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, Mohammad Balabandian, Fatemeh Sodeifian, Negin Rezaei, Mohammad Reza Rostami,
Multiple Sclerosis and Related Disorders, Volume 62; https://doi.org/10.1016/j.msard.2022.103795

The publisher has not yet granted permission to display this abstract.
, Frauke Nees
Published: 24 March 2022
Neuroforum, Volume 28, pp 105-116; https://doi.org/10.1515/nf-2021-0034

Abstract:
According to best current estimates, approximately 10% of those infected with SARS-CoV-2-virus experience long-term clinical and nonspecific neurological symptoms that may last for several weeks or months. This is currently referred to as “Long-COVID” or “Post-COVID-Syndrome”. Based on current knowledge, the most common long-term symptoms of COVID-19 disease include fatigue and poor concentration, but particularly also headache and musculoskeletal pain. However, given the novelty of COVID-19, only a few studies have systematically evaluated the central nervous alterations in the pain processing structures of our brain. Those first insights are yet important in order to offer patients adequate therapeutic options. Based on a systematic review of the literature, we will therefore provide an overview of the central nervous alterations in the brain described in the context of SARS-CoV-2 infection, focusing on findings with brain imaging.
, , Chisato Shimizu, Ottavia M. Delmonte, Kerry Dobbs, Valentina Discepolo, Andrea Lo Vecchio, Alfredo Guarino, Francesco Licciardi, Ugo Ramenghi, et al.
Published: 11 March 2022
Frontiers in Immunology, Volume 13; https://doi.org/10.3389/fimmu.2022.841126

Abstract:
The antibody profile against autoantigens previously associated with autoimmune diseases and other human proteins in patients with COVID-19 or multisystem inflammatory syndrome in children (MIS-C) remains poorly defined. Here we show that 30% of adults with COVID-19 had autoantibodies against the lung antigen KCNRG, and 34% had antibodies to the SLE-associated Smith-D3 protein. Children with COVID-19 rarely had autoantibodies; one of 59 children had GAD65 autoantibodies associated with acute onset of insulin-dependent diabetes. While autoantibodies associated with SLE/Sjögren’s syndrome (Ro52, Ro60, and La) and/or autoimmune gastritis (gastric ATPase) were detected in 74% (40/54) of MIS-C patients, further analysis of these patients and of children with Kawasaki disease (KD), showed that the administration of intravenous immunoglobulin (IVIG) was largely responsible for detection of these autoantibodies in both groups of patients. Monitoring in vivo decay of the autoantibodies in MIS-C children showed that the IVIG-derived Ro52, Ro60, and La autoantibodies declined to undetectable levels by 45-60 days, but gastric ATPase autoantibodies declined more slowly requiring >100 days until undetectable. Further testing of IgG and/or IgA antibodies against a subset of potential targets identified by published autoantigen array studies of MIS-C failed to detect autoantibodies against most (16/18) of these proteins in patients with MIS-C who had not received IVIG. However, Troponin C2 and KLHL12 autoantibodies were detected in 2 of 20 and 1 of 20 patients with MIS-C, respectively. Overall, these results suggest that IVIG therapy may be a confounding factor in autoantibody measurements in MIS-C and that antibodies against antigens associated with autoimmune diseases or other human proteins are uncommon in MIS-C.
Alessandro Padovani, Antonio Canale, Lorenzo Schiavon, Stefano Masciocchi, Alberto Imarisio, Barbara Risi, Giulio Bonzi, Valeria De Giuli, Monica Di Luca, Nicholas J. Ashton, et al.
Published: 27 January 2022
Alzheimer's & Dementia; https://doi.org/10.1002/alz.12554

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Margarita Kirienko, , Roland Hustinx, Jamshed B. Bomanji, Arturo Chiti, Stefano Fanti
Published: 1 January 2022
Seminars in Nuclear Medicine, Volume 52, pp 17-24; https://doi.org/10.1053/j.semnuclmed.2021.06.022

Abstract:
The COVID-19 pandemic has profoundly changed hospital activities, including nuclear medicine (NM) practice. This review aimed to determine and describe the impact of COVID-19 on NM in Europe and critically discuss actions and strategies applied to face the pandemic. A literature search for relevant articles was performed on PubMed, covering COVID-19 studies published up until January 21, 2021. The findings were summarized according to general and specific activities within the NM departments. The pandemic strongly challenged NM departments: a reduction in the workforce has been experienced in almost every center in Europe due to personnel diagnosed with COVID-19 and other reasons related to the coronavirus. NM departments introduced procedures to limit COVID-19 transmission, including environmental and personal hygiene, social distancing, rescheduling of non–high-priority procedures, the correct use of personal protective equipment, and prompt identification of suspect COVID-19 cases. A proportion of the departments experienced a delay in radiopharmaceuticals supply or technical assistance during the pandemic. Furthermore, the pandemic resulted in a significant reduction of diagnostic and therapeutic NM procedures, as well as a reduced level of care for patients affected by diseases other than COVID-19, such as cancer or acute cardiovascular disease. Telemedicine services have been set up to maintain medical assistance for patients. COVID-19 pandemic has reshaped human work resources, patient's diagnostic and therapeutic management, operative models, radiopharmaceutical supplies, teaching, training and research of NM departments. Limits of availability of resources emerged. Nonetheless, we have to provide continuity in care, especially for fragile patients, maintaining infection control measures. Challenges that have been faced should reshape our vision and get us prepared for the future.
, Andrea Stabile, Claudia Balducci, , Adriana Patruno, Roberto Rona, Michela Bombino, Cristina Capraro, Francesca Andreetta, Paola Cavalcante, et al.
Annals of Clinical and Translational Neurology, Volume 8, pp 2314-2318; https://doi.org/10.1002/acn3.51479

