Tourettes experimentally being treated with Mirapex

[guy123]

Source: http://www.news-medical.net/?id=43658

 

Kurlan and his colleagues are studying a drug called Mirapex (pramipexole). The drug is approved by the Food and Drug Administration for use in patients with Parkinson's disease and restless leg syndrome.Mirapex is a dopamine agonist; it stimulates dopamine production in the brain. Small pilot studies with the drug in TS patients have shown good outcomes and few side effects. Mirapex is investigational in patients with Tourette's syndrome.

 

"It would seem to be counter-intuitive to stimulate more chemical activity in the brain when we know that there already is an imbalance in Tourette's patients," said Kurlan. "However, we believe that this might actually cause the dopamine receptors in the brain to adapt and desensitize so that they start reacting less to the overactive dopamine."

 

I bolded the important parts, and I understand theoretically how that would work.

 

My question is, then, when someone comes off the medication, do they experience Parkinsonism? It sounds like after being on the medication for a while, the brain would have adapted to the increased dopamine by desensitizing or downregulating or whatever it does in the presence of too much of something. So it's returned to "baseline" but with more dopamine. Now you remove the medication, suddenly the brain is experiencing "not enough dopamine (relative to "baseline") = Parkinsons.

 

I wonder what the chances are if I emailed the doctor in that study my question that I would get a reply. I'm gonna try.

[Chemar]

many Parkinson's forums have some very alarming reports about Mirapex and reckless/compulsive behavior side effect

 

here is the legal side

http://injury-law.freeadvice.com/drug-toxi...rex-warning.htm

 

more information

http://www.mirapex-rx-for-disaster.net/mir...de_effects.html

 

with the frequency of severe compulsive disorders comorbid with TS this would seem very problematic to me

[kim]

will be interesting to read what Cheri posted when I get a chance.

 

Guy,

 

 

Guy

 

Hey, I thought your med chart was fabulous!

 

My thoughts on this are the same as with most of the drugs used for movement disorders. Good luck to them. Long term, these things just don't seem to work very well. If my understanding of the term "plastic" is correct, the brain has a great ability to change. If this would work, why wouldn't it happen normally? Too much dopamine.... theoretically, the brain should down (regulate) dopamine receptors (or presynaptic release of dopamine) on it's own in the first place, no?

 

A young friend of mine pops to mind. He was placed on two drugs that worked on blockade of the same receptors. His neuro saw what he was on and asked if the prescribing physician was crazy and made the remark that he would have parkinson's by the time he was 30. Seems the likelyhood of Parkinson's would depend on how many receptors were reduced (or the amount of presynaptic realease possibly increasing the amt of post synaptic receptors), and if they have the ability to return to an altered baseline and "stick" once the med was discontinued, if that's the intention. I suspect that first they are trying to see what happens with continuous use at a certain level, not with the intention of altering pathways then discontinuing drug use.

 

I have to think about TD here too. How is it that long term use of a dopamine antagonist can cause symptoms that are almost indistinguishable from origninal sysmptoms? TD sometimes remits and sometimes it doesn't. Why? Individual levels of brain plasticity makes the most sense to me, and how can that be determined until it's too late? Would luv to hear any of your thoughts on my ramblings Guy!

[guy123]

My thoughts on this are the same as with most of the drugs used for movement disorders. Good luck to them. Long term, these things just don't seem to work very well. If my understanding of the term "plastic" is correct, the brain has a great ability to change. If this would work, why wouldn't it happen normally? Too much dopamine.... theoretically, the brain should down (regulate) dopamine receptors (or presynaptic release of dopamine) on it's own in the first place, no?

 

I've heard that offered as a hypothesis why some people "grow out" of TS as they reach adulthood. The brain is too sensitive to dopamine (or whatever is going on) during youth, and so it "auto-compensates" by making itself less sensitive (or downregulating, or whatever it does) as the brain matures. I believe it was also used to support the idea that TS that persists into adulthood rarely goes away (the brain is already "developed" how it's going to develop, with the dopamine abnormality (or whatever is causing the TS)).

 

This is why I wonder if stem cells hold a possible solution. Get some stem cells to regrow/repair the basal ganglia (or whatever part of the brain is affected) correctly, instead of with the TS defect. Problem solved (theoretically). That would be a legit "cure." No more maintenance medication, no more symptom-suppression medication. The brain would now be operating correctly on its own.

 

A young friend of mine pops to mind. He was placed on two drugs that worked on blockade of the same receptors. His neuro saw what he was on and asked if the prescribing physician was crazy and made the remark that he would have parkinson's by the time he was 30. Seems the likelyhood of Parkinson's would depend on how many receptors were reduced (or the amount of presynaptic realease possibly increasing the amt of post synaptic receptors), and if they have the ability to return to an altered baseline and "stick" once the med was discontinued, if that's the intention. I suspect that first they are trying to see what happens with continuous use at a certain level, not with the intention of altering pathways then discontinuing drug use.

Do you recall what drugs he was on? Were they for TS?

 

I have to think about TD here too. How is it that long term use of a dopamine antagonist can cause symptoms that are almost indistinguishable from origninal sysmptoms? TD sometimes remits and sometimes it doesn't. Why? Individual levels of brain plasticity makes the most sense to me, and how can that be determined until it's too late? Would luv to hear any of your thoughts on my ramblings Guy!

 

Supposedly one of the conditions that www.23andme.com can genetically test a predisposition for is Tardive Dyskinesia. I think such testing should be mandatory before use of neuroleptics, at least so the patient has an idea if they are at significant risk for developing TD.