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Limbic Encephalitis

Limbic Encephalitis (Autoimmune) — Comprehensive Disease Characteristics Report

2026-05-16
Falcon MONDO:0015588 Model: Edison Scientific Literature 44 citations

Limbic Encephalitis (Autoimmune) — Comprehensive Disease Characteristics Report

Target Disease

  • Disease name: Limbic encephalitis (LE)
  • Category: Autoimmune (often antibody-mediated; can be paraneoplastic)
  • MONDO ID: Not retrieved in the tool-accessible evidence for this run (explicit MONDO mapping not available from the sources accessed).

Executive summary (current understanding)

Autoimmune limbic encephalitis is a subacute inflammatory syndrome affecting limbic structures (especially the medial temporal lobes) that commonly presents with memory deficits, seizures, and/or psychiatric symptoms. A widely used operational definition is the 2016 Graus et al. “definite autoimmune limbic encephalitis” criteria, which integrates clinical syndrome, medial temporal MRI (or FDG-PET) abnormalities, supportive CSF/EEG evidence, and exclusion of alternative causes. Autoimmune LE encompasses both (i) neuronal cell-surface/synaptic antibody–associated disease (often treatment-responsive) and (ii) paraneoplastic/intracellular onconeural antibody–associated disease (more often cancer-associated and less responsive to immunotherapy). (graus2016aclinicalapproach pages 6-7, graus2016aclinicalapproach pages 7-9)

1. Disease information

1.1 What is the disease?

Definite autoimmune limbic encephalitis (Graus 2016) requires all four of the following: (1) subacute onset (<3 months) of working memory deficits, seizures, or psychiatric symptoms suggesting limbic involvement; (2) bilateral medial temporal lobe abnormalities on T2/FLAIR MRI (or FDG-PET substitute); (3) at least one of CSF pleocytosis (>5 cells/mm³) or EEG with temporal epileptic/slow activity; and (4) reasonable exclusion of alternative causes. (graus2016aclinicalapproach pages 6-7)

Clinical concept: LE is a syndrome that can arise from infectious encephalitis (notably HSV) or autoimmune mechanisms; the Graus framework is intended to support early diagnosis and empiric immunotherapy once infectious causes are reasonably excluded because delays can worsen outcomes. (graus2016aclinicalapproach pages 2-4)

1.2 Key identifiers (OMIM, Orphanet, ICD-10/ICD-11, MeSH, MONDO)

In the retrieved tool-accessible full texts for this run, specific codes/IDs (OMIM, Orphanet, ICD-10/ICD-11, MeSH, MONDO) for limbic encephalitis were not explicitly provided. Accordingly, this report does not assert specific identifiers without evidence.

1.3 Common synonyms / alternative names

  • Autoimmune limbic encephalitis
  • Paraneoplastic limbic encephalitis (when associated with high-risk intracellular/onconeural antibodies and cancer)
  • Antibody-mediated encephalitis with limbic involvement (used in some reviews/guidelines) (graus2016aclinicalapproach pages 7-9)

1.4 Evidence provenance

Information in this report is derived from aggregated disease-level resources (international diagnostic criteria and national consensus guidelines) and cohort studies (multicenter and single-center), plus mechanistic reviews synthesizing in vitro and in vivo models. (graus2016aclinicalapproach pages 6-7, hahn2024canadianconsensusguidelines pages 8-9, dutra2024brazilianconsensusrecommendations pages 1-2, rada2024riskofseizure pages 1-2, ryding2023pathophysiologicaleffectsof pages 4-5)

2. Etiology

2.1 Disease causal factors

Autoimmune mechanisms dominate “autoimmune LE,” frequently mediated by autoantibodies against neuronal cell-surface/synaptic proteins (e.g., LGI1, CASPR2, GABABR, AMPAR, NMDAR) that can directly perturb synaptic function. (li2024clinicalcharacteristicsand pages 1-2, graus2016aclinicalapproach pages 29-29, ryding2023pathophysiologicaleffectsof pages 4-5)

Paraneoplastic etiologies occur when LE is associated with intracellular/onconeural antibodies (e.g., Hu, Ma2) and underlying cancer; these forms are generally less responsive to immunotherapy and require tumor-directed care. (graus2016aclinicalapproach pages 7-9, hahn2024canadianconsensusguidelines pages 8-9)

2.2 Risk factors

  • Neoplasm/cancer association: In multi-antibody AE (which can include LE phenotypes), ~46.9% (39/83) were confirmed/suspected to have a tumor; lung cancer was most common (33.7%, 28/83). (zhou2024clinicalcharacteristicsof pages 1-2)
  • Autoantibody subtype: Certain antibodies have high tumor associations per Graus’ summary table (e.g., AMPAR ~65% with thymoma/SCLC; GABABR ~50% with SCLC). (graus2016aclinicalapproach pages 29-29)

2.3 Protective factors

No protective factors (genetic or environmental) were identified in the retrieved sources for this run.

2.4 Gene–environment interactions

Not specifically addressed in retrieved sources for this run.

3. Phenotypes

3.1 Core phenotype spectrum and suggested HPO terms

Syndromic core (Graus 2016): subacute onset of - Memory deficits / working memory impairment (HPO: HP:0002354 Memory impairment) - Seizures (HPO: HP:0001250 Seizures) - Psychiatric symptoms (e.g., psychosis, behavioral change) (HPO: HP:0000708 Behavioral abnormality; HP:0000738 Hallucinations) (graus2016aclinicalapproach pages 6-7)

Seizure-related phenotypes: Seizures are common early in autoimmune encephalitis, reported in 42–100% of patients; <15% may develop chronic epilepsy. (li2024clinicalcharacteristicsand pages 1-2)

Subtype-linked phenotype example (LGI1): In an anti-LGI1 cohort (n=45), seizures occurred in 100%; cognitive dysfunction 82.2%; psychiatric disturbance 66.7%; sleep disorder 54.5%; hyponatremia 66.7%. Suggested HPO additions: HP:0002360 Sleep disturbance; HP:0002902 Hyponatremia. (li2021clinicalcharacteristicsand pages 1-2)

EEG phenotype: “Extreme delta brush” is noted in up to 30% of NMDAR antibody encephalitis cases. (hahn2024canadianconsensusguidelines pages 6-7)

3.2 Age of onset / progression patterns

LE typically presents with subacute onset (criterion: <3 months). (graus2016aclinicalapproach pages 6-7) Late-onset anti-NMDAR encephalitis (>45 years in one series) may be oligosymptomatic, has different tumor associations, and worse outcomes in some reports summarized in a 2024 review. (ferreira2024recentadvancesin pages 1-2)

3.3 Quality-of-life and functional impact

Long-term morbidity is substantial in anti-LGI1 encephalitis (a leading LE cause): residual moderate-to-severe cognitive impairment reported in 28.0–66.7%; only 24–43% returned to premorbid activities in cited series; visually detectable hippocampal atrophy in 77.8–88.9%. (li2021clinicalcharacteristicsand pages 1-2)

4. Genetic / molecular information

4.1 Causal genes / pathogenic variants

Autoimmune LE is not typically a monogenic disorder in the retrieved sources. Instead, disease is defined by autoantibody specificity (e.g., anti-LGI1, anti-CASPR2, anti-GABABR, anti-AMPAR, anti-NMDAR) and immune dysregulation.

