Restless Legs Syndrome (RLS) Discussion Board

For RLS - is it possible for the legs to be better i.e. no twitching, pain etc but the sleep problems persist?

I suspect that the answer to that is yes, but I don't know for sure. However, there are other things that can disturb sleep, such as sleep apnea. When I first saw a sleep doctor and went through a sleep study, the results showed that I had two separate conditions. I have a form of sleep apenea specific to thin people and PLMD. Of course, I also have RLS when I am awake and trying to go to asleep.

fuz_mind wrote:For RLS - is it possible for the legs to be better i.e. no twitching, pain etc but the sleep problems persist?

Absolutely yes. This is actually the usual pattern of people with moderate to severe RLS. Leg jumping (urge to move) controlled with medicine, but sleep still a serious problem.

It is known that the urge to move symptom is primarily mediated via the dopamine pathways, which are what the DAs (dopamine agonists like Requip and pramipexole) primarily work on. The sleep pathways are mostly mediated via the glutamatergic pathways, which the dopamine agonists don't have much effect on. Gabapentin, Lyrica, and Horizant help those. Also sleep seems to get better with THC, kratom, and dipyridamole. Dipyridamole is an adenosine booster and improves both the dopamine pathway and glutamatergic pathway. IV iron addresses the underlying problem (Brain Iron Deficiency) and via adenosine and the dopamine and glutamatergic pathways, improves both urge to move and sleep.

stjohnh wrote: The sleep pathways are mostly mediated via the glutamatergic pathways, which the dopamine agonists don't have much effect on. Gabapentin, Lyrica, and Horizant help those. Also sleep seems to get better with THC, kratom, and dipyridamole. Dipyridamole is an adenosine booster and improves both the dopamine pathway and glutamatergic pathway. IV iron addresses the underlying problem (Brain Iron Deficiency) and via adenosine and the dopamine and glutamatergic pathways, improves both urge to move and sleep.

Everybody is different. I had the same issues (RLS very well controlled through opioids but insomnia), but Gabapentin/Lyrica did nothing for me (except causing depression). But there are other options, at least in some cases: Apparently I have a melatonin deficit, I''m sleeping a lot better (though not nearly as good as healthy people) taking melantonin, tryptophan, and a teaspoon of gaba (Gamma-Aminobutyric acid) at night. (Tryptophan is required to produce melatonin, so that one boosts melatonin too.) But my doctor says that a melatonin deficit is fairly rare in his opionion. I do need the mix however, tryptophan alone helped for a couple of days but lost efficiency quickly, the melatonin helped a bit, but the gaba is the thing that nudges me into sleep.

thanks so much for the replies.

the information is really helpful for me to understand and normalise things a bit! from my doc's reaction, i was starting to wonder if this was (i.e. am I) even normal or possible.....given how much medication I'm taking.

i'm so exhausted that it's really not funny at all.....

Frunobulax wrote:

stjohnh wrote: The sleep pathways are mostly mediated via the glutamatergic pathways, which the dopamine agonists don't have much effect on. Gabapentin, Lyrica, and Horizant help those. Also sleep seems to get better with THC, kratom, and dipyridamole. Dipyridamole is an adenosine booster and improves both the dopamine pathway and glutamatergic pathway. IV iron addresses the underlying problem (Brain Iron Deficiency) and via adenosine and the dopamine and glutamatergic pathways, improves both urge to move and sleep.

Everybody is different. I had the same issues (RLS very well controlled through opioids but insomnia), but Gabapentin/Lyrica did nothing for me (except causing depression). But there are other options, at least in some cases: Apparently I have a melatonin deficit, I''m sleeping a lot better (though not nearly as good as healthy people) taking melantonin, tryptophan, and a teaspoon of gaba (Gamma-Aminobutyric acid) at night. (Tryptophan is required to produce melatonin, so that one boosts melatonin too.) But my doctor says that a melatonin deficit is fairly rare in his opionion. I do need the mix however, tryptophan alone helped for a couple of days but lost efficiency quickly, the melatonin helped a bit, but the gaba is the thing that nudges me into sleep.

I don’t believe GABA crosses the blood brain barrier, so you are better off supplementing with a GABA precursor. You can find that information the web. With your doctor’s consent, you may want to add magnesium to the mix and ensure your bedroom temperature is cool enough, 60-67 degrees is recommended. That will help your circadian rhythm stay balanced which facilitates better melatonin production.

