Cognitive impairments are one of the most common, insidious, and disabling symptoms of post-COVID-19 syndrome (PC-19), which have been correlated with damage to different brain structures.

To describe cognitive impairments in PC-19, identify associated variables, and compare the impact of mechanical ventilation on cognitive and neuroimaging outcomes.

A cohort of COVID-19 survivors was evaluated with neuropsychological tests (NPT) and cranial magnetic resonance imaging (MRI) 12 weeks after hospital discharge. Patients were classified into two groups based on whether they required invasive mechanical ventilation (IMV) or non-invasive mechanical ventilation (NIMV).

60 patients completed the study, 41 received IMV and 19 NIMV, with an average age of 57.11 years. 66% scored below 26 points on the MoCA test and 83.3% reported everyday memory failures (EMF). 85% showed impairments in at least one NPT. When comparing results between groups, significant differences were observed in the total MoCA test score (p = 0.045) and EMF (p = 0.032). Significant relationships were observed between the Boston Naming Test (-0.287; p = 0.035), the Rey Figure Recall Test (-0.324; p = 0.017) with parietal atrophy, as well as phonological verbal fluency with frontal atrophy (-0.276; p = 0.042). The HVLT (learning trial) test was related to hippocampal hyperintensity (-0.266; p = 0.050) and cingulate hyperintensity (0.311; p = 0.021). The TMT-B test was related to white matter hyperintensity (0.345; p = 0.010). The presence of poor functional prognosis was correlated with anxiety (p < 0.001), depression (p < 0.001), elevated D-dimer levels (p = 0.002) and the increase in days of intubation (p = 0.005).

Our study suggests that COVID-19 survivors who had moderate-to-severe infection experience subjective complaints and cognitive impairments in executive function, attention, and memory, regardless of whether invasive mechanical ventilation was used during treatment. We found white matter lesions and cerebral atrophy in frontal and parietal regions that were associated with cognitive deficits. Our findings highlight the clinical need for longitudinal programmes capable of evaluating the real impact of SARS-CoV-2 infection on the central nervous system, particularly in the cognitive and emotional domains.

Neurologic impairment is common in patients with acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection. While patients with severe COVID have a higher prevalence of neurologic symptoms, as many as one in five patients with mild COVID may also be affected, exhibiting impaired memory as well as other cognitive dysfunctions.

To characterize the effect of COVID on the brain, the current study recruited a group of adults with post-COVID cognitive complaints but with mild, non-hospitalized cases. They were then evaluated through formal neuropsychological testing and underwent functional MRI of the brain. The participants in our study performed nearly as expected for cognitively intact individuals. Additionally, we characterized the functional connectivity of the default mode network (DMN), which is known for cognitive functions including memory as well as the attention functions involved in normal aging and degenerative diseases.

Along with the retention of functional connectivity in the DMN, our results found the DMN to be associated with neurocognitive performance through region-of-interest and whole-brain analyses. The connectivity between key nodes of the DMN was positively correlated with cognitive scores (r = 0.51, p = 0.02), with higher performers exhibiting higher DMN connectivity.

Our findings provide neuroimaging evidence of the functional connectivity of brain networks among individuals experiencing cognitive deficits beyond the recovery of mild COVID. These imaging outcomes indicate expected functional trends in the brain, furthering understanding and guidance of the DMN and neurocognitive deficits in patients recovering from COVID.

Post-COVID syndrome manifests with numerous neurological and cognitive symptoms, the precise origins of which are still not fully understood. As females and older adults are more susceptible to developing this condition, our study aimed to investigate how post-COVID syndrome alters intrinsic brain dynamics in older adults and whether biological sex and cognitive training might modulate these effects, with a specific focus on older females. The participants, aged between 60 and 75 years, were divided into three experimental groups: healthy old female, post-COVID old female and post-COVID old male. They underwent an adaptive task-switching training protocol. We analysed multiscale entropy and spectral power density of resting-state EEG data collected before and after the training to assess neural signal complexity and oscillatory power, respectively. We found no difference between post-COVID females and males before training, indicating that post-COVID similarly affected both sexes. However, cognitive training was effective only in post-COVID females and not in males, by modulating local neural processing capacity. This improvement was further evidenced by comparing healthy and post-COVID females, wherein the latter group showed increased finer timescale entropy (1-30 ms) and higher frequency band power (11-40 Hz) before training, but these differences disappeared following cognitive training. Our results suggest that in older adults with post-COVID syndrome, there is a pronounced shift from more global to local neural processing, potentially contributing to accelerated neural aging in this condition. However, cognitive training seems to offer a promising intervention method for modulating these changes in brain dynamics, especially among females.

During the first wave of the COVID-19 outbreak in China, the surge of COVID-19 cases was rapid and drastic. Emerging evidence suggests that beyond the acute phase, patients with COVID-19 may experience a wide range of postacute or long COVID sequelae. However, the mechanism and burden of COVID-19, especially long COVID, have not yet been comprehensively clarified. To fill this knowledge gap, this large prospective follow-up study aims to investigate the short-term and long-term effects of COVID-19, explore the underlying biological mechanism and identify predictive neuroimaging and haematological biomarkers associated with these effects.

This multicentre study will recruit patients infected during the first wave of COVID-19 in China and healthy controls (HCs) with no history of COVID-19 infection from nine participating hospitals. Confirmed patients with mild or moderate COVID-19 will complete the following programmes during the acute infection phase and at 3, 12 and 24 months after infection: (a) blood test at the local laboratory, (b) multimodal brain and spine MRI scan and (c) the neuropsychological scales and questionnaires. Similarly, the uninfected HCs will complete the same programmes as the infected group mentioned above at the time of inclusion. At the first time point, 501 participants (418 patients and 83 HCs) from nine recruiting hospitals have been observed. Ultimately, all of these results will be analysed to explore the short-term and long-term effects of COVID-19.

