ArticleInternational journal of molecular sciences2025
Autoimmune Encephalitis with Neuronal Surface Autoantibodies and Other Suspected Cases of Autoimmune Etiology: A Single-Center Experience in Poland.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoimmune encephalitis (AE) is an autoantibody-mediated central nervous system disorder with diverse neuropsychiatric and neurological manifestations, and should be considered in the differential diagnosis of acute and subacute neurological or psychiatric syndromes. In this retrospective study, we analyzed 65 patients: 54 with AE (47 antibody-positive, seven antibody-negative) and 11 antibody-positive without AE. The most frequently detected antibodies targeted N-methyl-D-aspartate receptor (NMDAR), leucine-rich glioma-inactivated protein 1 (LGI1), and contactin-associated protein-like 2 (CASPR2)-key synaptic and axonal membrane proteins involved in excitatory neurotransmission, neuronal signaling, and synaptic plasticity. Clinical presentations were heterogeneous, ranging from common neuropsychiatric, cognitive, and seizure manifestations to atypical brainstem or cerebellar features. Symptom distribution analysis further demonstrated distinct patterns among Ab-positive AE, Ab-negative AE, and Ab-positive non-AE groups, with specific symptom-antibody associations providing potential diagnostic clues. Diagnostic complexity was underscored by unusual age at onset, overlap with multiple sclerosis, cases preceded by herpes labialis, and dual-antibody detection. A subset of antibody-positive patients had alternative diagnoses, highlighting the need for careful clinical correlation and cautious interpretation of antibody results. These findings illustrate the diagnostic challenges and broad clinical spectrum of AE, emphasizing the importance of integrating serological, clinical, and imaging data to improve diagnostic accuracy and guide management.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.