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Hallucinations Lead to Ovarian Cancer Diagnosis for Young Woman

Hallucinations Lead to Ovarian Cancer Diagnosis for Young Woman | AntiNMDA | Scoop.it
Lauren went from a psychiatric ward in a local hospital to the ICU....
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Count Down to WED Conference Saturday, 20 February 2021: Meet Dr. Tom Pollak

Count Down to WED Conference Saturday, 20 February 2021: Meet Dr. Tom Pollak | AntiNMDA | Scoop.it
We are delighted to spotlight Dr. Tom Pollak from the UK. Thanks to his engagement and research, many more are now getting the help they ...Read More...
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Imaging of Creutzfeldt-Jakob Disease: Imaging Patterns and Their Differential Diagnosis | RadioGraphics

Imaging of Creutzfeldt-Jakob Disease: Imaging Patterns and Their Differential Diagnosis | RadioGraphics | AntiNMDA | Scoop.it
The article provides an update on Creutzfeldt-Jakob disease (CJD), reviewing prion biology, subtypes of sporadic CJD, and the clinical aspects and molecular basis of this entity, with a comprehensi...
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Seizures in autoimmune encephalitis—A systematic review and quantitative synthesis - Yeshokumar - - Epilepsia

Seizures in autoimmune encephalitis—A systematic review and quantitative synthesis - Yeshokumar - - Epilepsia | AntiNMDA | Scoop.it
Abstract Objective This study aimed to evaluate the proportion of patients with seizures and electroencephalography (EEG) abnormalities in autoimmune encephalitis (AE) and its most common subtypes....
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High serum creatinine is associated with reduction of psychiatric symptoms in female patients with anti-NMDAR encephalitis - ScienceDirect

High serum creatinine is associated with reduction of psychiatric symptoms in female patients with anti-NMDAR encephalitis - ScienceDirect | AntiNMDA | Scoop.it
Serum creatinine (SCR) has been shown to be associated with many neurodegenerative diseases.In this study, we investigated the relationship between S…...
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Oophorectomy in NMDA receptor encephalitis and negative pelvic imaging | Practical Neurology

