I have spoken to my neurologist today re my rls and insomnia
I have been taking Pregabalin 200mg and 30mg codeine for some time now and still suffer with both symptoms when I did increase the Pregabalin to 300 mg I suffered heart palpitations and had to reduce back down to 200mg but with no success
My neurologist suggests going back on to pramepaxole after I stopped taking it a year ago and going on to a low dose and gradually reducing the Pregabalin
I don’t have much choice but I’m reluctant to go back on to pramipexole having suffered severe augmentation last time
Any suggestions gratefully received
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Hoochybaby
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Difficult! I can imagine your reluctance to return to the pramipexole.
Have you discussed a stronger opioid? Like oxycodon or Temgesic? I had some insomnia on the oxycodone, but it helped to wait with going to bed until really sleepy.
Also, given that your RLS is still not sufficiently under control maybe that has to take priority over the insomnia? I do know that even when we think we don't sleep, we often still get some, sometimes far more than we think. Based on results from sleep studies compared to subjective classification of one's sleep.
Insomnia and rls can be caused by high carb diets which cause high insulin levels in the blood. Insulin drives the cells, and when you're lying in bed the muscles aren't moving so it drives rhe nerves and your brain is a big bunch of nerves. It also causes inflammation which makes the nerves more sensitive and causes rls.
As Lotte says, difficult. It's a shame the pregabalin doesn't suit you.
Also as Lotte suggests, codeine doesn't seem to be the best opioid for RLS. A low dose of a more potent opioid may be more effective and with less side effects. Targinact (oxycodone) is licensed for RLS in the UK and temgesic is becoming more accepted.
You may also be able to continue a (lower dose of) pregabalin in combination.
Your choice if you decide to start taking a low dose of a dopamine agonist again. In which case ropinirole may have a less risk of augmentation than pramipexole.
Hopefully you're aware of the roleof iron and vitamin deficiencies in RLS.
Blood tests for haemoglobin, ferritin, vitamin B12 and D would be a good idea.
If your ferritin is below 75ug/L then an oral iron supplement may help.
Reducing your carbohydrate intake may help, especially simple carbs i.e. sugars.
Pregabalin I have seen reports of addiction to Pregabalin
I have been taking 200mg Pregabalin and 60 mg codeine nightly for some time. Theses drugs are considered pain killers and as such classified as possible addictive drugs
What do you make of this report and also should the be taken in conjunction
I have also read that pregabalin is potentially addictive and possibly moreso gabapentin.
However, I believe they're only addictive if they're abused, i.e. taken to get a "high".
I've never had a high from gabapentin and to get one I think you'd need to do more than swallow the capsules.
They are dependency producing however, which is only usually a problem if you need to stop taking them.
Codeine is also dependency producing and potentially addictive. It's less than ideal for RLS in any event. Low dose methadone, oxycodone or buprenorphine are preferable. As they're more potent, then you only need a lower dose.
Generally speaking addiction is much less likely if you only take a drug exactly as prescribed.
The term "painkiller" covers a wide variety of meficines that act in different ways. The way they reduce pain may therefore be different and they may be used for other issues as well.
Pregabalin/gabapentin reduce glutamate levels and hence desensitise nerves. Hence they are used for epilepsy and nerve pain. They incidentally relieve anxiety and promote sleep.
Paracetamol and ibuprofen can be called "painkillers" but their primary action is to reduce inflammation, they can also help treat a high temperature.
Aspirin is a "painkiller", but is now more commonly used as a mild anticoagulant..
Cocaine and it's derivatives are used medically as "painkillers" but in this case as local anaesthetics.
Opioids are known as "painkillers" too, but they a used for other reasons e.g. in a very strong cough medicine or to control diarrhoea.
I guess dopamine agonists, gabapentinoids and opioids can be taken in a combination of any two.
Personally I'd only take a dopamine agonist again if everything else failed.
