How TMS Developed as a Treatment for Depression

In my previous posts I shared some of the scientific background and history of transcranial magnetic stimulation (TMS). Now I’m going to share a bit about how it got started as a treatment for depression, and how it’s evolved since its beginnings.

To give you a sense for how the science around TMS for depression has developed over the years, I’ll give you a visual snapshot. Here’s a quick Excel plot of the studies indexed in the leading medical research database, PubMed, that came up when I did a search today using the phrase “transcranial magnetic stimulation depression”:

The total number of published papers in the graph is 4,634. That’s a lot of scientific activity, and it’s been steadily increasing! (The 2024 bar shows only studies published up to the day I wrote this post, at the beginning of April.)

I was telling you in my last post that the pioneer of the use of TMS as a clinical treatment for mental health conditions was Dr. Mark S. George of the Medical University of South Carolina. Dr. George is an eminent scientist, and has remained a leading figure in the field right up to today. His initial treatment target, the left dorsolateral prefrontal cortex (DLPFC), has stood up really well. It is, in fact, still the most common TMS target for depression.

That’s the spot!

So why the DLPFC? And why the left? At the time, there was a general idea among researchers that depression may be caused by an underactive left frontal lobe (relative to the right frontal lobe). So, when TMS was first applied for depression, researchers looked to “speed up” the left frontal lobe by using rapidly pulsed TMS. Within a few years, additional studies started coming out in which authors also got antidepressant effects when they “slowed down” the right frontal lobe – by using slowly pulsed TMS (at 1 pulse per second). This lent further support to the idea that depression was associated with the two frontal lobes being out of balance.

That hemispheric-imbalance idea has come under some criticism since; I’d say the best you can say of it now is that it’s a much more complex picture than people originally thought. But the clinical benefits of both excitatory (speed-up) TMS on the left and inhibitory (slow-down) TMS on the right have remained solid through more than two decades of study. Things get a wee bit complicated, because some studies have also suggested that excitatory treatment on the right may also have benefits, which is the opposite of what you might expect based on the imbalance hypothesis.

What we can say with lots of confidence at this point is that the DLPFC in general participates in important brain circuits for emotion and mood regulation. More on that to come!

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