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Medicina
Special Issues
Neuroinflammatory Disorders: New Insights and Future Directions
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Neuroinflammatory Disorders: New Insights and Future Directions

A special issue of Medicina (ISSN 1648-9144). This special issue belongs to the section "Neurology".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 1958

Special Issue Editors

Dr. Stefania Kalampokini

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Guest Editor
First Department of Neurology, Aristotle University of Thessaloniki, AHEPA University Hospital, Stilponos Kyriakidi 1, 54636 Thessaloniki, Greece
Interests: movement disorders; phenotype-genotype correlations; biomarkers; neuroinflammation; neuroimmunology; multiple sclerosis
Special Issues, Collections and Topics in MDPI journals
Dr. Effrosyni Koutsouraki

E-Mail Website
Guest Editor
First Department of Neurology, Aristotle University of Thessaloniki, AHEPA University Hospital, 54636 Thessaloniki, Greece
Interests: multiple sclerosis; cognitive disorders in multiple sclerosis; dementia; mild cognitive impairment; Alzheimer disease; neurocognitive disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroinflammatory disorders are a major concern for clinicians and particularly neurologists, as they are, in most cases, treatable diseases. Various neurological and/or psychiatric symptoms of subacute onset with or without systemic symptoms are proven to be of neuroimmunological origin, with a steadily expanding spectrum of antibodies related to immune-mediated disorders.

This Special Issue will cover, but is not restricted to, topics such as multiple sclerosis, neuromyelitis optica spectrum disorders, myelitis, autoimmune encephalitis, immune-mediated movement disorders, vaccine-related neurological manifestations, and inflammatory polyneuropathies. Our understanding of the mechanisms, pathophysiology, and therapeutic potential of these diseases is steadily increasing. A particularly interesting development is the evolution of diagnostic and treatment guidelines for conditions such as autoimmune encephalitis, which take into account the phenotypes of acute, short-term, and long-term sequelae. Moreover, interest in inflammatory sequelae of viral illnesses, such as SARS-CoV-2, has significantly increased, especially since the beginning of the COVID-19 pandemic and the recognition of the role of the Epstein–Barr virus in the pathophysiology of multiple sclerosis.

This Special Issue, entitled “Neuroinflammatory Disorders: New Insights and Future Directions”,  focuses on the pathophysiology, clinical presentation, including newly described clinical phenotypes, diagnostic biomarkers, and therapeutic management of inflammatory disorders that affect the central and peripheral nervous system. We will accept the submission of all types of articles (original research, reviews, communications, etc.) to this Special Issue.

Dr. Stefania Kalampokini
Dr. Effrosyni Koutsouraki
Guest Editors

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 250 words) can be sent to the Editorial Office for assessment.

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. Medicina is an international peer-reviewed open access monthly 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 2200 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

  • multiple sclerosis
  • neuromyelitis optica spectrum disorders
  • autoimmune encephalitis
  • myelitis
  • immune-mediated movement disorders
  • inflammatory polyneuropathies
  • vaccine-related

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Published Papers (3 papers)

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Research

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18 pages, 5116 KB  
Article
Amantadine Attenuates Secondary Oxidative and Inflammatory Injury by Modulating the HIF-1α/BNIP3L/HMGB1 Axis in Rat Model of Traumatic Brain Injury
by Ahmet Bindal, Pinar Karabacak, Halil Asci, Ilter Ilhan, Muhammet Yusuf Tepebasi, Orhan Imeci, Ahmet Yunus Hatip and Ozlem Ozmen
Medicina 2026, 62(2), 362; https://doi.org/10.3390/medicina62020362 - 11 Feb 2026
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Abstract
Background and Objectives: Traumatic brain injury (TBI) triggers oxidative stress, mitochondrial dysfunction, and sterile inflammation. Amantadine (ATD), a weak NMDA receptor antagonist, has shown neuroprotective potential, but its mechanistic basis remains unclear. This study examined whether ATD treatment is associated with changes in [...] Read more.
Background and Objectives: Traumatic brain injury (TBI) triggers oxidative stress, mitochondrial dysfunction, and sterile inflammation. Amantadine (ATD), a weak NMDA receptor antagonist, has shown neuroprotective potential, but its mechanistic basis remains unclear. This study examined whether ATD treatment is associated with changes in molecular and histological markers related to the HIF-1α/BNIP3L/HMGB1-mediated hypoxia–mitophagy–inflammation response in a rat TBI model. Materials and Methods: Thirty-two Wistar rats were assigned to four groups: sham, trauma, trauma + ATD (1 day), and trauma + ATD (7 days). TBI was induced using the impact-acceleration model, and ATD (45 mg/kg, i.p.) was administered post-injury. Oxidative stress indices (TOS, TAS, OSI), histopathology, inflammatory/apoptotic markers (CRP, TNF-α, Caspase-3), and gene expression (HIF-1α, BNIP3L, HMGB1) were evaluated. Results: ATD improved oxidative balance and histopathological integrity while reducing TNF-α, CRP, and Caspase-3 immunoreactivity. qPCR analysis showed lower HIF-1α, BNIP3L, and HMGB1 expression in ATD-treated groups, which is consistent with attenuation of hypoxia-related, mitochondrial stress-associated, and damage-associated molecular pattern-associated signaling after injury. Conclusions: In this experimental model, amantadine ameliorated oxidative, inflammatory, and apoptotic markers and was associated with reduced expression of HIF-1α, BNIP3L, and HMGB1. These findings support a mechanistic correlation between ATD treatment and suppression of secondary injury signatures; however, causal pathway relationships and functional neurological outcomes were not assessed. Full article
(This article belongs to the Special Issue Neuroinflammatory Disorders: New Insights and Future Directions)
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Review

