Electroconvulsive therapy
Electroconvulsive therapy (ECT) or electroshock therapy (EST) is a psychiatric treatment where a generalized seizure (without muscular convulsions) is electrically induced to manage refractory mental disorders.[1] Typically, 70 to 120 volts are applied externally to the patient's head, resulting in approximately 800 milliamperes of direct current passing between the electrodes, for a duration of 100 milliseconds to 6 seconds, either from temple to temple (bilateral ECT) or from front to back of one side of the head (unilateral ECT). However, only about 1% of the electrical current crosses the bony skull into the brain because skull impedance is about 100 times higher than skin impedance.[2]
"Electroshock" redirects here. For other uses, see Electroshock (disambiguation).
Aside from effects on the brain, the general physical risks of ECT are similar to those of brief general anesthesia.[3]: 259 Immediately following treatment, the most common adverse effects are confusion and transient memory loss.[4][5] Among treatments for severely depressed pregnant women, ECT is one of the least harmful to the fetus.[6]
ECT is often used as an intervention for major depressive disorder, mania, and catatonia.[4] The usual course of ECT involves multiple administrations, typically given two or three times per week until the patient no longer has symptoms. ECT is administered under anesthesia with a muscle relaxant.[7] ECT can differ in its application in three ways: electrode placement, treatment frequency, and the electrical waveform of the stimulus. These treatment parameters can pose significant differences in both adverse side effects and symptom remission in the treated patient.
Placement can be bilateral, where the electric current is passed from one side of the brain to the other, or unilateral, in which the current is solely passed across one hemisphere of the brain. High-dose unilateral ECT has some cognitive advantages compared to moderate-dose bilateral ECT while showing no difference in antidepressant efficacy.[8]
Mechanism of action[edit]
Despite decades of research, the exact mechanism of action of ECT remains elusive. A review from 2022 of neuroimaging studies based on a global data collaboration resulted in a model of temporary disruption of neural circuits followed by augmented neuroplasticity and rewiring.[32]
Society and culture[edit]
Controversy[edit]
Surveys of public opinion, the testimony of former patients, legal restrictions on the use of ECT and disputes as to the efficacy, ethics and adverse effects of ECT within the psychiatric and wider medical community indicate that the use of ECT remains controversial.[122][123][124][125][126][127][128] This is reflected in the January 2011 vote by the FDA's Neurological Devices Advisory Panel to recommend that FDA maintain ECT devices in the Class III device category for high risk devices, except for patients with catatonia, major depressive disorder, and bipolar disorder.[129] This may result in the manufacturers of such devices having to do controlled trials on their safety and efficacy for the first time.[4][130][131] In justifying their position, panelists referred to the memory loss associated with ECT and the lack of long-term data.[132]