Talkington Grant McGee, Kolluru Paresh, Gressett Timothy E, Ismael Saifudeen, Meenakshi Umar, Acquarone Mariana, Solch-Ottaiano Rebecca J, White Amanda, Ouvrier Blake, Paré Kristina, Parker Nicholas, Watters Amanda, Siddeeque Nabeela, Sullivan Brooke, Ganguli Nilesh, Calero-Hernandez Victor, Hall Gregory, Longo Michele, Bix Gregory J
Department of Neurosurgery, Clinical Neuroscience Research Center, Tulane University School of Medicine, New Orleans, LA, United States.
Tulane Brain Institute, Tulane University, New Orleans, LA, United States.
Front Neurol. 2025 Feb 7;15:1465787. doi: 10.3389/fneur.2024.1465787. eCollection 2024.
One lingering effect of the COVID-19 pandemic created by SARS-CoV-2 is the emergence of Long COVID (LC), characterized by enduring neurological sequelae affecting a significant portion of survivors. This review provides a thorough analysis of these neurological disruptions with respect to cognitive dysfunction, which broadly manifest as chronic insomnia, fatigue, mood dysregulation, and cognitive impairments with respect to cognitive dysfunction. Furthermore, we characterize how diagnostic tools such as PET, MRI, EEG, and ultrasonography provide critical insight into subtle neurological anomalies that may mechanistically explain the Long COVID disease phenotype. In this review, we explore the mechanistic hypotheses of these neurological changes, which describe CNS invasion, neuroinflammation, blood-brain barrier disruption, and gut-brain axis dysregulation, along with the novel vascular disruption hypothesis that highlights endothelial dysfunction and hypoperfusion as a core underlying mechanism. We lastly evaluate the clinical treatment landscape, scrutinizing the efficacy of various therapeutic strategies ranging from antivirals to anti-inflammatory agents in mitigating the multifaceted symptoms of LC.
由严重急性呼吸综合征冠状病毒2（SARS-CoV-2）引发的新冠疫情的一个持续影响是长期新冠（LC）的出现，其特征是持久的神经后遗症影响着很大一部分幸存者。本综述全面分析了这些与认知功能障碍相关的神经功能紊乱，认知功能障碍广泛表现为慢性失眠、疲劳、情绪失调以及认知障碍。此外，我们描述了正电子发射断层扫描（PET）、磁共振成像（MRI）、脑电图（EEG）和超声检查等诊断工具如何为可能从机制上解释长期新冠疾病表型的细微神经异常提供关键见解。在本综述中，我们探讨了这些神经变化的机制假说，这些假说描述了中枢神经系统入侵、神经炎症、血脑屏障破坏和肠脑轴失调，以及强调内皮功能障碍和灌注不足作为核心潜在机制的新型血管破坏假说。我们最后评估了临床治疗情况，仔细审查了从抗病毒药物到抗炎药物等各种治疗策略在减轻长期新冠多方面症状方面的疗效。