4.2 Susceptibility genetics

A 2024 review notes HLA associations for anti-LGI1, anti-CASPR2, anti-IgLON5, and anti-GAD syndromes. (ferreira2024recentadvancesin pages 1-2)

4.3 Molecular targets (key “genes” as antigen names)

See antibody table artifact below for major targets, tumor links, and mechanisms.

Table (click to expand)
Antibody/target Antigen location Typical syndrome/notes Common tumor associations and approximate positivity rates if provided Key mechanistic effect Key evidence type Primary sources
LGI1 Cell-surface/synaptic VGKC-complex–associated protein Classic autoimmune limbic encephalitis; prominent seizures, memory impairment, psychiatric/behavioral change; faciobrachial dystonic seizures (FBDS) are highly specific; hyponatremia common (graus2016aclinicalapproach pages 6-7, li2021clinicalcharacteristicsand pages 1-2) Thymoma reported; approximate tumor positivity 5–10% in Graus table (graus2016aclinicalapproach pages 29-29) Predominantly IgG4-mediated disruption of LGI1–ADAM22/ADAM23 interactions; reduction of synaptic AMPAR and Kv1 channel clusters; impaired LTP; increased excitability; some models suggest BBB tight-junction breakdown and possible complement/inflammatory effects (ryding2023pathophysiologicaleffectsof pages 4-5, ryding2023pathophysiologicaleffectsof pages 8-10, ryding2023pathophysiologicaleffectsof pages 6-8) Human clinical cohorts + in vitro/in vivo mechanistic models Graus 2016, doi: https://doi.org/10.1016/S1474-4422(15)00401-9; Li 2021, doi: https://doi.org/10.3389/fneur.2021.674368; Ryding 2023, doi: https://doi.org/10.3390/cells13010015 (graus2016aclinicalapproach pages 6-7, li2021clinicalcharacteristicsand pages 1-2, ryding2023pathophysiologicaleffectsof pages 4-5)
CASPR2 Cell-surface/paranodal-synaptic protein Limbic encephalitis spectrum with seizures/cognitive symptoms; can overlap with Morvan syndrome; relevant limbic involvement in autoimmune encephalitis panels (graus2016aclinicalapproach pages 29-29, rada2024riskofseizure pages 1-2) Thymoma reported; approximate tumor positivity 20–50% in Graus table (graus2016aclinicalapproach pages 29-29) Disruption of CASPR2–contactin-2 interactions and/or CASPR2 internalization; altered Kv1.2 surface expression, neuronal hyperexcitability, reduced AMPAR currents/LTP, memory impairment; glial activation and increased complement C3 in models (ryding2023pathophysiologicaleffectsof pages 4-5, ryding2023pathophysiologicaleffectsof pages 10-11, ryding2023pathophysiologicaleffectsof pages 8-10) Human clinical cohorts + in vitro/in vivo mechanistic models Graus 2016, doi: https://doi.org/10.1016/S1474-4422(15)00401-9; Rada 2024, doi: https://doi.org/10.1212/NXI.0000000000200225; Ryding 2023, doi: https://doi.org/10.3390/cells13010015 (graus2016aclinicalapproach pages 29-29, rada2024riskofseizure pages 1-2, ryding2023pathophysiologicaleffectsof pages 10-11)
GABABR Cell-surface/synaptic receptor Autoimmune limbic encephalitis with early and prominent seizures; often included among core limbic AE antibodies (graus2016aclinicalapproach pages 29-29, rada2024riskofseizure pages 1-2) Small-cell lung carcinoma common; approximate tumor positivity ~50% in Graus table (graus2016aclinicalapproach pages 29-29) Evidence supports direct inhibition/signaling blockade of receptor function rather than major receptor-expression loss (ryding2023pathophysiologicaleffectsof pages 5-6) Human clinical association + mechanistic in vitro evidence/review synthesis Graus 2016, doi: https://doi.org/10.1016/S1474-4422(15)00401-9; Rada 2024, doi: https://doi.org/10.1212/NXI.0000000000200225; Ryding 2023, doi: https://doi.org/10.3390/cells13010015 (graus2016aclinicalapproach pages 29-29, rada2024riskofseizure pages 1-2, ryding2023pathophysiologicaleffectsof pages 5-6)
AMPAR Cell-surface/synaptic glutamate receptor Limbic encephalitis with memory disturbance, seizures, psychiatric symptoms; important cell-surface limbic AE subtype (graus2016aclinicalapproach pages 29-29) Thymoma and small-cell lung cancer reported; approximate tumor positivity ~65% in Graus table (graus2016aclinicalapproach pages 29-29) Receptor internalization and lysosomal degradation, reduced AMPAR-mediated currents, impaired LTP, memory deficits (ryding2023pathophysiologicaleffectsof pages 4-5, ryding2023pathophysiologicaleffectsof pages 10-11, ryding2023pathophysiologicaleffectsof pages 8-10) Human clinical association + in vitro/in vivo mechanistic models Graus 2016, doi: https://doi.org/10.1016/S1474-4422(15)00401-9; Ryding 2023, doi: https://doi.org/10.3390/cells13010015 (graus2016aclinicalapproach pages 29-29, ryding2023pathophysiologicaleffectsof pages 10-11)
NMDAR (NR1) Cell-surface/synaptic glutamate receptor Broader autoimmune encephalitis phenotype; may involve limbic symptoms including memory deficits, seizures, psychiatric symptoms; anti-NMDAR is a major AE subtype and included in limbic differential/criteria (graus2016aclinicalapproach pages 6-7, ferreira2024recentadvancesin pages 1-2) Ovarian teratoma association; positivity varies with age/sex in Graus table; review notes ovarian teratoma in nearly 50% of cases in some series, with lower tumor rates (~10%) in some countries (graus2016aclinicalapproach pages 29-29, ferreira2024recentadvancesin pages 1-2) IgG1-mediated cross-linking, internalization, and lysosomal degradation of NMDAR; suppression of NMDAR-dependent plasticity/LTP; altered excitability and receptor trafficking (ryding2023pathophysiologicaleffectsof pages 4-5, ryding2023pathophysiologicaleffectsof pages 6-8) Human clinical cohorts + strong in vitro/in vivo mechanistic evidence Graus 2016, doi: https://doi.org/10.1016/S1474-4422(15)00401-9; Ferreira 2024, doi: https://doi.org/10.1055/s-0044-1793933; Ryding 2023, doi: https://doi.org/10.3390/cells13010015 (graus2016aclinicalapproach pages 29-29, ferreira2024recentadvancesin pages 1-2, ryding2023pathophysiologicaleffectsof pages 6-8)
Ma2 Intracellular/onconeural antigen Paraneoplastic limbic encephalitis; intracellular-antibody subgroup generally less responsive to immunotherapy than cell-surface forms (graus2016aclinicalapproach pages 7-9, graus2016aclinicalapproach pages 29-29) Testicular seminoma; Graus table reports positivity >95% by Western blot (graus2016aclinicalapproach pages 29-29) Primarily a marker of T-cell–mediated paraneoplastic autoimmunity rather than a directly pathogenic surface-antibody mechanism (ryding2023pathophysiologicaleffectsof pages 1-2, graus2016aclinicalapproach pages 7-9) Human clinical/paraneoplastic evidence Graus 2016, doi: https://doi.org/10.1016/S1474-4422(15)00401-9; Ryding 2023, doi: https://doi.org/10.3390/cells13010015 (graus2016aclinicalapproach pages 7-9, graus2016aclinicalapproach pages 29-29, ryding2023pathophysiologicaleffectsof pages 1-2)
Hu (ANNA-1) Intracellular/onconeural antigen Classic paraneoplastic limbic encephalitis/encephalomyelitis spectrum; intracellular high-risk antibody category with poorer response to immunotherapy (graus2016aclinicalapproach pages 7-9, hahn2024canadianconsensusguidelines pages 8-9) Strongly cancer-associated; Graus identifies Hu as an onconeuronal antibody linked to cancer, though the supplied excerpt does not give a percentage for Hu specifically (graus2016aclinicalapproach pages 7-9) Mainly reflects cytotoxic T-cell–mediated neuronal injury rather than receptor internalization/signaling blockade (ryding2023pathophysiologicaleffectsof pages 1-2, graus2016aclinicalapproach pages 7-9) Human clinical/paraneoplastic evidence Graus 2016, doi: https://doi.org/10.1016/S1474-4422(15)00401-9; Canadian guideline 2024, doi: https://doi.org/10.1017/cjn.2024.16; Ryding 2023, doi: https://doi.org/10.3390/cells13010015 (graus2016aclinicalapproach pages 7-9, hahn2024canadianconsensusguidelines pages 8-9, ryding2023pathophysiologicaleffectsof pages 1-2)
GAD65 Intracellular enzyme antigen Limbic encephalitis/autoimmune epilepsy subgroup with predominant seizures; often younger median age in Graus discussion; usually no cancer, but cancer risk higher in older patients or with coexisting GABABR antibodies (graus2016aclinicalapproach pages 7-9) Graus table reports approximate positivity ~25% and associations with thymoma and small-cell lung carcinoma (graus2016aclinicalapproach pages 29-29) Intracellular target; direct pathogenicity less established than for surface antibodies, often treated as part of broader autoimmune process rather than classic receptor-internalization mechanism (ryding2023pathophysiologicaleffectsof pages 2-4, ryding2023pathophysiologicaleffectsof pages 1-2) Human clinical evidence; mechanistic evidence less definitive Graus 2016, doi: https://doi.org/10.1016/S1474-4422(15)00401-9; Ryding 2023, doi: https://doi.org/10.3390/cells13010015 (graus2016aclinicalapproach pages 7-9, graus2016aclinicalapproach pages 29-29, ryding2023pathophysiologicaleffectsof pages 2-4)

