Antiglutamatergic agents, despite many initial hopes and several compounds tested, are not a mainstay of treatment of CP and are only infrequently used. The antiglutamatergic drug of choice remains parenteral ketamine. However, ketamine is a drug of addiction with neurotoxic (particularly with intrathecal/epidural administration) effects and unpleasant psychiatric side effects (e.g., somnolence, feelings of insobriety, nausea/vomiting, hallucinations, depersonalization/derealization, and drowsiness), most commonly in anxious and apprehensive individuals. On the other hand, acute administration of low dosages of ketamine has procognitive effects . Renal damage and cystitis are known toxicities with repeated administrations. Rapid-acting routes of administration (e.g., intranasal) should be avoided and doses kept as low as possible. Ketamine (4 mg/kg PO = 0.4 mg/kg IM) can (rarely) induce hepatic failure; it has a low bioavailability (ca. 15%) and is rapidly metabolized to the much weaker norketamine. Long-term subcutaneous ketamine may lead to painful indurations. Ketamine is best reserved for parenteral in-hospital administration for urgent pain control and pharmacologic dissection. Recommended parenteral and oral dosages are from 0.05 to 0.5 mg/kg/h (intravenous or subcutaneous) and 0.2–0.5 mg/kg/dose PO two to three times daily with a maximum of 50 mg/dose three times daily, respectively. A study in a 51-strong mixed chronic pain group found that outpatient ketamine infusions significantly reduced VAS from 7 to 6.06 and improved sleep and enjoyment of life, but had no effect on general activity, mood, walking, work, and social interaction . This is in line with controlled studies that do not find ketamine, however administered, particularly effective for CP. Nonetheless, some patients report pain abatement during IV challenge (Tables 12.1, 12.2, 12.3, 12.4, and 12.5).
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