Clinical and Experimental Neuroimmunology最新文献

{"title":"Trial of cytotoxic T cell induction in mice as an ex vivo model of paraneoplastic neurologic syndrome with anti-Hu antibodies","authors":"Keiko Tanaka,&nbsp;Takashi Tani,&nbsp;Katsuhiko Ogawa,&nbsp;Masako Kinoshita,&nbsp;Masami Tanaka","doi":"10.1111/cen3.12702","DOIUrl":"10.1111/cen3.12702","url":null,"abstract":"<p>The pathogenesis of neuronal damage in anti-Hu-antibody-positive paraneoplastic neurologic syndrome (Hu-PNS) is thought to be mediated by cytotoxic T lymphocyte (CTL). However, there is no direct evidence showing that antigen-specific T cells are the effector against neurons. Antigen-specific CTL-mediated cell death has been observed in cancer immunology, but not as a neurological disease model. The CTL-mediated etiology in PNS should be confirmed using in vivo model systems in the future. Herein, we present an ex vivo model of antigen-specific CTL against cultured neurons. A previous study showed the CTL activity of CD8⁺ T cells taken from the peripheral blood of patients with Hu-antibody-positive PNS against Hu-protein-derived-peptide-expressing autologous fibroblasts. Results revealed that the HuD peptide, which can bind to major histocompatibility complex (MHC) class I of Balb/c mice, stimulated CD8⁺ T cells collected from mice immunized with peptide-bound self-activated dendritic cells with murine CD40 ligand-transduced adenovirus vectors (AdmCD40L). Moreover, CTL activity against autologous neurons in culture was observed. Hence, this result could be used in the development of an in vivo model of CTL-induced neurological disorders, which can help in further understanding the pathogenesis of PNS.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47213572","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":"The coincidence of Guillain-Barré syndrome and myasthenia gravis","authors":"Majed Alluqmani","doi":"10.1111/cen3.12699","DOIUrl":"10.1111/cen3.12699","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The occurrence of both Guillain-Barré syndrome (GBS) and myasthenia gravis (MG) in the same individual is rare. The underlying pathophysiology of this case was assumed to be an autoimmune humoral mechanism. Molecular mimicry, in which a cross-reaction occurs between autoantibodies and the myelin sheath of peripheral nerves and acetylcholine receptors of the neuromuscular junction, cannot be excluded as an underlying cause.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case presentation</h3>\u0000 \u0000 <p>An 18-year-old female presented with symptoms of generalized weakness and distal weakness in both upper and lower extremities, more pronounced on the right side, and with associated right foot drop and bilateral ptosis. An electrophysiological study was performed and the acetylcholine receptor antibody titer determined. The patient was diagnosed with GBS and MG.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>GBS and MG are two different neurological entities with different pathophysiologies. New-onset or persistence of symptoms in a patient with GBS treated with intravenous immunoglobulins or plasmapheresis should prompt a probe for another autoimmune neurological illness, particularly autoimmune neuromuscular disorders such as MG.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46645819","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":"Weston Hurst hemorrhagic leukoencephalitis: A novel association with mixed connective tissue disease: uncloaking the “unholy” etiology underneath","authors":"Ritwik Ghosh,&nbsp;Subhankar Chatterjee,&nbsp;Dipayan Roy,&nbsp;Josef Finsterer,&nbsp;Durjoy Lahiri,&nbsp;Souvik Dubey,&nbsp;Julián Benito-León","doi":"10.1111/cen3.12701","DOIUrl":"10.1111/cen3.12701","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Weston Hurst syndrome (WHS), also known as acute hemorrhagic leukoencephalitis (AHLE), has not been previously associated with mixed connective tissue disease (MCTD), a rare rheumatologic disorder.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case presentation</h3>\u0000 \u0000 <p>We report a case of a 35-year-old female who presented with deep coma with features of previously undiagnosed MCTD and responded favorably to intravenous immunoglobulin (IVIG) therapy. On detailed historical enquiry, clinical examination, and investigation, AHLE was diagnosed. Furthermore, our patient showed significant improvement with IVIG administration, even though initial steroid therapy was unsuccessful.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>AHLE, an associated novel neurological manifestation of MCTD, can be responsive to IVIG, which makes this case reportable from the diagnostic as well as the therapeutic point of view.