Intracranial aneurysms (IAs) may afflict up to 5% of the general population, or up to 15 million individuals in the US. The two forms of IAs that can be recognized by their shape are saccular and nonsaccular IAs, with uncommon aneurysm types, fusiform and dissecting aneurysms, comprising 13% of nonsaccular IAs. Conceivably, among the various risk factors for IA development, vessel wall inflammation represents a major cause. Accordingly, IAs may not necessarily be the result of passive widening of vessel wall structures, but may also be the result of inflammation and tissue degeneration. Thus, flow-induced vascular remodeling during IA pathogenesis may reflect immune cell infiltration and consequent release of proinflammatory cytokine, chemokine, and matrix metalloproteinase that contribute to vessel wall degeneration and weakening. Thus, infiltrating neutrophils, macrophages, T-lymphocytes and complement factors, and the resulting immune microenvironment may be pertinent in IA pathogenesis.
{"title":"Immunocellular microenvironment of the vascular wall of cerebral aneurysms: What is the role of inflammatory cells in aneurysmal remodeling?","authors":"Vivig Shantha Kumar, Nerella Resheek, Vignarth Shantha Kumar, Ruthvik Thaghalli Sunil Kumar","doi":"10.1111/cen3.12789","DOIUrl":"https://doi.org/10.1111/cen3.12789","url":null,"abstract":"<p>Intracranial aneurysms (IAs) may afflict up to 5% of the general population, or up to 15 million individuals in the US. The two forms of IAs that can be recognized by their shape are saccular and nonsaccular IAs, with uncommon aneurysm types, fusiform and dissecting aneurysms, comprising 13% of nonsaccular IAs. Conceivably, among the various risk factors for IA development, vessel wall inflammation represents a major cause. Accordingly, IAs may not necessarily be the result of passive widening of vessel wall structures, but may also be the result of inflammation and tissue degeneration. Thus, flow-induced vascular remodeling during IA pathogenesis may reflect immune cell infiltration and consequent release of proinflammatory cytokine, chemokine, and matrix metalloproteinase that contribute to vessel wall degeneration and weakening. Thus, infiltrating neutrophils, macrophages, T-lymphocytes and complement factors, and the resulting immune microenvironment may be pertinent in IA pathogenesis.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 2","pages":"135-147"},"PeriodicalIF":0.0,"publicationDate":"2024-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143919404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yukihiro Nishikawa, Kimiko Hasegawa, Hiroki Abe, Shun Matsuzawa, Takuya Isayama, Ran Nakashima, Yoshihiko Saito, Ichizo Nishino, Masataka Kuwana
Objectives
A variety of myositis-specific autoantibodies have been identified in sera from patients with idiopathic inflammatory myopathies, and they play a crucial role in tailoring personalized disease management. In particular, autoantibodies against 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) are now recognized as a key tool for diagnosing immune-mediated necrotizing myopathy. The current gold standard for detecting anti-HMGCR autoantibodies involves immunoprecipitation (IP) using radiolabeled proteins from cell extracts or purified proteins produced by in vitro transcription/translation (IVTT). Unfortunately, this radioisotope labeling is technically intricate and not suitable for routine laboratory use. To address this, we developed a novel assay called “Bio-IVTT-IP” for detecting anti-HMGCR autoantibodies, which uses a nonradioactive biotinylated recombinant HMGCR protein produced by IVTT.
Methods
We collected 14 clinical specimens containing anti-HMGCR autoantibodies from patients with immune-mediated necrotizing myopathy, which were validated using the gold standard IP assay, and a set of 35 control samples from patients with other autoimmune diseases, such as systemic lupus erythematosus.
Results
The Bio-IVTT-IP assay successfully identified 14 clinical samples positive for anti-HMGCR. We confirmed that the performance of the Bio-IVTT-IP assay was completely consistent with that of the gold standard IP assay using radiolabeled proteins. Notably, no immunoprecipitates were found in control samples from patients with other autoimmune diseases.
Conclusions
These findings show that the Bio-IVTT-IP assay can serve as a potential alternative to the gold standard IP assay for detecting anti-HMGCR autoantibodies. It can be considered a practical immunodiagnostic tool for diagnosing immune-mediated necrotizing myopathy, particularly owing to its accessibility in routine laboratory settings.
