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Acute Disseminated Encephalomyelitis

Acute Disseminated Encephalomyelitis (ADEM): Comprehensive Disease Characteristics Report

2026-05-15
Falcon MONDO:0019383 Model: Edison Scientific Literature 60 citations

Acute Disseminated Encephalomyelitis (ADEM): Comprehensive Disease Characteristics Report

Executive summary (current understanding)

Acute disseminated encephalomyelitis (ADEM) is an immune-mediated inflammatory demyelinating disorder of the central nervous system (CNS) classically presenting as a first, polyfocal demyelinating event with encephalopathy and characteristic MRI abnormalities, most often in children. Operational pediatric definitions (International Pediatric Multiple Sclerosis Study Group; IPMSSG) emphasize encephalopathy “that cannot be explained by fever” and typical large, poorly demarcated white-matter lesions on MRI (krupp2013internationalpediatricmultiple pages 2-3). The modern landscape of “ADEM” is increasingly shaped by antibody-defined subgroups—especially myelin oligodendrocyte glycoprotein antibodies (MOG-IgG), which are detected in >50% of pediatric ADEM cohorts and are associated with higher relapse risk (dong2023clinicalradiologicaltherapeutic pages 1-2).

Evidence inventory and limitations

This report is based on the retrieved peer-reviewed literature and ClinicalTrials.gov records contained in the tool context (2023–2024 prioritized where available). Important limitation: using the available tools and retrieved corpus, I could not reliably extract MONDO ID, Orphanet ID, or MeSH unique ID for ADEM; therefore, this report emphasizes ICD-based identifiers and consensus clinical criteria (boesen2018implicationsofthe pages 3-4, xiu2021incidenceandmortality pages 1-2).

1. Disease information

1.1 Disease overview / definition

  • ADEM is an immune-mediated inflammatory/demyelinating CNS disorder. In a nationwide Chinese registry-based study, ADEM is defined as “an immune-mediated demyelinating disorder characterized by a widespread attack of inflammation in the brain and spinal cord that damages myelin” (xiu2021incidenceandmortality pages 1-2).
  • In the SARS-CoV-2 infection/vaccination context, ADEM is described as “an acute-onset demyelinating disease that involves a rapid evolution and multifocal neurological deficits” (stoian2023theoccurrenceof pages 1-2).

1.2 Key identifiers and classification systems (available in retrieved evidence)

The most consistently retrievable identifiers in the current evidence are ICD-10 codes used for registry ascertainment and IPMSSG 2013 clinical criteria used for case definition.

Table (click to expand)
Identifier system Code/term Notes/definition snippet Primary supporting source (with URL and year)
ICD-10 G04.0 Used as the core discharge/registry code for ADEM ascertainment in nationwide studies; one study identified ADEM-related hospitalizations using ICD-10 code “G04.0” and defined ADEM as “an immune-mediated demyelinating disorder characterized by a widespread attack of inflammation in the brain and spinal cord that damages myelin” (xiu2021incidenceandmortality pages 1-2) Xiu Y et al. Incidence and Mortality of Acute Disseminated Encephalomyelitis in China: A Nationwide Population-Based Study. 2021. https://doi.org/10.1007/s12264-021-00642-7
ICD-10 G04.0, G04.8, G04.9 Danish pediatric registry validation study used ADEM-related ICD-10 codes “G04.0, G04.8, G04.9” for case finding; unspecified encephalitis codes G04.0/G04.8/G04.9 were included in capture before record-level validation against clinical/IPMSSG criteria (boesen2018implicationsofthe pages 3-4, boesen2018implicationsofthe pages 2-2) Boesen MS et al. Implications of the International Paediatric Multiple Sclerosis Study Group consensus criteria for paediatric acute disseminated encephalomyelitis: a nationwide validation study. 2018. https://doi.org/10.1111/dmcn.13798
IPMSSG 2013 pediatric criteria Pediatric ADEM IPMSSG operational definition requires “A first polyfocal, clinical CNS event with presumed inflammatory demyelinating cause” plus “Encephalopathy that cannot be explained by fever,” no new clinical/MRI findings for at least 3 months, and acute-phase abnormal brain MRI (krupp2013internationalpediatricmultiple pages 2-3) Krupp LB et al. International Pediatric Multiple Sclerosis Study Group criteria for pediatric multiple sclerosis and immune-mediated central nervous system demyelinating disorders: revisions to the 2007 definitions. 2013. https://doi.org/10.1177/1352458513484547
IPMSSG 2013 MRI characterization Typical pediatric ADEM MRI Typical MRI lesions are described as “diffuse, poorly demarcated, large (>1–2 cm) lesions involving predominantly the cerebral white matter”; “T1 hypointense lesions in the white matter are rare,” and deep gray matter lesions may occur (krupp2013internationalpediatricmultiple pages 2-3, krupp2013internationalpediatricmultiple pages 6-7) Krupp LB et al. International Pediatric Multiple Sclerosis Study Group criteria for pediatric multiple sclerosis and immune-mediated central nervous system demyelinating disorders: revisions to the 2007 definitions. 2013. https://doi.org/10.1177/1352458513484547
Registry/clinical classification label Clinical ADEM vs IPMSSG ADEM Registry validation work distinguishes physician-diagnosed “Clinical ADEM” from stricter “IPMSSG ADEM,” highlighting that many coded/clinical ADEM cases do not fulfill mandatory encephalopathy/polyfocal-deficit criteria (boesen2018implicationsofthe pages 4-4, boesen2018implicationsofthe pages 1-2, boesen2018implicationsofthe pages 6-7) Boesen MS et al. Implications of the International Paediatric Multiple Sclerosis Study Group consensus criteria for paediatric acute disseminated encephalomyelitis: a nationwide validation study. 2018. https://doi.org/10.1111/dmcn.13798
Abbreviation / disease term ADEM = acute disseminated encephalomyelitis Standard expansion used in registry and clinical studies; defined as an immune-mediated inflammatory/demyelinating CNS disorder, often characterized by encephalopathy, multifocal deficits, and large poorly demarcated white-matter MRI lesions (boesen2018implicationsofthe pages 1-2, xiu2021incidenceandmortality pages 1-2) Boesen MS et al. 2018. https://doi.org/10.1111/dmcn.13798 ; Xiu Y et al. 2021. https://doi.org/10.1007/s12264-021-00642-7

Table: This table summarizes the key coding and classification systems used for ADEM in the available evidence, highlighting ICD-10 codes used in registry studies and the defining IPMSSG 2013 pediatric criteria. It is useful for mapping disease terminology across clinical, epidemiologic, and knowledge-base contexts.

Interpretation note (registry vs clinical definitions): Danish validation work highlights that physician-diagnosed “Clinical ADEM” can diverge substantially from IPMSSG ADEM because encephalopathy/polyfocal deficits may not be enforced in routine practice; this is critical for building EHR/claims phenotypes (boesen2018implicationsofthe pages 1-2).