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41739663","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":"Post-infectious cerebellar ataxia following COVID-19 in a patient with epilepsy","authors":"Sidhartha Chattopadhyay,&nbsp;Judhajit Sengupta,&nbsp;Sagar Basu","doi":"10.1111/cen3.12700","DOIUrl":"10.1111/cen3.12700","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Various neurological manifestations have been described in relation to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and coronavirus disease 2019 (COVID-19). However, the development of cerebellar ataxia after recovery from COVID-19 is rare. We present a case of cerebellar ataxia 3 weeks after recovery from COVID-19.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>A 70-year-old male patient from an urban area of India presented with ataxia. He was hypertensive and had been receiving treatment for post-traumatic epilepsy for the previous 3 years. He had previously had laboratory-confirmed COVID-19 infection with mild symptoms that resolved within 2 weeks. However, 3 weeks after symptom improvement, he developed severe pan-cerebellar ataxia. Investigations were suggestive of post-infectious cerebellar ataxia. Other causes of ataxia were excluded. He responded well to pulse methylprednisolone therapy and was discharged with mild tremor and ataxia.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Post-infectious cerebellar ataxia is an unusual presentation after COVID-19. The clinician should be aware of such complications following COVID-19 infection as early diagnosis and proper management leads to better outcomes in many patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.12700","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84609674","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":"Prominent D-dimer elevation and pretibial edema related to alemtuzumab treatment: A case report and literature review","authors":"Merve Aktan Suzgun,&nbsp;Sami Omerhoca,&nbsp;Nilufer Kale,&nbsp;Ugur Uygunoglu","doi":"10.1111/cen3.12698","DOIUrl":"10.1111/cen3.12698","url":null,"abstract":"<p>Alemtuzumab is one of the most effective agents in the treatment of multiple sclerosis (MS). On the other hand, the spectrum of possible side effects is wide and carries the potential to cause a variety of inflammatory and thrombotic complications. In this report firstly, a case who developed a systemic thrombotic and inflammatory response after alemtuzumab administration and then presented with pretibial edema in a period of 1 month is discussed. Then, based on the findings detected via this case, the possible side effects of alemtuzumab, both during drug infusion and in the early and late periods after administration, were classified. This classification was created by compiling the reported adverse effects in the literature related to the use of alemtuzumab for the treatment of multiple sclerosis. This presented case shows that prothrombotic predisposition after alemtuzumab administration may result in peripheral microvascular circulatory disorders even in the long term and one of them is pretibial edema. According to the current literature data, side effects of alemtuzumab treatment which is used for multiple sclerosis are categorized as follows: (i) infusion-related reactions, (ii) acute/subacute inflammatory and pro-thrombotic effects, (iii) immunosuppression-related opportunistic infections, (iv) immune reconstitution-related secondary autoimmune disorders. Increasing awareness of the possible side effects of alemtuzumab treatment used in the course of multiple sclerosis will enable both the development of possible prophylactic treatment options and the early control of emerging complications.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42420876","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":"Familial cold autoinflammatory syndrome and multiple sclerosis","authors":"Syed Basharat Ali,&nbsp;Debajyoti Chaudhuri,&nbsp;Deborah Field,&nbsp;Pravin Hissaria","doi":"10.1111/cen3.12697","DOIUrl":"10.1111/cen3.12697","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Cryopyrin-associated periodic syndrome (CAPS) is an autoinflammatory disorder with a spectrum ranging from the milder familial cold auto-inflammatory syndrome (FCAS) phenotype to the more severe Muckle–Wells Syndrome. Although headaches are the most common neurological symptoms, neuroinflammatory diseases such as multiple sclerosis (MS) have only been reported in the more severe phenotypes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>We describe a 43-year-old male diagnosed with relapse-remitting MS who developed cold-induced arthralgias and urticaria. He initially presented with facial numbness and arthralgias in his late teenage years, and brain magnetic resonance imaging (MRI) demonstrated multiple lesions with periventricular white matter extension. Oligoclonal bands were detected in the cerebrospinal fluid (CSF). Symptoms gradually improved, and a decade later he presented with numbness at upper limbs and tongue. Brain and spine MRI showed new lesions, but CSF was unremarkable. He was started on interferon β-1a with symptomatic improvement until another flare around 13 years later. Treatment was changed to dimethyl fumarate. During this hospitalization, urticaria was problematic and particularly associated with cold temperatures. This raised suspicion for possible CAPS and subsequently confirmed with an A439V mutation in the <i>NLRP3</i> gene, consistent with FCAS. Anakinra was started but was not tolerated because of localized reactions despite desensitization. His serum amyloid A was mildly elevated at 9 mg/L (reference range 0–6). He remains stable from a neurological perspective, including imaging, and continues dimethyl fumarate.