Table: This table summarizes major antibody-defined subtypes relevant to autoimmune limbic encephalitis, including antigen class, typical clinical patterns, tumor associations, and supported mechanisms. It is useful for comparing cell-surface/synaptic versus intracellular paraneoplastic forms and linking subtype to diagnosis and management.

5. Environmental information

5.1 Infectious triggers

Infectious encephalitis (notably HSV) is a major differential; HSV PCR may be falsely negative early (<24h) and repeat testing is emphasized in diagnostic reasoning. (graus2016aclinicalapproach pages 6-7) The Canadian guideline notes an infectious prodrome is common in autoimmune encephalitis broadly. (hahn2024canadianconsensusguidelines pages 1-2)

5.2 Lifestyle/other exposures

Not identified in retrieved sources for this run.

6. Mechanism / pathophysiology

6.1 Causal chains (examples)

Cell-surface/synaptic antibody LE (often more treatment-responsive): 1) Immune activation leads to production of IgG autoantibodies against neuronal surface/synaptic targets (e.g., NMDAR, AMPAR, LGI1, CASPR2). (li2024clinicalcharacteristicsand pages 1-2, ryding2023pathophysiologicaleffectsof pages 1-2) 2) Antibodies bind accessible extracellular epitopes → functional effects including receptor cross-linking/internalization (NMDAR/AMPAR), disruption of protein–protein interactions (LGI1/CASPR2), or direct signaling blockade (GABABR). (ryding2023pathophysiologicaleffectsof pages 4-5, ryding2023pathophysiologicaleffectsof pages 6-8, ryding2023pathophysiologicaleffectsof pages 5-6) 3) Synaptic dysfunction (impaired LTP, altered excitability) → limbic symptoms: memory deficits, seizures, psychiatric changes. (ryding2023pathophysiologicaleffectsof pages 4-5, ryding2023pathophysiologicaleffectsof pages 6-8)

Intracellular/onconeural paraneoplastic LE (often less treatment-responsive): 1) Tumor expression of neuronal antigens → immune response; intracellular antibodies serve as markers of paraneoplastic autoimmunity. 2) Strong cancer association and poorer immunotherapy response relative to cell-surface forms; tumor resection/oncologic therapy becomes central. (graus2016aclinicalapproach pages 7-9, hahn2024canadianconsensusguidelines pages 8-9)

