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Objective To explore the individual features of acute symptomatic seizures across various subtypes of antibody-mediated autoimmune encephalitis (AE), and to identify the influencing factors for the progression to chronic epilepsy. Methods A total of 84 patients diagnosed with antibody-mediated AE at The First Affiliated Hospital of Dalian Medical University from January 2016 to December 2024 were included. The data collected encompassed society demographic information, clinical manifestations, long-term video-electroencephalography (LT-VEEG), MRI, treatment and prognostic outcomes. Univariate and multivariate stepwise Logistic regression analyses were conducted to identify influencing factors for the progression from acute symptomatic seizures to chronic epilepsy. Furthermore, the receiver operating characteristic (ROC) curve was drawn, and the area under the curve (AUC) was calculated to determine the predictive efficacy of the influencing factors Results 1) The incidence of acute symptomatic seizures in antibody-mediated AE by different antibody subtypes was 85.71% (72/84). The primary seizure types were generalized tonic-clonic seizures (GTCS; 72.22%, 52/72), focal impaired consciousness seizure (FIC; 51.39%, 37/72), focal preserved consciousness seizure (FPC; 41.67%, 30/72), and focal to bilateral tonic-clonic seizure (FBTCS; 43.06%, 31/72), with status epilepticus (SE; 29.17%, 21/72) and subclinical electrical seizures (8.33%, 6/72) were also frequently observed. Among them, the acute symptomatic seizures in anti-leucine-rich glioma-inactivated 1 (LGI1) antibody-associated encephalitis (n=35) manifested as mesial temporal lobe epilepsy (mTLE)-like seizures, faciobrachial dystonic seizures (FBDS), or both. In anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis (n=16) and anti-myelin oligodendrocyte glycoprotein (MOG) antibody encephalitis (n=5), acute symptomatic seizures were primarily GTCS, often accompanied by focal seizures of neocortical origin, and were prone to SE. In anti-γ-aminobutyric acid receptor type B (GABABR, n=12) antibody-associated encephalitis and anti-glutamic acid decarboxylase 65 (GAD65) antibody-associated encephalitis (n=10), acute symptomatic seizures often presented as mTLE-like seizures. 2) Of the 72 patients with acute symptomatic seizures, 23 (31.94%) developed chronic epilepsy; among them, anti-GAD65 and anti-GABABR antibody-associated encephalitis had the highest proportions (8/8 and 8/12, respectively). 3) Logistic regression analysis showed limbic system atrophy was identified as risk factor (OR=24.985, 95%CI: 2.873-217.304; P=0.004)，while a normal blood neutrophil count was protective factor (OR=0.172, 95%CI: 0.038-0.786; P=0.023) for the progression from acute symptomatic seizures to chronic epilepsy. ROC curve showed that the AUC of limbic system atrophy and normal blood neutrophil count were 0.654 and 0.638, respectively. The AUC of the combined indicator increased to 0.784, indicating improved predictive efficacy (Z=2.310, P=0.021; Z=2.715, P=0.007). Conclusions Acute symptomatic seizures in antibody-mediated AE by various subtypes of antibodies exhibit both shared and distinct characteristics. Among them, patients with anti-GAD65 and anti-GABABR antibody-associated encephalitis have the highest proportions of developing chronic epilepsy. Limbic system atrophy serves as an independent risk factor, whereas a normal blood neutrophil count acts as an independent protective factor against the progression of acute symptomatic seizures to chronic epilepsy. The combined index has better predictive efficacy.