View clinical trials related to Encephalitis.
Filter by:Using a retrospective cohort of 501 patients with anti-NMDAR encephalitis to assess clinical and immunological prognostic biomarkers
Autoimmune encephalitis (AE) and paraneoplastic neurological syndromes (PNS) are rare neuroimmune syndromes with a wide range of clinical presentation but without pathognomonic clinical sign facilitating the diagnosis. A lot of differential diagnoses are possible such as neurodegenerative diseases or viral infections. Although rare the diagnosis of AE or PNS is essential because despite severe neurological symptoms, patients can be cured by appropriate immunotherapy. Autoantibodies highly specific of AE and PNS has been described in the serum and cerebrospinal fluid of the patients and can be used as biomarkers of the disease. Their presence can predict an autoimmune origin and in many cases a good prognosis after immunotherapy. However, if some autoantibodies are now well-characterized and industrial kits have been developed to detect them, in numerous cases of highly suspect AE or PNS no specific autoantibodies are identified leading frequently to an inappropriate treatment. Furthermore, as the mechanisms of AE and PNS is still unknown, treatments are not optimal and in some cases inefficient. There is no prognosis biomarker able to predict the patient's sensitivity to immunotherapy and there are only few clues to know how the immune system can provoke the neuropsychiatric symptoms observed in the patients. The investigators will use this project to better characterize AE and PNS patients to identify new diagnostic and prognostic biomarkers and develop new diagnostic tools.
Epilepsy is a disorder of the brain in which people have repeated seizures. Autoimmune encephalitis (AE) is a rare cause of epilepsy. It is an inflammatory disease of the brain. This means that the body's own immune system attacks healthy brain tissue, just like it would if it were infected by a virus or a bacteria, by producing an army of proteins called 'antibodies' which go on to 'attack' healthy tissues. Seizures in AE typically do not respond well to classic 'anti-seizure medications'. Instead, medications which suppress the immune system are used. These can have significant side-effects and some patients will still continue to have seizures or experience a recurrence of AE-related epilepsy despite treatment. It is difficult to accurately predict who will experience these outcomes. This study aims to find ways of predicting and monitoring which people with AE are at greatest risk of these outcomes, so we can better direct them towards appropriate treatments. We will collect clinical information and samples of blood and cerebrospinal fluid (CSF, fluid surrounding the brain and spinal cord) from people with AE and 'control' participants with other neurological illnesses. Samples will be analysed for markers which may help predict or correlate with outcomes in AE and better understand this condition.
Paraneoplastic neurological syndromes (PNS) are rare complications of cancer occurring in 0.01% of cases. Their clinical, biological and radiological presentation is heterogeneous and may constitute a diagnostic challenge. Anti-Ma2 PNS are rare diseases with a guarded prognosis. They are most often associated with a seminoma-like testicular tumor but can also be associated with lung cancer. Classically, they present as limbic, diencephalic and/or brainstem encephalitis. Anti-Ma2 antibodies target intracellular receptors and are characteristic of a particular form of encephalitis. Atypical manifestations including narcolepsy-cataplexy, weight gain, sexual dysfunction and motor neuron syndrome have been described and explain the difficulty in diagnosing anti-Ma2 associated PNS. It seems interesting to better characterize the phenotypes of Ma2 patients in order to optimize the diagnosis and follow-up.
This study aims to evaluate the diagnostic and prognostic performance of a novel mRNA diagnostic/prognostic classifier (interprets the expression of 29 host response mRNA biomarkers) from whole blood in adult patients presenting to emergency departments (ED) with suspected infection.
Tick-borne encephalitis (TBE) is a zoonosis mainly transmitted to humans by the bite of ticks of the genus Ixodes and, to a lesser extent, by the consumption of contaminated and unpasteurized dairy products. During the last decade, the epidemiology of this arbovirosis has changed profoundly with the discovery of new human cases and/or new areas of circulation of tick-borne encephalitis virus (TBEV) throughout Europe and particularly in France. Historically, Alsace is the main endemic area for this pathology in France. The pathology is notifiable since June 2021 in France. Although TBEV infection in children seems to lead to a milder clinical presentation, data are much less abundant than in adults and only a few cases reported in infants under 1 year old have been published. Data from the most recent ECDC Annual Epidemiological Report on TBE (2019) showed incidence rates of approximately 0.2 and 0.5 per 100,000 population in patients younger than 5 and 15 years, respectively. However, several observations may moderate and challenge both the low incidence rate and the less severe clinical presentation reported in children
The number of acute encephalitides diagnosed each year is gradually increasing, reaching approximately 5 to 10/100,000 per year; more than 50% of etiologies currently remain unknown. The majority of them are acute encephalitis of infectious origin, but it is estimated that 20% of encephalitis in northern Europe is related to an autoimmune mechanism with the majority of encephalitis with anti-NMDA Ac discovered recently in 2007. The study of a large American encephalitis cohort showed a death rate of 3% to 7% in cases of autoimmune encephalitis. Furthermore, delay in the initiation of effective treatment (tumor removal or immunotherapy) beyond 4 weeks is associated with a poor prognosis at 1 year. It is therefore necessary to better understand the signs of autoimmune encephalitis in order to recognize the disease quickly and to start a treatment quickly; in order to improve the management and the prognosis of these children.
