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Clinical and imaging features of children with autoimmune encephalitis and MOG antibodies | Neurology Neuroimmunology & Neuroinflammation

Clinical and imaging features of children with autoimmune encephalitis and MOG antibodies | Neurology Neuroimmunology & Neuroinflammation | AntiNMDA | Scoop.it
From nn.neurology.org - May 11, 2020 11:17 AM
Abstract Objective To describe the presentations, radiologic features, and outcomes of children with autoimmune encephalitis associated with myelin oligodendrocyte glycoprotein antibodies (MOG abs). Methods Identification of children fulfilling the diagnostic criteria for possible autoimmune encephalitis (AE) and testing positive for serum MOG abs. Chart review and comprehensive analysis of serum MOG abs using live cell assays and rat brain immunohistochemistry. Results Ten children (4 girls, 6 boys) with AE and serum MOG abs were identified. The median age at onset was 8.0 years (range: 4–16 years). Children presented with a combination of encephalopathy (10/10), headache (7/10), focal neurologic signs (7/10), or seizures (6/10). CSF pleocytosis was common (9/10, median 80 white cell count/μL, range: 21–256). Imaging showed cortical and deep gray matter involvement in all in addition to juxtacortical signal alterations in 6/10 children. No involvement of other white matter structures or contrast enhancement was noted. MOG abs were detected in all children (median titer 1:640; range: 1:320–1:10,540). Nine children had a favorable outcome at discharge (modified Rankin scale of < 2). Five of 10 children had up to 3 additional demyelinating relapses associated with persisting MOG abs. One child had NMDA receptor (NMDAR) abs at initial presentation. A second child had a third demyelinating episode with MOG abs with overlapping NMDAR encephalitis. Discussion AE associated with serum MOG abs represents a distinct form of autoantibody-mediated encephalitis in children. We therefore recommend including MOG abs testing in the workup of children with suspected AE. Glossary ab=antibody; ADEM=acute disseminated encephalomyelitis; ADS=acquired demyelinating syndrome; AE=autoimmune encephalitis; AQP4=aquaporin 4; CBA=cell-based assay; FLAIR=fluid-attenuated inversion recovery; FLAMES=unilateral FLAIR-hyperintense Lesions in Anti-MOG-associated Encephalitis with seizures; HSV=herpes simplex virus; IVIG=IV immunoglobulins; IVMP=IV methylprednisolone; MOG=myelin oligodendrocyte glycoprotein; MOG-SD=MOG spectrum disease; mRS=modified Rankin scale; NMDAR=NMDA receptor; NMOSD=neuromyelitis optica spectrum disorders; ON=optic neuritis; TBA=tissue-based screening; WCC=white cell count During the past decade, antibodies (abs) against myelin oligodendrocyte glycoprotein (MOG) have been described in different subgroups of acquired demyelinating syndromes (ADSs) distinct from aquaporin 4 (AQP4) abs-associated syndromes and MS.1,2 MOG spectrum diseases (MOG-SDs) manifest primarily in children with isolated or recurrent optic neuritis (ON), isolated or combined with myelitis, or acute disseminated encephalomyelitis (ADEM).3,–,7 The defining features of ADEM are the presence of encephalopathy, polyfocal neurologic signs, and typical MRI findings.8,9 Relapsing forms other than MS in children which are nearly always associated with MOG abs include multiphasic ADEM, ADEM followed by optic neuritis (ADEMON), and AQP-4 negative neuromyelitis optica spectrum diseases (NMOSDs).5,10,11 More recently, adult studies described patients with autoimmune encephalitis (AE), MOG abs, and MRI features such as cortical involvement of the brain.12,–,14 One study reported 3 adult patients with encephalitis, unilateral cerebral cortical lesions, and epileptic seizures in association with MOG abs.12 Recently, Budhram et al.15 reported an adult patient with MOG abs, encephalitis, seizures, and unilateral cortical involvement terming the acronym FLAMES (unilateral fluid-attenuated inversion recovery [FLAIR]-hyperintense Lesions in Anti-MOG-associated Encephalitis with seizures) after a detailed literature review of similar cases. Reports of children with clinical and radiologic presentations in the context of MOG abs are limited. In a recent study of 18 patients with ab-mediated encephalitis, 2 children with unilateral cortical involvement on MRI and MOG abs were identified.16 The aim of this study was to describe the clinical features, treatment response, outcome, and the neuroradiologic features of 10 children presenting with encephalitis associated with MOG abs. Methods Patients We identified 10 pediatric patients who (1) fulfilled the criteria of possible AE,17 (2) were tested positive for serum MOG abs, (3) had brain MRI findings primarily restricted to the cortical and deep gray matter structures, and (4) showed no involvement of deep white or periventricular white matter areas, cerebellum, brainstem, or spinal cord at initial presentation, thus failing the classification criteria for ADEM. Nine children were followed prospectively, and one child was identified retrospectively (Pat 1, table). Three children were primarily seen at the Children's Hospital Datteln (A.W.-P., A.B., and K.R.) where testing of MOG abs is routinely performed in patients with ADS and encephalitis. One child was initially included in the GENERATE study—a study focusing on patients presenting with encephalitis in which testing for MOG abs is also included. In the remaining 6 children, MOG ab testing was performed as part of a locally established protocol and discovered by chance with the exception of patient 7 who had previously a MOG ab-positive ON. All 7 children were referred to the attention of the senior author (K.R.) because of the unusual combination of clinical findings, MOG ab positivity, and cortical involvement as seen on MRI. All children had virologic, bacterial, and immunologic workup according to the local guidelines. Clinical features, laboratory, and neuroimaging findings performed in the first 48 hours of clinical presentation and outcome of all children were reviewed. Severity at onset and outcome at the last clinical evaluation was measured with the modified Rankin scale (mRS).18 View inline View popup Table Demographic, clinical data, laboratory findings, and MRI features of children with MOG-E Serological studies In 9 children, serum MOG ab testing was performed using live cell-based assays (CBAs), and end point titrations were performed as previously described.19 Median titers in patients with and without relapses were compared using Mann-Whitney U tests (GraphPad Prism 8). Serum MOG abs were tested in one child with a fixed CBA (Euroimmun, Lübeck, Germany), and this titer was not included in the statistics. CSF was available in 7 children and tested with live CBAs.19 Tissue-based screening (TBA) for neuronal surface abs in serum and CSF using rat brain was performed in 7/10 children. Nine of 10 children (7 serum and CSF, 2 serum only) were examined by commercially available biochips (Euroimmun) for the following antigens: NMDA receptor (NMDAR) consisting of NR1 subunits only, GAD65, LGI1, CASPR2, AMPAR subunit 2, γ-aminobutyric acid-B receptors, and glycine receptors.20 MRI MRI scans were evaluated by 3 neuroradiologists (A.W.-P., R.C., and M.B.). All reviewers were blinded for the patients' clinical data. Minimum requirements of the brain MRI sequences for inclusion were axial T2, axial FLAIR, sagittal T2, diffusion-weighted, and contrast-enhanced axial T1 images, which were not administered in one child. In 2 children, the MRI was performed on scanners with a field strength of 1.0 T, in 6 with 1.5 T and in 2 with 3.0 T. In 8 patients, spinal cord MRI was performed. Distribution of lesions was assessed regarding the involvement of certain regions such as cortical gray matter, juxtacortical, deep and periventricular white matter, corpus callosum, thalamus, basal ganglia, brainstem, and cerebellum.21 Furthermore, the following features were recorded: (1) areas of restricted diffusion (high signal on diffusion-weighted imaging and low signal on apparent diffusion coefficient) and (2) gadolinium-enhancing lesions. Spinal MRI was analyzed for the presence of transverse myelitis (figure 1). Figure 1 Clinical details and brain MRI from patient 1 with autoimmune encephalitis and serum myelin oligodendrocyte glycoprotein (MOG) antibodies Cerebral MRI of a 14-year-old girl (Pat 1) who presented to the emergency department with severe headache, mental status changes, and seizures. Fluid-attenuated inversion recovery image shows pronounced signal alterations and effacement of the cortical gray matter, particularly in the right temporal-parietal lobe (A). In addition, increased signal intensity was noted on signal diffusion weighted-imaging, but no corresponding hypointense apparent diffusion coefficient areas reflecting vasogenic edema rather than cytotoxic injury (B and C). Contrast enhancement of the right temporal-parietal lobe was not seen (D). Four months later, she developed a third episode with sudden onset of memory problems, aggression, sleeping problems, and social withdrawal. Autoantibody studies in CSF and serum revealed NMDA receptor antibodies (abs) in addition to serum MOG abs. MRI of the brain showed a new and large T2 signal alteration in the pons with contrast enhancement (E and F). She was treated with steroids and rituximab. A fourth episode occurred 2 years and 10 months after the initial onset with dizziness and ataxia. Cerebral MRI showed a new patchy T2-hyperintense signal in the right pons and in the left cerebellar white matter (G and H). All lesions resolved completely without residuals. Since the third relapse, she was treated with subcutaneous immunoglobulins. Standard protocol approvals, registrations, and patient consents This study was approved by the Ethics Committee of the Witten/Herdecke University, Germany (BIOMARKER-Study number AN4059). All caregivers gave informed consent. One patient was included in the GENERATE-study (study number EK 26-16) approved by the Ethics Committee of the Medical University RWTH Aachen, Germany. Data availability All relevant data generated or analyzed are included in this published article. Further anonymized data will be shared upon request from any qualified investigator. Results We identified 10 children fulfilling the criteria of possible AE17 in whom as part of the workup serum MOG abs were found. The cohort consisted of 4 female and 6 male patients with a median age at onset of 8.0 years (range: 4–16 years). Five of 10 children had signs of a mild preceding infection affecting the upper respiratory or gastrointestinal tract (table and figure 2). Figure 2 Clinical details and brain MRI from patient 2 with autoimmune encephalitis and serum myelin oligodendrocyte glycoprotein antibodies First cerebral MRI of a 12-year-old boy (Pat 2) with encephalopathy, fever, and ataxia reveals generalized edema of the cerebral cortex and the basal ganglia including the caudate nucleus, putamen, and globus pallidum. The initial examination was superimposed with strong movement artifacts, despite which the cortical edema can still be noted in the shown fluid-attenuated inversion recovery images (A and B). The second MRI of the brain performed 7 days later after treatment with high-dose cortisone and immunoglobulins still showed cortical involvement of the right fronto-temporal lobe (C). In the diffusion-weighted images, “T2-shine-through” (D) but no apparent diffusion coefficient (ADC) signal depression was found. In addition, a single new central pontine lesion was noted in the sagittal T2 images with increased signal intensity in diffusion-weighted imaging and ADC signal depression this time as a sign of cytotoxic injury (E and F) but still without contrast enhancement. In the third MRI of the brain performed 18 days after admission, the central pontine lesion was still present (G and H) associated with ADC depression (not shown). All children presented with signs of encephalopathy associated with fever (temperature > 38.5°C) (8/10), severe headache (7/10), febrile or afebrile seizures (6/10), and neurologic symptoms, including ataxia, hemiparesis, or dysarthria (7/10). The modified Rankin scale (mRS) in the initial phase was 3 (n = 1), 4 (n = 7), and 5 (n = 2). Four children were referred temporarily to the intensive care unit. CSF pleocytosis (>4 white cell count/μL) was detected in 9/10 children with a median of 80 cells/μL (range: 21–256). CSF protein was elevated in 3 children (range: 56–120 mg/dL). EEG was performed in 9 children, revealing generalized or focal slowing in 7/9 children in the first 48 hours of the presentation. Epileptic discharges were recorded only in one child in the acute phase. EEG recording in all children normalized after steroid treatment. Search for different pathogens in stool, throat swab, serum, and CSF was undertaken in all children including Herpes simplex virus (HSV)-PCR, which was negative in all. In addition to antibiotic and antiviral therapy, 8/10 children were treated with high-dose IV methylprednisolone (IVMP) for 3 to 5 days with a daily dose of 20 mg/kg (maximum 1 g/d). One child received IV immunoglobulins (IVIG; 2 g/kg/bodyweight) given for 5 days. At 4 weeks, 9 children had a favorable neurologic outcome (mRS 1), and one child had a residual left-sided hemiparesis (mRS 2) needing further rehabilitation. This child only received the diagnosis of MOG encephalitis 4 years later and had not been treated with IVMP nor IVIG at the time (supplementary file 1, Pat 1, links.lww.com/NXI/A245). The follow-up interval was between 6 and 48 months in all children with an average follow-up of 20 months. Five children had a monophasic disease course, and 5 children relapsed. Time to 1 relapse was between 2 and 30 months. Two children developed one relapse, one child had 2 relapses, and one child had 3 relapses, and all were diagnosed with relapsing MOG-SD. In one child (Pat 7), MOG encephalitis developed after an initial episode of unilateral ON 3 months earlier. Two children with relapsing episodes were started on disease-modifying therapies. One child receives monthly subcutaneous immunoglobulins (0.85 g/kg/mo) (table, Pat 1). The other child was started on rituximab with a dose of 375 mg/m2 body surface area and 7 consecutive applications (table, Pat 5). Serum MOG abs were detected in the acute phase in all children with a median titer of 1:640 (range: 1:320–1:10,240). In the 5 children with a monophasic course, all serum MOG ab titers declined to below 1:160 during the median follow-up interval of 11 months (range: 6–24). In 2 children with one further relapsing event, serum MOG abs dropped to undetectable levels (<1:40) after 6 and 10 months, respectively. In the other 3 children with relapsing events, MOG ab titers remained in the range of 1:320 and 1:640 over a follow-up period of 33 months (range: 9–48 months). At the time of the last relapse or last follow-up, median MOG serum titers were higher in patients with relapses (median 640, 95% CI 320–10,240) than in patients without relapses (median 60, 95% CI 20–160, p = 0.016). In 7 children, MOG abs were also tested in CSF (table) with no apparent intrathecal synthesis. Serum and/or CSF samples of 3/7 children reacted strongly with rat epitopes of MOG, showing a myelin staining pattern, which was not observed in any of the other 4/7 children tested using rat brain immunohistochemistry. Of note, one child also had NMDAR abs in serum and CSF (titer 1:10 in CBA and confirmed in TBA). Interestingly, although this child presented primarily with somnolence, increasing headache, and seizures, hallucinations were also described in the acute phase (table, Pat 4). NMDAR abs were found in one other child in CSF and serum who developed symptoms suggestive of NMDAR encephalitis in addition to MOG encephalitis (Pat 1, see below). In both children, subsequent testing for serum NMDAR abs 12 (Pat 1) and 4 months later was negative (Pat 4). MRI findings in children with encephalitis and MOG abs at disease onset MRI was performed in 6 different hospitals. All children had involvement of the cerebral cortex and to a lesser extent of deep gray matter structures, including the thalami (3/10). In addition to cortical involvement, a small rim of the adjacent juxtacortical white matter was affected in 6/10 children. In none of the children additional lesions in the corpus callosum, deep, or periventricular white matter were detected. Involvement of the optic nerves, brainstem, cerebellum, or spinal cord was also not noted. Bilateral limbic involvement