Electroconvulsive therapy (ECT) is a crude but effective treatment for depression. It consists of applying a brief alternating current to the brain in order to induce a generalized seizure, which usually lasts for less than half a minute. It looks nothing like the picture to the left.
ECT is typically given three times per week, and a dozen sessions are enough to produce a dramatic improvement in depression in most cases. However, how it works is entirely mysterious. There are plenty of theories. An important little study from Duke University psychiatrists Cassidy et al (including Bernard Carroll) has just ruled out one of them.
Monoamines are a class of neurotransmitters: serotonin, dopamine and noradrenaline. They're involved in various aspects of mood, although the picture is very complicated, and almost all antidepressant drugs target one or more monoamines. Could ECT act by increasing monoamine levels? It's as good a theory as any, and there's some evidence for it.
However, Cassidy et al's data suggest it's not the case. They took 9 volunteers who had been severely depressed, but had recently responded well to a course of ECT. They gave them combined serotonin depletion, with the tryptophan depletion method, and dopamine/noradrenaline depletion with the drug AMPT. As a placebo comparison, they used diphenhydramine, aka Benadryl, a mildly sedative antihistamine; this is because AMPT is a sedative, and they wanted to control for active placebo effects. Few psychopharmacology studies are so well controlled.
These depletion techniques, given separately, are known to cause temporary relapses in about 50% of people who've responded to antidepressants targeting the corresponding monoamine, and also in some people who used to be depressed but are no longer taking medication. If monoamines are involved in the response to ECT, depleting all of them at once should definitely cause relapse.
What happened? Nothing. No-one experienced even a partial return of their depression with either the real or the placebo treatments. These depletions don't put levels of the neurotransmitters down to zero, but Cassidy et al. used the same doses that have caused dramatic relapses in susceptible people.
This strongly suggests that monoamines are not required for the clinical response to ECT, at least not in any straightforward more-is-better way. Given that ECT works faster than antidepressants and more often (the controversial side effects are the main reason it's used only as a last resort), this is a blow for the monoamine hypothesis of depression... like I said, it is complicated.
And how does ECT work? We still don't know. This study narrows down the possibilities.
Monoamine Shock
13.12
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