6.2 Antibody-specific mechanistic highlights (selected)

6.3 Suggested ontology terms (mechanisms, cells)

GO biological processes (suggested, based on mechanisms described): - Synaptic signaling / glutamatergic transmission; synaptic plasticity / long-term potentiation (LTP) (ryding2023pathophysiologicaleffectsof pages 4-5, ryding2023pathophysiologicaleffectsof pages 6-8) - Receptor-mediated endocytosis / receptor internalization (NMDAR/AMPAR) (ryding2023pathophysiologicaleffectsof pages 10-11, ryding2023pathophysiologicaleffectsof pages 6-8) - Complement activation / innate immune response (subset of AE mechanisms) (ryding2023pathophysiologicaleffectsof pages 4-5, ryding2023pathophysiologicaleffectsof pages 1-2)

Cell Ontology (CL) cell types (suggested): - Hippocampal pyramidal neurons (inferred from hippocampal involvement and LTP mechanisms) (ryding2023pathophysiologicaleffectsof pages 6-8) - Microglia (glial activation in CASPR2 models) (ryding2023pathophysiologicaleffectsof pages 4-5) - Astrocytes (morphologic changes in CASPR2 models) (ryding2023pathophysiologicaleffectsof pages 10-11) - Oligodendrocytes (NMDAR effects on oligodendrocyte GLUT1 described) (ryding2023pathophysiologicaleffectsof pages 6-8)

7. Anatomical structures affected

7.1 Primary localization

  • Medial temporal lobes (limbic structures) as the key imaging localization: bilateral medial temporal T2/FLAIR abnormalities are a defining criterion for definite autoimmune LE. (graus2016aclinicalapproach pages 6-7)

7.2 Suggested UBERON terms

  • Hippocampus (UBERON:0001954)
  • Temporal lobe (UBERON:0001874) (These are ontology suggestions; explicit UBERON IDs were not provided in the retrieved sources.)

8. Temporal development

8.1 Onset pattern

8.2 Course patterns

9. Inheritance and population

9.1 Epidemiology

9.2 Population/subtype demographics

Anti-NMDAR encephalitis commonly affects young women and may be associated with ovarian teratoma in nearly 50% of cases in some series; other series report up to 40% male and ~10% neoplasia rates. (ferreira2024recentadvancesin pages 1-2)

10. Diagnostics

10.1 Standardized criteria and core workup

The Graus criteria provide a widely used framework for definite autoimmune limbic encephalitis (see Section 1). (graus2016aclinicalapproach pages 6-7)

National consensus guidelines emphasize a pragmatic workup incorporating MRI/EEG/CSF, paired serum+CSF antibody testing, and malignancy screening.

Table (click to expand)
Framework/source Intended diagnosis level Criteria/workup elements Notes/thresholds Source URL + publication month/year
Graus et al. 2016, A clinical approach to diagnosis of autoimmune encephalitis Definite autoimmune limbic encephalitis 1) Subacute onset of working memory deficits, seizures, or psychiatric symptoms suggesting limbic system involvement; 2) Bilateral brain abnormalities on T2-weighted FLAIR MRI highly restricted to the medial temporal lobes; 3) At least one of: CSF pleocytosis or EEG with epileptic/slow-wave activity involving temporal lobes; 4) Reasonable exclusion of alternative causes (graus2016aclinicalapproach pages 6-7, graus2016aclinicalapproach pages 2-4) Symptom onset should be <3 months; CSF pleocytosis threshold >5 cells/mm³; 18F-FDG-PET can substitute for criterion 2 if MRI unavailable/negative in some cases; if one of first 3 criteria is missing, diagnosis of definite LE requires detection of antibodies against cell-surface, synaptic, or onconeural proteins (graus2016aclinicalapproach pages 6-7, graus2016aclinicalapproach pages 7-9) https://doi.org/10.1016/S1474-4422(15)00401-9 — Apr 2016 (graus2016aclinicalapproach pages 6-7, graus2016aclinicalapproach pages 2-4)
Graus et al. 2016, syndrome-based AE approach Possible autoimmune encephalitis / early diagnostic framework Use clinical syndrome + conventional tests rather than waiting for antibody confirmation: neurologic assessment, MRI, CSF, EEG, differential diagnosis, and staged evidence levels (possible/probable/definite) (graus2016aclinicalapproach pages 2-4) Designed to avoid over-reliance on antibody tests and treatment response; supports early immunotherapy once mimics are excluded because delayed treatment worsens outcomes (graus2016aclinicalapproach pages 2-4) https://doi.org/10.1016/S1474-4422(15)00401-9 — Apr 2016 (graus2016aclinicalapproach pages 2-4)
Canadian Consensus Guidelines 2024 Adult AE diagnostic workup in acute care Core workup includes MRI brain, EEG, CSF, neural antibody testing, repeat/follow-up MRI if initial imaging is unrevealing, and consideration of FDG-PET and malignancy screening where appropriate (hahn2024canadianconsensusguidelines pages 1-2, hahn2024canadianconsensusguidelines pages 6-7) FDG-PET reported as more sensitive than MRI (87% vs 25–50%) but should not be used alone for diagnosis; whole-body FDG-PET is useful for occult malignancy, especially with intermediate-/high-risk antibodies; EEG contributes to definite limbic AIE criteria (hahn2024canadianconsensusguidelines pages 6-7) https://doi.org/10.1017/cjn.2024.16 — Feb 2024 (hahn2024canadianconsensusguidelines pages 1-2, hahn2024canadianconsensusguidelines pages 6-7)
Canadian Consensus Guidelines 2024 Ancillary test interpretation EEG abnormalities support diagnosis; specific recognition of extreme delta brush in anti-NMDAR encephalitis; imaging and antibody results should be interpreted in clinical context (hahn2024canadianconsensusguidelines pages 6-7) Extreme delta brush occurs in up to 30% of anti-NMDAR encephalitis cases; clinicians should contact testing laboratories for unexpected antibody results and consider confirmatory testing ("TIIF/IHC") for broad neural antibody panels (hahn2024canadianconsensusguidelines pages 6-7) https://doi.org/10.1017/cjn.2024.16 — Feb 2024 (hahn2024canadianconsensusguidelines pages 6-7)
Brazilian Consensus Recommendations 2024 Possible or definite AE diagnostic workup Initial investigations should include brain MRI, EEG, CSF analysis, oligoclonal bands, IgG index, and CSF PCR for herpesviruses; collect paired serum and CSF for antineuronal antibody testing before treatment when feasible (dutra2024brazilianconsensusrecommendations pages 7-8) MRI findings suggestive of AIE include medial temporal T2/FLAIR hyperintensities and multifocal inflammatory/demyelinating changes; herpes simplex and other herpesvirus encephalitides should be excluded with CSF PCR (dutra2024brazilianconsensusrecommendations pages 7-8) https://doi.org/10.1055/s-0044-1788586 — Jul 2024 (dutra2024brazilianconsensusrecommendations pages 7-8)
Brazilian Consensus Recommendations 2024 Antibody-confirmed AE / comprehensive laboratory workup Test serum and CSF using both tissue-based assay (TBA) and cell-based assay (CBA); CBA specifically recommended for anti-MOG and anti-glycine receptor antibodies; children should also be screened for anti-MOG (dutra2024brazilianconsensusrecommendations pages 1-2, dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11) Combined TBA + CBA improves sensitivity/specificity; TBA (rat-brain immunohistochemistry) may detect noncommercial/novel antibodies; the panel recommended against anti-VGKC testing; low-titer serum-only antibodies and low-titer anti-CASPR2 require cautious interpretation (dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11) https://doi.org/10.1055/s-0044-1788586 — Jul 2024 (dutra2024brazilianconsensusrecommendations pages 1-2, dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11)
Brazilian Consensus Recommendations 2024 Cancer/paraneoplastic workup Perform neoplasm screening at presentation and repeat surveillance for antibodies linked to cancer; use contrast-enhanced CT chest/abdomen/pelvis or MRI if CT contraindicated; consider whole-body FDG-PET if CT is negative (dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11) Screening at presentation had 100% panel agreement; CT chest/abdomen/pelvis 92% agreement; whole-body FDG-PET after negative CT 84% agreement; repeat cancer screening annually for 4 years for tumor-associated antibodies (dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11) https://doi.org/10.1055/s-0044-1788586 — Jul 2024 (dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11)
Practical cross-framework synthesis Real-world diagnostic implementation for autoimmune limbic encephalitis Suspected limbic encephalitis should be approached with rapid syndrome recognition, MRI/EEG/CSF, paired serum+CSF antibody testing, selective FDG-PET when MRI is negative or malignancy is suspected, and prompt exclusion of infectious mimics (graus2016aclinicalapproach pages 6-7, hahn2024canadianconsensusguidelines pages 6-7, dutra2024brazilianconsensusrecommendations pages 7-8) Key thresholds/features: subacute <3 months, CSF >5 cells/mm³, bilateral medial temporal FLAIR lesions, temporal EEG slow waves/epileptiform activity, extreme delta brush mainly in anti-NMDAR, and annual tumor surveillance for high-risk antibodies (graus2016aclinicalapproach pages 6-7, hahn2024canadianconsensusguidelines pages 6-7, dutra2024brazilianconsensusrecommendations pages 10-11) Graus 2016: https://doi.org/10.1016/S1474-4422(15)00401-9 (Apr 2016); Canadian 2024: https://doi.org/10.1017/cjn.2024.16 (Feb 2024); Brazilian 2024: https://doi.org/10.1055/s-0044-1788586 (Jul 2024) (graus2016aclinicalapproach pages 6-7, hahn2024canadianconsensusguidelines pages 6-7, dutra2024brazilianconsensusrecommendations pages 10-11)

