The COVID-19 pandemic, caused by SARS-CoV-2, has had profound global impacts since its emergence in late 2019. Whilst acute symptoms are well-documented, increasing evidence suggests long-term consequences extending beyond the acute phase. This study aimed to investigate the long-term cognitive and autonomic effects of COVID-19 in young adults.

We conducted a cross-sectional study comparing young adults with a history of COVID-19 (n = 34) to matched controls (n = 34). Cognitive function was assessed using the Sternberg Task, Stroop Task, and Go/No-Go Task (GNG). Autonomic function was evaluated using heart rate variability (HRV) parameters.

The average time interval between COVID-19 infection and testing was 28.2 months. The COVID-19 group showed significantly increased reaction time in the 2-item absent condition (p = 0.044) and errors in the 4-item present condition (p = 0.012) of the Sternberg Task and increased neutral response time (p = 0.028) and the normalized time for completing the task (p = 0.022) in the Stroop Task. No significant differences were found in the GNG Task. HRV parameters did not differ significantly between groups, although trends toward higher overall HRV were observed in the COVID-19 group.

Young adults who had COVID-19 infection approximately 28 months ago show minimal long-term impact on cognitive function and autonomic regulation. However, subtle cognitive inefficiencies persist, particularly in working memory and executive function tasks. These findings suggest a generally favorable long-term prognosis for young adults following mild to moderate COVID-19 but highlight the need for further investigation into persistent subtle cognitive effects and autonomic effects.

This study aimed to compare the prevalence of insomnia, lung function, inspiratory muscle function, functional capacity, and quality of life in individuals with and without post-COVID-19 fatigue.

Thirty-four post-COVID-19 individuals participated in the study, 20 with fatigue (32 ± 12 years old, 15% male) and 14 without fatigue (31 ± 12 years old, 42.9% male). The Chalder Fatigue Scale (CFS) was employed to categorize the volunteers into two groups: those with fatigue (score ≥4) and those without fatigue (score <4). The Insomnia Severity Index (ISI) and the Epworth Sleepiness Scale (ESS) were used to assess insomnia and excessive daytime sleepiness, respectively. Pulmonary function was evaluated by spirometry, inspiratory muscle strength was assessed by the maximum inspiratory pressure (MIP), and inspiratory endurance was evaluated by maintaining an inspiratory load of 60% of MIP until fatigue. The 6-min walk test (6MWT) was used to evaluated functional capacity, while the WHOQOL-BREF questionnaire assessed quality of life.

Individuals with post-COVID-19 fatigue demonstrated a higher prevalence of insomnia (80% vs. 49%) and excessive daytime sleepiness (45% vs. 7%), as well as lower MIP, shorter distance covered in the 6MWT, and lower FEV1/FVC (forced expired volume in the first second divided by forced vital capacity), and FEV1/FVC% of predicted. Additionally, they exhibited poorer quality of life in the physical and environmental domains. CFS demonstrated a direct correlation with ISI (r=0.436, p=0.01) and ESS (r=0.593, p=0.001), as well as an inverse correlation with the distance covered in the 6MWT (r=-0.398, p=0.022) and FEV1 (r=-0.412, p=0.01). ISI was an independent predictor of CFS, with 62% of CFS variance explained by ISI variance.

Individuals with symptoms of post-COVID-19 fatigue may have a higher prevalence of insomnia, reduced inspiratory muscle strength, functional capacity, and Tiffeneau index, along with impaired quality of life. ISI is an independent predictor of post-COVID-19 fatigue.

Major depressive episodes (MDE) following COVID-19 have been described in approximately 30 % of cases. A clinical picture characterized by physical and cognitive symptoms with underlying immune-inflammatory changes has been reported. However, a comparison of post-COVID-19 MDE with non-post-COVID-19 depression is still lacking. This study aims to characterize 209 patients with MDE, post-COVID-19 vs. non-post-COVID-19, focusing on physical and cognitive symptomatology evaluated through Hamilton Depression (HDRS) and Anxiety Rating Scales (HARS), Digit Symbol Substitution Test (DSST), Perceived Deficits Questionnaire-Depression 5-items (PDQ-D5). Inflammatory levels were assessed with blood count-derived indexes. Post-COVID-19 group (46.9 % of patients) displayed higher rates of first-onset depressive episodes (p = 0.001), an older age at onset (p = 0.006), more physical and cognitive features according to subitems of HDRS (p = 0.001), HARS (p < 0.001), and PDQ-D5 scores (p = 0.019), as well as higher inflammatory indexes (p < 0.001). Logistic regression showed a significant association of post-COVID-19 MDE with physical symptomatology (p = 0.02) and Systemic Immune-Inflammatory Index (p = 0.04). Receiver Operating Characteristic (ROC) curves displayed a discriminative potential for this association (AUC = 0.921). These results highlight the specific clinical presentation of post-COVID-19 MDE, with prominent physical symptoms and increased inflammation levels, suggesting that a more careful characterization might inform personalized interventions and promote full functional recovery in these patients.

SARS-CoV-2 is a neurotrophic and pro-inflammatory virus, with several acute and more persistent neuropsychiatric sequelae reported. There are limited data from African cohorts and few acute illness biomarkers of persistent neuropsychiatric symptoms.

To examine the association of neuropsychiatric outcomes with clinical illness severity, systemic inflammation, cardiovascular and renin-angiotensin-system (RAS) biomarkers. Second, to determine the prevalence of neuropsychiatric symptoms in a cohort of South African SARS-CoV-2 PCR positive patients at least six months following infection/hospitalization.

SARS-CoV-2 PCR positive patients were recruited prospectively from Cape Town, South Africa, including hospitalized patients from ancestral, beta and delta-dominant COVID-19 waves (pre-vaccine rollout); and asymptomatic/mild SARS-CoV-2 positive patients. The 96-protein O-link inflammation and cardiovascular panels, RAS fingerprinting, and antibody responses were measured in serum samples collected at peak severity and recovery (>3 months post-infection). Telephonic interviews were conducted at least six months post infection/hospitalization. Validated measures employed were: WHO Self-Report Questionnaire (SRQ-20), Generalized Anxiety Disorder Scale (GAD-7), Chalder Fatigue Scale (CFS-11) and Telephonic Montreal Cognitive Assessment (T-MoCA).

