ADEM, transverse myelitis, MS, GBS and acute ataxia in children

ADEM

The tree sorts acute neurologic deficits by MRI: lesions with encephalopathy (ADEM), a cord lesion (transverse myelitis), optic nerve or long cord lesions (antibody disorders), new lesions over time (MS), and a normal MRI with psychosis (anti-NMDA receptor encephalitis).

ADEM typically follows an infection by days to weeks and is most common in young children.

• Encephalopathy (confusion, irritability, drowsiness) is required and separates ADEM from transverse myelitis or a first MS attack.
• Multifocal deficits: ataxia, weakness, cranial nerve palsies, seizures.
• MRI: large, poorly defined, bilateral white-matter lesions, often also deep gray matter.
• Treatment: high-dose IV methylprednisolone, then an oral taper; IVIG or plasma exchange if the response is poor.
• Usually a single episode; test MOG antibodies, since MOG-positive children are more likely to relapse.

Transverse myelitis

Picture: back pain, then paraparesis, a truncal sensory level (for example T7) and urinary retention or other sphincter problems over hours to days.

• First step: emergency spine MRI with and without contrast, to exclude cord compression (tumor, abscess, hematoma), which needs surgery.
• MRI: swollen, T2-bright cord segment; a normal early MRI does not exclude myelitis when the clinical picture fits; repeat it.
• CSF: mild lymphocytic pleocytosis and mildly raised protein.
• Treatment: high-dose IV methylprednisolone; plasma exchange for severe disease or no response.
• Supportive care: bladder catheterization, bowel care, early rehabilitation.

NMOSD and MOG antibody disease

• Optic neuritis plus longitudinally extensive myelitis: test serum aquaporin-4 IgG; a positive result confirms NMOSD.
• MOG antibody-associated disease (MOGAD): ADEM, optic neuritis or myelitis with MOG antibodies; common in children.
• Test both antibodies in children with myelitis or optic neuritis: the features overlap, and the results predict relapse and chronic disease.
• Attack: IV methylprednisolone, with plasma exchange if severe.
• Aquaporin-4-positive NMOSD needs long-term immunosuppression to prevent relapses; MS disease-modifying drugs can worsen it.

Pediatric multiple sclerosis

Think of MS in a teen with a past attack, such as optic neuritis, who now has a new deficit and an MRI with both old and new lesions. Onset is usually around 11–14 years.

• McDonald criteria idea: lesions in separate CNS areas (dissemination in space), plus separate times or supportive CSF evidence.
• The 2024 McDonald revision adds the optic nerve as a fifth area, so dissemination in space means typical lesions in at least 2 of 5 areas (periventricular, cortical or juxtacortical, infratentorial, spinal cord, optic nerve).
• CSF oligoclonal bands are supportive, not specific; they alone do not establish MS.
• Relapse: high-dose IV methylprednisolone.
• Start disease-modifying therapy early to reduce relapses and disability.

Guillain–Barré syndrome vs spinal cord disease

Guillain–Barré syndrome (GBS) often follows Campylobacter jejuni diarrhea or a viral illness. Weakness ascends from the legs, reflexes are lost, and back or leg pain is common in children.

• CSF: high protein with normal or few white cells (albuminocytologic dissociation); protein may be normal in the first week.
• A distinct truncal sensory level or early bladder dysfunction suggests spinal cord disease, not typical GBS: get an urgent spine MRI.
• Monitor closely: breathing (vital capacity, negative inspiratory force) and autonomic instability (arrhythmia, blood pressure swings).
• Treatment for a child who cannot walk or is getting worse: IVIG (2 g/kg over 2–5 days) or plasma exchange.
• Corticosteroids do not help GBS.

Acute ataxia

Acute cerebellar ataxia is the most common cause of acute ataxia in toddlers. It follows varicella or another viral illness by days to a few weeks.

• Wide-based, unsteady gait, often truncal ataxia, sometimes nystagmus; the child is alert, with normal sensation and reflexes.
• Recovery over weeks is the rule; no specific treatment.
• Red flags needing urgent imaging and work-up: altered consciousness, severe headache, focal weakness, papilledema or progressive course.
• Also consider ingestion, posterior fossa tumor, stroke, opsoclonus-myoclonus (neuroblastoma) and GBS variants.
• Slowly progressive ataxia with areflexia and lost vibration and position sense: Friedreich ataxia.

Common questions

Sources

• Montalban X et al. Diagnosis of multiple sclerosis: 2024 revisions of the McDonald criteria (Lancet Neurol 2025)
• Krupp LB et al. International Pediatric MS Study Group criteria for pediatric MS and immune-mediated CNS demyelinating disorders (Mult Scler 2013)
• Leonhard SE et al. Diagnosis and management of Guillain–Barré syndrome in ten steps (Nat Rev Neurol 2019)

Written for Pedemy in our own words from the sources above; checked November 2026. For education only, not medical advice; check doses and local protocols before treating a patient. Pedemy is independent and not affiliated with or endorsed by the organizations cited.