BehindTheMedspeak: How Electroconvulsive Therapy (ECT) Works in Depression

ECT remains one of the most controversial areas in medicine, and certainly in the field of psychiatry both its advocates and detractors are loud and legion.

Many theories exist as to how and why a week–long series of powerful 30–second–long daily jolts of electricity to the brain alleviate depression — but there is no question that they do.

Now comes a Swedish scientist with a novel explanation: Dr. Johan Hellsten of Lund University in Sweden has just published a paper which implies that ECT causes new blood vessels to grow in brain regions particularly affected by depression, and that this regeneration may be related to the alleviation of depression.

Here's a news story about the work: it's from the current (September 15) issue of the Economist.

Shocking Treatment

How ECT works

Ernest Hemingway underwent 20 gruelling rounds of electroconvulsive therapy (ECT) to cure him of his depression.

Having lost many of his memories as a result, he said, "It was a brilliant cure but we lost the patient," and took a shotgun to his head not long afterwards.

Ever since ECT was pioneered by Ugo Cerletti, an Italian neurosurgeon, in the late 1930s, it has had a bad press.

In books ("The Bell Jar", "Zen and the Art of Motorcycle Maintenance"), in song ("Electric Co" by U2) and in film ("One Flew Over the Cuckoo's Nest" and "Tarnation"), it has been portrayed as a sinister procedure that leaves the patient a dribbling dullard.

But in spite of this, ECT remains one of the fastest-acting and most effective antidepressant treatments known.

Why it should be so effective, though, is an enigma.

On the face of it, running a current of almost an amp through someone's brain seems a silly thing to do.

But a study by Johan Hellsten of Lund University in Sweden has cast some light on the question.

Dr Hellsten has shown that ECT leads to the generation of new blood vessels in part of the brain implicated in depression.

Previous brain-imaging studies have shown that patients with long-term depression have a smaller hippocampus (part of the brain that deals with emotion and memory) than average.

But, while it is possible to use scanners to look at brain volume in people, it is impossible to examine what is going on at a cellular level.

For this reason, Dr Hellsten used rats.

There were two groups of rats in his experiment.

The test group received ECT once a day for ten days while the control group received a sham treatment.

On the eleventh day, the rats were killed and examined.

Dr Hellsten found a 20-fold increase in the number of endothelial cells (the cells that line blood vessels) in the hippocampuses of the test rats, compared with the control rats.

He also found a 16% increase in the total length of the blood vessels in their hippocampuses.

If the blood vessels of any organ—including the hippocampus—are reduced, that organ begins to atrophy.

ECT appears to reverse this atrophy.

This study is the first to show an increase in blood-vessel production in connection with an anti-depressive treatment.

Why ECT has this effect is still a subject of speculation, but Dr Hellsten suspects that what is happening is a consequence of the brain trying to protect itself.

ECT works by creating an artificial epileptic seizure.

Natural seizures, which often last much longer than the 30 seconds or so employed for ECT, result in the production of chemicals called growth factors that stimulate cell division and growth.

This response helps to compensate for the damage that a seizure can do.

Though modern ECT does not last long enough to cause damage, it nevertheless provokes the damage-limitation response.

ECT, invented in a more brutal age, was originally seen as a way to control unruly patients, often against their will.

Ironically, it now serves to give will back to those who have lost it.

Here's a link to the September 8 Lund University press release about the study. (I hope your Swedish is better than mine 'cause that's the language it's in.)

The entire field of brain research and psychiatry is in the midst of an epochal shift in its basic focus.

During the second half of the 20th century the rise of what I will call the "neurotransmitter hypothesis" occupied pride of place in research laboratories.

Long story short: the key to mood and behavioral disorders lay in how much serotonin, dopamine, epinenphrine and their ilk are present at brain synapses.

The 21st century finds a new focus: the various drugs and treatments used in psychiatry now appear to cause structural changes in the brain resulting in the formation of new brain cells and neural pathways.

The old model pictured the brain as a static organ with its full complement of cells present at birth; after birth, the brain gradually lost function, with little — if any — capacity for growth or regeneration.

The new paradigm sees the brain as a vital, changing, plastic, living thing with unlimited, largely still–hidden capabilities including growth and modification of basic circuitry and synaptic pathways.

The article cited above illustrates this new way of thinking.

We enter an era of potentially enormous progress in the treatment of mental disorders, still among the most devastating scourges of mankind.