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Anti-NMDA Receptor Encephalitis

Anti‑NMDA Receptor Encephalitis (Autoimmune) — Comprehensive Disease Characteristics Report

2026-05-16
Falcon MONDO:0021081 Model: Edison Scientific Literature 46 citations

Anti‑NMDA Receptor Encephalitis (Autoimmune) — Comprehensive Disease Characteristics Report

1. Disease Information

Overview / definition

Anti‑N‑methyl‑D‑aspartate receptor (NMDAR) encephalitis is a subacute, rapidly progressive autoimmune encephalitis characterized by neuropsychiatric symptoms (often prominent), seizures, movement disorders/dyskinesias, altered consciousness, and autonomic/respiratory dysfunction, associated with IgG autoantibodies targeting the GluN1 (NR1) subunit of the NMDAR and typically detected most reliably in CSF (nguyen2023antinmdareceptorautoimmune pages 1-2, nguyen2023antinmdareceptorautoimmune pages 3-5, gong2021longtermfunctionaloutcomes pages 1-2).

Key identifiers

  • MONDO: MONDO_0021081 (“anti‑NMDA receptor encephalitis”) (OpenTargets Search: Anti-NMDA receptor encephalitis).
  • Orphanet / MeSH / OMIM / ICD‑10/ICD‑11: Not retrieved in the available tool context; therefore not reported here.

Synonyms / alternative names (used in evidence base)

Evidence source types

This report integrates (i) human cohort/registry studies and systematic reviews, (ii) mechanistic in vitro and passive‑transfer animal model studies, and (iii) clinical trial registry information (ClinicalTrials.gov) (gong2021longtermfunctionaloutcomes pages 1-2, alsalek2024racialandethnic pages 1-2, dalmau2016nmdareceptorencephalitis pages 7-9, NCT03274375 chunk 1).

2. Etiology

Primary causal factors / triggers (current understanding)

Anti‑NMDAR encephalitis is primarily antibody‑mediated and frequently linked to antigenic triggers, particularly: - Ovarian teratoma (key paraneoplastic trigger in subsets of patients) (nguyen2023antinmdareceptorautoimmune pages 5-6, alsalek2024racialandethnic pages 1-2). - Herpes simplex encephalitis (HSE) as a post‑infectious trigger for secondary anti‑NMDAR encephalitis (dumez2024specificclinicaland pages 1-2, alsalek2024racialandethnic pages 1-2).

Risk factors (human clinical/epidemiologic)

Environmental / spatial & climatic factors

A 2023 systematic review/meta‑analysis reported that incidence estimates varied across regions and were associated with geography/climate: - higher reported incidence in Oceania (0.2/100,000 person‑years) and South America (0.16/100,000 person‑years) than Europe/North America (0.06/100,000 person‑years) (alentorn2023spatialandecological pages 1-2). - a strong negative correlation with latitude (Pearson’s R = −0.88) and seasonal peaks during warm months; extreme heat in France associated with incidence (p = 0.03) (alentorn2023spatialandecological pages 1-2).

Protective factors / gene–environment interactions

No protective factors or explicit gene–environment interaction data were retrieved in the current tool context.

3. Phenotypes

Core phenotype domains (with selected frequencies)

Common clinical manifestations include psychiatric/behavioral symptoms, seizures, movement disorders/dyskinesias, speech dysfunction, decreased consciousness, autonomic instability, and central hypoventilation (nguyen2023antinmdareceptorautoimmune pages 3-5, xu2020antinmdarencephalitis pages 1-2).

Selected quantitative phenotype frequencies from cohorts: - Psychosis/behavioral symptoms: 82.7% psychosis in a prospective China cohort (n=220, 2011–2017) (xu2020antinmdarencephalitis pages 1-2); behavioral changes 74.5% in an East China cohort (n=106) (wang2020influencingelectroclinicalfeatures pages 1-2). - Seizures: 80.9% in the prospective China cohort (n=220) (xu2020antinmdarencephalitis pages 1-2); 67% in the East China cohort (n=106), with 54.9% focal among those with seizures (wang2020influencingelectroclinicalfeatures pages 1-2). - Prodrome: a prodromal phase occurs in 40–70% of patients (review synthesis) (nguyen2023antinmdareceptorautoimmune pages 3-5).

Age-related clinical patterning (review synthesis): teenagers/adults commonly develop psychiatric/behavioral symptoms early (~90%), whereas young children more often present with neurologic features such as seizures/abnormal movements rather than frank psychiatric syndromes (nguyen2023antinmdareceptorautoimmune pages 3-5).