The publisher has not yet granted permission to display this abstract.
, Elham Rostami, Eva Kumlien, Nicholas J. Ashton, Sven Jackmann, Radu Pavel, Kaj Blennow, , Miklos Lipcsey, Robert Frithiof, et al.
Published: 18 November 2021
The publisher has not yet granted permission to display this abstract.
, Benjamin Cross, Danish Hafeez, Mao Fong Lim, Hamilton Morrin, Emma Rachel Rengasamy, Tom Pollak, Timothy R. Nicholson
Published: 11 November 2021
Psychiatric Clinics of North America, Volume 45, pp 29-43; https://doi.org/10.1016/j.psc.2021.11.001

, , Chisato Shimizu, Ottavia M. Delmonte, Kerry Dobbs, Valentina Discepolo, Andrea Lo Vecchio, Alfredo Guarino, Francesco Licciardi, Ugo Ramenghi, et al.
Published: 4 November 2021
Abstract:
The autoantibody profile associated with known autoimmune diseases in patients with COVID-19 or multisystem inflammatory syndrome in children (MIS-C) remains poorly defined. Here we show that adults with COVID-19 had a moderate prevalence of autoantibodies against the lung antigen KCNRG, and SLE-associated Smith autoantigen. Children with COVID-19 rarely had autoantibodies; one of 59 children had GAD65 autoantibodies associated with acute insulin-dependent diabetes. While autoantibodies associated with SLE/Sjögren’s syndrome (Ro52, Ro60, and La) and/or autoimmune gastritis (gastric ATPase) were detected in 74% (40/54) of MIS-C patients, further analysis of these patients and of children with Kawasaki disease (KD), showed that the administration of intravenous immunoglobulin (IVIG) was largely responsible for detection of these autoantibodies in both groups of patients. Monitoring in vivo decay of the autoantibodies in MIS-C children showed that the IVIG-derived Ro52, Ro60, and La autoantibodies declined to undetectable levels by 45-60 days, but gastric ATPase autoantibodies declined more slowly requiring >100 days until undetectable. Together these findings demonstrate that administration of high-dose IVIG is responsible for the detection of several autoantibodies in MIS-C and KD. Further studies are needed to investigate autoantibody production in MIS-C patients, independently from IVIG administration.
, Pattana Wangaryattawanich, Jason Hartman, Christopher G. Filippi, Daniel S. Hippe, Nathan M. Cross
The British Journal of Radiology, Volume 94; https://doi.org/10.1259/bjr.20210149

Abstract:
We reviewed the literature to describe outcomes associated with abnormal neuroimaging findings among adult COVID-19 patients. We performed a systematic literature review using PubMed and Embase databases. We included all studies reporting abnormal neuroimaging findings among hospitalized patients with confirmed COVID-19 and outcomes. Data elements including patient demographics, neuroimaging findings, acuity of neurological symptoms and/or imaging findings relative to COVID-19 onset (acute, subacute, chronic), and patient outcomes were recorded and summarized. After review of 775 unique articles, a total of 39 studies comprising 884 COVID-19 patients ≥ 18 years of age with abnormal neuroimaging findings and reported outcomes were included in our analysis. Ischemic stroke was the most common neuroimaging finding reported (49.3%, 436/884) among patients with mortality outcomes data. Patients with intracranial hemorrhage (ICH) had the highest all-cause mortality (49.7%, 71/143), followed by patients with imaging features consistent with leukoencephalopathy (38.5%, 5/13), and ischemic stroke (30%, 131/436). There was no mortality reported among COVID-19 patients with acute disseminated encephalomyelitis without necrosis (0%, 0/8) and leptomeningeal enhancement alone (0%, 0/12). Stroke was a common acute or subacute neuroimaging finding, while leukoencephalopathy was a common chronic finding. Among hospitalized COVID-19 patients with abnormal neuroimaging findings, those with ICH had the highest all-cause mortality; however, high mortality rates were also seen among COVID-19 patients with ischemic stroke in the acute/subacute period and leukoencephalopathy in the chronic period. Specific abnormal neuroimaging findings may portend differential mortality outcomes, providing a potential prognostic marker for hospitalized COVID-19 patients.
, , Jacqueline Fernandes Do Nascimento
Published: 28 October 2021
Psychiatry Research Communications, Volume 1; https://doi.org/10.1016/j.psycom.2021.100004

The publisher has not yet granted permission to display this abstract.
, Gundega Ķauķe, Krista Skrējāne, Līga Jaunozoliņa,
Published: 16 October 2021
European Journal of Neurology, Volume 28, pp 3870-3872; https://doi.org/10.1111/ene.14966

The publisher has not yet granted permission to display this abstract.
Gul Moonis, Christopher G. Filippi, Claudia F. E. Kirsch, Suyash Mohan, Evan G. Stein, Joshua A. Hirsch, Amit Mahajan
American Journal of Roentgenology, Volume 217, pp 959-974; https://doi.org/10.2214/ajr.20.24839

