The aim of ECT is to induce a therapeutic clonic seizure (a seizure where the person loses consciousness and has convulsions) lasting for at least 15 seconds. Although a large amount of research has been carried out, the exact mechanism of action of ECT remains elusive. The main reasons for this are that the human brain can not be studied directly before and after ECT and therefore scientists rely on animal models of depression and ECT, with major limitations. While animal models are acknowledged to model merely aspects of depressive illness, human and animal brains are very similar at a molecular level, enabling detailed study of the molecular mechanisms involved in ECT.

There is a vast literature on the effects of Electroconvulsive Shock (ECS) in animals. In animal models of depression, particularly "Learned helplessness" and "Social defeat", there is evidence of pruning of normally dense synaptic connections in the hippocampus, a richly connected area deep in the temporal lobe which is vital in controlling both mood and memory. ECS has been shown to increase levels of Brain-derived neurotrophic factor (BDNF) and Vascular Endothelial Growth Factor (VEGF) in the rodent hippocampus. This reverses the toxic effects of depression on this area of the brain, increasing both new synapse formation and the formation of new brain cells (hippocampal neurogenesis).

Both these effects have been noted to be present in antidepressant-treated animals, however they are neither necessary nor sufficient for antidepressant response. ECT is a more robust inducer of these neuroplastic effects than antidepressants. Electroconvulsive Therapy (ECT) has also been shown to increase serum brain-derived neurotrophic factor (BDNF) in drug resistant depressed patients. This suggests a common molecular mechanism of action, albeit in need of much further study.

The American Psychiatric Association (APA) 2001 guidelines give the primary indications for ECT among patients with depression as a lack of response to, or intolerance of, antidepressant medications; a good response to previous ECT; and the need for a rapid and definitive response (e.g. because of psychosis or a risk of suicide).

The decision to use ECT depends on several factors, including the severity and chronicity of the depression, the likelihood that alternative treatments would be effective, the patient's preference and capacity to consent, and a weighing of the risks and benefits.

In recent years, ECT has much improved. Before treatment, which is done under brief anesthesia, patients are given a muscle relaxant. Electrodes are placed at precise locations on the head to deliver electrical impulses. The stimulation causes a brief (about 30 seconds) generalized seizure within the brain, which is necessary for therapeutic efficacy. The person receiving ECT does not consciously experience the electrical stimulus.

A typical course of ECT entails six to 12 treatments, administered at a rate of three times per week, on either an inpatient or outpatient basis. To sustain the response to ECT, continuation treatment, often in the form of antidepressant and/or mood stabilizer medication, must be instituted. Some individuals may require maintenance ECT (MECT), which is delivered on an outpatient basis at a rate usually of one treatment weekly, tapered off to bi weekly to monthly for up to one year.Pros for this therapy

Pros for this therapy

ECT often is effective in cases where antidepressant medications do not provide sufficient relief of symptoms. The American Psychiatric Association guidelines advocate ECT treatment for severe major depression with psychotic features, manic delirium, or catatonia.

Cons for this therapy

The acute effects of ECT can include amnesia, both retrograde (for events occurring before the treatment) and anterograde (for events occurring after the treatment).There are risks and side effects associated with ECT. Although rare, people have suffered anesthesia reactions and anaphylaxis, cardiovascular outcomes such as arrythmias, heart attack, and blood pressure changes, physical trauma from restrained muscle contraction and dental/oral trauma from intubation, neurological complications such as stroke and seizure. More common is the risk of amnesia, memory loss, and cognitive decline, although these risks are controversial. If memory loss occurs, it usually resolves in the days to weeks after treatment.

ECT was first introduced in 1938 by Italian neuropsychiatrists Ugo Cerletti and Lucio Bini, and gained widespread use as a form of treatment in the 1940s and 1950s.

The steady growth of antidepressant use along with negative depictions of ECT in the mass media led to a marked decline in the use of ECT during the 1950s to the 1970s.

(ECT) for years had a poor reputation with many negative depictions in popular culture. However, the procedure has improved significantly since its initial use and is safe and effective. People who undergo ECT do not feel any pain or discomfort during the procedure.

Electroconvulsive Therapy (ECT) is another treatment option that may be particularly useful for individuals whose depression is severe or life threatening, or who cannot take antidepressant medication. 

(ECT) can be a very effective and safe treatment for depression. ECT uses electric currents to cause a seizure in patients. This current produces many changes in the chemistry and functioning of the brain. Although a large amount of research has been carried out, the exact mechanism of action of ECT remains elusive. ECT doctors claim it may "jumpstart the brain", helping boost neurotransmission. The brain changes help the patient to fight depression. 

Today, ECT is most often recommended for use as a treatment for severe depression that has not responded to other treatment, and is also used in the treatment of mania and catatonia.

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Review Date: 
February 15, 2012