TABLE 2223 Causes of Acute Ataxia in Children Roughly in Order of Frequency

Intoxications are a cause of ataxia in children, and the ingestion may be surreptitious. Though ethanol may be suspected by odor, other drugs such as phenytoin or carbamazepine will not be detected in that manner. History should include queries about any medications in the household.

Unusual metabolic disorders such as pyruvate decarboxylase complex deficiency may present with ataxia. Family history may or may not suggest a metabolic disorder. Typically, the onset is gradual, but abrupt decompensations may occur. Other systemic or CNS abnormalities will be present.

Posterior fossa mass lesions and other CNS masses may present with ataxia, though usually some abnormality of cranial nerves or strength will be discovered with careful examination. Attention is needed to exclude abnormalities on physical examination that might suggest problems not localized to the cerebellum. Abnormal ocular movements should increase the suspicion of a mass lesion.

Rarely, ataxia can follow immunizations, viral illnesses, or varicella but also has been rarely reported in the preeruptive phase of varicella. 8 Most children are in the 2-to 4-year-old range. The onset of gait ataxia is abrupt, and only occasionally is fever present at the time ataxia begins. The latency from the prodromal illness to the onset of ataxia is from 2 days to 2 weeks. Other neurologic findings encountered included truncal ataxia, dysmetria and, uncommonly, cranial nerve abnormalities. Varicella patients appear to have uniform excellent recovery compared with patients with acute cerebellar ataxia from other causes that may have some residual problems.9 Little workup is needed if the ataxia occurs in the convalescent phase of varicella, and antiviral medications are not indicated. Otherwise, neuroimaging, lumbar puncture, and consultation are advisable. One study showed that while roughly half of the patients had cerebrospinal fluid inflammatory changes with pleocytosis or elevated immunoglobulin G index, magnetic resonance imaging (MRI) identified inflammatory changes in the cerebellum in only a minority of cases. 9 Another small report noted MRI abnormalities not only in the cerebellum but in other areas of the CNS. This "syndrome" may in fact consist of several subgroups, some of which involve transient demyelination.10

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