Oophorectomy in NMDA receptor encephalitis and negative pelvic imaging | Practical Neurology | AntiNMDA | Scoop.it
A difficult case Oophorectomy in NMDA receptor encephalitis and negative pelvic imaging http://orcid.org/0000-0003-1078-7217Dustin Anderson1, http://orcid.org/0000-0001-6446-1146Nabeela Nathoo2, Monica Henry1, George Wood3, Penelope Smyth2, Jennifer McCombe2 Critical Care, University of Alberta, Edmonton, Canada Medicine (Neurology), University of Alberta, Edmonton, Canada Department of Laboratory Medicine & Pathology, University of Alberta, Edmonton, Canada Correspondence to Jennifer McCombe, 7-132D Clinical Sciences Building, 11350 83 Avenue, Edmonton, T6G 2G3, Canada; jmccombe{at}ualberta.ca Abstract Ovarian teratomas are found in one-third of females presenting with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis. When a teratoma is detected on imaging, its removal is first-line therapy. Even with multiple imaging modalities, occasionally, the teratoma is found only on subsequent imaging, long after initial presentation. Very rarely, patients have undergone oophorectomy despite negative imaging, with pathology demonstrating teratoma, and resulting clinical improvement. We present a patient in whom removal of a teratoma, not visible on conventional imaging, resulted in marked clinical improvement. Such cases present a major clinical challenge, needing to consider the risks of oophorectomy, including sterilisation and early menopause, versus the possibility of death in the absence of response to first-line (eg, corticosteroids, plasma exchange, intravenous immunoglobulin), second-line (eg, rituximab) and third-line (eg, bortezomib) immunosuppression. This decision is made more difficult as patients are usually females of childbearing age who at the time lack capacity to make medical decisions. This case also highlights the lack of consensus and guidelines for imaging modalities used to detect teratoma and when to pursue oophorectomy. View Full Text Statistics from Altmetric.com View Full Text Footnotes DA and NN contributed equally Contributors DA, NN and JM drafted the original manuscript. All authors were directly involved in the patient’s care and management, provided intellectual content for the manuscript, and edited the manuscript. Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors. Competing interests None declared. Patient consent for publication Consent obtained from parent(s)/guardian(s). Ethics approval The patient’s mother provided consent for publication of this case. Provenance and peer review Not commissioned. Externally peer reviewed by Adam Al-Diwani, Oxford, UK. Data availability statement Not applicable. Request Permissions If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways. Copyright information: © Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ. Linked Articles Editors’ commentary Phil E M Smith Geraint N Fuller Practical Neurology 2021; 21 1-1 Published Online First: 19 Jan 2021. doi: 10.1136/practneurol-2020-002894 Read the full text or download the PDF: Subscribe Log in Other content recommended for you Rapid recovery from catastrophic paraneoplastic anti-NMDAR encephalitis secondary to an ovarian teratoma following ovarian cystectomy Charuwan Tantipalakorn et al., BMJ Case Reports, 2016 Encephalitis on deployment in Kenya: think beyond the infections Daniel Cameron Thompson et al., Journal of the Royal Army Medical Corps, 2019 Clinical approach to the diagnosis and successful management of anti-NMDA receptor encephalitis when antibody testing is not possible Anil Frank Ramlackhansingh et al., BMJ Case Reports, 2019 Differential expression of antibodies to NMDA receptor in anti-NMDA receptor encephalitis and in neuropsychiatric systemic lupus erythematosus Shunsei Hirohata et al., Lupus Science & Medicine, 2019 Primary lateral sclerosis - like picture in a patient with a remote history of anti-N - methyl - D - aspartate receptor (anti - NMDAR) antibody encephalitis Mubeen Janmohamed et al., BMJ Case Reports, 2018 Successful treatment of anti-N - methyl - D - aspartate receptor encephalitis presenting with catatonia M Schimmel et al., Archives of Disease in Childhood, 2009 Neurogenic bladder in an adolescent woman with an ovarian tumour: an unusual presentation of anti-NMDA - receptor encephalitis Natasha Soong-Ying Liou et al., BMJ Case Reports, 2019 Fluorodeoxyglucose positron emission tomography in anti-N - methyl - D - aspartate receptor encephalitis: distinct pattern of disease Frank Leypoldt et al., Journal of Neurology, Neurosurgery & Psychiatry, 2012 NMDAR (N - methyl - D - aspartate receptor) encephalitis in a patient with MS (multiple sclerosis): a rare and challenging case Sadia Suleman et al., BMJ Case Reports, 2018 Treatment responsive opsoclonus – ataxia associated with ovarian teratoma I Kawachi et al., Journal of Neurology, Neurosurgery & Psychiatry, 2010
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Autoimmune encephalitis and epilepsy: evolving definition and clinical spectrum

Autoimmune encephalitis and epilepsy: evolving definition and clinical spectrum | AntiNMDA | Scoop.it
Advances in autoimmune encephalitis studies in the past 10 years have led to the identification of new syndromes and biomarkers that have transformed the diagnostic approach to the disorder.The disorder or syndrome has been linked to a wide variety of pathologic processes associated with the neuron...
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Correction to: Refractory anti‑NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review | SpringerLink

Correction to: Refractory anti‑NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review | SpringerLink | AntiNMDA | Scoop.it
The authors would like to correct some errors in the publication of the original article. The corrected and updated details are given below for your reading.
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Ca V α2δ Autoimmune Encephalitis: A Novel Antibody and its Characteristics

Ca V α2δ Autoimmune Encephalitis: A Novel Antibody and its Characteristics | AntiNMDA | Scoop.it
Here, we found a novel autoimmune encephalitis associated with anti-Ca<sub>V</sub> α2δ antibody. Further analysis of the antibody in autoimmune encephalitis might promote the early diagnosis and treatment.
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Clinical features and management of coexisting anti-N-methyl-D-aspartate receptor encephalitis and myelin oligodendrocyte glycoprotein antibody-associated encephalomyelitis: a case report and revie...

Clinical features and management of coexisting anti-N-methyl-D-aspartate receptor encephalitis and myelin oligodendrocyte glycoprotein antibody-associated encephalomyelitis: a case report and revie... | AntiNMDA | Scoop.it
The rates of coexisting anti-NMDA receptor encephalitis and MOG antibody-associated encephalomyelitis may be underestimated.Clinical symptoms such as seizures and cognitive decline accompanied by atypical central nervous system demyelination serve as warning signs of possible coexisting anti-NMDA...
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The Antibodies Contributing to focal Epilepsy Signs and symptoms (ACES) score - Bruijn - - Annals of Neurology