of both hippocampi was present in one patient (table, Pat 3, figure 3). Figure 3 Clinical details and brain MRI from patient 3 with autoimmune encephalitis and serum myelin oligodendrocyte glycoprotein (MOG) antibodies MRI of the brain of a previously healthy 16-year-old boy (Pat 3) who presented to the emergency department with a 6-day history of severe right-sided headache shows bilateral signal alterations in both hippocampi, particularly in the coronal fluid-attenuated inversion recovery sequences more pronounced on the right than left side (A). In the T2-weighted images, the alterations are less pronounced (C). Diffusion restriction or contrast medium enhancement was not noted in this patient (B and D). Follow-up MRI of the brain 3 months later did not reveal any abnormalities (not shown). Diffusion restrictions were not found, and pathologic contrast enhancement was absent in all patients, except for a single case with presumed hemorrhagic and unilateral encephalitis (table, Pat 4, figure 4D) in whom vascular leakage resulted in contrast medium accumulation with no lesion-specific pattern. This child had a single lesion affecting the left temporal cortical and juxtacortical region. Figure 4 Clinical details and brain MRI from patient 4 with autoimmune encephalitis and serum myelin oligodendrocyte glycoprotein antibodies Brain MRI of a 10-year-old boy (Pat 4) with focal seizures, encephalopathy, and fever revealed a large hyperintense lesion of the right insular cortex and the adjacent juxtacortical white matter (A, fluid-attenuated inversion recovery). In the diffusion-weighted images, there is “T2-shine-through” but no apparent diffusion coefficient signal depression and therefore no diffusion restriction (B and C). This was the only patient in whom after administration of contrast agent, a streaky, garland-like contrast enhancement in the area of the insular cortex and the juxtacortical white matter on the right was noted (D). We assume that vascular leakage resulted in contrast medium accumulation with no lesion-specific pattern. In this patient, no other areas of the brain were affected. Distribution of lesions was unilateral in 4 children and bilateral in 6 children. The anatomical localization of the cortical changes in the initial MRI of the brain was mostly parietal (8/10), less frequently frontal (7/10), temporal (5/10), and occipital (3/10). The insular cortex was affected in 6 children. In the first available MRI study, several radiologic features were noted in all children: (1) involvement of cortical and deep gray matter structures often associated with juxtacortical signal changes, (2) absent diffusion restriction, (3) no involvement of the optic nerves or other white matter structures such as deep white and periventricular matter, spinal cord, and (4) no lesional contrast enhancement. Case presentation of 3 children with MOG encephalitis In the supplemental material, we describe the clinical presentations and further course of 3 patients (see supplementary file 1, links.lww.com/NXI/A245, Pat 1–3, table). Discussion Here, we describe the clinical characteristics, neuroimaging features, and outcome of children presenting with AE associated with MOG abs, which were distinct from ADEM associated with MOG abs. All children had a brief prodromal period associated often with severe headache, followed by impairment of consciousness associated with other neurologic symptoms and seizures. All children fulfilled the criteria for possible AE as proposed by Graus et al.17 Children presenting with a presumed encephalitis require immediate treatment to improve neurologic outcome. The differential diagnosis entails pathogen-driven diseases and autoimmune-mediated diseases. In particular, ab-mediated forms of encephalitis have been shown in several studies to be important causes.17,22 On clinical grounds and standard laboratory testing, the different entities cannot be separated with a high degree of certainty. MRI plays an important role in the first assessment of patients presenting with clinical signs of encephalitis. Our analysis of the imaging studies of children with MOG encephalitis shows that these children have a radiologic pattern that is distinct from pathogen-induced encephalitis, other forms of ab-mediated AE or ADEM. All children in our sample showed involvement of cortical region with absent diffusion restriction and contrast enhancement. In addition to optic nerves, white matter structures such as deep white were not affected initially, which is in contrast to children with ADEM and MOG abs. Imaging in MOG-positive ADEM is characterized by hazy, large lesions confined to subcortical and deep white areas in addition to areas including the spinal cord. Here, cortical areas can be affected too but not exclusively, as shown previously.9,10 MRI findings in HSV encephalitis are mainly restricted to the temporal lobes affecting cortical and white matter areas and are associated with features indicating substantial structural damage such as an increased signal intensity on diffusion-weighted imaging and contrast-medium enhancement. MRI in children with NMDAR encephalitis is often unremarkable, with one-third of patients showing only unspecific MRI changes and very rarely cortical enhancement.23,24 Our study further shows that MOG encephalitis in children can (1) occur as a monophasic disease, (2) can continue as a relapsing disease in half of all children with different demyelinating syndromes, and (3) present with features of NMDAR encephalitis at the same time (Pat 1, 4) (table). In one study, 2 children with encephalitis, unilateral cortical involvement on MRI, and MOG abs were reported, confirming the presence of MOG encephalitis in children.16 Budhram et al. reviewed the literature of patients with serum MOG abs, encephalitis, and seizures. They found that MRI in these patients often reveals a unilateral cortical involvement and coined the acronym FLAMES (unilateral FLAIR-hyperintense Lesions in Anti-MOG-associated Encephalitis with seizures).15 Two further single cases were recently published, describing children with symptoms suggestive of encephalitis associated with MOG abs but with MRI features more reminiscent of ADEM underscoring the need for precise terminology and diagnostic standards for children with MOG-SD.25,26 Recently, Armangue et al. showed that the spectrum of MOG-SD is wider than previously reported including children with encephalitis.27 In their large cohort of children with ADS and encephalitis, they found that 22/296 children with definite or possible AE harbored MOG abs. We could not delineate serologic or CSF findings specific to MOG encephalitis in comparison to other MOG-SD. Reaction with rat epitopes has been described as associated with NMOSD phenotype, yet we did observe this in 3/7 of our patients,28 supporting the notion of including TBA using rat brain sections in the workup of pediatric AE. Intrathecal synthesis of MOG abs has been speculated earlier to be associated with ADEM in contrast to NMOSD phenotypes, yet this was not observed in any of the 7 patients with testing available in CSF and serum.29 Another interesting observation in our case series is that 2 children with MOG encephalitis either had NMDAR abs in serum and CSF at initial presentation or presented with a severe clinical manifestation of NMDAR encephalitis 4 months later. In adults, the occurrence of overlapping demyelinating syndromes associated with MOG or AQP4 abs and subsequent episodes of encephalitis with NMDAR abs has been described.30 The simultaneous presence of both abs was also reported recently in a large study of children with NMDAR encephalitis, which found that more than 10% of affected children also harbored MOG abs.16 There was no difference in the CSF cell count of children with MOG encephalitis in our cases series compared with children with ADEM or NMDAR encephalitis.7 Encephalitis in children remains a severe disease despite recent advances. Timely diagnosis is of utmost importance, and delay may thus contribute to significant long-term sequelae. The differential diagnosis is broad, ranging from viral, bacterial, fungal, and parasitic infections to possible and definite cases of AE and other forms of immune-mediated diseases such as ADEM. Metagenomic next-generation sequencing is emerging as a new approach for the diagnosis of infectious causes which can be identified by using a single assay, most likely increasing the detection rate of pathogen-induced encephalitis.31 In addition, novel neuronal cellsurface and synaptic autoantibodies have been identified in recent years expanding the spectrum of definite causes of AE.32,–,34 MOG abs directed against epitopes of MOG of the myelin sheath of oligodendrocytes appears to be another culprit in the events leading to the manifestation of an AE. In contrast to the variable clinical manifestation in NMDAR encephalitis, children with MOG encephalitis, as far as we observed, present commonly with fever, headache, somnolence, seizures, and a characteristic imaging pattern with good response to steroids. Limitations that need to be addressed as follows: (1) small sample size and a lack of comparison with other children who fulfill the diagnostic criteria for AE but do not have MOG abs, (2) not all children were followed prospectively, and (3) children with a monophasic disease course had shorter follow-up period compared with the one with a relapsing disease course. In addition, (4) not in all children, autoantibody testing for neuronal antigens was performed in the CSF, thus leading to an underestimate of other autoantibodies involved. Finally, (5) the outcome was tested only with mRS, thereby not accurately assessing cognitive function in this form of encephalitis. AE with serum MOG abs represents a further form of autoantibody-mediated encephalitis in children and MOG encephalitis should therefore be considered in the differential diagnosis, particularly in the presence of cortical involvement on MRI. Diagnostic workup of pediatric patients with suspected AE should include TBA using rat brain immunohistochemistry and live cell MOG abs assays. Author contributions A. Wegener-Panzer and K. Rostásy designed and directed the study. K. Rostásy wrote the first draft of the manuscript. R. Höftberger, F. Leypoldt, and M. Reindl conducted the serologic testing of patient samples and revised the manuscript. All authors contributed and analyzed the data and read and revised the manuscript. Study funding This study is supported by grants numbers 14158 and 15918 (K. Rostasy) and 16919 (R. Höftberger) from the Jubilaeumsfonds of the Austrian National Bank and research grant “BIG WIG MS” from the Austrian Federal Ministry of Science, Research and Economy (Markus Reindl). Disclosure A. Wegener-Panzer, R. Cleaveland, E.-M. Wendel, M. Baumann, A. Bertolini, M. Häusler, E. Knierim, E. Reiter-Fink, M. Breu, Ö. Sönmez, A. Della Marina, R. Peters, C. Lechner, M. Piepkorn, C. Roll, and R. Höftberger report no disclosures related to the present work. F. Leypoldt reports speaker honoraria from Grifols, Teva, Biogen, Bayer, Roche, Novartis, Fresenius, travel funding from Merck, Grifols and Bayer and serving on advisory boards for Roche, Biogen and Alexion. K. Rostásy received speaker's honoraria from Novartis and served on the advisory board of the PARADIGM study. M. Reindl receives payments for ab assays (MOG, AQP4, and other autoantibodies) and for MOG and AQP4 ab validation experiments organized by Euroimmun (Lübeck, Germany). Go to Neurology.org/NN for full disclosures. Acknowledgment The authors thank the children and their families who agreed to take part in this study. Footnotes Go to Neurology.org/NN for full disclosures. Funding information is provided at the end of the article. The Article Processing Charge was funded by authors. Received February 17, 2020. Accepted in final form March 25, 2020. Copyright © 2020 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND), which permits downloading and sharing the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. References 1.↵Ketelslegers IA, Van Pelt DE, Bryde S, et al. Anti-MOG antibodies plead against MS diagnosis in an acquired demyelinating syndromes cohort. Mult Scler 2015;12:1513–2030.OpenUrl 2.↵Hacohen Y, Absoud M, Deiva K, et al. Myelin oligodendrocyte glycoprotein antibodies are associated with a non-MS course in children. Neurol Neuroimmunol Neuroinflamm 2015;2:e81. doi: 10.1212/NXI.0000000000000081. 3.↵Pröbstel AK, Dornmair K, Bittner R, et al. Antibodies to MOG are transient in childhood acute disseminated encephalomyelitis. 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Pediatric autoimmune encephalitis: case series from two Chinese Tertiary Pediatric Neurology Centers. Front Neurol 2019;10:906.OpenUrl 17.↵Titulaer MJ, Balu R, et alGraus F, Titulaer MJ, Balu R, et al. A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurol 2016;15:391–404.OpenUrlCrossRefPubMed 18.↵Patel N, Rao VA, Heilman-Espinoza ER, et al. Simple and reliable determination of the modified Rankin scale score in neurosurgical and neurological patients. Neurosurgery 2012;71:971–975.OpenUrlCrossRefPubMed 19.↵Mader S, Gredler V, Schanda K, et al. Complement activating antibodies to myelin oligodendrocyte glycoprotein in neuromyelitis optica and related disorders. J Neuroinflammation 2011;8:184.OpenUrlCrossRefPubMed 20.↵Dalmau J, Lancaster E, Martinez-Hernandez E, Rosenfeld MR, Balice-Gordon R. Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis. Lancet Neurol 2011;10:63–74.OpenUrlCrossRefPubMed 21.↵Verhey LH, Branson HM, Laughlin S, et al. Development of a standardized MRI scoring tool for CNS demyelinationin children. AJNR Am J Neuroradiol 2013;34:1271–1277. 22.↵Venkatesan A, Tunkel AR, Bloch KC, et al; International Encephalitis Consortium. Case definitions, diagnostic algorithms, and priorities in encephalitis: consensus statement of the International Encephalitis. Clin Infect Dis 2013;8:1114–1128.OpenUrl 23.↵Armangue T, Titulaer MJ, Málaga I, et al. Pediatric anti-N-methyl-D-aspartate receptor encephalitis—clinical analysis and novel findings in a series of 20 patients. J Pediatr 2013;162:850–856.OpenUrlCrossRefPubMed 24.↵Wright S, Hacohen Y, Jacobson L, et al. N-methyl-D-aspartate receptor antibody-mediated neurological disease: results of a UK-based surveillance study in children. Arch Dis Child 2015;100:521–526. 25.↵Zhong X, Chang Y, Tan S. Relapsing optic neuritis and meningoencephalitis in a child: case report of delayed diagnosis of MOG-IgG syndrome. BMC Neurol 2019;11:94.OpenUrl 26.↵Tani H, Ishikawa N, Kobayashi Y, et al. Anti-MOG antibody encephalitis mimicking neurological deterioration in a case of Rett syndrome with MECP2 mutation. Brain Dev 2018;10:943–946.OpenUrl 27.↵Armangue T, Olivé-Cirera G, Martinez-Hernandez E, et al. Associations of paediatric demyelinating and encephalitic syndromes with myelin oligodendrocyte glycoprotein antibodies: a multicentre observational study. Lancet Neurol 2020;19:234–246.OpenUrl 28.↵Sepúlveda M, Armangue T, Martinez-Hernandez E, et al. Clinical spectrum associated with MOG autoimmunity in adults: significance of sharing rodent MOG epitopes. J Neurol 2016;263:1349–1360.OpenUrl 29.↵Körtvélyessy P, Breu M, Pawlitzki M, et al. ADEM-like presentation, anti-MOG antibodies, and MS pathology: TWO case reports. Neurol Neuroimmunol Neuroinflamm 2017;4:e335. doi: 10.1212/NXI.0000000000000335. 30.↵Titulaer MJ, Höftberger R, Isuka T, et al. Overlapping demyelinating syndromes and anti–N-methyl-D-aspartate receptor encephalitis. Ann Neurol 2014;75:411–428.OpenUrlCrossRefPubMed 31.↵Wilson MR, Sample HA, Zorn KC, et al. Clinical metagenomic sequencing for diagnosis of meningitis and encephalitis. N Engl J Med 2019;380:2327–2340.OpenUrlCrossRef 32.↵Petit-Pedrol M, Armangue T, Peng X, et al. Encephalitis with refractory seizures, status epilepticus, and antibodies to the GABAA receptor: a case series, characterisation of the antigen, and analysis of the effects of antibodies. Lancet Neurol 2014;13:276–286.OpenUrlCrossRefPubMed 33.↵Lancaster E, Martinez-Hernandez E, Titulaer MJ, et al. Antibodies to metabotropic glutamate receptor 5 in the Ophelia syndrome. Neurology 2011;77:1698–1701.OpenUrlCrossRefPubMed 34.↵Nosadini M, Toldoa I, Tasciniaet B, et al. LGI1 and CASPR2 autoimmunity in children: systematic literature review and report of a young girl with Morvan syndrome. J Neuroimmunol 2019;335:577008.OpenUrl
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Josep Dalmau receives the “Scientific Breakthrough 2023” Award from the American Brain Foundation