Ethics approval was granted by Ethics Committee of the First Affiliated Hospital of Xi'an Jiaotong University (XJTU1AF2023LSK-013). Findings will be presented at national and international conferences, as well as published in peer-reviewed scientific journals.

NCT05745805.

Demyelination is among the most conspicuous neurological sequelae of SARS-CoV-2 infection (COVID-19) in both the central (CNS) and peripheral (PNS) nervous systems. Several hypotheses have been proposed to explain the mechanisms underlying demyelination in COVID-19. However, none have considered the SARS-CoV-2's effects on the renin-angiotensin-aldosterone system (RAAS). Therefore, our objective in this review is to evaluate how RAAS imbalance, caused by direct and indirect effects of SARS-CoV-2 infection, could contribute to myelin loss in the PNS and CNS. In the PNS, we propose that demyelination transpires from two significant changes induced by SARS-CoV-2 infection, which include upregulation of ADAM-17 and induction of lymphopenia. Whereas, in the CNS, demyelination could result from RAAS imbalance triggering two alterations: (1) a decrease in angiotensin type II receptor (AT2R) activity, responsible for restraining defense cells' action on myelin; (2) upregulation of ADAM-17 activity, leading to impaired maturation of oligodendrocytes and myelin formation. Thus, we hypothesize that increased ADAM-17 activity and decreased AT2R activity play roles in SARS-CoV-2 infection-mediated demyelination in the CNS.

This study systematically reviews the available evidence on resting-state functional magnetic resonance imaging (rs-fMRI) related to neurological symptoms and cognitive declines in COVID-19 patients. We followed PRISMA guidelines and looked up the PubMed, and Scopus databases for articles search on COVID-19 patients with neurological impairments, and functional connectivity alteration using rs-fMRI technique. Articles published between January 1, 2020, and May 31, 2024, are included in this study. The Quality Assessment Tool for Observational Prospective and Cross-Sectional Studies from the National Heart, Lung, and Blood Institute (NHLBI) was used to assess the quality of papers. A total of 15 articles met the inclusion criteria. The result reveals that the most prevalent neurological impairment associated with COVID-19 was cognitive decline, encompassing issues in attention, memory, processing speed, executive functions, language, and visuospatial ability. The brain connectivity results reveal that two brain areas were functionally altered; the prefrontal cortex and parahippocampus. The functional connectivity mainly increased in the frontal, temporal, and anterior piriform cortex, and reduced in the cerebellum, superior orbitofrontal cortex, and middle temporal gyrus, which also correlated with cognitive decline. The findings of neurological symptoms indicate one study reported a Disorder of Consciousness (DoC), and four studies reported COVID-19 patients with olfactory dysfunction. The present study concludes that COVID-19 can alter brain functional connectivity and offers significant insight into how COVID-19 affects the neuronal foundation of cognitive decline and other neurological impairments.

Demyelinating diseases including multiple sclerosis are associated with prior infectious exposures, so we assessed whether SARS-CoV-2 infection is associated with subsequent diagnoses of non-multiple sclerosis demyelinating diseases and multiple sclerosis. All residents of Sweden aged 3-100 years were followed between 1 January 2020 and 30 November 2022, excluding those with demyelinating disease prior to 2020, comprising 9 959 818 individuals divided into uninfected and those who were infected were categorized into those with and without hospital admission for the infection as a marker of infection severity. Cox regression assessed the risk of two separate outcomes: hospital diagnosed non-multiple sclerosis demyelinating diseases of the CNS and multiple sclerosis. The exposures were modelled as time-varying covariates (uninfected, infection without hospital admission and infected with hospital admission). Hospital admission for COVID-19 was associated with raised risk of subsequent non-multiple sclerosis demyelinating disease, but only 12 individuals had this outcome among the exposed, and of those, 7 has an unspecified demyelinating disease diagnosis. Rates per 100 000 person-years (and 95% confidence intervals) were 3.8 (3.6-4.1) among those without a COVID-19 diagnosis and 9.0 (5.1-15.9) among those admitted to hospital for COVID-19, with an adjusted hazard ratio and (and 95% confidence interval) of 2.35 (1.32-4.18, P = 0.004). Equivalent associations with multiple sclerosis (28 individuals had this outcome among the exposed) were rates of 9.5 (9.1-9.9) and 21.0 (14.5-30.5) and an adjusted hazard ratio of 2.48 (1.70-3.61, P < 0.001). Only a small number of non-multiple sclerosis demyelinating disease diagnoses were associated with hospital admission for COVID-19, and while the number with multiple sclerosis was somewhat higher, longer duration of follow-up will assist in identifying whether the associations are causal or due to shared susceptibility or surveillance bias, as these diseases can have long asymptomatic and prodromal phases.

