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Acute Disseminated Encephalomyelitis (ADEM)

Monophasic immune-mediated demyelination of the CNS

Written by: Saygı Hospital Health Guide Editorial Board
Last updated:

This content has been compiled by the Saygı Hospital Health Guide Editorial Board and is periodically reviewed by a specialist physician.

References (5)

This content is for informational purposes only and does not constitute medical advice. You can book an appointment at our Nöroloji department. Book Appointment →

What is Acute Disseminated Encephalomyelitis (ADEM)?

ADEM is most commonly post-infectious (especially after viral upper respiratory infection or measles, rubella, mumps, varicella, EBV, Mycoplasma) but can follow vaccination.

The pathophysiology involves immune cross-reactivity to CNS myelin antigens (molecular mimicry), causing inflammation and demyelination.

Most cases are monophasic; recurrent or multiphasic disease, or progression to MS or MOG-antibody disease, occurs in a minority.

MRI shows large, multifocal, often bilateral and asymmetric T2/FLAIR hyperintense lesions in white matter, basal ganglia, thalamus and brainstem, often with mild contrast enhancement.

Most patients recover substantially with treatment, though some retain neurologic deficits.

Symptoms

Encephalopathy: confusion, lethargy, irritability, behavioral change, decreased consciousness — required for diagnosis
Multifocal neurologic deficits: hemiparesis, ataxia, cranial nerve palsies, optic neuritis, seizures
Acute onset over hours to days, usually 1–4 weeks after preceding illness or vaccination
Headache, fever, neck stiffness, vomiting (often initial features)
Spinal cord involvement (transverse myelitis pattern) in some cases: limb weakness, sensory level, bladder dysfunction
Visual loss from optic neuritis (uni- or bilateral)

Risk Factors

Recent (1–4 weeks) viral or bacterial infection (URI, GI infection)
Recent vaccination (rare association — incidence is much lower than ADEM after natural infection)
Pediatric age group (peak 3–8 years), but adult cases occur
MOG antibody seropositivity in some patients (overlapping syndromes)
No clear genetic predisposition

When to See a Doctor?

If you experience any of the following symptoms, seek medical attention promptly:

  • Acute alteration of consciousness with multifocal neurologic deficits
  • New seizures with encephalopathy
  • Optic neuritis or transverse myelitis with confusion or behavioral change
  • Recent infection or vaccination followed by acute neurologic syndrome
  • Pediatric patient with rapidly evolving neurologic features and altered mental state

Treatment Methods

01
Urgent brain and spinal MRI (essential for diagnosis), CSF analysis (mild pleocytosis, normal/elevated protein, no oligoclonal bands typically)
02
Exclude infectious causes: HSV PCR, bacterial cultures, Lyme, syphilis depending on context
03
Test for MOG antibodies and AQP4 antibodies for differential and prognostic assessment
04
First-line treatment: high-dose intravenous methylprednisolone (30 mg/kg/day for children, 1 g/day for adults) for 3–7 days, followed by oral taper over 4–6 weeks
05
Second-line for severe or refractory cases: intravenous immunoglobulin (IVIG) 2 g/kg or plasma exchange
06
Supportive care: seizure control, ICU admission for severe cases, swallowing assessment, rehabilitation
07
Long-term follow-up: serial MRI, monitoring for relapse or progression to MS or MOGAD; pediatric neuropsychologic assessment

Which Department to Visit?

You can visit our Nöroloji department for these complaints. Our specialist physicians will create the most suitable treatment plan for you.

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Health Disclaimer: The information on this page is prepared for general informational purposes only. It does not replace medical diagnosis and treatment. Please consult your physician for your complaints. Saygı Hospital does not accept responsibility for actions taken based on the information on this page.