From www.clinicbarcelona.org - May 23, 2023 2:38 PM
The accolade recognises the commitment of this Clínic Barcelona-IDIBAPS researcher to deepening our understanding of autoimmune neurological diseases such...
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IDIBAPS creates three multidisciplinary research programs to encourage collaboration among its groups

From www.clinicbarcelona.org - September 5, 2023 11:21 AM
They are the Translational cancer research program, the Synaptic autoimmunity in neurology, psychiatry and cognitive neuroscience program and the Lymphoid...
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ExTINGUISH: A Beacon of Hope for NMDAR Encephalitis

From youtu.be - August 6, 2023 7:10 PM
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MR Imaging Findings in a Large Population of Autoimmune Encephalitis | American Journal of Neuroradiology

MR Imaging Findings in a Large Population of Autoimmune Encephalitis | American Journal of Neuroradiology | AntiNMDA | Scoop.it
From www.ajnr.org - July 27, 2023 11:18 AM
Research ArticleAdult Brain MR Imaging Findings in a Large Population of Autoimmune Encephalitis S. Gillon, M. Chan, J. Chen, E.L. Guterman, X. Wu, C.M. Glastonbury and Y. Li American Journal of Neuroradiology July 2023, 44 (7) 799-806; DOI: https://doi.org/10.3174/ajnr.A7907 ArticleFigures & DataInfo & MetricsReferences PDF This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased. AbstractBACKGROUND AND PURPOSE: Autoimmune encephalitis is a rare condition in which autoantibodies attack neuronal tissue, causing neuropsychiatric disturbances. This study sought to evaluate MR imaging findings associated with subtypes and categories of autoimmune encephalitis.MATERIALS AND METHODS: Cases of autoimmune encephalitis with specific autoantibodies were identified from the medical record (2009–2019). Cases were excluded if no MR imaging of the brain was available, antibodies were associated with demyelinating disease, or >1 concurrent antibody was present. Demographics, CSF profile, antibody subtype and group (group 1 intracellular antigen or group 2 extracellular antigen), and MR imaging features at symptom onset were reviewed. Imaging and clinical features were compared across antibody groups using χ2 and Wilcoxon rank-sum tests.RESULTS: Eighty-five cases of autoimmune encephalitis constituting 16 distinct antibodies were reviewed. The most common antibodies were anti-N-methyl-D-aspartate (n = 41), anti-glutamic acid decarboxylase (n = 7), and anti-voltage-gated potassium channel (n = 6). Eighteen of 85 (21%) were group 1; and 67/85 (79%) were group 2. The median time between MR imaging and antibody diagnosis was 14 days (interquartile range, 4–26 days). MR imaging had normal findings in 33/85 (39%), and 20/33 (61%) patients with normal MRIs had anti-N-methyl-D-aspartate receptor antibodies. Signal abnormality was most common in the limbic system (28/85, 33%); 1/68 (1.5%) had susceptibility artifacts. Brainstem and cerebellar involvement were more common in group 1, while leptomeningeal enhancement was more common in group 2.CONCLUSIONS: Sixty-one percent of patients with autoimmune encephalitis had abnormal brain MR imaging findings at symptom onset, most commonly involving the limbic system. Susceptibility artifact is rare and makes autoimmune encephalitis less likely as a diagnosis. Brainstem and cerebellar involvement were more common in group 1, while leptomeningeal enhancement was more common in group 2.ABBREVIATIONS:AIEautoimmune encephalitisanti-Gq1banti-ganglioside Q1banti-LGI1anti-leucine-rich glioma inactivated 1CASPR2contactin-associated protein-like 2GABAgamma-aminobutyric acidGADglutamic acid decarboxylaseGFAPglial fibrillary acidic proteinNMDAN-methyl-D-aspartatePD-1programmed cell death protein 1VGCCvoltage gated calcium channelVGKCvoltage-gated potassium channel© 2023 by American Journal of NeuroradiologyView Full Text Log in using your username and password Username * Password * Forgot your user name or password? PreviousNext Back to top In this issue American Journal of Neuroradiology Vol. 44, Issue 7 1 Jul 2023 Table of ContentsIndex by authorComplete Issue (PDF) Print Download PDF Email Article Citation Tools Share Tweet WidgetFacebook LikeGoogle Plus One Purchase Related ArticlesNo related articles found.PubMedGoogle Scholar Cited By...No citing articles found.CrossrefGoogle Scholar More in this TOC Section Cost-Effectiveness Analysis of 68Ga-DOTATATE PET/MRI in Radiotherapy Planning in Patients with Intermediate-Risk Meningioma Choroid Plexus Calcification Correlates with Cortical Microglial Activation in Humans: A Multimodal PET, CT, MRI Study Show more ADULT BRAIN Similar Articles
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Elevated blood and cerebrospinal fluid biomarkers of microglial activation and blood‒brain barrier disruption in anti-NMDA receptor encephalitis | Journal of Neuroinflammation | Full Text

Elevated blood and cerebrospinal fluid biomarkers of microglial activation and blood‒brain barrier disruption in anti-NMDA receptor encephalitis | Journal of Neuroinflammation | Full Text | AntiNMDA | Scoop.it
From jneuroinflammation.biomedcentral.com - July 27, 2023 11:01 AM
Background Anti-NMDA receptor (NMDAR) encephalitis is an autoimmune disease characterized by complex neuropsychiatric syndrome and cerebrospinal fluid (CSF) NMDAR antibodies. Triggering receptor expressed on myeloid cells 2 (TREM2) has been reported to be associated with inflammation of the...
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Anti-N-methyl-d-aspartate receptor encephalitis and positive human herpesvirus-7 deoxyribonucleic acid in cerebrospinal fluid: a case report | Journal of Medical Case Reports | Full Text

Anti-N-methyl-d-aspartate receptor encephalitis and positive human herpesvirus-7 deoxyribonucleic acid in cerebrospinal fluid: a case report | Journal of Medical Case Reports | Full Text | AntiNMDA | Scoop.it
From jmedicalcasereports.biomedcentral.com - July 14, 2023 2:17 PM
Background Anti-N-methyl-d-aspartate receptor encephalitis is a neuroautoimmune syndrome typically presenting with seizures, psychiatric symptoms, and autonomic dysfunction. Human herpesvirus-7 is often found with human herpesvirus-6 and infects leukocytes such as T-cells, monocytes–macrophages,...
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We have a winner! - The Anti-NMDA Receptor Encephalitis Foundation Prize, 2023

We have a winner! - The Anti-NMDA Receptor Encephalitis Foundation Prize, 2023 | AntiNMDA | Scoop.it
From www.antinmdafoundation.org - June 25, 2023 2:58 PM
It’s that time of year again, when the Foundation is delighted to offer its annual Anti-NMDA Receptor Encephalitis Foundation Prize to a promising neurology trainee ...Read More...
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Antibodies Associated With Autoimmune Encephalitis in Patients With Presumed Neurodegenerative Dementia | Neurology Neuroimmunology & Neuroinflammation

