ReviewNature reviews. Disease primers2025
Autoimmune encephalitis.
Review in Nature reviews. Disease primers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed.
- Diagnosing autoimmune encephalitis in psychiatry: clinical recommendations and unresolved challenges from the GENERATE network.Molecular psychiatry · 2026Review
- The cascade to pathogenicity in autoantibody-mediated CNS diseases.Brain : a journal of neurology · 2026Review
- Bipolar disorder in oncology: Considerations for the psychiatrist.Journal of mood and anxiety disorders · 2026Review
- Copine-5-IgG-related autoimmune encephalitis: a novel paraneoplastic neurological syndrome with a strong melanoma association.Journal of neuroinflammation · 2026Article
- Autoimmune encephalitis in eastern China over last decade: a multi-center retrospective study.Journal of neurology · 2026Article
- Research Advances and Biological Features of IgA for Immune-Related Diseases.International journal of molecular sciences · 2026Review
- Minimally Clinically Important Difference of the Clinical Assessment Scale in Autoimmune Encephalitis.Annals of clinical and translational neurology · 2026Article
- Article
- Parvovirus B19 DNA Detected in Ovarian Teratomatous Tissue in Anti-NMDAR Encephalitis: A Case Report.Viruses · 2026Article
- Association of Autoimmune Diseases With Pancreatic Cancer: A Nationwide Follow-Up Study From Sweden.Cancer medicine · 2026Article
- Review
- HLA polymorphism in neuroimmune diseases: linking antigen presentation to neuroinflammatory programs.Frontiers in immunology · 2026Review
- Case Report: Mercury exposure and anti-LGI1/Caspr2 autoimmune encephalitis: a case series and literature review on the paradoxical worsening after chelation therapy.Frontiers in immunology · 2026Review
- Multimodal temporal dissociation in anti-GABAFrontiers in immunology · 2026Article
- Total cerebrospinal fluid IgA as a candidate adjunctive biomarker associated with autoimmune encephalitis: a retrospective case-control study.Frontiers in neurology · 2026Article
- Anti-DPPX antibody-associated encephalitis with the first detected anti-Yo antibody during one-year follow-up: a case report.Frontiers in immunology · 2026Review
- Case Report: A case of paraneoplastic autoimmune encephalitis with concurrent anti-GABABR and anti-SOX1 antibody positivity.Frontiers in cellular neuroscience · 2026Article
- Clinical heterogeneity and treatment optimization in anti-KLHL11 encephalitis: two case reports and literature review.Frontiers in immunology · 2026Review
- Neuroinflammation and Mental Health in Multiple Sclerosis and Autoimmune Encephalitis: Bridging Biological Mechanisms and Psychosocial Factors.Archives of internal medicine research · 2026Article
- Burden level and influencing factors of caregivers for patients with autoimmune encephalitis.Frontiers in neurologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoimmune encephalitis (AE) is a treatable neuro-inflammatory disorder that is increasing in incidence. AE can be associated with malignancy (paraneoplastic), but in many patients no tumour is present. The disease presentation of AE can be heterogeneous depending on the type of antibody involved. AE is often caused by neuronal antibodies that bind to extracellular autoantigens (that is, N-methyl-D-aspartate receptor (NMDAR) and LGI1). Binding of these antibodies causes dysfunction of synaptic receptors, which leads to neurological symptoms. In these patients, treatment with immunosuppressive therapies is believed to decrease inflammation and deplete antibodies, and is essential for recovery. AE can also occur in patients with antibodies against intracellular antigens (such as Hu and Ri), often in the setting of malignancy. In these patients, tumour treatment is essential for stabilization or improvement. The most frequent symptoms of AE are cognitive problems, behavioural changes and seizures. Rapid recognition of AE syndromes is essential as earlier treatment of AE leads to better outcomes. For a definite diagnosis, the identification of an autoantibody is essential; however, some patients have seronegative AE. Most patients are severely affected during the acute disease stage, but long-term functional recovery is often good, particularly for patients without cancer. Nevertheless, residual anxiety, fatigue and cognitive problems can considerably affect quality of life. Research focuses on improving the understanding of pathophysiological processes, establishing patient-tailored outcome measures, optimizing treatment prediction models and studying different therapeutic regimens, all aiming to improve treatment and long-term outcomes.
Indexed as
Identifiers
40935848What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.