Table: This table condenses the core diagnostic criteria for definite autoimmune limbic encephalitis from Graus 2016 and aligns them with 2024 Canadian and Brazilian consensus diagnostic workup recommendations. It is useful for quickly comparing formal criteria, practical testing steps, thresholds, and malignancy-screening guidance.

10.2 Imaging

  • MRI: bilateral medial temporal T2/FLAIR hyperintensity is central to definite LE criteria. (graus2016aclinicalapproach pages 6-7)
  • FDG-PET: Canadian guideline reports brain FDG-PET may be more sensitive than MRI (87% vs 25–50%) but should not be used alone for diagnosis; whole-body FDG-PET is useful for occult malignancy in higher-risk antibody contexts. (hahn2024canadianconsensusguidelines pages 6-7)

10.3 CSF / EEG

10.4 Antibody testing (real-world implementation)

Brazilian 2024 consensus recommends testing paired serum and CSF using both tissue-based assay (TBA) and cell-based assay (CBA); TBA can detect noncommercial/novel antibodies; and it recommends against anti-VGKC testing. (dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11)

10.5 Differential diagnosis

HSV and other infections are key mimics; Graus notes HSV PCR can be falsely negative if performed within 24 hours. (graus2016aclinicalapproach pages 6-7)

11. Outcome / prognosis

11.1 Seizure outcomes (quantitative)

A multicenter cohort (n=981 across NMDAR/LGI1/CASPR2/GABABR) estimated the probability of remaining seizure-free for 12 months after achieving 3 months seizure freedom as: NMDAR 0.89, LGI1 0.84, CASPR2 0.82, GABABR 0.76 (Kaplan–Meier). (rada2024riskofseizure pages 1-2)

11.2 Mortality / severe outcomes

In a cohort of AE patients with co-existing multiple neuronal antibodies (n=83), 31.3% (26/83) died during treatment or follow-up; 68.6% had partial/complete recovery. (zhou2024clinicalcharacteristicsof pages 1-2)

11.3 Relapse

Anti-LGI1 relapse rates in literature are reported as 12.5%–35.3%; in one cohort (n=45), ~13% relapsed over follow-up 32.8±13.5 months. (li2021clinicalcharacteristicsand pages 1-2)

11.4 Prognostic factors

A 2024 seizure-focused cohort study in AE found poor prognosis associated with status epilepticus, complications, intubation, higher mRS at discharge, and higher APE2/RITE2 scores; intensive care and higher albumin were associated with reduced risk. (li2024clinicalcharacteristicsand pages 1-2)

12. Treatment

12.1 Consensus treatment algorithms (real-world practice)

Both Canadian (2024) and Brazilian (2024) guidance emphasize early empiric immunotherapy once infection is reasonably excluded and recommend tiered escalation (first-line → second-line → third-line), incorporating cancer treatment when appropriate.

