During the coronavirus disease 2019 (COVID-19) pandemic, Long COVID syndrome, which impairs patients through cognitive deficits, fatigue, and exhaustion, has become increasingly relevant. Its underlying pathophysiology, however, is unknown. In this study, we assessed cognitive profiles and regional cerebral glucose metabolism as a biomarker of neuronal function in outpatients with long-term neurocognitive symptoms after COVID-19. Methods: Outpatients seeking neurologic counseling with neurocognitive symptoms persisting for more than 3 mo after polymerase chain reaction (PCR)–confirmed COVID-19 were included prospectively between June 16, 2020, and January 29, 2021. Patients (n = 31; age, 53.6 ± 2.0 y) in the long-term phase after COVID-19 (202 ± 58 d after positive PCR) were assessed with a neuropsychologic test battery. Cerebral ¹⁸F-FDG PET imaging was performed in 14 of 31 patients. Results: Patients self-reported impaired attention, memory, and multitasking abilities (31/31), word-finding difficulties (27/31), and fatigue (24/31). Twelve of 31 patients could not return to the previous level of independence/employment. For all cognitive domains, average group results of the neuropsychologic test battery showed no impairment, but deficits (z score < –1.5) were present on a single-patient level mainly in the domain of visual memory (in 7/31; other domains ≤ 2/31). Mean Montreal Cognitive Assessment performance (27/30 points) was above the cutoff value for detection of cognitive impairment (<26 points), although 9 of 31 patients performed slightly below this level (23–25 points). In the subgroup of patients who underwent ¹⁸F-FDG PET, we found no significant changes of regional cerebral glucose metabolism. Conclusion: Long COVID patients self-report uniform symptoms hampering their ability to work in a relevant fraction. However, cognitive testing showed minor impairments only on a single-patient level approximately 6 mo after the infection, whereas functional imaging revealed no distinct pathologic changes. This clearly deviates from previous findings in subacute COVID-19 patients, suggesting that underlying neuronal causes are different and possibly related to the high prevalence of fatigue.

在 2019 年冠状病毒病 (COVID-19) 大流行期间，通过认知缺陷、疲劳和疲惫影响患者的长期 COVID 综合征变得越来越重要。然而，其潜在的病理生理学尚不清楚。在这项研究中，我们评估了 COVID-19 后出现长期神经认知症状的门诊患者的认知特征和局部脑葡萄糖代谢作为神经元功能的生物标志物。方法：在 2020 年 6 月 16 日至 2021 年1月 29 日期间，前瞻性纳入了在聚合酶链反应 (PCR) 确认的 COVID-19 后神经认知症状持续超过 3 个月且寻求神经系统咨询的门诊患者。= 31; 年龄，53.6 ± 2.0 岁）在 COVID-19 后的长期阶段（阳性 PCR 后 202 ± 58 天）用神经心理学测试电池进行评估。31 名患者中有 14 名进行了脑¹⁸ F-FDG PET 成像。结果：患者自述注意力、记忆力和多任务处理能力受损 (31/31)、找词困难 (27/31) 和疲劳 (24/31)。31 名患者中有 12 名无法恢复到以前的独立/就业水平。对于所有认知领域，神经心理学测试组的平均组结果显示没有损伤，但有缺陷（z分数 < –1.5）主要存在于视觉记忆领域（7/31；其他领域≤2/31）。平均蒙特利尔认知评估表现（27/30 分）高于检测认知障碍的临界值（<26 分），尽管 31 名患者中有 9 名的表现略低于该水平（23-25 分）。^在接受18 F-FDG PET的患者亚组中，我们发现局部脑葡萄糖代谢没有显着变化。结论：长期 COVID 患者自我报告统一的症状阻碍了他们在相关部分工作的能力。然而，认知测试仅在感染后约 6 个月显示单个患者水平的轻微损伤，而功能成像显示没有明显的病理变化。这显然不同于之前在亚急性 COVID-19 患者中的发现，这表明潜在的神经元原因是不同的，并且可能与疲劳的高患病率有关。