Quality of life and long-term functional/cognitive impacts

A 2024 nationwide cohort study of 92 patients reported that although most had “favorable” functional outcome by mRS, long-term deficits were common: - beyond 36 months, 34% had persistent cognitive impairment (z < −1.5 SD) and 65% scored below average in ≥1 domain; memory and language were most affected (brenner2024longtermcognitivefunctional pages 1-2). - 30% did not resume school/work and 18% needed adjustments; patient‑reported outcomes showed reduced emotional well‑being, social functioning, energy, and quality of life compared to norms (brenner2024longtermcognitivefunctional pages 1-2).

Suggested HPO terms (examples; see ontology table)

Examples include Seizure (HP:0001250), Psychiatric symptoms (HP:0000708), Dyskinesia (HP:0100660), Autonomic dysfunction (HP:0002271), Central hypoventilation (HP:0007110), Memory impairment (HP:0002354), Language impairment (HP:0002465) (artifact-01).

4. Genetic/Molecular Information

Causal genes

Anti‑NMDAR encephalitis is not typically a Mendelian monogenic disorder; it is defined by autoantibodies to the NMDAR (GluN1 subunit) rather than pathogenic variants in a causal gene (balu2019ascorethat pages 1-2, dalmau2017autoantibodiestosynaptic pages 8-10).

Target antigen and epitope information

  • Structural epitope mapping indicates most autoantibodies target a conformational epitope in the amino‑terminal domain (ATD) of GluN1, including residues N368/G369; point mutations at these residues abolish binding (dalmau2017autoantibodiestosynaptic pages 8-10).

Modifier genes / protective variants / allele frequencies

Not retrieved in the available tool context.

5. Environmental Information

Infectious triggers

Climate/ecological signals (population level)

Incidence appears associated with geographic/climatic variables including latitude, higher temperatures, and UV exposure in a systematic review/meta‑analysis (alentorn2023spatialandecological pages 1-2).

Lifestyle/toxin exposures were not retrieved.

6. Mechanism / Pathophysiology

Causal chain (current consensus)

1) Trigger/antigen exposure (e.g., ovarian teratoma or post‑HSV inflammation) can initiate/boost autoreactive B‑cell responses (nguyen2023antinmdareceptorautoimmune pages 5-6, dalmau2017autoantibodiestosynaptic pages 8-10). 2) Autoreactive B cells/plasma cells generate IgG targeting extracellular NMDAR epitopes; intrathecal synthesis is supported by cloning of recombinant antibodies from CSF cells and by intrathecal immune activity models (dalmau2017autoantibodiestosynaptic pages 37-38, dalmau2017autoantibodiestosynaptic pages 8-10). 3) Antibodies bind cell-surface NMDAR and induce receptor crosslinking and internalization, reducing surface and synaptic receptor density, producing reversible synaptic dysfunction (dalmau2017autoantibodiestosynaptic pages 34-35, dalmau2016nmdareceptorencephalitis pages 7-9). 4) Network-level consequences include impaired hippocampal synaptic plasticity (LTP) and cognitive/behavioral phenotypes, consistent with functional NMDAR hypofunction (dalmau2016nmdareceptorencephalitis pages 7-9, dalmau2016nmdareceptorencephalitis pages 2-3).

Key mechanistic findings (authoritative sources)

  • Crosslinking-dependent internalization: internalization is not blocked by NMDA receptor antagonism and is not reproduced by Fab fragments that cannot crosslink, implicating crosslinking as a mechanism (dalmau2017autoantibodiestosynaptic pages 34-35).
  • Internalization kinetics and trafficking: internalization begins within ~2 hours and peaks by ~12 hours; internalized receptors traffic preferentially to Rab11-positive recycling endosomes more than lysosomes, with evidence of enhanced degradation (dalmau2017autoantibodiestosynaptic pages 34-35).
  • Passive-transfer model reversibility and EphB2 pathway modulation: chronic infusion of patient CSF causes progressive antibody binding (maximal ~day 18), synaptic NMDAR loss, impaired LTP, and memory impairment, with reversibility after cessation; co-infusion of soluble ephrin‑B2 prevents pathogenic effects, implicating NMDAR–EphB2 synaptic interactions (dalmau2016nmdareceptorencephalitis pages 7-9, dalmau2017autoantibodiestosynaptic pages 37-38).

Blood–brain barrier (BBB) and immune trafficking

BBB dysfunction is proposed as enabling movement of antibodies and immune cells into the CNS. The BBB is described as “crucial for antibodies and immune cells to enter or exit the CNS,” with evidence supporting intrathecal B-cell involvement and cytokine signals consistent with BBB involvement (gong2023antinmdarantibodiesthe pages 1-2).

