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Journal articles on the topic 'Encephalitis'

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Published: 4 June 2021
Last updated: 30 July 2024

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1

Badenoch, James, Tamara Searle, Iona Watson, and Andrea E. Cavanna. "Tics in patients with encephalitis." Neurological Sciences 42, no. 4 (January 23, 2021): 1311–23. http://dx.doi.org/10.1007/s10072-021-05065-w.

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Abstract Background Movement disorders have been described in the context of different types of encephalitis. Among hyperkinetic manifestations, tics have sporadically been reported in cases of encephalitis resulting from a range of aetiologies. Objective This review aimed to assess the prevalence and characteristics of tics in patients with encephalitis. Methods We conducted a systematic literature review of original studies on the major scientific databases, according to the standards outlined in the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Results In addition to the established association between tics and encephalitis lethargica, our literature search identified reports of tics in patients with immune-mediated pathologies (including autoimmune encephalitides affecting the N-methyl-d-aspartate receptor, voltage-gated potassium channels, and glycine receptors) and infective processes (ranging from relatively common viral pathogens, such as herpes simplex, to prions, as in Creutzfeldt-Jakob disease). Tics were most commonly reported in the post-encephalitic period and involvement of the basal ganglia was frequently observed. Discussion The association of new-onset tics and encephalitis, in the background of other neuropsychiatric abnormalities, has practical implications, potentially improving the detection of encephalitis based on clinical features. Future research should focus on the categorisation and treatment of hyperkinetic movement disorders associated with encephalitis.
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2

Stavrou, Maria, Jing Ming Yeo, Alexander David Slater, Sarosh Irani, and Peter Foley. "060 Fulminant meningitis as a presenting feature of anti-NMDA receptor encephalitis." Journal of Neurology, Neurosurgery & Psychiatry 90, no. 12 (November 14, 2019): A24.2—A24. http://dx.doi.org/10.1136/jnnp-2019-abn-2.79.

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Anti-NMDA receptor encephalitis is a well-recognised immunotherapy-responsive condition which often occurs as a paraneoplastic phenomenon. A typical presentation is in a young individual with a viral-like prodrome followed by the development of severe psychiatric symptoms, memory loss, seizures, reduced consciousness and sometimes orofacial dyskinesias, and progression to autonomic and respiratory instability. Fulminant meningitis is a very rare presenting feature of anti-NMDA receptor encephalitis with our literature search only revealing one other reported case.We present a case of a 33-year old Caucasian woman who initially presented with lymphocytic meningitis but subsequently developed clinical and investigative features consistent with anti-NMDA receptor encephalitis. Through this case, we aim to present and discuss possible mechanisms1–3underlying this atypical presentation and to highlight frank meningitis as an atypical presenting feature of anti-NMDA-receptor encephalitis. Clinicians should consider autoimmune encephalitides in individuals with meningitis, particularly where extensive investigations fail to identify a causative micro-organism and there is rapid development of an encephalitic phenotype. A multidisciplinary approach is required to address the neurological, gynaecological, oncological, and neuropsychiatric aspects of this challenging and incompletely understood disorder.ReferencesBektaş Ö, et al.Neuropediatrics2014;45(6):396–401Irani SR, et al.Brain2010;133(Pt 6):1655–67Dalmau J, et al.Lancet Neurol2008;7(12):1091–8
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3

Akinsulie, Olalekan Chris, Ridwan Olamilekan Adesola, Victor Ayodele Aliyu, Ifeoluwa Peace Oladapo, and Abdulafees Hamzat. "Epidemiology and Transmission Dynamics of Viral Encephalitides in West Africa." Infectious Disease Reports 15, no. 5 (September 5, 2023): 504–17. http://dx.doi.org/10.3390/idr15050050.

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Encephalitis is an inflammation of the brain, often caused by an autoimmune reaction, or in most cases because of a direct viral, bacterial, or parasitic infection. Viral encephalitides (VE) presents a significant public health concern globally, especially in West Africa. There are more than five hundred known arthropod-borne viruses (arboviruses), with over a hundred of them identified to cause encephalitic diseases in humans and animals, giving rise to a tremendous burden of the diseases and socioeconomic strains in tropical and subtropical regions worldwide. Despite their importance, few effective preventive and control measures in the form of vaccines and therapies are available, and when they are, their use is limited. These limitations are largely hinged on the paucity of information about the molecular epidemiology and transmission patterns of VE in West Africa. Here, we reviewed the transmission dynamics, molecular epidemiology, and the ecological drivers of VE in West Africa. Collectively, timely and accurate interventions are essential for encephalitic viral disease control. Moreover, the integrated health system approach, combining surveillance, vaccination, vector control, and community engagement, could be effective in preventing viral encephalitis globally.
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4

Gleadle, Jonathan, Christine Dixon, Martin M. Brown, and Frederick Schon. "The Use of Acyclovir in Suspected Encephalitis." Journal of the Royal Society of Medicine 87, no. 1 (January 1994): 7–8. http://dx.doi.org/10.1177/014107689408700105.

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The early use of intravenous acyclovir in herpes simplex encephalitis (HSE) is essential. However, rapid diagnostic tests are not freely available. Hence, all patients with suspected encephalitis may need to be commenced on acyclovir. In our study, of 34 patients with suspected encephalitis, only two eventually had HSE confirmed, 19 had encephalitis not due to herpes simplex and in 13 a non-encephalitic illness was finally diagnosed. Guidelines for the use of acyclovir in suspected encephalitis are given aimed at minimizing the drug cost whilst still protecting all cases of presumed HSE.
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5

Bradshaw, Michael, and Jenny Linnoila. "An Overview of Autoimmune and Paraneoplastic Encephalitides." Seminars in Neurology 38, no. 03 (June 2018): 330–43. http://dx.doi.org/10.1055/s-0038-1660821.

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AbstractThe understanding of the manifestations, mechanisms, and management of autoimmune encephalitis has expanded dramatically in recent decades. Immune-mediated encephalitides are comparable in incidence and prevalence to infectious etiologies, and are associated with significant morbidity, especially when there is a delay in recognition and treatment. As such, clinicians from many specialties must develop a functional understanding of these disorders. Herein we provide an overview of the autoimmune and paraneoplastic encephalitides, including those associated with either intracellular or cell surface/synaptic neuronal autoantibodies. After briefly reviewing the current understanding of the pathobiology of autoimmune encephalitis, we combine a neuroanatomical approach with specific antibody syndromes to provide the reader with a clinically relevant review of these disorders. The clinical manifestations, diagnosis, and management of autoimmune encephalitis are reviewed, with an emphasis on clinical relevance. We also introduce updates in the field, including autoimmune encephalitis associated with novel cancer immunotherapies, infectious triggers of autoimmune encephalitis, and autoimmune encephalitis with demyelinating overlap syndromes.
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6

Toledano, Michel, and Nicholas W. S. Davies. "Infectious encephalitis: mimics and chameleons." Practical Neurology 19, no. 3 (March 16, 2019): 225–37. http://dx.doi.org/10.1136/practneurol-2018-002114.

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‘Query encephalitis’ is a common neurological consultation in hospitalised patients. Identifying the syndrome is only part of the puzzle. Although historically encephalitis has been almost synonymous with infection, we increasingly recognise parainfectious or postinfectious as well as other immune-mediated causes. We must also distinguish encephalitis from other causes of encephalopathy, including systemic infection, metabolic derangements, toxins, inherited metabolic disorders, hypoxia, trauma and vasculopathies. Here, we review the most important differential diagnoses (mimics) of patients presenting with an encephalitic syndrome and highlight some unusual presentations (chameleons) of infectious encephalitis.
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7

Cartwright, Haley N., Dominique J. Barbeau, Joshua D. Doyle, Ed Klein, Mark T. Heise, Martin T. Ferris, and Anita K. McElroy. "Genetic diversity of collaborative cross mice enables identification of novel rift valley fever virus encephalitis model." PLOS Pathogens 18, no. 7 (July 14, 2022): e1010649. http://dx.doi.org/10.1371/journal.ppat.1010649.