1.3 Common synonyms / alternative names (within retrieved corpus)

1.4 Evidence sources: individual vs aggregated

2. Etiology

2.1 Primary causal factors / triggers

ADEM is widely conceptualized as a post-infectious or post-immunization immune-mediated demyelinating syndrome. - Pediatric cohort/review descriptions: ADEM “typically occurs after a viral infection or recent vaccination” (mukhtiar2024clinicalpatternneuroimaging pages 1-2). - COVID context review: ADEM usually develops following viral/bacterial infection and “less frequently” after vaccination; historical vaccine associations listed include influenza, varicella, measles, mumps, rabies, hepatitis B, diphtheria, and tetanus (stoian2023theoccurrenceof pages 2-4).

2.2 Risk factors

Age: ADEM is predominantly pediatric, with median onset often cited around 5–8 years (pediatric cohort/review) (mukhtiar2024clinicalpatternneuroimaging pages 1-2, paolilo2020acutedisseminatedencephalomyelitis pages 3-5).

Antecedent infections: A preceding infection/illness is frequently reported (review-level estimates 70–80%) with neurologic onset often 2–21 days after infection (paolilo2020acutedisseminatedencephalomyelitis pages 3-5).

SARS-CoV-2 infection/vaccination: Systematic reviews catalog ADEM cases after infection and vaccination; in one review cohort of 74 ADEM cases, 60.81% followed SARS-CoV-2 infection and 39.19% followed vaccination (stoian2023theoccurrenceof pages 23-26).

2.3 Protective factors

No robust protective genetic variants or environmental protective exposures were extractable from the retrieved evidence.

2.4 Gene–environment interactions

The strongest “molecular-by-exposure” interaction in the retrieved corpus is the MOG-IgG-defined subgroup interacting with common immune triggers (infection/vaccination) in shaping relapse risk and phenotype (pediatric ADEM >50% MOG-IgG positivity; relapse associations) (dong2023clinicalradiologicaltherapeutic pages 1-2).

3. Phenotypes (clinical presentation) and suggested HPO terms

ADEM typically presents as an acute/subacute encephalopathic illness with polyfocal deficits.

Table (click to expand)
Feature Type (symptom/sign/lab/imaging) Suggested HPO term Evidence summary with numbers Source (URL, year)
Encephalopathy / Altered consciousness Symptom/Sign HP:0002243, HP:0004372 Requisite for pediatric ADEM per IPMSSG (not explained by fever); includes irritability, lethargy, or coma. Reported as the most frequent presenting feature (18.5% to >50% depending on cohort). (nabizadeh2023acutedisseminatedencephalomyelitis pages 1-3, mukhtiar2024clinicalpatternneuroimaging pages 1-2, krupp2013internationalpediatricmultiple pages 2-3) Krupp et al., 2013 (https://doi.org/10.1177/1352458513484547); Mukhtiar et al., 2024 (https://doi.org/10.12669/pjms.40.7.8015)
Pyramidal signs / Motor deficit Sign HP:0002493, HP:0003470 Observed in 68.7% of adult ADEM cases; 53.5% of pediatric cases in a single-center cohort. Often presents as polyfocal weakness or paresis. (mukhtiar2024clinicalpatternneuroimaging pages 1-2, li2022clinicalpresentationand pages 1-2) Li et al., 2022 (https://doi.org/10.3389/fimmu.2022.870867); Mukhtiar et al., 2024 (https://doi.org/10.12669/pjms.40.7.8015)
Fever and Headache Symptom HP:0001945, HP:0002315 Very common prodromal and presenting features; typically lasting 3-4 days before progressing to encephalopathy. (mukhtiar2024clinicalpatternneuroimaging pages 1-2) Mukhtiar et al., 2024 (https://doi.org/10.12669/pjms.40.7.8015)
Seizures Sign HP:0001250 Reported in ~9.2% of post-vaccine cases; observed at a significantly lower frequency in MOG-seropositive pediatric ADEM compared to MOG-seronegative cases. (nabizadeh2023acutedisseminatedencephalomyelitis pages 1-3, dong2023clinicalradiologicaltherapeutic pages 1-2) Nabizadeh et al., 2023 (https://doi.org/10.1016/j.jocn.2023.03.008); Dong et al., 2023 (https://doi.org/10.3389/fnins.2023.1128422)
Large, diffuse white matter lesions Imaging HP:0002500, HP:0011036 Abnormal brain MRI in 91.6% of adults (87.1% show white matter lesions). Lesions are typically bilateral, asymmetrical, poorly demarcated, >1-2 cm, and hyperintense on T2/FLAIR. T1 hypointensity is rare (unlike in MS). (krupp2013internationalpediatricmultiple pages 2-3, stoian2023theoccurrenceof media 322d56fe, li2022clinicalpresentationand pages 4-5) Krupp et al., 2013 (https://doi.org/10.1177/1352458513484547); Li et al., 2022 (https://doi.org/10.3389/fimmu.2022.870867)
Deep gray matter involvement Imaging HP:0012750 Frequent involvement of the thalamus and basal ganglia; the corpus callosum is typically spared and Dawson fingers are absent (helpful to differentiate from MS). (krupp2013internationalpediatricmultiple pages 2-3, stoian2023theoccurrenceof media 322d56fe) Krupp et al., 2013 (https://doi.org/10.1177/1352458513484547); Stoian et al., 2023 (https://doi.org/10.3390/vaccines11071225)
CSF pleocytosis and elevated protein Lab HP:0002128, HP:0002922 Abnormal CSF found in 46.6% to 80% of cases. In adults, pleocytosis occurs in 51.8% and elevated protein in 39.1%. (mukhtiar2024clinicalpatternneuroimaging pages 1-2, li2022clinicalpresentationand pages 4-5, stoian2023theoccurrenceof pages 31-32) Li et al., 2022 (https://doi.org/10.3389/fimmu.2022.870867); Mukhtiar et al., 2024 (https://doi.org/10.12669/pjms.40.7.8015)
Oligoclonal bands (OCB) absence Lab HP:0003261 OCB positivity is low in ADEM (~20% to 23.9% in adults) compared to MS (>80%), serving as a key diagnostic differentiator. (li2022clinicalpresentationand pages 6-7, li2022clinicalpresentationand pages 4-5) Li et al., 2022 (https://doi.org/10.3389/fimmu.2022.870867)
MOG-IgG Seropositivity Lab N/A Detectable in >50% of pediatric ADEM cases; strongly associated with multiphasic disease and higher relapse risk, though onset disability is often milder. (dong2023clinicalradiologicaltherapeutic pages 1-2) Dong et al., 2023 (https://doi.org/10.3389/fnins.2023.1128422)

Table: A summary of the core clinical symptoms, imaging findings, and laboratory test results characteristic of ADEM, including differences from MS and corresponding HPO terms.

3.1 Common clinical features and frequencies (examples from recent/large cohorts)

  • Pediatric single-center cohort (Pakistan, 2018–2022): fever, headache, altered consciousness were most common; motor deficits occurred in 53.5%; CSF abnormal in 46.6%; bilateral/multifocal MRI lesions in 78.6%; brainstem involvement 25%; improvement 89.3%; residual weakness at discharge 26%; one death (mukhtiar2024clinicalpatternneuroimaging pages 1-2).
  • Post-COVID vaccination ADEM case review (54 cases): muscle weakness 22.2%, unconsciousness 18.5%, urinary complaints 16.6%, visual impairment 16.6%, seizures 9.2%; clinical improvement 85.1%; deaths reported (4 cases per excerpt) (nabizadeh2023acutedisseminatedencephalomyelitis pages 1-3).