Abstract:
Neurologic involvement is well-recognized in coronavirus disease (COVID-19). This article reviews the neuroimaging manifestations of COVID-19 on CT and MRI, presenting cases from the New York City metropolitan region encountered by the authors during the first surge of the pandemic. The most common neuroimaging manifestations are acute infarcts with large clot burden and intracranial hemorrhage, including microhemorrhages. However, a wide range of additional imaging patterns occur, including leukoencephalopathy, global hypoxic injury, acute demyelinating encephalomyelitis, cytotoxic lesions of the corpus callosum, olfactory bulb involvement, cranial nerve enhancement, and Guillain Barré syndrome. The described central nervous system abnormalities largely represent secondary involvement from immune activation that leads to a prothrombotic state and cytokine storm; evidence for direct neuroinvasion is scant. Comorbidities such as hypertension, complications of prolonged illness and hospitalization, as well as associated supportive treatments, also contribute to the central nervous system involvement in COVID-19. Routine, long-term, neurologic follow-up may be warranted, given emerging evidence of long-term microstructural and functional changes on brain imaging, after COVID-19 recovery.
Anne Melhuish, Fiona McGill
Published: 25 September 2021
The publisher has not yet granted permission to display this abstract.
Wei Lin, Chien-An Ko, Yueh-Feng Sung, Yeu-Chin Chen, Jiunn-Tay Lee, Yun-Qian Lin, Yu-Kai Lin
Published: 24 September 2021
Frontiers in Neurology, Volume 12; https://doi.org/10.3389/fneur.2021.738329

Abstract:
Objective: Coronavirus disease (COVID-19) vaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare but fatal complication observed within 2 weeks of adenovirus-vectored vaccination. Case Report: A 52-year-old male patient, with a family history of autoimmune diseases, presented with a new onset of worsening headache with nausea and vomiting post-vaccination. The patient was diagnosed with VITT based on laboratory findings demonstrating thrombocytopenia, elevated D-dimer, and dural sinus thrombosis identified on neuroimaging. The patient was successfully treated with high-dose immunoglobulin, steroids, and non-heparin anticoagulants, without any neurologic sequelae. Finally, a confirmatory test with anti-platelet factor 4 antibody was strongly positive. Conclusion: Physicians should be vigilant when treating patients presenting with new-onset thunderclap headache, progressive worsening headache, and awakening headache accompanied by nausea or vomiting after vaccination, even if no definite clinical neurological deficits are identified. Emergency laboratory test results for demonstrating elevated D-dimer levels, decreased platelet count, and neuroimaging correlation are integral for diagnosis and must be the standard protocol. Treatment with non-heparin anticoagulants, high-dose intravenous immunoglobulin, and steroids that halt or slow the immune-mediated prothrombotic process should be initiated immediately. Considering the high mortality rate of VITT, treatment should be initiated prior to confirmatory test results.
Published: 9 September 2021
Abstract:
Minor neurological symptoms such as anosmia are relatively common manifestations of coronavirus disease 2019 (COVID-19). However, severe affection of the central nervous system (CNS) occurs in a minority of cases and its treatment and pathophysiology is not yet well understood. It has been described that encephalitis due to COVID-19 may be caused by the proinflammatory state due to the cytokine storm or direct invasion of the virus in the CNS. Here we present a case of a 66-year-old man with bipolar disorder and moderate respiratory COVID-19 symptoms who presented to the emergency department with a decreased level of consciousness. Brain computerized tomography (CT) showed no acute pathology. A thorough investigation of other possible causes of CNS affection was negative. The patient was treated with pulse therapy with methylprednisolone and presented a significant improvement of his neurological condition, being discharged with a complete neurological recovery five days after the start of the treatment. This case illustrates the importance of a high index of suspicion in diagnosing severe CNS impairment in mild respiratory COVID-19 cases. Also, this case corroborates with previous reports of glucocorticoid response in CNS impairment associated with COVID-19, although more robust studies are required to confirm this relation.
Yumin Wang, Yanchao Wang, Liang Huo, Qiang Li, Jichao Chen,
Published: 30 August 2021
Journal of Neurology, Volume 269, pp 1071-1092; https://doi.org/10.1007/s00415-021-10771-8

The publisher has not yet granted permission to display this abstract.
, Nathan Praschan, Gregory Fricchione, Scott Beach
Journal of the Academy of Consultation-Liaison Psychiatry, Volume 62, pp 625-633; https://doi.org/10.1016/j.jaclp.2021.08.009

The publisher has not yet granted permission to display this abstract.
, Laura Faiver, Andrew M. Nguyen, Lauren Ottenhoff,
Published: 24 August 2021
The Neurohospitalist, Volume 12, pp 31-37; https://doi.org/10.1177/19418744211034815

Abstract:
Background and Purpose: A variety of neurological manifestations have been attributed to COVID-19, but there is currently limited evidence regarding risk factors and outcomes for delirium in critically ill patients with COVID-19. The purpose of this study was to identify delirium in a large cohort of ICU patients with COVID-19, and to identify associated features and clinical outcomes at the time of hospital discharge. Methods: This is an observational cohort study of 213 consecutive patients admitted to an ICU for COVID-19 respiratory illness. Delirium was diagnosed by trained abstractors using the CHART-DEL instrument. The associations between key clinical features, sedation and delirium were examined, as were the impacts of delirium on clinical outcomes. Results: Delirium was identified in 57.3% of subjects. Delirious patients were more likely to receive mechanical ventilation, had lower P: F ratios, higher rates of renal replacement therapy and ECMO, and were more likely to receive enteral benzodiazepines. Only mechanical ventilation remained a significant predictor of delirium in a logistic regression model. Mortality was not significantly different, but delirious patients experienced greater mechanical ventilation duration, ICU/hospital lengths of stay, worse functional outcomes at discharge, and were less likely to be discharged home. Conclusions: Delirium is common in critically ill patients with COVID-19 and appears to be associated with greater disease severity. When present, delirium is associated with worse functional status at discharge, but not increased mortality. Additional studies are necessary to determine the generalizability of these results and the impact of delirium on longer-term cognitive and functional outcomes.
, Vincenzo Silani, Alessandro Padovani, Paolo Barone, Paolo Calabresi, Paolo Girlanda, Leopnardo Lopiano, Luca Massacesi, Salvatore Monaco, Marco Onofrj, et al.
Published: 10 August 2021
Neurological Sciences, Volume 42, pp 4425-4431; https://doi.org/10.1007/s10072-021-05346-4