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Rift Valley fever (RVF) is an arboviral disease of humans and livestock responsible for severe economic and human health impacts. In humans, RVF spans a variety of clinical manifestations, ranging from an acute flu-like illness to severe forms of disease, including late-onset encephalitis. The large variations in human RVF disease are inadequately represented by current murine models, which overwhelmingly die of early-onset hepatitis. Existing mouse models of RVF encephalitis are either immunosuppressed, display an inconsistent phenotype, or develop encephalitis only when challenged via intranasal or aerosol exposure. In this study, the genetically defined recombinant inbred mouse resource known as the Collaborative Cross (CC) was used to identify mice with additional RVF disease phenotypes when challenged via a peripheral foot-pad route to mimic mosquito-bite exposure. Wild-type Rift Valley fever virus (RVFV) challenge of 20 CC strains revealed three distinct disease phenotypes: early-onset hepatitis, mixed phenotype, and late-onset encephalitis. Strain CC057/Unc, with the most divergent phenotype, which died of late-onset encephalitis at a median of 11 days post-infection, is the first mouse strain to develop consistent encephalitis following peripheral challenge. CC057/Unc mice were directly compared to C57BL/6 mice, which uniformly succumb to hepatitis within 2–4 days of infection. Encephalitic disease in CC057/Unc mice was characterized by high viral RNA loads in brain tissue, accompanied by clearance of viral RNA from the periphery, low ALT levels, lymphopenia, and neutrophilia. In contrast, C57BL/6 mice succumbed from hepatitis at 3 days post-infection with high viral RNA loads in the liver, viremia, high ALT levels, lymphopenia, and thrombocytopenia. The identification of a strain of CC mice as an RVFV encephalitis model will allow for future investigation into the pathogenesis and treatment of RVF encephalitic disease and indicates that genetic background makes a major contribution to RVF disease variation.
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8

Bagic, Anto, Eilis A. Boudreau, Jacquelyn Greenfield, and Susumu Sato. "Electro‐clinical evolution of refractory non‐convulsive status epilepticus caused by West Nile virus encephalitis." Epileptic Disorders 9, no. 1 (March 2007): 98–103. http://dx.doi.org/10.1684/epd.2007.0056.

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ABSTRACT West Nile virus (WNV) has re‐emerged with a much wider geographic distribution and a higher incidence than ever. In spite of some recent reports on the neurological manifestations and EEG changes caused by WNV encephalitis, there are few data on the incidence of seizures, status epilepticus or post‐encephalitic epilepsy. There is also no systematic review of EEG changes caused by WNV encephalitis that is based on a large series of patients. Here, we review the pertinent literature, and report the electroclinical evolution and therapeutic complexity of a patient with WNV encephalitis who developed refractory, non‐convulsive status epilepticus.
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9

Jawad, Fazal, Sadiq Nouman, Bowen Michael, Muhammad Wasim Wali, Sawlani Vijay, and Jacob Saiju. "WED 148 Imaging findings in autoimmune encephalitis: a retrospective review." Journal of Neurology, Neurosurgery & Psychiatry 89, no. 10 (September 13, 2018): A17.2—A17. http://dx.doi.org/10.1136/jnnp-2018-abn.62.

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BackgroundNeuroimaging findings in autoimmune encephalitis may include normal MRI as well as limbic and extra-limbic involvement. Prompt recognition allows early immunosuppression and improved outcomes.MethodsRetrospective review of patients with Autoimmune encephalitis over the last 5 years.ResultsWe identified N-methyl-d-aspartate receptor (NMDAR) n=8, voltage gated potassium channel (VGKC) n=11, and leucine-rich glioma inactivated 1 (LGI1) n=11 encephalitis patients. 1/8 NMDAR encephalitis patients had abnormal MRI findings of T2 hyper intense signal in right anterior temporal and bilateral frontal and left insular lobe. DWI sequence showed restricted diffusion. 4/11 with VGKC encephalitis had positive MRI findings. Two patients had limbic involvement while one also had involvement of basal ganglia. Two patients had modest cerebral atrophy. Four patients had normal MRI findings. MRI scan was not available for three patients. 5/11 LGI1 encephalitis patients had bilateral mesial temporal lobe changes. In one patient, MRI could not be done due to permanent pacemaker. Five patients had normal MRI findings.ConclusionsIn our series, 33% patients had abnormal MRI findings consistent with a diagnosis of autoimmune encephalitis, which is lower than reported in literature. High clinical suspicion should lead to prompt diagnosis even in the absence of typical encephalitic changes on MRI.
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10

AbdulJabbar, Mohammad, Ibrahim Ghozi, Anwar Haq, and Hanz Korner. "Sudden ‘Stroke-Like’ Onset of Hemiparesis Due to Herpetic Encephalitis." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 22, no. 4 (November 1995): 320–21. http://dx.doi.org/10.1017/s0317167100039573.

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AbstractBackground/ObjectiveHerpes simplex encephalitis usually has a progressive cause. Sudden neurological deficits are unusual.MethodCase study.ResultsA 17-year-old girl presented with an acute onset focal neurological deficit followed one week later by the more classical feature of altered level of consciousness, fever and focal seizures. The diagnosis of hepetic encephalitis was made by magnetic resonance imaging (MRI) and by the significant increase in cerebrospinal fluid titres of antibodies against herpes simplex type I.ConclusionHerpetic encephalitis should be considered in the differential diagnosis of acute stroke in young patients even in the absence of encephalitic features, if common etiological factors such as embolization and intracerebral bleed are excluded.
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11

Bartlett, Maggie, Heather Poeck-Goux, Linwood Johnson Johnson, Kevin Scully, Amy Vittor, Ronald Hayes, Jean-Paul Carrera, and Darci R. Smith. "Biomarkers of Neurological Injury for Emerging Viral Threats and Post Viral Disease." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 235.23. http://dx.doi.org/10.4049/jimmunol.210.supp.235.23.

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Abstract Neurotropic viral infection and the ensuant immune response are a significant cause of morbidity and mortality worldwide, which can range in severity from mild to permanent central nervous system (CNS) damage and death. Encephalitic alphaviruses include Venezuelan and eastern equine encephalitis viruses (VEEV and EEEV; Alphavirus; Togaviridae). Injury to the CNS is an important determinant of poor outcome and tools to predict this outcome are lacking. Neurons are the primary target cells of encephalitic alphaviruses where cytopathology plays a major role in CNS dysfunction. Proteins are released following cell death, such as ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) and glial fibrillary acidic protein (GFAP) are neuromarkers of CNS tissue injury which could serve as biomarkers to assess injury severity, monitor disease progression, direct treatment, and as reliable endpoints to help develop novel medical countermeasures. Recent advances in the use of blood-based biomarkers for diagnosis of traumatic brain injury (TBI) which have FDA approved assays have provided a scientific foundation for expanding the biomarker technology to brain damage caused by other CNS pathologies like viral encephalitis. Here we evaluated the ability to detect these biomarkers for encephalitic alphaviruses, encephalitis of unknown origin, and hospitalized patients with severe coronavirus disease (COVID-19). Higher levels of specific biomarkers were detected in patients diagnosed with alphavirus or unknown encephalitis which may be useful in prognosis and treatment guidance of post viral disease. Collectively, our results suggest that these blood-based biomarkers may be a good indicator for brain injury resulting from viral infection.
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12

Suri, Vinit, Swapnil Jain, Mohit Kalangi Venkata Naga, Sudheer Tyagi, Aditendraditya Singh Bhati, and Kanika Suri. "Decompressive craniectomy in herpes simplex encephalitis: a case report." International Journal of Research in Medical Sciences 8, no. 7 (June 26, 2020): 2705. http://dx.doi.org/10.18203/2320-6012.ijrms20202923.

