Neuroinflammatory

Acute disseminated encephalomyelitis (ADEM)

A monophasic, post-infectious or post-immunisation multifocal demyelinating illness — encephalopathy plus multifocal CNS signs — usually with full recovery after high-dose steroids.

Acute disseminated encephalomyelitis (ADEM) is a monophasic, post-infectious inflammatory demyelinating disease of the central nervous system that occurs most often in children, usually 5–14 days after a viral illness or, very rarely, after immunisation. It presents acutely with encephalopathy (depressed level of consciousness, irritability or behavioural change — a mandatory diagnostic criterion) plus multifocal neurological signs (cranial nerve palsies, hemiparesis, ataxia, transverse myelitis, optic neuritis) developing over hours to days. MRI shows multiple, large, fluffy, often subcortical T2/FLAIR-hyperintense lesions, frequently involving the basal ganglia, thalami, brainstem and spinal cord. Most cases are monophasic and recover with high-dose IV methylprednisolone followed by an oral taper; a minority go on to have further demyelinating events, in which case the diagnosis is often revised to MOGAD, multi-phasic disseminated encephalomyelitis (MDEM), or paediatric MS. The 2023 MOGAD criteria show that around half of paediatric ADEM is now attributable to MOG-IgG.

At a glance

Onset: Typically 5–14 days after viral illness or (rarely) immunisation
Mandatory feature: Encephalopathy — depressed consciousness, irritability or behavioural change
Common signs: Multifocal: ataxia, hemiparesis, cranial nerve palsies, transverse myelitis, optic neuritis
MRI: Multiple, large, fluffy T2/FLAIR lesions; basal ganglia, thalami, brainstem, cord often involved
Treatment: IV methylprednisolone 5 days + oral taper 4–6 weeks; IVIG or plasma exchange in steroid-refractory cases

What it is

ADEM is an acute, immune-mediated demyelinating illness of the central nervous system. In most cases it follows a viral upper respiratory or gastrointestinal infection by 1–2 weeks; very rarely it follows a vaccination. The triggering antigen is thought to share epitopes with myelin (molecular mimicry), prompting an autoimmune attack against oligodendrocytes and myelin. About half of paediatric ADEM is now known — using the 2023 International MOGAD Panel criteria — to be MOG-IgG-positive, placing it within the MOGAD spectrum; the remaining 'classical' ADEM is MOG-negative and usually monophasic.

How it presents

The presentation is acute (hours to days) and quite stereotyped:

Prodrome — viral illness 1–2 weeks before, often resolved by the time neurological symptoms begin
Encephalopathy — mandatory for the diagnosis. Sleepiness, irritability, confusion, or coma. This is the feature that separates ADEM from isolated optic neuritis or transverse myelitis
Multifocal neurological signs — ataxia (very common), hemiparesis, cranial nerve palsies (commonly facial weakness, eye movement abnormalities), dysarthria, sensory disturbance, transverse myelitis (paralysis, urinary retention), optic neuritis (visual loss)
Headache, vomiting, low-grade fever
Seizures in about 25%, more frequent in younger children

Diagnosis

The International Pediatric MS Study Group consensus criteria require: (1) first polysymptomatic acute or subacute episode of inflammatory demyelinating disease; (2) clinical encephalopathy that is not explained by fever; (3) multifocal lesions on MRI; (4) no new symptoms, signs or MRI findings appearing 3 months after onset.

MRI is the key investigation: multiple, large, ill-defined, asymmetric T2/FLAIR-hyperintense lesions in the white matter, often with cortical, basal ganglia, thalamic, brainstem and cord involvement. Contrast enhancement is variable. The lesions are typically simultaneously acquired (in contrast to MS, where lesions accumulate over time).

CSF: mild lymphocytic pleocytosis in two-thirds, mildly elevated protein, oligoclonal bands less common than in MS (about 10–20%).

Antibody testing: MOG-IgG by cell-based assay (about 50% positive); AQP4-IgG (rarely positive); anti-NMDAR (when encephalopathy is severe or features overlap).

Differential: bacterial or viral encephalitis (especially HSV, where the imaging picture overlaps), autoimmune encephalitis, paediatric multiple sclerosis (no encephalopathy), MOGAD, vascular causes.

Treatment

Treatment is built on prompt high-dose corticosteroids:

IV methylprednisolone 30 mg/kg/day (max 1 g/day) for 3–5 days, followed by an oral prednisolone taper over 4–6 weeks. This long taper differs from MS practice and reflects the recognition that abrupt steroid withdrawal is associated with early relapse in ADEM/MOGAD
IVIG 2 g/kg over 2–5 days — used in steroid-refractory or steroid-contraindicated cases; many centres now use IVIG as first-line in younger children
Plasma exchange (5–7 sessions) — for severe, steroid-refractory disease
Supportive care — antiseizure medicines for seizures, ITU support for reduced consciousness, physiotherapy, occupational therapy and speech and language therapy from early in the recovery
Antibiotics or aciclovir initially in many cases until bacterial / viral encephalitis is excluded

Course and prognosis

Most children with ADEM recover well — about 70–80% with little or no residual deficit. Recovery is usually rapid in the first weeks, then gradual over months. Mortality is now under 5% with modern care.

Key follow-up question: is this monophasic or the first attack of a relapsing disease? Children who relapse with the same features within 3 months are considered to still be in the same ADEM attack; later relapses with new symptoms may indicate MDEM (multiphasic ADEM), MOGAD (especially if MOG-IgG-positive at presentation) or paediatric MS. A follow-up MRI at 3 and 12 months is therefore recommended, along with re-testing for MOG-IgG.

Cognitive and behavioural outcomes

Even when motor recovery is excellent, around 20–30% of children with ADEM have measurable long-term differences in attention, processing speed, executive function and academic performance. Neuropsychological assessment at 6 and 12 months and educational support are now part of routine ADEM follow-up.

How an educational review can help

ADEM families face the rapid transition from a viral illness to an ITU admission and then a long recovery, with the open question of whether further attacks will follow. An educational review can place the diagnosis in the current diagnostic framework (including the 2023 MOGAD criteria), summarise the steroid-taper and follow-up plan, and help you prepare focused questions for your treating team about MOG-IgG retesting, MRI surveillance and rehabilitation.

It is an educational second opinion — not a diagnosis, treatment or prescription — and it does not replace the care of your child's own clinicians.

Selected sources

Krupp LB et al. International Pediatric MS Study Group criteria for paediatric multiple sclerosis and immune-mediated central nervous system demyelinating disorders: revisions to the 2007 definitions. Mult Scler. 2013.
Tenembaum S et al. Acute disseminated encephalomyelitis. Lancet Neurol. 2007 / 2024 update.
Banwell B et al. Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: International MOGAD Panel proposed criteria. Lancet Neurol. 2023; 22: 268–282.
Hahn JS, Pohl D, Rensel M. Practice parameter: acute disseminated encephalomyelitis in children. Pediatr Neurol. 2019; updated 2023.

Last reviewed: 2026-05-27

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