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16 pages, 1995 KB  
Review
Current and Future Biomarkers in the Diagnosis of Autoimmune Encephalitis: A Review of Biomarker Detection Techniques and Their Performance
by Patricija Plačenytė, Nataša Giedraitienė and Mantas Vaišvilas
Medicina 2026, 62(5), 896; https://doi.org/10.3390/medicina62050896 - 6 May 2026
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Abstract
Autoimmune encephalitis is an increasingly recognized cause of encephalitis. Detection of disease-specific antibodies is the cornerstone of diagnosis. Despite growing clinical awareness and the routine availability of antibody assays in most centers, diagnosis remains challenging due to diverse clinical presentations, the low diagnostic [...] Read more.
Autoimmune encephalitis is an increasingly recognized cause of encephalitis. Detection of disease-specific antibodies is the cornerstone of diagnosis. Despite growing clinical awareness and the routine availability of antibody assays in most centers, diagnosis remains challenging due to diverse clinical presentations, the low diagnostic yield of commercial antibody kits, difficulties in interpreting antibody results, and a substantial proportion of paraclinically silent patients. This narrative review summarizes current diagnostic approaches to autoimmune encephalitis, with particular emphasis on antibody detection strategies, the diagnostic yield of different techniques, serum vs. cerebrospinal fluid testing, and the diagnostic value of supportive cerebrospinal fluid biomarkers. In addition, we discuss patients with seronegative or paraclinically silent disease, in whom diagnosis relies primarily on clinical criteria and the exclusion of alternative etiologies. Finally, we outline future perspectives, including advanced immunological techniques and machine learning-based diagnostic models, which may facilitate earlier identification and more accurate classification of autoimmune encephalitis. Improved integration of clinical assessment with cerebrospinal fluid biomarkers and novel analytical tools may reduce diagnostic delay and support the timely initiation of immunotherapy, ultimately improving neurological outcomes. Full article
(This article belongs to the Special Issue Neuroinflammatory Disorders: New Insights and Future Directions)
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Other

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17 pages, 758 KB  
Systematic Review
Movement Disorders in MOGAD: A Systematic Review
by Stefania Kalampokini, Antonis Frontistis, Antonis Pilavas, Iraklis Keramidiotis, Marianthi Arnaoutoglou, Vasilios K. Kimiskidis and Effrosyni Koutsouraki
Medicina 2026, 62(4), 693; https://doi.org/10.3390/medicina62040693 - 4 Apr 2026
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Abstract
Background and objectives: Movement disorders are an underrecognized phenomenon in Myelin Oligodendrocyte Glycoprotein-Associated Disease (MOGAD). The aim of this paper was to summarize all movement disorders previously described in MOGAD. Materials and Methods: We conducted a systematic literature search in PubMed, Web of [...] Read more.
Background and objectives: Movement disorders are an underrecognized phenomenon in Myelin Oligodendrocyte Glycoprotein-Associated Disease (MOGAD). The aim of this paper was to summarize all movement disorders previously described in MOGAD. Materials and Methods: We conducted a systematic literature search in PubMed, Web of Science, and Scopus in English, focusing on patients with MOGAD exhibiting a movement disorder, i.e., ataxia, tremor, dystonia, parkinsonism, chorea, athetosis, myoclonus, ballism, tics, stereotypies, dyskinesia. Results: We included 58 studies, with a total of 91 patients with MOGAD and a movement disorder (45.6% male, 54.4% female). Movement disorders had a mean latency of 2.1 years (±6.9, 0–42) after MOGAD onset; however, they could be the presenting feature (in approximately 70% of cases), especially in pediatric patients. Cerebellar ataxia was the most common movement disorder, occurring in 77 patients (84.6%). Tremor, postural and/or kinetic, was the second most common movement disorder (15%). Dystonia was reported in 8.8%, presenting as cervical, or limb dystonia or stereotyped dystonic episodes. Myoclonus and hypokinetic movement disorders were rare. Subcortical (in 60%), brainstem and cerebellar lesions (in 50% respectively) were the most common imaging findings. The most common accompanying symptoms were encephalopathy, fever and headache. Approximately half of the patients made a full recovery, and the other half showed a significant improvement in the movement disorder after immunomodulatory treatment, most commonly steroids. Conclusions: The new onset of a movement disorder, especially ataxia, in a young patient should prompt the search for MOGAD or can indicate a relapse in patients with an established diagnosis. Full article
(This article belongs to the Special Issue Neuroinflammatory Disorders: New Insights and Future Directions)
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