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Department of Psychiatry, National Centre Hospital for Mental, Nervous and Muscular Disorders, National Centre of Neurology and Psychiatry (NCNP), and Department of Neuropsychiatry, Keio University School of Medicine, Tokyo
Department of Psychiatry, National Centre Hospital for Mental, Nervous and Muscular Disorders, Tokyo
Department of Anaesthesiology, National Centre Hospital for Mental, Nervous and Muscular Disorders, NCNP, Tokyo, and Department of Anaesthesiology, Yokohama City University School of Medicine, Yokohama
Department of Radiology, National Centre Hospital for Mental, Nervous and Muscular Disorders, NCNP, Tokyo
Department of Neuropsychiatry, Keio University School of Medicine, Tokyo
Department of Radiology, National Centre Hospital for Mental, Nervous and Muscular Disorders, NCNP, Tokyo, Japan
Correspondence: Dr N. Motohashi, Department of Neuropsychiatry, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, 1110 Shimokato, Chuo City, Yamanashi 409-3898, Japan. Tel: +81 55 273 9847; fax: +81 55 273 6765; email: motohashi{at}yamanashi.ac.jp
Declaration of interest None. Funding detailed in Acknowledgements.
Background Although electroconvulsive therapy (ECT) is widely used to treat psychiatric disorders such as depression, its precise neural mechanisms remain unknown.
Aims To investigate the time course of changes in cerebral blood flow during acute ECT.
Method Cerebral blood flow was quantified serially prior to, during and after acute ECT in six patients with depression under anaesthesia using [15O]H2O positron emission tomography (PET).
Results Cerebral blood flow during ECT increased particularly in the basal ganglia, brain-stem, diencephalon, amygdala, vermis and the frontal, temporal and parietal cortices compared with that before ECT. The flow increased in the thalamus and decreased in the anterior cingulate and medial frontal cortex soon after ECT compared with that before ECT.
Conclusions These results suggest a relationship between the centrencephalic system and seizure generalisation. Further, they suggestthat some neural mechanisms of action of ECT are mediated via brain regions including the anterior cingulate and medial frontal cortex and thalamus.
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