Table (click to expand)
Framework/source Treatment tier / decision point Recommended strategy Timing for escalation / treatment failure Dosing examples provided Neoplasm / other key management notes Source URL + publication date
Canadian consensus guidelines Empiric initiation Start early empiric immunotherapy for suspected autoimmune encephalitis once infectious causes are reasonably excluded; do not delay while awaiting neural antibody results (hahn2024canadianconsensusguidelines pages 8-9, hahn2024canadianconsensusguidelines pages 6-7) Treatment should begin promptly in the acute setting; delay is associated with worse prognosis in guideline rationale (hahn2024canadianconsensusguidelines pages 1-2, hahn2024canadianconsensusguidelines pages 6-7) Severe AIE combination therapy example: IV methylprednisolone 1 g daily for 5 days plus IVIG 2 g/kg over 2–5 days (hahn2024canadianconsensusguidelines pages 6-7) Early tumor removal in paraneoplastic encephalitis is crucial; malignancy search is part of workup, especially with intermediate/high-risk neural antibodies (hahn2024canadianconsensusguidelines pages 6-7) https://doi.org/10.1017/cjn.2024.16; Feb 2024 (hahn2024canadianconsensusguidelines pages 8-9, hahn2024canadianconsensusguidelines pages 6-7)
Canadian consensus guidelines First-line therapy Steroids, IVIG, and/or plasma exchange (PLEX); in severe disease, guideline supports combination therapy rather than waiting for monotherapy failure (hahn2024canadianconsensusguidelines pages 8-9, hahn2024canadianconsensusguidelines pages 6-7) First-line failure defined as lack of improvement or worsening at 5–10 days in severe AIE and 2–4 weeks in mild/moderate AIE; objective measures such as seizure frequency and cognitive testing recommended (hahn2024canadianconsensusguidelines pages 8-9) IV methylprednisolone 1 g/day ×5 days; IVIG 2 g/kg over 2–5 days; repeat high-dose steroids or repeat PLEX/IVIG can be considered if previously effective (hahn2024canadianconsensusguidelines pages 8-9, hahn2024canadianconsensusguidelines pages 6-7) Follow-up MRI if initial MRI negative but suspicion remains; FDG-PET may be more sensitive than MRI but should not be used alone for diagnosis (hahn2024canadianconsensusguidelines pages 6-7) https://doi.org/10.1017/cjn.2024.16; Feb 2024 (hahn2024canadianconsensusguidelines pages 8-9, hahn2024canadianconsensusguidelines pages 6-7)
Canadian consensus guidelines Second-line therapy: cell-surface antibody or antibody-negative AIE Prefer rituximab because of efficacy/safety profile in cell-surface antibody disease and antibody-negative AIE (hahn2024canadianconsensusguidelines pages 8-9) Escalate after first-line failure using above timing windows; failure after second-line is harder to define because onset of action is variable and treatments overlap (hahn2024canadianconsensusguidelines pages 8-9) Specific rituximab dose not stated in extracted Canadian text (hahn2024canadianconsensusguidelines pages 8-9) Can use rituximab when cyclophosphamide is contraindicated (hahn2024canadianconsensusguidelines pages 8-9) https://doi.org/10.1017/cjn.2024.16; Feb 2024 (hahn2024canadianconsensusguidelines pages 8-9)
Canadian consensus guidelines Second-line therapy: paraneoplastic / intracellular high-risk antibody AIE Prefer cyclophosphamide for paraneoplastic cases and intracellular high-risk antibodies such as Hu or Yo (hahn2024canadianconsensusguidelines pages 8-9) Escalate after first-line failure; specialist input recommended in severe/refractory disease (hahn2024canadianconsensusguidelines pages 8-9) Specific cyclophosphamide dose not stated in extracted Canadian text (hahn2024canadianconsensusguidelines pages 8-9) Strong recommendation for tumor resection and oncology involvement in paraneoplastic encephalitis (hahn2024canadianconsensusguidelines pages 8-9, hahn2024canadianconsensusguidelines pages 6-7) https://doi.org/10.1017/cjn.2024.16; Feb 2024 (hahn2024canadianconsensusguidelines pages 8-9, hahn2024canadianconsensusguidelines pages 6-7)
Canadian consensus guidelines Third-line / refractory disease Tocilizumab or bortezomib used for refractory disease after failure of second-line therapy; myeloablative cyclophosphamide may be considered in selected severe cases with specialist input (hahn2024canadianconsensusguidelines pages 8-9) No fixed universal failure interval after second-line because response kinetics vary (hahn2024canadianconsensusguidelines pages 8-9) Specific tocilizumab/bortezomib doses not stated in extracted Canadian text (hahn2024canadianconsensusguidelines pages 8-9) Guideline notes evidence base is limited and largely observational/consensus-driven, except one positive RCT for IVIG in LGI1/CASPR2-seropositive patients (hahn2024canadianconsensusguidelines pages 6-7) https://doi.org/10.1017/cjn.2024.16; Feb 2024 (hahn2024canadianconsensusguidelines pages 8-9, hahn2024canadianconsensusguidelines pages 6-7)
Brazilian consensus recommendations Empiric initiation Treat possible or definite AIE; consensus states treatment should be started within the first 4 weeks of symptoms and should not wait for complete antibody confirmation when suspicion is high (dutra2024brazilianconsensusrecommendations pages 1-2, dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11) If there is no satisfactory clinical/functional improvement within 10–14 days, start second-line therapy (dutra2024brazilianconsensusrecommendations pages 7-8) First-line usually combines methylprednisolone with IVIG or plasmapheresis (dutra2024brazilianconsensusrecommendations pages 1-2, dutra2024brazilianconsensusrecommendations pages 8-10) Prognosis is associated with treatment within the first 4 weeks; panel recommends neoplasm screening at presentation (dutra2024brazilianconsensusrecommendations pages 10-11) https://doi.org/10.1055/s-0044-1788586; Jul 2024 (dutra2024brazilianconsensusrecommendations pages 1-2, dutra2024brazilianconsensusrecommendations pages 8-10, dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11)
Brazilian consensus recommendations First-line therapy Preferred first-line is combination therapy: methylprednisolone + IVIG or methylprednisolone + plasmapheresis; MP, IVIG, and PLEX may be given concomitantly depending on availability/experience (dutra2024brazilianconsensusrecommendations pages 1-2, dutra2024brazilianconsensusrecommendations pages 8-10, dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11) Assess for clinical/functional response over 10–14 days (dutra2024brazilianconsensusrecommendations pages 7-8) IVIG 2 g/kg over 2–5 days; IV methylprednisolone adults 1,000 mg/day for 3–5 days; children 20–30 mg/kg/day, max 1 g/day for 3–5 days; plasmapheresis 5–7 sessions over 7–14 days (dutra2024brazilianconsensusrecommendations pages 8-10) Rule out herpesvirus encephalitis with CSF PCR; MRI/EEG/CSF are part of parallel workup (dutra2024brazilianconsensusrecommendations pages 8-10, dutra2024brazilianconsensusrecommendations pages 7-8) https://doi.org/10.1055/s-0044-1788586; Jul 2024 (dutra2024brazilianconsensusrecommendations pages 8-10, dutra2024brazilianconsensusrecommendations pages 7-8)
Brazilian consensus recommendations Second-line therapy Rituximab and/or cyclophosphamide for refractory disease or inadequate response to first-line therapy (dutra2024brazilianconsensusrecommendations pages 1-2, dutra2024brazilianconsensusrecommendations pages 8-10, dutra2024brazilianconsensusrecommendations pages 10-11) Start after 10–14 days without satisfactory improvement (dutra2024brazilianconsensusrecommendations pages 7-8) Rituximab: acceptable regimens include 500–1,000 mg twice 2 weeks apart or 375 mg/m² weekly ×4; cyclophosphamide 500–1,000 mg/m² IV monthly pulses (dutra2024brazilianconsensusrecommendations pages 8-10) Rituximab supported by better functional outcomes and fewer relapses, especially in anti-NMDAR; cyclophosphamide favored when rituximab unavailable or in selected refractory patients >16 years (dutra2024brazilianconsensusrecommendations pages 8-10, dutra2024brazilianconsensusrecommendations pages 10-11) https://doi.org/10.1055/s-0044-1788586; Jul 2024 (dutra2024brazilianconsensusrecommendations pages 8-10, dutra2024brazilianconsensusrecommendations pages 10-11)
Brazilian consensus recommendations Third-line therapy Tocilizumab and bortezomib are third-line options for refractory disease (dutra2024brazilianconsensusrecommendations pages 1-2, dutra2024brazilianconsensusrecommendations pages 8-10, dutra2024brazilianconsensusrecommendations pages 10-11) Used after failure of second-line therapy in refractory cases (dutra2024brazilianconsensusrecommendations pages 1-2, dutra2024brazilianconsensusrecommendations pages 8-10) Tocilizumab: monthly IV dosing with pediatric/adult weight-based regimens; bortezomib: 3 cycles of 21 days, given subcutaneously on days 1, 4, 8, 11 (dutra2024brazilianconsensusrecommendations pages 8-10) Intended for highly refractory disease; evidence base remains limited compared with first-/second-line treatments (dutra2024brazilianconsensusrecommendations pages 8-10, dutra2024brazilianconsensusrecommendations pages 10-11) https://doi.org/10.1055/s-0044-1788586; Jul 2024 (dutra2024brazilianconsensusrecommendations pages 8-10, dutra2024brazilianconsensusrecommendations pages 10-11)
Brazilian consensus recommendations Maintenance / long-term therapy Maintenance may include monthly IVIG in selected cases; routine long-term azathioprine/mycophenolate is not supported by current evidence, and oral immunosuppressants should not be used in anti-NMDAR according to panel consensus (dutra2024brazilianconsensusrecommendations pages 1-2, dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11) Long-term strategy individualized after acute response (dutra2024brazilianconsensusrecommendations pages 7-8) No standardized dose extracted for monthly IVIG maintenance (dutra2024brazilianconsensusrecommendations pages 7-8) ASMs are for seizure control; most seizures are acute symptomatic and may be weaned after acute stage (dutra2024brazilianconsensusrecommendations pages 1-2, dutra2024brazilianconsensusrecommendations pages 8-10, dutra2024brazilianconsensusrecommendations pages 10-11) https://doi.org/10.1055/s-0044-1788586; Jul 2024 (dutra2024brazilianconsensusrecommendations pages 1-2, dutra2024brazilianconsensusrecommendations pages 8-10, dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11)
Brazilian consensus recommendations Neoplasm management Screen for neoplasia at presentation in all patients; for antibodies commonly linked to cancer, continue surveillance (dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11) Repeat screening annually for 4 years when antibodies are commonly tumor-associated (dutra2024brazilianconsensusrecommendations pages 7-8, dutra2024brazilianconsensusrecommendations pages 10-11) Initial screening examples: contrast-enhanced CT chest/abdomen/pelvis; MRI if CT contraindicated; consider whole-body FDG-PET if CT is negative (dutra2024brazilianconsensusrecommendations pages 10-11) Integrates AE care with oncology; parallels Canadian emphasis on early tumor treatment in paraneoplastic disease (hahn2024canadianconsensusguidelines pages 8-9, hahn2024canadianconsensusguidelines pages 6-7, dutra2024brazilianconsensusrecommendations pages 10-11) https://doi.org/10.1055/s-0044-1788586; Jul 2024; https://doi.org/10.1017/cjn.2024.16; Feb 2024 (hahn2024canadianconsensusguidelines pages 8-9, hahn2024canadianconsensusguidelines pages 6-7, dutra2024brazilianconsensusrecommendations pages 10-11)

