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ischemic stroke due to vertebral artery dissection is traumatic in half of cases and
often presents with ataxia, headache, vomiting, cranial nerve deficits, and
hemiparesis. Rarely, cerebral sinovenous thrombosis can manifest with isolated
cerebellar venous infarction.
On rare occasions, ataxia can be part of the initial clinical manifestations of
opsoclonus-myoclonus syndrome, often associated with neuroblastoma.

FIGURE 15.1 Acute ataxia diagnostic pathway.

MANAGEMENT CONSIDERATIONS
Posterior fossa masses and cerebellar edema due to stroke or cerebellitis may
manifest with signs of ICP, often associated with ataxia, altered mental status, and
other neurologic signs. In these instances, consideration of the increased ICP
must be foremost. Deferring LP in a child with concern for increased ICP is
imperative to prevent herniation and its potential morbidity and mortality. If there
is any concern clinically for a mass, hemorrhage, or other space occupying CNS
lesion, imaging should precede LP. If a child is found to have increased ICP,
treatment with hypertonic saline or mannitol and other acute neurologic
precautions should be undertaken (see Chapter 97 Neurologic Emergencies ).
Consultation with neurology and/or neurosurgery may be warranted.
Treatment for GBS or its variants is mostly supportive, and in up to 10% to
20% of cases may require ventilator support. Children with reduced vital capacity
(≤20 mL/kg) generally progress to respiratory failure. This needs to be evaluated