3.2 Quality of life impact

Direct standardized QoL instruments (EQ-5D, PROMIS) were not extractable from the retrieved cohort texts. However, pediatric cohorts report long-term issues such as poor scholastic performance and behavioral problems (functional outcomes consistent with QoL impact) (mukhtiar2024clinicalpatternneuroimaging pages 1-2).

4. Genetic / molecular information

4.1 Causal genes

ADEM is generally not a monogenic disease; no causal gene list (OMIM-style) was supported by the retrieved evidence.

4.2 Key molecular biomarkers: MOG-IgG and antibody-defined disease boundaries

A major development in “ADEM” classification is overlap with MOG antibody-associated disease (MOGAD). - Pediatric ADEM cohort: MOG antibodies can be detected in >50% of children with ADEM; in one cohort, 35/62 (≈56%) were MOG-seropositive (dong2023clinicalradiologicaltherapeutic pages 1-2). - Prognosis: in this cohort, MOG-seropositive children were more likely to relapse (P=0.017) (dong2023clinicalradiologicaltherapeutic pages 1-2).

4.3 Diagnostic interpretation (2023 MOGAD criteria context; 2024 evidence)

A clinically actionable 2024 test-performance study quantified how MOG-IgG positivity predicts “true MOGAD” under 2023 criteria: - Overall PPV 78.3% for MOG-IgG seropositivity. - PPV by titer: 52.6% for low titer vs 90.1% for high titer. - PPV in children vs adults: 93.9% vs 67.2%. - PPV without a core clinical demyelinating attack: 6.3%. (nguyen2024thepositivepredictive pages 1-2) These findings support expert recommendations to interpret low-titer MOG-IgG cautiously, especially when a core demyelinating attack phenotype is absent (nguyen2024thepositivepredictive pages 1-2).

4.4 Modifier genes / HLA

No ADEM-specific modifier gene or HLA association statistics were extractable from the retrieved evidence.

5. Environmental information

5.1 Infectious agents (triggers)

Multiple viral infections are cited as antecedent triggers in reviews of ADEM, including influenza and Epstein–Barr virus (EBV) among others (stoian2023theoccurrenceof pages 2-4).

5.2 Vaccination and immune stimulation

The post-vaccination ADEM literature remains dominated by case reports/series; a 2023 systematic review identified 54 cases after COVID-19 vaccination and concluded that causality is not established (“it is not clear that ADEM could be a potential complication of COVID-19 vaccination based on the current evidence”) (nabizadeh2023acutedisseminatedencephalomyelitis pages 1-3).

5.3 Other environmental/lifestyle factors

No reproducible toxin, occupational, dietary, or lifestyle exposures were extractable from the retrieved evidence.

6. Mechanism / pathophysiology

6.1 Causal chain (conceptual model)

  1. Triggering immune event (often viral infection; less commonly vaccination) → (stoian2023theoccurrenceof pages 2-4)
  2. Aberrant immune activation (molecular mimicry and immune cross-reactivity hypothesized in SARS-CoV-2 settings) → BBB dysfunction/neuroinflammation (stoian2023theoccurrenceof pages 30-31, stoian2023theoccurrenceof pages 1-2)
  3. CNS demyelinating inflammation with perivenous/perivascular pathology and multifocal lesions → MRI T2/FLAIR hyperintensities, encephalopathy, polyfocal deficits (krupp2013internationalpediatricmultiple pages 2-3, stoian2023theoccurrenceof pages 31-32)
  4. In a subset, antibody-mediated disease biology (MOG-IgG) is associated with relapse propensity and overlapping phenotypes (ADEM, optic neuritis, myelitis, cortical encephalitis) (dong2023clinicalradiologicaltherapeutic pages 1-2, kim2024pediatricmogab–associatedencephalitis pages 1-2).

6.2 Immune system involvement and candidate pathways

Ontology suggestions (mechanism): - GO Biological Process (examples): - “immune system process” (GO:0002376) - “inflammatory response” (GO:0006954) - “demyelination” (GO:0042552) - “leukocyte migration” (GO:0050900) - Cell Ontology (examples): - microglia (CL:0000129) - T cell (CL:0000084) - B cell (CL:0000236) - macrophage (CL:0000235) - UBERON anatomy (examples): - brain (UBERON:0000955) - spinal cord (UBERON:0002240) - cerebral white matter (UBERON:0006120)

6.3 Molecular profiling / omics

Direct transcriptomic/proteomic datasets were not present in the retrieved literature; however, a 2025 recruiting interventional study explicitly aims to identify relapse-predictive biomarkers using high-throughput omics in PBMCs across ADEM-MOGAD and control demyelinating phenotypes (NCT06863974) (NCT06863974 chunk 1).

7. Anatomical structures affected

7.1 Organ/system level

7.2 Tissue/cell level

7.3 MRI localization patterns (key differentiators)

Typical ADEM MRI lesions are diffuse, poorly demarcated, large (>1–2 cm) and predominantly in cerebral white matter; deep gray matter lesions may occur and T1 hypointense “black holes” are rare (krupp2013internationalpediatricmultiple pages 2-3). Lesion patterns can aid differential diagnosis vs MS (periventricular lesions, black holes, lack of bilateral diffuse pattern) (krupp2013internationalpediatricmultiple pages 2-3, stoian2023theoccurrenceof pages 31-32).

Visual evidence (diagnostic criteria and MRI features): key figure/table regions summarizing diagnostic criteria and MRI lesion distributions were retrieved from a 2023 systematic review (stoian2023theoccurrenceof media 322d56fe, stoian2023theoccurrenceof media df3808bd, stoian2023theoccurrenceof media ee7112b9).