The purpose of this study is to longitudinally characterize and evaluate changes in synaptic density in the brain using novel positron-emission tomography (PET) scans; magnetic resonance imaging (MRI), and clinical laboratory markers associated with HIV-related injury in the central nervous system. This study will test hypotheses relating to the presence and mechanisms of aberrant brain structure at the synaptic level in living humans with virologically controlled HIV on antiretroviral therapy. To evaluate associations between PET imaging radiotracers [11C]UCB-J, a ligand for presynaptic vesicle protein 2A (SV2A), a vesicle membrane protein expressed in synapses, and PET [11C]PBR28 a measure of microglia function in the brain, the Yale PET center has developed an advanced approach of combining multiple distinct ligands in coordinated same-day PET imaging. Additionally, the study will evaluate the associations of this novel synaptic density marker with well-established clinical measures of neurocognitive performance and laboratory measures of blood and cerebrospinal fluid (CSF).
Background and objective From this April, there was a COVID-19 outbreak in Taiwan. The first fatal case of pediatric COVID-19 encephalitis was reported on April 19, 2022 and fatal fulminant cerebral edema in other 4 children with COVID-19 encephalitis was reported within 1 month from Taiwan CDC registry. To date, around 700,000 children got COVID-19 recently. Several children developed MIS-C (multi-system inflammatory syndrome in children)-related shock about 2-6 weeks after COVID-19. Since both COVID-19 associated encephalopathy/ encephalitis and MIS-C are life-threatening, it is urgent to delineate its prognostic biomarker, host genetic factors, immunopathogenesis and viral pathogenesis. Methods Pediatricians will enroll cases of both COVID-19 associated encephalopathy/ encephalitis and MIS-C from several hospitals and medical centers. Their clinical manifestations, lab findings, severity and outcomes will be collected. Clinical assessment of all the systems will be performed. Blood, nasopharyngeal swab and stool will be collected at acute, subacute and convalescent stages for whole exome sequencing, immunopathogenesis including chemokine/cytokine, T/B lymphocyte subset, SARS-CoV2 specific Ab/T/B cell, T and B cell repertoire, viral pathogenesis including multiple viral detection, persistence of fecal SARS-COVID-2 as well as respiratory and gut microbiota. We will establish the animal models for COVID-19 associated encephalopathy/encephalitis and MIS-C, based on the K18-hACE2 or R26R-AGP mouse models established in NTU animal center. Moreover, specific viral or host factors involved in regulating the pathogenesis and immune responses can be investigated, to optimize the protocol for further improvement of the animal models and also to help identify the putative therapeutic targets. Expected results We will delineate the clinical and laboratory characteristics of COVID-19 associated encephalopathy and encephalitis, the role of immune, virology, genetics mechanism in pathophysiology, and will optimize the treatment algorithm based on the result of this study. We also expect that the important biomarkers and risk factors associated with clinical outcome and severity, the immunopathogenesis of MIS-C, host genetic factors and the viral pathogenesis and microbiota associated with MIS-C will be found.
We hypothesize that a high CD4+ and CD8+ T cell count will reduce viremia upon challenge with a structurally heterologous virus, and correspondingly result in reduced magnitude of host response to challenge infection. Primary Objective: To compare, after challenge with a structurally heterologous vaccine, the differences in levels of viremia between healthy adults who received primary vaccination with either YF17D vaccine, chimeric JE-YF17D vaccine, or inactivated JE vaccine. 58 subjects will be randomised into 1 of 2 arms (Arm B1 and Arm B2) in a 1:1 ratio, in a double-blind fashion. Subjects in Arm B1 will receive JE-YF17D vaccine (Imojev, Sanofi Pasteur) on Day 0 followed by YF17D vaccine (Stamaril, Sanofi Pasteur) on Day 28. Subjects in Arm B2 will receive Stamaril on Day 0 followed by Imojev on Day 28. Arm B3 will be conducted as a separate single-arm open label design in 14 subjects. Subjects in Arm B3 will receive inactivated JE vaccine (Ixiaro, Valneva) on Day 0 followed by Stamaril on Day 28. The rationale for these three study arms is as follows: Arm B1 will show the impact low levels of viremia, and the resultant low levels of virus-specific CD4+ and CD8+ T cells, would have on YF17D infection. In contrast, YF17D vaccination in Arm B2 would produce high levels of viremia, and in turn high levels virus-specific T cells, thus likely ameliorating JE-YF17D infection. Arm B3 will serve as the control arm, as vaccination with inactivated JE vaccine would not produce any YF17D-specific T cell response. Notably, the first vaccination in Arms B1 and B2 would also provide the viremia response in the absence of virus-specific T cells, which would serve as a reference point to interpret the outcome of the second vaccination.