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  • BDD Moderators: Keif’ Richards | negrogesic

What causes RLS during opiate withdrawal?

pema

Bluelighter
Joined
Feb 15, 2012
Messages
60
What is the cause of the Restless Leg Syndrome?
RLS is a big problem for me during withdrawal. I have to find something to alleviate my withdrawal RLS. But I don't want to eat a hundred tablets and hope that one will work. If possible I don't want to take muscle relaxants like tetrazepam or any other benzodiazepines. If possible I don't want to take any medicaments which need to be prescribed.

First of all the most important question is surely: Is it really RLS? Is that what tortures us during withdrawal really RLS? Is it the same illness or a completely other thing that we just call the same?
Or maybe it is akathisia? Or PLMS? (I don't know if PLMS is the right abbreviation. The German expression is "periodische Beinbewegungen im Schlaf". Translated that would be: Periodic Leg Movements during Sleep)?
Is it really RLS? Is withdrawal-RLS the same as "normal" RLS? If it is the same, I can be treated the same way. If it is something else with just the same symptoms, I probably has to be treated somehow different.

Can magnesium and calcium help? When I have no deficiency, than probably taking magnesium/calcium will not help?
But maybe I get such a deficiency in withdrawal? A found a study that tells something about changed mineral levels during withdrawal. I do not know how this can be. I have no idea what could be the cause but it seems that some mineral/trace element levels change during withdrawal. (How can that be?)
Furthermore, in withdrawal syndrome, Fe, Mg, Mn, and Ti levels were diminished and Al, Ca, and Cu levels were increased ... Moreover, Mg, Mn, and Se levels were also diminished and Al level was increased
Source:
Cemek M, Büyükokuroglu ME, Hazman Ö, Bulut S, Konuk M, Birdane Y. Antioxidant enzyme and element status in heroin addiction or heroin withdrawal in rats: effect of melatonin and vitamin E plus Se. Biol Trace Elem Res. 2011 Jan;139(1):41-54. Epub 2010 Feb 24.
OK. Those are rats in the study. Needn't be the same in humans but seems so be interessting. Let's assume it is the same with humans.
Then could a mineral deficiency cause RLS? I think I read that an iron deficiency could be a cause of RLS. And magnesium deficiency could be a cause, too (or was magnesium only a cause of muscle cramps?)
Then it is maybe possible to defeit RLS with iron or magnesium supplements. But I am not sure if this is really the cause. I'm just trying to find possible causales.
Are there any studies on mineral/vitamine/trace elements levels during withdrawal in humans? I couldn't find anything.

Or maybe withdrawal-RLS has something to do with dopamine levels? Something like temporarily parkinsons disease? Then could L-Dopa treatment help?
Withdrawal and dopamine levels seem to correleate in some way. Dopamine agonists help with parkinson and with opiate withdrawal.
But again I am not sure if maybe a too low dopamine level could be the cause of the RLS.
It seems like medical doctors are not really sure what causes RLS and then maybe they know even less what causes RLS during withdrawal. But maybe somebody knows more than me. Or mabe there are some clinical studies that I could not find.

BTW: I always suffer from RLS during withdrawal and all the addicts I know have the same problem. When I read in internet forums, it seemed for me that RLS is a "usual" withdrawal symptom. But now I found this study:
Scherbaum N, Stüper B, Bonnet U, Gastpar M.: Transient restless legs-like syndrome as a complication of opiate withrawal. Pharmacopsychiatry. 2003 Mar-Apr;36(2):70-2.
This analysis revealed 15 out of 120 patients who had described the symptoms of transient RLS emerging during opiate detoxification treatment.
Only 15 out of 120 patients?? That would be only 12,5%. I really thought, that nearly every addict had this problem. Not? Wrong numbers?
Do you suffer from RLS during withdrawal? Any experiences?


Has anybody found a remedy that really help with RLS during withdrawal?
I thought of trying L-Dopa because it is easy to get in form of mucuna pruriens extract capsules. But those capsules alone would be useless to increase dopamine in the brain. It makes no sense without a decarboxylase inhibitor and no doctor would prescribe this to me. Maybe it is possible to prevent L-Dopa from getting metabolized to early so it can pass whe blood brain barrier with the help of green tea extract?



The website www.rlcure.com claims to have "an absolute cure for RLS". Following the author, RLS is caused by inflammation processes in the body.
I know that there are diseases like rheumatism or arthritis are caused by inflammation processes in the body. But I don't know if this can be THE cause of RLS, too.
I think, some doctor should have realized it. It is possible to detect inflammations in the body by some blood values.
And I think that some RLS patients should have realized it, too. If RLS would have been caused by inflammation then it should probably stop, when a patient takes glucocorticoids like cortisol/hydrocortisone, prednisolone, ... So the inflammation theory sounds a little bit unlogical. But I had only a short look on this website.
When I have a little more time, I will read it more precisely.
 
I'm guessing it has to do with a lack of dopamine because anti-psychotics such as Olanzapine antagonize dopamine receptors and are known to cause RLS.
 
Interesting read...

I thought the following article was an interesting read in relation to what causes RLS during opiate WD:

A narcotic addict experiences this "jerking" due to the abrupt cessation on the endorphins the brain was receiving from an outside source. The body and brain are finely tuned and during the abuse of narcotics, the brain slowed down on production as it sensed the outside source of dopamine (endorphins). The brain will heal fortunately to the degree that the brain will begin producing adequate endorphins again. The incidence of RLS among addicts who exercise is less than among addicts who are sedentary. During withdrawals, exercise can help produce the much needed endorphins and can actually reduce the symptoms of RLS for the recovering addict.