Antibodies Associated With Autoimmune Encephalitis in Patients With Presumed Neurodegenerative Dementia | Neurology Neuroimmunology & Neuroinflammation | AntiNMDA | Scoop.it
From nn.neurology.org - June 19, 2023 9:45 PM
AbstractBackground & Objectives Autoimmune encephalitis (AIE) may present with prominent cognitive disturbances without overt inflammatory changes in MRI and CSF. Identification of these neurodegenerative dementia diagnosis mimics is important because patients generally respond to immunotherapy. The objective of this study was to determine the frequency of neuronal antibodies in patients with presumed neurodegenerative dementia and describe the clinical characteristics of the patients with neuronal antibodies.Methods In this retrospective cohort study, 920 patients were included with neurodegenerative dementia diagnosis from established cohorts at 2 large Dutch academic memory clinics. In total, 1,398 samples were tested (both CSF and serum in 478 patients) using immunohistochemistry (IHC), cell-based assays (CBA), and live hippocampal cell cultures (LN). To ascertain specificity and prevent false positive results, samples had to test positive by at least 2 different research techniques. Clinical data were retrieved from patient files.Results Neuronal antibodies were detected in 7 patients (0.8%), including anti-IgLON5 (n = 3), anti-LGI1 (n = 2), anti-DPPX, and anti-NMDAR. Clinical symptoms atypical for neurodegenerative diseases were identified in all 7 and included subacute deterioration (n = 3), myoclonus (n = 2), a history of autoimmune disease (n = 2), a fluctuating disease course (n = 1), and epileptic seizures (n = 1). In this cohort, no patients with antibodies fulfilled the criteria for rapidly progressive dementia (RPD), yet a subacute deterioration was reported in 3 patients later in the disease course. Brain MRI of none of the patients demonstrated abnormalities suggestive for AIE. CSF pleocytosis was found in 1 patient, considered as an atypical sign for neurodegenerative diseases. Compared with patients without neuronal antibodies (4 per antibody-positive patient), atypical clinical signs for neurodegenerative diseases were seen more frequently among the patients with antibodies (100% vs 21%, p = 0.0003), especially a subacute deterioration or fluctuating course (57% vs 7%, p = 0.009).Discussion A small, but clinically relevant proportion of patients suspected to have neurodegenerative dementias have neuronal antibodies indicative of AIE and might benefit from immunotherapy. In patients with atypical signs for neurodegenerative diseases, clinicians should consider neuronal antibody testing. Physicians should keep in mind the clinical phenotype and confirmation of positive test results to avoid false positive results and administration of potential harmful therapy for the wrong indication.GlossaryAD=Alzheimer dementia; AIE=autoimmune encephalitis; CBA=cell-based assays; DLB=dementia with Lewy bodies; IHC=immunohistochemistry; LN=live hippocampal cell cultures; PPA=primary progressive aphasia; PSP=progressive supranuclear palsy; RPD=rapidly progressive dementia; VGCC=voltage-gated calcium channelCognitive dysfunction can be the presenting and most prominent symptom in patients with autoimmune encephalitis (AIE).1,2 In contrast to neurodegenerative diseases, patients with antibody-mediated encephalitis might benefit from immunotherapy and improve considerably.3,4 The presence of neuronal antibodies has been reported predominantly in rapidly progressive dementia (RPD).5,6 However, AIE can present less fulminantly and is therefore potentially missed, resulting in diagnosis and treatment delay or even misdiagnosis.7,8 We hypothesized that a small—but not insignificant—part of dementia syndromes is indeed caused by antibody-mediated encephalitis and underdiagnosed, withholding these patients' available treatments. The wish to diagnose every single patient with autoimmune encephalitis is in opposition with the risk for false positive tests.9 Therefore, we strictly adhere to confirmation of positive test results with 2 different test techniques. In this study, we describe the frequency of neuronal antibodies in a cohort of patients diagnosed with various dementia syndromes in a memory clinic. In addition, we present clues to improve clinical recognition of AIE in dementia syndromes.MethodsPatients and Laboratory StudiesIn this retrospective multicenter study, we tested for the presence of neuronal antibodies in serum and CSF samples from patients diagnosed with neurodegenerative dementia diagnosis, included earlier prospectively in established cohorts at 2 large Dutch academic memory clinics (Erasmus University Medical Center, Amsterdam University Medical Centers, location VUmc)10 between 1998 and 2016 (84% last 10 years). All patients fulfilled the core clinical criteria for dementia, as defined by the National Institutes of Aging-Alzheimer Association workgroups.11 Patients were classified into 4 subgroups (based on diagnostic criteria): Alzheimer dementia (AD), frontotemporal dementia (FTD; both behavioral variant and primary progressive aphasia [PPA]), dementia with Lewy bodies (DLB), and other dementia syndromes.11,-,14 Rapidly progressive dementia was defined as dementia within 12 months or death within 2 years after the appearance of the first cognitive symptoms.15 Patients with vascular dementia were not included. Clinic information was retrieved from the prospectively collected data. A subacute deterioration was defined as a marked progression of symptoms in 3 months and a fluctuating course as a disease course fluctuating over a longer period (e.g., weeks to months; different from the fluctuations within a day as seen in some patients with DLB). Dementia markers were scored according to the reference values (per year and per center; included in Table 1).View inline View popup Table 1 Patient Characteristics of Auto-antibody Positive PatientsAll samples, stored in both cohorts' biobanks, were screened for immunoreactivity with immunohistochemistry (IHC), as previously described.16 Preferably, paired serum and CSF were tested for optimal sensitivity and specificity. Samples that were showing a positive or questionable staining pattern were tested more extensively using validated commercial cell-based assays (CBA) and in-house CBA (eTable 1, links.lww.com/NXI/A869). In addition, these samples were tested with live hippocampal cell cultures (LN).16,17 To ascertain specificity, only samples that could be confirmed by CBA or LN were scored as positive because there is a higher risk for false-positive test results in this population with a low a priori chance to have encephalitis.9,18 If IHC was suggestive for antibodies against intracellular (paraneoplastic) targets, this was explored by a different IHC technique.19 Anti-thyroid peroxidase (TPO), voltage-gated calcium channel (VGCC), or low titer glutamic acid decarboxylase antibodies were not tested for because these are generally nonspecific at these ages and are not associated with dementia syndromes.Antibody-positive patients were described exploratory and compared with a randomly selected antibody-negative group (ratio 1:4) matched for memory clinic, dementia subtype, sex, and age (±5 years). For these comparisons, medical records were additionally assessed for both the antibody-positive and antibody-negative patients. All antibody-positive patients were reviewed by a panel consisting of neurologists specialized in neurodegenerative (F.J., H.S., J.S.) or autoimmune diseases (J.V., P.S.S., M.T.), and a consensus classification of AIE vs AIE with a neurodegenerative dementia comorbidity was reached.Statistical AnalysisWe used IBM SPSS 25.0 (SPSS Inc) and Prism 8.4.3 (GraphPad) for statistical analysis. Baseline characteristics were analyzed using the Fisher exact test, the Fisher-Freeman-Halton test, or the Kruskal-Wallis test, when appropriate. For group comparisons, encompassing categorical data, we used the Pearson χ2 test or the Fisher-Freeman-Halton test, when appropriate. Continuous data were analyzed using the Mann-Whitney U test. All p-values were two-sided and considered statistically significant when below 0.05. We applied no correction for multiple testing, and therefore, p values between 0.05 and 0.005 should be interpreted carefully.Standard Protocol Approvals, Registrations, and Patient ConsentsThe study was approved by The Institutional Review Boards of Erasmus University Medical Center Rotterdam and Amsterdam University Medical Center, location VUmc. Written informed consent was obtained from all patients.Data AvailabilityAny data not published within this article are available at the Erasmus MC University Medical Center. Patient-related data will be shared on reasonable request from any qualified investigator, maintaining anonymization of the individual patients.ResultsIn total, 1,398 samples from 920 patients were tested (Figure; in 478, both CSF and serum [52%]). Three-hundred fifty-eight patients were classified as AD (39%), 283 FTD (31%), and 161 DLB (17%). The fourth subgroup with other dementia syndromes consisted of 118 patients (13%), including progressive supranuclear palsy (n = 48, 5%) and corticobasal syndrome (n = 29, 3%). The median age at disease onset was 62 years (range 16–90 years). Male patients were overrepresented (n = 542, 59%), and 60 patients (7%) fulfilled the criteria for rapidly progressive dementia (RPD; eTable 2, links.lww.com/NXI/A869).