Levodopa was the first drug formally studied to treat restless legs syndrome (RLS). Also called L-dopa, it was first discovered as a treatment for the symptoms of Parkinson's disease over 50 years ago and then was tried on RLS patients. It works fairly quickly to reduce RLS symptoms and improve sleep quality. Sinemet is a combination of levodopa and carbidopa. This was the first medication I used years ago. I switched to pramipexole because it quit working. When I got off of Sinemet I did not suffer augmentation. Maybe this would be better for you. I am currently suffering from augmentation due to 1.5 mg of pramipexole. I went down to l mg and my body went crazy, so now down to 1.25 mg. ♥Also, what helps me is I bind my legs with ace bandages kind of tight until they calm down. I hope this helps. Many blessings your way.
Just to say, you do not get augmentation from getting off a drug. When you reduce or stop taking a dopaminergic drug, agonist or L dopa, you get withdrawal effects and possibly even DAWS.
Dopaminergic augmentation is caused by taking a drug, not stopping it.
Of all the drugs used (or once used), for RLS rotigotine is the least likely to cause augmentation, ropinirole is more likely to cause it and pramipexole the worst agonist for augmentation.
L dopa is the very worst for augmentation, surpassing all agonists.
L dopa should never be taken regularly for RLS, only intermittently 2 or 3 times a month.
I believe melatonin can make RLS wose because it inhibits dopamine.
However if you do want to boost your melatoin levels - at night, the natural way is to ensure you're exposed to full spectrum daylight during the day and avoid it at night.
Keep houselights dim in the evening and night. LED lighting and floursecent are the worst.
Avoid using any backlit device 2 hours before bed, TV, PC, Laptop, Smartphone etc. Some devices have a facility for filtering out the blue end of the sepctrum and this is better.
Light inhibits the release of melatonin.
This is one of the sleep hygiene measures.
Others include -
If you don't get to sleep in fifteen minutes, get up!
Always go to bed and get up at the same time.
Make sure the room is cool but not cold.
Make sure the room is dark.
Bed is for sleep and intimacy only : nothing else, no reading, watching movies etc.
There are dopamine rich foods, I'm not sure if they actually help boost dopamine levels.
Dopamine is made in the body from two amino acids. Amino acids come from digested protein. I'm not sure then if you eat adequate protein, that extra dopamine in the diet is necessary.
Interesting that I've just read that a lack of gut microbiota can inhibit this synthesis.
That is right Manerva; from what I have read, augmentation occurs while on the dopamine agonist drugs. These drugs somehow create additional receptor sites in the brain as one uses them over time. These receptor sites are what causes one to augment or easier said.. causes one to require a higher dosage to satisfy the new receptor sites, so yes, augmentation occurs while a person is taking the drug.
I'm afraid what you say isn't accurate. RLS is largely due to a lack of dopamine receptor sites, rather than a lack of dopamine.
The agonists compensate for this by stimulating the receptor sites which can relieve the symptoms.
However, this can raise dopamine levels. It has been shown that long term heightened levels of dopamine and long term use of agonists downregulates receptor sites.
This means that there are less functional receptor sites which means symptoms get worse - augmentation.
At this point increasing the agonist any more causes more downregulation and hence worsens the augmentation.
The solution to this is to reduce the agonist, which will restore function to some receptor sites.
However, it seems the agonist can cause permanent loss of some receptor sites so after having once augmented you are more.prone to augmentation in the future.
Dopamine agonists do not increase receptor sites, in effect they do the opposite.
The picture is further complicated in that another neurotransmitter, glutamate, is involved in RLS.
Some aspects of RLS are due to an excess of glutamate. Glutamate makes nerves more excitable or oversensitive and this can cause the insomnia aspect of RLS. Drugs which reduce glutamate levels can help control symptoms, relieve anxiety and promote sleep.
Hi Manerva, I will have to find the research article where I read that dopamine agonist have been discovered to actually create new additional receptor sites... I seem to recall that scientists at either John Hopkins or the Mayo Clinic here in the US gave the new sites a D1 or D2 name.... they contributed the need for higher dosages to the new discovery of additional receptor sites as well as what you have explained in your post. I'll see if I can dig it up.. I appreciate all the help this site offers and I would hope I am not posting incorrect information... will look a little deeper. Thks!
