[Acute onset ataxia in infancy: its aetiology, treatment and follow-up]

Acute childhood ataxia is a cause of referency to the pediatric emergency room. AIM. To characterize the etiology, clinical picture, management, and outcome of acute ataxia in our hospital.

A prospective study was undertaken including 39 children with acute ataxia who were admitted between January 1, 2001 and December 31, 2003.

During the study period 159,002 episodes were evaluated, 39 children (0.024%) with acute ataxia. The most common diagnoses were post-infectious ataxia (51.2%) and toxic exposure (25.6%). The mean age at presentation in post-infectious ataxia was 55 +/- 27.61 months, 60% females. A prodromal febrile illness was noted in 95%: varicella (10), nonspecific viral infection (6), mycoplasma, enterovirus, and Epstein-Barr virus. The latency from the prodromal illness to the onset of ataxia was 5.86 +/- 3.78 days. Lumbar punctures were altered in 11/17. All computed tomography scans performed were normal. At follow up, one boy presented asymmetric signs of cerebellar dysfunction secondary to hemicerebellitis. The media of the patient who showed full-gait recovery was 18 days, and was complete in all children, except one boy who presented hemophagocytic lymphohistiocytosis. Toxic ingestion was the second most common cause. Boys less than 6 years were more commonly affected.

Acute childhood ataxia are an uncommon cause of presentation to our pediatric emergency room. Postinfectious ataxia and drug ingestion are the most common diagnosis, with a usually benign and self-limited process. A thorough history and neurology examination should be guided to etiology. Neuroimaging studies and hospitalization are needed only if atypical presentation, asymmetric neurologic examination and prolonged ataxia.