The Antibodies Contributing to focal Epilepsy Signs and symptoms (ACES) score - Bruijn - - Annals of Neurology | AntiNMDA | Scoop.it
Objective Diagnosing autoimmune encephalitis (AIE) is difficult in patients with less fulminant diseases, like epilepsy. However, recognition is important, as patients require immunotherapy. This s...
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Can You Identify Autoimmune Psychosis? | Psychiatric News

Can You Identify Autoimmune Psychosis? | Psychiatric News | AntiNMDA | Scoop.it
Patients with a rare neurological condition known as anti-NMDA receptor encephalitis often present first with psychosis.
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Good Article! It used to be that relapse rates were between 15-25%. In this report, Dalmau refers to a 10% relapse rate. 

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Infiltration of plasma cells in colorectal adenocarcinoma associated with autoimmune encephalitis

Infiltration of plasma cells in colorectal adenocarcinoma associated with autoimmune encephalitis | AntiNMDA | Scoop.it
Paraneoplastic autoimmune encephalitis (PAE) represents a group of rare neurological syndromes associated with neoplastic diseases.Here, we report a case that multiple anti-neuronal antibodies were present in a patient with PAE who developed both small cell lung cancer and colorectal adenocarcinoma...
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Unremitting diarrhoea in a girl diagnosed anti-N-methyl-D-aspartate-receptor encephalitis: A case report | Read by QxMD

Unremitting diarrhoea in a girl diagnosed anti-N-methyl-D-aspartate-receptor encephalitis: A case report | Read by QxMD | AntiNMDA | Scoop.it
Create a free QxMD account to take advantage of the features offered by Read like saving your papers and creating collections. Get Started Unremitting diarrhoea in a girl diagnosed anti-N-methyl-D-aspartate-receptor encephalitis: A case report Norrapat Onpoaree, Montida Veeravigrom, Anapat Sanpavat, Narissara Suratannon, Palittiya Sintusek World Journal of Clinical Cases 2020 October 26, 8 (20): 4866-4875 BACKGROUND: Asymptomatic cytomegalovirus (CMV) infection is common in children; in contrast, in children with a weakened immune system, invasive CMV can occur. This is the first case report of a severe manifestation of CMV esophago-enterocolitis in a girl diagnosed with anti-N-methyl-D-aspartate-receptor (anti-NMDAR) encephalitis who received only a moderate dose of corticosteroid therapy. CASE SUMMARY: A 12-year-old-Thai girl presented with acute behavioural change and headache for 6 d. Electroencephalogram and positivity for NMDAR autoantibodies were compatible with anti-NMDAR encephalitis. Hence, she received pulse methylprednisolone 10 mg/kg per day for 4 d and continued with prednisolone 1.2 mg/kg per day. On day 42 of corticosteroid therapy, she developed unremitting vomiting and diarrhoea. Endoscopy showed multiple ulcers and erythaematous mucosa along the gastrointestinal tract. Tissue CMV viral load and viral-infected cells confirmed CMV esophago-enterocolitis. Therefore, the patient received ganciclovir 5 mg/kg per dose every 12 h for 3 wk and then 5 mg/kg per dose once daily for 3 wk. Unremitting diarrhoea slowly improved from stool output 1-4 L per day to 1-2 L per day after 3 wk of treatment. Pulse methylprednisolone 20 mg/kg for 5 d was initiated and continued with prednisolone 1 mg/kg per day. After this repeated pulse methylprednisolone treatment, surprisingly, diarrhoea subsided. Immunologic work-up was performed to rule out underlying immune deficiency with unremarkable results. CONCLUSION: Unremitting diarrhoea from CMV esophago-enterocolitis subsided with antiviral and methylprednisolone therapy, implying the immune and NMDAR dysregulation in anti-NMDAR encephalitis. Full Text Links We have located links that may give you full text access. Additional links Discussion You are not logged in. Sign Up or Log In to join the discussion. Trending Papers 2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Steve R Ommen, Seema Mital, Michael A Burke, Sharlene M Day, Anita Deswal, Perry Elliott, Lauren L Evanovich, Judy Hung, José A Joglar, Paul Kantor, Carey Kimmelstiel, Michelle Kittleson, Mark S Link, Martin S Maron, Matthew W Martinez, Christina Y Miyake, Hartzell V Schaff, Christopher Semsarian, Sorajja Paul Circulation 2020 November 20, : CIR0000000000000938 Effectiveness of Adding a Mask Recommendation to Other Public Health Measures to Prevent SARS-CoV-2 Infection in Danish Mask Wearers : A Randomized Controlled Trial. Henning Bundgaard, Johan Skov Bundgaard, Daniel Emil Tadeusz Raaschou-Pedersen, Christian von Buchwald, Tobias Todsen, Jakob Boesgaard Norsk, Mia M Pries-Heje, Christoffer Rasmus Vissing, Pernille B Nielsen, Ulrik C Winsløw, Kamille Fogh, Rasmus Hasselbalch, Jonas H Kristensen, Anna Ringgaard, Mikkel Porsborg Andersen, Nicole Bakkegård Goecke, Ramona Trebbien, Kerstin Skovgaard, Thomas Benfield, Henrik Ullum, Christian Torp-Pedersen, Kasper Iversen Annals of Internal Medicine 2020 November 18 How to ventilate obstructive and asthmatic patients. Alexandre Demoule, Laurent Brochard, Martin Dres, Leo Heunks, Amal Jubran, Franco Laghi, Armand Mekontso-Dessap, Stefano Nava, Lamia Ouanes-Besbes, Oscar Peñuelas, Lise Piquilloud, Theodoros Vassilakopoulos, Jordi Mancebo Intensive Care Medicine 2020 November 9 Volume overload in hemodialysis: diagnosis, cardiovascular consequences, and management. Charalampos Loutradis, Pantelis A Sarafidis, Charles J Ferro, Carmine Zoccali Nephrology, Dialysis, Transplantation 2020 November 13 Clinical Management of Hyperkalemia. Biff F Palmer, Juan Jesus Carrero, Deborah J Clegg, Gates B Colbert, Michael Emmett, Steven Fishbane, Debra J Hain, Edgar Lerma, Macaulay Onuigbo, Anjay Rastogi, Simon D Roger, Bruce S Spinowitz, Matthew R Weir Mayo Clinic Proceedings 2020 November 4 Comparing Laparoscopic Elective Sigmoid Resection With Conservative Treatment in Improving Quality of Life of Patients With Diverticulitis: The Laparoscopic Elective Sigmoid Resection Following Diverticulitis (LASER) Randomized Clinical Trial. Alexandre Santos, Panu Mentula, Tarja Pinta, Shamel Ismail, Tero Rautio, Risto Juusela, Aleksi Lähdesmäki, Tom Scheinin, Ville Sallinen JAMA Surgery 2020 November 18
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Frontiers | Clinical and Radiological Features of Adult Onset Bilateral Medial Frontal Cerebral Cortical Encephalitis With Anti-myelin Oligodendrocyte Glycoprotein Antibody | Neurology