Abstract:
Background The coronavirus disease 2019 (COVID-19) pandemic has severely impacted the Italian healthcare system, underscoring a dramatic shortage of specialized doctors in many disciplines. The situation affected the activity of the residents in neurology, who were also offered the possibility of being formally hired before their training completion. Aims (1) To showcase examples of clinical and research activity of residents in neurology during the COVID-19 pandemic in Italy and (2) to illustrate the point of view of Italian residents in neurology about the possibility of being hired before the completion of their residency program. Results Real-life reports from several areas in Lombardia—one of the Italian regions more affected by COVID-19—show that residents in neurology gave an outstanding demonstration of generosity, collaboration, reliability, and adaptation to the changing environment, while continuing their clinical training and research activities. A very small minority of the residents participated in the dedicated selections for being hired before completion of their training program. The large majority of them prioritized their training over the option of earlier employment. Conclusions Italian residents in neurology generously contributed to the healthcare management of the COVID-19 pandemic in many ways, while remaining determined to pursue their training. Neurology is a rapidly evolving clinical field due to continuous diagnostic and therapeutic progress. Stakeholders need to listen to the strong message conveyed by our residents in neurology and endeavor to provide them with the most adequate training, to ensure high quality of care and excellence in research in the future.
Laura Zelada-Ríos, , Milagros Galecio-Castillo, Cesar Yamunaqué-Chunga, Kelvin Álvarez-Toledo,
Published: 26 July 2021
Journal of Neuroimmunology, Volume 359, pp 577674-577674; https://doi.org/10.1016/j.jneuroim.2021.577674

The publisher has not yet granted permission to display this abstract.
Bahar Bahranifard, Somayeh Mehdizadeh, Ali Hamidi, Alireza Khosravi, Ramin Emami, Kamran Mirzaei, Reza Nemati, Fatemeh Nemati, Majid Assadi, Ali Gholamrezanezhad
The Neuroradiology Journal, Volume 35, pp 3-24; https://doi.org/10.1177/19714009211029177

Abstract:
Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to various neurological manifestations. There is an urgent need for a summary of neuroimaging findings to accelerate diagnosis and treatment plans. We reviewed prospective and retrospective studies to classify neurological abnormalities observed in patients with the SARS-CoV-2 infection. Methods: The relevant studies published in Scopus, PubMed and Clarivate Analytics databases were analysed. The search was performed for full-text articles published from 23 January 2020 to 23 February 2021. Results: In 23 studies the number of patients with SARS-CoV-2 infection was 20,850 and the number of patients with neurological manifestations was 1996 (9.5%). The total number of patients with neuroradiological abnormalities was 602 (2.8%). SARS-CoV-2 has led to various neuroimaging abnormalities which can be categorised by neuroanatomical localisation of lesions and their main probable underlying pathogenesis. Cranial nerve and spinal root abnormalities were cranial neuritis and polyradiculitis. Parenchymal abnormalities fell into four groups of: (a) thrombosis disorders, namely ischaemic stroke and sinus venous thrombosis; (b) endothelial dysfunction and damage disorders manifested as various types of intracranial haemorrhage and posterior reversible encephalopathy syndrome; (c) hypoxia/hypoperfusion disorders of leukoencephalopathy and watershed infarction; and (d) inflammatory disorders encompassing demyelinating disorders, encephalitis, vasculitis-like disorders, vasculopathy and cytotoxic lesions of the corpus callosum. Leptomeninges disorders included meningitis. Ischaemic stroke was the most frequent abnormality in these studies. Conclusion: The review study suggests that an anatomical approach to the classification of heterogeneous neuroimaging findings in patients with SARS-CoV-2 and neurological manifestations would lend itself well for use by practitioners in diagnosis and treatment planning.
Amelia K. Boehme, Kevin Doyle, Kiran T. Thakur, David Roh, Soojin Park, Sachin Agarwal, Angela G. Velazquez, Jennifer A. Egbebike, Caroline Der Nigoghossian, Morgan L. Prust, et al.
Published: 28 June 2021
Neurocritical Care pp 1-8; https://doi.org/10.1007/s12028-021-01256-7

The publisher has not yet granted permission to display this abstract.
, Rajan Jain, Jennifer Frontera, Dimitris G. Placantonakis, Steven Galetta, Laura Balcer,
Published: 8 June 2021
Journal of Neuroimaging, Volume 31, pp 826-848; https://doi.org/10.1111/jon.12880

