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Background. Systemic lupus erythematosus (SLE) patients (pts) often suffered from an impairment in cognitive functions, but a universal definition of “brain fog” does not exist. The objective of the study was to evaluate the prevalence of subjective impairment and objective mental alterations (depression, cognition, fatigue) adopting screening tools validated in SLE; also we aimed to investigate which factors were associated with brain fog.   Methods. A Cross-sectional study was conducted enrolling adult SLE pts. Brain fog referred to the presence of mental alterations (i.e.; memory, concentration, attention...) as reported by SLE participants. To minimize contribution of type B symptoms, we made a subanalysis of brain fog involving pts with active disease, namely lupus fog. Demographic, clinical, therapeutic data were collected (Table). Serum anti-ribosomal P antibodies (anti-RibP) were quantified using ELISA kits. Cognitive deficits were assessed by a neuropsychologist exploring deficits in 8 cognitive domains with a battery of neuropsychological tests and screened using the Montreal Cognitive Assessment (MoCA) test performed by certified personnel (cut-off<26/30). Depressive symptoms were evaluated using the Center for Epidemiologic Studies Depression Scale (CES-D) (>15). Fatigue was measured using FACIT-F (<34). Chi-squared test and the Mann-Whitney test were used for univariate analysis (UV-A); multivariate analysis (MV-A) was performed building logistic regression models including variables showing p <0.10.   Results. 114 SLE pts were enrolled (Table), 105 female (92.1%), mean age 43.7 years (+-12.2). Brain fog was found in 54% pts, with memory deficit reported in 49.1%, attention in 38.6%, concentration in 10.5% and afasia nominum in 5.3%. CES-D>15 was altered in 53.3%, MoCA<26 in 45% and FACIT<34 in 52.9%. At UV-A, an association emerged between the presence of brain fog and CES-D (Fig1A, score p<0.001), FACIT (Fig1A, score p=0.012), fibromyalgia (p<0.001), the neuropsychiatric involvement (p=0.015), anti-RNP (p=0.014), anti Rib-P (p=0.018) and disease duration (p=0.045). No association was found with MoCA test, the battery of neuropsychological test, disease activity scores or treatment. At MV-A, an independent association between brain fog and fibromyalgia (OR=34.6; 95%CI 2.3-523.1, p=0.011), CES-D score (OR=1.1 per unit, 95%CI 1.0-1.2, p=0.033) and disease duration (OR=1.1 per year, 95%CI 1.0-1.2, p=0.038) emerged. Out of 46 pts with clinically active disease, 21 were classified as lupus fog, resulting associated at UV-A with CES-D (Fig2A, score p=0.034), FACIT (Fig2A, score p=0.024) , fibromyalgia (p=0.017). MV-A showed independent association between lupus fog and FACIT score (OR=-0.146; 95%CI -0.275 to -0.017).   Conclusion. Brain fog is frequent in SLE pts, but did not correlate with cognitive dysfunction, but with longer disease duration, depressive symptoms, fibromyalgia and in active pts with fatigue. Our findings suggest that SLE pts may have a negative perception about proper cognitive performances, without having a real impairment, supporting the need for assessing depressive and fatigue symptoms during clinical visits.

The development of long-term symptoms of coronavirus disease 2019 (COVID-19) more than four weeks after primary infection, termed “long COVID” or post-acute sequela of COVID-19 (PASC), can implicate persistent neurological complications in up to one third of patients and present as fatigue, “brain fog”, headaches, cognitive impairment, dysautonomia, neuropsychiatric symptoms, anosmia, hypogeusia, and peripheral neuropathy. Pathogenic mechanisms of these symptoms of long COVID remain largely unclear; however, several hypotheses implicate both nervous system and systemic pathogenic mechanisms such as SARS-CoV2 viral persistence and neuroinvasion, abnormal immunological response, autoimmunity, coagulopathies, and endotheliopathy. Outside of the CNS, SARS-CoV-2 can invade the support and stem cells of the olfactory epithelium leading to persistent alterations to olfactory function. SARS-CoV-2 infection may induce abnormalities in innate and adaptive immunity including monocyte expansion, T-cell exhaustion, and prolonged cytokine release, which may cause neuroinflammatory responses and microglia activation, white matter abnormalities, and microvascular changes. Additionally, microvascular clot formation can occlude capillaries and endotheliopathy, due to SARS-CoV-2 protease activity and complement activation, can contribute to hypoxic neuronal injury and blood–brain barrier dysfunction, respectively. Current therapeutics target pathological mechanisms by employing antivirals, decreasing inflammation, and promoting olfactory epithelium regeneration. Thus, from laboratory evidence and clinical trials in the literature, we sought to synthesize the pathophysiological pathways underlying neurological symptoms of long COVID and potential therapeutics.

