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Background: Cognitive deficits are commonly reported after COVID-19 recovery, but little is known in the older population. This study aims to investigate possible cognitive damage in older adults 6 months after contracting COVID-19, as well as individual risk factors. Methods: This cross-sectional study involved 70 participants aged 60-78 with COVID-19 6 months prior and 153 healthy controls. Montreal Cognitive Assessment-Basic (MoCA-B) screened for cognitive impairment; Geriatric Depression Scale and Geriatric Anxiety Inventory screened for depression and anxiety. Data were collected on demographics and self-reports of comorbid conditions. Results: The mean age of participants was 66.97 ± 4.64 years. A higher proportion of individuals in the COVID group complained about cognitive deficits (χ2 = 3.574; p = 0.029) and presented with deficient MoCA-B scores (χ2 = 6.098, p = 0.014) compared to controls. After controlling for multiple variables, all the following factors resulted in greater odds of a deficient MoCA-B: COVID-19 6-months prior (OR, 2.44; p = 0.018), age (OR, 1.15; p < 0.001), lower income (OR, 0.36; p = 0.070), and overweight (OR, 2.83; p = 0.013). Further analysis pointed to individual characteristics in COVID-19-affected patients that could explain the severity of the cognitive decline: age (p = 0.015), lower income (p < 0.001), anxiety (p = 0.049), ageusia (p = 0.054), overweight (p < 0.001), and absence of cognitively stimulating activities (p = 0.062). Conclusion: Our study highlights a profile of cognitive risk aggravation over aging after COVID-19 infection, which is likely mitigated by wealth but worsened in the presence of overweight. Ageusia at the time of acute COVID-19, anxiety, being overweight, and absence of routine intellectual activities are risk factors for more prominent cognitive decline among those infected by COVID-19.
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Introduction: Sleep problems are one of the most persistent symptoms of post-COVID syndrome in adults. However, most recent research on sleep quality has relied on the impact of the pandemic, with scarcely any data for older adults on the long-term consequences of COVID infection. This study aims to understand whether older individuals present persistently impaired sleep quality after COVID-19 infection and possible moderators for this outcome. Methods: This is a cross-sectional analysis of a longitudinal cohort study with 70 elders with 6-month-previous SARS-CoV-2 infection and 153 controls. The Pittsburgh Sleep Quality Index (PSQI) was used to assess sleep quality; Geriatric Depression Scale and Geriatric Anxiety Inventory for screening depression and anxiety. Demographics and comorbid conditions were collected. Results: The mean age of participants was 66,97 ± 4,64 years. There were no statistical differences in depression and anxiety between groups. Poor sleep quality was found in 52,9% and 43,8% of the COVID and control groups (p=.208). After controlling for multiple variables, all the following factors resulted in greater chances of poor sleep quality: female gender (OR, 2.12; p=.027), memory complaints (OR, 2.49; p=.074), insomnia (OR, 3.66; p=.032), anxiety (OR, 5.46; p<.001), depression (OR, 7.26; p=.001), joint disease (OR, 1.80; p=.050), glucose intolerance (OR, 2.20; p=.045), psychoactive drugs (OR, 8.36; p<.001), diuretics (OR, 2.46; p=.034), and polypharmacy (OR, 2.84; p=.016). Conclusion: Psychosocial burden in the context of the COVID-19 pandemic and pre-existing conditions seems to influence the sleep quality of older adults more than SARS-CoV-2 infection.
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Background: Chikungunya fever is a disabling articular disease caused by chikungunya virus (CHIKV). In the past decade it has affected millions of people across America, Africa, Asia, and Europe, turning this infection into a public health concern. The acute phase of chikungunya infection is usually self-limiting, characterized by severe arthralgia, fever, chills, myalgia, headache, and rash. CHIKV neurovirulence is evident and seems to be higher among elders. Considering their susceptibility to cognitive decline and dementia, the aim of our study was to investigate whether CHIKV infection might cause long-term cognitive impairment in aged people. Methods: A cross-sectional study was conducted with volunteers aged from 60 to 90 who had been affected by chikungunya and also with healthy controls. A structured questionnaire was used to record demographic and clinical data, functional status, and depression. Global cognitive function was assessed through MoCA. A comprehensive neuropsychological battery was performed to assess specific cognitive functions. Results: Subjective memory complaints were present in 70% of subjects with previous chikungunya. This group had a poorer performance in MoCA (p = 0.000) and specific cognitive tests: Semantic (p = 0.05) and Phonemic Verbal Fluency (p = 0.003), 5-Digit (choice, reading, counting and alternance, p = 0.003, p = 0.014, p = 0.021, and p = 0.021, respectively), Stroop test (time, errors and interference, p = 0.000, p = 0.027 and p = 0.015, respectively), and RAVLT (word total session p = 0.05). These tests reflect performance on general executive functions, cognitive flexibility, inhibitory control, processing speed, semantic memory and episodic memory. Conclusion: Our data suggest that CHIKV infection may cause long-term cognitive decline in aged people and might be a risk factor for future dementia in this population.
