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Neurology International
Special Issues
COVID-19, Neuroinflammation and Therapeutics, 2nd Edition
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COVID-19, Neuroinflammation and Therapeutics, 2nd Edition

A special issue of Neurology International (ISSN 2035-8377).

Deadline for manuscript submissions: 31 October 2024 | Viewed by 3420

Special Issue Editor

Dr. Yasir Rehman

E-Mail Website
Guest Editor
Department of Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, ON, Canada
Interests: anatomy; physiology; pathology; neuromuscular examination
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are living in the throes of COVID-19, with new variants and complications emerging regularly. With a continuously growing knowledge base due to information gathered from epidemiological studies, randomized controlled trials (RCTs), observational studies, case reports, and meta-analytical reviews, new light has been shed on different aspects of the direct and indirect disease burden associated with COVID-19. Although primarily a disease of the respiratory system, systematic inflammatory and immune responses have also emerged as a result of COVID-19; this indicates that its manifestations are diverse and affect multiple systems, including the nervous system.

This Special Issue aims to fill knowledge gaps on COVID-19. We are inviting research papers, including reports, observational studies, RCTs, reviews (including narrative reviews), and meta-analytical reviews, that provide novel insights into the clinical features, treatments, therapeutics, and inflammatory biomarkers of COVID-19 (e.g., through laboratory-, neuroimaging-, or neurophysiology-based approaches).

Bringing this new research to the forefront of the scientific community will enhance our understanding of this virus and its effects, especially those related to its neurological complications.

Dr. Yasir Rehman
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Neurology International is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • COVID-19
  • SARS-CoV-2 infection
  • neuroinflammation
  • neuroimaging
  • neurophysiology

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Published Papers (3 papers)

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Research

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13 pages, 1724 KiB  
Article
Cerebrovascular Reactivity Assessed by Breath-Hold Functional MRI in Patients with Neurological Post-COVID-19 Syndrome—A Pilot Study
by Leonie Zerweck, Uwe Klose, Annerose Mengel, Tobias Hoheisel, Melinda Eikemeier, Vivien Richter, Natalie Sophie Joos, Ulrike Ernemann, Benjamin Bender and Till-Karsten Hauser
Neurol. Int. 2024, 16(5), 992-1004; https://doi.org/10.3390/neurolint16050075 - 9 Sep 2024
Viewed by 293
Abstract
Endothelial dysfunction represents a potential pathomechanism of neurological post-COVID-19 syndrome (PCS). A recent study demonstrated reduced cerebrovascular reactivity (CVR) in patients with PCS. The aim of this pilot study was to prospectively assess CVR in patients with PCS using breath-hold functional MRI (bh-fMRI). [...] Read more.
Endothelial dysfunction represents a potential pathomechanism of neurological post-COVID-19 syndrome (PCS). A recent study demonstrated reduced cerebrovascular reactivity (CVR) in patients with PCS. The aim of this pilot study was to prospectively assess CVR in patients with PCS using breath-hold functional MRI (bh-fMRI). Fourteen patients with neurological PCS and leading symptoms of fatigue/memory issues/concentration disorder (PCSfmc), 11 patients with PCS and leading symptoms of myopathy/neuropathy (PCSmn), and 17 healthy controls underwent bh-fMRI. Signal change and time to peak (TTP) were assessed globally and in seven regions of interest and compared between the subgroups using one-way ANCOVA adjusting for age, time since infection, Fazekas score, and sex. No significant differences were observed. In PCS patients, the global CVR exhibited a slight, non-significant tendency to be lower compared to healthy controls (PCSfmc: 0.78 ± 0.11%, PCSmn: 0.84 ± 0.10% and 0.87 ± 0.07%). There was a non-significant trend towards lower global TTP values in the PCS subgroups than in the control group (PCSfmc: 26.41 ± 1.39 s, PCSmn: 26.32 ± 1.36 s versus 29.52 ± 0.93 s). Endothelial dysfunction does not seem to be the sole pathomechanism of neurological symptoms in PCS. Further studies in larger cohorts are required. Full article
(This article belongs to the Special Issue COVID-19, Neuroinflammation and Therapeutics, 2nd Edition)
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16 pages, 522 KiB  
Article
Long Neurocognitive and Neuropsychiatric Sequelae in Participants with Post-COVID-19 Infection: A Longitudinal Study
by Marta Almeria, Juan Carlos Cejudo, Joan Deus and Jerzy Krupinski
Neurol. Int. 2024, 16(4), 853-868; https://doi.org/10.3390/neurolint16040064 - 16 Aug 2024
Viewed by 580
Abstract
Objective: To evaluate and characterize the cognitive changes in COVID-19 participants at 6-month follow-up, and to explore a possible association with clinical symptoms, emotional disturbance and disease severity. Methods: This single-center longitudinal cohort study included participants aged 20 and 60 years old to [...] Read more.
Objective: To evaluate and characterize the cognitive changes in COVID-19 participants at 6-month follow-up, and to explore a possible association with clinical symptoms, emotional disturbance and disease severity. Methods: This single-center longitudinal cohort study included participants aged 20 and 60 years old to exclude cognitive impairment age-associated with confirmed COVID-19 infection. The initial evaluation occurred 10 to 30 days after hospital or ambulatory discharge, with a subsequent follow-up at 6 months. Patients who had a history of cognitive impairment, neurological conditions, or serious psychiatric disorders were not included. Information on demographics and laboratory results was gathered from medical records. Cognitive outcomes were assessed with a neuropsychological battery including attention, verbal and visual memory, language and executive function tests. Results: A total of 200 participants were included in the study, and 108 completed the follow-up visit. At the 6-month follow-up, comparing the means from baseline with those of the follow-up evaluation, significant overall improvement was observed in verbal and visual memory subtests (p = 0.001), processing speed (p = 0.001), executive function (p = 0.028; p = 0.016) and naming (p = 0.001), independently of disease severity and cognitive complaints. Anxiety and depression were significantly higher in groups with Subjective Cognitive Complaints (SCC) compared to those without (p < 0.01 for both). Conclusions: Persistent symptoms are common regardless of disease severity and are often linked to cognitive complaints. Six months after COVID-19, the most frequently reported symptoms included headache, dyspnea, fatigue, cognitive complaints, anxiety, and depression. No cognitive impairment was found to be associated with the severity of COVID-19. Overall, neuropsychological and psychopathological improvement was observed at 6 months regardless of disease severity and cognitive complaints. Full article
(This article belongs to the Special Issue COVID-19, Neuroinflammation and Therapeutics, 2nd Edition)
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Review