Suggested GO biological process / CL cell type terms

Examples include receptor internalization (GO:0031623), regulation of synaptic plasticity (GO:0048167), B cell mediated immunity (GO:0019724), immunoglobulin production (GO:0002377), and cell types B cell (CL:0000236) and plasma cell (CL:0000786) (artifact-01).

7. Anatomical Structures Affected

Organ/system level

Tissue/cell level

8. Temporal Development

Onset pattern

Typically subacute (rapid progression) with prodrome in a substantial fraction (40–70%) (nguyen2023antinmdareceptorautoimmune pages 3-5). Diagnostic criteria frameworks emphasize symptom accumulation within weeks and rapid onset within <3 months (nguyen2023antinmdareceptorautoimmune pages 3-5).

Post‑infectious timing

In post‑HSE anti‑NMDAR encephalitis, median time between HSE and NMDARE onset was 30 days (21–46) (dumez2024specificclinicaland pages 1-2).

Recovery trajectory

Cognitive recovery may continue for years; in one nationwide cohort, improvements continued up to 36 months, with persistent impairments common beyond 36 months (brenner2024longtermcognitivefunctional pages 1-2).

9. Inheritance and Population

Epidemiology (recent quantitative data)

A compact table of recent quantitative incidence/outcomes is provided below.

Table (click to expand)
Study (first author year, journal) Design/setting N Key population notes Incidence/prevalence (with units) Tumor frequency Relapse frequency Mortality/fatality Key prognostic factors/notes URL/DOI
Nguyen 2023, Int J Gen Med Review summarizing epidemiology and management NR Median age 21; 81% female in summarized data Olmsted County incidence 0.4/100,000 (1995–2005) rising to 1.2/100,000 (2006–2015); autoimmune encephalitis prevalence 13.7/100,000 in 2014; anti-NMDAR prevalence 0.6/100,000 NR in excerpt 10–30% of cases, mostly within first 2 years NR CSF antibody testing more sensitive/specific than serum; all patients should be screened at least once for neoplasm (nguyen2023antinmdareceptorautoimmune pages 1-2) https://doi.org/10.2147/IJGM.S397429
Alsalek 2024, Neurol Neuroimmunol Neuroinflamm Retrospective population-based cohort, Kaiser Permanente Southern California, 2011–2022 70 Median age at onset 23.7 years; 64% female; >10 million person-years Age- and sex-standardized incidence per 1 million person-years: Black 2.94 (95% CI 1.27–4.61), Hispanic 2.17 (1.51–2.83), Asian/Pacific Islander 2.02 (0.77–3.28), White 0.40 (0.08–0.72) Ovarian teratomas in 58.3% of Black female individuals; 21 female patients overall had ovarian teratoma NR NR CSF pleocytosis 70%, abnormal EEG 73%, abnormal MRI 40%; median time symptom onset to diagnosis 17 days; most patients (61.4%) had no identifiable trigger (alsalek2024racialandethnic pages 1-2) https://doi.org/10.1212/NXI.0000000000200255
Alentorn 2023, Biomedicines Systematic review/meta-analysis of incidence studies NR Higher incidence reported in southern hemisphere regions; warm-month peak Oceania 0.2/100,000 person-years; South America 0.16/100,000 person-years; Europe/North America 0.06/100,000 person-years About half of cases associated with ovarian teratoma NR NR Strong negative correlation with latitude (Pearson R = −0.88); positive association with extreme heat in France (p = 0.03) (alentorn2023spatialandecological pages 1-2) https://doi.org/10.3390/biomedicines11061525
Dumez 2024, J Neurol Retrospective comparative cohort of post-HSE anti-NMDAR encephalitis 13 post-HSE cases among 375 NMDARE patients Median age 19 years; 31% children <4 years; 54% male; median latency 30 days after HSE HSE incidence noted as 2–4 per million/year NR NR NR Worse 12-month mRS than regular NMDARE; behavioral changes 92%, movement disorders 62%, dysautonomia 54%; extensive MRI lesions 100% vs 48% and bilateral DWI abnormalities 90% vs 29% versus regular HSE comparators (dumez2024specificclinicaland pages 1-2) https://doi.org/10.1007/s00415-024-12615-7
Xu 2020, Neurol Neuroimmunol Neuroinflamm Single-center prospective cohort, China, 2011–2017 220 Acute onset with characteristic neuropsychiatric manifestations NR 19.5% had neoplasm; ovarian teratoma was 100% of tumors in females 17.3% during first 12 months 2.3% died within first 12 months 94.1% improved during first 12 months; 92.7% had favorable outcome (mRS ≤2) at 12 months; 99.5% received first-line therapy; 7.3% received second-line therapy (xu2020antinmdarencephalitis pages 1-2) https://doi.org/10.1212/NXI.0000000000000633
Gong 2021, Neurol Neuroimmunol Neuroinflamm Prospective observational cohort, Western China 244 Median age 26; 52.45% female; median follow-up 40 months NR 15.57% had tumors 15.9%; 82.0% of first relapses within 24 months 6.96% fatality 84.8% improved within 4 weeks after immunotherapy; 80.7% and 85.7% had substantial recovery at 12 and 24 months; disturbance of consciousness in first month independently predicted poor outcome (OR 2.91, 95% CI 1.27–6.65); female sex and delayed treatment linked to relapse (gong2021longtermfunctionaloutcomes pages 1-2) https://doi.org/10.1212/NXI.0000000000000958
Balu 2019, Neurology Multicenter cohort developing prognostic score 382 Anti-GluN1 antibody-associated disease NR NR NR NR NEOS score predictors: ICU admission, treatment delay >4 weeks, lack of improvement within 4 weeks, abnormal MRI, CSF WBC >20 cells/μL; poor 1-year outcome ranged from 3% (0–1 points) to 69% (4–5 points) (balu2019ascorethat pages 1-2) https://doi.org/10.1212/WNL.0000000000006783
Brenner 2023, Neurology Retrospective biomarker study with healthy references 71 patients; 61 references 75% female; mean age 31.4 years; paired CSF available in 33 NR NR Reported 12% relapse within 2 years in background summary NR Serum NfL 19.5 pg/mL vs 6.4 pg/mL in references (p < 0.0001); CSF-serum NfL correlation R = 0.84; post-HSV patients 248.8 vs 14.1 pg/mL; association with 12-month mRS largely confounded by age (brenner2023predictivevalueof pages 1-2) https://doi.org/10.1212/WNL.0000000000207221
Brenner 2024, Neurology Nationwide cross-sectional/prospective cohort 92 Mean age 29 ± 2 years; 77% female NR NR NR NR Recovery continued up to 36 months; beyond 36 months, 34% had persistent impairment and 65% scored below average in ≥1 cognitive domain; 91% had favorable mRS ≤2, yet 30% did not resume school/work and 18% needed adjustments (nguyen2023antinmdareceptorautoimmune pages 1-2) https://doi.org/10.1212/WNL.0000000000210109

