with cognitive decline, increased risk of dementia, and potential for new therapeutic targets.
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Brainstem infarcts can be categorized into several types based on their location and MRI patterns. A study involving 28 patients identified six topographical types of infarcts in the lower brainstem: small midlateral, dorsolateral, inferolateral, large inferodorsolateral, dorsal, and paramedian infarcts. The most common types were small midlateral, dorsolateral, inferolateral, and inferodorsolateral, often associated with Wallenberg's syndrome. Dorsal infarcts were frequently accompanied by cerebellar infarcts in the posterior inferior cerebellar artery (PICA) territory, while paramedian infarcts led to crossed tongue and sensorimotor hemiplegia. Atheromatosis was the most frequent cause, accounting for 72% of cases, with vertebral artery dissection and cardioembolism also contributing.
Genome-wide association studies (GWAS) have explored the genetic underpinnings of covert MRI-defined brain infarcts. A meta-analysis from the CHARGE consortium identified significant associations with specific single nucleotide polymorphisms (SNPs), particularly rs2208454, which was linked to a lower risk of MRI infarcts. However, replication in independent samples was inconsistent, highlighting the need for further research to confirm these genetic associations.
Watershed infarcts occur in the border zones between major cerebral arteries and account for approximately 10% of all brain infarcts. These infarcts can be caused by systemic hypotension or microembolism, although the exact mechanisms remain debated. They are more easily recognized in the brain due to the well-defined course of cerebral arteries.
Cerebral infarction involves complex biochemical and molecular changes. Following artery occlusion, a severely ischemic core and a moderately ischemic penumbra develop. The penumbra is potentially salvageable with timely intervention. Reperfusion alters genomic properties, inducing stress proteins that help mitigate neuronal injury. Apoptosis and inflammatory reactions also play significant roles in the expansion of infarction, presenting potential targets for therapeutic intervention.
Longitudinal studies have shown that brain infarcts are associated with cognitive decline and an increased risk of dementia. Men are at higher risk of developing new infarcts compared to women. Subcortical infarcts, in particular, are strongly linked to incident dementia, suggesting that small vessel disease may play a crucial role in cognitive deterioration.
In focal cerebral ischemia models, brain edema can significantly affect the measurement of infarct volume. Traditional direct measurement methods may overestimate infarct size due to edema. Indirect measurement techniques, which account for non-infarcted cortex volume, provide more accurate assessments and are less influenced by edema.
Silent brain infarcts, detected through advanced imaging techniques, are prevalent in up to 50% of certain patient populations. Although they lack overt stroke symptoms, they are associated with subtle cognitive and physical deficits and significantly increase the risk of subsequent stroke and dementia. This underscores the importance of early detection and potential intervention to mitigate long-term consequences.
The number and location of cerebral infarcts are critical determinants of cognitive performance. Infarcts in multiple locations are associated with poorer memory, processing speed, and executive function. Subcortical and cortical infarcts, in particular, have a significant impact on cognitive abilities, independent of other vascular risk factors.
Research on brain infarcts highlights the complexity of their types, causes, and consequences. From the genetic factors influencing covert infarcts to the biochemical changes during cerebral ischemia, understanding these mechanisms is crucial for developing effective interventions. Silent brain infarcts, despite their lack of immediate symptoms, pose significant risks for cognitive decline and dementia, emphasizing the need for proactive management and further research.
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