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14 pages, 969 KiB  
Review
Decoding Post-Viral Fatigue: The Basal Ganglia’s Complex Role in Long-COVID
by Thorsten Rudroff
Neurol. Int. 2024, 16(2), 380-393; https://doi.org/10.3390/neurolint16020028 - 28 Mar 2024
Viewed by 2013
Abstract
Long-COVID afflicts millions with relentless fatigue, disrupting daily life. The objective of this narrative review is to synthesize current evidence on the role of the basal ganglia in long-COVID fatigue, discuss potential mechanisms, and highlight promising therapeutic interventions. A comprehensive literature search was [...] Read more.
Long-COVID afflicts millions with relentless fatigue, disrupting daily life. The objective of this narrative review is to synthesize current evidence on the role of the basal ganglia in long-COVID fatigue, discuss potential mechanisms, and highlight promising therapeutic interventions. A comprehensive literature search was conducted using PubMed, Scopus, and Web of Science databases. Mounting evidence from PET, MRI, and functional connectivity data reveals basal ganglia disturbances in long-COVID exhaustion, including inflammation, metabolic disruption, volume changes, and network alterations focused on striatal dopamine circuitry regulating motivation. Theories suggest inflammation-induced signaling disturbances could impede effort/reward valuation, disrupt cortical–subcortical motivational pathways, or diminish excitatory input to arousal centers, attenuating drive initiation. Recent therapeutic pilots targeting basal ganglia abnormalities show provisional efficacy. However, heterogeneous outcomes, inconsistent metrics, and perceived versus objective fatigue discrepancies temper insights. Despite the growing research, gaps remain in understanding the precise pathways linking basal ganglia dysfunction to fatigue and validating treatment efficacy. Further research is needed to advance understanding of the basal ganglia’s contribution to long-COVID neurological sequelae and offer hope for improving function across the expanding affected population. Full article
(This article belongs to the Special Issue COVID-19, Neuroinflammation and Therapeutics, 2nd Edition)
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