Frontiers | Clinical and Radiological Features of Adult Onset Bilateral Medial Frontal Cerebral Cortical Encephalitis With Anti-myelin Oligodendrocyte Glycoprotein Antibody | Neurology | AntiNMDA | Scoop.it
Objective: To clarify the clinical and radiological features of adult onset anti-myelin oligodendrocyte glycoprotein (MOG) antibody-associated bilateral medial frontal cerebral cortical encephalitis (BFCCE).Methods: We systematically reviewed the literature for patients with anti-MOG...
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Paediatric multiple sclerosis and antibody-associated demyelination: clinical, imaging, and biological considerations for diagnosis and care

Paediatric multiple sclerosis and antibody-associated demyelination: clinical, imaging, and biological considerations for diagnosis and care | AntiNMDA | Scoop.it
The field of acquired CNS neuroimmune demyelination in children is transforming. Progress in assay development, refinement of diagnostic criteria, increased biological insights provided by advanced neuroimaging techniques, and high-level evidence for the therapeutic efficacy of biological agents...
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Antineuronal antibodies and epilepsy: treat the patient, not the lab | Journal of Neurology, Neurosurgery & Psychiatry

The study results implicate that starting immunosppressive treatment in new-onset epilepsy should be guided by clinics, not simply antibody presence Epilepsy affects about 70–80 million people worldwide; about one-third of patients cannot become seizure free. New diagnostic and therapeutic avenues to improve this situation are welcome. The impact of autoimmune phenomena on pathogenesis of some epilepsies increasingly gained attention as these mechanisms open the door for alternative medical treatments beyond antiseizure medications, that is, immunosuppressants. Thus, ‘autoimmune’ has become one of the six aetiologic categories of the new Intenational League Against Epilepsy classification of seizures and epilepsies. Numerous neuronal surface autoantibodies (NSAbs) identified in the past years cause autoimmune encephalitis (AE),1 often associated with severe seizures and status epilepticus. Additionally, the prevalence of NSAbs in patients with chronic epilepsies of unknown aetiology yielded a prevalence between 3% and 21%, but the question whether all epilepsy patients with NSAbs or only those with pharmacoresistant epilepsy (PRE) and/or additional signs of AE warrant immunosuppressants remained unresolved yet. A study looking at the presence of NSAbs in PRE found that 62% of patients responded to immunotherapy, and 34% even became seizure free, indicating that a trial may be justfied.2 But how does this result relate to patients with new-onset focal epilepsy (NFE)? The paper by Mc Ginty et al,3 tackles this issue by prospectively looking at those patients with NFE and a test positive for at least one NSAbs. The authors established an NSAbs prediction score based on clinical and paraclinical information and evaluated the value of immunotherapy in patients with NFE. About 10% of their cohort was NSAbs positive and 40% of them were diagnosed with AE. They identified six features which in combination were highly predictive for the presence of NSAbs, that is, age >54 years, ictal piloerection, self-reported lowered mood, MRI changes in the limbic system, the absence of ‘conventional’ epilepsy risk factors and intact attention. This ‘NSAbs-detecting’ Score compared better with the recently published ‘antibody prevalence in epilepsy and encephalopathy’ (APE2) Score4 in terms of forecasting AE, but worse in predicting presence of NSAbs. According to the present study (with an admittedly small sample of patients), immunotherapy could be omitted in those patients with NSAbs-positive new-onset epilepsy without signs or symptoms of AE. Conversely, the study also indicates that immunosuppressants are warranted in patients with even subtle AE. This is in line with another study where patients with AE even without NSAbs benefitted from immunosuppressants.5 The authors conclude that the administration of immunotherapy in NSAbs-positive patients should be guided by clinical signs for (subtle or obvious) AE and not only by NSAbs positivity per se. The study did not rely on cerebrospinal fluid data, probably leading to some missed cases of NSAbs positivity and AE. It is also interesting that 5/16 NSAbs positive, but AE-negative patients had mRS >0 and, thus, likely were pharmacoresistant, although this information was not exactly verifiable without follow-up phone interview. Statistically, this would exactly fit the one-third of patients basically becoming pharmacoresistant in chronic epilepsy of various aetiologies. Thus, future trials should test whether immunotherapy given to these patients would prevent pharmacoresistancy despite the fact that outcome without such treatment was mostly promising in this study.
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The Anti-NMDA Receptor Encephalitis Prize 2021 / Le prix de l'encéphalite à anticorps antirécepteurs nmda 2021

The Anti-NMDA Receptor Encephalitis Prize 2021 / Le prix de l'encéphalite à anticorps antirécepteurs nmda 2021 | AntiNMDA | Scoop.it
We are immensely proud to offer for the 3rd year in a row, The Anti-NMDA Receptor Encephalitis prize, in collaboration with the Canadian Neurological Society ...Read More...
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COVID Can Cause Forgetfulness, Psychosis, Mania or a Stutter - Scientific American