Background Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is characterized by persistent physical and mental fatigue. The post-COVID-19 condition patients refer physical fatigue and cognitive impairment sequelae. Given the similarity between both conditions, could it be the same pathology with a different precipitating factor? Objective To describe the cognitive impairment, neuropsychiatric symptoms, and general symptomatology in both groups, to find out if it is the same pathology. As well as verify if the affectation of smell is related to cognitive deterioration in patients with post-COVID-19 condition. Methods The sample included 42 ME/CFS and 73 post-COVID-19 condition patients. Fatigue, sleep quality, anxiety and depressive symptoms, the frequency and severity of different symptoms, olfactory function and a wide range of cognitive domains were evaluated. Results Both syndromes are characterized by excessive physical fatigue, sleep problems and myalgia. Sustained attention and processing speed were impaired in 83.3% and 52.4% of ME/CFS patients while in post-COVID-19 condition were impaired in 56.2% and 41.4% of patients, respectively. Statistically significant differences were found in sustained attention and visuospatial ability, being the ME/CFS group who presented the worst performance. Physical problems and mood issues were the main variables correlating with cognitive performance in post-COVID-19 patients, while in ME/CFS it was anxiety symptoms and physical fatigue. Conclusions The symptomatology and cognitive patterns were similar in both groups, with greater impairment in ME/CFS. This disease is characterized by greater physical and neuropsychiatric problems compared to post-COVID-19 condition. Likewise, we also propose the relevance of prolonged hyposmia as a possible marker of cognitive deterioration in patients with post-COVID-19.

Berlin Electropolisties the German discourse on nervousness in the late nineteenth and early twentieth centuries to Berlin's transformation into a capital of the second industrial revolution. Focusing on three key groups-railway personnel, soldiers, and telephone operators-Andreas Killen traces the emergence in the 1880s and then later decline of the belief that modernity caused nervous illness. During this period, Killen explains, Berlin became arguably the most advanced metropolis in Europe. A host of changes, many associated with breakthroughs in technologies of transportation, communication, and leisure, combined to radically alter the shape and tempo of everyday life in Berlin. The resulting consciousness of accelerated social change and the shocks and afflictions that accompanied it found their consummate expression in the discourse about nervousness. Wonderfully researched and clearly written, this book offers a wealth of new insights into the nature of the modern metropolis, the psychological aftermath of World War I, and the operations of the German welfare state. Killen also explores cultural attitudes toward electricity, the evolution of psychiatric thought and practice, and the status of women workers in Germany's rapidly industrializing economy. Ultimately, he argues that the backlash against the welfare state that occurred during the late Weimar Republic brought about the final decoupling of modernity and nervous illness.

It has been more than three years since COVID-19 impacted the lives of millions of people, many of whom suffer from long-term effects known as long-haulers. Notwithstanding multiorgan complaints in long-haulers, signs and symptoms associated with cognitive characteristics commonly known as “brain fog” occur in COVID patients over 50, women, obesity, and asthma at excessive. Brain fog is a set of symptoms that include cognitive impairment, inability to concentrate and multitask, and short-term and long-term memory loss. Of course, brain fog contributes to high levels of anxiety and stress, necessitating an empathetic response to this group of COVID patients. Although the etiology of brain fog in COVID-19 is currently unknown, regarding the mechanisms of pathogenesis, the following hypotheses exist: activation of astrocytes and microglia to release pro-inflammatory cytokines, aggregation of tau protein, and COVID-19 entry in the brain can trigger an autoimmune reaction. There are currently no specific tests to detect brain fog or any specific cognitive rehabilitation methods. However, a healthy lifestyle can help reduce symptoms to some extent, and symptom-based clinical management is also well suited to minimize brain fog side effects in COVID-19 patients. Therefore, this review discusses mechanisms of SARS-CoV-2 pathogenesis that may contribute to brain fog, as well as some approaches to providing therapies that may help COVID-19 patients avoid annoying brain fog symptoms.

Post-acute sequelae of SARS-CoV-2 (PASC) is a poorly understood condition with significant impact on quality of life. We aimed to better understand the lived experiences of patients with PASC, focusing on the impact of cognitive complaints (“brain fog”) and fatigue on (1) daily activities, (2) work/employment, and (3) interpersonal relationships. We conducted semi-structured qualitative interviews with 15 patients of a Midwestern academic hospital’s post-COVID-19 clinic. We audio-recorded, transcribed, and analyzed interviews thematically using a combined deductive-inductive approach and collected participants’ characteristics from chart review. Participants frequently used descriptive and metaphorical language to describe symptoms that were relapsing-remitting and unpredictable. Fatigue and brain fog affected all domains and identified subthemes included symptoms’ synergistic effects, difficulty with multitasking, lack of support, poor self-perception, and fear of loss of income and employment. Personal relationships were affected with change of responsibilities, difficulty parenting, social isolation, and guilt due to the burdens placed on family. Furthermore, underlying social stigma contributed to negative emotions, which significantly affected emotional and mental health. Our findings highlight PASC’s negative impact on patients’ daily lives. Providers can better support COVID-19 survivors during their recovery by identifying their needs in a sensitive and timely manner.