Ninety-seven participants completed telephonic interviews. The median (IQR) age was 48 (37-59) years, and 54 % were female. There were no significant associations between neuropsychiatric outcomes and illness severity, systemic inflammation, cardiovascular and/or renin-angiotensin-system (RAS) biomarkers from either peak illness or recovery samples. More than half of this SA COVID-19 cohort had one or more persistent neuropsychiatric symptoms >6 months post vaccine-naïve infection. On the T-MoCA, 44 % of participants showed evidence of cognitive and/or memory impairments.

The high prevalence of persistent neuropsychiatric symptoms in this African cohort supports ongoing attention to long COVID. Acute and early serum protein biomarkers were not associated with persistent neuropsychiatric outcomes post-COVD-19.

To assess the impact of post-COVID clinics by examining the association between their early usage and downstream health care utilization.

In a case-control study spanning data from March 11, 2020 to June 1, 2023, patients with Long COVID were identified from a major health system using diagnosis codes. The Fast, Large-Scale Almost Matching Exactly algorithm was used to match patients who presented early to post-COVID clinics with patients with Long COVID who did not attend such clinics. Matching was performed on demographic characteristics, acute COVID severity, comorbidities, diagnosis date, and vaccination, to reduce confounders for the comparison of the health care utilization and mortality between cohorts.

When exactly matching on all 46 features, the algorithm yielded 2814 matched patients, of whom 692 (24.6%; 66.6% females; mean [SD] age, 48.8 [14.5] years) were seen in post-COVID clinics within the first 6 months and 2122 (75.4%; 64.1% females; mean [SD] age, 49.7 [15.2] years) who were not. The average treatment effect (95% CI) of early post-COVID clinic usage was -0.60 (-0.83 to -0.39) on inpatient visits, -0.19 (-0.26 to -0.11) on emergency department visits, 7.62 (6.96-8.56) on outpatient visits, -$3467 (-$6267 to -$754) on estimated costs, and -0.006 (-0.010 to -0.003) on mortality.

Early usage of post-COVID clinics by patients with Long COVID is associated with not only fewer downstream inpatient stays, emergency department visits, estimated costs, and reduced mortality within the first 6 months but also greater outpatient utilization. Results suggest early post-COVID clinic involvement shifts care to outpatient settings, potentially reducing costs and mortality.

Golden Syrian hamsters are an often-overlooked model in behavioral testing. While previously utilized for research examining circadian rhythms and mammalian reproduction, they are less common than murine models in both infectious disease and behavioral studies. However, coronavirus disease-19 (COVID-19) quickly pushed hamster modeling to the forefront due to its myriad of advantages over mice in recapitulating human pathology and transmission. At least 10 % of COVID-19 survivors suffer from post-acute sequelae of COVID-19 (PASC), a collection of some 200 sequelae with neurologic sequelae (neuro-PASC) presenting with potentially debilitating symptomology. This presents a clear need for a small animal model that recapitulates human disease with the ability to assess any potential long term neurological changes. We adapted and optimized a panel of behavioral tests from previously accepted murine models utilizing the golden Syrian hamster model for use within biocontainment facilities. Our panel includes grip strength, Porsolt forced swim, and novel object recognition testing to measure muscle fatigue or weakness, depression, and memory loss or cognitive impairment, respectively. Apart from severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), this panel of tests is applicable to other pathogens that cause neurologic sequelae, such as Nipah or eastern equine encephalitis viruses, or any other model systems that require the use of hamsters. In this manuscript, we detail the methods for each of these three behavioral tests, how to interpret and analyze the resulting data, and emphasize additional factors for consideration. We also provide baseline data for both male and female golden Syrian hamsters.

To describe the experiences of people living with neuropsychological symptomatology associated with long-COVID, as well as identifying the barriers they encounter in their daily lives and the strategies they develop to deal with them.

Descriptive qualitative study following an interpretative phenomenological perspective.

Primary Care Centres in the Northern Metropolitan Area of Barcelona and the Germans Trias i Pujol University Hospital (Badalona), Spain.

34 adults with any persistent neuropsychological symptoms of COVID-19 (>12 weeks since disease onset).

In-depth individual interviews were conducted following a script of open-ended questions to elicit their narratives around the research objective.

3 clusters detailing the life impact of long-COVID and its neuropsychological symptomatology were identified: long-COVID as life-breaking and life-changing; coping strategies; and (ac)knowledge (of) the emerging subjectivity.

From the participants' accounts and the existing literature emerges the relevance of critically integrating lessons learned from analogous syndromes such as fibromyalgia and chronic fatigue, as well as involving patients in the design and implementation (even at the consultation level) of clinical practices that raise awareness of these neuropsychological sequelae (psychoeducation) both to other patients and to caregivers and professionals. This would facilitate a greater and better specialised psychological approach and reduce the stigma that still accompanies the condition.

A few studies have reported conjunctivitis is a complication associated with acute COVID-19. It is unknown whether SARS-CoV-2 infection increases the risk of conjunctivitis post-COVID-19 long term.

This study investigated the incidence of new-onset conjunctivitis 3.5 years post SARS-CoV-2 infection and compared it with patients without SARS-CoV-2 infection.

This retrospective study consisted of 67 702 patients who tested positive for COVID-19 (defined by a positive PCR test), and 1 391 135 COVID-19-negative patients with no prior records of conjunctivitis in the Montefiore Health System from 11 March 2020 to 31 December 2022. The study included adult patients re-presenting to our centre with conjunctivitis. Outcome was new conjunctivitis between 14 days and 3.5 years post index date. Analysis was performed with unmatched and matched cohorts. Matching was done for age, sex, race and ethnicity. Cumulative incidence and hazard ratio (HR) with and without adjustment for competitive risks were analysed.

There were 1154 (2.27%) individuals with COVID-19 and contemporary 13 899 (1.57%) controls who developed new conjunctivitis. COVID-19-positive patients had a significantly higher risk of developing new incident conjunctivitis (unmatched cohort adjusted HR 1.11 (95% CI 1.04 to 1.17), matched cohort adjusted HR 1.10 (95% CI 1.02 to 1.16)) compared with COVID-19-negative patients.

COVID-19-positive patients had significantly higher risk of developing new conjunctivitis compared with contemporary COVID-19-negative controls. Identifying risk factors for developing new-onset conjunctivitis may draw clinical attention for careful follow-up in at-risk individuals for ocular infections.

