Opioid Tolerance

[Oozz]

I started to ask the very first question above and figured that the poster had no idea why the doc said that. I REALLY want to know if there are any studies...I surely haven't seen any!

I bet a lot of it is just personal experience. Which shouldn't be discarded lightly. Even though I fully agree that we need more studies

My neurologist (who is a RLS specialist) is dead set against changing anything in my medication, on account that my RLS is contained right now. (I wanted to change something several times, so I had many discussions.) He says that he has seen patients struggle for months and years even after seemingly simple changes as going from one opioid to another, or being exposed to higher doses for a short time (for example in patients who got oxycodone after surgery). Yet I don't know any literature on that.

To say that something is truth, however, means you have proof. No doctor should say that something is X without qualification if there isn't proof. All the doc has to say is, "In my experience, when we use opioids to control the symptoms prior to getting the dopaminergic out of the system, the person has more problems and for longer. Blah blah blah. That is why we do XYZ." (Or whatever the experience is).

This is basically what my doctor said. He is very well known for RLS. He said in, his experience, that it could have an impact and gave a theoretical basis for why this could be the case. Generally, he does not recommend patients go from medication to medication without taking a drug holiday to return to baseline.

[Oozz]

I was told my doctor that going straigh ... baseline.

When I hear this sort of statement, I often wonder several things:

1. Does the doctor have any studies or data to justify the statement?
2. Does the doctor apply this equally to all patients, regardless of the severity of their RLS, their max DA dose, the length of time they were augmented, etc.?
3. Does the doctor understand the degree of suffering that a patient with severe or very severe RLS will undergo during a month long withdrawal and drug holiday?
4. How much of this is being done to justify the doctor's theory of the use of drug holidays, which do not appear to be supported by all of the RLS experts?

He’s very experienced treating RLS. I think his approach is justified and his rationale makes sense - particularly, given the context of my situation.

I’m not here to advise people in the wrong direction; however, I do share whatever new information comes my way and this was one thing that could help someone out with a similar problem.

[debbluebird]

I take gabapentin 1800mg at 7:30 pm. Originally I took 600mg three times a day. My pain Doctor had me take it all three times a day. I had stopped methadone and got a spinal stimulator to replace the methadone.
I also later added buprenorphine film .5mg at 2:30 pm to prevent insomnia.
You might have to switch your codeine to something better.
I started with Darvocet years ago. You can't get it anymore. Then methadone. I couldn't get it anymore after I moved to NM.
Good luck

[Oozz]

I’m wondering if the tolerance is at the opioid receptor or if it’s somewhere else in the RLS dysfunction.

[Oozz]

I figured out what caused this for me so I will update this post in case anyone else experiences this.

D1 super sensitivity. I basically developed augmentation in another part of my brain, most likely the nucleus acumben.

I was able to counteract the hyperarousal I was experience from any dopaminergic mediation with very low doses of Dipiridyamole - 18mg/night. I usually have to redose once during the night. It’s important to keep your Dipiridyamole dose as low as possible since you will develop tolerance.

[badnights]

I figured out what caused this for me so I will update this post in case anyone else experiences this.

D1 super sensitivity. I basically developed augmentation in another part of my brain, most likely the nucleus acumben.

I was able to counteract the hyperarousal I was experience from any dopaminergic mediation with very low doses of Dipiridyamole - 18mg/night. I usually have to redose once during the night. It’s important to keep your Dipiridyamole dose as low as possible since you will develop tolerance.

I am interested in this but I don't quite understand. I think this is what you're saying, please confirm or clarify: you developed augmentation from methadone.( This augmentation consisted of the typical augmentation cycle of symptoms worsening, dose increase, further worsening, etc.) Your RLS specialist theorizes that by starting methadone while still augmented from a DA, your dopamine receptors never normalized, and that this might have somehow caused or contributed to the opioid augmentation. You have now figured out that your opioid augmentation was caused by super-sensitivity of the D1 dopamine receptors - ? Could you please clarify this for me?

I understand that dopamine receptors are down-regulated, particularly in the nucleus accumbens, after chronic methadone use, but your augmentation happened within a few months, is that long enough to be say your methadone use was chronic?

I missed something else in your story, probably because I was off the board for so long; are you now taking dopaminergic meds?
Thanks

[Oozz]

I developed augmentation in another part of my brain. I.e, The pathological presentation of augmentation occurred in another part of my brain. It presented as a constant hyperarousal which prevents me from sleeping. My akathisia was entirely controlled, but I could not sleep. It was not “alerting” from opioids. Low dose Dipiridyamole, which can activates the A1 receptor, counteracts it. As does clozapine, a d1 antagonist.

I, with the help of chatGPT Pro, figured out the solution. Hours and hours of research, various experiments… I have not been entirely happy with the support I have received from RLS experts, many just tossed up their hands and said they could not help me. Honestly, many outright dismissed me. Despite this, one was open-minded enough to listen and I’ll forever be grateful.

[badnights]

Wow. I'm reading this while brain-dead so I will have to come back to it when I'm more normal.

I used to get (still get?) alerting from my opioid medication. It was a "constant hyperarousal which prevented me from sleeping" - akathisia entirely controlled but unable to sleep. What, then, is the difference between what I call hyper-alertness from opioids and what you are calling augmentation in another part of the brain? Could they be the same thing?

Since augmentation is by definition a worsening of the WED/RLS disease, which consists primarily of an urge to move (usually accompanied by nasty sensations), can the constant hyperarousal you experienced with methadone properly be called augmentation?

But whatever it's called, it's fascinating that the dipyridamole counteracts it. I wish there were more studies being done to chase all these things down.

one was open-minded enough to listen and I’ll forever be grateful.

Love that.