Adverse effects on the CNS occur in 40 to 50 percent of patients with clinical digitalis toxicity and may develop before, with, or after signs of cardiac toxicity. Neurological complications include nausea, vomiting, visual disturbances, seizures, confusion, delirium, mania, hallucinosis, and syncope. Explanations for the high frequency of neurotoxicity with digitalis have been inadequate, and the few pathological studies compiled have not demonstrated consistent lesions. '1

The most frequent and often the first neurotoxic reaction is nausea due to direct stimulation of the medullary chemoreceptor trigger zone. Nausea associated with digitalis toxicity is often accompanied by vomiting, and when vomiting is chronic, it may lead to malnourishment and cachexia. The incidence of digitalis-related visual disturbances has been estimated at 40 percent. Clinically, it presents with blurred vision, scotomas, diplopia, defects of color vision, and amaurosis. Electrodiagnostic and labeled tracer studies have implicated retinal dysfunction in the pathogenesis. y

Seizures are most commonly seen in the pediatric population. The mechanism by which digitalis induces seizures has been postulated to involve inhibition of membrane ATPase and subsequent neuronal irritability. Confusion, delirium, mania, and hallucinosis have been reported in as many as 15 percent of patients with digitalis toxicity. '1! Although the mechanism for the symptoms is unknown, they are not the result of altered cardiac function. On the other hand, transient cognitive changes that are believed to be due to intermittent cerebral hypoperfusion can resemble transient global amnesia or be manifested as syncope.

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