Abstract:
We reviewed the literature to evaluate cerebrospinal fluid (CSF) results from patients with coronavirus disease 2019 (COVID‐19) who had neurological symptoms and had an MRI that showed (1) central nervous system (CNS) hyperintense lesions not attributed to ischemia and/or (2) leptomeningeal enhancement. We sought to determine if these findings were associated with a positive CSF severe acute respiratory syndrome associated coronavirus 2 (SARS‐CoV‐2) polymerase chain reaction (PCR). We performed a systematic review of Medline and Embase from December 1, 2019 to November 18, 2020. CSF results were evaluated based on the presence/absence of (1) ≥ 1 CNS hyperintense lesion and (2) leptomeningeal enhancement. In 117 publications, we identified 193 patients with COVID‐19 who had an MRI of the CNS and CSF testing. There were 125 (65%) patients with CNS hyperintense lesions. Patients with CNS hyperintense lesions were significantly more likely to have a positive CSF SARS‐CoV‐2 PCR (10% [9/87] vs. 0% [0/43], p = 0.029). Of 75 patients who had a contrast MRI, there were 20 (27%) patients who had leptomeningeal enhancement. Patients with leptomeningeal enhancement were significantly more likely to have a positive CSF SARS‐CoV‐2 PCR (25% [4/16] vs. 5% [2/42], p = 0.024). The presence of CNS hyperintense lesions or leptomeningeal enhancement on neuroimaging from patients with COVID‐19 is associated with increased likelihood of a positive CSF SARS‐CoV‐2 PCR. However, a positive CSF SARS‐CoV‐2 PCR is uncommon in patients with these neuroimaging findings, suggesting they are often related to other etiologies, such as inflammation, hypoxia, or ischemia.
Lars Christian Lund, Jesper Hallas, Henrik Nielsen, Anders Koch, Stine Hasling Mogensen, Nikolai Constantin Brun, Christian Fynbo Christiansen, Reimar Wernich Thomsen,
Published: 10 May 2021
The Lancet Infectious Diseases, Volume 21, pp 1373-1382; https://doi.org/10.1016/s1473-3099(21)00211-5

The publisher has not yet granted permission to display this abstract.
Claudia Carrarini, Mirella Russo, Fedele Dono, Filomena Barbone, Marianna G. Rispoli, Laura Ferri, Martina Di Pietro, Anna Digiovanni, Paola Ajdinaj, Rino Speranza, et al.
Published: 16 April 2021
Frontiers in Neurology, Volume 12; https://doi.org/10.3389/fneur.2021.644317

Abstract:
Agitation is a behavioral syndrome characterized by increased, often undirected, motor activity, restlessness, aggressiveness, and emotional distress. According to several observations, agitation prevalence ranges from 30 to 50% in Alzheimer's disease, 30% in dementia with Lewy bodies, 40% in frontotemporal dementia, and 40% in vascular dementia (VaD). With an overall prevalence of about 30%, agitation is the third most common neuropsychiatric symptoms (NPS) in dementia, after apathy and depression, and it is even more frequent (80%) in residents of nursing homes. The pathophysiological mechanism underlying agitation is represented by a frontal lobe dysfunction, mostly involving the anterior cingulate cortex (ACC) and the orbitofrontal cortex (OFC), respectively, meaningful in selecting the salient stimuli and subsequent decision-making and behavioral reactions. Furthermore, increased sensitivity to noradrenergic signaling has been observed, possibly due to a frontal lobe up-regulation of adrenergic receptors, as a reaction to the depletion of noradrenergic neurons within the locus coeruleus (LC). Indeed, LC neurons mainly project toward the OFC and ACC. These observations may explain the abnormal reactivity to weak stimuli and the global arousal found in many patients who have dementia. Furthermore, agitation can be precipitated by several factors, e.g., the sunset or low lighted environments as in the sundown syndrome, hospitalization, the admission to nursing residencies, or changes in pharmacological regimens. In recent days, the global pandemic has increased agitation incidence among dementia patients and generated higher distress levels in patients and caregivers. Hence, given the increasing presence of this condition and its related burden on society and the health system, the present point of view aims at providing an extensive guide to facilitate the identification, prevention, and management of acute and chronic agitation in dementia patients.
, Enrico Premi, Andrea Pilotto, Viviana Cristillo, , Ilenia Libri, Marcello Giunta, H. Jeremy Bockholt, Jingyu Liu, Riccardo Campora, et al.
Published: 13 April 2021
Neurobiology of Stress, Volume 14; https://doi.org/10.1016/j.ynstr.2021.100326

The publisher has not yet granted permission to display this abstract.
Kuaikuai Duan, Enrico Premi, Andrea Pilotto, Viviana Cristillo, Alberto Benussi, Ilenia Libri, Marcello Giunta, H. Jeremy Bockholt, Jingyu Liu, Riccardo Campora, et al.
Published: 13 April 2021
Abstract:
COVID-19, the infectious disease caused by the most recently discovered severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has become a global pandemic. It dramatically affects people's health and daily life. Neurological complications are increasingly documented for patients with COVID-19. However, the effect of COVID-19 on the brain is less studied, and existing quantitative neuroimaging analyses of COVID-19 were mainly based on the univariate voxel-based morphometry analysis (VBM) that requires corrections for a large number of tests for statistical significance, multivariate approaches that can reduce the number of tests to be corrected have not been applied to study COVID-19 effect on the brain yet. In this study, we leveraged source-based morphometry (SBM) analysis, a multivariate extension of VBM, to identify changes derived from computed tomography scans in covarying gray matter volume patterns underlying COVID-19 in 120 neurological patients (including 58 cases with COVID-19 and 62 patients without COVID-19 matched for age, gender and diseases). SBM identified that lower gray matter volume (GMV) in superior/medial/middle frontal gyri was significantly associated with a higher level of disability (modified Rankin Scale) at both discharge and six months follow-up phases even when controlling for cerebrovascular diseases. GMV in superior/medial/middle frontal gyri was also significantly reduced in patients receiving oxygen therapy compared to patients not receiving oxygen therapy. Patients with fever presented significant GMV reduction in inferior/middle temporal gyri and fusiform gyrus compared to patients without fever. Patients with agitation showed GMV reduction in superior/medial/middle frontal gyri compared to patients without agitation. Patients with COVID-19 showed no significant GMV differences from patients without COVID-19 in any brain region. Results suggest that COVID-19 may affect the frontal-temporal network in a secondary manner through fever or lack of oxygen.
, on behalf of the “Cognitive and Behavioral Neurology” Study Group of the Italian Neurological Society, Gabriella Bottini, Maria Guarino, Eugenio Magni, Leonardo Pantoni
Published: 12 April 2021
Neurological Sciences pp 1-9; https://doi.org/10.1007/s10072-021-05231-0