Long COVID, a condition characterized by persistent symptoms after COVID-19 infection, is increasingly being recognized worldwide. Neurologic symptoms are frequently reported in survivors of COVID-19, making it crucial to better understand this phenomenon both on a societal scale and for the quality of life of these patients. Between January 1, 2020, and July 31, 2022, Illinois (IL) had a standardized cumulative death rate that ranked it 24th out of the 51 states in the United States (US). However, the US had one of the highest per capita COVID-19 death rates among large, high-income countries. [Bollyky T. et al. 2023] As a result of the increased number of COVID-19 infections, there was a rise in the number of patients experiencing Long COVID. At our neuro-infectious disease clinic in Chicago (IL), we observed an increasing number of patients presenting with cognitive and other neurologic symptoms after contracting COVID-19. Initially, we needed to provide these individuals with a better understanding of their condition and expected outcomes. We were thus motivated to further evaluate this group of patients for any patterns in presentation, neurologic findings, and diagnostic testing that would help us better understand this phenomenon. We aim to contribute to the growing body of research on Long COVID, including its presentation, diagnostic testing results, and outcomes to enlighten the long COVID syndrome. We hypothesize that the neurological symptoms resulting from long COVID persist for over 12 months. We conducted a retrospective analysis of clinical data from 44 patients with long-COVID. Cognitive symptoms were the most common presenting concern. Abnormalities in Montreal Cognitive Assessment, electroencephalogram, serum autoantibody testing, and cerebrospinal fluid were found in minority subsets of our cohort. At 12 months, most patients continue to experience neurologic symptoms, though more than half reported moderate or marked improvement compared to initial presentation. Although most of the patients in this study did not show a consistent occurrence of symptoms suggesting a cohesive underlying etiology, our clinical data demonstrated some features of Long COVID patients in Chicago (IL) that could lead to new research avenues, helping us better understand this syndrome that affects patients worldwide.

Acute coronavirus disease 2019 (COVID-19) is paralleled by a rise in the peripheral levels of neurofilament light chain (NfL), suggesting early nervous system damage. In a cohort of 103 COVID-19 patients, we studied the relationship between the NfL and peripheral inflammatory markers. We found that the NfL levels are significantly predicted by a panel of circulating cytokines/chemokines, including CRP, IL-4, IL-8, IL-9, Eotaxin, and MIP-1ß, which are highly up-regulated during COVID-19 and are associated with clinical outcomes. Our findings show that peripheral cytokines influence the plasma levels of the NfL, suggesting a potential role of the NfL as a marker of neuronal damage associated with COVID-19 inflammation.

The COVID-19 pandemic has underscored the critical interplay between systemic infections and neurological complications, notably cerebral microbleeds. This comprehensive review meticulously aggregates and analyses current evidence on cerebral microbleeds' prevalence, pathophysiological underpinnings and clinical implications within COVID-19 cohorts. Our findings reveal a pronounced correlation between cerebral microbleeds and increased severity of COVID-19, emphasizing the role of direct viral effects, inflammatory responses and coagulation disturbances. The documented association between cerebral microbleeds and elevated risks of morbidity and mortality necessitates enhanced neurological surveillance in managing COVID-19 patients. Although variability in study methodologies presents challenges, the cumulative evidence substantiates cerebral microbleeds as a critical illness manifestation rather than mere coincidence. This review calls for harmonization in research methodologies to refine our understanding and guide targeted interventions. Prioritizing the detection and study of neurological outcomes, such as cerebral microbleeds, is imperative for bolstering pandemic response strategies and mitigating the long-term neurological impact on survivors.

Observational studies have reported structural changes in the brains of patients with coronavirus disease 2019 (COVID-19); it remains unclear whether these associations are causal.

We evaluated the causal effects of COVID-19 susceptibility, hospitalization and severity on cortical structures.

Mendelian randomization (MR) study.

Data on the different COVID-19 phenotypes were obtained from the latest large-scale genome-wide association study (R7) of the COVID-19 Host Genetics Initiative. Brain structure data, including cortical thickness (TH) and surface area (SA), were obtained from the ENIGMA Consortium. Additionally, we employed the round 5 dataset released in January 2021 as the validation cohort. The inverse-variance weighted (IVW) method was used as the primary analysis in MR. Sensitivity analyses were conducted to evaluate heterogeneity and pleiotropy. We performed enrichment analysis on the MR analyses that passed the sensitivity analysis filtering.

After IVW and sensitivity analyses, we observed causal associations between COVID-19 susceptibility and rostral middle frontal SAw (P = 0.0308, β = -39.1236), cuneus THw (P = 0.0170, β = -0.0121), medial orbitofrontal THw (P = 0.0002, β = 0.0225), postcentral THw (P = 0.0217, β = -0.0106), temporal pole THw (P = 0.0077, β = 0.0359), medial orbitofrontal SAnw (P = 0.0106, β = -24.0397), medial orbitofrontal THnw (P = 0.0007, β = 0.0232), paracentral SAnw (P = 0.0483, β = -20.1442), rostral middle frontal SAnw (P = 0.0368, β = -81.9719) and temporal pole THnw (P = 0.0429, β = 0.0353). COVID-19 hospitalization had causal effects on medial orbitofrontal THw (P = 0.0053, β = 0.0063), postcentral THw (P = 0.0143, β = -0.0042), entorhinal THnw (P = 0.0142, β = 0.0142), medial orbitofrontal THnw (P = 0.0147, β = 0.0065) and paracentral SAnw (P = 0.0119, β = -7.9970). COVID-19 severity had causal effects on rostral middle frontal SAw (P = 0.0122, β = -11.8296), medial orbitofrontal THw (P = 0.0155, β = 0.0038), superior parietal THw (P = 0.0291, β = -0.0021), lingual SAnw (P = 0.0202, β = -11.5270), medial orbitofrontal THnw (P = 0.0290, β = 0.0039), paracentral SAnw (P = 0.0180, β = -5.7744) and pars triangularis SAnw (P = 0.0151, β = -5.4520).

Our MR results demonstrate a causal relationship between different COVID-19 phenotypes and cortical structures.