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Herpes Simplex Encephalitis is the commonest form of sporadic encephalitis. Availability of effective antiviral therapy viz Acyclovir has significantly reduced the mortality of Herpes Simplex Encephalitis. Elevated intracranial pressure resulting in herniation syndromes continues to be an important cause of mortality. Antiviral therapy and medical measures for managing raised intracranial pressure including osmotic diuretics, careful usage of steroids and controlled hyperventilation continue to be the cornerstones in management of these patients. Authors present a 38-year-old male patient with Cerebrospinal fluid Meningo-encephalitic panel positivity for herpes simplex virus 1 and bilateral temporal lobe lesions with secondary decline due to impending herniation syndrome despite osmotic diuretics and steroids with patient survival and complete recovery following decompressive hemicraniectomy.
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13

Tan, CT, and KT Wong. "Nipah Encephalitis Outbreak in Malaysia." Annals of the Academy of Medicine, Singapore 32, no. 1 (January 15, 2003): 112–17. http://dx.doi.org/10.47102/annals-acadmedsg.v32n1p112.

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Introduction: Between September 1998 and June 1999, there was a severe outbreak of viral encephalitis among the pig farm workers in Malaysia. Methods: This is a review of the published literature related to the outbreak with the focus on human diseases. Results: The encephalitis was caused by a newly discovered paramyxovirus related to Hendra virus, later named Nipah virus. There were 265 patients with acute encephalitis. The disease is thought to spread from pig to man through close contact. The risk of human-to-human spread is thought to be low. The disease affected mainly adult Chinese males, half of whom had affected family members. The disease presented mainly as acute encephalitis with a short incubation period of less than two weeks, with the main symptoms of fever, headache, and giddiness followed by coma. Distinctive clinical signs include segmental myoclonus, areflexia and hypotonia, hypertension, and tachycardia. Initial cerebrospinal fluid was abnormal in 75% of patients. Serology was helpful in confirming the diagnosis. Magnetic resonance imaging showed distinctive changes of multiple, discrete, and small high signal lesions, best seen with fluid-attenuated inversion recovery (FLAIR) sequences. Mortality was high at 40% and death was probably due to severe brainstem involvement. The main necropsy finding in acute encephalitis was that of disseminated microinfarction associated with vasculitis and direct neuronal involvement. Ribavirin was able to reduce the mortality by 36%. Relapse encephalitis was seen in 7.5% of those who recovered from acute encephalitis, and late-onset encephalitis in 3.4% of those with initial non-encephalitic or asymptomatic diseases. The mean interval between initial illness and the onset of the complication was 8.4 months. The relapse and late-onset encephalitis which manifested as focal encephalitis arose from recurrent infection. Conclusion: Nipah virus, a recently discovered paramyxovirus, causes a unique encephalitis with high mortality as well as relapse and late-onset encephalitis. The infection is mainly spread from pigs to man.
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Chouhan, Dr Arpan Singh. "Dengue Encephalitis." Journal of Medical Science And clinical Research 04, no. 12 (December 30, 2016): 14287. http://dx.doi.org/10.18535/jmscr/v4i12.02.

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15

Johnson, John, and P. A. Lucey. "Encephalitis Lethargica, a Contemporary Cause of Catatonic Stupor." British Journal of Psychiatry 151, no. 4 (October 1987): 550–52. http://dx.doi.org/10.1192/bjp.151.4.550.

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Two cases of catatonic stupor are described due to presumed encephalitis lethargica. Catatonic and obsessional phenomena in the setting of a depressive psychosis associated with a movement disorder may constitute a post-encephalitic syndrome.
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16

Rickards, Hugh, Saiju Jacob, Belinda Lennox, and Tim Nicholson. "Autoimmune encephalitis: a potentially treatable cause of mental disorder." Advances in Psychiatric Treatment 20, no. 2 (March 2014): 92–100. http://dx.doi.org/10.1192/apt.bp.113.011304.

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SummaryAutoimmune encephalitides can present with altered mental states, particularly psychosis and delirium. Psychiatrists need to be particularly vigilant in cases of first-episode psychosis and to look out for other, sometimes subtle, features of encephalitis. Encephalitis related to N-methyl-d-aspartate (NMDA) receptor autoantibodies is the most common autoimmune cause of isolated psychosis, the second being related to voltage-gated potassium channel (VGKC)-complex antibodies. Psychiatrists should note ‘red flag’ signs of seizures, autonomic instability, movement disorders and sensitivity to antipsychotic medication (including neuroleptic malignant syndrome). They should also be aware that, in some cases, encephalitis is a non-metastatic manifestation of malignancy. Treatment primarily involves suppression of immunity and is often successful if delivered early. There is accumulating evidence that isolated psychiatric syndromes can be caused by autoimmunity and this could potentially signal a significant change in the approach to disorders such as schizophrenia. Psychiatrists and neurologists need to work together to diagnose, manage and understand this group of conditions.LEARNING OBJECTIVES•Consider ‘red flags' for the diagnosis of autoimmune encephalitis presenting to general psychiatric practice.•Understand the investigations required to diagnose autoimmune encephalitis.•Become familiar with the basics of treatment of autoimmune encephalitis.
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Nissen, Mette Scheller, Matias Ryding, Morten Meyer, and Morten Blaabjerg. "Autoimmune Encephalitis: Current Knowledge on Subtypes, Disease Mechanisms and Treatment." CNS & Neurological Disorders - Drug Targets 19, no. 8 (December 24, 2020): 584–98. http://dx.doi.org/10.2174/1871527319666200708133103.

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Autoimmune Encephalitides (AE) comprises a group of diseases with antibodies against neuronal synaptic and cell surface antigens. Since the discovery of the most common subtype, NMethyl- D-Aspartate (NMDA) receptor encephalitis, an astonishing number of novel disease-causing antibodies have been described. This includes other glutamatergic and GABAergic receptor antibodies and antibodies against various other surface proteins. Many of these novel conditions present as limbic encephalitis with memory impairment, psychiatric features and epileptic seizures, often alongside subtype specific clinical features. Others present with a clinical disease course specific to the antibody. In contrast to the well-known paraneoplastic syndromes with antibodies directed against intracellular antigens (e.g. limbic encephalitis with Hu antibodies), autoimmune encephalitides are often highly responsive to immunotherapy, with a good outcome if diagnosed and treated early. Prognosis depends on aggressive immunotherapy, often with a combination of corticosteroids, intravenous immunoglobulin, plasma exchange or in some cases anti-CD20 therapy and cyclophosphamide. Other treatment regimens exist, and prognosis varies between disease subtypes and occurrence of underlying cancer. We review current knowledge on subtype-specific clinical presentation, disease mechanisms, diagnosis including pitfalls, treatment paradigms and outcome in autoimmune encephalitides, and provide suggestions for future research.
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18

Kumar, Dr Surender. "Rasmussen's Encephalitis - Chronic Focal Encephalitis (CFE) - A Rare Entity." Journal of Medical Science And clinical Research 05, no. 03 (March 22, 2017): 19229–34. http://dx.doi.org/10.18535/jmscr/v5i3.145.