COVID Can Cause Forgetfulness, Psychosis, Mania or a Stutter - Scientific American | AntiNMDA | Scoop.it
Patrick Thornton, a 40-year-old math teacher in Houston, Tex., relies on his voice to clearly communicate with his high school students. So when he began to feel he was recovering from COVID, he was relieved to get his voice back a month after losing it. Thornton got sick in mid-August and had symptoms typical of a moderate case: a sore throat, headaches, trouble breathing. By the end of September, “I was more or less counting myself as on the mend and healing,” Thornton says. “But on September 25, I took a nap, and then my mom called.” As the two spoke, Thornton’s mother remarked that it was great that his voice was returning. Something was wrong, however. “I realized that some of the words didn’t feel right in my mouth, you know?” he says. They felt jumbled, stuck inside. Thornton had suddenly developed a severe stutter for the first time in his life. “I got my voice back, but it broke my mouth,” he says. After relaying the story over several minutes, Thornton sighs heavily with exhaustion. The thought of going back to teaching with his stutter, “that was terrifying,” he says. In November Thornton still struggled with low energy, chest pain and headaches. And “sometimes my heart rate [would] just decide that we’re being chased by a tiger out of nowhere," he adds. His stutter only worsened by that time, Thornton says, and he worried that it reflected some more insidious condition in his brain, despite doctors’ insistence that the speech disruption was simply a product of stress. A growing body of evidence warns that the legacy of the pandemic does not necessarily disappear when the novel coronavirus, or SARS-CoV-2, is cleared from the body. Among the millions of people who have survived respiratory complications from COVID-19, many still live with lingering symptoms in the wake of even a mild case of the disease. Neurological symptoms, ranging from fatigue to brain fog to loss of smell, persist after the virus is gone from the body. An early survey of 153 COVID-19 patients in the U.K. and a more recent preprint study of people hospitalized with the disease in Italy both found that about a third had neurological symptoms of some kind. Other estimates have trended even higher. “There’s a really wide spectrum of [neurological] manifestations of COVID,” says Thomas Pollak, a neuropsychiatrist at King’s College London and a co-author of the U.K. study. “Some are totally devastating, like stroke or encephalitis, and some are much more subtle.” Increasingly common symptoms include fatigue and memory problems—and, at times, new cases of psychosis or mania. Some neurological manifestations of post-COVID, such as stuttering, are more bizarre than others. But Houston’s Thornton is not the only one afflicted. Soo-Eun Chang, a neuroscientist at the University of Michigan, is among the few researchers investigating stutter. “While stress and anxiety are not the cause of stutter, they do exacerbate it,” Chang says, and that is true for Thornton. But she says the origins of the disorder lie in complex circuits of the brain that coordinate the millions of neuronal connections needed for human speech. While most people develop this disruption of speech when they learn to talk, around age two, neurogenic stutter can arise after brain trauma, such as an injury. Chang says her colleagues in clinical practice have reported seeing an increase in cases of stuttering during the pandemic—mostly in people whose existing stutter worsened or whose childhood stutter returned.* Having the virus, she says, could lead to conditions that disrupt speech. “Speech is one of the more complex movement behaviors that humans perform,” Chang says. “There are literally 100 muscles involved that have to coordinate on a millisecond time scale, so it’s a significant feat. And it depends on a well-functioning brain.” COVID’s inflammatory response could undermine the efficiency of these circuits. “An immune-mediated attack on synaptic connections could lead to a change in brain function,” she says. The idea that SARS-CoV-2 can get into the human brain is mainly supported by autopsy studies, such as one by Frank Heppner, a neuropathologist at Charité–University Medicine Berlin, and his colleagues. The researchers found evidence of the virus in specific areas of the brain, probably near the sites of entry. One could be the lining of the nasal passage, the olfactory mucosa, which is in close contact with neuronal cells that could provide a route to the brain. “We started at that region and then physically mapped [a pathway through] the regions up to the olfactory bulb and further to brain stem nuclei,” Heppner says. The researchers found evidence of viral protein in those distant brain stem regions but not in other areas of the brain. “This told us, or made it likely, that the virus used the transmucosal route along the olfactory nerve as a port of entry,” Heppner adds. They also saw viral particles in trigeminal nerves, which are sensory nerves that enter the brain and transmit the pain of headache. Heppner says his team also discovered hints that the virus could get into the brain through blood vessels. But autopsies were undertaken in those with severe disease, and it is uncertain whether the virus gets into the brain in milder cases. For most people, the symptoms brought on by COVID are likely the result of immune system activity. “The virus gets cleared from the lungs, but the immune system is triggered and doing harmful things,” Heppner says. “The same could be true for the central nervous system. It’s a fair speculation. It could explain very well the long COVID symptoms like chronic fatigue and problems in concentration.” William Banks, who studies the blood-brain barrier (BBB) at the Department of Veterans Affairs Puget Sound Health Care System in Washington State and the University of Washington Medical School, says, “The virus doesn’t have to get into the brain to muck up function. We know there’s a big cytokine storm,” meaning the release of inflammatory signals by immune cells in serious cases. Even mild cases provoke cytokine release, however. And Banks says it is well established that “cytokines can cross the blood-brain barrier and cause depressionlike symptoms.” Researchers refer to those symptoms—including a loss of interest in life, an increased desire to rest and sleep and cognitive impairments—as “sickness behavior,” which often accompanies a flu or cold. Those symptoms could drag on if cytokines continue to be released after the infection has passed. Yet another possibility is that the virus itself does not cross the BBB but that a viral