Table: This table summarizes consensus treatment pathways for autoimmune encephalitis and limbic encephalitis from the 2024 Canadian and Brazilian guidelines. It highlights empiric treatment timing, escalation thresholds, drug tiers, dosing examples where available, and tumor-management recommendations.

12.2 Key guideline points (selected)

12.3 MAXO (suggested) terms

  • High-dose intravenous corticosteroid therapy
  • Intravenous immunoglobulin therapy
  • Therapeutic plasma exchange
  • B-cell depletion therapy (rituximab)
  • Alkylating agent immunosuppression (cyclophosphamide)
  • IL-6 receptor inhibitor therapy (tocilizumab; satralizumab investigational)
  • Proteasome inhibitor therapy (bortezomib) (These are ontology suggestions; MAXO IDs were not provided in retrieved sources.)

12.4 Recent developments / latest research (2023–2024 prioritized)

Targeted cytokine pathway therapy in trials: The Phase 3 basket RCT CIELO (NCT05503264) evaluates satralizumab (IL-6R inhibition) in NMDAR-IgG+ or LGI1-IgG+ autoimmune encephalitis; primary endpoint includes ≥1-point mRS improvement and no rescue at Week 24; the design allows background immunosuppression and rescue therapies to mirror real-world care. (lee2024innovationandoptimization pages 1-2, lee2024innovationandoptimization pages 3-4)

13. Prevention

There are no established primary prevention strategies for autoimmune LE in the retrieved sources. Secondary/tertiary prevention in practice centers on: - Early recognition and early immunotherapy (avoid delayed treatment). (graus2016aclinicalapproach pages 2-4, hahn2024canadianconsensusguidelines pages 6-7) - Cancer screening and surveillance in tumor-associated antibody contexts (annual for 4 years in Brazilian consensus). (dutra2024brazilianconsensusrecommendations pages 10-11)

14. Other species / natural disease

Not addressed in retrieved sources for this run.