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19

Ryding, Matias, Anne With Mikkelsen, Mette Scheller Nissen, Anna Christine Nilsson, and Morten Blaabjerg. "Pathophysiological Effects of Autoantibodies in Autoimmune Encephalitides." Cells 13, no. 1 (December 20, 2023): 15. http://dx.doi.org/10.3390/cells13010015.

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The heterogeneity of autoantibody targets in autoimmune encephalitides presents a challenge for understanding cellular and humoral pathophysiology, and the development of new treatment strategies. Thus, current treatment aims at autoantibody removal and immunosuppression, and is primarily based on data generated from other autoimmune neurological diseases and expert consensus. There are many subtypes of autoimmune encephalitides, which now entails both diseases with autoantibodies targeting extracellular antigens and classical paraneoplastic syndromes with autoantibodies targeting intracellular antigens. Here, we review the current knowledge of molecular and cellular effects of autoantibodies associated with autoimmune encephalitis, and evaluate the evidence behind the proposed pathophysiological mechanisms of autoantibodies in autoimmune encephalitis.
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20

Schmitt, LM, E. Balcom, M. Doan, WG Branton, J. Jovel, G. Blevins, B. Edguer, et al. "Clinical, neuropathological and molecular features of fatal human pegivirus-associated encephalitis." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 46, s2 (September 2019): S66. http://dx.doi.org/10.1017/cjn.2019.271.

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Flaviviruses include many viruses causing encephalitis, including West Nile encephalitis, St. Louis encephalitis, tick-borne encephalitis and Japanese encephalitis. Human pegivirus genotype-1 (HPgV-1) is a lesser known member of the Flaviviridae family and has been identified in human serum, cerebrospinal fluid and brain tissue. Here, we describe two adult patients with fatal HPgV-1-associated encephalitis. Neuroimaging revealed multifocal lesions, initially present in the periventricular and brain stem white matter, then one year later throughout the corona radiata bilaterally with marked involvement of the brainstem and cervical spinal cord. Phylogenetic analyses of HPgV-1 showed clustering of brain-derived sequences from both patients with other human pegiviruses. In both patients, a novel 87-nucleotide deletion in the viral NS2 gene was detected. The presence of positive and negative strand HPgV-1 RNA and viral antigens in both patients indicated viral persistence and replication in the CNS. Autopsy showed lymphocyte infiltration and gliosis predominantly in white matter of the brain and brain stem but, to a lesser extent, also in grey matter. Immunofluorescence revealed HPgV-1 NS5A antigen in lymphocytes as well as in astrocytes and oligodendrocytes. Thus, we hypothesize that the novel deletion in the NS2 coding region may have caused HPgV-1 neuroadaptation or might represent a yet unrecognized genotype of human pegivirus.LEARNING OBJECTIVESThis presentation will enable the learner to:1.Describe the clinical and neuropathological features of fatal human pegivirus-associated encephalitis2.Recognize the importance of molecular analysis in encephalitis cases with unknown etiology
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Hara, Makoto, Eugenia Martinez-Hernandez, Helena Ariño, Thais Armangué, Marianna Spatola, Mar Petit-Pedrol, Albert Saiz, Myrna R. Rosenfeld, Francesc Graus, and Josep Dalmau. "Clinical and pathogenic significance of IgG, IgA, and IgM antibodies against the NMDA receptor." Neurology 90, no. 16 (March 16, 2018): e1386-e1394. http://dx.doi.org/10.1212/wnl.0000000000005329.

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ObjectiveTo determine the frequency and clinical relevance of immunoglobulin (Ig)G, IgA, and IgM N-methyl-d-aspartate receptor (NMDAR) antibodies in several diseases, and whether the IgG antibodies occur in disorders other than anti-NMDAR encephalitis.MethodsEvaluation of IgG, IgA, and IgM NMDAR antibodies in serum of 300 patients with anti-NMDAR encephalitis, stroke, dementia, schizophrenia, or seronegative autoimmune encephalitis. Antibodies and their effect on cultured neurons were examined with cell-based assays and brain and live neuronal immunostaining. Retrospective analysis of the clinical diagnoses of a cohort of 1,147 patients with IgG NMDAR antibodies identified since 2005.ResultsAmong the 300 patients studied, IgG NMDAR antibodies were only identified in those with anti-NMDAR encephalitis and all reacted with brain and live neurons. By cell-based assay, IgA or IgM antibodies were detected in 22 of 300 patients (7%) with different diseases, but only 10 (3%) reacted with brain and 7 (2%) with live neurons. In cultured neurons, IgG but not IgA or IgM antibodies caused a decrease of synaptic and extrasynaptic NMDAR. Among the cohort of 1,147 patients with IgG NMDAR antibodies, 1,015 (88.5%) had anti-NMDAR encephalitis, 45 (3.9%) a limited form of the disease, 41 (3.6%) autoimmune post–herpes simplex encephalitis, 37 (3.2%) overlapping syndromes (anti-NMDAR encephalitis and demyelinating disease), and 9 (0.8%) atypical encephalitic syndromes; none had schizophrenia.ConclusionsIgG NMDAR antibodies are highly specific for anti-NMDAR encephalitis and cause a decrease of the levels of NMDAR. In contrast, IgA or IgM antibodies occur infrequently and nonspecifically in other diseases and do not alter the receptor levels.
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Das, SK, D. Lau, R. Cooper, J. Chen, VL Sim, JA McCombe, GJ Tyrrell, et al. "Mycobacterium chimaera encephalitis following cardiac surgery in three adult immunocompetent patients: first detailed neuropathological report." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 46, s2 (September 2019): S65—S66. http://dx.doi.org/10.1017/cjn.2019.270.

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Non-tuberculous mycobacterium encephalitis is rare. Since 2013, a global outbreak of Mycobacterium chimaera infection has been attributed to point-source contamination of heater cooler units used in cardiac surgery. Disseminated M. chimaera infection has presented many unique challenges, including non-specific clinical presentations with delays in diagnosis, and a high mortality rate among predominantly immunocompetent adults. Here, we describe three patients with fatal disseminated Mycobacterium chimaera infection showing initially non-specific, progressively worsening neurocognitive decline, including confusion, delirium, depression and apathy. Autopsy revealed widespread granulomatous encephalitis of the cerebrum, brain stem and spinal cord, along with granulomatous chorioretinitis. Cerebral involvement and differentiation between mycobacterial granulomas and microangiopathic changes can be assessed best on MRI with contrast enhancement. The prognosis of M. chimaera encephalitis appears to be very poor, but might be improved by increased awareness of this new syndrome and timely antimicrobial treatment.LEARNING OBJECTIVESThis presentation will enable the learner to:1.Describe the clinical, radiological and neuropathological findings of Mycobacterium chimaera encephalitis2.Be aware of this rare form of encephalitis, and explain its diagnosis, prognosis and management
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23

d’Offay, Jean M., Richard E. Mock, and Robert W. Fulton. "Isolation and characterization of encephalitic bovine herpesvirus type 1 isolates from cattle in North America." American Journal of Veterinary Research 54, no. 4 (April 1, 1993): 534–39. http://dx.doi.org/10.2460/ajvr.1993.54.04.534.