protein, perhaps shed from a dying virus, might do so. Banks and his colleagues showed as much in a recent paper in Nature Neuroscience. They injected mice with S1, which makes up half of SARS-CoV-2’s “spike” protein, and found that it readily crossed the BBB. Michelle Erickson, who works with Banks at the VA Puget Sound and the University of Washington Medical School, says that the work “adds, at least in mice, a defined route by which the virus can get into brain, importantly, in the absence of inflammation,” when the blood-brain barrier might be leaky. “We saw that spike can get into the intact BBB,” she adds. “Often infiltration is almost entirely due to BBB disruption. But here it was only slightly disrupted, which was quite surprising to us.” The results hint that not only the S1 protein but potentially the virus itself could cross the BBB. A viral protein could cause damage by binding to proteins on neurons and other critical brain cells. “We know these binding proteins are very neurotoxic; they’re stress inducing,” Banks says. And the presence of any viral material could “shoot off the immune system.” There is yet another possibility: the virus could lead the immune system to produce damaging autoantibodies. These proteins bind not only to the virus but to other proteins in the body as well, either disrupting their function directly or triggering an immune attack on cells. “COVID wreaks havoc with the immune system,” says neuropsychiatrist Pollak. “There’s a huge surge in various inflammatory mediators.” Some early evidence suggests that anti-SARS-CoV-2 antibodies may react to tissues in the brain and body, he says, and that could possibly occur at neurons. Autoantibodies are the culprit in a recently described neurological disease called anti-NMDA receptor encephalitis, which can cause fatigue, brain fog, and even psychosis and coma. The immune system proteins bind to NMDA receptors that are critical for neuronal signaling. “Binding to neuronal proteins tends to disrupt synaptic function, like in the case of anti-NMDA receptor antibodies,” Pollak says. “That leads to signaling dysfunction, and information processing gets out of whack.” The autoantibody hypothesis still warrants further research. “It’s probably the most speculative and the one we know the least about,” Banks says.  Fatigue, brain fog and other symptoms probably arise from multiple different immune-mediated mechanisms. But researchers agree that synapses, where brain signals are passed from neuron to neuron, are probably disrupted. “We’re a long way off from understanding exactly how these nebulous responses arise,” Pollak says. “But the general principle is that if you create a perturbation in the system or the brain, you’ll affect its computational ability.” Recent preprint work by Andrew Yang at the laboratory of Tony Wyss-Coray of Stanford University also hints that the brain undergoes widespread changes in the wake of COVID-19 that could contribute to neurological symptoms. Yang and his colleagues found altered patterns of genes switching on and off in cells from the brains of patients who had died of the disease. These differences were observed in neurons and other brain cells—glia and immune cells called microglia. The genetic activation patterns differed from those observed in people who died of the flu or nonviral causes. Yang’s team examined an area of the cortex and saw dramatic gene expression changes in neurons in a specific region called cortical layer 2/3. These neurons have been recently implicated as playing a pivotal role in the complex processing required for human thought, so disruption of their activity could lead to mental fuzziness. The patterns of genetic changes the researchers saw in the cortex mirrored genetic pathways mapped out in mental illnesses such as schizophrenia and depression. In addition, Yang also found gene-expression changes in microglia, which clean up waste and eat dead cells in a process called phagocytosis. Microglia can consume, or phagocytose, neuron bodies and synapses, reshaping neural circuits if the cells are dying or even when they are under stress. Neurons generally do not regenerate, so cognitive function may be impaired. It is not only neurological symptoms that afflict patients. More common mental illnesses are affecting people with COVID, too. A study published in the Lancet Psychiatry showed that having the disease led to greater risk for anxiety, depression and sleep disorders. Paul Harrison of the University of Oxford and his colleagues sifted through the electronic health records of nearly 70 million Americans and identified more than 62,000 people who had been diagnosed with COVID-19. In the three months following diagnosis, “we found that COVID was associated with roughly twice the incidence of common psychiatric diagnoses, compared with other health conditions,” Harrison says. Why COVID increased the risk for mental illness remains unclear. But Harrison says the virus itself is probably not directly responsible. He points to the psychological consequences of having a potentially fatal illness that could prevent you from returning from the hospital to your family. “There are all sorts of acute stresses associated with the diagnosis,” he says. “I think those factors are going to be the most important explanation for the association we observed.” Still, Harrison adds that the immune response provoked by the virus may have also had an effect on the brain that could have triggered psychiatric symptoms. He has a study underway to investigate the longer-term mental health effects of COVID-19, including symptoms such as brain fog and fatigue. The legacy of COVID will undoubtedly persist. Although Thornton was still struggling by December, his stutter and energy level had improved, and he had gone back to teaching. “The kids have been really good about it,” he says. “It’s been a rocky road, but there’s light at the end.” Still, the lasting effects could mean not just bothersome symptoms for a few people but a public mental health crisis, Banks says. “It could ultimately turn out that—as horrible as the death rate is, with perhaps one in 1,000 Americans having died—in the end there, could be this legacy affecting up to one in 10,” he adds. “And it’s probably rooted in neuroimmunity.” Read more about the coronavirus outbreak from Scientific American here. And read coverage from our international network of magazines here. *Editor’s Note (1/22/21): This sentence was edited after posting to correct the description of Soo-Eun Chang’s comments regarding an increase in cases of stuttering.
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Count Down to WED Conference 2021: Meet Dr. Jérôme Honnorat