<img class="highwire-fragment fragment-image" alt="Figure" width="440" height="305" src="https://nn.neurology.org/content/nnn/10/5/e200137/F1.medium.gif">Download figure Open in new tab Download powerpoint Figure Flowchart of Patient Inclusion With Antibody ResultsIn total, 920 patients (1,398 samples) with a presumed neurodegenerative dementia syndrome were tested for the presence of neuronal antibodies in serum and CSF. Neuronal antibodies were detected in 7 patients (0.8%, 95% CI 0.2–1.3); five among the 358 Alzheimer disease patients. Subclassification of the ‘other’ group is provided in supplementary table eTable 2 (links.lww.com/NXI/A869). AD = Alzheimer disease; DLB = diffuse Lewy body dementia; DPPX = dipeptidyl aminopeptidase-like protein 6; FTD = frontotemporal dementia; IgLON5 = Ig-like domain-containing protein family member 5; LGI1 = leucin-rich glioma inactivated protein 1; NMDAR = N-methyl-d-aspartate receptor; S = serum.Neuronal antibodies were detected in 7 patients (0.8%; 5 in the AD group: 1.4%; Figure), including anti-IgLON5 (n = 3), anti-LGI1 (n = 2), anti-DPPX (n = 1), and anti-NMDAR antibodies (n = 1; Table 1). Among these 7, 4 patients were diagnosed retrospectively with an exclusive diagnosis of AIE, while 3 patients were classified to have AIE (anti-IgLON5 [n = 2] and anti-NMDAR antibodies [n = 1]) with a neurodegenerative dementia comorbidity. No patients with antibodies fulfilled the criteria for RPD, yet a subacute deterioration later in the disease was reported in 3 patients. Atypical clinical signs for neurodegenerative diseases were present in 7 of 7 antibody-positive patients (100% vs 21% in antibody-negative patients, p = 0.0003; Table 2). These included a subacute deterioration (n = 3), myoclonus (n = 2), a fluctuating disease course over months (n = 1), a history of autoimmune disease (n = 2), and epileptic seizures (n = 1; Table 1). Brain MRI of none of the patients demonstrated abnormalities suggestive for active AIE, in particular no hippocampal swelling nor increased T2-signal intensity. CSF pleocytosis was found in 1 patient. CSF biomarkers (t-tau, p-tau, and Aβ42) were tested in 5 of 7 patients, and t-tau and p-tau were increased in 4, while a low Aβ42 was seen in 2. Of note, only 1 patient had the combination of reduced Aβ42 and increased p-tau/t-tau, and was diagnosed with a comorbid AD. No patient received immunotherapy. Two patients still alive (1 anti-LG1, 1 anti-DPPX positive) were contacted but refused to visit our clinic to try very delayed immunotherapy trials. It is of interest that the patient with anti-DPPX antibodies showed spontaneous improvement of cognitive disturbances, atypical for a pure neurodegenerative disease.View inline View popup Table 2 Comparisons Between Patients With Neuronal Auto-antibodies and Antibody-Negative PatientsCompared with the patients without neuronal antibodies, subacute cognitive deterioration or fluctuating course was present more frequently (4/7 [57%] vs 2/28 [7%], p = 0.009). Although movement disorders (myoclonus) and autoimmune disorders were present in 2 of 7 patients each, this did not reach significance (Table 2).DiscussionIn this large, multicenter, cohort study consisting of patients with a presumed neurodegenerative dementia diagnosis, we show that a small, but clinically relevant proportion (0.8%) have neuronal antibodies. In this particular group, 4 of 7 antibody-positive patients presented with an atypical clinical course (subacute deterioration or fluctuating disease course), which is considered as a clinical clue (‘red flag’) for an antibody-mediated etiology of dementia.4 It is important that a fluctuating disease course was observed over a longer period (e.g., weeks or months) in AIE and should not be confused with shorter fluctuations of cognition or alertness (over the day) in DLB. Other known red flags, which we observed in these 7 patients, were myoclonus, epilepsy, pleocytosis, or a history of autoimmune disorders, as described earlier.1,4,-,6 Compared with antibody-negative patients, no significant difference was found related to these symptoms alone, probably due to the low number of positive patients and related low power. However, atypical clinical signs for neurodegenerative diseases together were seen significantly more frequently in the antibody-positive group. Within this cohort mostly devoid of patients with RPD, none of the antibody-positive patients fulfilled the criteria for RPD, nor ancillary testing showed specific signs for AIE in most patients. This implicates that AIE can resemble more protracted, progressive neurodegenerative dementia syndromes, as we reported earlier.1Three antibody-positive patients had IgLON5 antibodies, which is a very rare and known to have heterogeneous (chronic) clinical manifestations, including pronounced sleep problems, cognitive dysfunction, and movement disorders.20,21 Misdiagnosis with progressive supranuclear palsy (PSP) is reported, mainly associated with the preceding movement disorders. In addition, half of the patients have cognitive impairment of whom 20% fulfilled clinical criteria for dementia.21 It is of interest that IgLON5 disease shares features with neurodegeneration because autopsy studies showed tau deposits.22 However, there is a strong HLA association,20 and studies show that antibodies directly bind to surface IgLON5 on neurons and directly alter neuronal function and structure,23 suggesting a primary inflammatory disease.In previous research, a notably higher frequency (14%) of neuronal antibodies in patients with dementia was reported by Giannocaro et al.24 The discrepancy with our test results is probably explained by differences in patient selection and antibody testing methodology. First, 30% of the patients in the cohort described by Giannocaro et al. demonstrated CSF inflammatory abnormalities, indicating a relatively high pretest probability of antibody-positivity compared with our study.24 A lack of CSF pleocytosis probably better represents the population of memory clinics. Second, the previous study exclusively tested serum by cell-based assay without confirmatory tests nor testing antibodies in CSF.24 We only considered antibody test results positive when confirmed by additional techniques to avoid suboptimal specificity and false-positive test results.9Previous studies, including our own, suggested RPD as a relevant red flag for AIE,1,4,9,25 but we cannot determine this from our study based on the design of our study. We included patients at tertiary memory clinics without overt signs or symptoms suggestive for encephalitis. Therefore, the amount of patients with RPD included was very limited (7%), comparable with other large dementia cohort studies, as was the amount of patients with abnormal ancillary testing suggestive for AIE because this would have prompted a different approach than referral to a tertiary memory clinic. These patients with RPD and ancillary testing suggestive of AIE were not included in our study. Inclusion of those patients would have likely increased our rate of positivity.The strength of our study is the large number of paired samples (serum and CSF combined) from a cohort with various presumed neurodegenerative diseases without AIE suspicion, representative for academic memory clinics. A limitation is the lack of neuropathologic data to support our findings and make diagnoses of neurodegeneration or inflammation definite. To confirm if the symptoms are related to the presence of antibodies, we tried to overcome this concern in different ways. First, the presence of antibodies in serum and CSF was confirmed by different techniques (cell-based assay, tissue immunohistochemistry, and cultured live neurons), indicating optimal test specificity. Second, afterward patients were thoroughly reviewed by a panel of neurologists specialized in neurodegenerative or autoimmune disease to detect atypical signs and symptoms related to AIE. This is a very large cohort of patients with dementia examined for the presence of neuronal antibodies. Nevertheless, an important limitation of this study is the small number of antibody-positive patients, underpowering the probability to identify significant differences between antibody-positive and antibody-negative patients. The low number of patients with RPD has probably added to this small number, and a prospective study including patients with RPD is recommended. Nevertheless, several probable red flags could be identified. Diagnosing AIE in patients with dementia is highly relevant because these patients might respond to immunotherapy. Therefore, clinicians should test for neuronal antibody in patients demonstrating red flags suggestive for an autoimmune etiology, if possible early in disease course. When profound temporal lobe atrophy already has developed, little effect is to be expected. Red flags identified in this study are subacute deterioration or fluctuating course. Other red flags described previously, we also see reflected in our study, are autoimmune disorders, myoclonus, seizures, and pleocytosis,1,4,-,6 Preferably, both serum and CSF should be tested and confirmed by additional techniques. Always consider the possibility of a false positive test result, especially when only using a single technique (like the commercial cell-based assay). If the clinical phenotype is atypical, confirmation in a research laboratory should be mandatory. The use of antibody panels is discouraged, especially including the paraneoplastic blots, because these are associated with higher risks of lack of clinical relevance.26 This caution is even more warranted for tests not associated with neurodegenerative syndromes, but with a history of nonspecificity, including VGKC (in the absence of LGI1 or CASPR2), VGCC, anti-TPO, and low-titer anti-GAD65.27,-,30 Further research should focus on improving clinical recognition of AIE in patients with dementia determining the effect of immunotherapy in this specific patient category and assessing the frequency of AIE in RPD.In conclusion, we have shown that a clinically relevant, albeit small proportion of patients with a suspected neurodegenerative disease and nonrapidly progressive course have neuronal antibodies indicative of AIE.Study FundingM.J. Titulaer was supported by an Erasmus MC fellowship and has received funding from the Netherlands Organization for Scientific Research (NWO, Veni incentive), ZonMw (Memorabel program), the Dutch Epilepsy Foundation (NEF 14-19 & 19-08), Dioraphte (2001 0403), and E-RARE JTC 2018 (UltraAIE, 90030376505). F. Leypoldt has received funding from the German Ministry of Education and Research (01GM1908A) and the Era-Net funding program (LE3064/2-1).DisclosureA.E.M. Bastiaansen reports no disclosures. R.W. van Steenhoven reports no disclosures. Research programs of Wiesje van der Flier have been funded by ZonMW, now, EUFP7, EU-JPND, Alzheimer Nederland, Hersenstichting CardioVascular Onderzoek Nederland, Health∼Holland, Topsector Life Sciences & Health, stichting Dioraphte, Gieskes-Strijbis fonds, stichting Equilibrio, Edwin Bouw fonds, Pasman stichting, stichting Alzheimer & Neuropsychiatrie Foundation, Philips, Biogen MA Inc, Novartis-NL, Life-MI, AVID, Roche BV, Fujifilm, and Combinostics. W.M. van der Flier holds the Pasman chair. W.M. van der Flier is recipient of ABOARD, which is a public-private partnership receiving funding from ZonMW (#73305095007) and Health Holland, Topsector Life Sciences & Health (PPP-allowance; #LSHM20106). All funding is paid to her institution. WF has performed contract research for Biogen MA Inc and Boehringer Ingelheim. All funding is paid to her institution. W.M. van der Flier has been an invited speaker at Boehringer Ingelheim, Biogen MA Inc, Danone, Eisai, WebMD Neurology (Medscape), and