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Summary Nine cns bovine herpesvirus type 1 (bhv-1) isolates, recovered from bovine brain samples submitted to the Texas Veterinary Medical Diagnostic Laboratories from 1974-1989, were compared by analyzing their dna restriction endonuclease (re) fragment migration pattern. Seven had pattern similar to that of the respiratory bhv-1 Cooper strain. The remaining 2 isolates, however, had variant patterns, similar to that of each other, but completely different from patterns for the other 7. The re patterns of these 2 variants were similar to published re patterns for 2 encephalitic or neuropathogenic bhv-1 strains — the Australian N-569 strain and the Argentine A-663 strain. One of the Texas encephalitic variants (No. 30326) was isolated from the cns of a calf that died during an epizootic of encephalitis in 1974. The other, designated TX-89, was isolated in 1989 from the cns of a 7-month-old feedlot steer with acute fatal encephalitis. Microscopic lesions of encephalitis with neuronal degeneration and intranuclear inclusions were observed for 3 of the 9 isolates, the 2 variant isolates (No. 30326 and TX-89), and a respiratory isolate. The remaining 6 cns isolates, all respiratory subtypes, were recovered from cattle that did not have clinical cns disease or gross or microscopic cns lesions; in 5 of these cattle, virus was recovered from at least 1 other organ (lungs) besides the cns. We conclude that the cns of calves can be naturally infected with 2 distinct bhv-1 subtypes, the respiratory and the encephalitic, and that the encephalitic subtype (subtype 3 or bhv-1.3) has been present in Texas cattle since at least 1974.
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Griesman, Trevor, Cynthia M. McMillen, Seble Getenet Negatu, Jesse J. Hulahan, Kanupriya Whig, Lenka Dohnalová, Mark Dittmar, et al. "The lipopeptide Pam3CSK4 inhibits Rift Valley fever virus infection and protects from encephalitis." PLOS Pathogens 20, no. 6 (June 27, 2024): e1012343. http://dx.doi.org/10.1371/journal.ppat.1012343.

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Rift Valley fever virus (RVFV) is an encephalitic bunyavirus that can infect neurons in the brain. There are no approved therapeutics that can protect from RVFV encephalitis. Innate immunity, the first line of defense against infection, canonically antagonizes viruses through interferon signaling. We found that interferons did not efficiently protect primary cortical neurons from RVFV, unlike other cell types. To identify alternative neuronal antiviral pathways, we screened innate immune ligands and discovered that the TLR2 ligand Pam3CSK4 inhibited RVFV infection, and other bunyaviruses. Mechanistically, we found that Pam3CSK4 blocks viral fusion, independent of TLR2. In a mouse model of RVFV encephalitis, Pam3CSK4 treatment protected animals from infection and mortality. Overall, Pam3CSK4 is a bunyavirus fusion inhibitor active in primary neurons and the brain, representing a new approach toward the development of treatments for encephalitic bunyavirus infections.
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Hudson, Arthur J., and George P. A. Rice. "Similarities of Guamanian ALS/PD to Post-Encephalitic Parkinsonism/ALS: Possible Viral Cause." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 17, no. 4 (November 1990): 427–33. http://dx.doi.org/10.1017/s0317167100031024.

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ABSTRACT:Guamanian amyotrophic lateral sclerosis with parkinsonism-dementia (ALS/PD) has been the subject of intensive study since its discovery in 1947 because of its extraordinarily high incidence in a small ethnic group (Chamorros) whose dietary lack and customs have suggested possible causes. As yet, these and other suspected causes have eluded proof. Because of marked similarities between Guamanian ALS/PD and late onset post-encephalitic (encephalitis lethargica) parkinsonism and ALS it is suggested that they have a common cause. The parkinsonism and ALS in the two disorders are clinically very similar and neuropathological studies have shown a very similar distribution of neurofibrillary tangles in neurons. Some clinical differences, such as ocular features in the post-encephalitic cases and dementia in Guamanian ALS/PD, can be explained by differences in the severity of infection and the interval between the encephalitis and onset of sequelae. Although unproven, influenza A (HswilNl strain) has long been suspected as the cause of encephalitis lethargica because of simultaneous pandemics of the two diseases in the 1920s. Because influenza A can persistently infect cells and has a marked propensity to mutate it is an optimal candidate among other RNA viruses for delayed nervous system infection as a possible cause of ALS/PD.
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Solomon, T. "Flavivirus encephalitis and other neurological syndromes (Japanese encephalitis, WNV, Tick borne encephalits, Dengue, Zika virus)." International Journal of Infectious Diseases 45 (April 2016): 24. http://dx.doi.org/10.1016/j.ijid.2016.02.086.

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Greenlee, John E. "Encephalitis and Postinfectious Encephalitis." CONTINUUM: Lifelong Learning in Neurology 18, no. 6 (December 2012): 1271–89. http://dx.doi.org/10.1212/01.con.0000423847.40147.06.

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Kumar, Rashmi. "Understanding and managing acute encephalitis." F1000Research 9 (January 29, 2020): 60. http://dx.doi.org/10.12688/f1000research.20634.1.

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Encephalitis is an important cause of morbidity, mortality, and permanent neurologic sequelae globally. Causes are diverse and include viral and non-viral infections of the brain as well as autoimmune processes. In the West, the autoimmune encephalitides are now more common than any single infectious cause, but, in Asia, infectious causes are still more common. In 2006, the World Health Organization coined the term “acute encephalitis syndrome”, which simply means acute onset of fever with convulsions or altered consciousness or both. In 2013, the International Encephalitis Consortium set criteria for diagnosis of encephalitis on basis of clinical and laboratory features. The most important infectious cause in the West is herpes simplex virus, but globally Japanese encephalitis (JE) remains the single largest cause. Etiologic diagnosis is difficult because of the large number of agents that can cause encephalitis. Also, the responsible virus may be detectable only in the brain and is either absent or transiently found in blood or cerebrospinal fluid (CSF). Virological diagnosis is complex, expensive, and time-consuming. Different centres could make their own algorithms for investigation in accordance with the local etiologic scenarios. Magnetic resonance imaging (MRI) and electroencephalography are specific for few agents. Clinically, severity may vary widely. A severe case may manifest with fever, convulsions, coma, neurologic deficits, and death. Autoimmune encephalitis (AIE) includes two major categories: (i) classic paraneoplastic limbic encephalitis (LE) with autoantibodies against intracellular neuronal antigens (Eg: Hu and Ma2) and (ii) new-type AIE with autoantibodies to neuronal surface or synaptic antigens (Eg: anti-N-methyl-D-aspartate receptor). AIE has prominent psychiatric manifestations: psychosis, aggression, mutism, memory loss, euphoria, or fear. Seizures, cognitive decline, coma, and abnormal movements are common. Symptoms may fluctuate rapidly. Treatment is largely supportive. Specific treatment is available for herpesvirus group and non-viral infections. Various forms of immunotherapy are used for AIE.
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Leong, Wan Yi, Abdul Hanif Khan Yusof Khan, Janudin Baharin, Chao Loh WeiAnna Misya’il Abdul Rashid, Anna Misya’il Abdul Rashid, Wan Aliaa Wan Sulaiman, Kee Hoo Fan, Hamidon Basri, Laila Mastura Ahmad Apandi, and Liyana Najwa Inche Mat. "Acute Mycoplasma Pneumoniae Encephalitis in an Adult." Malaysian Journal of Medicine and Health Sciences 18, no. 5 (September 15, 2022): 222–24. http://dx.doi.org/10.47836/mjmhs.18.5.31.

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Mycoplasma pneumonia is an atypical bacterium that causes mild respiratory tract infections, especially in the upper respiratory system. Mycoplasma pneumoniae infection is infrequently associated with various CNS manifestations such as encephalitis, meningoencephalitis, myelitis, Guillain-Barre syndrome and acute disseminated encephalomyelitis (ADEM). Here we report a rare case of mycoplasma encephalitis in an adult who presented with a first episode of seizure following fever and neck stiffness for one week. Mycoplasma pneumoniae antibody titer was markedly elevated at >1:320 and MRI brain revealed encephalitic changes with a lesion in the splenium. Interestingly, there was no associated respiratory infection and his stay in the hospital was also complicated by SIADH. The patient improved after treatment with a macrolide antibiotic.
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Stone, E. Taylor, and Amelia K. Pinto. "T Cells in Tick-Borne Flavivirus Encephalitis: A Review of Current Paradigms in Protection and Disease Pathology." Viruses 15, no. 4 (April 13, 2023): 958. http://dx.doi.org/10.3390/v15040958.