Hospitalized patients with COVID-19 have an increased risk of developing psychiatric symptoms associated with post-COVID-19 syndrome. We aimed to evaluate the impact of COVID-19 hospitalization on neuropsychiatric healthcare utilization as well as new-onset depression and dementia. This nationwide, retrospective, observational cohort study included hospitalized COVID-19 patients aged 18 years or older across the Veterans Health Administration database from January 1st, 2020 through January 1st, 2022. The COVID-19 group consisted of patients hospitalized with COVID-19 with a positive test within seven days of the hospitalization. The control group consisted of patients hospitalized for reasons other than COVID-19 without a prior positive test or during the study duration. Propensity scores were utilized for 1:1 matching. This study included 50,805 patients in each matched cohort. Average patient population was 69 years old with ∼93 % male. The primary outcome of psychiatry-related hospitalization incidence rates were significantly higher in the COVID-19 group at both 90 days and 180 days. There was also a significant increase in the incidence outpatient mental health visits at 180 days in the COVID-19 cohort. Significantly higher risk of new-onset depression and new-onset dementia in the COVID-19 hospitalization group at 180 days as compared to the non-COVID-19 cohort was noted.

Although COVID-19 is primarily an acute respiratory infection, 5%-40% of patients develop late and prolonged symptoms with frequent neurological complaints, known as long COVID syndrome. The presentation of the disease suggests that COVID infection may cause functional and/or morphological central nervous system alterations, but studies published in the literature report contradictory findings.

To investigate the chronic effects of COVID-19 on cerebral grey matter in a group of young patients without comorbidities, with mild course of COVID infection and no medical complaints at the time of examination.

Prospective.

Thirty-eight young (age = 26.6 ± 5.0 years; male/female = 14/24), adult participants who recovered from mild COVID infection without a history of clinical long COVID and 37 healthy control subjects (age = 25.9 ± 2.8 years; male/female = 14/23).

Three Tesla, 3D T1-weighted magnetization-prepared rapid gradient-echo, 2D T2-weighted turbo spin-echo.

MRI-based morphometry and volumetry along with neuropsychological testing and self-assessed questionnaire.

Fisher's exact test, Mann-Whitney U-test, and multiple linear regression analyses were used to assess differences between COVID and healthy control groups. P < 0.05 was used as cutoff for significance.

In the COVID group, significantly lower bilateral mean cortical thickness (left/right-hemisphere: 2.51 ± 0.06 mm vs. 2.56 ± 0.07 mm, η2 p = 0.102/2.50 ± 0.06 mm vs. 2.54 ± 0.07 mm, η2 p = 0.101), lower subcortical gray matter (57881 ± 3998 mm3 vs. 60470 ± 5211 mm3, η2 p = 0.100) and lower right olfactory bulb volume (52.28 ± 13.55 mm3 vs. 60.98 ± 15.8 mm3, η2 p = 0.078) were found. In patients with moderate to severe anosmia, cortical thickness was significantly lower bilaterally, as compared to patients without olfactory function loss (left/right-hemisphere: 2.50 ± 0.06 mm vs. 2.56 ± 0.05 mm, η2 = 0.173/2.49 ± 0.06 mm vs. 2.55 ± 0.05 mm, η2 = 0.189). Using further exploratory analysis, significantly reduced cortical thickness was detected locally in the right lateral orbitofrontal cortex in the COVID group (2.53 ± 0.10 mm vs. 2.60 ± 0.09 mm, η2 p = 0.112).

Even without any subjective or objective neurological complaints at the time of the MR scan, subjects in the COVID group showed gray matter alterations in cortical thickness and subcortical gray matter volume.

2 TECHNICAL EFFICACY: Stage 3.

Amid the ongoing global repercussions of SARS-CoV-2, it is crucial to comprehend its potential long-term psychiatric effects. Several recent studies have suggested a link between COVID-19 and subsequent mental health disorders. Our investigation joins this exploration, concentrating on Schizophrenia Spectrum and Psychotic Disorders (SSPD). Different from other studies, we took acute respiratory distress syndrome (ARDS) and COVID-19 lab-negative cohorts as control groups to accurately gauge the impact of COVID-19 on SSPD. Data from 19,344,698 patients, sourced from the N3C Data Enclave platform, were methodically filtered to create propensity matched cohorts: ARDS (n = 222,337), COVID-19 positive (n = 219,264), and COVID-19 negative (n = 213,183). We systematically analyzed the hazard rate of new-onset SSPD across three distinct time intervals: 0-21 days, 22-90 days, and beyond 90 days post-infection. COVID-19 positive patients consistently exhibited a heightened hazard ratio (HR) across all intervals [0-21 days (HR: 4.6; CI: 3.7-5.7), 22-90 days (HR: 2.9; CI: 2.3 -3.8), beyond 90 days (HR: 1.7; CI: 1.5-1.)]. These are notably higher than both ARDS and COVID-19 lab-negative patients. Validations using various tests, including the Cochran Mantel Haenszel Test, Wald Test, and Log-rank Test confirmed these associations. Intriguingly, our data indicated that younger individuals face a heightened risk of SSPD after contracting COVID-19, a trend not observed in the ARDS and COVID-19 negative groups. These results, aligned with the known neurotropism of SARS-CoV-2 and earlier studies, accentuate the need for vigilant psychiatric assessment and support in the era of Long-COVID, especially among younger populations.

The severe acute respiratory syndrome coronavirus 2 virus has, up to the time of this article, resulted in >770 million cases of COVID-19 illness worldwide, and approximately 7 million deaths, including >1.1 million in the United States. Although defined as a respiratory virus, early in the pandemic, it became apparent that considerable numbers of people recovering from COVID-19 illness experienced persistence or new onset of multi-system health problems, including neurologic and cognitive and behavioral health concerns. Persistent multi-system health problems are defined as Post-COVID-19 Condition (PCC), Post-Acute Sequelae of COVID-19, or Long COVID. A significant number of those with PCC report cognitive problems. This paper reviews the current state of scientific knowledge on persisting cognitive symptoms in adults following COVID-19 illness. A brief history is provided of the emergence of concerns about persisting cognitive problems following COVID-19 illness and the definition of PCC. Methodologic factors that complicate clear understanding of PCC are reviewed. The review then examines research on patterns of cognitive impairment that have been found, factors that may contribute to increased risk, behavioral health variables, and interventions being used to ameliorate persisting symptoms. Finally, recommendations are made about ways neuropsychologists can improve the quality of existing research.