The publisher has not yet granted permission to display this abstract.
, MRCP Benedict D. Michael PhD, Erica Westenberg Msc, Andrea S. Winkler Md, Global COVID‐19 Neuro Research Coalition, Benedict D. Michael, Tom Solomon, Erica Westenberg, Samuel Knauss, Jim Sejvar, et al.
Published: 9 April 2021
Annals of Neurology, Volume 89, pp 1059-1067; https://doi.org/10.1002/ana.26076

Abstract:
There is an accumulating volume of research into neurological manifestations of COVID‐19. However, inconsistent study designs, inadequate controls, poorly‐validated tests, and differing settings, interventions, and cultural norms weaken study quality, comparability, and thus the understanding of the spectrum, burden and pathophysiology of these complications. Therefore, a global COVID‐19 Neuro Research Coalition, together with the WHO, has reviewed reports of COVID‐19 neurological complications and harmonised clinical measures for future research. This will facilitate well‐designed studies using precise, consistent case definitions of SARS‐CoV2 infection and neurological complications, with standardised forms for pooled data analyses that non‐specialists can use, including in low‐income settings.
Neuroimaging of Covid-19. First Insights based on Clinical Cases pp 3-15; https://doi.org/10.1007/978-3-030-67521-9_2

The publisher has not yet granted permission to display this abstract.
, Benedict D Michael
Published: 1 March 2021
The Lancet Neurology, Volume 20, pp 172-172; https://doi.org/10.1016/s1474-4422(21)00040-5

The publisher has not yet granted permission to display this abstract.
, Romain Sonneville, Sérafima Vledouts, Pierre Jaquet, Anny Rouvel-Tallec, Marie-Pia D’Ortho
Published: 19 February 2021
Frontiers in Physiology, Volume 11; https://doi.org/10.3389/fphys.2020.622466

Abstract:
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread worldwide since the end of year 2019 and is currently responsive for coronavirus infectious disease 2019 (COVID-19). The first reports considered COVID-19 as a respiratory tract disease responsible for pneumonia, but numerous studies rapidly emerged to warn the medical community of COVID-19-associated neurological manifestations, including encephalopathy at the acute phase and other postinfectious manifestations. Using standard visual analysis or spectral analysis, recent studies reported electroencephalographic (EEG) findings of COVID-19 patients with various neurological symptoms. Most EEG recordings were normal or revealed non-specific abnormalities, such as focal or generalized slowing, interictal epileptic figures, seizures, or status epilepticus. Interestingly, novel EEG abnormalities over frontal areas were also described at the acute phase. Underlying mechanisms leading to brain injury in COVID-19 are still unknown and matters of debate. These frontal EEG abnormalities could emphasize the hypothesis whereby SARS-CoV-2 enters the central nervous system (CNS) through olfactory structures and then spreads in CNS via frontal lobes. This hypothesis is reinforced by the presence of anosmia in a significant proportion of COVID-19 patients and by neuroimaging studies confirming orbitofrontal abnormalities. COVID-19 represents a new viral disease characterized by not only respiratory symptoms but also a systemic invasion associated with extra-respiratory signs. Neurological symptoms must be the focus of our attention, and functional brain evaluation with EEG is crucial, in combination with anatomical and functional brain imaging, to better understand its pathophysiology. Evolution of symptoms together with EEG patterns at the distance of the acute episode should also be scrutinized.
Dean W. A. Walton, Kiran T. Thakur, Arun Venkatesan, Gerome Breen, Tom Solomon,
Published: 10 February 2021
Frontiers in Neurology, Volume 12; https://doi.org/10.3389/fneur.2021.637586