{"title":"Development of an immunoprecipitation assay for detecting anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase autoantibodies using a non-radioactive biotinylated recombinant protein","authors":"Yukihiro Nishikawa, Kimiko Hasegawa, Hiroki Abe, Shun Matsuzawa, Takuya Isayama, Ran Nakashima, Yoshihiko Saito, Ichizo Nishino, Masataka Kuwana","doi":"10.1111/cen3.12810","DOIUrl":"https://doi.org/10.1111/cen3.12810","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>A variety of myositis-specific autoantibodies have been identified in sera from patients with idiopathic inflammatory myopathies, and they play a crucial role in tailoring personalized disease management. In particular, autoantibodies against 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) are now recognized as a key tool for diagnosing immune-mediated necrotizing myopathy. The current gold standard for detecting anti-HMGCR autoantibodies involves immunoprecipitation (IP) using radiolabeled proteins from cell extracts or purified proteins produced by <i>in vitro</i> transcription/translation (IVTT). Unfortunately, this radioisotope labeling is technically intricate and not suitable for routine laboratory use. To address this, we developed a novel assay called “Bio-IVTT-IP” for detecting anti-HMGCR autoantibodies, which uses a nonradioactive biotinylated recombinant HMGCR protein produced by IVTT.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We collected 14 clinical specimens containing anti-HMGCR autoantibodies from patients with immune-mediated necrotizing myopathy, which were validated using the gold standard IP assay, and a set of 35 control samples from patients with other autoimmune diseases, such as systemic lupus erythematosus.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The Bio-IVTT-IP assay successfully identified 14 clinical samples positive for anti-HMGCR. We confirmed that the performance of the Bio-IVTT-IP assay was completely consistent with that of the gold standard IP assay using radiolabeled proteins. Notably, no immunoprecipitates were found in control samples from patients with other autoimmune diseases.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These findings show that the Bio-IVTT-IP assay can serve as a potential alternative to the gold standard IP assay for detecting anti-HMGCR autoantibodies. It can be considered a practical immunodiagnostic tool for diagnosing immune-mediated necrotizing myopathy, particularly owing to its accessibility in routine laboratory settings.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 2","pages":"88-97"},"PeriodicalIF":0.0,"publicationDate":"2024-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.12810","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143919856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stroke and traumatic brain injury leave many survivors with permanent neurological disabilities, and the development of therapeutics to enhance functional recovery is needed. Both residential and infiltrating immune cells participate in the acute inflammation after brain injury, exacerbating functional outcomes; however, some immune cells have been reported to alter their characteristic to a reparative phenotype. This review focused on the recent findings of the reparative immunity of myeloid cells. Functional recovery after injury is achieved through the combination of resolution of inflammation, reorganization of neuronal network, white matter repair, angiogenesis and extracellular matrix reorganization. In each process, myeloid cells play vital roles in leading to functional recovery. Further research on the diversity of immune cells implicated in neural repair will be promising to develop therapeutics enhancing functional recovery after brain tissue injuries.
{"title":"Role of myeloid cells in neural repair after brain tissue injury","authors":"Ryuki Koyama, Takashi Shichita","doi":"10.1111/cen3.12808","DOIUrl":"https://doi.org/10.1111/cen3.12808","url":null,"abstract":"<p>Stroke and traumatic brain injury leave many survivors with permanent neurological disabilities, and the development of therapeutics to enhance functional recovery is needed. Both residential and infiltrating immune cells participate in the acute inflammation after brain injury, exacerbating functional outcomes; however, some immune cells have been reported to alter their characteristic to a reparative phenotype. This review focused on the recent findings of the reparative immunity of myeloid cells. Functional recovery after injury is achieved through the combination of resolution of inflammation, reorganization of neuronal network, white matter repair, angiogenesis and extracellular matrix reorganization. In each process, myeloid cells play vital roles in leading to functional recovery. Further research on the diversity of immune cells implicated in neural repair will be promising to develop therapeutics enhancing functional recovery after brain tissue injuries.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"15 4","pages":"215-221"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Eculizumab use throughout pregnancy in two patients with aquaporin-4-positive neuromyelitis optica spectrum disorder","authors":"Takeshi Fujimoto, Yasuhiro Maeda","doi":"10.1111/cen3.12809","DOIUrl":"https://doi.org/10.1111/cen3.12809","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 1","pages":"6"},"PeriodicalIF":0.0,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143456002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lucas C. Adam, Lana Gilly, Joerg Mueller, Joerg Wissel, Anatol Kivi
Background
Rasmussen's encephalitis (RE) is a rare autoimmune encephalopathy typically manifesting in early childhood, causing unilateral autoimmune inflammation of the cerebral cortex, leading to progressive neurological deficits, notably focal epileptic seizures. The late-onset variant of RE in adults progresses slower and presents atypical features. Despite extensive research, the etiology remains elusive, hindering accurate diagnosis and treatment options.