Table: This table compiles the main quantitative epidemiology, trigger, relapse, mortality, and prognosis figures for anti-NMDA receptor encephalitis from the retrieved evidence. It is useful as a compact reference for populating disease knowledge-base fields with explicitly supported numbers.

Key recent statistics include: - US population-based incidence disparities (2011–2022): standardized incidence per 1 million person‑years: Black 2.94; Hispanic 2.17; Asian/PI 2.02; White 0.40 (alsalek2024racialandethnic pages 1-2). - Climate/geography associations: incidence estimates and latitude/temperature associations in systematic review/meta-analysis (alentorn2023spatialandecological pages 1-2).

10. Diagnostics

Clinical criteria and practical diagnostic approach

Guidelines emphasize exclusion of infectious mimics (notably HSV encephalitis), with routine blood/CSF analysis and MRI often sufficient to evaluate alternative causes; importantly, HSV CSF PCR can be negative early and may need repeating if suspicion remains high (graus2016aclinicalapproach pages 6-7).

Anti‑NMDAR encephalitis can be approached with syndrome-based criteria for probable diagnosis and confirmed via antibody testing; supportive findings include abnormal EEG and CSF inflammatory markers (nguyen2023antinmdareceptorautoimmune pages 3-5).

Antibody testing: CSF vs serum

CSF testing is more sensitive and specific than serum. Review synthesis reports serum false-positives (up to 23.2%) and some serum reactivity in healthy controls; a substantial fraction of patients may be CSF‑only positive (reported 28–38.2% across series), supporting testing of both CSF and serum (nguyen2023antinmdareceptorautoimmune pages 3-5).

CSF abnormalities

Across cohorts, CSF pleocytosis has been reported in ~47–91% and oligoclonal bands in ~25–62.6% (nguyen2023antinmdareceptorautoimmune pages 3-5). In the Kaiser Permanente cohort, CSF pleocytosis was present in 70% (alsalek2024racialandethnic pages 1-2).

EEG and MRI

  • EEG is abnormal in most cases; one review notes EEG abnormality in 83.6% and describes extreme delta brush as a specific pattern, defined as “rhythmic delta activity at 1–3 Hz with bursts of rhythmic beta activity,” occurring in ~6.7% (nguyen2023antinmdareceptorautoimmune pages 5-6).
  • Brain MRI can be normal in many patients; in Kaiser Permanente, abnormal MRI was 40% (alsalek2024racialandethnic pages 1-2).