Rustsmith wrote:I suspect that the answer to that is yes, but I don't know for sure. However, there are other things that can disturb sleep, such as sleep apnea. When I first saw a sleep doctor and went through a sleep study, the results showed that I had two separate conditions. I have a form of sleep apenea specific to thin people and PLMD. Of course, I also have RLS when I am awake and trying to go to asleep.

Hi Rustsmith

I just took a double take at your reply. you have sleep apenea specific to thin pple? No intention of being instrusive or rude here, but just curious that there is a condition like this?

I think that medications also add to the complexity. They change our brain chemistry, make us more or less able to stay asleep, more or less able to awaken, more or less able to get the necessarily phases of sleep...etc. Combine it all? Who knows what any one person ends up with and how different it might be than the next person.

I just took a double take at your reply. you have sleep apenea specific to thin pple? No intention of being instrusive or rude here, but just curious that there is a condition like this?

rustsmith is on holidays and may answer more fully when he returns. He was diagnosed with Upper Airway Resistance Syndrome (UARS). (I was also diagnosed with it.) It was controversial at the time - some doctors thought it wasn't a thing, others were adamant that it was. I don't know if it's still as controversial. Some sites now describe it as on the spectrum between normal sleep breathing and obstructive sleep apnea. The key difference is that breathing doesn't actually stop (i.e. there are no apneas), but there are episodes when breathing is abnormally shallow - one could say, it almost stops (i.e. there are hypopneas)

ViewsAskew wrote:I think that medications also add to the complexity. They change our brain chemistry, make us more or less able to stay asleep, more or less able to awaken, more or less able to get the necessarily phases of sleep...etc. Combine it all? Who knows what any one person ends up with and how different it might be than the next person.

For me this is so true. It's the meds that cause insomnia. I hate it. I get my legs calmed down, then I'm wide awake. My solution which works most of the time, is to space out the drugs over 24 hours.

For me this is so true. It's the meds that cause insomnia. I hate it. I get my legs calmed down, then I'm wide awake.

Me too!!!

Hi Rustsmith

I just took a double take at your reply. you have sleep apenea specific to thin pple? No intention of being instrusive or rude here, but just curious that there is a condition like this?

Beth's reply about UARS is the condition that I have. It still remains somewhat controversial, mostly because the number of sleep labs that can actually test for it is still extremely limited. It involves a lesser form of apnea that does not result in oxygen loss like standard obstructive sleep apnea. However, it is more likely to cause micro-awakenings each time there is an event, which is very problematic when you also have severe PLMS. In my sleep test (at a lab that was set up for monitoring for UARS), I was being awakened by UARS or PLMS about every six minutes. So it wasn't any wonder that I was so sleep deprived.

Treatment for UARS is also very controversial since there have been so few studies and this means that insurance will not cover anything. Sometimes CPAP is recommended and other times they suggest a dental device. The extreme is a surgical procedure that is supposed to help, but the reviews that I saw more often than not reported on serious side effects with little benefit for the UARS.

I found adding dipyridamole to my combination of meds had a very beneficial impact on my general sense of well-being and of feeling rested and ‘myself’ during the day. This has persisted even though I discontinued dipyridamole after about 10 months. In general I would observe though that rls is a very idiosyncratic condition and individual response to the various treatment options seems to vary widely.

thanks for all the explaination and sharing!

sorry that I have been off the boards for a while again hence delayed response

Oozz wrote:

Frunobulax wrote: Apparently I have a melatonin deficit, I''m sleeping a lot better (though not nearly as good as healthy people) taking melantonin, tryptophan, and a teaspoon of gaba (Gamma-Aminobutyric acid) at night.

I don’t believe GABA crosses the blood brain barrier, so you are better off supplementing with a GABA precursor. You can find that information the web. With your doctor’s consent, you may want to add magnesium to the mix and ensure your bedroom temperature is cool enough, 60-67 degrees is recommended. That will help your circadian rhythm stay balanced which facilitates better melatonin production.

I know that GABA is not supposed to cross the blood brain barrier, but I do get an immediate reaction if I take it in large enough quantities. (Immediate means after 15-30 minutes.) So either taking a large quantity brings a bit into the brain via diffusion, or something else is working here.

I take large quantities of magnesium. If only the bedroom temperature would help I suffer from CFS and all my neurotransmitters are way down, despite supplementing all the precursers like Tryptophane and Tyrosine in large quantities.