Case Presentation
We present a biopsy-confirmed late-onset variant of RE case in a 71-year-old man with a disease course of 12 years. After the initiation of intravenous immunoglobulin therapy and immunosuppressive treatment, disease stabilization was achieved, as evidenced by clinical assessments and imaging. Initially, the affected hemisphere swelled hyperacutely, followed by years of atrophic encephalopathy stabilizing into a residual state, with emerging focal disease signs in the contralateral hemisphere. Multimodal rehabilitation and immune therapy attenuated brain atrophy and reduced signal enhancement.
Conclusions
Late-onset variant of RE rehabilitation remains underdeveloped, focusing on symptom management and functional recovery post-surgery. Longitudinal imaging is crucial for monitoring immune therapy response in clinical practice.
拉斯穆森脑炎（Rasmussen's encephalitis，RE）是一种罕见的自身免疫性脑病，通常在儿童早期发病，引起单侧大脑皮层自身免疫性炎症，导致进行性神经功能缺损，尤其是局灶性癫痫发作。成人的晚发性变异型 RE 进展较慢，并表现出非典型特征。尽管进行了大量研究，但病因仍然难以捉摸，妨碍了准确诊断和治疗方案的选择。我们报告了一例经活检证实的晚发型RE病例，患者为一名71岁的男性，病程长达12年。在接受静脉注射免疫球蛋白治疗和免疫抑制治疗后，病情趋于稳定，临床评估和影像学检查均证实了这一点。起初，受影响的半球出现急性肿胀，随后经过多年的萎缩性脑病稳定为残留状态，对侧半球出现病灶性疾病征兆。多模式康复和免疫疗法减轻了脑萎缩，降低了信号增强。晚发性变异性RE康复治疗仍未得到充分发展，主要集中在症状管理和术后功能恢复方面。在临床实践中，纵向成像对于监测免疫疗法的反应至关重要。
{"title":"Longitudinal imaging for monitoring disease activity in late-onset Rasmussen's encephalitis during multimodal rehabilitation and immune therapy","authors":"Lucas C. Adam, Lana Gilly, Joerg Mueller, Joerg Wissel, Anatol Kivi","doi":"10.1111/cen3.12805","DOIUrl":"10.1111/cen3.12805","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Rasmussen's encephalitis (RE) is a rare autoimmune encephalopathy typically manifesting in early childhood, causing unilateral autoimmune inflammation of the cerebral cortex, leading to progressive neurological deficits, notably focal epileptic seizures. The late-onset variant of RE in adults progresses slower and presents atypical features. Despite extensive research, the etiology remains elusive, hindering accurate diagnosis and treatment options.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>We present a biopsy-confirmed late-onset variant of RE case in a 71-year-old man with a disease course of 12 years. After the initiation of intravenous immunoglobulin therapy and immunosuppressive treatment, disease stabilization was achieved, as evidenced by clinical assessments and imaging. Initially, the affected hemisphere swelled hyperacutely, followed by years of atrophic encephalopathy stabilizing into a residual state, with emerging focal disease signs in the contralateral hemisphere. Multimodal rehabilitation and immune therapy attenuated brain atrophy and reduced signal enhancement.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Late-onset variant of RE rehabilitation remains underdeveloped, focusing on symptom management and functional recovery post-surgery. Longitudinal imaging is crucial for monitoring immune therapy response in clinical practice.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 1","pages":"35-41"},"PeriodicalIF":0.0,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.12805","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141828015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Response to: Eculizumab use throughout pregnancy in two patients with aquaporin-4-positive neuromyelitis optica spectrum disorder","authors":"Ilya Kister, Alla Wilson","doi":"10.1111/cen3.12807","DOIUrl":"10.1111/cen3.12807","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 1","pages":"4-5"},"PeriodicalIF":0.0,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141661504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Myasthenia gravis (MG) is an autoimmune disorder mediated by antibodies against the acetylcholine receptor (AChR), muscle specific kinase (MuSK), and other antigens in the neuromuscular junction. Antibody production is influenced by T lymphocytes. The T helper 17 (Th17) subset, an inflammatory lineage of Th cells, is associated with several autoimmune diseases. Functional interactions between T lymphocytes and pathogenic antibody responses including aberrant Th17 cell responses have been reported in MG. However, the precise mechanism(s) underlying the activation and/or pathogenic transformation of Th17 cells are not clearly known. The current study aimed at simultaneously exploring the roles of the inducers, master regulator transcription factors, and effectors of Th17 cells in patients with MG.
Methods
In this cross-sectional study, quantification of gene expression of IL6, IL17A, STAT3, and RORC in the peripheral mononuclear cells by quantitative polymerase chain reaction (qPCR) as well as estimation of plasma levels of IL-1β, IL-6, and IL-17A cytokines by multiplex suspension assay were carried out in 59 patients with MG and 61 healthy controls.
