✅ Model Answer:
• Diagnosis: Acute post-infectious cerebellar ataxia — most common cause of acute ataxia in children (peak age 3-5 years). Truncal ataxia, nystagmus, vomiting following viral URI (varicella, EBV, enterovirus, influenza). Normal inflammatory markers, normal MRI. Afebrile and alert (excludes CNS infection).
• Any other test: CSF analysis (may show mild lymphocytic pleocytosis — optional if diagnosis is clear), urine toxicology (to rule out ingestion), serum glucose, ammonia, lactate (metabolic screen). Consider viral serologies if not already done.
• What to do next: Supportive care — hydration, rest, physical therapy. No specific antiviral or immunomodulatory therapy is needed. If opsoclonus/myoclonus present, evaluate for neuroblastoma (urine VMA/HVA, chest/abdomen imaging).
• Follow-up plan: Clinical improvement over days to weeks (usually 2-4 weeks). If worsens or fails to improve after 2-3 weeks, repeat MRI to rule out tumor, demyelination, or other progressive disorders. Most children recover completely.

✅ Model Answer:
• Acute post-infectious cerebellar ataxia is a self-limited neurological disorder characterized by sudden onset of ataxia following a viral infection.
• Age: Most common in children 1-5 years (peak 3-5 years).
• Causes:
- Viral infections: Varicella-zoster (most common), Epstein-Barr virus (EBV), enterovirus, influenza, coxsackievirus, echovirus, mumps, measles, HIV.
- Post-vaccination: Rare — after varicella, MMR, or other vaccines.
- Bacterial infections: Mycoplasma pneumoniae, Lyme disease.
• Mechanism: Immune-mediated inflammation of the cerebellum (not direct viral invasion).
• Time course: Symptoms appear 1-3 weeks after the precipitating infection.

✅ Model Answer:
• Core features:
- Truncal ataxia: Unsteady gait, wide-based stance, difficulty sitting or standing.
- Limb ataxia: Dysmetria (finger-to-nose test), intention tremor, dysdiadochokinesia.
- Nystagmus: Horizontal or vertical (cerebellar type).
- Vomiting: Often prominent (due to cerebellar dysfunction or raised ICP).
- Dysarthria: Slurred, scanning speech (less common in young children).
• Key distinguishing features (from other causes):
- Alert and afebrile: No altered sensorium or fever.
- Normal tone and reflexes: No weakness or hyperreflexia (differentiates from Friedreich ataxia).
- No opsoclonus: Absence of dancing eyes (differentiates from OMAS).
- Self-limited: Gradual improvement over days to weeks.

✅ Model Answer:
• Differential diagnosis:
- Acute post-infectious cerebellar ataxia — most common, self-limited.
- Opsoclonus-myoclonus-ataxia syndrome (OMAS): Dancing eyes, myoclonus, neuroblastoma (urine VMA/HVA ↑).
- Acute disseminated encephalomyelitis (ADEM): Encephalopathy, multifocal deficits, MRI shows white matter lesions.
- Miller Fisher syndrome: Ophthalmoplegia, ataxia, areflexia — GQ1b antibody positive.
- Intoxication: Alcohol, benzodiazepines, antihistamines, carbamazepine, phenytoin.
- CNS infection: Meningitis, encephalitis, cerebellar abscess (fever, altered sensorium).
- Cerebellar tumor: Medulloblastoma, astrocytoma (progressive, morning headache, vomiting).
- Posterior fossa stroke: Acute onset, focal deficits, vascular risk factors.
- Metabolic disorders: GLUT1 deficiency (episodic, low CSF glucose), Wilson disease.
- Migraine: Episodic ataxia, headache, visual aura.

✅ Model Answer:
• MRI Brain (with and without contrast): The imaging modality of choice.
• In acute post-infectious cerebellar ataxia: Usually normal (no cerebellar enhancement or atrophy).
• If abnormal, consider:
- ADEM: T2/FLAIR hyperintensities in white matter, basal ganglia, brainstem.
- Cerebellar tumor: Mass lesion, hydrocephalus.
- Stroke: Restricted diffusion (DWI) in vascular territory.
- Demyelination: Multiple sclerosis, acute disseminated encephalomyelitis.
• CT Head: Less sensitive than MRI; may be used as an initial screen if MRI is unavailable, but MRI is preferred.
• Indications for repeat MRI: If symptoms worsen, fail to improve after 2-3 weeks, or atypical features (opsoclonus, encephalopathy, focal deficits).

✅ Model Answer:
• Management is supportive:
- Hydration: IV or oral fluids to maintain hydration (especially if vomiting).
- Nutritional support: Ensure adequate intake.
- Physical therapy: Early mobilization, gait training, balance exercises.
- Occupational therapy: Activities of daily living.
- Pain management: Headache (if present) with acetaminophen/ibuprofen.
• No specific treatment: Antivirals, steroids, or immunoglobulins are NOT indicated for typical post-infectious cerebellar ataxia.
• Admission: If vomiting prevents oral intake, significant dehydration, or if the diagnosis is uncertain.
• Reassurance: Parents should be reassured about the self-limited nature and excellent prognosis.

✅ Model Answer:
• Excellent: Most children recover completely within 2-4 weeks.
• Mild residual ataxia: May persist for up to 6 months in a small percentage.
• Recurrence: Rare (<5%).
• Permanent sequelae: Uncommon (<10%) — more likely if underlying cause is not post-infectious (tumor, demyelination, metabolic).
• Prognostic factors:
- Age: Younger children (<3 years) may have slightly longer recovery time.
- Severity: Severe ataxia may take longer to resolve.
- Underlying infection: Varicella often has a good prognosis.
• Follow-up: If symptoms do not improve within 2-3 weeks, consider repeat MRI and further investigations (genetic testing, metabolic workup).

✅ Model Answer:
• Red flags (alternative diagnosis):
- Opsoclonus or myoclonus: Suggests OMAS (neuroblastoma).
- Encephalopathy: Altered consciousness, confusion, irritability (think ADEM, meningitis, encephalitis).
- Fever: Suggests CNS infection (meningitis, encephalitis, abscess).
- Focal deficits: Weakness, hemiparesis (think stroke, tumor, ADEM).
- Progressive symptoms: Worsening over days to weeks (think tumor, metabolic disease).
- Morning headache + vomiting: Suggests increased ICP (tumor, hydrocephalus).
- History of ingestion: Toxin exposure (alcohol, drugs).
- Immunosuppression: Increased risk of opportunistic infections.
- Abnormal MRI: Mass lesion, white matter changes (not typical for post-infectious ataxia).
- No improvement after 3 weeks: Consider alternative diagnosis.