Many Coronavirus Disease 2019 (COVID-19) patients are suffering from long-term neuropsychological sequelae. These patients may benefit from a better understanding of the underlying neuropathophysiological mechanisms and identification of potential biomarkers and treatment targets. Structural clinical neuroimaging techniques have limited ability to visualize subtle cerebral abnormalities and to investigate brain function. This scoping review assesses the merits and potential of advanced neuroimaging techniques in COVID-19 using literature including advanced neuroimaging or postmortem analyses in adult COVID-19 patients published from the start of the pandemic until December 2023. Findings were summarized according to distinct categories of reported cerebral abnormalities revealed by different imaging techniques. Although no unified COVID-19-specific pattern could be subtracted, a broad range of cerebral abnormalities were revealed by advanced neuroimaging (likely attributable to hypoxic, vascular, and inflammatory pathology), even in absence of structural clinical imaging findings. These abnormalities are validated by postmortem examinations. This scoping review emphasizes the added value of advanced neuroimaging compared to structural clinical imaging and highlights implications for brain functioning and long-term consequences in COVID-19.

This systematic review is aimed at synthesising the literature base to date on the frequency and topographical distribution of neuroanatomical changes seen on imaging following COVID-19 invasion with a focus on both the acute and chronic phases of the disease.

In this study, 8 databases were systematically searched to identify relevant articles published from December 2019 to March 2022 and supplemented with a manual reference search. Data were extracted from the included studies and narrative synthesis was employed to integrate the findings.

A total of 110 studies met the inclusion criteria and comprised 119,307 participants (including 31,073 acute and 143 long COVID-19 patients manifesting neurological alterations) and controls. Considerable variability in both the localisation and nature of neuroanatomical abnormalities are noted along the continuum with a wide range of neuropathologies relating to the cerebrovascular/neurovascular system, (sub)cortical structures (including deep grey and white matter structures), brainstem, and predominant regional and/or global alterations in the cerebellum with varying degrees of spinal involvement.

Structural regional alterations on neuroimaging are frequently demonstrated in both the acute and chronic phases of SARS-CoV‑2 infection, particularly prevalent across subcortical, prefrontal/frontal and cortico-limbic brain areas as well as the cerebrovascular/neurovascular system. These findings contribute to our understanding of the acute and chronic effects of the virus on the nervous system and has the potential to provide information on acute and long-term treatment and neurorehabilitation decisions.

Imaging has been demonstrated to play a crucial role in both the diagnosis and management of COVID-19. Depending on resources, pre-test probability, and risk factors for severe disease progression, real-time polymerase chain reaction (RT-PCR) testing may be followed by chest radiography (CXR) or chest computed tomography (CT) to further aid in diagnosis or excluding COVID-19 disease. SARS-CoV-2 has been shown not only to pathologically impact the pulmonary system, but also the cardiovascular, gastrointestinal, and neurological systems to name a few. Imaging has again proven useful in further investigating and managing extrapulmonary disease, with the use of echocardiogram, CT angiography of the cardiovascular and cerebrovascular structures, MRI of the brain, as well as ultrasound of the abdomen and CT of the abdomen and pelvis proving particularly useful. Research in artificial intelligence and its application in the diagnosis of COVID-19 and disease severity prediction is underway, and point-of-care ultrasound is an emerging bedside technique that may allow for more efficient and timely diagnosis of COVID-19.

Cerebral hypoperfusion has been described in both severe and mild forms of symptomatic Coronavirus Disease 2019 (COVID-19) infection. The purpose of this study was to investigate global and regional cerebral blood flow (CBF) in asymptomatic COVID-19 patients.

Cases with mild COVID-19 infection and age-, sex-, and race-matched healthy controls were drawn from the Aging Brain Consortium at The University of South Carolina data repository. Demographics, risk factors, and data from the Montreal Cognitive Assessment were collected. Mean CBF values for gray matter (GM), white matter (WM), and the whole brain were calculated by averaging CBF values of standard space-normalized CBF image values falling within GM and WM masks. Whole brain region of interest-based analyses were used to create standardized CBF maps and explore differences between groups.

Twenty-eight cases with prior mild COVID-19 infection were compared with 28 controls. Whole-brain CBF (46.7 ± 5.6 vs. 49.3 ± 3.7, p = .05) and WM CBF (29.3 ± 2.6 vs. 31.0 ± 1.6, p = .03) were noted to be significantly lower in COVID-19 cases as compared to controls. Predictive models based on these data predicted COVID-19 group membership with a high degree of accuracy (85.2%, p < .001), suggesting CBF patterns are an imaging marker of mild COVID-19 infection.

In this study, lower WM CBF, as well as widespread regional CBF changes identified using quantitative MRI, was found in mild COVID-19 patients. Further studies are needed to determine the reliability of this newly identified COVID-19 brain imaging marker and determine what drives these CBF changes.

Concerns about potential increases in suicidal behavior during the coronavirus disease 2019 (COVID-19) pandemic arose in response to reported widespread mental health deterioration. Although early data did not corroborate such concerns, suicide remains a significant cause of preventable deaths worldwide and is of significant interest to public health in the setting of a pandemic. In this study, we present 17 cases of COVID-19-related suicides seen in our West Michigan Medical Examiner's office from 2020 to 2022, which exhibit the complex relationship between mental health and pandemic-related psychological, social, and economic stressors. The relationships were generally categorized as increased anxiety and/or stress due to COVID-19 (5/17 [29.4%]), the loss of social support and/or social isolation occurring as a result of COVID-19 restrictions (5/17 [29.4%]), financial concerns or loss of income as a result of COVID-19 policies (3/17 [17.6%]), grief related specifically to COVID-19 (2/17 [11.8%]), and purported neuropsychiatric sequelae of a prior COVID-19 infection (2/17 [11.8%]). By examining these cases, we highlight ways in which public health systems might prepare for and respond to mental health crises during current or future pandemics and the need for increased collaboration between forensic pathologists and epidemiologists in collating high-quality data during death investigations.