Abstract:
Over a century since the H1N1 influenza pandemic of 1918, we are in the midst of another global pandemic: COVID-19, caused by Severe Acute Respiratory Syndrome- Coronavirus−2 (SARS-CoV-2). While predominantly a respiratory illness, evidence of neurological conditions is arising and we are seeing a plethora of heterogeneous neurology with COVID-19. Analysis of past communicable disease outbreaks and contemporaneous reports will allow us to better understand the potential role of direct neuroinvasion. Encephalitis has been observed in previous viral pandemics and epidemics as well as seasonal Coronavirus outbreaks in rare cases. In three cases of encephalopathy with seizures Severe Acute Respiratory Syndrome- Coronavirus-1 (SARS-CoV-1) was identified through brain culture and reverse-transcription polymerase chain reaction (RT-PCR) of CSF (1–3). Three cases of Middle Eastern Respiratory Syndrome (MERS) displayed features of Acute Disseminated Encephalomyelitis (ADEM) and Bickerstaff's Encephalitis but did not find CSF evidence of viral nucleic acid by RT-PCR (4, 5). During the Influenza A pandemic of 2009 (H1N1), cases of Influenza-associated encephalopathy (IAE) increased nearly 7-fold compared to the average over the previous five seasons and seizures and encephalopathy were a common initial presentation among children (6–8). Furthermore, a seasonal coronavirus (OC43) is documented to have caused encephalitis in two immunodeficient children (9, 10). Lastly, although never proven, the 1918 pandemic caused by the H1N1 virus has been associated with the wave of encephalitis lethargica observed at the time (11). Given this history and these significant findings it is perhaps not surprising that we are seeing a multitude of neurological sequelae associated with the COVID-19 pandemic. However, correlation does not equal causation, and the challenge is distinguishing between neurological complications secondary to critical illness and those directly linked to the virus itself (12). The encephalitis syndromes seen with COVID-19 are heterogenous in their presentation (13). This undoubtedly represents varied underlying neuropathogenesis. Acute presentations are potentially a consequence of systemic pro-inflammatory cytokines transcending the blood-brain barrier (BBB) or due to direct viral invasion of the central nervous system (CNS) in a small number of cases (12, 14). Later, post-infectious presentations are more likely to be due to immune mediated processes operating through cellular or antibody pathways (6, 15). Since the first case of COVID-19 encephalitis was reported (16), in whom SARS-CoV-2 RNA was detected in CSF but not on nasopharyngeal RT-PCR, several other case studies have corroborated this phenomenon and demonstrated potential viral invasion as the cause in these cases by positive SARS-CoV-2 RT-PCR in CSF and tissue samples, and evidence of viral particles in neural cell bodies (1, 17, 18). A review article of 21 case reports, found that in 10 patients with proposed encephalitis in whom CSF RT-PCR for SARS-CoV-2 was performed, four were positive and the majority also tested positive for nasopharyngeal RNA (19). The review was critical of attributing symptomology to parenchymal invasion and support for this skepticism also comes from post-mortem data. A study of 43 patients observed marked neuroinflammation in the brainstem of COVID-19 patients at post-mortem with microglia activation and cytotoxic T cell infiltration (20). However, only 21 had evidence of SARS-CoV-2 RNA in post-mortem tissue by PCR and this was not associated with the severity of inflammatory histopathological changes. Moreover, detection of viral RNA in CNS tissue may reflect virus in the blood vessels of cerebral vasculature (as most tissues will have not undergone whole body perfusion via the left ventricle as would be undertaken in murine models) or passive viral entry through a disrupted BBB. Indeed, there is increasing evidence of BBB disruption in COVID-19 (21, 22). In addition to representing an alternative viral entry pathway to the CNS these presentations may represent systemic pro-inflammatory cytokines affecting the CNS, and hence para-infectious, inflammation and maybe also post-infectious antibody response directed against CNS antigens (12). A further case series of eight patients that examined SARS-CoV-2 antibody (Ab) titres in CSF and serum of COVID-19 patients found detectable SARS-CoV-2 Ab in the CSF of all eight patients but these samples were negative for SARS-CoV-2 by PCR (21). They also demonstrated high CSF titres comparable to serum in four of these patients and evidence of intrathecal synthesis in one patient. This scarcity of detecting SARS-CoV-2 by RT-PCR in CSF of encephalitis cases may reflect disease mechanisms other than direct invasion but alternatively could question the sensitivity of the test itself. Taken together, these findings highlight the importance of testing the CSF by both PCR and IgG/IgM, and of interpreting antibody findings relative to the concurrent serum titer and to the CSF:serum albumin ratio using Rieber's formula to confirm true intrathecal synthesis. Even prior to COVID-19, many cases of viral encephalitis were well-recognized to be negative in CSF by PCR but antibody positive, such as West Nile virus, and many other flaviviridae and coronaviridea. Nevertheless, in emerging zoonotic infections, such as SARS-CoV-2, in which the pathophysiology is in question, direct visualization of the virus, such as with fluorescent in-situ hybridization, remains the gold standard for confirming encephalitis with direct viral neurotropic invasion. There are now multiple case reports related to post-infectious phenomenon, such as ADEM (17, 23), limbic encephalitis (13, 24), autoimmune encephalitis (25, 26), and in some cases specific autoantibodies directed against CNS antigens have been identified (27). In the face of amassing evidence of encephalitis in COVID-19, rigorous critique of these case reports and series is needed as several studies lack vital investigations and report diagnoses with minimal evidence (13, 19). However, a common finding among multiple studies is that the presence of neurological complications in COVID-19 has a negative impact on outcomes and delays recovery, although the long-term impact of these complications is not yet known and whether delayed emergent, post-infectious, complications develop is unclear (28–30). As SARS-CoV-2 continues its unrelenting march we will undeniably see further evidence of neurological complications. Currently, while encephalitis cases are sparse it is pertinent that subsequent cases are all identified and meticulously documented in order to classify neurological sequelae in COVID-19. Standardized diagnostic frameworks, such as that proposed by Ellul et al., which utilize the World Health Organization COVID-19 case definitions and apply them to cover neurological clinical syndromes will be valuable for international comparisons of reported cases, case series, and cohort studies (11). In particular, it is important to distinguish between non-specific symptoms associated with critical illness regardless of etiology and those linked with SARS-CoV-2 directly or indirectly (12). Once classified, consolidating cases and the information they provide is imperative to draw comparisons, appreciate patterns and better understand the neuropathogenesis of COVID-19. Already there are examples of national observational, prospective multi-center, prospective cohort studies (15, 28, 31) that are evaluating the prevalence and outcomes of neurological complications in COVID-19. Efforts to systematically categorize and analyse all relevant publications on a weekly basis is also underway (32). Furthermore, national surveillance programmes that collect and collate neurological cases by allowing clinicians to easily and quickly identify patients in real time are powerful tools for timely appreciation of potential neurological complications of COVID-19; and those which span the clinical neurosciences—including psychiatry and neurosurgery—are of particular value when combating such a rapidly progressing global threat (33). Lastly, on-going research concerning longer term sequelae and underlying biology is necessary (34–36), especially since the H1N1 pandemic was followed by a wave of encephalitis lethargica that put a considerable strain on health services (37). While the end of this current pandemic often feels distant, we are hopeful that in the coming months more evidence will be accumulated for potential vaccine candidates. When this pandemic is over, we will need to prepare for future pandemics and epidemics, and ask ourselves- what can we learn from our experience of COVID-19's effects on the brain? In order to become more proficient and expedient at addressing viral outbreaks we must learn from current events; what has been done well in addition to shortcomings (36). Rapid and early identification of novel zoonoses or mutations is vital to limit spread; containment alone however may prove difficult, as demonstrated by SARS-CoV-2. Once a new threat has reached pandemic proportions, emphasis should turn toward international collaborative efforts of identification, classification, and knowledge sharing, especially with neurological complications where caseloads may be smaller (36, 38). It is only by implementing a worldwide collaborative response across the neuroscience community that we can tackle such a global disease. Even though this task appears daunting, with the tireless efforts of scientists, medical professionals and researchers what we learn now from this pandemic, even more than in previous pandemics, has the potential for us to be much better prepared for those pandemics yet to come. The final draft was written, reviewed, and approved by all authors. KT was supported by NINDS/NIH 1K23NS105935-01. AV was supported by research grants from the NIH, Maryland Stem Cell Research Fund, and U.S. Department of Defense. TS was supported by the European Union's Horizon 2020 research and innovation programme, ZikaPLAN (Preparedness Latin America Network; grant 734584), the National Institute for Health Research (NIHR) Global Health Research Group on Brain Infections (17/63/110) and the NIHR Health Protection Research Unit in Emerging and Zoonotic Infections at University of Liverpool. BM was supported by grants from the UKRI/MRC (COVID-CNS; MR/V03605X/1), Medical Research Council, Wellcome, and NIHR. 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This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. *Correspondence: Benedict Daniel Michael, [email protected]
, , Silvia Canovetti, Enrico Tagliaferri, Francesco Turco, Stefano Verdenelli, , Marta Franchi, Enrica Bonanni, Francesco Menichetti, et al.
Published: 24 January 2021
Brain, Behavior, & Immunity - Health, Volume 12, pp 100210-100210; https://doi.org/10.1016/j.bbih.2021.100210

