How does ECT work?
The short answer: no one knows.
The long answer:
Richard Abrams acknowledges that despite years of study, researchers only have ideas, but no answers:
It is further notable that a comprehensive review of the data supporting a neurobiologic mechanism for the therapeutic effects of ECT in man failed to uncover a single candidate for the magic bullet, concluding that "Despite considerable investigation, the mechanism of antidepressant (sic) effect of ECT is still a mystery."
(The main theories of how ECT works) are either too narrow, premature, unconfirmed, or just plain wrong.
It should be clear from this brief review that no coherent general neurochemical theory of the action of ECT yet exists.
Modern ECT researchers, regardless of their species of redilection, have hardly more insight into the relationship between brain biological events and treatment response in ECT than they did at the time of the first edition of this book -- which is to say, very little, indeed. Moreover, modern neurohumoral theories of the action of ECT -- even as formulated by sophisticated investigators with impeccable credentials -- have not surpassed in conceptual elegance the 18th century claim that things burned because they contained phlogiston; ECT awaits its Lavoisier. (1)
There are three main hypotheses of how ECT works. There have been other hypotheses that have come and gone as well, but these are the current crop.
I emphasize that none of these are proven to be true, but the ECT industry has tended to pick the theory that fit the current trend and pass it off to the public as fact. While some ECT critics have done the same, the difference is that when an "expert" and someone with Dr. attached (whether MD, DO or Ph.D.) to his/her name, it is accepted by the public and media as fact, never questioned.
1. The brain damage theory - this theory has been around the longest, and was championed by the "Grandfather of American ECT," Dr. Max Fink. This theory holds that ECT traumatizes the brain, making it unable to feel the emotions that were considered the problem. For decades, Dr. Fink (www.electroshock.org, no longer in service) claimed (and showed scientifically) that "craniocerebral trauma" was the goal. (2) In fact, he was quite prolific through the 1970s, writing about the damaging effects on the brain. He stated that the many abnormalities in the brain post-ECT show that "induced convulsions in man are more similar to cerebral trauma than to spontaneous seizures." (3)
Critics of ECT point to the common use of 'suprathreshold' doses of electricity (determining the dose needed to produce convulsion, then multiplying that amount by as much as 500 percent) as concrete evidence that brain damage is necessary to get the desired effect in ECT. Otherwise, say critics, why wouldn't the dose simply be the amount needed to produce the convulsion? (4,5)
2. The anticonvulsant theory says that during the first several ECT treatments, the patient's seizure threshold increases, meaning that it takes more ECT stimulus to produce a seizure. Certain changes in the brain occur, in an effort to stop the seizures: cerebral blood flow decreases, with the decrease in blood flow perhaps lasting several months; brain waves change; and certain chemicals (neurotransmitters and neuropeptides) are released. (6) It is hypothesized that these chemicals inhibit the seizure and cause, or at least substantially contribute to, the desired effect of ECT. Variations on this hypothesis seem to be in vogue currently.
3. The neurotransmitter theory holds that ECT works by causing the release of neurotransmitters in the brain which reduce depression. This has often been touted as fact by the ECT industry, despite no scientific evidence to prove it. Claims are continually made that studies are underway to "prove" this is how ECT works. However, despite those many studies for decades and millions of dollars, it remains unproven and still remains a hypothesis. (7)
Despite the abundance of professional literature that clearly states the mechanism of action of ECT is still unknown, many laypersons believe that number three is a proven fact. The likely reason for that is it appears in many patient pamphlets without clarification and is part of the standard homily given by recommending psychiatrists to patients.
Here is only a small sampling of what's said amid ECT professionals versus what the public hears:
||For the public
|Despite being in use for over 70 years, its mechanism of action (MOA) is still not clearly understood. Various theories on MOA of ECT have been proposed over the years. These have included looking at psychological, neurophysiological, neurochemical, neuroendocrine, and neuropeptides mechanisms. (7)
||Max Fink: When a person has a mental illness, their neuroendocrine system is markedly disturbed. The hypothalamus and the pituitary of the brain and the adrenal glands (called the "HPA" axis) are affected. As a consequence, the functions of the thyroid, testes and ovaries are disturbed. In severe depression, melancholia and psychotic depression the HPA axis functions poorly. Within 6 ECT treatments the neuroendocrine system reverses itself and the patient feels much better as a result. (8)
|Although there are active steps within the NIMH to address these issues and provide more focused research in ECT, an understanding of the basic mechanisms by which ECT exerts its effect is still unclear. (9)
||Kellner: The brain is releasing the chemicals that control emotions that are deficient in the depressed state. ECT has a potent effect on the brain chemicals that control emotions and what it does is that it causes the release of neurotransmitters like serotonin and norepinephrine in a way similar to the way the antidepressant drugs work, but ECT is much more powerful than the antidepressant drugs. (10)
And of course my favorite example, as always, is Richard Abrams, co-owner of Somatics, Inc. (One of the main device manufacturers)
The quotes at the top (italics) of this page are only a small portion of the very eloquent explanation Abrams has for his fellow ECT practitioners on why there is still no definitive answer to the question of how ECT works.
Despite that admission in the textbook, the patient brochure (also written by Richard Abrams and made available through Somatics, Inc.) says something very different:
"The resultant nerve-cell activity releases chemicals in the brain and helps restore normal functioning."
Tucked away on the back of the brochure, however, Abrams does clarify that "exactly how this interaction is therapeutic needs further investigation. We believe..."
He then goes on to add that a "number of rigorously-designed research projects are underway to study this question." (11)
After decades of study, they are still underway and have yet to figure it out.
1. Abrams R: Electroconvulsive Therapy. USA, Oxford University Press, 2002
2. Fink M: A unified theory of the action of the physiodynamic therapies. Journal of Hillside Hospital 1957; 6:197206
3. Fink M: Cholinergic aspects of convulsive therapy. Journal of Nervous and Mental Disease 1966; 142:475484
4. Cameron D: ECT: Sham Statistics, the Myth of Convulsive Therapy, and the Case for Consumer Misinformation. Journal of Mind and Behavior 1994; Vol. 15(Nos. 1 and 2):177-198
5. Fink M: Ref: 21 CFR Part 882 Docket # 82P-0316. Edited by Administration FaD. Rockville, 1990, p Personal Communication
6. Sackeim H: The anticonvulsant hypothesis of the mechanisms of action of ECT: current status. J ECT 1999; 15(1):5-26
7. Grover S, Mattoo SK, Gupta N: Theories on Mechanism of Action of Electroconvulsive Therapy German Journal of Psychiatry 2005
8. CBS: CBS Cares Depression: Other Treatment Options, unknown date, likely 2002-2004
9. Davis KL, Charney D, Coyle JT, Nemeroff C: Neuropsychopharmacology: The Fifth Generation of Progress. Lippincott Williams & Wilkins, 2002
10. Elliot G: Gordon Elliot Show, Electroconvulsive Therapy, 1996
11. Schwartz C, Abrams R: Somatics Patient Brochure. 1994