8. Temporal development

8.1 Onset

8.2 Course and progression

9. Inheritance and population

9.1 Epidemiology (incidence, mortality, outcomes)

Table (click to expand)
Population/setting Study type (cohort/meta-analysis/systematic review) N Incidence (with units) Mortality Residual deficits/long-term sequelae Notes Source (URL, year)
Children, general/pediatric ADEM (global estimates cited in reviews) Narrative review / review of epidemiology NR 0.07–0.9 per 100,000 children/year NR ICU needed in ~15% of pediatric cases; recovery usually over weeks; multiphasic course or later MS can occur in a minority Median onset 5–8 years; male:female reported from 1:0.8 to 2.3:1; identifiable trigger in up to 50–85%, preceding infection/illness in 70–80% (paolilo2020acutedisseminatedencephalomyelitis pages 3-5) Paolilo R et al. https://doi.org/10.3390/children7110210 (2020)
Children, single-center Pakistan cohort Retrospective cohort 30 Background estimate cited: 0.07–0.9 per 100,000 children/year 1/30 (3.3%) Residual weakness at discharge 8/30 (26%); long-term sequelae included motor deficits, seizures, poor scholastic performance, behavioral problems Mean age 6.43 years; immediate clinical improvement in 25/28 evaluable or 89.3% as reported (mukhtiar2024clinicalpatternneuroimaging pages 1-2) Mukhtiar K et al. https://doi.org/10.12669/pjms.40.7.8015 (2024)
Adults worldwide Systematic review and meta-analysis 437 NR 7.8% (95% CI 3.3–13.5) Residual deficits 47.5% (95% CI 31.8–63.4) Pooled adult features included white matter lesions 87.1%, polyfocal onset 80.5%, pyramidal signs 68.7%; adults had worse outcomes than children (li2022clinicalpresentationand pages 1-2) Li K et al. https://doi.org/10.3389/fimmu.2022.870867 (2022)
Adults worldwide Systematic review and meta-analysis 437 NR 7.8% overall; 4.3% within 3 months; 11.0% after >3 months; Asia subgroup 14.5% Nearly half had residual deficits at mean follow-up 2.8 ± 3.6 years Recurrence 7.2%; mean hospital stay 23.1 days; ICU 39.7%; preceding infection ~25.7%, vaccination ~2.9% (li2022clinicalpresentationand pages 4-5, li2022clinicalpresentationand pages 5-6) Li K et al. https://doi.org/10.3389/fimmu.2022.870867 (2022)
Nationwide China, tertiary hospitals Population-based cohort / registry study 2,265 newly diagnosed cases; 3,101 total patients; 6,978 hospitalizations Provincial annual incidence examples: Beijing 0.066 per 100,000 person-years (95% CI 0.046–0.086); Heilongjiang 0.027 per 100,000 person-years (95% CI 0.018–0.037) NR in excerpt NR in excerpt Cases identified with ICD-10 G04.0 across 1,665 tertiary hospitals; study also cited prior pediatric incidences: Europe 0.07–0.51, North America 0.2–0.6, Japan ~0.4 per 100,000 (xiu2021incidenceandmortality pages 1-2) Xiu Y et al. https://doi.org/10.1007/s12264-021-00642-7 (2021)
Denmark, pediatric registry validation Nationwide validation cohort NR for full national cohort; incidence analysis reported for clinical/IPMSSG subsets Clinical ADEM 0.54 per 100,000 person-years; IPMSSG ADEM 0.19 per 100,000 person-years NR NR Shows how stricter IPMSSG criteria reduce estimated incidence; registry pull used ICD-10 G04.0/G04.8/G04.9 among others (boesen2018implicationsofthe pages 3-4) Boesen MS et al. https://doi.org/10.1111/dmcn.13798 (2018)
SARS-CoV-2-associated ADEM/AHLE Systematic review 48 NR 5/48 (10%) died in hospital Poor outcome on discharge in 31/48 (64%); only 15% full recovery Median age 44 years; 19% were children; outcomes worse than classic ADEM (wang2022sarscov2associatedacutedisseminated pages 18-19) Wang Y et al. https://doi.org/10.1007/s00415-021-10771-8 (2022)
COVID-19 infection or vaccination-associated ADEM Systematic review 74 NR 8 deaths reported across review cohort Average recovery 1–6 months in treated cases; permanent neurological disability can occur 45 followed infection, 29 vaccination; 13/74 (17.33%) AHLE; poor outcome linked to coma/AHLE, extensive lesions, brainstem involvement, ICU admission (stoian2023theoccurrenceof pages 1-2, stoian2023theoccurrenceof pages 31-32) Stoian A et al. https://doi.org/10.3390/vaccines11071225 (2023)
Post-COVID-19 vaccination ADEM Systematic review of case reports 54 NR 4 deaths (reported as 13.8% in excerpt) Clinical improvement in 46 cases (85.1%); MRI improvement in 44 cases (81.4%) Median interval from vaccination to neurologic symptoms 14 days; most cases after first dose (45/54, 85.1%) (nabizadeh2023acutedisseminatedencephalomyelitis pages 1-3) Nabizadeh F et al. https://doi.org/10.1016/j.jocn.2023.03.008 (2023)

Table: This table compiles the main epidemiology and outcomes statistics for acute disseminated encephalomyelitis from the retrieved cohort studies, meta-analyses, and systematic reviews. It is useful for quickly comparing pediatric, adult, and COVID-associated ADEM burden, mortality, and sequelae across settings.

Key epidemiologic statistics from the retrieved evidence: - Pediatric incidence (general estimates): 0.07–0.9 per 100,000 children/year (pediatric cohort/review) (mukhtiar2024clinicalpatternneuroimaging pages 1-2, paolilo2020acutedisseminatedencephalomyelitis pages 3-5). - Population-based incidence (China, tertiary hospitals): provincial annual incidence examples include Beijing 0.066 per 100,000 person-years and Heilongjiang 0.027 per 100,000 person-years (xiu2021incidenceandmortality pages 1-2). - Adults (meta-analysis): mortality 7.8% (95% CI 3.3–13.5) and residual deficits 47.5% (95% CI 31.8–63.4) (li2022clinicalpresentationand pages 1-2).

9.2 Sex ratio

Male predominance is suggested in pediatric reviews (range reported male:female 1:0.8 to 2.3:1) (paolilo2020acutedisseminatedencephalomyelitis pages 3-5).

9.3 Geographic distribution

Incidence varies geographically and has been reported to be higher with increasing distance from the equator (review summary) (paolilo2020acutedisseminatedencephalomyelitis pages 3-5).

10. Diagnostics

10.1 Clinical criteria (IPMSSG 2013 pediatric ADEM)

The IPMSSG operational definition requires all of: - “A first polyfocal, clinical CNS event with presumed inflammatory demyelinating cause” - “Encephalopathy that cannot be explained by fever” - No new clinical and MRI findings for ≥3 months - Abnormal brain MRI in the acute (3-month) phase and typical MRI lesions described as “diffuse, poorly demarcated, large (>1–2 cm) lesions involving predominantly the cerebral white matter” (krupp2013internationalpediatricmultiple pages 2-3).

10.2 Imaging

MRI is central: - Lesions commonly appear as multifocal, bilateral T2/FLAIR hyperintensities, often involving white matter with possible deep gray involvement; contrast enhancement varies (e.g., 36.48% in a COVID-associated systematic review cohort) (stoian2023theoccurrenceof pages 23-26).

10.3 CSF and laboratory

  • CSF abnormalities can occur (pleocytosis, elevated protein), but may be absent in a subset; OCBs are generally less common than in MS (adult meta-analysis OCB ~23.9%) (li2022clinicalpresentationand pages 4-5).

10.4 Differential diagnosis

11. Outcome / prognosis

11.1 Pediatric outcomes

Pediatric cohorts often report favorable short-term outcomes but nontrivial residual deficits: - Improvement 89.3% with residual weakness 26% at discharge in one cohort (mukhtiar2024clinicalpatternneuroimaging pages 1-2).

11.2 Adult outcomes

Adults have worse prognosis: - Mortality 7.8% and residual deficits 47.5% in meta-analysis (li2022clinicalpresentationand pages 1-2).

11.3 COVID-associated outcomes

COVID-associated ADEM/AHLE series show notably worse outcomes than “classic” pediatric ADEM: - Poor outcome 64%, death 10%, only 15% full recovery in one systematic review cohort (wang2022sarscov2associatedacutedisseminated pages 18-19).

