Journal
JOURNAL OF ECT
Volume 28, Issue 3, Pages 157-161Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/YCT.0b013e31824f8296
Keywords
ECT; ketamine; rapid; antidepressant; barbiturate
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Funding
- State of Connecticut, Department of Mental Health and Addiction Services through Connecticut Mental Health Center
- National Institute of Mental Health [K02 MH076222-04]
- National Institute on Drug Abuse [T32-DA022975]
- Abbott
- AstraZeneca
- Avanier Pharmaceuticals
- Bristol-Myers Squibb
- Evotec
- Eli Lilly Co
- Hoffman La-Roche
- Johnson Johnson
- Novartis
- Novum Pharmaceuticals
- Merck Co
- Sepracor Inc
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Objectives: Studies now provide strong evidence that the N-methyl-D-aspartate receptor antagonist ketamine possesses rapidly acting antidepressant properties. This study aimed to determine if a low dose of ketamine could be used to expedite and augment the antidepressant effects of electroconvulsive therapy (ECT) treatments in patients experiencing a severe depressive episode. Materials and Methods: Subjects with major depressive disorder or bipolar disorder referred for ECT treatment of a major depressive episode were randomized to receive thiopental alone or thiopental plus ketamine (0.5 mg/kg) for anesthesia before each ECT session. The Hamilton Depression Rating Scale (HDRS) was administered at baseline and at 24 to 72 hours after the first and sixth ECT sessions. Results: Electroconvulsive therapy exerted a significant antidepressant effect in both groups (F-2,F-24 = 14.35, P < 0.001). However, there was no significant group effect or group-by-time interaction on HDRS scores. In addition, post hoc analyses of the time effect on HDRS showed no significant HDRS reduction after the first ECT session for either group. Conclusions: The results of this pilot study suggest that ketamine, at a dose of 0.5 mg/kg, given just before ECT, did not enhance the antidepressant effect of ECT. Interestingly, the results further suggest that the coadministration of ketamine with a barbiturate anesthetic and ECT may attenuate the immediate antidepressant effects of the N-methyl-D-aspartate antagonist.
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