Objective COVID-19 (SARS-CoV-2) has been associated with neurological sequelae even in those patients with mild respiratory symptoms. Patients experiencing cognitive symptoms such as “brain fog” and other neurologic sequelae for 8 or more weeks define “long haulers”. There is limited information regarding damage to grey matter (GM) structures occurring in COVID-19 “long haulers”. Advanced imaging techniques can quantify brain volume depletions related to COVID-19 infection which is important as conventional Brain MRI often fails to identify disease correlates. 3-dimensional voxel-based morphometry (3D VBM) analyzes, segments and quantifies key brain volumes allowing comparisons between COVID-19 “long haulers” and normative data drawn from healthy controls, with values based on percentages of intracranial volume. Methods This is a retrospective single center study which analyzed 24 consecutive COVID-19 infected patients with long term neurologic symptoms. Each patient underwent Brain MRI with 3D VBM at median time of 85 days following laboratory confirmation. All patients had relatively mild respiratory symptoms not requiring oxygen supplementation, hospitalization, or assisted ventilation. 3D VBM was obtained for whole brain and forebrain parenchyma, cortical grey matter (CGM), hippocampus, and thalamus. Results The results demonstrate a statistically significant depletion of CGM volume in 24 COVID-19 infected patients. Reduced CGM volume likely influences their long term neurological sequelae and may impair post COVID-19 patient’s quality of life and productivity. Conclusion This study contributes to understanding effects of COVID-19 infection on patient’s neurocognitive and neurological function, with potential for producing serious long term personal and economic consequences, and ongoing challenges to public health systems.

The incidence of long COVID is substantial, even in people with mild to moderate acute COVID-19. The role of early viral kinetics in the subsequent development of long COVID is largely unknown, especially in individuals who were not hospitalized for acute COVID-19. Seventy-three non-hospitalized adult participants were enrolled within approximately 48 hours of their first positive SARS-CoV-2 RT-PCR test, and mid-turbinate nasal and saliva samples were collected up to 9 times within the first 45 days after enrollment. Samples were assayed for SARS-CoV-2 using RT-PCR and additional SARS-CoV-2 test results were abstracted from the clinical record. Each participant indicated the presence and severity of 49 long COVID symptoms at 1-, 3-, 6-, 12-, and 18-months post-COVID-19 diagnosis. Time from acute COVID-19 illness onset to SARS-CoV-2 RNA clearance greater or less than 28 days was tested for association with the presence or absence of each of 49 long COVID symptoms at 90+ days from acute COVID-19 symptom onset. Self-reported brain fog and muscle pain at 90+ days after acute COVID-19 onset were negatively associated with viral RNA clearance within 28 days of acute COVID-19 onset with adjustment for age, sex, BMI ≥ 25, and COVID vaccination status prior to COVID-19 (brain fog: aRR 0.46, 95% CI 0.22-0.95; muscle pain: aRR 0.28, 95% CI 0.08-0.94). Participants reporting higher severity brain fog or muscle pain at 90+ days after acute COVID-19 onset were less likely to have cleared SARS-CoV-2 RNA within 28 days. The acute viral RNA decay trajectories of participants who did and did not later go on to experience brain fog 90+ days after acute COVID-19 onset were distinct. This work indicates that at least two long COVID symptoms - brain fog and muscle pain - at 90+ days from acute COVID-19 onset are specifically associated with prolonged time to clearance of SARS-CoV-2 RNA from the upper respiratory tract during acute COVID-19. This finding provides evidence that delayed immune clearance of SARS-CoV-2 antigen or greater amount or duration of viral antigen burden in the upper respiratory tract during acute COVID-19 are directly linked to long COVID. This work suggests that host-pathogen interactions during the first few weeks after acute COVID-19 onset have an impact on long COVID risk months later.

The coronavirus disease 2019 (COVID-19) pandemic caused by SARS-CoV-2 has been defined as the greatest global health and socioeconomic crisis of modern times. While most people recover after being infected with the virus, a significant proportion of them continue to experience health issues weeks, months and even years after acute infection with SARS-CoV-2. This persistence of clinical symptoms in infected individuals for at least three months after the onset of the disease or the emergence of new symptoms lasting more than two months, without any other explanation and alternative diagnosis have been named long COVID, long-haul COVID, post-COVID-19 conditions, chronic COVID, or post-acute sequelae of SARS-CoV-2 (PASC). Long COVID has been characterized as a constellation of symptoms and disorders that vary widely in their manifestations. Further, the mechanisms underlying long COVID are not fully understood, which hamper efficient treatment options. This review describes predictors and the most common symptoms related to long COVID’s effects on the central and peripheral nervous system and other organs and tissues. Furthermore, the transcriptional markers, molecular signaling pathways and risk factors for long COVID, such as sex, age, pre-existing condition, hospitalization during acute phase of COVID-19, vaccination, and lifestyle are presented. Finally, recommendations for patient rehabilitation and disease management, as well as alternative therapeutical approaches to long COVID sequelae are discussed. Understanding the complexity of this disease, its symptoms across multiple organ systems and overlapping pathologies and its possible mechanisms are paramount in developing diagnostic tools and treatments.