Reb, I think you are right. I read something along those lines as well. It has to do with the different dopamine receptor sites. If I recall correctly, DAs stimulates receptors D3 (and D2?) and after a while te non-stimulated D1 receptors get upregulated. Something lime that - from the top of my head.
I think I read a summary of it in Nightwalkers. Shall have a look an report back.
From Nightwalkers winter 2021 on a study by Dr William Ondo on dopamine receptor 1/5 antagonist ecopipam:
"..based on studies in our lab, we theorize that augmentation is a result of an increase in activity at the D1 receptors in the brain and spinal chord. We postulate that dopaminergic drugs [...] stimulate the D2/D3 receptors, which improves RLS, but they also stimulate D1 receptors to a lesser extent, which seems to worsen RLS. After time, when D1 receptors are upregulated, the drugs produce contradictory results."
Personally, even though being a scientist, I find this text a bit difficult to follow. I assume they left out some essential steps to keep the article concise. I'll fond the original paper; it was published in Journal of the Neurological Sciences.
Thank you Lotte - I agree, this particular article is a little difficult to interpret precisely. The article I read was a different article but along similar lines.
Hi Manerva, so sorry it has taken a while to get back on the article about augmentation creating new additional receptor sites. Work got the best of me the past few days. I went through my entire "Research File" on RLS last night and unfortunately I must not have printed and saved the article. I weaned myself off Ropinerole because I had augmented just a month or so prior to seeing the article so perhaps I didn't have the need to save it at the moment. So sorry I can't substantiate what I remember reading but will continue to do some research. My doctor says if I go back on medication we will try gabapentin. At this stage since we've discovered I have Helicobactor Pylori (currently being treated) we feel this was the trigger for my 7 months of agony with all the different RLS symptoms every single night. I wasn't absorbing iron orally so I had an iron transfusion. We can't rule out that I don't have the genetic genes for RLS but we can say with documented research that the H. Pylori could have brought on this bout. I have done an awful lot of research since on H. Pylori and this bacteria in the stomach can and likely did contribute to all the RLS symptoms. There are 3 or 4 mechanisms by which it does this by aggravating the CNSystem and the pheripheral nervous system. My symptoms are nearly gone, thank God. But now I'm aware I do have PLMovement. Oh well, I'll take that any day over the restless legs (and back and shoulders). This site is probably the best site I've been on in terms of trying to share factful information rather than just constantly giving complaints.
Hi. I've done a bit more reading on this and wish I hadn't.
The plot thickens!
I do know that both too much dopamine and also too little glutamate are associated with schizophrenia. I have also read that dopamine agonists have been considered as a treatment for schizophrenia as they downregulate dopamine receptors.
Unfortunately, I didn't save the link for the first article I found.
Although it may be that this downregulation is only true for D2 receptors.
I haven't yet found anything that says DAs upregulate DI receptors.
Interestingly, I've found evidence that glutamate (indirectly) alters the balance between dopamine D1 and D2 receptor signaling, i.e. upregulates D1 receptors.
Excess glutamate is also associated with RLS.
Trying to make sense of the story so far then
If D1 upregulation as well as D2 downregulation can lead to audgmentation
and
If DAs can cause DI upregulation of D1 as well as D2 downregulation
and
If excess glutamate also causes D1 upregulation
Then. as is already a recommendation, alpha 2 delta lignads should be used as a first treatment for RLS in order to avoid dopaminergic augmentation.
By inhibiting glutamate the ligands can prevent D1 upregulation and don't cause D2 downregulation.
BUT, if you're digging a hole and starts getting dark, time to stop digging!
WOW! and the wheel goes round and round... it does make me dizzy. You are quite the investigator so if anyone can make some linear sense out of it perhaps it will be you. Sometimes articles can be so poorly written that one's interpretation can be opposite other articles written on the same topic. I dig on the internet all the time; sure wish I could find that darn article!
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