Lockdown Brain fog
237640870
The Pandemic Brain: neuroinflammation in healthy, non infected individuals during the COVID 19 pandemic
The impact of COVID 19 on human health extends beyond the morbidity and death toll directly caused by the SARS CoV 2 virus. In fact, accumulating evidence indicates a global increase in the incidence of fatigue, brain fog and depression, including among non infected, since the pandemic onset. Motivated by previous evidence linking those symptoms to neuroimmune activation in other pathological contexts, we hypothesized that subjects examined after the enforcement of lockdown/stay at home measures would demonstrate increased neuroinflammation. We performed simultaneous brain Positron Emission Tomography Magnetic Resonance Imaging in healthy volunteers either before (n=57) or after (n=15) the 2020 Massachusetts lockdown, using [11C]PBR28, a radioligand for the glial marker 18 kDa translocator protein (TSPO) First, we compared [11C]PBR28 signal across pre and post lockdown cohorts. Then, we evaluated the link between neuroinflammatory signals and scores on a questionnaire assessing mental and physical impacts of the pandemic. Further, we investigated multivariate associations between the spatial pattern of [11C]PBR28 post lockdown changes and constitutive brain gene expression in post mortem brains (Allen Human Brain Atlas) Finally, in a subset (n=13 pre lockdown; n=11 post lockdown) we also used magnetic resonance spectroscopy to quantify brain (thalamic) levels of myoinositol (mIns) another neuroinflammatory marker. Both [11C]PBR28 and mIns signals were overall stable pre lockdown, but markedly elevated after lockdown, including within brain regions previously implicated in stress, depression and 'sickness behaviors' Moreover, amongst the post lockdown cohort, subjects endorsing higher symptom burden showed higher [11C]PBR28 PET signal compared to those reporting little/no symptoms. Finally, the post lockdown [11C]PBR28 signal changes were spatially aligned with the constitutive expression of several genes highly expressed in glial/immune cells and/or involved in neuroimmune signaling. Our results suggest that pandemic related stressors may have induced sterile neuroinflammation in healthy individuals that were not infected with SARS CoV 2. This work highlights the possible impact of the COVID 19 pandemic related lifestyle disruptions on human brain health.
medRxiv
Ludovica Brusaferri Zeynab Alshelh Diana Martins Akila Weerasekera Heather H Housman E J Morrisey Paulina Knight Kelly A Castro-Blanco Daniel S Albrecht Nicole R Zurcher Eva-Marie Ratai Oluwaseun Johnson-Akeju N Mercaldo Nouchine Hadjikhani Mattia Veronese Frederico Turkheimer B R Rosen Jacob M Hooker Marco L Loggia
233565619
Effects of COVID 19 related stay at home order on neuropsychophysiological response to urban spaces: Beneficial role of exposure to nature?
Abstract Background The COVID 19 pandemic has had severe negative effects on populations worldwide. The seriousness of the pandemic necessitated local and even national lockdowns. In Singapore a national lockdown with aStay at Home Order (SHO) lasted for over 7 weeks. The impact of the pandemic and of the long SHO period on neuropsychophysiological functioning remains unknown. Studies prior to the pandemic highlighted the beneficial role of nature exposure on mental health and well being, although this has not yet been explored in the post pandemic world. This is the first study to investigate the longitudinal changes in (1) brain frontal alpha asymmetry (FAA; neuroelectric marker of approach related motivation) (2) depressive mood and (3) symptoms, and (4) emotional response to videos of various urban spaces from before COVID 19 to immediately after the SHO in Singapore was over. Finally, we examined whether higher vs lower exposure to nature during the SHO moderated changes over time. Methods The sample included 25 healthy adult Singaporeans (56% female, Mage 40.4 y, SD 17.8) who attended two electroencephalography (EEG) lab sessions, within a year before the COVID 19 pandemic (T1) and immediately following the SHO (T2) The participants viewed 9 fixed frame videos, filmed before the pandemic, from 3 urban public spaces (Busy Downtown, Residential Green, Lush Garden) on the roll up screen. They rated their emotional response (arousal, valence) after each video and completed Becks Depression Inventory II (BDI II) as a measure of depressive symptoms, Profile of Mood Scale (POMS) as a measure of momentary mood, and self reported the frequency and duration of their nature visits during the SHO. Results Linear mixed models were fitted to examine changes over time, and effect moderation by amount of nature exposure during the SHO. The results showed decrease in FAA (p Conclusions Post SHO, brain activity and responsiveness to landscapes changed, and showed a general reduction in positive emotions and increased depressive symptoms among participants. The higher nature exposure during the SHO did not help mitigate this depressive symptoms, as previous research would suggest. This can be due to the modified quality of nature exposure during lockdown, which highlights the importance of high quality nature experience in cities and the provision of diversified visual exposures. Potential neuropsychophysiological consequences of SHO should be considered by policy makers in the post COVID 19 world.
