Most patients hospitalized at tertiary care pediatric institutions receive at least 1 medication outside the terms of the Food and Drug Administration product license. Substantial variation in the frequency of off-label use was observed across diagnostic categories and drug classes. Despite the frequent off-label use of drugs, using an administrative database, we cannot determine which of these treatments are unsafe or ineffective and which treatments result in substantial benefit to the patient.

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MTX is used in the treatment of several childhood cancers and has side effects of varying severity [1]. Neurotoxicity can occur in up to 15% of patients receiving high-dose MTX [2, 3]. Elevated homocysteine in CSF are documented in such cases. Dextromethorphan, an NMDA receptor antagonist, suppresses homocysteine activity and is the initial treatment. Ketamine, also an NMDA receptor antagonist, may be considered as an optimal treatment choice in intubated patients requiring sedation. We describe the use of ketamine in a pediatric patient with methotrexate-induced neurotoxicity. Ketamine as treatment of MTX-induced neurotoxicity has not been described in the literature.

Cocaine (1.5 mg/kg i.v.) was administered to awake newborn piglets that were pretreated with either intravenous saline (placebo) or SCH23390, a dopamine antagonist, to study dopamine’s role in cocaine’s vascular and behavioral actions. In the placebo group, cocaine increased the locomotor activity and cerebellar and cardiac blood flow (31 ± 36 and 72 ± 66%), but decreased choroid plexus and renal blood flow (47 ± 23 and 18 ± 19%). In the SCH23390-treated group, cocaine did not affect organ blood flow or locomotor activity. Cocaine transiently increased the mean arterial blood pressure in both groups (10 ± 7 and 18 ± 13%). These data indicate that the behavioral and blood flow responses to cocaine in cerebellum, choroid plexus, heart, and kidneys are mediated by dopamine, whereas the arterial pressor response to cocaine is not.

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