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>To date, FCAS and possible association with MS has not been described. The case raises challenges in the diagnosis of concurrent disease processes. It also highlights that neurological sequelae should be considered in all spectrums of CAPS, and distinctions with MS should be made where possible.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.12697","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48133131","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 “Nerve conduction studies support the classification of SARSCoV-2 associated Guillain-Barre subtypes”","authors":"Gustavo Figueiredo da Silva,&nbsp;Caroline Figueiredo da Silva,&nbsp;Raddib Eduardo Noleto da Nobrega Oliveira,&nbsp;Fabiana Romancini,&nbsp;Rafael Marques Mendes,&nbsp;Amanda Locks,&nbsp;Maria Francisca Moro Longo,&nbsp;Carla Heloisa Cabral Moro,&nbsp;Alexandre Luiz Longo,&nbsp;Vera Lucia Braatz","doi":"10.1111/cen3.12696","DOIUrl":"10.1111/cen3.12696","url":null,"abstract":"<p>We read with interest the comments made by Finsterer et al.<span>¹</span> on our previously published case report “Guillain–Barré syndrome after coronavirus disease 2019 vaccine: A temporal association”.<span>²</span> We understand that the comments made are interesting points of discussion.</p><p>The main point questioned by Finsterer et al., the diagnosis of Guillain-Barré syndrome (GBS) as a temporal association, not necessarily causal, can be elucidated due to several components. First, due to the time the article was written, in which there were not as many cases reported in the literature as currently, as correctly described in the letter “In a recent review of the neurological side effects of SARS-CoV-2 vaccines, 300 cases of SC2VaG were described”.<span>¹</span> Second, due to limited diagnostic resources in the case, a public hospital in southern Brazil. The absence of diagnostic tests, such as those mentioned by Finsterer et al. (electroneuromyography, investigation of cytokines, chemokines and glial markers in the CSF), are factors that must be highlighted before defining the causality of the association. Added to the two previous points is the sensitivity to the moment of the pandemic in which the article was produced. The beginning of an important vaccination campaign, in the midst of the growth of anti-vaccine groups, inspires caution when associating causality without the possibility of ruling out, through more elaborate tests, other causes. Finally, the level of evidence that a case report has in comparison to other scientific productions is highlighted. Then, for a reliable correlation between the SARS-CoV-2 vaccine and GBS, studies with a higher level of evidence are necessary, such as randomized clinical trials and systematic reviews.<span>³</span></p><p>Furthermore, it is noteworthy that the delay between the onset of symptoms and diagnosis was due to the patient having interpreted the initial changes as of psychiatric origin, taking 2 months to seek the medical service of reference in the region. Thus, there is a consensus among us authors that the delay in diagnosis and treatment, as well highlighted by Finsterer et al., may have been one of the factors that led to worse outcome. The authors also emphasize that the findings of the patient's neurological physical examination are those described in the article, so, those not mentioned, such as the involvement of several pairs of cranial nerves, were not present.</p><p>Therefore, for all the reasons mentioned above and despite the interesting and pertinent comments made by Finsterer et al., the authors adopted a more cautious approach and, thus, defined the case as a temporal association, not necessarily a causal one.</p><p>None declared.</p><p>All authors are in agreement with the content of the manuscript. All authors participated in the data acquisition and analysis, and contributed to the drafting of the manuscript.</p><p>All i","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.12696","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88201654","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":"Efficacy of monoclonal antibodies in neuromyelitis optica: An updated systematic review with meta-analysis","authors":"Prajjwol Luitel,&nbsp;Anup Ghimire,&nbsp;Devansh Upadhyay,&nbsp;Rajeev Ojha","doi":"10.1111/cen3.12695","DOIUrl":"10.1111/cen3.12695","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This is a critical review of studies aiming to assess the safety and efficacy of monoclonal antibodies as compared with the classical regimen in patients with neuromyelitis optica spectrum disorder.