Real-world diagnostic implementation notes

11. Outcome / Prognosis

Functional outcomes and relapse

Prognostic scores

The NEOS score (anti‑NMDAR Encephalitis One‑Year Functional Status) uses five predictors: ICU admission, treatment delay >4 weeks, lack of improvement within 4 weeks, abnormal MRI, and CSF WBC >20 cells/µL; poor 1‑year outcome probability ranged from 3% (0–1 points) to 69% (4–5 points) (balu2019ascorethat pages 1-2).

Biomarkers (recent developments)

A 2023 Neurology study evaluated serum neurofilament light chain (NfL): serum NfL at diagnosis was higher in patients (mean 19.5 pg/mL) than references (mean 6.4 pg/mL, p<0.0001) and correlated with CSF NfL (R=0.84); post‑HSV cases had markedly higher levels (mean 248.8 vs 14.1 pg/mL) (brenner2023predictivevalueof pages 1-2).

12. Treatment

Current standard treatment strategy (real-world implementation)

A widely used approach is escalation of immunotherapy plus trigger removal (e.g., teratoma removal). First-line therapies include high-dose corticosteroids, IVIG, and plasma exchange; second-line therapies include rituximab or cyclophosphamide; refractory options may include bortezomib and tocilizumab (nguyen2023antinmdareceptorautoimmune pages 1-2, nguyen2023antinmdareceptorautoimmune pages 6-7).

A key implementation point is that decisions should be guided by clinical status rather than serial antibody titers: titers have limited correlation with severity and serum titers are unreliable; CSF titers may be more useful for relapse assessment when compared to earlier samples (nguyen2023antinmdareceptorautoimmune pages 6-7).

Visual evidence: treatment options table

Nguyen & Wang (2023) provide a detailed “Table 2 Summary of Treatment Options,” including regimens and adverse effects (nguyen2023antinmdareceptorautoimmune media a2c6c545, nguyen2023antinmdareceptorautoimmune media e857af28).

Suggested MAXO terms

Examples include corticosteroid therapy, intravenous immunoglobulin therapy, plasma exchange therapy, rituximab therapy, cyclophosphamide therapy, tumor resection, and tumor screening (artifact-01).

13. Prevention

No established primary prevention is supported in the retrieved evidence base. Practical prevention focuses on secondary/tertiary prevention: early recognition, prompt immunotherapy escalation when needed, and evaluation for/removal of triggering tumors to reduce morbidity and relapse risk (nguyen2023antinmdareceptorautoimmune pages 6-7, xu2020antinmdarencephalitis pages 1-2).

14. Other Species / Natural Disease

No naturally occurring disease in other species was retrieved in the available evidence context.

15. Model Organisms

Mechanistic work includes passive-transfer models (e.g., chronic infusion of patient CSF) demonstrating reversible synaptic receptor loss, impaired LTP, and behavioral deficits; these are frequently used to interrogate synaptic mechanisms and potential rescue strategies (e.g., ephrin‑B2) (dalmau2016nmdareceptorencephalitis pages 7-9, dalmau2017autoantibodiestosynaptic pages 37-38).

Recent developments and latest research highlights (2023–2024 prioritized)

Current applications and real-world implementations

Clinical trials / registries (ClinicalTrials.gov)

  • NCT03274375 (Phase 2; recruiting; start 2021‑06‑23; est. completion 2026‑06): immunoadsorption sessions + rituximab in severe pediatric disease (NCT03274375 chunk 1).
  • NCT06183788 (AMENDS) (recruiting; start 2023‑01‑16): remote cognitive rehabilitation and biomarker/mechanism characterization in post‑acute stage (NCT06183788 chunk 1).
  • NCT06023160 (NEOSII) (observational; 714 participants): develop NEOS2 score for outcome and first-line response prediction (NCT06023160 chunk 1).
  • NCT02559089 and NCT02443350 (China/Beijing registries; ~400 enrollment each): clinical registries to build databases and evaluate outcomes (e.g., death endpoints) (NCT02559089 chunk 1, NCT02443350 chunk 1).
  • NCT04339127 (retrospective; ~12 participants): post‑herpetic anti‑NMDAR encephalitis characterization (NCT04339127 chunk 1).