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Tremor and Other Hyperkinetic Movements, Volume 11; https://doi.org/10.5334/tohm.595

Abstract:
Movement disorders are increasingly described in hospitalized and milder cases of SARS-CoV-2 infection, despite a very low prevalence compared to the total patients. We reviewed the scientific literature published in English, spanning from the initial descriptions of COVID-19 until January 25, 2021, in the PubMed/MEDLINE database. We identified 93 new-onset movement disorders cases (44 articles) from 200 papers screened in the database or reference lists. Myoclonus was present in 63.4% (n = 59), ataxia in 38.7% (n = 36), action/postural tremor in 10.8% (n = 10), rigid-akinetic syndrome in 5.38% (n = 5), oculomotor abnormalities in 20.4% (n = 19), catatonia in 2.1% (n = 2), dystonia in 1.1% (n = 1), chorea in 1.1% (n = 1), functional (psychogenic) movement disorders in 3.2% (n = 3) of the reported COVID-19 cases with any movement disorder. Encephalopathy was a common association (n = 37, 39.78%). Comprehensive neurophysiological, clinical, and neuroimaging descriptions of movement disorders in the setting of SARS-CoV-2 infection are still lacking, and their pathophysiology may be related to inflammatory, postinfectious, or even indirect mechanisms not specific to SARS-CoV-2, such as ischemic-hypoxic brain insults, drug effects, sepsis, kidney failure. Cortical/subcortical myoclonus, which the cited secondary mechanisms can largely cause, seems to be the most common hyperkinetic abnormal movement, and it might occur in association with encephalopathy and ataxia. This brief review contributes to the clinical description of SARS-CoV-2 potential neurological manifestations, assisting clinical neurologists in identifying features of these uncommon syndromes as a part of COVID-19 symptomatology. - Movement disorders are probably uncommon neurological manifestations in SARS-CoV-2 infection;- Myoclonus is the most reported movement disorder associated with COVID-19, its clinical complications or pharmacological management;- The pathophysiology is yet not well-understood but can include systemic inflammation, autoimmune mechanisms, or hypoxia.
Ishita Desai, Rajat Manchanda, , Ashutosh Tiwari,
Published: 11 January 2021
Neurological Sciences, Volume 42, pp 773-785; https://doi.org/10.1007/s10072-020-04964-8

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