12. Treatment

Table (click to expand)
Intervention Indication/setting Mechanism/class Typical regimen/dose (as available) Evidence/outcomes Trial identifiers/status (if any) Source (URL, year) with pqac citations
IV methylprednisolone (IVMP) First-line acute treatment for ADEM; also used in MOGAD/MOG-related ADEM attacks High-dose corticosteroid; broad anti-inflammatory and immunosuppressive therapy 1–2 g/day for 3–5 days then oral taper in adults/reviews; pediatric dosing commonly 30 mg/kg/day (max 1000 mg) for 3–5 days, followed by oral prednisone taper over 4–6 weeks (stoian2023theoccurrenceof pages 31-32, paolilo2020acutedisseminatedencephalomyelitis pages 7-9, mahapure2021covid19associatedacutedisseminated pages 10-11, vempati2023acutedisseminatedencephalomyelitis pages 4-8) Favorable response in about two-thirds of cases; steroids shorten disease duration and halt progression; early treatment associated with better outcomes; rapid taper/early discontinuation may increase relapse risk in MOGAD/ADEM-spectrum disease (stoian2023theoccurrenceof pages 31-32, paolilo2020acutedisseminatedencephalomyelitis pages 7-9, mahapure2021covid19associatedacutedisseminated pages 10-11, misu2025myelinoligodendrocyteglycoprotein pages 7-8) Standard of care; no dedicated ADEM RCT retrieved Stoian et al. https://doi.org/10.3390/vaccines11071225 (2023); Paolilo et al. https://doi.org/10.3390/children7110210 (2020); Mahapure et al. https://doi.org/10.4103/ajns.ajns_406_20 (2021); Vempati et al. https://doi.org/10.7759/cureus.42070 (2023) (stoian2023theoccurrenceof pages 31-32, paolilo2020acutedisseminatedencephalomyelitis pages 7-9, mahapure2021covid19associatedacutedisseminated pages 10-11, vempati2023acutedisseminatedencephalomyelitis pages 4-8)
Oral corticosteroid taper after IVMP Post-acute ADEM and MOGAD-related ADEM to reduce rebound/relapse Corticosteroid continuation/taper Prednisone taper over 4–6 weeks commonly recommended; in one MOGAD-related source, relapse trends noted when prednisolone dropped below 10 mg/day within 2 months (paolilo2020acutedisseminatedencephalomyelitis pages 7-9, misu2025myelinoligodendrocyteglycoprotein pages 7-8) Used routinely in practice; slower taper in MOG-seropositive pediatric ADEM was observed, but relapse risk remained higher in that group (dong2023clinicalradiologicaltherapeutic pages 1-2) Standard practice; no dedicated trial retrieved Paolilo et al. https://doi.org/10.3390/children7110210 (2020); Misu https://doi.org/10.3390/ijms26178538 (2025); Dong et al. https://doi.org/10.3389/fnins.2023.1128422 (2023) (paolilo2020acutedisseminatedencephalomyelitis pages 7-9, misu2025myelinoligodendrocyteglycoprotein pages 7-8, dong2023clinicalradiologicaltherapeutic pages 1-2)
IVIG Second-line or adjunctive therapy for steroid-unresponsive ADEM; part of first-line immunotherapy set in suspected immune-mediated MOG-Ab encephalitis Pooled immunoglobulin; immunomodulatory Total dose 2 g/kg over 2–5 days in review guidance; COVID-ADEM reviews also describe IVIG as next-line after steroids (paolilo2020acutedisseminatedencephalomyelitis pages 7-9, mahapure2021covid19associatedacutedisseminated pages 10-11) Generally well tolerated; used for steroid-unresponsive, recurrent, or steroid-dependent disease; in pediatric MOG-Ab encephalitis, should not be delayed once infections are reasonably excluded and immune-mediated disease suspected (paolilo2020acutedisseminatedencephalomyelitis pages 7-9, mahapure2021covid19associatedacutedisseminated pages 10-11, kim2024pediatricmogab–associatedencephalitis pages 1-2) Standard practice; no dedicated ADEM IVIG trial retrieved Paolilo et al. https://doi.org/10.3390/children7110210 (2020); Mahapure et al. https://doi.org/10.4103/ajns.ajns_406_20 (2021); Kim et al. https://doi.org/10.1212/nxi.0000000000200323 (2024) (paolilo2020acutedisseminatedencephalomyelitis pages 7-9, mahapure2021covid19associatedacutedisseminated pages 10-11, kim2024pediatricmogab–associatedencephalitis pages 1-2)
Plasma exchange / therapeutic plasma exchange (PLEX/TPE) Escalation therapy for severe or steroid-refractory ADEM; also considered in severe MOGAD attacks Apheresis; removal of pathogenic antibodies, immune complexes, cytokines In classic RCT, exchanges every 2 days for 7 exchanges; pediatric series often 4–5 sessions after steroid/IVIG failure (bhardwaj2024evaluatingtherapeuticplasma pages 4-5, NCT00004645 chunk 1) Recommended when inadequate response to steroids/IVIG; mixed neuroimmunology series reported immediate improvement in 95% and sustained significant improvement in 78% at follow-up; small pediatric ADEM series showed progressive clinical improvement in all patients, though some retained deficits (bhardwaj2024evaluatingtherapeuticplasma pages 4-5, bhardwaj2024evaluatingtherapeuticplasma pages 5-6) NCT00004645, Phase 3, randomized double-blind sham-controlled, status unknown/previously active-not-recruiting; included ADEM among acute severe inflammatory demyelinating attacks refractory to IVMP (NCT00004645 chunk 1) Bhardwaj et al. https://doi.org/10.7759/cureus.64190 (2024); ClinicalTrials.gov NCT00004645 (1995) (bhardwaj2024evaluatingtherapeuticplasma pages 4-5, bhardwaj2024evaluatingtherapeuticplasma pages 5-6, NCT00004645 chunk 1)
Early first-line immunotherapy bundle (steroids, IVIG, plasma exchange) Pediatric suspected MOG-Ab encephalitis/ADEM spectrum, including initially normal MRI Acute immunosuppression strategy No single fixed regimen; recommendation is to start first-line immunotherapy once HSV PCR/Gram stain are negative and infection no longer explains presentation (kim2024pediatricmogab–associatedencephalitis pages 1-2) Real-world implication: many children were initially misdiagnosed as infective meningoencephalitis (67%); delayed steroids were associated with encephalitis phenotype compared with ADEM phenotype (median 16.6 vs 9.6 days) (kim2024pediatricmogab–associatedencephalitis pages 1-2) Not a trial; practice recommendation from multicenter cohort Kim et al. https://doi.org/10.1212/nxi.0000000000200323 (2024) (kim2024pediatricmogab–associatedencephalitis pages 1-2)
Azathioprine Relapse prevention after first MOGAD attack / recurrent MOGAD including MOG-related ADEM phenotypes Purine antimetabolite immunosuppressant Trial dosing: 100 mg/day if ≤50 kg and 150 mg/day if >50 kg, orally, plus associated prednisone taper over 6 months (NCT05349006 chunk 1) Trial aims to determine whether early azathioprine prevents relapse and disability accrual; secondary outcomes include EDSS, visual outcomes, MRI lesions, QoL, and MOG-Ab titers (NCT05349006 chunk 1) NCT05349006, Phase 3, RECRUITING, estimated enrollment 126 (NCT05349006 chunk 1) ClinicalTrials.gov NCT05349006 (2023) (NCT05349006 chunk 1)
Satralizumab MOGAD relapse prevention in adolescents/adults, relevant to relapsing MOG-related ADEM phenotypes Anti-IL-6 receptor monoclonal antibody Subcutaneous loading at weeks 0, 2, 4, then every 4 weeks; monotherapy or add-on to baseline therapy (NCT05271409 chunk 1) Primary outcome is time to first adjudicated MOGAD relapse; key secondary outcomes include ARR, active MRI lesions, rescue therapy use, and hospitalization rate (NCT05271409 chunk 1) NCT05271409 (Meteoroid), Phase 3, RECRUITING, estimated enrollment 152 (NCT05271409 chunk 1) ClinicalTrials.gov NCT05271409 (2022) (NCT05271409 chunk 1)
Rozanolixizumab Adult MOGAD relapse prevention, applicable to relapsing MOG-related ADEM spectrum FcRn inhibitor reducing pathogenic IgG Subcutaneous infusion/administration in randomized placebo-controlled design; exact dose not given in retrieved chunk (NCT05063162 chunk 1) Primary endpoint is time to first centrally adjudicated relapse; secondary measures include EDSS, low-contrast visual acuity, hospitalizations, ARR, and TEAEs (NCT05063162 chunk 1) NCT05063162 (cosMOG), Phase 3, ACTIVE_NOT_RECRUITING, enrollment 113 (NCT05063162 chunk 1) ClinicalTrials.gov NCT05063162 (2022) (NCT05063162 chunk 1)
Tocilizumab MOGAD patients, generally for relapse prevention or refractory disease Anti-IL-6 receptor monoclonal antibody Regimen not available in retrieved chunk Trial listed as evaluating safety and efficacy in MOGAD; detailed endpoints not retrieved in current context (from clinical trial search summary) NCT06452537, Phase 2/3, ACTIVE_NOT_RECRUITING, enrollment 102 ClinicalTrials.gov NCT06452537 (trial registry summary from search results) ()
High-throughput omics biomarker study (blood/PBMC profiling) First demyelinating attack in children to predict relapse in ADEM/MOGAD network Biomarker discovery / immune-cell multi-omics Serial blood collection at inclusion, 6 months, and 24 months; PBMC sampling before immunomodulatory treatment for retrospective inclusions (NCT06863974 chunk 1) Objective is early identification of biomarkers predicting MOGAD recurrence after first attack; outcomes include EDSS and number/type of demyelinating relapses (NCT06863974 chunk 1) NCT06863974 (HOT-BRAIN), interventional, RECRUITING, enrollment 20 (NCT06863974 chunk 1) ClinicalTrials.gov NCT06863974 (2025) (NCT06863974 chunk 1)