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The family Flaviviridae is comprised of a diverse group of arthropod-borne viruses that are the etiological agents of globally relevant diseases in humans. Among these, infection with several of these flaviviruses—including West Nile virus (WNV), Zika virus (ZIKV), Japanese encephalitis virus (JEV), tick-borne encephalitis virus (TBEV), and Powassan virus (POWV)—can result in neuroinvasive disease presenting as meningitis or encephalitis. Factors contributing to the development and resolution of tick-borne flavivirus (TBEV, POWV) infection and neuropathology remain unclear, though many recently undertaken studies have described the virus–host interactions underlying encephalitic disease. With access to neural tissues despite the selectively permeable blood–brain barrier, T cells have emerged as one notable contributor to neuroinflammation. The goal of this review is to summarize the recent advances in tick-borne flavivirus immunology—particularly with respect to T cells—as it pertains to the development of encephalitis. We found that although T cell responses are rarely evaluated in a clinical setting, they are integral in conjunction with antibody responses to restricting the entry of TBFV into the CNS. The extent and means by which they can drive immune pathology, however, merits further study. Understanding the role of the T cell compartment in tick-borne flavivirus encephalitis is instrumental for improving vaccine safety and efficacy, and has implications for treatments and interventions for human disease.
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Cheng, Keat Moh, Calvin Ke Wen Wong, and Bee Ker Hong. "Dengue Encephalopathy or Japanese Encephalitis? Co-Infection or Serologic Cross- Reactivity?" NOVEMBER ISSUE 18, no. 6 (November 11, 2022): 344–46. http://dx.doi.org/10.47836/mjmhs.18.6.44.

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Dengue infection has a wide clinical spectrum ranging from asymptomatic presentation to life-threatening severe dengue with multiorgan failure, and increasingly recognized neurological presentation in the past decade. Japanese encephalitis on the other hand is another common mosquitoes-borne flavivirus infection endemic in Southeast Asia, which share some similar clinical features. We report a case of a 38-year-old male patient who presented to us with complaints of fever and acute encephalitis syndrome with positive dengue NS1 antigen, and positive cerebrospinal fluid serologies for both dengue and JE immunoglobulins. Magnetic Resonance Imaging findings were suggestive of encephalitic changes. Co-infection and serology cross-reactivity of these two flaviviruses is not uncommon in countries where both dengue and Japanese encephalitis are endemic, and thus, the treating clinician should have a high index of suspicion if clinical and serological evidence are present whilst treating the patient.
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Jhan, Ming-Kai, Chia-Ling Chen, Ting-Jing Shen, Po-Chun Tseng, Yung-Ting Wang, Rahmat Dani Satria, Chia-Yi Yu, and Chiou-Feng Lin. "Polarization of Type 1 Macrophages Is Associated with the Severity of Viral Encephalitis Caused by Japanese Encephalitis Virus and Dengue Virus." Cells 10, no. 11 (November 15, 2021): 3181. http://dx.doi.org/10.3390/cells10113181.

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Infection with flaviviruses causes mild to severe diseases, including viral hemorrhagic fever, vascular shock syndrome, and viral encephalitis. Several animal models explore the pathogenesis of viral encephalitis, as shown by neuron destruction due to neurotoxicity after viral infection. While neuronal cells are injuries caused by inflammatory cytokine production following microglial/macrophage activation, the blockade of inflammatory cytokines can reduce neurotoxicity to improve the survival rate. This study investigated the involvement of macrophage phenotypes in facilitating CNS inflammation and neurotoxicity during flavivirus infection, including the Japanese encephalitis virus, dengue virus (DENV), and Zika virus. Mice infected with different flaviviruses presented encephalitis-like symptoms, including limbic seizure and paralysis. Histology indicated that brain lesions were identified in the hippocampus and surrounded by mononuclear cells. In those regions, both the infiltrated macrophages and resident microglia were significantly increased. RNA-seq analysis showed the gene profile shifting toward type 1 macrophage (M1) polarization, while M1 markers validated this phenomenon. Pharmacologically blocking C-C chemokine receptor 2 and tumor necrosis factor-α partly retarded DENV-induced M1 polarization. In summary, flavivirus infection, such as JEV and DENV, promoted type 1 macrophage polarization in the brain associated with encephalitic severity.
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Lin, Chiou-Feng. "Targeting TNF-α against dengue virus-induced neurotoxicity and acute viral encephalitis-like symptoms." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 182.33. http://dx.doi.org/10.4049/jimmunol.200.supp.182.33.

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Abstract Pro-inflammatory tumor necrosis factor α (TNF-α) facilitates dengue virus (DENV) infection in endovascular dysfunction and neurotoxicity. The introduction of TNF-α blocking therapy with antibodies and antagonists is performed for testing its therapeutic effects in this study. In DENV-infected mice, TNF-α was produced in the brains accompanied by the progression of neurotoxicity and encephalitis. DENV infection caused loss in hippocampal neurons with TNF-α expression around the damaged regions. Additionally, immunostaining showed the induction of apoptosis in hippocampal neurons. TNF-α was expressed in active microglia as well as astrocytes of DENV-infected mice. TNF-α facilitated DENV-induced neurotoxicity in vitro in murine Neuro-2a cells. By using a currently established encephalitic mice model that DENV infection caused progressive hunchback posture, limbic seizures, limbic weakness, paralysis, and lethality 7 days post-infection, TNF-α transgenic mice represented the progressive disease development while administration of neutralizing TNF-α antibody reduced dengue encephalitis and mortality. These results demonstrate an immunopathogenesis of TNF-α for mediating DENV-induced encephalitis-associated neurotoxicity and targeting TNF-α can be used as a strategy against dengue encephalitis.
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34

Dehority, Walter, Andrew B. Janowski, Kevin Messacar, Kevin Messacar, Philip M. Polgreen, and Susan E. Beekmann. "355. Variability in the Current Evaluation and Management of Pediatric Encephalitis: Survey Results from an Emerging Infections Network Survey." Open Forum Infectious Diseases 7, Supplement_1 (October 1, 2020): S246—S247. http://dx.doi.org/10.1093/ofid/ofaa439.550.