Results
Gene expression levels of IL17A were significantly upregulated in patients as compared to healthy controls. The plasma levels of IL-1β, IL-6, and IL-17A were significantly elevated in patients compared to healthy controls. IL17A as well as RORC gene expressions correlated with the clinical features. IL17A gene expression levels were higher in AChR-MG patients.
Conclusion
The present study supports the crucial role of the Th17 pathway in the pathobiology of MG, including its potential influence on disease severity.
{"title":"Th17 pathway-related immune signatures in the pathobiology of myasthenia gravis: Integrating the roles of regulatory/effector cytokines and transcription factors","authors":"Nibu Varghese, Madhu Nagappa, Nikhitha Sreenivas, Saikat Dey, Thrinath Mullapudi, Anagha Pettututhazhe Kuniyil, Sumanth Shivaram, Doniparthi V. Seshagiri, Binu Valsalakumari Sreekumaran Nair, Monojit Debnath","doi":"10.1111/cen3.12804","DOIUrl":"10.1111/cen3.12804","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Myasthenia gravis (MG) is an autoimmune disorder mediated by antibodies against the acetylcholine receptor (AChR), muscle specific kinase (MuSK), and other antigens in the neuromuscular junction. Antibody production is influenced by T lymphocytes. The T helper 17 (Th17) subset, an inflammatory lineage of Th cells, is associated with several autoimmune diseases. Functional interactions between T lymphocytes and pathogenic antibody responses including aberrant Th17 cell responses have been reported in MG. However, the precise mechanism(s) underlying the activation and/or pathogenic transformation of Th17 cells are not clearly known. The current study aimed at simultaneously exploring the roles of the inducers, master regulator transcription factors, and effectors of Th17 cells in patients with MG.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this cross-sectional study, quantification of gene expression of <i>IL6, IL17A, STAT3,</i> and <i>RORC</i> in the peripheral mononuclear cells by quantitative polymerase chain reaction (qPCR) as well as estimation of plasma levels of IL-1β, IL-6, and IL-17A cytokines by multiplex suspension assay were carried out in 59 patients with MG and 61 healthy controls.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Gene expression levels of <i>IL17A</i> were significantly upregulated in patients as compared to healthy controls. The plasma levels of IL-1β, IL-6, and IL-17A were significantly elevated in patients compared to healthy controls. <i>IL17A</i> as well as <i>RORC</i> gene expressions correlated with the clinical features. <i>IL17A</i> gene expression levels were higher in AChR-MG patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The present study supports the crucial role of the Th17 pathway in the pathobiology of MG, including its potential influence on disease severity.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 1","pages":"7-18"},"PeriodicalIF":0.0,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141667298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Bickerstaff brainstem encephalitis (BBE) is an autoimmune disease affecting the brainstem, typically caused by a prior infection. However, BBE after coronavirus disease 2019 (COVID-19) infection is rare. Here, we present a severe case of BBE after COVID-19 infection, highlighted by increased levels of CXCL-10.
Case Presentation
A 28-year-old woman presented with symptoms of cold and fever lasting 5 days, accompanied by numbness, weakness and unsteadiness in the distal parts of her limbs before being admitted. Upon admission, her condition was classified with a Glasgow Coma Scale score of E1V1M4, absence of bilateral ocular cephalic reflexes, eyes fixed in the midline position and pathological reflex in lower limbs. COVID-19 antigen tests were positive, and cerebrospinal fluid CXCL-10 levels were elevated. Positive serum anti-GQ1b antibodies, along with other clinical findings, confirmed the diagnosis of BBE. Initial treatment with high-dose intravenous immunoglobulin was ineffective, leading to mechanical ventilation on day 2 from admission. Additional steroid pulse therapy and plasmapheresis were initiated on day 7. Communication abilities were restored by day 19, and the patient was extubated on day 21. Continuous alleviation of symptoms was observed, with no sequelae at discharge on day 42.
Conclusions
BBE related to COVID-19 with high CXCL-10 levels can become severe. However, early intensive immunotherapy, including plasmapheresis, might result in favorable prognosis.