Table: This table summarizes acute real-world treatment strategies for ADEM and MOGAD-related ADEM, including escalation approaches and selected ongoing or recent clinical trials. It is useful for connecting current standard care with emerging targeted and biomarker-driven interventions.

12.1 Current standard acute management (real-world implementation)

12.2 MAXO (Medical Action Ontology) suggestions

(Exact MAXO IDs are not available in the retrieved evidence; terms below are suggested action concepts.) - High-dose intravenous corticosteroid therapy - Intravenous immunoglobulin therapy - Therapeutic plasma exchange - Immunosuppressive therapy (azathioprine) - Anti–IL-6 receptor monoclonal antibody therapy (satralizumab/tocilizumab in MOGAD trials)

13. Prevention

No established primary prevention exists beyond reducing risk of triggering infections through general public health measures. The retrieved evidence does not support definitive causal attribution of routine vaccination to ADEM and includes systematic-review caution on causality in COVID vaccine-associated case reports (nabizadeh2023acutedisseminatedencephalomyelitis pages 1-3).

14. Other species / natural disease

Not addressed in retrieved evidence.

15. Model organisms

Not directly addressed in retrieved evidence. (Historically, experimental autoimmune encephalomyelitis is often discussed as a demyelinating model, but model-organism specifics were not extractable from the retrieved ADEM-focused corpus.)

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

  1. Case-aggregated safety signal characterization: systematic reviews of ADEM after COVID-19 infection and vaccination have provided aggregate clinical, imaging, and outcome summaries, including proportions of ADEM vs hemorrhagic variants and treatment patterns (stoian2023theoccurrenceof pages 23-26, stoian2023theoccurrenceof pages 1-2).
  2. Post-vaccination case aggregation with outcome statistics: 2023 systematic review of 54 post-COVID vaccination ADEM cases reported 85.1% clinical improvement and deaths among reported cases, while emphasizing causality uncertainty (nabizadeh2023acutedisseminatedencephalomyelitis pages 1-3).
  3. Operationalization of MOG antibody testing interpretation under 2023 MOGAD criteria: 2024 multi-center analysis quantified PPV and demonstrated strong dependence on titer and presence of a core demyelinating attack—critical for avoiding false-positive MOGAD labeling in ADEM-spectrum presentations (nguyen2024thepositivepredictive pages 1-2).
  4. Expanding phenotypic boundaries (MOG-Ab encephalitis phenotype): 2024 multicenter pediatric cohort argues for broad MOG-Ab testing in suspected encephalitis even with initially normal MRI and for timely immunotherapy initiation once key infectious tests are negative (kim2024pediatricmogab–associatedencephalitis pages 1-2).

Reference URLs and publication dates (selected key sources)

References

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  2. (dong2023clinicalradiologicaltherapeutic pages 1-2): Xue-yan Dong, Yan-yan Jiang, Ping Yuan, Xiaoming Fan, Jiannan Ma, Peng Wu, Li Jiang, and Xiu-juan Li. Clinical, radiological, therapeutic and prognostic differences between mog-seropositive and mog-seronegative pediatric acute disseminated encephalomyelitis patients: a retrospective cohort study. Frontiers in Neuroscience, May 2023. URL: https://doi.org/10.3389/fnins.2023.1128422, doi:10.3389/fnins.2023.1128422. This article has 9 citations and is from a peer-reviewed journal.

  3. (boesen2018implicationsofthe pages 3-4): Magnus S Boesen, Morten Blinkenberg, Nils Koch‐Henriksen, Lau C Thygesen, Peter V Uldall, Melinda Magyari, and Alfred P Born. Implications of the international paediatric multiple sclerosis study group consensus criteria for paediatric acute disseminated encephalomyelitis: a nationwide validation study. Developmental Medicine & Child Neurology, 60:1123-1131, Nov 2018. URL: https://doi.org/10.1111/dmcn.13798, doi:10.1111/dmcn.13798. This article has 53 citations and is from a highest quality peer-reviewed journal.

  4. (xiu2021incidenceandmortality pages 1-2): Yuwen Xiu, Hongqiu Gu, Xindi Li, Zixiao Li, Wei-Na Jin, Qiang Liu, and Fu-Dong Shi. Incidence and mortality of acute disseminated encephalomyelitis in china: a nationwide population-based study. Neuroscience Bulletin, 37:804-808, Mar 2021. URL: https://doi.org/10.1007/s12264-021-00642-7, doi:10.1007/s12264-021-00642-7. This article has 6 citations and is from a peer-reviewed journal.