Substantial numbers of individuals who contract COVID-19 experience long-lasting cognitive symptoms such as brain fog. Yet research to date has not compared these patients with healthy controls with a history of laboratory-confirmed COVID-19 infection, making it difficult to understand why certain COVID patients develop post-COVID cognitive symptoms while others do not. The objective of this pilot study was to compare two groups of laboratory-confirmed post-COVID patients, with and without cognitive symptoms, on measures of cognitive and psychological functioning, self-reported perceptions of functional status and quality of life, and biomarkers of stress, inflammation, and neuroplasticity. Using a case-control design, 17 participants were recruited from a healthcare system in western Michigan, USA in 2022-2024. All participants were aged 25-65 and had a positive polymerase chain reaction (PCR) test confirming previous COVID-19 infection. Ten participants reported cognitive symptoms (long COVID group) while seven were fully recovered with no residual symptoms (controls). All participants underwent an interview on their self-rated health and quality of life, a battery of neurocognitive tests, and blood draw for biomarker analysis. No group differences were detected for neuropsychological test measures except for letter fluency where the long COVID group scored significantly lower (p < .05). The long COVID group had significantly lower ratings than controls on quality of life, physical health, emotional functioning, and psychological well-being. Serum levels of nerve growth factor (NGF), a biomarker of brain plasticity, were significantly lower in the long COVID group, which was significantly more likely than controls to have serum levels of inflammatory marker (interleukin (IL)-10) values greater than or equal to the median (p = 0.015). Biomarker analyses suggest possible prolonged inflammatory processes in long COVID patients compared to fully recovered patients. Results of decreased neuroplastic functioning give credence to patients' reports of post-COVID changes in brain function.

Neuropathic pain is a recognized and debilitating symptom of SARS-CoV-2 infection across acute, post-acute, and long-COVID phases. Initially emerging as acute or subacute symptoms, these neuropathic manifestations can evolve into chronic conditions, with approximately 10% of all SARS-CoV-2 cases (estimated 65 million individuals globally) developing post-acute SARS-CoV-2 (PASC) neuropathic sequalae. Given the limited literature specifically addressing neuropathic pain related to PASC, a deeper understanding is needed to improve management and reduce patient burden.

PASC symptoms are associated with disease severity, elevated body mass indexes, preexisting psychological conditions, and addiction history. Sex differences appear to influence prevalence, and the multisystem nature of PASC complicates symptom presentation, with mood disorders, fatigue, and cognitive dysfunction contributing to altered pain perception. Proposed mechanisms include immune dysregulation, persistent viral protein effects, and neuroanatomical changes. Management typically involves a multimodal approach.

This review examines SARS-CoV-2 neuropathic pain across the illness trajectory, examining its pathophysiology, prevalence, and treatment. It highlights the potential for subacute neuropathic symptoms to become chronic and calls for future research to refine long-term management strategies and assess broader healthcare implications.

People with long COVID report prolonged, multisystem involvement and significant disability. This study aimed to determine long COVID prevalence and factors associated with it among US adults using nationally representative data.

This cross-sectional analysis utilized data from 2022 Behavioral Risk Factor Surveillance System survey, a nationally representative telephone survey conducted among noninstitutionalized adults aged ≥ 18 years residing in the United States. Age-adjusted prevalence of long COVID was calculated using weighted survey analysis. Poisson regression was employed to assess adjusted prevalence ratios (aPRs) associated with long COVID across various demographic, socioeconomic and health-related characteristics.

Among 390,233 participants, 120,178 reported COVID-19, with 25,582 experiencing long COVID. Age-adjusted prevalence of self-reported COVID-19 and long COVID were estimated at 34.1% (95% CI, 33.7-34.4%) and 7.2% (95% CI, 7.0-7.4%) as of 2022, respectively. Among adults reporting COVID-19, 20.9% (95% CI, 20.5-21.4%) had ever experienced long COVID. An inverted U-shaped association was observed between long COVID risk and age, with the highest prevalence (23.5%) in the 45-54 age group. Long COVID was more prevalent among women (aPR, 1.40 [95% CI, 1.34-1.47]), individuals without a spouse (aPR, 1.06 [95% CI, 1.00-1.13]), uninsured (aPR, 1.16 [95% CI, 1.06-1.27]), and those with a high school education (aPR, 1.17 [95% CI, 1.12-1.23]), cardiovascular disease (aPR, 1.17 [95% CI, 1.09-1.25]), depressive disorder (aPR, 1.41 [95% CI, 1.34-1.48]), chronic obstructive pulmonary disease (aPR, 1.33 [95% CI, 1.24-1.43]), asthma (aPR, 1.28 [95% CI, 1.21-1.35]), and kidney disease (aPR, 1.11 [95% CI, 1.01-1.21]). Long COVID was less prevalent among non-Hispanic Black (aPR, 0.87 [95% CI, 0.81-0.95]), students (aPR, 0.87 [95% CI, 0.76-0.99]) or retired individuals (aPR, 0.89 [95% CI, 0.82-0.98]), and those with household incomes ≥$100,000 (aPR, 0.85 [95% CI, 0.79-0.92]).

Long COVID affects 7.2% of US adults, with higher vulnerability among women, middle-aged individuals, White individuals, socioeconomically disadvantaged groups, and those with chronic conditions. These findings underscore the need for targeted public health strategies to address disparities in long COVID burden and support high-risk populations.

Cognitive impairment, including deficits in attention, memory, executive function, and processing speed, is common in post-COVID-19 conditions, though language performance remains less studied. The present study examined the long-term effects of COVID-19 condition on cognition and language - communication, and its associations with disease severity, Body Mass Index (BMI), inflammatory markers, and quality of life.

Nighty eight Greek participants under 65 years of age were recruited for this study. Forty-seven participants were allocated in the COVID-19 group and 51 served as cognitively healthy controls. The COVID-19 group was categorized by disease severity and long COVID status. Assessments occurred 12 weeks post-infection, with 12 patients reevaluated after another 12 weeks. Neurocognitive tests included ABCD-II, verbal fluency, CCT, SDMT, and Euro QoL EQ-5D. Blood samples were analyzed for inflammatory markers.