Springer Healthcare. All funding is paid to her institution. W.M. van der Flier is consultant to Oxford Health Policy Forum CIC, Roche, and Biogen MA Inc. All funding is paid to her institution. W.M. van der Flier participated in advisory boards of Biogen MA Inc and Roche. All funding is paid to her institution. W.M. van der Flier is a member of the steering committee of PAVE and Think Brain Health. W.M. van der Flier was an associate editor of Alzheimer, Research & Therapy in 2020/2021. W.M. van der Flier is an associate editor at Brain. Research of C. Teunissen was supported by the European Commission (Marie Curie International Training Network, Grant Agreement No. 860197 (MIRIADE)), Innovative Medicines Initiatives 3TR (Horizon 2020, Grant No. 831434), EPND (IMI 2 Joint Undertaking (JU) under Grant Agreement No. 101034344) and JPND (bPRIDE), National MS Society (Progressive MS alliance) and Health Holland, the Dutch Research Council (ZonMW), Alzheimer Drug Discovery Foundation, The Selfridges Group Foundation, Alzheimer Netherlands, and Alzheimer Association. C. Teunissen is recipient of ABOARD, which is a public-private partnership receiving funding from ZonMW (#73305095007) and Health∼Holland, Topsector Life Sciences & Health (PPP-allowance, #LSHM20106). ABOARD also receives funding from Edwin Bouw Fonds and Gieskes-Strijbisfonds. C. Teunissen has a collaboration contract with ADx Neurosciences, Quanterix, and Eli Lilly, performed contract research or received grants from AC-Immune, Axon Neurosciences, Bioconnect, Bioorchestra, Brainstorm Therapeutics, Celgene, EIP Pharma, Eisai, Grifols, Novo Nordisk, PeopleBio, Roche, Toyama, and Vivoryon. She serves on editorial boards of Medidact Neurologie/Springer, Alzheimer Research and Therapy, and Neurology: Neuroimmunology & Neuroinflammation and is an editor of a Neuromethods book Springer. She had speaker contracts for Roche, Grifols, and Novo Nordisk. E. de Graaff holds a patent for the detection of anti-DNER antibodies. M.M.P. Nagtzaam reports no disclosures. M. Paunovic reports no disclosures. S. Franken reports no disclosures. M.W.J. Schreurs reports no disclosures. F. Leypoldt has received speakers honoraria from Grifols, Roche, Novartis, Alexion, and Biogen and serves on an advisory board for Roche and Biogen. He works for an academic institution (University Hospital Schleswig-Holstein) which offers commercial autoantibody testing. P.A.E. Sillevis Smitt holds a patent for the detection of anti-DNER and received research support from Euroimmun. J.M. de Vries reports no disclosures. H. Seelaar reports no disclosures. J.C. van Swieten reports no disclosures. F.J. de Jong reports no disclosures. Y.A.L. Pijnenburg Research of Alzheimer center Amsterdam is part of the neurodegeneration research program of Amsterdam Neuroscience. Alzheimer Center Amsterdam is supported by Stichting Alzheimer Nederland and Stichting VUmc fonds. The chair of Wiesje van der Flier is supported by the Pasman stichting. M.J. Titulaer has filed a patent, on behalf of the Erasmus MC, for methods for typing neurologic disorders and cancer, and devices for use therein, and has received research funds for serving on a scientific advisory board of Horizon Therapeutics, for consultation at Guidepoint Global LLC, for consultation at UCB, for teaching colleagues by Novartis. MT has received an unrestricted research grant from Euroimmun AG and from CSL Behring. Go to Neurology.org/NN for full disclosure.AcknowledgmentThe authors thank all patients for their participation. The authors also thank Esther Hulsenboom and Ashraf Jozefzoon-Aghai for their technical assistance. M.W.J. Schreurs, F. Leypoldt, P.A.E. Sillevis Smitt, J.M. de Vries, and M.J. Titulaer of this publication are members of the European Reference Network for Rare Immunodeficiency, Autoinflammatory, and Autoimmune Diseases—Project ID No. 739543 (ERN-RITA; HCP Erasmus MC and University Hospital Schleswig-Holstein). H. Seelaar, J.C. van Swieten, and F.J. de Jong of this publication are members of the European Reference Network for Rare Neurological Diseases—Project ID 73910. Research of the VUmc Alzheimer center is part of the neurodegeneration research program of Amsterdam Neuroscience. The Alzheimer Center VUmc is supported by Alzheimer Nederland and Stichting VUmc Fonds. The clinical database structure was developed with funding from Stichting Dioraphte.Appendix Authors<img class="highwire-fragment fragment-image" alt="Table" src="https://nn.neurology.org/content/nnn/10/5/e200137/T3.medium.gif"; width="599" height="2531">FootnotesGo to Neurology.org/NN for full disclosures. Funding information is provided at the end of the article.The Article Processing Charge was funded the authors.Submitted and externally peer reviewed. The handling editor was Editor Josep O. Dalmau, MD, PhD, FAAN.Received December 8, 2022.Accepted in final form May 8, 2023.Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND), which permits downloading and sharing the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.References1.↵Bastiaansen AEM, van Steenhoven RW, de Bruijn M, et al. Autoimmune encephalitis resembling dementia syndromes. Neurol Neuroimmunol Neuroinflamm. 2021;8(5):e1039.OpenUrlAbstract/FREE Full Text2.↵Lancaster E, Lai M, Peng X, et al. Antibodies to the GABA(B) receptor in limbic encephalitis with seizures: case series and characterisation of the antigen. Lancet Neurol. 2010;9(1):67-76.OpenUrlCrossRefPubMed3.↵Titulaer MJ, McCracken L, Gabilondo I, et al. Treatment and prognostic factors for long-term outcome in patients with anti-NMDA receptor encephalitis: an observational cohort study. Lancet Neurol 2013;12(2):157-165.OpenUrlCrossRefPubMed4.↵Flanagan EP, McKeon A, Lennon VA, et al. Autoimmune dementia: clinical course and predictors of immunotherapy response. Mayo Clin Proc. 2010;85(10):881-897.OpenUrlCrossRefPubMed5.↵Geschwind MD, Tan KM, Lennon VA, et al. Voltage-gated potassium channel autoimmunity mimicking creutzfeldt-jakob disease. Arch Neurol. 2008;65(10):1341-1346.OpenUrlCrossRefPubMed6.↵Grau-Rivera O, Sanchez-Valle R, Saiz A, et al. Determination of neuronal antibodies in suspected and definite Creutzfeldt-Jakob disease. JAMA Neurol. 2014;71(1):74-78.OpenUrl7.↵Titulaer MJ, McCracken L, Gabilondo I, et al. Late-onset anti-NMDA receptor encephalitis. Neurology. 2013;81(12):1058-1063.OpenUrlAbstract/FREE Full Text8.↵Gaig C, Graus F, Compta Y, et al. Clinical manifestations of the anti-IgLON5 disease. Neurology. 2017;88(18):1736-1743.OpenUrlAbstract/FREE Full Text9.↵Bastiaansen AEM, de Bruijn M, Schuller SL, et al. Anti-NMDAR encephalitis in The Netherlands, focusing on late-onset patients and antibody test accuracy. Neurol Neuroimmunol Neuroinflamm. 2022;9(2):e1127.OpenUrl10.↵van der Flier WM, Scheltens P. Amsterdam dementia cohort: performing research to optimize care. J Alzheimers Dis. 2018;62(3):1091-1111.OpenUrl11.↵McKhann GM, Knopman DS, Chertkow H, et al. The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011;7(3):263-269.OpenUrlCrossRefPubMed12.↵Rascovsky K, Hodges JR, Knopman D, et al. Sensitivity of revised diagnostic criteria for the behavioural variant of frontotemporal dementia. Brain. 2011;134(Pt 9):2456-2477.OpenUrlCrossRefPubMed13.↵Gorno-Tempini ML, Hillis AE, Weintraub S, et al. Classification of primary progressive aphasia and its variants. Neurology. 2011;76(11):1006-1014.OpenUrlAbstract/FREE Full Text14.↵McKeith IG, Boeve BF, Dickson DW, et al. Diagnosis and management of dementia with Lewy bodies: fourth consensus report of the DLB Consortium. Neurology. 2017;89(1):88-100.OpenUrlAbstract/FREE Full Text15.↵Geschwind MD. Rapidly progressive dementia. Continuum (Minneap Minn). 2016;22(2 Dementia):510-537.OpenUrl16.↵Ances BM, Vitaliani R, Taylor RA, et al. Treatment-responsive limbic encephalitis identified by neuropil antibodies: MRI and PET correlates. Brain. 2005;128(Pt 8):1764-1777.OpenUrlCrossRefPubMed17.↵Gresa-Arribas N, Titulaer MJ, Torrents A, et al. Antibody titres at diagnosis and during follow-up of anti-NMDA receptor encephalitis: a retrospective study. Lancet Neurol. 2014;13(2):167-177.OpenUrlCrossRefPubMed18.↵Martinez-Martinez P, Titulaer MJ. Autoimmune psychosis. Lancet Psychiatry. 2020;7(2):122-123.OpenUrl19.↵van Coevorden-Hameete MH, Titulaer MJ, Schreurs MW, et al. Detection and characterization of autoantibodies to neuronal cell-surface antigens in the central nervous system. Front Mol Neurosci. 2016;9:37.OpenUrl20.↵Sabater L, Gaig C, Gelpi E, et al. A novel non-rapid-eye movement and rapid-eye-movement parasomnia with sleep breathing disorder associated with antibodies to IgLON5: a case series, characterisation of the antigen, and post-mortem study. Lancet Neurol. 2014;13(6):575-586.OpenUrlCrossRefPubMed21.↵Gaig C, Compta Y, Heidbreder A, et al. Frequency and characterization of movement disorders in anti-IgLON5 disease. Neurology. 2021;97(14):e1367–e1381.OpenUrlAbstract/FREE Full Text22.↵Gelpi E, Hoftberger R, Graus F, et al. Neuropathological criteria of anti-IgLON5-related tauopathy. Acta Neuropathol. 2016;132(4):531-543.OpenUrlCrossRefPubMed23.↵Landa J, Gaig C, Plaguma J, et al. Effects of IgLON5 antibodies on neuronal cytoskeleton: a link between autoimmunity and neurodegeneration. Ann Neurol. 2020;88(5):1023-1027.OpenUrlCrossRefPubMed24.↵Giannoccaro MP, Gastaldi M, Rizzo G, et al. Antibodies to neuronal surface antigens in patients with a clinical diagnosis of neurodegenerative disorder. Brain Behav Immun. 2021;96:106-112.OpenUrl25.↵Hermann P, Zerr I. Rapidly progressive dementias - aetiologies, diagnosis and management. Nat Rev Neurol. 2022;18(6):363-376.OpenUrl26.↵Dechelotte B, Muniz-Castrillo S, Joubert B, et al. Diagnostic yield of commercial immunodots to diagnose paraneoplastic neurologic syndromes. Neurol Neuroimmunol Neuroinflamm. 2020;7(3):e701.OpenUrlAbstract/FREE Full Text27.↵van Sonderen A, Schreurs MW, de Bruijn MA, et al. The relevance of VGKC positivity in the absence of LGI1 and Caspr2 antibodies. Neurology. 2016;86(18):1692-1699.OpenUrlCrossRefPubMed28.↵Muñoz Lopetegi A, Boukhrissi S, Bastiaansen A, et al. Neurological syndromes related to anti-GAD65: clinical and serological response to treatment. Neurol Neuroimmunol Neuroinflamm. 2020;7(3):e696.OpenUrlAbstract/FREE Full Text29.↵Mattozzi S, Sabater L, Escudero D, et al. Hashimoto encephalopathy in the 21st century. Neurology. 2020;94(2):e217-e224.OpenUrlAbstract/FREE Full Text30.↵Flanagan EP, Geschwind MD, Lopez-Chiriboga AS, et al. Autoimmune encephalitis misdiagnosis in adults. JAMA Neurol. 2023;80(1):30-39.OpenUrl
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Research study - can you help?