15. Model organisms

Mechanistic understanding is supported by in vitro neuronal culture models, passive transfer approaches, and in vivo mouse models showing receptor internalization, synaptic dysfunction, memory deficits, and seizure phenotypes for several antibody types (e.g., NMDAR, LGI1, CASPR2, AMPAR). (ryding2023pathophysiologicaleffectsof pages 4-5, ryding2023pathophysiologicaleffectsof pages 10-11, ryding2023pathophysiologicaleffectsof pages 6-8)

Figures / tables (visual evidence)

  • Diagnostic criteria and antibody–tumor association table from Graus 2016 were retrieved as cropped images supporting (i) possible AE criteria, (ii) definite autoimmune limbic encephalitis criteria, and (iii) antibody/tumor associations. (graus2016aclinicalapproach media eb6ebeb5, graus2016aclinicalapproach media fdd6abe4, graus2016aclinicalapproach media be8b1f92, graus2016aclinicalapproach media 2946d09a)

Evidence gaps and limitations for knowledge-base population

  • Disease identifiers (MONDO/MeSH/ICD/Orphanet/OMIM): not present in the retrieved full texts; therefore not asserted.
  • PMIDs: The tool outputs provided DOIs/URLs and bibliographic metadata but did not provide PMIDs; therefore PMIDs are not asserted.
  • Environmental/lifestyle risk and protective factors, gene–environment interactions, and cross-species models: not supported by retrieved evidence in this run.

References

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  17. (ryding2023pathophysiologicaleffectsof pages 5-6): Matias Ryding, Anne With Mikkelsen, Mette Scheller Nissen, Anna Christine Nilsson, and Morten Blaabjerg. Pathophysiological effects of autoantibodies in autoimmune encephalitides. Cells, 13:15, Dec 2023. URL: https://doi.org/10.3390/cells13010015, doi:10.3390/cells13010015. This article has 16 citations.

  18. (ryding2023pathophysiologicaleffectsof pages 1-2): Matias Ryding, Anne With Mikkelsen, Mette Scheller Nissen, Anna Christine Nilsson, and Morten Blaabjerg. Pathophysiological effects of autoantibodies in autoimmune encephalitides. Cells, 13:15, Dec 2023. URL: https://doi.org/10.3390/cells13010015, doi:10.3390/cells13010015. This article has 16 citations.

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  20. (hahn2024canadianconsensusguidelines pages 1-2): Christopher Hahn, Adrian Budhram, Katayoun Alikhani, Nasser AlOhaly, Grayson Beecher, Gregg Blevins, John Brooks, Robert Carruthers, Jacynthe Comtois, Juthaporn Cowan, Paula de Robles, Julien Hébert, Ronak K. Kapadia, Sarah Lapointe, Aaron Mackie, Warren Mason, Brienne McLane, Alexandra Muccilli, Ilia Poliakov, Penelope Smyth, Kimberly G. Williams, Christopher Uy, and Jennifer A. McCombe. Canadian consensus guidelines for the diagnosis and treatment of autoimmune encephalitis in adults. Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques, 51:734-754, Feb 2024. URL: https://doi.org/10.1017/cjn.2024.16, doi:10.1017/cjn.2024.16. This article has 33 citations.

  21. (dutra2024brazilianconsensusrecommendations pages 7-8): Lívia Almeida Dutra, Pedro Victor de Castro Silva, João Henrique Fregadolli Ferreira, Alexandre Coelho Marques, Fabio Fieni Toso, Claudia Cristina Ferreira Vasconcelos, Doralina Guimarães Brum, Samira Luisa dos Apóstolos Pereira, Tarso Adoni, Leticia Januzi de Almeida Rocha, Leticia Pereira de Brito Sampaio, Nise Alessandra de Carvalho Sousa, Renata Barbosa Paolilo, Angélica Dal Pizzol, Bruna Klein da Costa, Caio César Diniz Disserol, Camila Pupe, Daniel Almeida do Valle, Denise Sisterolli Diniz, Fabiano Ferreira de Abrantes, Felipe da Rocha Schmidt, Fernando Cendes, Francisco Tomaz Meneses de Oliveira, Gabriela Joca Martins, Guilherme Diogo Silva, Katia Lin, Lécio Figueira Pinto, Mara Lúcia Schimtz Ferreira Santos, Marcus Vinícius Magno Gonçalves, Mariana Braatz Krueger, Michel Elyas Jung Haziot, Orlando Graziani Povoas Barsottini, Osvaldo José Moreira do Nascimento, Paulo Ribeiro Nóbrega, Priscilla Mara Proveti, Raphael Machado do Castilhos, Vanessa Daccach, and Felipe von Glehn. Brazilian consensus recommendations on the diagnosis and treatment of autoimmune encephalitis in the adult and pediatric populations. Arquivos de Neuro-Psiquiatria, 82:001-015, Jul 2024. URL: https://doi.org/10.1055/s-0044-1788586, doi:10.1055/s-0044-1788586. This article has 11 citations and is from a peer-reviewed journal.

  22. (dutra2024brazilianconsensusrecommendations pages 10-11): Lívia Almeida Dutra, Pedro Victor de Castro Silva, João Henrique Fregadolli Ferreira, Alexandre Coelho Marques, Fabio Fieni Toso, Claudia Cristina Ferreira Vasconcelos, Doralina Guimarães Brum, Samira Luisa dos Apóstolos Pereira, Tarso Adoni, Leticia Januzi de Almeida Rocha, Leticia Pereira de Brito Sampaio, Nise Alessandra de Carvalho Sousa, Renata Barbosa Paolilo, Angélica Dal Pizzol, Bruna Klein da Costa, Caio César Diniz Disserol, Camila Pupe, Daniel Almeida do Valle, Denise Sisterolli Diniz, Fabiano Ferreira de Abrantes, Felipe da Rocha Schmidt, Fernando Cendes, Francisco Tomaz Meneses de Oliveira, Gabriela Joca Martins, Guilherme Diogo Silva, Katia Lin, Lécio Figueira Pinto, Mara Lúcia Schimtz Ferreira Santos, Marcus Vinícius Magno Gonçalves, Mariana Braatz Krueger, Michel Elyas Jung Haziot, Orlando Graziani Povoas Barsottini, Osvaldo José Moreira do Nascimento, Paulo Ribeiro Nóbrega, Priscilla Mara Proveti, Raphael Machado do Castilhos, Vanessa Daccach, and Felipe von Glehn. Brazilian consensus recommendations on the diagnosis and treatment of autoimmune encephalitis in the adult and pediatric populations. Arquivos de Neuro-Psiquiatria, 82:001-015, Jul 2024. URL: https://doi.org/10.1055/s-0044-1788586, doi:10.1055/s-0044-1788586. This article has 11 citations and is from a peer-reviewed journal.

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