Covid-19 survivors experienced significant cognitive deficits compared to healthy controls, particularly in processing speed, memory, and verbal fluency. Long COVID patients showed notably lower scores in processing speed and QoL, compared to those without Long COVID. However, no significant differences were observed between groups on episodic memory and executive functions tasks. Cognitive deficits were associated with biomarkers such as d-dimers and C-Reactive protein, with elevated d-dimers linked to poorer performance on generative drawing and cognitive flexibility. Higher education served as a protective factor, and was associated with higher scores in tasks such as story retelling, confrontation naming, generative drawing and reading comprehension. Older age and higher Body Mass Index were associated with poorer cognitive performance, especially on processing speed. Sex appears to influence language comprehension outcomes, with males exhibiting enhanced performance on the reading comprehension-sentence task. Disease severity negatively affected performance on the Symbol Digit Modalities Test and generative naming, indicating that greater severity was linked to poorer outcomes in these domains. Follow-up evaluations of recovered COVID-19 patients revealed significant improvements in processing speed and recall, suggesting partial recovery in these areas, although some deficits persisted over time.

The study supports findings that the prolonged effects of COVID-19 markedly impaired neurocognitive functions in recovering patients, especially those with severe or long COVID syndrome. Moreover, while several cognitive domains may improve over time, many other domains remain impaired and vulnerable.

Inflammation is associated with a range of neuropsychiatric symptoms, but the issue of causality remains unclear. We used complementary non-genetic, genetic risk score (GRS), and Mendelian randomization (MR) analyses to examine whether inflammatory markers are associated with affect, depressive and anxiety disorders, and cognition. We tested in ≈55,098 (59% female) individuals from the Dutch Lifelines cohort the concurrent/prospective associations of C-reactive protein (CRP) with: depressive and anxiety disorders; positive/negative affect; and attention, psychomotor speed, episodic memory, and executive functioning at baseline and a follow-up assessment occurring 3.91 years later (SD = 1.21). Additionally, we examined the association between inflammatory GRSs (CRP, interleukin-6 [IL-6], IL-6 receptor [IL-6R and soluble IL-6R (sIL-6R)], glycoprotein acetyls [GlycA]) on these same outcomes (Nmin = 35,300; Nmax = 57,946), followed by MR analysis examining evidence of causality of CRP on outcomes (Nmin=22,154; Nmax = 23,268). In non-genetic analyses, higher CRP was associated with depressive disorder, lower positive/higher negative affect, and worse executive function, attention, and psychomotor speed after adjusting for potential confounders. In genetic analyses, CRPGRS was associated with any anxiety disorder (β = 0.002, p = 0.037) whereas GlycAGRS was associated with major depressive disorder (β = 0.001, p = 0.036). Both CRPGRS (β = 0.006, p = 0.035) and GlycAGRS (β = 0.006, p = 0.049) were associated with greater negative affect. Inflammatory GRSs were not associated with cognition, except sIL-6RGRS which was associated with poorer memory (β = -0.009, p = 0.018). There was a non-significant CRP-anxiety association using MR (β = 0.12; p = 0.054). Genetic and non-genetic analyses provide consistent evidence for an association between CRP and negative affect. These results suggest that inflammation may impact a broad range of trans-diagnostic affective symptoms.

Attention/ processing speed deficits with or without executive function and episodic memory deficits have been suggested as a relatively characteristic cognitive profile of people with post-COVID condition (PCC). Most studies have been performed using standardized paper and pencil neuropsychological assessment. Sensitive and applicable tests are needed to improve the diagnostic capacity of patients with PCC.

In this study, we aimed to investigate the dimensions of a comprehensive computerized neuropsychological battery and to characterize the cognitive characteristics of patients with PCC.

Five hundred and eight participants were enrolled in the study (PCC = 227, Healthy Controls, HC = 281) and underwent cognitive assessment focused on attention, concentration, executive functions, and episodic memory. We conducted a multi-group confirmatory factor analysis. Factor scores were obtained to compare the PCC and HC groups and partial invariance analysis was performed to identify relevant cognitive processes that differentiate the two groups.

The proposed four-factor model showed adequate fit indices. There were differences in attention, concentration, and executive functions factor scores with small to moderate effect sizes and with a particular implication of attention processes based on measurement invariance analysis. Impairments in reaction times and divided attention were especially relevant in patients with PCC.

The battery revealed four factors representing attention, concentration, executive functions, and episodic memory. The PCC group performed worse than the HC group in attention, concentration, and executive functions. These findings suggest the validity of computerized neuropsychological assessment, which could be particularly useful in PCC.

There is limited information on new-onset mental disorders in adults with metabolic diseases following the COVID-19 pandemic. Here, we aimed to examine the changes in mental health following the COVID-19 pandemic and identify factors associated with the development of new-onset mental disorders. Among 90,580 UK Biobank participants diagnosed with COVID-19 between Jan 31, 2020 and Oct 31, 2022, those who completed both baseline and follow-up mental health questionnaires in 2016-2017 and 2022-2023 were included in the analysis. New-onset depression, anxiety, and alcohol use disorder following the COVID-19 pandemic, as well as changes in mental health scores, were assessed. Furthermore, their association with sociodemographic, clinical, and self-perceived emotional state-related exposures was examined. Prevalent metabolic diseases were significantly associated with a higher risk of new-onset depression (hypertension: odds ratio [OR], 1.22; 95% CI 1.01-1.47; diabetes: OR 1.8; 95% CI 1.25-2.6; obesity: OR 1.66; 95% CI 1.43-1.95) and anxiety (hypertension: OR 1.32; 95% CI 1.06-1.63; diabetes: OR 1.66; 95% CI 1.06-2.62; obesity: OR 1.2; 95% CI 0.99-1.44) following COVID-19 pandemic. There was a significant increase of Patient Health Questionnaire-9 (PHQ-9; beta, 0.32; 95% CI 0.29-0.35) and Generalized Anxiety Disorder-7 (GAD-7; beta, 0.10; 95% CI 0.06-0.13) scores throughout the COVID-19 pandemic, while Alcohol Use Disorder Identification Test (AUDIT) score decreased over time (beta, - 0.24; 95% CI - 0.30 to - 0.18). Preexisting metabolic diseases were associated with the accelerated increase in the PHQ-9 and GAD-7 scores following the pandemic. Adults with metabolic diseases are associated with an increased risk of new-onset depression, anxiety, and alcohol use disorders following the COVID-19 pandemic.