Research study - can you help? | AntiNMDA | Scoop.it
From www.encephalitis.info - June 19, 2023 9:38 PM
Researchers at Kings College London are looking for young people to travel to London and help with an encephalitis study...
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Sociocultural Influences in Autoimmune Encephalitis Without Neurologic Symptoms

Sociocultural Influences in Autoimmune Encephalitis Without Neurologic Symptoms | AntiNMDA | Scoop.it
From www.psychiatrist.com - June 19, 2023 9:33 PM
This complex case highlights barriers to identifying autoimmune encephalitis when no neurologic symptoms are present, which are normally central to disease detection.
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Anti N-Methyl-D-Aspartate receptor antibody associated Acute Demyelinating Encephalomyelitis in a patient with COVID-19: a case report | Journal of Medical Case Reports | Full Text

Anti N-Methyl-D-Aspartate receptor antibody associated Acute Demyelinating Encephalomyelitis in a patient with COVID-19: a case report | Journal of Medical Case Reports | Full Text | AntiNMDA | Scoop.it
From jmedicalcasereports.biomedcentral.com - June 19, 2023 9:27 PM
Background Anti N-Methyl-D-Aspartate (NMDA) receptor antibody associated ADEM is a diagnosis that was first described relatively recently in 2007 by Dalmau et al. The recent COVID-19 pandemic has resulted in multiple neurological complications being reported.
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Autoimmune Encephalitis Consensus Criteria | Neurology Clinical Practice