{"title":"Successful treatment with plasmapheresis of severe Bickerstaff brainstem encephalitis with high cerebrospinal fluid CXCL-10 levels after COVID-19 infection: A case report","authors":"Naoki Iijima, Kenzo Sakurai, Riyoko Ko, Kenji Isahaya, Yoshihisa Yamano","doi":"10.1111/cen3.12806","DOIUrl":"10.1111/cen3.12806","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Bickerstaff brainstem encephalitis (BBE) is an autoimmune disease affecting the brainstem, typically caused by a prior infection. However, BBE after coronavirus disease 2019 (COVID-19) infection is rare. Here, we present a severe case of BBE after COVID-19 infection, highlighted by increased levels of CXCL-10.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>A 28-year-old woman presented with symptoms of cold and fever lasting 5 days, accompanied by numbness, weakness and unsteadiness in the distal parts of her limbs before being admitted. Upon admission, her condition was classified with a Glasgow Coma Scale score of E1V1M4, absence of bilateral ocular cephalic reflexes, eyes fixed in the midline position and pathological reflex in lower limbs. COVID-19 antigen tests were positive, and cerebrospinal fluid CXCL-10 levels were elevated. Positive serum anti-GQ1b antibodies, along with other clinical findings, confirmed the diagnosis of BBE. Initial treatment with high-dose intravenous immunoglobulin was ineffective, leading to mechanical ventilation on day 2 from admission. Additional steroid pulse therapy and plasmapheresis were initiated on day 7. Communication abilities were restored by day 19, and the patient was extubated on day 21. Continuous alleviation of symptoms was observed, with no sequelae at discharge on day 42.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>BBE related to COVID-19 with high CXCL-10 levels can become severe. However, early intensive immunotherapy, including plasmapheresis, might result in favorable prognosis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 1","pages":"30-34"},"PeriodicalIF":0.0,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141668079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cerebrovascular alterations in acute bacterial meningitis significantly contribute to adverse patient outcomes, with reported complication rates ranging from 10% to 29%. Focal alterations in arterial lumens, leading to vasoconstriction, are common in cerebral ischemic and inflammatory conditions, such as bacterial meningitis, presenting neurological complications, such as seizures, brain swelling, hydrocephalus, hearing loss and ischemic or hemorrhagic brain damage. The observed arterial narrowing during meningitis is attributed to diverse factors, including direct encroachment by inflammatory exudate, vascular wall edema, vasospasm, and vasculitis due to cellular infiltration and vessel remodeling. Early-stage constriction might result from a watery exudate's encroachment, whereas persistent inflammation leads to thicker exudates, attracting inflammatory cells and inducing arteriopathic growth factor synthesis. This process promotes structural modifications in the vessel wall, progressing from subintimal infiltration to organic intimal thickening, culminating in vasculitis and the risk of cerebral ischemia. Accordingly, this review seeks to more clearly delineate the intricate relationship between subarachnoid space inflammation and acute and chronic vessel wall remodeling during bacterial meningitis. Conceivably, understanding this pathological process holds promise in unveiling potential treatment avenues to improve patient outcomes, and reduced morbidity and mortality associated with cerebrovascular complications during bacterial meningitis.
{"title":"Intensity of subarachnoid space inflammation corresponds to the evolution of vessel wall remodeling during the acute and chronic phases of bacterial meningitis","authors":"Vivig Shantha Kumar, Vignarth Shantha Kumar, Ruthvik Thaghalli Sunil Kumar","doi":"10.1111/cen3.12794","DOIUrl":"10.1111/cen3.12794","url":null,"abstract":"<p>Cerebrovascular alterations in acute bacterial meningitis significantly contribute to adverse patient outcomes, with reported complication rates ranging from 10% to 29%. Focal alterations in arterial lumens, leading to vasoconstriction, are common in cerebral ischemic and inflammatory conditions, such as bacterial meningitis, presenting neurological complications, such as seizures, brain swelling, hydrocephalus, hearing loss and ischemic or hemorrhagic brain damage. The observed arterial narrowing during meningitis is attributed to diverse factors, including direct encroachment by inflammatory exudate, vascular wall edema, vasospasm, and vasculitis due to cellular infiltration and vessel remodeling. Early-stage constriction might result from a watery exudate's encroachment, whereas persistent inflammation leads to thicker exudates, attracting inflammatory cells and inducing arteriopathic growth factor synthesis. This process promotes structural modifications in the vessel wall, progressing from subintimal infiltration to organic intimal thickening, culminating in vasculitis and the risk of cerebral ischemia. Accordingly, this review seeks to more clearly delineate the intricate relationship between subarachnoid space inflammation and acute and chronic vessel wall remodeling during bacterial meningitis. Conceivably, understanding this pathological process holds promise in unveiling potential treatment avenues to improve patient outcomes, and reduced morbidity and mortality associated with cerebrovascular complications during bacterial meningitis.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 1","pages":"19-29"},"PeriodicalIF":0.0,"publicationDate":"2024-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141670127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号