  5. (stoian2023theoccurrenceof pages 1-2): Adina Stoian, Zoltan Bajko, Mircea Stoian, Roxana Adriana Cioflinc, Raluca Niculescu, Emil Marian Arbănași, Eliza Russu, Marian Botoncea, and Rodica Bălașa. The occurrence of acute disseminated encephalomyelitis in sars-cov-2 infection/vaccination: our experience and a systematic review of the literature. Vaccines, 11:1225, Jul 2023. URL: https://doi.org/10.3390/vaccines11071225, doi:10.3390/vaccines11071225. This article has 36 citations.

  6. (boesen2018implicationsofthe pages 2-2): Magnus S Boesen, Morten Blinkenberg, Nils Koch‐Henriksen, Lau C Thygesen, Peter V Uldall, Melinda Magyari, and Alfred P Born. Implications of the international paediatric multiple sclerosis study group consensus criteria for paediatric acute disseminated encephalomyelitis: a nationwide validation study. Developmental Medicine & Child Neurology, 60:1123-1131, Nov 2018. URL: https://doi.org/10.1111/dmcn.13798, doi:10.1111/dmcn.13798. This article has 53 citations and is from a highest quality peer-reviewed journal.

  7. (krupp2013internationalpediatricmultiple pages 6-7): Lauren B Krupp, Marc Tardieu, Maria Pia Amato, Brenda Banwell, Tanuja Chitnis, Russell C Dale, Angelo Ghezzi, Rogier Hintzen, Andrew Kornberg, Daniela Pohl, Kevin Rostasy, Silvia Tenembaum, and Evangeline Wassmer. International pediatric multiple sclerosis study group criteria for pediatric multiple sclerosis and immune-mediated central nervous system demyelinating disorders: revisions to the 2007 definitions. Multiple Sclerosis Journal, 19:1261-1267, Apr 2013. URL: https://doi.org/10.1177/1352458513484547, doi:10.1177/1352458513484547. This article has 1386 citations.

  8. (boesen2018implicationsofthe pages 4-4): Magnus S Boesen, Morten Blinkenberg, Nils Koch‐Henriksen, Lau C Thygesen, Peter V Uldall, Melinda Magyari, and Alfred P Born. Implications of the international paediatric multiple sclerosis study group consensus criteria for paediatric acute disseminated encephalomyelitis: a nationwide validation study. Developmental Medicine & Child Neurology, 60:1123-1131, Nov 2018. URL: https://doi.org/10.1111/dmcn.13798, doi:10.1111/dmcn.13798. This article has 53 citations and is from a highest quality peer-reviewed journal.

  9. (boesen2018implicationsofthe pages 1-2): Magnus S Boesen, Morten Blinkenberg, Nils Koch‐Henriksen, Lau C Thygesen, Peter V Uldall, Melinda Magyari, and Alfred P Born. Implications of the international paediatric multiple sclerosis study group consensus criteria for paediatric acute disseminated encephalomyelitis: a nationwide validation study. Developmental Medicine & Child Neurology, 60:1123-1131, Nov 2018. URL: https://doi.org/10.1111/dmcn.13798, doi:10.1111/dmcn.13798. This article has 53 citations and is from a highest quality peer-reviewed journal.

  10. (boesen2018implicationsofthe pages 6-7): Magnus S Boesen, Morten Blinkenberg, Nils Koch‐Henriksen, Lau C Thygesen, Peter V Uldall, Melinda Magyari, and Alfred P Born. Implications of the international paediatric multiple sclerosis study group consensus criteria for paediatric acute disseminated encephalomyelitis: a nationwide validation study. Developmental Medicine & Child Neurology, 60:1123-1131, Nov 2018. URL: https://doi.org/10.1111/dmcn.13798, doi:10.1111/dmcn.13798. This article has 53 citations and is from a highest quality peer-reviewed journal.

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  12. (wang2022sarscov2associatedacutedisseminated pages 18-19): Yumin Wang, Yanchao Wang, Liang Huo, Qiang Li, Jichao Chen, and Hongquan Wang. Sars-cov-2-associated acute disseminated encephalomyelitis: a systematic review of the literature. Journal of Neurology, 269:1071-1092, Aug 2022. URL: https://doi.org/10.1007/s00415-021-10771-8, doi:10.1007/s00415-021-10771-8. This article has 64 citations and is from a domain leading peer-reviewed journal.

  13. (nabizadeh2023acutedisseminatedencephalomyelitis pages 1-3): Fardin Nabizadeh, Maryam Noori, Shayan Rahmani, and Helia Hosseini. Acute disseminated encephalomyelitis (adem) following covid-19 vaccination: a systematic review. Journal of Clinical Neuroscience, 111:57-70, May 2023. URL: https://doi.org/10.1016/j.jocn.2023.03.008, doi:10.1016/j.jocn.2023.03.008. This article has 40 citations and is from a peer-reviewed journal.

  14. (mukhtiar2024clinicalpatternneuroimaging pages 1-2): Khairunnisa Mukhtiar, Mohammad Raza, Sidra Ishaque, Quratulain Maha, and Ayesha Noor. Clinical pattern, neuroimaging findings and outcome of acute disseminated encephalomyelitis in children: a retrospective study. Pakistan Journal of Medical Sciences, 40:1479-1484, Jun 2024. URL: https://doi.org/10.12669/pjms.40.7.8015, doi:10.12669/pjms.40.7.8015. This article has 10 citations and is from a peer-reviewed journal.

  15. (stoian2023theoccurrenceof pages 2-4): Adina Stoian, Zoltan Bajko, Mircea Stoian, Roxana Adriana Cioflinc, Raluca Niculescu, Emil Marian Arbănași, Eliza Russu, Marian Botoncea, and Rodica Bălașa. The occurrence of acute disseminated encephalomyelitis in sars-cov-2 infection/vaccination: our experience and a systematic review of the literature. Vaccines, 11:1225, Jul 2023. URL: https://doi.org/10.3390/vaccines11071225, doi:10.3390/vaccines11071225. This article has 36 citations.

  16. (paolilo2020acutedisseminatedencephalomyelitis pages 3-5): Renata Barbosa Paolilo, Kumaran Deiva, Rinze Neuteboom, Kevin Rostásy, and Ming Lim. Acute disseminated encephalomyelitis: current perspectives. Children, 7:210, Nov 2020. URL: https://doi.org/10.3390/children7110210, doi:10.3390/children7110210. This article has 118 citations.

  17. (stoian2023theoccurrenceof pages 23-26): Adina Stoian, Zoltan Bajko, Mircea Stoian, Roxana Adriana Cioflinc, Raluca Niculescu, Emil Marian Arbănași, Eliza Russu, Marian Botoncea, and Rodica Bălașa. The occurrence of acute disseminated encephalomyelitis in sars-cov-2 infection/vaccination: our experience and a systematic review of the literature. Vaccines, 11:1225, Jul 2023. URL: https://doi.org/10.3390/vaccines11071225, doi:10.3390/vaccines11071225. This article has 36 citations.