Excess weight has been identified as a potential risk factor for post-COVID-19 condition (PCC). This systematic review and meta-analysis aimed to investigate whether excess weight is associated with the development or experience of neurological and neuropsychiatric symptoms in PCC.

We conducted a comprehensive search of eight databases (PubMed, Embase, Scopus, Web of Science, VHL, Google Scholar, ProQuest, and medRxiv) for studies published up to July 2023. Studies were included if they assessed PCC symptoms in relation to nutritional status, specifically the development of neurological and neuropsychiatric symptoms more than 12 weeks post-infection. The analysis compared exposure and controls groups (excess weight vs. normal weight; obesity vs. non-obesity). Data were synthesized using a random-effects model.

Of the 10,122 abstracts screened, 18 studies (n = 139,091 adults) were included. These studies included 79,050 individuals with excess weight vs 57,926 normal-weight individuals and 30,694 individuals with obesity vs 107,612 non-obese individuals. The presence of excess weight in PCC was significantly associated with persistent depression (RR = 1.21; 95% CI: 1.03-1.42), headache (OR = 1.23; 95% CI: 1.10-1.37), memory issues (RR = 1.43; 95% CI: 1.24-1.65), sleep disturbance (RR = 1.31; 95% CI: 1.16-1.48), and vertigo (RR = 1.21; 95% CI: 1.04-1.41). Obesity was significantly associated with persistent headache (OR = 1.45; 95% CI: 1.37-1.53), numbness (RR = 1.61; 95% CI: 1.46-1.78), smell disorder (OR = 1.16; 95% CI: 1.11-1.22), taste disorder (OR = 1.22; 95% CI: 1.08-1.38), and vertigo (RR = 1.44; 95% CI: 1.35-1.53).

Excess weight, including overweight and obesity, is associated with experiencing neuro-symptoms related to PCC. Individuals with these conditions urgently need enhanced personalized care management in current post-pandemic context.

Objective: Objective cognitive impairment has been shown in a minority of hospitalized COVID-19 patients, and longitudinal studies with a relatively long follow-up duration are scarce. We sought to investigate the presence and long-term change of objective cognitive functioning. Method: Forty-six initially hospitalized (18 ± 19 days) COVID-19 survivors (male/female: 30/16; age: 61 ± 11) underwent extensive neuropsychological assessment (including performance validity) approximately 1 (T1) and 2.5 years (T2) post-infection. Cognitive domains assessed were: memory, attention, executive functioning, processing speed, and language (n = 14 (sub)tests). We used normative data to derive age, sex, and education-adjusted T-scores (T ≤ 35 [≤-1.5SD], deficit cut-off). Repeated measures AN(C)OVAs were used to investigate cognitive functioning over time. Results: Mean neuropsychological performance (n = 14 tests) was within normal range at both timepoints, and number of individuals with objective cognitive deficits ranged from 0-20% (T1), and 2-22% (T2). Number of subjective cognitive complaints remained unchanged. A minority (17%) showed objective cognitive deficits on ≥2 tests at both 1 and 2.5 years post-infection, but not consistently within one cognitive domain. Longitudinal analyses on the total sample showed improvement in performance over time on phonemic fluency (p<.001), but stable cognitive performance on all other tests, independent of prior comorbidities, subjective cognitive complaints, depressive symptoms, and ICU admission. Conclusions: There were no consistent objective cognitive deficits or major cognitive disorders years after SARS-CoV-2 infection in the majority of cases. Neuropsychological functioning remained essentially unchanged over time. Future larger longitudinal studies are necessary to unravel COVID-19-related cognitive phenotypes of persisting deficits and how these can be modulated.

Post-COVID-19 condition (PCC) is a serious debilitating condition that develops after the resolution of an acute infection of severe acute respiratory syndrome-associated coronavirus 2. Some commonly reported symptoms include fatigue and cognitive deficits. Multiple lines of evidence have indicated fatigue to be associated with cognitive deficits in the general population. Herein, we perform a secondary analysis of the effects of fatigue on subjective and objective cognition in persons with PCC using a generalized linear model. In this study, fatigue was measured using the Fatigue Severity Scale (FSS) and cognition was measured using the Digit-Symbol Substitution Test (DSST) and the Trails Making Test parts A and B (TMT-A/B). FSS had a statistically significant negative correlation with DSST and TMT-A/B scores. Fatigue serves as a possible target for the development of PCC therapeutics. Fatigue and cognition correlates should be further investigated for underlying neurobiological substrates in persons with PCC.

COVID-19 survivors may present with cognitive and psychiatric symptoms long after the acute phase of SARS-CoV-2 infection.

To determine subjective cognitive, psychiatric, and fatigue symptoms two years after COVID-19, and their change from six months to two years.

We assessed three COVID-19 patient groups of different acute disease severity (ICU-treated, ward-treated, home-isolated) concerning subjective cognitive functioning (AB Neuropsychological Assessment Schedule), anxiety (Generalised Anxiety Disorder 7), depression (Patient Health Questionnaire 9), post-traumatic stress (Impact of Event Scale 6), and fatigue (Multidimensional Fatigue Inventory) with a mailed questionnaire approximately two years after acute COVID-19. We compared the results with those obtained six months after the acute disease. We studied whether any change emerged in the scores of symptomatic patients between six- and 24-month follow-ups.

Two years post-COVID-19, 58 ICU-treated, 35 ward-treated, and 28 home-isolated patients responded to the questionnaire. Subjective cognitive symptoms and fatigue emerged as the most common problems occurring in 30.6 and 35.5% of patients, respectively. In patients with clinically significant symptoms at six months, symptom scores for depression, anxiety, and post-traumatic stress decreased at two years.

Two years after COVID-19, particularly self-reported cognitive symptoms and fatigue remained clinically significant, but also some recovery was evident in depression, anxiety, and post-traumatic stress.

Patients with pre-existing Parkinson's disease (PD) face higher risks of severe acute COVID-19 outcomes than matched controls, but long-term post-COVID-19 outcomes remain largely unknown. This study investigated clinical outcomes up to 3.5 years post-infection in a Bronx inner-city PD population.

