Sorry I haven’t been here in a while! Yesterday I gave my senior seminar—a 45 minute literature review presentation in front of my peers, all the faculty in the discipline, and my parents—so I’ve been a bit preoccupied with that during the last few weeks. I’m DONE and I think it went well. I slept in this morning and missed PZ’s class (sorry, PZ!), but I was really wiped and, dammit, I deserved it.
Anyway, today I’m writing about electroconvulsive therapy (ECT), or, in the vernacular, electroshock. Try to wipe your mind of what you think you know about ECT from movies. The media has not been kind in its representation of this therapy, and the therapy itself is not what it was fifty years ago.
ECT is the stimulation of a grand mal seizure in a patient by electricity applied through electrodes placed on the scalp. The patient is unconscious, having received a short-acting anesthetic, and his or her muscles do not convulse because a muscle relaxant is also administered.
ECT is still an important therapy in use today. As many as one in five patients experiencing major depressive disorder are classified as having treatment-resistant depression (estimates vary because criteria for this classification are not consistent). Pharmacological and psychotheraputic treatments are not effective for these individuals, but ECT can often help. However, in spite of its well-known effectiveness and its long history of use, we still do not understand how ECT manifests its antidepressant effects in the brain. We do, however, have some hypotheses.
One is that ECT alters the neurotransmitter levels in the brain. The concentration of GABA has been shown to increase following ECT. As well, the monamine neurotransmitters—serotonin, dopamine, and norepinephrine—have been shown to be affected by ECT. The 5-HT1A serotonin receptor is sensitized by ECT, and both dopamine levels and dopamine receptors are affected by ECT. Repeated ECT treatments enhance dopamine binding to receptors.
Interestingly, ECT has been demonstrated to have neurogenic effects. One study in animals found increased neurotrophic factors and cell proliferation in the subgranular zone in the dentate gyrus of the hippocampus.
These don’t seem to be articulated hypotheses, you say. It’s true, they aren’t. This is basically a list of things we’ve shown that ECT does in the brain. We need some more data, and then we may be able to put this information together in a meaningful hypothesis on how ECT does it antidepressant thang in the brain.
The brain is really complicated. REALLY complicated. We don’t understand more than a small fraction of its workings. We also don’t really understand depression. We know that people who have depression seem to have lower levels of serotonin, dopamine, and norepinephrine, but that’s not even close to the whole story. So, given our poor comprehension of this thing called The Brain (seems it ought to be capitalized, mighty as it is), it’s not at all surprising that we don’t understand ECT.
Merkl, A.; Heuser, I.; Bajbouj, M., Antidepressant electroconvulsive therapy: Mechanism of action, recent advances and limitations. Experimental Neurology 2009, 219 (1), 20-26.