It is known that there can be neurologic complications related to acute infection with SARS-CoV-2, the virus that causes COVID-19. Currently, there is a growing body of evidence that postacute sequelae of SARS-CoV-2 infection can manifest as neurologic sequelae as a result of direct neuroinvasion, autoimmunity, and possibly lead to chronic neurodegenerative processes. Certain complications can be associated with worse prognosis, lower functional outcome, and higher mortality. This article provides an overview of the known pathophysiology, symptoms presentation, complications and treatment approaches of the post-acute neurologic and neuromuscular sequelae of SARS-CoV-2 infection.

Neurological symptoms are prevalent in both the acute and post-acute phases of coronavirus disease 2019 (COVID-19), and they are becoming a major concern for the prognosis of COVID-19 patients. Accumulation evidence has suggested that metal ion disorders occur in the central nervous system (CNS) of COVID-19 patients. Metal ions participate in the development, metabolism, redox and neurotransmitter transmission in the CNS and are tightly regulated by metal ion channels. COVID-19 infection causes neurological metal disorders and metal ion channels abnormal switching, subsequently resulting in neuroinflammation, oxidative stress, excitotoxicity, neuronal cell death, and eventually eliciting a series of COVID-19-induced neurological symptoms. Therefore, metal homeostasis-related signaling pathways are emerging as promising therapeutic targets for mitigating COVID-19-induced neurological symptoms. This review provides a summary for the latest advances in research related to the physiological and pathophysiological functions of metal ions and metal ion channels, as well as their role in COVID-19-induced neurological symptoms. In addition, currently available modulators of metal ions and their channels are also discussed. Collectively, the current work offers a few recommendations according to published reports and in-depth reflections to ameliorate COVID-19-induced neurological symptoms. Further studies need to focus on the crosstalk and interactions between different metal ions and their channels. Simultaneous pharmacological intervention of two or more metal signaling pathway disorders may provide clinical advantages in treating COVID-19-induced neurological symptoms.

Hypertension is considered one of the most critical risk factors for COVID-19. Evidence suggests that SARS-CoV-2 infection produces intense effects on the cardiovascular system by weakening the wall of large vessels via vasa-vasorum. In this commentary, we propose that SARS-CoV-2 invades carotid and aortic baroreceptors, leading to infection of the nucleus tractus solitari (NTS) and paraventricular hypothalamic nucleus (PVN), and such dysregulation of NTS and PVN following infection causes blood pressure alteration at the central level. We additionally explored the hypothesis that SARS-CoV-2 favors the internalization of membrane ACE2 receptors generating an imbalance of the renin-angiotensin-aldosterone system (RAAS), increasing the activity of angiotensin II (ANG-II), disintegrin, and metalloproteinase 17 domain (ADAM17/TACE), eventually modulating the integration of afferents reaching the NTS from baroreceptors and promoting increased blood pressure. These mechanisms are related to the increased sympathetic activity, which leads to transient or permanent hypertension associated with SARS-CoV-2 invasion, contributing to the high number of deaths by cardiovascular implications.

Long COVID patients have experienced a decline in their quality of life due to, in part but not wholly, its negative emotional impact. Some of the most prevalent mental health symptoms presented by long COVID patients are anxiety, depression, and sleep disorders. As such, the need has arisen to analyze the personal experiences of these patients to understand how they are managing their daily lives while dealing with the condition. The objective of this study is to increase understanding about the emotional well-being of people diagnosed with long COVID.

A qualitative design was created and carried out using 35 patients, with 17 participants being interviewed individually and 18 of them taking part in two focus groups. The participating patients were recruited in November and December 2021 from Primary Health Care (PHC) centers in the city of Zaragoza (Northern Spain) and from the Association of Long COVID Patients in Aragon. The study topics were emotional well-being, social support networks, and experience of discrimination. All an inductive thematic content analyses were performed iteratively using NVivo software.

The Long COVID patients identified low levels of self-perceived well-being due to their persistent symptoms, as well as limitations in their daily lives that had been persistent for many months. Suicidal thoughts were also mentioned by several patients. They referred to anguish and anxiety about the future as well as a fear of reinfection or relapse and returning to work. Many of the participants reported that they have sought the help of a mental health professional. Most participants identified discriminatory situations in health care.

It is necessary to continue researching the impact that Long COVID has had on mental health, as well as to provide Primary Health Care professionals with evidence that can guide the emotional treatment of these patients.

Many people with coronavirus disease 2019 (COVID-19) report varying degrees of memory impairment. Neuroimaging techniques such as MRI and PET have been utilized to shed light on how COVID-19 affects brain function in humans, including memory dysfunction. In this PRISMA-based systematic review, we compared and summarized the current literature looking at the relationship between COVID-19-induced neuropathological changes by neuroimaging scans and memory symptoms experienced by patients who recovered from COVID-19. Overall, this review suggests a correlational trend between structural abnormalities (e.g., cortical atrophy and white matter hyperintensities) or functional abnormalities (e.g., hypometabolism) in a wide range of brain regions (particularly in the frontal, parietal and temporal regions) and memory impairments in COVID-19 survivors, although a causal relationship between them remains elusive in the absence of sufficient caution. Further longitudinal investigations, particularly controlled studies combined with correlational analyses, are needed to provide additional evidence.