This retrospective study evaluated 3512 patients with PD in the Montefiore Health System (January 2016-July 2023), which serves a large diverse population and was an epicenter of the early COVID-19 pandemic and subsequent infection surges. Comparisons were made with PD patients without a positive SARS-CoV-2 test (defined by polymerase chain reaction test). Outcomes were post-index date all-cause mortality, major adverse cardiovascular events (MACE), altered mental status, fatigue, dyspnea, headache, psychosis, dementia, depression, anxiety, dysphagia, falls, and orthostatic hypotension. Changes in Levodopa prescriptions were also tabulated. Adjusted hazard ratios (aHR) were computed accounting for competing risks.

PD patients with COVID-19 had similar demographics but a higher prevalence of pre-existing comorbidities compared to PD patients without COVID-19. PD patients with COVID-19 had greater risk of mortality (aHR = 1.58 [95% CI: 1.03, 2.41]), MACE (aHR = 1.57 [1.19, 2.07]), dyspnea, fatigue, and fall compared to PD patients without COVID-19. Levodopa dose adjustment was higher post-infection in the COVID-19 cohort.

Among PD patients, COVID-19 was associated with a higher risk of adverse long-term outcomes. PD patients who survive COVID-19 may benefit from heightened clinical awareness and close follow-up. Findings highlight the need to improve post-COVID care for PD patients to mitigate disease progression and maintain quality of life.

Post-COVID-19 Syndrome (PCS) is defined as symptoms persisting beyond 12 weeks from the onset of symptoms. Notably, COVID-19 has been associated with long-term effects on the brain and mental health. This cross-sectional study aims to investigate depression, fatigue, sleep quality, and cognitive dysfunction, particularly working memory, in individuals with PCS compared to a healthy control group.

Between April and December 2021, 45 COVID-19 individuals and 60 healthy individuals met the eligibility criteria. Demographic information and the Montreal Cognitive Assessment were collected. Two visual working memory tasks, Delayed Match-to-Sample (DMS) and n-back, were performed, along with self-report questionnaires: Beck Depression Inventory, Modified Fatigue Impact Scale, and Pittsburgh Sleep Quality Index.

A total of 105 participants were enrolled. Findings reveal that the PCS group exhibited notably higher levels of cognitive impairment (13.3% vs. 1.6%, p = 0.04), depression (53.9% vs. 25.9%, p = 0.03), and sleep disturbances (53.9% vs. 18.6%, p = 0.01) compared to the healthy control group. Sleep latency and sleep duration were particularly affected. No significant differences in working memory function were observed between the two groups (p = 0.90 for DMS and p = 0.98 for n-back).

The study highlights the higher prevalence of sleep disturbance, depression, and cognitive impairment in the PCS phase, with inflammation likely playing a significant role. Moreover, the study suggests that untreated depression and sleep disturbances may pose long-term risks for dementia. Understanding the underlying mechanisms is crucial for developing effective interventions and support for individuals recovering from the infection. Prospective longitudinal studies with larger and more diverse samples are warranted to confirm and expand upon these findings.

After a COVID-19 infection, some patients experience long-term consequences known as Post-Covid Syndrome, which often includes cognitive impairment. We investigated the congruence between subjectively experienced and objectively measured cognitive deficits after a COVID-19 infection in an unselected, successively admitted cohort of 46 patients reporting subjective cognitive complaints (SCC).

We employed a comprehensive neuropsychological test battery to assess objective cognitive impairment across various cognitive domains. Three different cut-off criteria were applied, commonly used in the literature to define objective neurocognitive disorder (NCD).

We observed a notably low congruence between SCC and NCD in Post-Covid Syndrome, regardless of the cut-off criterion. Depending on the cognitive domain, only 4% to maximally 40% of the SCC could be objectified.

One possible explanation for this discrepancy could be the high rate of depressive symptoms observed in the group of patients studied, which may negatively influence the perception of one's cognitive abilities. These findings emphasize the need for careful evaluation of SCC in Post-Covid Syndrome and suggest that treating depressive symptoms may also alleviate some of the perceived cognitive deficits.

'Brain fog' is commonly reported in more than a dozen chronic diseases, but what is it? We review research across conditions which has characterised brain fog and evaluate its definitions and objective correlates. Brain fog has been used to refer to a variable set of overlapping symptoms implicating cognition, fatigue, and affect. It has been defined as a distinct symptom, a syndrome, or a nonspecific term. We consider the evidence that brain fog is a transdiagnostic entity with a common phenomenology and profile of objective cognitive deficits. We discuss where these commonalities arise and argue that linguistic ambiguity, shared cognitive impairments, and noncognitive factors are more likely than shared neurobiology. We suggest how future research might apply existing tools to disambiguate the phenomena that brain fog conflates.

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic debilitating condition with no cure that shares commonality with long-COVID. This review examines current understanding of long-COVID symptoms, characteristics of the affected population, the connection with ME/CFS, and the potential for salubrinal, an agent known for its influence on cellular stress pathways, to mitigate these disorders It also describes the historical development and mechanism of action of salubrinal, to mitigate endoplasmic reticulum (ER)/cellular stress responses, that could potentially contribute to symptom improvement in both ME/CFS and long-COVID patients. Further research and clinical trials are warranted to advance our understanding of the potential role of salubrinal in improving the quality of life for individuals with long-COVID-related ME/CFS symptoms as well as ME/CFS patients.

Objective: The coronavirus disease-2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has had a profound global impact on individual health and well-being in adults and children. While most fully recover from COVID-19, a relatively large subgroup continues to experience persistent physical, cognitive, and emotional/behavioral symptoms beyond the initial infection period. The World Health Organization has termed this phenomenon "Post-COVID-19 Condition" (PCC), better known as "Long COVID." Due to the cognitive and psychosocial symptoms, neuropsychologists often assess and recommend treatment for individuals with Long COVID. However, guidance for neuropsychologists' involvement in clinical care, policy-making, and research has not yet been developed. The authors of this manuscript convened to address this critical gap and develop guidance for clinical neuropsychologists working with patients presenting with Long COVID. Method: Authors include pediatric and adult neuropsychologists with expertise in Long COVID and behavioral health. All authors have been engaged in clinical and research efforts examining the impact of COVID-19. Authors summarized the literature-to-date pertinent to the neuropsychiatric sequelae of Long COVID and developed guidance for neuropsychologists working with individuals with Long COVID. Conclusions: Research findings regarding neuropsychiatric symptoms associated with Long COVID are mixed and limited by methodological differences. As they practice and conduct research, neuropsychologists should remain mindful of the evolving and tenuous nature of the literature.