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Abstract Background Childhood encephalitis causes severe morbidity and mortality. Difficulty identifying causative organisms and a lack of effective therapies leads to variability in management. The recent emergence of novel diagnostic tools and the increased recognition of auto-immune encephalitides has the potential to change the approach to this disease. Our objective was to assess the current evaluation and management of childhood encephalitis. Methods An 11-question confidential, web-based survey was distributed by the Emerging Infections Network (EIN) of the Infectious Disease Society of America to 370 Pediatric Infectious Disease (ID) physicians between January 29th and February 17th, 2020. Respondents were characterized by practice region, experience since fellowship, place of employment and primary hospital type. Responses were analyzed with SAS, v 9.4. Results Responses were obtained from 222 of 370 members (60%) (Table). Of the 222 respondents, 196 (88%) reported caring for children with suspected encephalitis and form the basis for this report. Multi-plex PCR testing of cerebrospinal fluid (CSF) in the initial evaluation of most children with suspected encephalitis was reported by 56% (with 65% of these respondents reporting the use of pathogen-specific confirmatory testing). CSF metagenomic next generation sequencing (mNGS) had been used by 47%, with 74% of all respondents stating they would use this test if likely diagnoses were excluded via standard testing (and 64% of these only using the test if the child was not improving). Variability in the interpretation of negative CSF mNGS results was reported (Fig 1a). Primary involvement of ID physicians in the diagnostic evaluation of auto-immune encephalitis was reported by 33%, yet only 55% of ID physicians reported feeling comfortable diagnosing this condition. Marked variation existed regarding criteria for the use of immunomodulating agents (Fig 1b) and the need for testing for autochthonous tropical viruses in the U.S. (Fig 1c). Background of 222 Respondents to an Emerging Infections Network Survey Assessing the Evaluation and Management of Pediatric Encephalitis. ID=Infectious Disease; VA=Veterans Affairs; DOD=Department of Defense *Respondents were significantly more likely than non-respondents to have <5 years of ID experience (p=0.04). Figure 1 Approaches to the Interpretation of CSF mNGS Results, Use of Immunomodulating Agents and Testing for Autochthonous Tropical Viral Pathogens in Children with Encephalitis Conclusion Variation exists in the evaluation and management of childhood encephalitis, including the application of new diagnostic modalities and management of autoimmune encephalitides. Updated standardized management guidelines may improve implementation of advances in this realm. Disclosures All Authors: No reported disclosures
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35

BG, Ranganath. "Japanese Encephalitis/Acute Encephalitis Syndrome: Prevention and Control Strategies in India." JOURNAL OF CLINICAL AND BIOMEDICAL SCIENCES 05, no. 03 (September 15, 2015): 98–106. http://dx.doi.org/10.58739/jcbs/v05i3.11.

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B.G, Dr Ranganath. "Acute Encephalitis Syndrome in India – Japanese Encephalitis, Polluted Water and Malnutrition." JOURNAL OF CLINICAL AND BIOMEDICAL SCIENCES 05, no. 2 (June 15, 2015): 52–53. http://dx.doi.org/10.58739/jcbs/v05i2.8.

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37

Bondre, Vijay P., Gajanan N. Sapkal, Prasanna N. Yergolkar, Pradip V. Fulmali, Vasudha Sankararaman, Vijay M. Ayachit, Akhilesh C. Mishra, and Milind M. Gore. "Genetic characterization of Bagaza virus (BAGV) isolated in India and evidence of anti-BAGV antibodies in sera collected from encephalitis patients." Journal of General Virology 90, no. 11 (November 1, 2009): 2644–49. http://dx.doi.org/10.1099/vir.0.012336-0.

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During investigations into the outbreak of encephalitis in 1996 in the Kerala state in India, an arbovirus was isolated from a Culex tritaeniorhynchus mosquito pool. It was characterized as a Japanese encephalitis and West Nile virus cross-reactive arbovirus by complement fixation test. A plaque reduction–neutralization test was performed using hyperimmune sera raised against the plaque-purified arbovirus isolate. The sera did not show reactivity with Japanese encephalitis virus and were weakly reactive with West Nile virus. Complete open reading frame sequence analysis characterized the arbovirus as Bagaza virus (BAGV), with 94.80 % nucleotide identity with African BAGV strain DakAr B209. Sera collected from the encephalitic patients during the acute phase of illness showed 15 % (8/53) positivity for anti-BAGV neutralizing antibodies. This is the first report of the isolation of BAGV from India. The presence of anti-BAGV neutralizing antibodies suggests that the human population has been exposed to BAGV.
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Diao, Xavier, and Milana Mor. "Anti-NMDA Receptor Encephalitis in a Patient with a History of Autism Spectrum Disorder." Adolescent Psychiatry 10, no. 3 (December 21, 2020): 231–35. http://dx.doi.org/10.2174/2211352517666190902144221.

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Background: Anti-NMDA receptor (NMDAR) encephalitis is an autoimmune syndrome characterized by a well-described constellation of neuropsychiatric symptoms. Its exact pathophysiology is poorly understood, but it is thought to be mediated by autoantibodies against NMDA (N-methyl-D-aspartate)-type glutamate receptors in the central nervous system. There is ongoing literature to suggest that patients with autism spectrum disorder (ASD) have evidence of neuroinflammation—or by definition, encephalitis. Objective: To investigate the link between autism spectrum disorder and autoimmune encephalitides. Methods: We present a case of anti-NMDA receptor encephalitis in a patient with autism spectrum disorder. “OP” is a 16-year-old male with a history of attention-deficit/ hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) who presented with a 3-day history of acute-onset altered mental status, electroencephalogram (EEG)-corroborated seizures, and slurred speech. Laboratory studies were significant for serum- and cerebrospinal fluid (CSF)-positive NMDA antibodies. The child psychiatry consult-liaison service was consulted for significant agitation and behavioral dyscontrol. We recommended 1:1 observation for safety, as well as antipsychotic agents titrated to clinical effect. The patient had a protracted hospital course, but was eventually discharged to an acute rehabilitation facility for continued stabilization and therapy. Conclusion: It remains to be seen if the relation between encephalitis and ASD is uni- or bidirectional, that is: whether children with ASD have a genetic diathesis to developing encephalitides (such as those mediated by the NMDAR), or conversely, if deranged or inflamed neuroreceptor processes are implicated in the development of ASD.
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Wang, Hsiuying. "Anti-NMDA Receptor Encephalitis: Efficacy of Treatment for Male Patients and miRNA Biomarker." Current Medicinal Chemistry 27, no. 24 (July 7, 2020): 4138–51. http://dx.doi.org/10.2174/0929867325666180221142623.

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Background: Anti-N-methyl-D-aspartate (NMDA) receptor encephalitis is an acute form of encephalitis. Treatments for the anti-NMDA receptor encephalitis usually include steroids, intravenous immunoglobulin, plasma exchange, plasmapheresis, rituximab, cyclophosphamide and tumor resection. Objective: We aimed to compare the efficacy of the treatments including intravenous immunoglobulin, plasma exchange, plasmapheresis, rituximab or cyclophosphamide for male anti- NMDA receptor encephalitis patients without tumor and to discuss potential biomarkers for this disease. Method: The Fisher exact test and the contingency table analysis were used to analyze the treatment efficacy for 43 male and 76 female patients. In addition, a hierarchical tree method was adopted to analyze the difference in the treatment efficacy between male and female patients. Results: The p-values of testing whether the efficacy rate of plasmapheresis (or plasma exchange) for the male patient is greater than a threshold are significantly different from the pvalues for the other two treatments. In addition, the hierarchical tree method shows that the treatment strategy associating with early recovery is different for male and female patients. Conclusion: The results revealed that the efficacy rate of plasmapheresis (or plasma exchange) is not inferior to that of intravenous immunoglobulin and rituximab (or cyclophosphamide) for male patients without tumor. In addition, B-cell attracting C-X-C motif chemokine 13 (CXCL13) and microRNA let-7b have the potential to be the treatment response biomarkers for anti-NMDA receptor encephalitis. They may not be useful prognostic biomarkers for this encephalitis unless they are not biomarkers for other autoimmune encephalitides.
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Sahu, Neelam, Pushpendra Nath Renjen, Avinash Goswami, Shams Kanuga, and Nidhi Goyal. "Anti-NMDA antibody autoimmune encephalitis post-HSV encephalitis: A rare case report." Edorium Journal of Neurology 9, no. 1 (March 13, 2024): 1–4. http://dx.doi.org/10.5348/100018n06ns2024cr.