Count Down to WED Conference 2021: Meet Dr. Jérôme Honnorat | AntiNMDA | Scoop.it
Dr. Honnorat has more than 25 years of experience in the field of paraneoplastic neurological syndromes (PNS) and autoimmune encephalitis (AE). The topic of his presentations will be the role of genetics in autoimmune encephalitis (AE). He is head of the Department of Neuro-Oncology at the neurological hospital, Hospices Civils de Lyon and a team leader of the “Synaptopathies and Autoantibodies (SynatAc)” at the Institute NeuroMyoGene (UMR INSERM U1217, CNRS 5310). He is also chair of the French rare disease reference center “paraneoplastic neurological syndrome and autoimmune encephalitis” since 2007, which collects samples from all over France and provides care and follow-up for people with rare diseases. He has been working on PNS and AE for more than 25 years. His main work combines Basic and Clinical Research at multiple levels (patient’s cohorts; biological collections; cellular and animal models; biomarkers...) to explore the pathophysiologies of both brain tumors and neuro-inflammatory diseases and to detect specific autoantibodies as biomarkers of these diseases and as tools to understand synaptic functions.  We invite you to register today for what promises to be just one of the fascinating presentations of the conference.
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Normally Sharp, He Was Chronically Confused. What Was Going On? - The New York Times