Post-COVID-19 condition refers to a range of persisting physical, neurocognitive, and neuropsychological symptoms after SARS-CoV-2 infection. Abnormalities in brain connectivity were found in recovered patients compared to non-infected controls. This study aims to evaluate the effect of hyperbaric oxygen therapy (HBOT) on brain connectivity in post-COVID-19 patients.

In this randomized, sham-controlled, double-blind trial, 73 patients were randomized to receive 40 daily sessions of HBOT (n = 37) or sham treatment (n = 36). We examined pre- and post-treatment resting-state brain functional magnetic resonance imaging (fMRI) and diffusion tensor imaging (DTI) scans to evaluate functional and structural connectivity changes, which were correlated to cognitive and psychological distress measures.

The ROI-to-ROI analysis revealed decreased internetwork connectivity in the HBOT group which was negatively correlated to improvements in attention and executive function scores (p < 0.001). Significant group-by-time interactions were demonstrated in the right hippocampal resting state function connectivity (rsFC) in the medial prefrontal cortex (PFWE = 0.002). Seed-to-voxel analysis also revealed a negative correlation in the brief symptom inventory (BSI-18) score and in the rsFC between the amygdala seed, the angular gyrus, and the primary sensory motor area (PFWE = 0.012, 0.002). Positive correlations were found between the BSI-18 score and the left insular cortex seed and FPN (angular gyrus) (PFWE < 0.0001). Tractography based structural connectivity analysis showed a significant group-by-time interaction in the fractional anisotropy (FA) of left amygdala tracts (F = 7.81, P = 0.007). The efficacy measure had significant group-by-time interactions (F = 5.98, p = 0.017) in the amygdala circuit.

This study indicates that HBOT improves disruptions in white matter tracts and alters the functional connectivity organization of neural pathways attributed to cognitive and emotional recovery in post-COVID-19 patients. This study also highlights the potential of structural and functional connectivity analysis as a promising treatment response monitoring tool.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first identified in December 2019 in Wuhan, China. Although coronavirus disease-19 (COVID-19) affects every population group, the sports community and athletes require special consideration of the effects on cardiovascular, musculoskeletal, neurologic, and respiratory systems. A comprehensive understanding of imaging indications, findings, and features of COVID-19 supports appropriate imaging utilization and effective patient management and treatment.

To review the spectrum of sports imaging in COVID-19 infection, organ system manifestations, vaccine effects, and complications in recreational and competitive athletes.

Narrative review.

Levels 4 and 5.

Based on a PubMed database search, studies describing the imaging findings of COVID-19 infection, organ system manifestations, vaccine effects, and complications in recreational and competitive athletes were included.

On March 11, 2020, World Health Organization officially declared COVID-19 a global pandemic. As of May 9, 2022, more than 515 million confirmed cases of COVID-19 were reported globally. While the multisystem effects of COVID-19 are incompletely understood, the role of imaging in diagnosing, monitoring, and prognosticating active disease, long-term effects, and complications is evolving. In the respiratory system, imaging plays an important role in diagnosing, characterizing, and monitoring pulmonary COVID-19 infections, barotrauma, and COVID-19-associated chronic pulmonary opacities and fibrotic-like lung changes. Ultrasonography, computed tomography, and magnetic resonance imaging aid in the timely diagnosis of ischemic, embolic, and thrombotic peripheral and central cardiovascular events, including deep venous thrombosis, pulmonary embolism, myocarditis, and stroke. COVID-19-associated musculoskeletal and peripheral nervous system manifestations include rhabdomyolysis and myonecrosis, plexus and peripheral neuropathies, Guillain-Barré syndrome, and shoulder injury related to vaccine administration.

In athletes, COVID-19 infections and associated effects on cardiovascular, musculoskeletal, neurologic, and respiratory systems require special consideration. With the increasing understanding of the multisystem effects of COVID-19, the role of imaging in diagnosing, monitoring, and prognosticating active disease, long-term effects, and complications is evolving. A comprehensive understanding of imaging indications, COVID-19 imaging features, and organ system effects aids in appropriate imaging utilization and effective patient management and treatments.

Few studies have reported specific attention deficits in post-COVID-19 patients. Attention consists of different subdomains. Disruptions to specific attention subdomains might impair a wide range of everyday tasks, including road safety. As there are millions of COVID-19 patients with different socio-economic backgrounds, screening of attentional performance less dependent on education is needed. Here, we verified if physically recovered COVID-19 inpatients showed specific attention decrements at discharge. The Continuous Visual Attention Test (CVAT) is a Go/No-go task which is independent of participants' schooling. It detects visuomotor reaction time (RT = intrinsic alertness), variability of reaction time (VRT = sustained attention), omission (focused-attention), and commission errors (response-inhibition). Thirty physically functional COVID-19 inpatients at discharge and 30 non-infected controls underwent the CVAT. A MANCOVA was performed to examine differences between controls and patients, followed by post-hoc ANCOVAs. Then, we identified the percentile score for each patient within the distribution of the CVAT performance of 211 subjects mentally capable of driving (reference group). COVID-19 patients at discharge showed greater RT and VRT, and more omission errors than controls. Twenty-two patients (73%) had performance below the 5th percentile of the reference group in one or more subdomains. As slow visuomotor RT, deficits in focusing and difficulties in keeping visual attention are associated with traffic accidents, we concluded that most COVID-19 patients at discharge had deficits that may increase the risk of road injuries. As these deficits will probably affect other daily activities, a routine assessment with the CVAT could provide useful information on whom to send to post-COVID centers.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of coronavirus disease 2019 (COVID-19), can trigger a myriad of neuropsychiatric manifestations. As a 2-year-old disease (at the writing of this manuscript), its long-term cognitive and neuropsychiatric implications, known as post-COVID-19 conditions, are incompletely recognized and mechanistically obscure.