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Introduction: Autoimmune encephalitis is a group of neuropsychiatric disorder in which antibodies interact directly to their target antigen and produce neuronal dysfunction. Generally herpes simplex encephalitis is a monophasic illness although in few patients neurological worsening can develop some weeks later. This worsening is generally due to autoimmune encephalitis after herpes simplex encephalitis (AEaHSE). Case Report: We report an interesting case report of 67 years old female patient who initially was diagnosed to have herpes simplex virus (HSV) encephalitis, showed improvement in her clinical status followed subsequently by deterioration in cognitive status. Anti-N-methyl-D-aspartate (NMDA) antibody was positive in cerebrospinal fluid (CSF) and serum. The patient was managed with intravenous immunoglobulin (IVIG) and subsequently showed improvement in her clinical state. Conclusion: The discovery and clinical application of anti-NMDA receptor antibodies has helped to define the mechanism behind immune-based relapse of herpes simplex virus encephalitis (HSVE). This case illustrates the usefulness of testing for anti-NMDA receptor antibodies following worsening few weeks after treatment of herpes simplex encephalitis.
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Urriola, Nicolás, Kavie Soosapilla, James Drummond, and Mark Thieben. "Fulminant thymomatous AMPAR-antibody limbic encephalitis with hypertonic coma, bruxism, an isoelectric electroencephalogram and temporal cortical atrophy, with recovery." BMJ Case Reports 12, no. 2 (February 2019): e227893. http://dx.doi.org/10.1136/bcr-2018-227893.

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Autoimmune encephalitides are a potentially devastating group of treatable disorders with a wide variety of clinical presentations. The most studied autoimmune encephalitis is caused by antibodies to the N-methyl-D-aspartate glutamate receptor. A rarer cause is due to antibodies against the evolutionarily related α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR). The full assortment of electroencephalogram (EEG) and clinical descriptions of the latter are yet to be fully described. A 44-year-old woman with impaired consciousness and subsequent coma characterised by an isoelectric EEG was diagnosed with AMPAR-antibody limbic encephalitis. MRI revealed temporal T2 hyperintensities that improved with immunosuppression, although leaving marked cortical atrophy. Gradual clinical improvement saw the development of aggressive bruxism requiring botulinum toxin injection with eventual meaningful clinical recovery. This case expands the clinical spectrum of AMPAR limbic encephalitis to include aggressive bruxism, and highlights that despite poor clinical and EEG findings at the outset, recovery is still possible.
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Storset, A. K., Ø. Evensen, and E. Rimstad. "Immunohistochemical Identification of Caprine Arthritis-Encephalitis Virus in Paraffin-embedded Specimens from Naturally Infected Goats." Veterinary Pathology 34, no. 3 (May 1997): 180–88. http://dx.doi.org/10.1177/030098589703400302.

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The expression of caprine arthritis-encephalitis virus capsid protein was studied in seropositive naturally infected asymptomatic goats (10), seropositive naturally infected encephalitic kids (12) and goats (4), and noninfected control goats (3). Rabbit antiserum to recombinant viral capsid and matrix proteins were used in a biotin-streptavidin-alkaline phosphatase complex immunohistochemical method on sections of formalin-and ethanol-fixed tissue specimens. Macrophages in inflamed areas of the lung (8/12), in the brain (5/16), and in the spinal cord (4/16) from encephalitic animals harbored viral antigens, as revealed by immunohistochemistry and use of a capsid protein-specific antiserum. Altogether 12/16 encephalitic animals tested positive for viral antigen. Viral antigens were found in 5/10 seropositive asymptomatic goats in macrophages located in the lung (3), the udder (1), and the medulla of lymph nodes (4). None of the control animals tested positive for viral antigen. Ethanol fixation showed highest sensitivity, and the lowest antigen concentration that revealed a positive signal discernible from background was twofold higher in ethanol-fixed specimens than in formalin-fixed specimens. The evaluation was performed on artificial antigen substrates embedded with defined concentrations of recombinant viral capsid protein. Immunohistochemistry is a valuable supplement to the methods presently available for diagnosis in cases suspicious of caprine arthritis-encephalitis.
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Ogawa, Ryo, Ichiro Nakashima, Toshiyuki Takahashi, Kimihiko Kaneko, Tetsuya Akaishi, Yoshiki Takai, Douglas Kazutoshi Sato, et al. "MOG antibody–positive, benign, unilateral, cerebral cortical encephalitis with epilepsy." Neurology - Neuroimmunology Neuroinflammation 4, no. 2 (January 16, 2017): e322. http://dx.doi.org/10.1212/nxi.0000000000000322.

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Objective:To describe the features of adult patients with benign, unilateral cerebral cortical encephalitis positive for the myelin oligodendrocyte glycoprotein (MOG) antibody.Methods:In this retrospective, cross-sectional study, after we encountered an index case of MOG antibody–positive unilateral cortical encephalitis with epileptic seizure, we tested for MOG antibody using our in-house, cell-based assay in a cohort of 24 consecutive adult patients with steroid-responsive encephalitis of unknown etiology seen at Tohoku University Hospital (2008–2014). We then analyzed the findings in MOG antibody–positive cases.Results:Three more patients, as well as the index case, were MOG antibody–positive, and all were adult men (median age 37 years, range 23–39 years). The main symptom was generalized epileptic seizure with or without abnormal behavior or consciousness disturbance. Two patients also developed unilateral benign optic neuritis (before or after seizure). In all patients, brain MRI demonstrated unilateral cerebral cortical fluid-attenuated inversion recovery hyperintense lesions, which were swollen and corresponded to hyperperfusion on SPECT. CSF studies showed moderate mononuclear pleocytosis with some polymorphonuclear cells and mildly elevated total protein levels, but myelin basic protein was not elevated. A screening of encephalitis-associated autoantibodies, including aquaporin-4, glutamate receptor, and voltage-gated potassium channel antibodies, was negative. All patients received antiepilepsy drugs and fully recovered after high-dose methylprednisolone, and the unilateral cortical MRI lesions subsequently disappeared. No patient experienced relapse.Conclusions:These MOG antibody–positive cases represent unique benign unilateral cortical encephalitis with epileptic seizure. The pathology may be autoimmune, although the findings differ from MOG antibody–associated demyelination and Rasmussen and other known immune-mediated encephalitides.
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Lewis, Paul, and Carol A. Glaser. "Encephalitis." Pediatrics in Review 26, no. 10 (September 30, 2005): 353–63. http://dx.doi.org/10.1542/pir.26-10-353.

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45

Beretta, Ruth. "Encephalitis." Nursing Standard 30, no. 23 (February 3, 2016): 61–62. http://dx.doi.org/10.7748/ns.30.23.61.s48.

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46

Gutierrez, Kathleen M., and Charles G. Prober. "Encephalitis." Postgraduate Medicine 103, no. 3 (March 1998): 123–43. http://dx.doi.org/10.3810/pgm.1998.03.413.

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47

&NA;. "Encephalitis." Pediatric Emergency Care 29, no. 2 (February 2013): 242–44. http://dx.doi.org/10.1097/01.pec.0000427421.57191.7c.

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48

Kamath, Priyanka N. "Encephalitis." Obstetrics & Gynecology 123 (May 2014): 29S. http://dx.doi.org/10.1097/01.aog.0000447295.23039.15.

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Guerci, Ingrid R. "Encephalitis." Neurology Now 5, no. 4 (July 2009): 6. http://dx.doi.org/10.1097/01.nnn.0000359071.09915.4b.

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Roos, Karen L. "ENCEPHALITIS." Neurologic Clinics 17, no. 4 (November 1999): 813–33. http://dx.doi.org/10.1016/s0733-8619(05)70168-7.

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You might also be interested in the bibliographies on the topic 'Encephalitis' for other source types:
Dissertations / Theses Books
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To the bibliography