  18. (stoian2023theoccurrenceof media 322d56fe): Adina Stoian, Zoltan Bajko, Mircea Stoian, Roxana Adriana Cioflinc, Raluca Niculescu, Emil Marian Arbănași, Eliza Russu, Marian Botoncea, and Rodica Bălașa. The occurrence of acute disseminated encephalomyelitis in sars-cov-2 infection/vaccination: our experience and a systematic review of the literature. Vaccines, 11:1225, Jul 2023. URL: https://doi.org/10.3390/vaccines11071225, doi:10.3390/vaccines11071225. This article has 36 citations.

  19. (li2022clinicalpresentationand pages 4-5): Kunyi Li, Mao-zhong Li, L. Wen, Qiancheng Wang, Xin Ding, and Jian Wang. Clinical presentation and outcomes of acute disseminated encephalomyelitis in adults worldwide: systematic review and meta-analysis. Frontiers in Immunology, Jun 2022. URL: https://doi.org/10.3389/fimmu.2022.870867, doi:10.3389/fimmu.2022.870867. This article has 43 citations and is from a peer-reviewed journal.

  20. (stoian2023theoccurrenceof pages 31-32): Adina Stoian, Zoltan Bajko, Mircea Stoian, Roxana Adriana Cioflinc, Raluca Niculescu, Emil Marian Arbănași, Eliza Russu, Marian Botoncea, and Rodica Bălașa. The occurrence of acute disseminated encephalomyelitis in sars-cov-2 infection/vaccination: our experience and a systematic review of the literature. Vaccines, 11:1225, Jul 2023. URL: https://doi.org/10.3390/vaccines11071225, doi:10.3390/vaccines11071225. This article has 36 citations.

  21. (li2022clinicalpresentationand pages 6-7): Kunyi Li, Mao-zhong Li, L. Wen, Qiancheng Wang, Xin Ding, and Jian Wang. Clinical presentation and outcomes of acute disseminated encephalomyelitis in adults worldwide: systematic review and meta-analysis. Frontiers in Immunology, Jun 2022. URL: https://doi.org/10.3389/fimmu.2022.870867, doi:10.3389/fimmu.2022.870867. This article has 43 citations and is from a peer-reviewed journal.

  22. (nguyen2024thepositivepredictive pages 1-2): Linda Nguyen, Sumit Singh, Fabricio S Feltrin, Lauren M Tardo, Rebekah L Clarke, Cynthia X Wang, and Benjamin M Greenberg. The positive predictive value of mog-igg testing based on the 2023 diagnostic criteria for mogad. Multiple Sclerosis Journal - Experimental, Translational and Clinical, Jul 2024. URL: https://doi.org/10.1177/20552173241274610, doi:10.1177/20552173241274610. This article has 7 citations.

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  24. (kim2024pediatricmogab–associatedencephalitis pages 1-2): Nee Na Kim, Dimitrios Champsas, Michael Eyre, Omar Abdel-Mannan, Vanessa Lee, Alison Skippen, Manali V. Chitre, Rob Forsyth, Cheryl Hemingway, Rachel Kneen, Ming Lim, Dipak Ram, Sithara Ramdas, Evangeline Wassmer, Siobhan West, Sukhvir Wright, Asthik Biswas, Kshitij Mankad, Eoin P. Flanagan, Jacqueline Palace, Thomas Rossor, Olga Ciccarelli, and Yael Hacohen. Pediatric mog-ab–associated encephalitis. Neurology Neuroimmunology & Neuroinflammation, Nov 2024. URL: https://doi.org/10.1212/nxi.0000000000200323, doi:10.1212/nxi.0000000000200323. This article has 21 citations.

  25. (NCT06863974 chunk 1): High-throughput Omic Technology for Identification of Biomarkers of Relapsing Acute Disseminated Encephalomyelitis in Immune Cell Network. University Hospital, Angers. 2025. ClinicalTrials.gov Identifier: NCT06863974

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  27. (stoian2023theoccurrenceof media ee7112b9): Adina Stoian, Zoltan Bajko, Mircea Stoian, Roxana Adriana Cioflinc, Raluca Niculescu, Emil Marian Arbănași, Eliza Russu, Marian Botoncea, and Rodica Bălașa. The occurrence of acute disseminated encephalomyelitis in sars-cov-2 infection/vaccination: our experience and a systematic review of the literature. Vaccines, 11:1225, Jul 2023. URL: https://doi.org/10.3390/vaccines11071225, doi:10.3390/vaccines11071225. This article has 36 citations.

  28. (li2022clinicalpresentationand pages 5-6): Kunyi Li, Mao-zhong Li, L. Wen, Qiancheng Wang, Xin Ding, and Jian Wang. Clinical presentation and outcomes of acute disseminated encephalomyelitis in adults worldwide: systematic review and meta-analysis. Frontiers in Immunology, Jun 2022. URL: https://doi.org/10.3389/fimmu.2022.870867, doi:10.3389/fimmu.2022.870867. This article has 43 citations and is from a peer-reviewed journal.

  29. (paolilo2020acutedisseminatedencephalomyelitis pages 7-9): Renata Barbosa Paolilo, Kumaran Deiva, Rinze Neuteboom, Kevin Rostásy, and Ming Lim. Acute disseminated encephalomyelitis: current perspectives. Children, 7:210, Nov 2020. URL: https://doi.org/10.3390/children7110210, doi:10.3390/children7110210. This article has 118 citations.

  30. (mahapure2021covid19associatedacutedisseminated pages 10-11): Kiran Mahapure, Anagha Prabhune, and Aradhana Chouvhan. Covid-19-associated acute disseminated encephalomyelitis: a systematic review. Asian Journal of Neurosurgery, 16:457-469, Sep 2021. URL: https://doi.org/10.4103/ajns.ajns_406_20, doi:10.4103/ajns.ajns_406_20. This article has 17 citations.

  31. (vempati2023acutedisseminatedencephalomyelitis pages 4-8): Roopeessh Vempati, Sri Harsha Narayana, Ritik Kathal, Juhi Chandra, Gazala Khan, Kritika Bhakoo, and Praveena Sunkara. Acute disseminated encephalomyelitis in a six-year-old child: a case report. Cureus, Jul 2023. URL: https://doi.org/10.7759/cureus.42070, doi:10.7759/cureus.42070. This article has 2 citations.

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  34. (NCT00004645 chunk 1): Phase III Randomized, Double-Blind, Sham-Controlled Study of Plasma Exchange for Acute Severe Attacks of Inflammatory Demyelinating Disease Refractory to Intravenous Methylprednisolone. National Institute of Neurological Disorders and Stroke (NINDS). 1995. ClinicalTrials.gov Identifier: NCT00004645

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  36. (NCT05349006 chunk 1): Azathioprine in MOGAD. Hospices Civils de Lyon. 2023. ClinicalTrials.gov Identifier: NCT05349006

  37. (NCT05271409 chunk 1): A Study to Evaluate the Efficacy, Safety, Pharmacokinetics, and Pharmacodynamics of Satralizumab in Participants With Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease. Hoffmann-La Roche. 2022. ClinicalTrials.gov Identifier: NCT05271409

  38. (NCT05063162 chunk 1): A Study to Evaluate the Efficacy and Safety of Rozanolixizumab in Adult Participants With Myelin Oligodendrocyte Glycoprotein (MOG) Antibody-associated Disease (MOGAD). UCB Biopharma SRL. 2022. ClinicalTrials.gov Identifier: NCT05063162

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