Post-acute sequelae of SARS-CoV-2 infection (Long COVID) in older adults
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Cited by 6 publications
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Neurologic Manifestations of Long COVID Disproportionately Affect Young and Middle‐Age Adults
ObjectiveTo investigate neurologic manifestations of post‐acute sequelae of SARS‐CoV‐2 infection (Neuro‐PASC) in post‐hospitalization Neuro‐PASC (PNP) and non‐hospitalized Neuro‐PASC (NNP) patients across the adult lifespan.MethodsCross‐sectional study of the first consecutive 200 PNP and 1,100 NNP patients evaluated at a Neuro‐coronavirus disease 2019 (COVID‐19) clinic between May 2020 and March 2023. Patients were divided into younger (18–44 years), middle‐age (45–64 years), and older (65+ years) age groups.ResultsYounger and middle‐age individuals accounted for 142 of 200 (71%) of PNP and 995 of 1100 (90.5%) of NNP patients. Significant age‐related differences in the frequencies of comorbidities and abnormal neurologic findings demonstrated higher prevalence in older patients. Conversely, 10 months from COVID‐19 onset, we found significant age‐related differences in Neuro‐PASC symptoms indicating lower prevalence, and therefore, symptom burden, in older individuals. Moreover, there were significant age‐related differences in subjective impression of fatigue (median [interquartile range (IQR)] patient‐reported outcomes measurement information system [PROMIS] score: younger 64 [57–69], middle‐age 63 [57–68], older 60.5 [50.8–68.3]; p = 0.04) and sleep disturbance (median [IQR] PROMIS score: younger 57 [51–63], middle‐age 56 [53–63], older 54 [46.8–58]; p = 0.002) in the NNP group, commensurate with higher impairment in quality of life (QoL) among younger patients. Finally, there were significant age‐related differences in objective executive function (median [IQR] National Institutes of Health [NIH] toolbox score: younger 48 [35–63], middle‐age 49 [38–63], older 54.5 [45–66.3]; p = 0.01), and working memory (median [IQR] NIH toolbox score: younger 47 [40–53], middle‐age 50 [44–57], older 48 [43–58]; p = 0.0002) in NNP patients, with the worst performance coming from the younger group.InterpretationYounger and middle‐age individuals are disproportionally affected by Neuro‐PASC regardless of acute COVID‐19 severity. Although older people more frequently have abnormal neurologic findings and comorbidities, younger and middle‐age patients suffer from a higher burden of Neuro‐PASC symptoms and cognitive dysfunction contributing to decreased QoL. Neuro‐PASC principally affects adults in their prime, contributing to profound public health and socioeconomic impacts warranting dedicated resources for prevention, diagnosis and interventions. ANN NEUROL 2024
Neurologic Manifestations of Long COVID Disproportionately Affect Young and Middle‐Age Adults
ObjectiveTo investigate neurologic manifestations of post‐acute sequelae of SARS‐CoV‐2 infection (Neuro‐PASC) in post‐hospitalization Neuro‐PASC (PNP) and non‐hospitalized Neuro‐PASC (NNP) patients across the adult lifespan.MethodsCross‐sectional study of the first consecutive 200 PNP and 1,100 NNP patients evaluated at a Neuro‐coronavirus disease 2019 (COVID‐19) clinic between May 2020 and March 2023. Patients were divided into younger (18–44 years), middle‐age (45–64 years), and older (65+ years) age groups.ResultsYounger and middle‐age individuals accounted for 142 of 200 (71%) of PNP and 995 of 1100 (90.5%) of NNP patients. Significant age‐related differences in the frequencies of comorbidities and abnormal neurologic findings demonstrated higher prevalence in older patients. Conversely, 10 months from COVID‐19 onset, we found significant age‐related differences in Neuro‐PASC symptoms indicating lower prevalence, and therefore, symptom burden, in older individuals. Moreover, there were significant age‐related differences in subjective impression of fatigue (median [interquartile range (IQR)] patient‐reported outcomes measurement information system [PROMIS] score: younger 64 [57–69], middle‐age 63 [57–68], older 60.5 [50.8–68.3]; p = 0.04) and sleep disturbance (median [IQR] PROMIS score: younger 57 [51–63], middle‐age 56 [53–63], older 54 [46.8–58]; p = 0.002) in the NNP group, commensurate with higher impairment in quality of life (QoL) among younger patients. Finally, there were significant age‐related differences in objective executive function (median [IQR] National Institutes of Health [NIH] toolbox score: younger 48 [35–63], middle‐age 49 [38–63], older 54.5 [45–66.3]; p = 0.01), and working