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Various electronic databases were searched for original articles reporting results from the use of monoclonal antibodies in neuromyelitis optica spectrum disorder. The Expanded Disability Status Scale and annualized relapse rate score before and after treatment were the primary effect measures. The pooled standardized mean difference with 95% CI was calculated using the random effects model. The heterogeneity of the included studies was calculated using Cochran's Q test and <i>I</i>² statistics.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Of 36 included studies, meta-analysis was carried out from 27 studies. The pooled analysis of 1010 patients showed a mean reduction in the mean annualized relapse rate ratio after tocilizumab therapy −2.45 (95% CI −3.13 to −1.77) to be higher compared with rituximab −1.49 (95% CI −1.81 to −1.17). Likewise, the mean reduction in the Expanded Disability Status Scale after tocilizumab was higher −1.10 (95% CI −1.75 to −0.44) compared with rituximab −0.80 (95% CI −1.11 to −0.48).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Tocilizumab has a greater effect than rituximab in terms of the reduction of the annualized relapse rate and Expanded Disability Status Scale in neuromyelitis optica spectrum disorder patients. The greater efficacy of tocilizumab could result from its multiple dynamic pharmacodynamics (i.e. its effect on interleukin-6-dependent inflammatory processes, involving CD20-negative plasmablasts, pathogenic T cells and regulatory T cells) and to some degree due to heterogeneity in our study. Satralizumab (monotherapy or add-on), eculizumab and inebilizumab (monotherapy) are effective in aquaporin-4-positive cases with good safety profiles. Ublituximab, bortezomib, bevacizumab and C1-esterase inhibitors are both effective and safe add-on drugs.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47131061","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":"Demyelinating neuropathy requires differential diagnosis with vasculitic neuropathy in rheumatoid arthritis: Significance of sural nerve electrophysiology findings","authors":"Masaki Kobayashi,&nbsp;Megumi Takeuchi,&nbsp;Miki Suzuki,&nbsp;Kazuo Kitagawa","doi":"10.1111/cen3.12694","DOIUrl":"10.1111/cen3.12694","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Neuropathy is considered a complication of rheumatoid arthritis (RA), whose underlying mechanisms are mainly entrapment, drug-induced and rheumatoid vasculitis (RV). At Tokyo Women's Medical University, for the purpose of diagnosing vasculitic neuropathy, we carried out nerve and muscle biopsies in nine RA patients. Unexpectedly, we found three cases of demyelinating neuropathy, together with six cases of RV. Our aim was to investigate the neurophysiological features of demyelinating neuropathy in patients with RA, compared with those of patients with RV.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We reviewed the pathological, clinical and electrophysiological findings in patients with RA who underwent nerve and muscle biopsies. We compared patient demographics and nerve conduction study findings between patients with RV and other patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The histological findings showed necrotizing vasculitis in six of nine patients. Vasculitis was absent in the other three patients, which showed evidence of demyelination and remyelination. The absence of a sensory nerve action potential and compound motor action potential were observed more frequently in the RV cohort. Sural sparing, shown as the sural-to-median sensory nerve action potential ratio, was significantly higher in demyelinating neuropathy patients. Treatment was corticosteroid and cyclophosphamide in RV patients, and intravenous immunoglobulin was administered to three demyelinating neuropathy patients. Treatment response was satisfactory in seven of the nine patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Demyelinating neuropathy was found more often in patients with RA neuropathy than expected. Sural nerve sparing, as well as the absence of sensory nerve action potential or compound motor action potential, are useful for the differential diagnosis of demyelinating neuropathy with RV in RA patients with neuropathy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41665364","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":"A thank you note to our reviewers","authors":"","doi":"10.1111/cen3.12689","DOIUrl":"10.1111/cen3.12689","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.12689","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41587506","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}