Normally Sharp, He Was Chronically Confused. What Was Going On? - The New York Times | AntiNMDA | Scoop.it
He was getting lost driving home from work. And he was having strange spasms. What was the cause?
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Leveraging molecular biomarkers to make the common diagnosis in the uncommon patient - ScienceDirect

Leveraging molecular biomarkers to make the common diagnosis in the uncommon patient - ScienceDirect | AntiNMDA | Scoop.it
The factors that predispose to relapse in patients recovering with autoimmune encephalitis (AE) are largely unknown, complicating efforts to distingui…...
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Flortaucipir (tau) PET in LGI1 antibody encephalitis - Day - - Annals of Clinical and Translational Neurology

Flortaucipir (tau) PET in LGI1 antibody encephalitis - Day - - Annals of Clinical and Translational Neurology | AntiNMDA | Scoop.it
Abstract The contributors to persistent cognitive impairment and hippocampal atrophy in leucine‐rich glioma‐inactivated 1 antibody encephalitis (LGI1) patients are unknown. We evaluated whether tau...
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Collection of Biological Samples From Patients With Rare Neurological...

The aim of this project is to improve biological collections of patients presenting rare neurological disorders with known or suspected autoimmune origin...
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Individuals with psychosis more likely to have certain antibodies

Individuals with psychosis more likely to have certain antibodies | AntiNMDA | Scoop.it
Individuals with psychosis were more likely to have a higher prevalence of a particular antibody vs. controls, according to results of a meta-analysis published in The Lancet Psychiatry.&ldquo;The discovery of an encephalitic syndrome driven by antibodies targeting the N-methyl-D aspartate receptor...
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Diagnosis of pediatric anti-NMDAR encephalitis at the onset: A clinical challenge - ScienceDirect

Diagnosis of pediatric anti-NMDAR encephalitis at the onset: A clinical challenge - ScienceDirect | AntiNMDA | Scoop.it
To investigate the clinical and instrumental features at the onset addressing to the diagnosis of anti-NMDAR encephalitis.Twenty children (age: 15 mon…...
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