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Re: Suggestions on treating Tardive Dyskinesia TD? SLS

Posted by undopaminergic on October 31, 2020, at 4:17:40

In reply to Re: Suggestions on treating Tardive Dyskinesia TD?, posted by SLS on October 30, 2020, at 15:25:04

> A friend of mine has been diagnosed as having Tardive Dyskinesia. She is being treated for depression (possibly bipolar). She took Abilify for a number of years, but has been off of it for at least a year. More recently, she has tried Latuda and Vraylar. Her symptoms so far are limited to some minor tongue movements.
> What do you think?
> 1. Using another AP?

APs can mask the symptoms, and therefore can offer some relief, but since they are also the *cause* of TD, I would worry they could make it worse.

> 2. Using an anticholinergic medication?

From what I've read, anticholinergics are effective for early antipyramidal symptoms, but not for tardive dyskinesia.

> 3. Alternative treatments - Vitamins? Supplements? Anti-oxidants?
> That's about all I know.

That is pretty much what I know too.

> ***** There are two new drugs approved specifically for treating TD *****
> 1. valbenazine (Ingrezza)
> 2. deutetrabenazine (Austedo)
> Your doctor has hopefully discussed this with you. They are probably prohibitively expensive. I dont know. Below, I wrote a brief descripton of the mechanism of action.
> Both of these drugs have the same novel mechanism of actions that doesnt involve dopamine receptors.

They affect dopamine receptors indirectly, by depleting presynaptic dopamine stores.

There is nothing novel about their mechanism of action. Reserpine has been known for ages, and tetrabenazine has also been known for a long time. In other words, the new agents you mention sound like "me too" drugs to me.

> TD presumably occurs because postsynaptic dopamine receptors become super-sensitive when they are blocked by an antipsychotics for too long.

That is the best theory.

> The mechanism of action of the new drugs involves preventing the presynaptic neuron from releasing too much dopamine into the synaptic cleft, which would otherwise overstimulate the postsynaptic receptors (the ones that became super-sensitive because of antipsychotic use). This is accomplished inside the presynaptic neuron by preventing dopamine from refilling the releasing vessicles. Technically, these drugs are both VMAT2 inhibitors.


> In other words, the neuron cant spit because its mouth is dry.

Beware though that these drugs, through the same mechanism of action, can worsen depression, especially anhedonia and apathy, but probably attention, concentration, and energy levels too.





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