Ontology mapping artifact

Table (click to expand)
Category Suggested ontology Term label Term ID Evidence-supported rationale
Disease MONDO anti-NMDA receptor encephalitis MONDO_0021081 OpenTargets identifies the disease as anti-NMDA receptor encephalitis with MONDO_0021081, matching the requested disease concept (OpenTargets Search: Anti-NMDA receptor encephalitis).
Anatomy UBERON brain UBERON:0000955 Anti-NMDAR encephalitis is a CNS autoimmune encephalitis with neuropsychiatric, seizure, and cognitive manifestations indicating primary brain involvement (nguyen2023antinmdareceptorautoimmune pages 1-2, gong2023antinmdarantibodiesthe pages 1-2).
Anatomy UBERON hippocampus UBERON:0001954 Mechanistic studies describe impaired hippocampal synaptic activity/plasticity and hippocampal binding of patient antibodies, supporting hippocampal involvement (gong2023antinmdarantibodiesthe pages 1-2, dalmau2016nmdareceptorencephalitis pages 7-9).
Anatomy UBERON cerebrospinal fluid UBERON:0001359 CSF is the preferred compartment for antibody detection and frequently shows pleocytosis or oligoclonal bands in this disease (nguyen2023antinmdareceptorautoimmune pages 3-5, nguyen2023antinmdareceptorautoimmune pages 5-6).
Anatomy UBERON blood-brain barrier UBERON:0013702 BBB dysfunction is implicated because the BBB is described as crucial for antibody and immune-cell trafficking into and out of the CNS (gong2023antinmdarantibodiesthe pages 1-2).
Anatomy UBERON ovary UBERON:0000992 Ovarian teratoma is the major tumor trigger, especially in female patients, supporting ovary as a key associated anatomical site (nguyen2023antinmdareceptorautoimmune pages 5-6, alsalek2024racialandethnic pages 1-2).
Cell type CL B cell CL:0000236 CNS B-cell expansion and intrathecal antibody production are described in anti-NMDAR encephalitis, making B cells a central disease-relevant cell type (gong2023antinmdarantibodiesthe pages 1-2, dalmau2017autoantibodiestosynaptic pages 8-10).
Cell type CL plasma cell CL:0000786 Intrathecal plasma cells are a reported source of GluN1 autoantibodies in mechanistic studies (dalmau2017autoantibodiestosynaptic pages 37-38, dalmau2017autoantibodiestosynaptic pages 8-10).
Cell type CL neuron CL:0000540 Patient antibodies bind neuronal surface NMDARs and alter synaptic receptor density and function, implicating neurons as the primary target cell type (dalmau2017autoantibodiestosynaptic pages 34-35, dalmau2016nmdareceptorencephalitis pages 2-3).
Subcellular GO synapse GO:0045202 Anti-NMDAR antibodies reduce synaptic NMDAR density and disrupt synaptic plasticity, so synapse is a core affected compartment (dalmau2017autoantibodiestosynaptic pages 37-38, gong2023antinmdarantibodiesthe pages 1-2).
Subcellular GO plasma membrane GO:0005886 The pathogenic antibodies bind cell-surface NMDARs and decrease surface receptor density/localization (dalmau2016nmdareceptorencephalitis pages 2-3, gong2023antinmdarantibodiesthe pages 1-2).
Subcellular GO recycling endosome GO:0055037 Internalized receptors preferentially traffic to Rab11-positive recycling endosomes in mechanistic studies (dalmau2017autoantibodiestosynaptic pages 34-35).
Phenotype HPO Psychiatric symptoms HP:0000708 Psychiatric/behavioral symptoms are among the most common presenting features, affecting about 90% of teenagers/adults in review data (nguyen2023antinmdareceptorautoimmune pages 3-5).
Phenotype HPO Seizure HP:0001250 Seizures are a core diagnostic manifestation and occurred in 80.9% of a 220-patient cohort and 67% of a 106-patient cohort (xu2020antinmdarencephalitis pages 1-2, wang2020influencingelectroclinicalfeatures pages 1-2).
Phenotype HPO Dyskinesia HP:0100660 Movement disorder, especially orolingual-facial dyskinesia, is characteristic of anti-NMDAR encephalitis (nguyen2023antinmdareceptorautoimmune pages 3-5).
Phenotype HPO Autonomic dysfunction HP:0002271 Autonomic dysfunction is included in diagnostic criteria and includes instability of temperature, salivation, blood pressure, heart rate, and continence (nguyen2023antinmdareceptorautoimmune pages 3-5, ho2017highsensitivityand pages 3-3).
Phenotype HPO Central hypoventilation HP:0007110 Central hypoventilation is a recognized core manifestation linked to ICU care and worse prognosis (nguyen2023antinmdareceptorautoimmune pages 3-5, ho2017highsensitivityand pages 3-3).