Fatigue, anxiety, depression, posttraumatic stress disorder, and cognitive dysfunction are reported more frequently in COVID-19 survivors than in matching, non-COVID-19 population. Risk factors are unclear, including comorbidities, age at COVID-19 onset, or disease severity; women, however, have been reported to be at increased risk than men. Although the frequency of these symptoms decreases over time, at least one in five will have persistent cognitive and neuropsychiatric manifestations one year after recovering from COVID-19.

Neurocognitive and psychiatric post-COVID-19 long-term conditions are frequent and complex multifactorial sequelae. Several acute and chronic factors such as hypoxemia, cerebral thrombotic and inflammatory endothelial damage, and disruption of the blood-brain barrier (leading to parenchymal translocation of pro-inflammatory molecules, cytokines, and cytotoxic T lymphocytes) are involved, leading to microglial activation and astrogliosis. As an evolving topic, evidence derived from prospective studies will expand our understanding of post-COVID-19 these long-term outcomes.

Radiology plays a crucial role for the diagnosis and management of COVID-19 patients during the different stages of the disease, allowing for early detection of manifestations and complications of COVID-19 in the different organs. Lungs are the most common organs involved by SARS-CoV-2 and chest computed tomography (CT) represents a reliable imaging-based tool in acute, subacute, and chronic settings for diagnosis, prognosis, and management of lung disease and the evaluation of acute and chronic complications. Cardiac involvement can be evaluated by using cardiac computed tomography angiography (CCTA), considered as the best choice to solve the differential diagnosis between the most common cardiac conditions: acute coronary syndrome, myocarditis, and cardiac dysrhythmia. By using compressive ultrasound it's possible to study the peripheral arteries and veins and to exclude the deep vein thrombosis, directly linked to the onset of pulmonary embolism. Moreover, CT and especially MRI can help to evaluate the gastrointestinal involvement and assess hepatic function, pancreas involvement, and exclude causes of lymphocytopenia, thrombocytopenia, and leukopenia, typical of COVID-19 patients. Finally, radiology plays a crucial role in the early identification of renal damage in COVID-19 patients, by using both CT and US. This narrative review aims to provide a comprehensive radiological analysis of commonly involved organs in patients with COVID-19 disease.

Background. Interest in electroencephalographic (EEG) coronavirus disease 2019 (COVID-19) findings has been growing, especially in the search for a specific-features EEG of encephalopathy. Methods. We made a retrospective analysis of 29 EEGs recorded in 15 patients with COVID-19 and neurological symptoms. We classified the EEGs as "Acute EEG" and "follow-up EEG." We did a statistical analysis between voltage and respiratory status of the patient, stay or not in the intensive care unit (ICU), days of stay in the ICU, sedative drugs, pharmacological treatment, type of symptoms predominating, and outcome. Results. We found EEG abnormalities in all patients studied. We observed the amplitude of background <20 µV at 93% of "acute EEG," versus only 21.4% of "follow-up EEG." The average voltage went from 12.33 ± 5.09 µV in the acute EEGs to 32.8 ± 20.13 µV in the follow-up EEGs. A total of 60% of acute EEGs showed an intermittent focal rhythmic. We have not found a statistically significant association between voltage of acute EEG and nonneurological clinical status (including respiratory) that may interfere with the EEG findings. Conclusions. Nonspecific diffuse slowing EEG pattern in COVID-19 is the most common finding reported, but we found in addition to that, as a distinctive finding, low voltage EEG, that could explain the low prevalence of epileptic activity published in these patients. A metabolic/hypoxic mechanism seems unlikely on the basis of our EEG findings. This pattern in other etiologies is reminiscent of severe encephalopathy states associated with poor prognosis. However, an unreactive low voltage pattern in COVID-19 patients is not necessarily related to poor prognosis.

Novel coronavirus disease 2019 (COVID-19) has been found to be associated with encephalopathy and brain imaging abnormalities. The identification of incident white matter lesions, known to be associated with cerebral microcirculatory failure and cerebrovascular disease, in COVID-19 patients is of clinical and scientific interest. We performed a meta-analysis to investigate the incidence of white matter lesions (WMLs) in hospitalized COVID-19 patients.

PubMed, EMBASE, and the Cochrane Library were searched for studies on brain imaging abnormalities in hospitalized COVID-19 patients. The terms used included "white matter lesions," "white matter hyperintensity," "COVID-19," "coronavirus," and "SARS-CoV-2." A random-effects meta-analysis was conducted to obtain a pooled estimate of WML prevalence in hospitalized COVID-19 patients.

A total of 4 eligible studies involving 362 patients (144 with WMLs and 218 without) were included in the meta-analysis. We found the pooled estimate of WML prevalence to be 20% (ES 0.20; 95% CI 0.00-0.54; p = .03).

The estimated pooled prevalence rate of WMLs was approximately 20% in hospitalized COVID-19 patients, albeit lower than the crude prevalence rate (39.8%).

The worldwide pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has infected an estimated 200 million people with over 4 million deaths. Although COVID-19, the disease caused by the SARS-CoV-2 virus, is primarily a respiratory disease, an increasing number of neurologic symptoms have been reported. Some of these symptoms, such as loss of smell or taste, are mild and non-life threatening, while others, such as stroke or seizure, are more critical. Many of these symptoms remain long after the acute illness has passed, a phenomenon known as "long COVID" or postacute sequelae of SARS-CoV-2 infection (PASC). Neurological symptoms can be difficult to study due to the complexity of the central and peripheral nervous system. These neurologic symptoms can be difficult to identify and quantitate. This narrative review will describe approaches for assessing neurologic manifestations of COVID-19, with examples of the data they provide, as well as some directions for future research to aid in understanding the pathophysiology of COVID-19-related neurological implications.