Agnieszka Olszewska-Guizzo Anna Fogel Nicolas Escoffier Roger Chun-Man Ho
225513416
From 'brain fog' to heart damage, COVID 19's lingering problems alarm scientists
Jennifer Couzin-Frankel
220681237
The influence of the COVID 19 pandemic on traumatic brain injuries in Tyrol: experiences from a state under lockdown
In February 2020, the federal state of Tyrol in Austria has become one of the epicenters of the COVID 19 pandemic. Tyrol is known for numerous skiing areas. Thus, winter sport resorts became a starting point for COVID 19 infections spreading towards the rest of the state, Austria and other countries, leading to a mandatory quarantine for almost a million people, who were placed under a curfew and restrictions in daily life. Additionally, all ski resorts and hotels were closed. We aimed to analyze the influence of the COVID 19 quarantine on traumatic brain injury (TBI) cases in Tyrol. We retrospectively compared demographical and injury characteristics from all TBI patients within the 2020 strict quarantine period with the respective time periods from 2016 to 2019. As our department is the only neurosurgical unit in Tyrol, all patients with moderate or severe TBI are transferred to our hospital. During 3 weeks of the full quarantine period, the weekly TBI cases load decreased significantly in comparison to the same time periods in the years 2016 2019. Furthermore, concomitant skull fractures decreased significantly (p 0.016) probably reflecting different causative mechanisms. The other demographical and injury characteristics and particularly falls at home stayed relatively unchanged. TBI remained an important contributor to the neurosurgical workflow during the COVID 19 pandemic. Strategies to ensure neurosurgical care also under pandemic induced lockdown are important.
European Journal of Trauma and Emergency Surgery
Daniel Pinggera Barbara E K Klein Claudius Thome Lukas Grassner
216367637
Brain fog in postural tachycardia syndrome: An objective cerebral blood flow and neurocognitive analysis
It remains unclear whether brain fog is related to impaired cerebral blood flow (CBF) in postural tachycardia syndrome (POTS) patients.
Journal of arrhythmia
Rachel Wells Felix Paterson Stephen Bacchi Amanda J Page Mathias Baumert Dennis H Lau
221365646
Brain fog and non coeliac gluten sensitivity: Proof of concept brain MRI pilot study
Aims Non Coeliac Gluten Sensitivity (NCGS) is poorly understood, particularly in terms of its neurological outcomes. We initially conducted a prospective postal survey to investigate its neurological presentation and symptom course. Results from this then motivated a follow up pilot study utilising brain MRI to characterise potential diagnostic biomarkers for future research. Methods Patients with NCGS were recruited from a specialist centre and completed a prospective postal questionnaire (N 125) This summarised symptoms experienced, their severity and their course. Onset time was compared by Chi squared analysis to data from the same centre concerning coeliac disease patients (N 224) Five respondents on a strict gluten free diet who self reported brain fog then attended a pilot study, completing MR brain imaging/questionnaires before/after a gluten challenge. "Baseline" data were assessed for abnormalities, while symptom severity and cerebral blood flow (CBF) were compared before/after challenge. Results Survey participants were aged 47 (85% female) Prevalence of neurological symptoms were: headaches (51% brain fog (48% balance issues (31% tingling (19% Median symptom resolution time was 48 hours, while onset was 90 minutes; onset pattern was not significantly different compared to CD patients (p 0.322) Extra intestinal symptoms worsened by 37% 28) during a typical reaction. Predominantly non statistical observations from the brain imaging study are discussed. Conclusions Neurological symptoms in NCGS are common, and onset time is comparable to that in CD. Brain imaging may be a useful future means of investigating physiological injury and responses to gluten in further study.
PloS one
Iain D Croall Nigel Hoggard Imran Aziz Marios Hadjivassiliou David S Sanders
218609373
MON 245 Brain Fog: An Important Cue to Neurosarcoidosis and Its Flare Up?