Phenotype HPO Memory impairment HP:0002354 Memory deficits are frequent in the acute syndrome and remain a major long-term deficit domain in survivors (brenner2024longtermcognitivefunctional pages 1-2, xu2020antinmdarencephalitis pages 1-2).
Phenotype HPO Language impairment HP:0002465 Language scores remain persistently reduced in long-term follow-up and speech dysfunction is a core diagnostic domain (brenner2024longtermcognitivefunctional pages 1-2, ho2017highsensitivityand pages 3-3).
Phenotype HPO Mutism HP:0002300 Speech dysfunction in anti-NMDAR encephalitis includes verbal reduction and mutism in clinical criteria/reviews (nguyen2023antinmdareceptorautoimmune pages 3-5).
Phenotype HPO Cerebrospinal fluid pleocytosis HP:0012675 CSF pleocytosis is common, with reported frequencies ranging from 47% to 91% across cohorts (nguyen2023antinmdareceptorautoimmune pages 3-5, alsalek2024racialandethnic pages 1-2).
Phenotype HPO Oligoclonal bands in cerebrospinal fluid HP:0032150 Positive CSF oligoclonal bands are reported in roughly 25% to 62.6% of cases across studies (nguyen2023antinmdareceptorautoimmune pages 3-5, nguyen2023antinmdareceptorautoimmune pages 5-6).
Phenotype HPO Abnormality of EEG HP:0002353 EEG is abnormal in most patients and supports diagnosis when antibody results are pending (nguyen2023antinmdareceptorautoimmune pages 5-6, alsalek2024racialandethnic pages 1-2).
Phenotype HPO Delta brush EEG pattern ID not retrieved Extreme delta brush is a disease-associated EEG pattern specifically highlighted in anti-NMDAR encephalitis diagnostic discussions (nguyen2023antinmdareceptorautoimmune pages 3-5, graus2016aclinicalapproach pages 6-7).
Process GO receptor internalization GO:0031623 Patient antibodies cause NMDAR loss primarily through receptor crosslinking and internalization rather than agonist activation (dalmau2017autoantibodiestosynaptic pages 34-35, dalmau2016nmdareceptorencephalitis pages 1-2).
Process GO regulation of synaptic plasticity GO:0048167 Loss of synaptic NMDARs impairs long-term potentiation and broader synaptic plasticity in passive-transfer studies (dalmau2016nmdareceptorencephalitis pages 7-9, dalmau2017autoantibodiestosynaptic pages 37-38).
Process GO trans-synaptic signaling GO:0099537 Reduced synaptic receptor density and altered hippocampal signaling support disruption of synaptic communication pathways (gong2023antinmdarantibodiesthe pages 1-2).
Process GO B cell mediated immunity GO:0019724 Disease pathogenesis involves autoreactive B cells and intrathecal antibody-producing cells targeting GluN1 (gong2023antinmdarantibodiesthe pages 1-2, dalmau2017autoantibodiestosynaptic pages 8-10).
Process GO immunoglobulin production GO:0002377 Intrathecal synthesis of anti-GluN1 antibodies by B cells/plasma cells is part of the proposed pathogenic cascade (dalmau2017autoantibodiestosynaptic pages 37-38, dalmau2017autoantibodiestosynaptic pages 8-10).
Process GO blood-brain barrier maintenance GO:1990961 BBB dysfunction is repeatedly proposed as enabling entry/exit of antibodies and immune cells in anti-NMDAR encephalitis (gong2023antinmdarantibodiesthe pages 1-2).
Treatment MAXO corticosteroid therapy ID not retrieved High-dose corticosteroids are standard first-line immunotherapy in anti-NMDAR encephalitis management algorithms (nguyen2023antinmdareceptorautoimmune pages 1-2, nguyen2023antinmdareceptorautoimmune pages 6-7).
Treatment CHEBI methylprednisolone CHEBI:6888 IV methylprednisolone is explicitly listed as a first-line treatment option and regimen in the treatment table (nguyen2023antinmdareceptorautoimmune pages 6-7, nguyen2023antinmdareceptorautoimmune media a2c6c545).
Treatment MAXO intravenous immunoglobulin therapy ID not retrieved IVIG is a standard first-line immunotherapy and commonly combined with steroids in clinical practice (nguyen2023antinmdareceptorautoimmune pages 1-2, nguyen2023antinmdareceptorautoimmune pages 6-7).
Treatment CHEBI immunoglobulin CHEBI:59132 IVIG is directly listed in treatment recommendations and Table 2 for anti-NMDAR encephalitis (nguyen2023antinmdareceptorautoimmune pages 6-7, nguyen2023antinmdareceptorautoimmune media a2c6c545).