Rehabilitation is an effective and feasible approach for post-COVID patients to improve mental health and cognitive complaints. However, knowledge regarding the long-term impact of rehabilitation on neuropsychological health of these patients is lacking.

This study aims to investigate psychological health, fatigue, and cognitive function 6 and 12 months after inpatient post-COVID rehabilitation of patients, who acquired COVID-19 in the workplace. In addition, group differences in these outcome parameters according to sex, age, acute COVID status, socioeconomic status, profession, and pre-existing diseases will be detected.

This longitudinal observational study examined the changes in mental and cognitive health of 127 patients with COVID-19 as an occupational disease or work accident. Symptoms of depression and anxiety, fatigue severity, somatic symptom severity, trauma-related symptoms, and cognitive functioning were assessed at the beginning as well as six and 12 months after rehabilitation. Group differences concerning sex, age, acute COVID status, socioeconomic status, occupational status, and existing diseases prior to COVID-19 were also analyzed.

The results showed that the improvements direct after rehabilitation in mental health and fatigue severity could not be maintained six and 12 months after rehabilitation discharge. Contrary, patients' cognitive function maintained stable during follow-up. Significant group differences were observed regarding age, sex, acute COVID status, socioeconomic status, occupational status, and pre-existing diseases.

This study highlights the importance of the aftercare process and the implementation of adequate and individualized therapeutic interventions such as psychological support and strengthen self-management skills.The study is registered in the German Clinical Trials Register with the identifier DRKS00022928.

A high number of individuals report suffering from physical and psychological sequelae symptoms after COVID-19-the so-called post COVID-19 condition. Commonly reported complaints include physical symptoms such as fatigue, headache, attention and concentration deficits or dyspnea and anxiety, symptoms of post-traumatic stress, or depression. Evidence-based treatment recommendations are still lacking up to this point. Associations between physical and psychological symptoms in chronic diseases are known for a long time. Support in coping with the disease and improvement of self-efficacy can have a positive effect on the course of diseases. For this reason, we designed a randomized, controlled explorative intervention trial as a treatment of bodily distress disorder in COVID-19 recovered persons.

Patients with a post COVID-19 condition meeting to the criteria of the WHO, along with a bodily distress disorder, are randomized in an intervention and control arm (TAU). Randomization takes place after a diagnostic interview, screening, and informed consent. In total, 60 patients will be included in the trial (30 per group). The intervention group receives a cognitive behavioral therapy as a video-conference-based group therapy (6 weeks) and mobile, respiratory biofeedback treatment (for 4 weeks). At several time points, both groups are assessed in terms of psychological and physical health status, treatment expectation, and satisfaction with the intervention. Furthermore, they will get biofeedback examination appointments. The primary outcome is the change in self-efficacy; secondary outcomes include assessed parameters of mental health, somatic symptoms, and satisfaction with the intervention. Data will be analyzed primarily using R and SPSS.

The randomized, controlled, explorative intervention trial POSITIV is one of the very first interventions for patients with post COVID-19 condition and psychological burden due to their different symptoms. The aim of the study is to generate new evidence and help patients to cope with the disease and thus, increase their quality of life and reduce symptomatology. We expect with a high probability that the patients' self-efficacy and health status will improve as a result of the intervention.

German Clinical Trial Register (DRKS); DRKS-ID: DRKS00030565. Registered on December 22, 2022.

A significant number of COVID-19 survivors continue to experience persistent physical, cognitive, and psychological symptoms up to one year after discharge. This study aimed to examine the frequency, severity, and progression of and risk factors for these symptoms. This single-centre retrospective cohort study included 126 COVID-19 patients admitted to the VieCuri Medical Centre between 2020 and 2022. Follow-up assessments were conducted at 3 and 12 months postdischarge, including pulmonary function tests, CT scans, bioimpedance analysis, and questionnaires on physical, cognitive, and psychological symptoms. At both follow-up assessments, 31-32% of patients reported moderate to severe physical symptoms, 26-27% reported multiple cognitive symptoms, and 14-18% experienced depressive or posttraumatic stress symptoms (PTSSs). Only anxiety symptoms significantly decreased between the 3-month follow-up and the 12-month follow-up (from 22 to 12%; p = .014). The persistence of symptoms at 12 months was significantly associated with premorbid conditions (chronic respiratory disease, multiple comorbidities), illness severity (infection during the third wave), physical factors (COVID-19-related pulmonary abnormalities, lower total lung capacity, and dyspnoea), and cognitive and psychological factors (cognitive symptoms, anxiety, depression, and PTSS) (p < .05). These findings suggest that a significant proportion of COVID-19 survivors continue to experience persistent symptoms due to biopsychosocial factors, thus emphasizing the need for a biopsychosocial approach in early screening and treatment.

The coronavirus disease 2019 (COVID-19) pandemic was a global health emergency that significantly affected both the wellbeing of individuals and the global economy.

The aim of this study was to evaluate the degree of SARS-CoV-2 involvement, viral load, and immunological response in adults aged 18-65 who performed essential tasks in the municipality of Andratx (Balearic Islands, Spain) compared to those who did not. Additionally, the study examined these factors in children aged 2-18 years from both groups, if there were any.

Both groups were monitored between July 2020 and February 2021, in which the degree of involvement, the viral load, and the immunological response to the SARS-CoV-2 were analyzed using questionnaires, polymerase chain reaction (PCR) tests, and ELISA serology tests.

A positive case of RT-PCR test was found in screening the general population. The highest 2019-nCoV(N)-Ig antibody levels in plasma were measured from 1 to 17 February 2021, with the following percentage of positives: 6.8% of essential workers, 9.5% of essential workers' sons, 7.3% of non-essential workers, and 2.2% of non-essential workers' sons. However, an increase in levels of anti-SARS-CoV-2 (N) immunoglobulin G (IgG) and anti-SARS-CoV-2 (N) immunoglobulin M (IgM) were produced in session 3, from 9 to 25 November 2020, in both cases in non-essential workers, with a mean of 218.1 ng/mL of anti-SARS-CoV-2 (N) IgG and 31.3 ng/mL of anti-SARS-CoV-2 (N) IgM.

The control measures taken to manage the COVID-19 pandemic in the municipality of Andratx, Mallorca, Spain, were effective.

