Tardive Dysphoria?

"Now Antidepressant-Induced Chronic Depression Has a Name: Tardive Dysphoria" read the title of the article in Psychology Today by Robert Whitaker (read it here). To me, this seemed an only natural light being shed on something that has been suspected and feared for a while now, that I felt I understood without even reading the article. For you, however, this might have very little meaning, so I thought I might try to explain some of the science behind it.

Synaptic Cleft

Your neurons can stretch for fairly long distances in your body (up to a metre). Messages are sent in the form of electrical signals, that flow down the long padded (myelenate) axons of the neuron. Neurons have endings that branch out like a tree, allowing them to send and receive messages to and from different neurons spanning different directions. At some point, though, the message must be passed on from one neuron (pre-synaptic) to the next (post-synaptic) and this happens at the synaptic cleft, the channel between them.

This area has been the focus of many of the drugs you may know, because it's a fairly simple concept of blocking or encouraging the mail man to deliver his message. The message, which could be a sensory one, such as pain, may still be happening but if it is not transmitted then the brain cannot interpret it and it is as if it never happened. Spooky.

SSRIs

Selective Seratonin Re-uptake Inhibitors work to maximize the transmission of Seratonin (sometimes called 5-HT) which is known as the well-being neurotransmitter (transmitter of neuron messages at the synaptic cleft). It is given to those who suffer severe depression, as it is meant to maximize their sensation of happiness with fewer side-effects than the alternatives.


At the synaptic cleft, electrical currents traveling along the pre-synaptic neuron cause neurotransmitters to be released into the void. There, they have a few options: they can be admitted into the next neuron (post-synaptic) or leftovers can be taken back into the the previous neuron (pre-synaptic) to be recycled or reused.

Now what if we blocked the second possibility? What if we only allowed for the neurotransmitter to travel forward, exciting the next cell, sending a message of well-being to the body and brain? That is the work of SSRIs, they bind to the re-uptake proteins, only allowing for continued release of Seratonin with no returns.


Tardive Dysphoria

If you have ever heard the word "tardive" before, it is possibly in the context of drugs for schizophrenia or parkinsons. Oliver Sacks writes beautifully about this effect in Awakenings, where parkinsonian patients were given a new medication (L-dopa) which "awoke" them from their slowed states. They were essentially "normal", for a time, but then they started to revert back, to a state sometimes worse than previously. So what happened? Part of what makes life so amazing on the planet is its ability to adapt to circumstances.

Basically, after prolonged and high dosage use, the body adapts to the effects of the medication. It says to itself, well, heck, if you're going to keep giving priority to these transmitters over those ones, I'm just going to slow down producing and releasing them!

Once taken off the drugs, the body does not seem to regain its abilities to produce and release seratonin the way it did before. This leads to the chronic depression known as tardive dysphoria, a state even more difficult to treat than untreated severe depression, because it has become resistant to the effect of the drugs.

Moral of the story, medication for depression is meant only in severe cases and should be considered a temporary aid to treatment (with a set goal to discontinue). Treatment must also include talk-therapy, cognitive reframing therapy or other alternatives, to ensure lasting positive outcomes.