Brief report Changes in brain metabolism after ECTPositron emission tomography in the assessment of changes in glucose metabolism subsequent to electroconvulsive therapy Lessons, limitations and future applications E.Z. Schmidt a, , B. Reininghaus a , C. Enzinger b , C. Ebner a , P. Hofmann a , H.P. Kapfhammer a a Department of Psychiatry, Medical University Graz, Auenbruggerplatz 31, 8036 Graz, Austria b Department of Neurology and Section of Neuroradiology, Department of Radiology, Medical University Graz, 8036 Graz, Austria Received 5 April 2007; received in revised form 19 June 2007; accepted 20 June 2007 Available online 26 July 2007 Abstract Background: Electroconvulsive therapy (ECT) has been used as an effective treatment option in severe and treatment resistant cases of depression for decades. However the mode of action of ECT is still not fully understood. Advances in neuroimaging created new possibilities to understand the functional changes of the human brain. Methods: Literature review of studies assessing possible changes in cerebral glucose metabolism pre- and post-ECT by PET, identified by PubMed. Results: Studies were limited by small sample size, inhomogeneous study population with uni- and bipolar depressive patients and methodological inconsistencies. Despite considerable variance, reduction in glucose metabolism after ECT in bilateral anterior and posterior frontal areas represented the most consistent findings. Conclusions: Future research into this issue should include larger and more consistent cohorts of patients. Assessing clinical improvement of depression after ECT should allow to correlate changes in brain glucose metabolism with functional scores. Follow up PET scans after six or twelve months should be performed to test if changes in brain metabolism are persistent. © 2007 Elsevier B.V. All rights reserved. Keywords: Electroconvulsive therapy (ECT); Depression; Positron emission tomography (PET); Glucose metabolism 1. Introduction A large body of evidence suggests electroconvulsive therapy (ECT) as an effective treatment especially for severe and treatment-refractory depression (Janicak et al., 1985; Pluijms et al., 2006; UK ECT Review Group, 2003; Prudic et al., 1996). ECT-induced seizures propagate from the site of initiation to other specific brain regions and induce decreases in cerebral blood flow (CBF) in cingulate and left dorsolateral frontal cortex suggesting cortico- cortical or cortico-thalamo-cortical networks mainly involved in the mechanism of ECT (Enev et al., 2007; McNally and Blumenfeld, 2004). Journal of Affective Disorders 106 (2008) 203 208 www.elsevier.com/locate/jad Corresponding author. Tel.: +43 385 86214. E-mail address: eva.schmidt@klinikum-graz.at (E.Z. Schmidt). 0165-0327/$ - see front matter © 2007 Elsevier B.V. All rights reserved. doi:10.1016/j.jad.2007.06.009