COVID-19’un Santral Sinir Sistemi Üzerine Etkileri ve Nörobilişsel Bozukluklar
Özet
COVID-19 pandemisi, akut solunum yolu bulgularının yanı sıra santral sinir sistemini de etkileyerek anksiyete, bilişsel bozukluklar, ensefalit ve deliryum gibi geniş bir yelpazede nöropsikiyatrik belirtilere yol açmaktadır. Bu semptomların patofizyolojisinde doğrudan nöral invazyon, sitokin fırtınasına bağlı sistemik inflamasyon, kan-beyin bariyeri hasarı, hipoksi, koagülopatiye ikincil iskemik değişiklikler ve otoimmünite gibi çoklu mekanizmalar öne sürülmektedir. Özellikle inflamatuar süreçler ve hipoksinin kan-beyin bariyerinin geçirgenliğini artırarak nörodejenerasyonu tetiklediği görülmektedir. Hastalığın akut, subakut ve post-COVID dönemlerinde yapılan araştırmalar; enfeksiyonu atlatan kişilerin önemli bir kısmında dikkat, yürütücü işlevler, bellek ve sözel akıcılık performanslarında belirgin düşüşler ve orta düzeyde bilişsel bozulmalar olduğunu doğrulamaktadır. DSM-5 kapsamında değerlendirilen nörobilişsel bozukluklardan deliryumun COVID-19 hastalarında influenza gibi diğer solunum yolu enfeksiyonlarına kıyasla daha yüksek oranda izlendiği ve mortaliteyi artırdığı saptanmıştır. Ayrıca, ApoE4-ε4 genotipi gibi genetik faktörlerin de etkisiyle demans ve Alzheimer hastalarının COVID-19’a yakalanma, hastaneye yatış ve ölüm risklerinin ciddi oranda yükseldiği; pandemi kısıtlamalarının ve izolasyonun bu hastalarda ajitasyon, anksiyete ve apati gibi nöropsikiyatrik semptomları kötüleştirdiği gözlenmiştir. Gelecekte, endotelyal disfonksiyon ve amiloid plak birikimi gibi mekanizmaların Alzheimer gelişimini hızlandırabileceği düşünülmektedir.
The COVID-19 pandemic leads to a wide spectrum of neuropsychiatric manifestations, including anxiety, cognitive impairments, encephalitis, and delirium, in addition to acute respiratory symptoms. Multiple mechanisms are proposed in the pathophysiology of these symptoms, such as direct neural invasion, cytokine storm-induced systemic inflammation, blood-brain barrier disruption, hypoxia, coagulopathy-related secondary ischemic changes, and autoimmunity. Inflammatory processes and hypoxia, in particular, appear to trigger neurodegeneration by increasing blood-brain barrier permeability. Research conducted across the acute, subacute, and post-COVID periods confirms that a significant portion of survivors exhibit marked declines in attention, executive functions, memory, and verbal fluency, alongside moderate cognitive impairment. Among neurocognitive disorders categorized under DSM-5, delirium is found to occur at a higher rate in COVID-19 patients compared to other respiratory infections like influenza, subsequently increasing mortality. Furthermore, driven partly by genetic factors such as the ApoE4-ε4 genotype, individuals with dementia and Alzheimer's face substantially elevated risks of contracting COVID-19, hospitalization, and mortality; additionally, pandemic restrictions and isolation have worsened neuropsychiatric symptoms like agitation, anxiety, and apathy in these patients. In the future, pathophysiological pathways including endothelial dysfunction and amyloid plaque accumulation are hypothesized to potentially accelerate the development of Alzheimer's dementia.
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