Searched over 200M research papers for "cerebral infarction"
10 papers analyzed
These studies suggest cerebral infarction has diverse subgroups, is linked to poor outcomes after aneurysmal subarachnoid hemorrhage, involves noncoding RNAs in neuroinflammation, can be influenced by psychological interventions, and is associated with factors like acute anemia, infections, and genomic changes in brain cells.
20 papers analyzed
Cerebral infarction, a leading cause of disability and death, can be classified into distinct subtypes based on the affected vascular territories. A community-based study of 675 patients identified four primary subtypes: total anterior circulation infarcts (TACI), partial anterior circulation infarcts (PACI), posterior circulation infarcts (POCI), and lacunar infarcts (LACI). Each subtype exhibits unique characteristics and outcomes. TACI, involving both cortical and subcortical regions, has a high mortality rate and poor functional outcomes. PACI, which affects predominantly cortical areas, shows a higher likelihood of early recurrent strokes. POCI, associated with the vertebrobasilar arterial territory, has the best chance of a good functional outcome despite a higher risk of recurrent stroke later in the first year. LACI, confined to deep perforating arteries, often results in substantial handicap despite the small size of the infarcts.
Cerebral infarction significantly impacts outcomes in patients with aneurysmal subarachnoid hemorrhage (SAH). A study involving 3567 patients found that cerebral infarction increased the odds of an unfavorable outcome by a factor of 5.4. Key predictors of cerebral infarction in these patients include older age, worse neurological grade on admission, history of hypertension or diabetes, larger aneurysm size, induced hypertension, high temperature post-SAH, and symptomatic vasospasm. Symptomatic vasospasm, in particular, is a critical treatable factor associated with infarction.
Acute anemia, particularly following significant blood loss, can also lead to cerebral infarction. A study of patients with acute anemia due to massive gastrointestinal bleeding or postoperative hematoma revealed that borderzone infarction is a common finding. The mean hemoglobin level at the time of infarction was critically low, indicating that reduced oxygen-carrying capacity and cerebral blood flow insufficiency are key mechanisms.
Neuroinflammation plays a crucial role in the pathophysiology of cerebral infarction. Following ischemic stroke, the innate immune response is activated, leading to the production of neurotoxic substances and the disruption of the blood-brain barrier. This process involves the infiltration of immune cells into brain tissue, which can exacerbate neuronal damage and neurological deficits. Non-coding RNAs (ncRNAs) have emerged as significant regulators of these inflammatory and immune responses, offering potential as biomarkers and therapeutic targets.
Psychological interventions can significantly enhance the rehabilitation outcomes for patients with cerebral infarction. A controlled study demonstrated that a 3-month psychological intervention program improved cognitive function, reduced depression, and enhanced daily living activities compared to traditional rehabilitation care. This suggests that addressing the psychological well-being of patients is crucial for comprehensive stroke recovery.
Cerebral infarction encompasses various subtypes, each with distinct prognostic implications. Understanding the predictors and mechanisms underlying cerebral infarction in conditions like SAH and acute anemia is essential for improving patient outcomes. Additionally, addressing neuroinflammation and incorporating psychological interventions can play a pivotal role in the holistic management of cerebral infarction. These insights underscore the importance of tailored therapeutic strategies to mitigate the impact of this debilitating condition.
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