Treatment MAXO plasma exchange therapy ID not retrieved Plasma exchange/PLEX is a recommended first-line therapy for acute disease (nguyen2023antinmdareceptorautoimmune pages 1-2, nguyen2023antinmdareceptorautoimmune pages 6-7).
Treatment MAXO rituximab therapy ID not retrieved Rituximab is the best-established second-line escalation therapy for refractory disease and relapse prevention (nguyen2023antinmdareceptorautoimmune pages 1-2, nguyen2023antinmdareceptorautoimmune pages 6-7).
Treatment CHEBI rituximab CHEBI:64357 Rituximab is specifically named in the treatment table as second-line immunotherapy (nguyen2023antinmdareceptorautoimmune pages 6-7, nguyen2023antinmdareceptorautoimmune media a2c6c545).
Treatment MAXO cyclophosphamide therapy ID not retrieved Cyclophosphamide is a recommended second-line agent for refractory anti-NMDAR encephalitis (nguyen2023antinmdareceptorautoimmune pages 1-2, nguyen2023antinmdareceptorautoimmune pages 6-7).
Treatment CHEBI cyclophosphamide CHEBI:4027 Cyclophosphamide appears in the treatment table as a second-line immunotherapy option (nguyen2023antinmdareceptorautoimmune pages 6-7, nguyen2023antinmdareceptorautoimmune media a2c6c545).
Treatment MAXO tocilizumab therapy ID not retrieved Tocilizumab is described as a complementary option in refractory cases beyond standard second-line therapy (nguyen2023antinmdareceptorautoimmune pages 1-2, nguyen2023antinmdareceptorautoimmune media a2c6c545).
Treatment CHEBI tocilizumab CHEBI:71416 Tocilizumab is included among escalation/refractory therapies in the visualized treatment table (nguyen2023antinmdareceptorautoimmune media a2c6c545, nguyen2023antinmdareceptorautoimmune media e857af28).
Treatment MAXO bortezomib therapy ID not retrieved Bortezomib is considered in refractory cases when standard escalation is insufficient (nguyen2023antinmdareceptorautoimmune pages 1-2, nguyen2023antinmdareceptorautoimmune media a2c6c545).
Treatment CHEBI bortezomib CHEBI:52717 Bortezomib is listed among additional escalation therapies in the treatment table (nguyen2023antinmdareceptorautoimmune media e857af28).
Treatment MAXO mycophenolate mofetil therapy ID not retrieved Mycophenolate mofetil is used as prolonged/maintenance immunotherapy in some cohorts and tables (xu2020antinmdarencephalitis pages 1-2, nguyen2023antinmdareceptorautoimmune media e857af28).
Treatment CHEBI mycophenolate mofetil CHEBI:31824 MMF is specifically listed as a maintenance therapy and was used >1 year in a large Chinese cohort (xu2020antinmdarencephalitis pages 1-2, nguyen2023antinmdareceptorautoimmune media e857af28).
Treatment MAXO azathioprine therapy ID not retrieved Azathioprine is used as long-term maintenance immunotherapy in some patients after the acute phase (xu2020antinmdarencephalitis pages 1-2, nguyen2023antinmdareceptorautoimmune media e857af28).
Treatment CHEBI azathioprine CHEBI:22636 Azathioprine is named in the treatment table and in long-term immunotherapy descriptions (xu2020antinmdarencephalitis pages 1-2, nguyen2023antinmdareceptorautoimmune media e857af28).
Treatment MAXO tumor resection ID not retrieved Treatment guidance emphasizes teratoma removal alongside immunotherapy when an ovarian teratoma is present (nguyen2023antinmdareceptorautoimmune pages 1-2, nguyen2023antinmdareceptorautoimmune pages 6-7).
Treatment MAXO tumor screening ID not retrieved All patients should be screened at least once for neoplasm, and female patients may need serial pelvic imaging because ovarian teratoma is a common trigger (nguyen2023antinmdareceptorautoimmune pages 1-2, nguyen2023antinmdareceptorautoimmune pages 5-6).

Table: This table maps key anti-NMDA receptor encephalitis concepts to suggested ontology terms across disease, anatomy, cell type, phenotype, process, and treatment categories. It is evidence-aligned to the retrieved literature and can help populate a structured disease knowledge base.

Notes on citation requirements (PMID)

Where possible, this report cites primary literature and major reviews with DOI and publication year/month extracted from the retrieved sources. PMIDs were not available in the current tool context for most items, so they are not included to avoid introducing unsupported identifiers.

References

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Artifacts