Medical Treating Depression with Deep Brain Stimulation

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Recent research highlighted in Scientific American Mind focuses on treating severe depression through deep-brain stimulation targeting Area 25, a brain region identified as overactive in depressed patients. Neuroimaging studies revealed that during depressive episodes, activity in the frontal cortex decreases while Area 25 becomes more active. To address this, researchers implanted electrodes in Area 25 and utilized a pacemaker to deliver electrical stimulation. Notably, some patients experienced immediate relief upon activation of the electrodes, with about two-thirds achieving normal mood and function within months. However, there remains uncertainty regarding the mechanism by which electrical stimulation inhibits neuronal firing in this area, with suggestions that excitation of certain neurons may inhibit neighboring ones or lead to a shutdown of the neurons themselves. The surgical team continues to investigate the underlying reasons for the treatment's effectiveness.
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I am reading an article in this month's SciAm mind about treating depression with deep-brain stimulation. Researchers found that an area known as Area 25 is overactive in patients with severe depression. From what I understand, this area is sort of a "traffic controller" for neural paths between the frontal cortex and the limbic system. They did some neuroimaging experiments and found that when a depression attack occurred, frontal cortex activity plummeted and Area 25 activity increased. As the depressive episode subsided, frontal activity revived and Area 25 activity settled down.

Anyway, what they did to treat these patients was implant electrodes into Area 25, and then used an implanted "pacemaker" to send current to them.

What I am not clear about is how the electrical stimulation inhibits rather than excites the firing in this area.
 
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Math Is Hard said:
I am reading an article in this month's SciAm mind about treating depression with deep-brain stimulation. Researchers found that an area known as Area 25 is overactive in patients with severe depression. From what I understand, this area is sort of a "traffic controller" for neural paths between the frontal cortex and the limbic system. They did some neuroimaging experiments and found that when a depression attack occurred, frontal cortex activity plummeted and Area 25 activity increased. As the depressive episode subsided, frontal activity revived and Area 25 activity settled down.

Anyway, what they did to treat these patients was implant electrodes into Area 25, and then used an implanted "pacemaker" to send current to them.

What I am not clear about is how the electrical stimulation inhibits rather than excites the firing in this area.
I remember seeing a show on Discovery Health about a man who was near suicide and had been severly depressed for many years until he got the implant. Now he lives a normal life. Very interesting.
 
They had some pretty amazing results. Some of the patients felt better as soon as they turned on the electrodes. 2/3 of them returned to normal mood and function within months.
 
excitation of some neurons might inhibit neighbouring ones...or the neurons them selves might shut off(not sure chemically) if neighbouring synapses are being excited.
 
neurocomp2003 said:
excitation of some neurons might inhibit neighbouring ones...or the neurons them selves might shut off(not sure chemically) if neighbouring synapses are being excited.
sounds a little like guess work. Of course, the surgeon did say she is still investigating why this worked.
 
I've been reading a bunch of articles in this month's Scientific American on Alzheimer's and ran across this article in a web feed that I subscribe to. The SA articles that I've read so far have touched on issues with the blood-brain barrier but this appears to be a novel approach to the problem - fix the exit ramp and the brain clears out the plaques. https://www.sciencealert.com/new-alzheimers-treatment-clears-plaques-from-brains-of-mice-within-hours The original paper: Rapid amyloid-β...

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