Acute ataxia Acute ataxia is usually the result of cerebellar dysfunction. However, it may also result from conditions affecting the vestibular apparatus, disorders of sensory input (from peripheral nerves, posterior roots, posterior columns), or abnormalities in the connections between the posterior columns and the parietal lobes. Although the most common causes (Table 16-1) are intoxications (alcohol, benzodiazepines, anticonvulsant medications) and parainfectious and viral infections, always consider a mass lesion (posterior fossa, brainstem, spinal cord), hydrocephalus, head trauma, meningitis, encephalitis, and a metabolic or vascular etiology. Clinical presentation Ataxia is manifested as an unsteady, reeling, wide-based gait or truncal instability (titubation). Dysmetria, tremor, slow, dysrhythmic “scanning” speech, and nystagmus may also be present. Parainfectious acute cerebellar ataxia Acute cerebellar ataxia most often occurs days to weeks after a viral infection such as varicella. Typically, a 1– 3-year-old presents with a short history (hours to days) of incoordination, unsteady gait, tremor, speech abnormalities, titubation, or nystagmus. The mental status and the rest of the examination are normal. The well appearance of the child helps distinguish this syndrome from encephalitis and meningitis. The ataxia may precede or follow the appearance of an exanthem. The CSF may be normal, or there may be a mild pleocytosis or elevation of the protein. Recovery is rapid (often within days, usually within 4– 6 weeks), but as many as 10– 20% of patients have sequelae of variable severity. Acute disseminated encephalomyelitis Acute disseminated encephalomyelitis (ADEM) is an inflammatory demyelinating disease of the CNS that often presents with ataxia after a viral infection or vaccination.
|Title of host publication||Clinical Manual of Emergency Pediatrics, Fifth Edition|
|Publisher||Cambridge University Press|
|Number of pages||41|
|State||Published - Jan 1 2010|