memory (median [IQR] NIH toolbox score: younger 47 [40–53], middle‐age 50 [44–57], older 48 [43–58]; p = 0.0002) in NNP patients, with the worst performance coming from the younger group.InterpretationYounger and middle‐age individuals are disproportionally affected by Neuro‐PASC regardless of acute COVID‐19 severity. Although older people more frequently have abnormal neurologic findings and comorbidities, younger and middle‐age patients suffer from a higher burden of Neuro‐PASC symptoms and cognitive dysfunction contributing to decreased QoL. Neuro‐PASC principally affects adults in their prime, contributing to profound public health and socioeconomic impacts warranting dedicated resources for prevention, diagnosis and interventions. ANN NEUROL 2024
The role of atrial fibrillation in vascular cognitive impairment and dementia: epidemiology, pathophysiology, and preventive strategies
The aging population in Europe faces a substantial burden from dementia, with vascular cognitive impairment and dementia (VCID) being a preventable cause. Atrial fibrillation (AF), a common cardiac arrhythmia, increases the risk of VCID through mechanisms such as thromboembolism, cerebral hypoperfusion, and inflammation. This review explores the epidemiology, pathophysiology, and preventive strategies for AF-related VCID. Epidemiological data indicate that AF prevalence rises with age, affecting up to 12% of individuals over 80. Neuroimaging studies reveal chronic brain changes in AF patients, including strokes, lacunar strokes, white matter hyperintensities (WMHs), and cerebral microbleeds (CMHs), while cognitive assessments show impairments in memory, executive function, and attention. The COVID-19 pandemic has exacerbated the underdiagnosis of AF, leading to an increase in undiagnosed strokes and cognitive impairment. Many elderly individuals did not seek medical care due to fear of exposure, resulting in delayed diagnoses. Additionally, reduced family supervision during the pandemic contributed to missed opportunities for early detection of AF and related complications. Emerging evidence suggests that long COVID may also elevate the risk of AF, further complicating the management of this condition. This review underscores the importance of early detection and comprehensive management of AF to mitigate cognitive decline. Preventive measures, including public awareness campaigns, patient education, and the use of smart devices for early detection, are crucial. Anticoagulation therapy, rate and rhythm control, and addressing comorbid conditions are essential therapeutic strategies. Recognizing and addressing the cardiovascular and cognitive impacts of AF, especially in the context of the COVID-19 pandemic, is essential for advancing public health.
Human herpesvirus reactivation and its potential role in the pathogenesis of post-acute sequelae of SARS-CoV-2 infection
The emergence of SARS-CoV-2 has precipitated a global pandemic with substantial long-term health implications, including the condition known as post-acute sequelae of SARS-CoV-2 infection (PASC), commonly referred to as Long COVID. PASC is marked by persistent symptoms such as fatigue, neurological issues, and autonomic dysfunction that persist for months beyond the acute phase of COVID-19. This review examines the potential role of herpesvirus reactivation, specifically Epstein-Barr virus (EBV) and cytomegalovirus (CMV), in the pathogenesis of PASC. Elevated antibody titers and specific T cell responses suggest recent herpesvirus reactivation in some PASC patients, although viremia is not consistently detected. SARS-CoV-2 exhibits endothelial trophism, directly affecting the vascular endothelium and contributing to microvascular pathologies. These pathologies are significant in PASC, where microvascular dysfunction may underlie various chronic symptoms. Similarly, herpesviruses like CMV also exhibit endothelial trophism, which may exacerbate endothelial damage when reactivated. Evidence suggests that EBV and CMV reactivation could indirectly contribute to the immune dysregulation, immunosenescence, and autoimmune responses observed in PASC. Additionally, EBV may play a role in the genesis of neurological symptoms through creating mitochondrial dysfunction, though direct confirmation remains elusive. The reviewed evidence suggests that while herpesviruses may not play a direct role in the pathogenesis of PASC, their potential indirect effects, especially in the context of endothelial involvement, warrant further investigation.
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