What is the mechanism of action for electroconvulsive therapy (ECT)?

Updated: Sep 24, 2019
  • Author: Mehul V Mankad, MD; Chief Editor: Dennis M Popeo, MD  more...
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The mechanism of action of ECT is not fully known. ECT affects multiple central nervous system components, including hormones, neuropeptides, neurotrophic factors, and neurotransmitters. [11]  

One theory of ECT efficacy is related to the "hyperconnectivity hypothesis." Functional MRI (fMRI) data suggests that patients with depression experience a localized increase in connectivity within the left dorsolateral prefrontal cortex. This hyperconnectivity is decreased in patients treated with ECT in a similar fashion to those individuals treated with chemical antidepressant treatment. [12]  

Positron emission tomography (PET) has been used to study the neurophysiological effects of ECT. In a literature review of studies assessing possible changes in cerebral glucose metabolism by PET before and after ECT, reduction in glucose metabolism after ECT in bilateral anterior and posterior frontal areas represented the most consistent findings. [13]

Nearly every neurotransmitter system is affected by ECT, including adrenergic, serotonin, muscarinic, cholinergic, and dopaminergic systems. Brain-derived neurotrophic factor (BDNF), [14, 15] second-messenger systems, and catechol-O-methyltransferase (COMT) polymorphisms [16] may play a role in ECT. An increase in gamma-aminobutyric acid (GABA) transmission and receptor antagonism has also been observed. [17]  Finally, ECT may also lead to an increase of endogenous opioids. [18, 19]

Although many biomarkers have been studied, no ECT biomarker is routinely used in current clinical practice. [15]

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