Abstract Introduction: Sarcoidosis is a multisystem inflammatory disorder characterized by noncaseating granulomas in various organ systems, mainly the lung and lymphatic system. Neurosarcoidosis (NS) involving central or peripheral nervous system is uncommon and Hypothalamic pituitary (HP) NS is rarer. Case: A 45 years old African American man presented with a few days' history of cognitive slowness (brain fog) and a sense of loss of direction. He was discharged a few months ago from another hospital after being admitted for shortness of breath and hypercalcemia of 13 mg/dl, which improved after hydration. CXR showed mediastinal and bilateral hilar enlargement. He was discharged home with outpatient pulmonary appointment but was readmitted to our hospital with altered mental status. Calcium level on this admission was 11.5 mg/dl. CT brain showed a sellar/suprasellar lesion, which was better visualized on MRI as enlargement and enhancement of pituitary gland, pituitary stalk, optic chiasm, left and right optic tract and nerves, and hypothalamus. He had left hemi temporal field defect. Work up revealed inappropriately high normal 1,25 vitamin D, low PTH, PTrp and vitamin D. He has anterior hypopituitarism and mildly elevated prolactin. EBUS with mediastinal lymph node biopsy was non diagnostic, however, excisional biopsy of mediastinal node showed non caseating granuloma. ACE level, flow cytometry, infectious work up and serum IgG4 were normal. Discussion: NS may present as cranial nerve palsy, chronic headache with incidental HP mass and endocrine dysfunction such as diabetes insipidus, hyperprolactinemia, and anterior hypopituitarism. Visual deficits from optic atrophy or neuropathy; or change in vision from anterior uveitis are present in 41% of patients. Other non specific presentations of NS include fatigue, cognitive difficulties (brain fog) such as impaired memory, slowed thinking, diminished attention and concentration. Hypercalcemia in sarcoidosis is due to increased intestinal absorption of calcium from increased 1,25 OH vitamin D. Though definitive diagnosis of NS is based on evidence of non caseating granulomas from neural tissue, probable diagnosis can be made from clinical and radiologic characteristics, non caseating granulomas at an extraneural site with no evidence of alternative disease. Steroid is the mainstay of treatment in NS and requires slow tapering. Other immunomodulators can be considered in worsening disease or patients with steroid adverse effect. Conclusion: Diagnosis of NS is challenging due to its rarity and difficult access to neural tissue for diagnosis. Though brain fog may not be specific for NS or its flare up, additional neurological test or imaging should be considered especially in African American patients with hilar lymphadenopathy as 20% of NS patients may simply present with non specific cognitive or behavioral complaints.
Journal of the Endocrine Society
Manasi S Shah Yin Htwe Oo
216647732
Palmitoylethanolamide counteracts brain fog improving depressive like behaviour in obese mice: Possible role of synaptic plasticity and neurogenesis
High fat diet (HFD) induced obesity is accompanied by metabolic and neurochemical changes that have been associated with depression. Recent studies indicate that palmitoylethanolamide (PEA) exerts metabolic effects and holds neuroprotective potential. However, studies on HFD exposure in mice which investigate the effects of PEA on monoamine system and synaptic plasticity are limited.
British journal of pharmacology
Adriano Lama Claudio Pirozzi Chiara Annunziata Maria Grazia Morgese Martina Senzacqua Ilenia Severi Antonio Calignano Luigia Trabace Antonio Giordano Rosaria Meli Giuseppina Mattace Raso
211556012
Accelerated immune aging was correlated with lupus associated brain fog in reproductive age systemic lupus erythematosus patients
Cognitive impairment is common in systemic lupus erythematosus (SLE) patients with substantial adverse effects on function and quality of life. One hypothesis to understand the mechanisms of cognitive impairment in SLE is accelerated immunosenescence. The aim of this study is to observe the correlation between immunosenescence with cognitive impairment in patients with SLE.
International journal of rheumatic diseases
Handono Kalim Mirza Zaka Pratama Ernes Mahardini Eden Suryoiman Winoto Pratista Adi Krisna Kusworini Handono
211072230
Can the light of immunometabolism cut through "brain fog"
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a highly debilitating disease with heterogeneous constitutional and neurological complaints. Infection like symptoms often herald disease onset, but no pathogen or immune defect has been conclusively linked. In this issue of the JCI, Mandarano et al. illuminate bioenergetic derangements of ME/CFS T cell subsets. CD4+ and CD8+ T cells had impaired resting glycolysis. CD8+ cells additionally showed activation related metabolic remodeling deficits and decreased mitochondrial membrane potential; a subset had increased resting mitochondrial mass. Immune senescence and exhaustion paradigms offer only partial explanations. Hence, unique mechanisms of disrupted immunometabolism may underlie the complex neuroimmune dysfunction of ME/CFS.
The Journal of clinical investigation
Mady Hornig