Dysregulation of autoimmune responses and the presence of autoantibodies (AA), particularly those related to the renin-angiotensin system (RAS), have been implicated in the acute phase of COVID-19, and persistent dysregulation of brain RAS by RAS-related autoantibodies may also contribute to neurological symptoms of post-COVID.

We analyzed levels of serum and CSF RAS AA in post-COVID patients with neurological symptoms, individuals who have fully recovered from COVID-19 (after-COVID controls), and uninfected individuals, and their possible correlations with the serum marker of neuroaxonal damage neurofilament light chain (NfL) and the degrees of cognitive deficit.

Both in serum and CSF, levels of AA agonists of the pro-inflammatory angiotensin II type 1 receptors (AT1-AA) were significantly elevated in this cohort of neurological post-COVID patients compared to both uninfected and after-COVID controls and correlated with serum levels of NfL. Changes in serum and CSF levels of AA promoting the RAS anti-inflammatory axis (upregulation of AA agonists of AT2 and Mas receptors, downregulation of AA antagonists of ACE2) suggest upregulation of the RAS compensatory response in this cohort of neurological post-COVID patients. Post-COVID patients with more pronounced cognitive impairment exhibited significantly higher CSF levels of MasR-AA and a trend toward elevated AT2-AA. Persistent brain RAS dysregulation, particularly persistent increase in AT1-AA, and its correlation with neuroaxonal damage markers and cognitive impairment, may play a significant role in neurological symptoms associated with post-COVID. Serum levels of NfL and AT1-AA may be interesting biomarkers for the early identification of CNS involvement in patients with neurological symptoms and a history of COVID-19. However, post-COVID is a highly heterogeneous entity and may result from various underlying mechanisms. The present study includes a cohort, which may differ from other cohorts with different clinical profiles, which may show different results on NfLs and CSF RAS autoantibodies, particularly AT1-AA.

These findings highlight the potential of targeting AT1 receptors as a therapeutic strategy for mitigating cognitive deficits in post-COVID patients showing upregulated AT1-AA levels.

Although COVID-19 is no longer a global public health threat, its consequences persist, with long COVID affecting at least 10% of patients and manifesting in various organ systems. National and international health agencies promoted vaccination to enhance population immunity, prioritizing healthcare personnel due to their high occupational risk. In a previous study, we found that the risk of SARS-CoV-2 transmission among dental teams in Germany was not higher than in the general population. This follow-up investigation aims to assess the vaccination status and the prevalence and severity of long COVID symptoms among dental teams in Germany. As part of a follow-up investigation involving the original cohort, 267 team members from 186 German dental practices previously included in the initial study completed an online questionnaire. The questionnaire covered three topics: (1) vaccination status, (2) confirmed COVID-19 diagnosis, and (3) self-reported long COVID symptoms. One hundred and seventy-two dentists (64.4%), 74 dental assistants (27.7%) and 21 dental hygienists (7.9%) completed the questionnaire. In total, 245 participants (91.8%) were at least once vaccinated. A COVID-19 infection after January 1st 2021 was reported by 146 (54.7%) participants, of which 33 participants (22.6%) suffered from long COVID symptoms. Our results showed lower vaccination rates among dental auxiliary personnel compared to dentists (95.9% vs. 84.2%). Individuals with long COVID symptoms were more often dental assistants (48.5% vs. 29.2%) or dental hygienists (15.2% vs. 8.0%) than dentists (36.4% vs. 62.8%) compared to the group not reporting long COVID symptoms (p = 0.025). In addition, it is unlikely that dental healthcare personnel are more prone to experiencing more severe symptoms compared to the general population. Vaccination against SARS-CoV-2 is likely to help against symptoms of long COVID.

To understand the impact of post-acute sequelae of COVID-19 (PASC) on quality of life (QOL) in a Midwestern community sample.

Anonymous online cross-sectional community survey.

Survey responses collected July 2023-October 2024 were examined from 1,564 individuals reporting prior COVID-19 positive test or diagnosis. Logistic regressions and sensitivity analyses using subset of data were conducted to identify symptoms significantly associated with perceived Current QOL (determined by "Taking everything in your life into account, please rate your current overall QOL") and Deteriorated QOL (i.e., Current QOL rated lower than QOL prior to SARS CoV-2 infection).

Current QOL was predicted by pre-infection QOL and more frequent experiences of work/school difficulties, challenges with shopping/cleaning/driving/meal-prep, anxiety, depression, fatigue/tiredness, light headedness/fainting/rapid heartbeat episodes, and diminished activity/exercise tolerance (C-statistic = 0.84). Compared to the full dataset's primary analyses, sensitivity analysis revealed all identified predictors except three physical symptoms remained significant Current QOL predictors. Deteriorated QOL after SARS-CoV-2 infection was predicted by pre-infection QOL, and more frequent experiences of work/school difficulties, diminished activity/exercise tolerance, anxiety, depression, trouble completing daily activities, fatigue/tiredness, and slow mental processing (C-statistic = 0.85). In contrast, sensitivity analysis revealed frequency of SARS-CoV-2 infection, pre-infection QOL, and more frequent challenges with shopping/cleaning/driving/meal-prep were the only significant predictors of Deteriorated QOL.

PASC negatively impacted QOL. Pre-infection QOL may influence perceived post-infection QOL.

Results make a compelling case for community nurses to identify PASC, rule-out underlying medical causes, and refer patients for interdisciplinary post-COVID rehabilitation to improve health outcomes and QOL.

Long COVID is characterized by debilitating fatigue, likely stemming from abnormal interactions among brain regions, but the neural mechanisms remain unclear. Here, we utilized a nested-spectral partition (NSP) approach to study the segregation and integration of resting-state brain functional networks in 34 patients with long COVID from acute to chronic phase post infection. Compared to healthy controls, patients with long COVID exhibited significantly higher fatigue scores and shifted the brain into a less segregated state at both 1 month and 3 months post infection. During the recovery of fatigue severity, there was no significant difference of segregation/integration. A positive correlation between network integration and fatigue was observed at 1 month, shifting to a negative correlation by 3 months. Gene Ontology analysis revealed that both acute and long-term effects of fatigue were associated with abnormal social behavior. Our findings reveal the brain network reconfiguration trajectories during post-viral fatigue progression that serve as functional biomarkers for tracking neurocognitive sequelae.