Autoimmune Encephalitis Consensus Criteria | Neurology Clinical Practice | AntiNMDA | Scoop.it
From cp.neurology.org - June 14, 2023 7:42 PM
June 2023; 13 (3) Editorial Autoimmune Encephalitis Consensus CriteriaLessons Learned From Real-World Practice View ORCID ProfileJeffrey M. Gelfand, Chu-Yueh Guo First published April 25, 2023, DOI: https://doi.org/10.1212/CPJ.0000000000200155 Full PDF Citation Permissions Make Comment See Comments Downloads133 Share Article Info & Disclosures This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased. Autoimmune encephalitis (AE) encompasses a spectrum of neurologic disorders caused by brain inflammation, a subset of which is associated with autoantibodies to neuronal cell-surface antigens such as anti-N-methyl-d-aspartate (NMDA) receptor AE or anti-leucine-rich glioma-inactivated 1 (LGI1) AE.1 Up to half of patients with AE, however, do not have abnormal neuronal or glial autoantibodies identified and are classified as having “seronegative” AE.2 Clinical antibody testing can take several days to result, a time in which clinicians caring for patients with suspected AE may wish to initiate empiric immunosuppressive therapy. Antibody testing is also not readily accessible in some health care settings and, even when technically available, may require time-consuming advocacy with local clinical laboratories to justify relatively costly send-out testing. To add further complexity, some patients with immunoreactive (e.g., laboratory true-positive) antibodies do not have clinical AE, and over-reliance and misapplication of antibody testing were identified as important contributors to AE misdiagnosis in a 2023 multicenter analysis.3FootnotesFunding information and disclosures are provided at the end of the article. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp.See page e200151© 2023 American Academy of NeurologyView Full Text AAN Members We have changed the login procedure to improve access between AAN.com and the Neurology journals. If you are experiencing issues, please log out of AAN.com and clear history and cookies. (For instructions by browser, please click the instruction pages below). After clearing, choose preferred Journal and select login for AAN Members. You will be redirected to a login page where you can log in with your AAN ID number and password. When you are returned to the Journal, your name should appear at the top right of the page. Google Safari Microsoft Edge Firefox Click here to login AAN Non-Member Subscribers Click here to login Purchase access For assistance, please contact: AAN Members (800) 879-1960 or (612) 928-6000 (International) Non-AAN Member subscribers (800) 638-3030 or (301) 223-2300 option 3, select 1 (international) Sign Up Information on how to subscribe to Neurology and Neurology: Clinical Practice can be found here Purchase Individual access to articles is available through the Add to Cart option on the article page. Access for 1 day (from the computer you are currently using) is US$ 39.00. Pay-per-view content is for the use of the payee only, and content may not be further distributed by print or electronic means. The payee may view, download, and/or print the article for his/her personal, scholarly, research, and educational use. Distributing copies (electronic or otherwise) of the article is not allowed. You May Also be Interested in Back to top Safety and Efficacy of Tenecteplase and Alteplase in Patients With Tandem Lesion Stroke: A Post Hoc Analysis of the EXTEND-IA TNK Trials Dr. Nicole Sur and Dr. Mausaminben Hathidara ► Watch Related Articles Autoimmune Encephalitis Criteria in Clinical Practice Topics Discussed All Clinical Neurology Autoimmune diseases Encephalitis Alert Me Alert me when eletters are published
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Predictive Value of Serum Neurofilament Light Chain Levels in Anti-NMDA Receptor Encephalitis

Predictive Value of Serum Neurofilament Light Chain Levels in Anti-NMDA Receptor Encephalitis | AntiNMDA | Scoop.it
From pubmed.ncbi.nlm.nih.gov - June 14, 2023 7:41 PM
Increased serum NfL levels reflect neuroaxonal damage in anti-NMDAR encephalitis. No relationship was identified with disease severity, whereas the association with outcome was confounded by age.The implied role of sampling timing on NfL levels also limits the applicability of NfL as a prognostic...
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Frontiers | The MOG antibody associated encephalitis preceded by COVID-19 infection; a case study and systematic review of the literature

Frontiers | The MOG antibody associated encephalitis preceded by COVID-19 infection; a case study and systematic review of the literature | AntiNMDA | Scoop.it
From www.frontiersin.org - September 5, 2023 11:22 AM
BackgroundNew neurological complications of COVID-19 infection have been reported in recent research. Among them, the spectrum of anti-MOG positive diseases, defined as anti-MOG antibody associated disease (MOGAD), is distinguished, which can manifest as optic neuritis, myelitis, or various forms...
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Enceph-IG Study - Institute of Infection, Veterinary and Ecological Sciences - University of Liverpool

Enceph-IG Study - Institute of Infection, Veterinary and Ecological Sciences - University of Liverpool | AntiNMDA | Scoop.it
From www.liverpool.ac.uk - August 6, 2023 7:27 PM
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A Rare Presentation of Steroid-responsive Encephalopathy Associated with Autoimmune Thyroiditis with Neuropsychiatric Symptoms: A Case Report

A Rare Presentation of Steroid-responsive Encephalopathy Associated with Autoimmune Thyroiditis with Neuropsychiatric Symptoms: A Case Report | AntiNMDA | Scoop.it
From touchneurology.com - July 27, 2023 11:22 AM
A 42-year-old woman presented in the emergency department with acute onset whole-body myoclonic jerks for 1 day.On enquiry, the patient’s parents advised...
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Pioneering Research in Autoimmune Neurology: Vanda Lennon, M.D., Ph.D.

Pioneering Research in Autoimmune Neurology: Vanda Lennon, M.D., Ph.D. | AntiNMDA | Scoop.it
From news.mayocliniclabs.com - July 27, 2023 11:05 AM
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New center to spotlight neurological autoimmune disorders

New center to spotlight neurological autoimmune disorders | AntiNMDA | Scoop.it
From bioengineer.org - July 14, 2023 2:19 PM
How do neurological disorders arise that are caused, triggered, or influenced by antibodies? What better possibilities are there for diagnosis – and above all for treatment? These are the questions addressed by the new Clinical Research Unit “BecauseY” headed by Charité – Universitätsmedizin Berlin.
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Progressive alliance advances science through patient-powered research

Progressive alliance advances science through patient-powered research | AntiNMDA | Scoop.it
From news.mayocliniclabs.com - July 14, 2023 2:16 PM
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ENCEPH-IG Trial: The Challenges Of Running A Rare Disease Trial - Centre for Trials Research

ENCEPH-IG Trial: The Challenges Of Running A Rare Disease Trial - Centre for Trials Research | AntiNMDA | Scoop.it
From blogs.cardiff.ac.uk - June 19, 2023 9:46 PM
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30 neurological disorders every doctor should know about –

30 neurological disorders every doctor should know about – | AntiNMDA | Scoop.it
From theneurologylounge.com - June 19, 2023 9:42 PM
Neurology is a jungle of disorders and syndromes. This creates a challenge for doctors and medical students... What to prioritise for learning and practice? *** To solve this conundrum... We combed the extensive database of Neurochecklists...
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A score that predicts 1-year functional status in patients with anti-NMDA receptor encephalitis

A score that predicts 1-year functional status in patients with anti-NMDA receptor encephalitis | AntiNMDA | Scoop.it
From pubmed.ncbi.nlm.nih.gov - June 19, 2023 9:34 PM
The NEOS score accurately predicts 1-year functional status in patients with anti-NMDAR encephalitis. This score could help estimate the clinical course following diagnosis and may aid in identifying patients who could benefit from novel therapies.
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Canadian Blood Services needs thousands more donors to roll up their sleeves | CBC News

Canadian Blood Services needs thousands more donors to roll up their sleeves | CBC News | AntiNMDA | Scoop.it
From www.cbc.ca - June 19, 2023 9:28 PM
Canadian Blood Services is looking to fill 150,000 appointments for people willing to donate their blood or plasma to tackle a shortage.
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A catatonic woman awakened after 20 years. Her story may change psychiatry – My Health CRM

A catatonic woman awakened after 20 years. Her story may change psychiatry – My Health CRM | AntiNMDA | Scoop.it
From myhealthcrm.com - June 14, 2023 7:43 PM
New research suggests that a subset of patients with psychiatric conditions such as schizophrenia may actually have autoimmune disease that attacks the brain...
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Case Report: Paroxysmal weakness of unilateral limb as an initial symptom in anti-LGI1 encephalitis: a report of five cases

Case Report: Paroxysmal weakness of unilateral limb as an initial symptom in anti-LGI1 encephalitis: a report of five cases | AntiNMDA | Scoop.it
From pubmed.ncbi.nlm.nih.gov - June 14, 2023 7:41 PM
Anti-leucine-rich glioma-inactivated 1 (LGI1) encephalitis is the second most common kind of autoimmune encephalitis following anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis.Anti-LGI1 encephalitis is characterized by cognitive impairment or rapid progressive dementia, psychiatric disorders...
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Medical Moment: The signs of ‘brain-on-fire’ disease

Medical Moment: The signs of ‘brain-on-fire’ disease | AntiNMDA | Scoop.it
From www.wndu.com - June 14, 2023 7:40 PM
(WNDU) - Imagine being totally fine one day, then the next, you’re having hallucinations, seizures, memory loss, and even trouble talking.It’s called “brain-on-fire” disease or anti-NMDA receptor encephalitis. It’s a rare neurological disorder that can cause inflammation in the brain.It occurs when the body’s immune system mistakenly attacks the NMDA receptors in the brain, which are responsible for regulating communication between nerve cells. Brain-on-fire disease is often misdiagnosed as other neurological disorders or psychiatric illnesses because its symptoms are similar to those of many other conditions.However, a blood or cerebrospinal fluid test can help diagnose the disease by detecting the presence of antibodies that attack the NMDA receptors in the brain. The disease is rare as it affects one in 1.5 million people a year.Katie Miller would be one of those people.Hunting, mountain biking, horseback riding - you name it, Katie Miler would do it... until she couldn’t.“I just didn’t feel like myself, like normal,” Katie recalled.“Katie said, ‘Mom, I feel like my brain snapped,’” said Colleen Miller, Katie’s mother.Local doctors admitted Katie into a psychiatric ward, but what was happening to Katie wasn’t mental; it was physical.“What happens is you’re perfectly normal one day, and suddenly overnight, this person can become paranoid, can start having visual hallucinations, auditory hallucinations,” explained Stacy Clardy, MD, PhD, an autoimmune neurologist at the University of Utah.Anti-NMDA receptor encephalitis is misdiagnosed as a psychiatric disorder in up to 40% of patients.“So, for many of the females, especially after puberty, they can develop what’s called an ovarian dermoid cyst or an ovarian teratoma,” Dr. Clardy said.These cysts often have hair and teeth in them. The immune system sees it as foreign and attacks it, but...“In these cysts, there is a component of tissue that really is brain tissue,” Dr. Clardy continued.Within four days, Katie was catatonic and needed a ventilator to breathe. There is no single approved treatment. That’s why a five-year, nationwide clinical trial is testing whether a drug called Inebilizumab will stop the assault on the brain. It has the potential to improve outcomes for patients who are not responding to other treatments and may also lead to fewer long-term neurological effects.Katie had her cyst removed; she can’t remember three months of her life. But now, with various medications, Katie is on her way to recovery.Up to 50% of patients can suffer long-term consequences, especially cognitive and mood symptoms.Copyright 2023 WNDU. All rights reserved.
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