The symptoms of the condition tend to occur at exactly the wrong time—when people are trying to relax or sleep. As quality and quantity of sleep become an issue, daytime fatigue and exhaustion follow, affecting work and mental performance

Although the cause of RLS is unknown, researchers believe that it results from abnormal functioning of the central nervous system. RLS produces excitability in a region of the brain known as the subcortical area. This excitability is caused by a dysfunction in a nerve-signaling chemical called dopamine. Dopamine is a central neurotransmitter that is particularly important in the regulation of movement.

The exact prevalence of RLS is undetermined. It may be more common than is currently thought because people may not report it to their physicians, and some physicians may wrongly attribute the symptoms to nervousness, insomnia, stress, arthritis, muscle cramps, or aging. RLS is associated with diabetes and smoking. Studies show that it affects between 1 percent and 5 percent of younger adults and up to 20 percent of adults older than 60 years. There is also a clear familial connection; about one third of patients with RLS have multiple family members who are also affected by the condition. There are those who suffer from RLS chronically and those who have it only temporarily, which incudes an addict during withdrawals.

Iron and Dopamine Abnormalities

The brains of patients with RLS exhibit abnormalities in the relationship between iron and dopamine. An enzyme involved in dopamine synthesis—tyrosine hydroxylase—requires iron for proper function. In animal studies, iron insufficiency appears to cause abnormal dopamine function. It is believed that patients with RLS may have impaired iron absorption in the brain . The iron deficiencies are pronounced in certain parts of the brain that help control body movement. In autopsies of people with RLS, iron levels have been particularly low in a region of the brain called the substantia nigra.

Further evidence of the relationship between iron deficiency and RLS is found in the three major secondary causes of RLS—end-stage renal disease, pregnancy, and iron deficiency, which all involve low levels of iron.

Source - http://www.medhelp.org/tags/health_...Leg-Syndrome-and-Opiate-Withdrawal?hp_id=1098
 
The problem is that I don't know if this is real RLS. Maybe it is akathisia? Or PLMS? Or something else.
Who said that this withdrawal symptom is really RLS? I could not find real medical texts.
All tese illnesses seem to be caused from different things and should probably not be treated the same way.
I would really be glad if I knew what causes this withdrawal RLS.
Until now I will assume it is (temporary) RLS.

I looked which possibilities there are to treat normal RLS.

Iron deficiency could be a cause. I found a study that said that Fe-levels are reduced in heroin addicts. So I tried to supplement iron. I took it for a month. No effect, I think. I don't know if my withdrawal RLS would be worse if I had not supplemented iron. But in any case: I reduced my methadone dose and I woke up with this ugly RLS which stopped after taking a little more methadone.

Then it is said that valerian root would help a lot of people suffering from (real) RLS.
So I took the strongest valerian root capsules that I could find. I took them nearly 2 weeks and reduced my methadone dose. Again I woke up with RLS. I did not help me.

Consider dietary supplements. Check with a doctor or nutritionist to find out if you’re low on iron, vitamin B, folic acid, or magnesium. Deficiencies can bring on restless legs syndrome (RLS).
- Iron did not work.
- I also supplemented magnesium and calcium (400mg magnesium daily and 800mg calcium). Some magnesium compounds are quickly absorbed by the body (e.g. magnesium citrate) while others take a quite long time. It is said that it should be necessary to take magnesium over longer time in order to fill the body storage. I took magnesium oxide and magnesium citrate for about one month. Maybe it helps to reduce muscle cramps (e.g. leg cramps) but still RLS began when I reduced my methadone dose.
- Vitamin B and folic acid. Folic acid is belongs to the vitamin b complex, too. I took a high dosed vitamin b complex which also contained folic acid. I took it for maybe 3 weeks. No effect for me. Again I woke up suffering from RLS.

Cut back on caffeine. Caffeine often makes the symptoms of restless legs syndrome (RLS) worse. Try reducing or eliminating your consumption of coffee, tea, soft drinks, and caffeine-containing foods such as chocolate.
I stopped drinking coffee last year. I usually drink tea but I stopped it. No tea, no coca cola. Nothing with caffeine. Neither chocolade, altough it contains nearly no caffeine.
It did not work. I cannot tell if RLS would be worse if I had not done this. But actually RLS was worse.

Alcohol and cigarettes shall be able to worsen RLS. I drank no alcohol since the beginning of this year.
But I still smoke...
Some medicaments shall also be able to worsen RLS, especially Diphenhydramine. I did not use this. (Actually I'm afraid of using it for withdrawal. I wanted to try it once in order to help me sleep, but a friend told me that it dreadfully increased his RLS. It seems that a lot of addicts have already made this experience. So I will not try.)

I tried to change my nutrition/diet. I ate as somebody who suffers from rheumatism. For example, I did not eat foods high in arachidonic acid. I did this for more than three weeks.
The same results. I cannot tell if it probably helped to decrease the severity but I stiff suffered from RLS and it was no fun. I would say it did not work.


Maybe all of those things together could help to decrease the severity of RLS. I have not tried it all together. But none of this methods alone was able to stop my RLS or to decrease it to a tolerable level.
But when my RLS starts, usually I also have leg cramps from time to time. I bought "Ben Gay" for that case and some quinine tablets. I realized that I did not need them. OK. When I woke up at night, suffering from RLS, I took another methadone dose in order to stop it.
Maybe this time was too short for leg cramps to occur. But usually this starts quickly for me. It seems that those methods were probably able to prevent leg cramps.


I do not believe in homeopathy. The theory behind this is unlogical. But I don't want to explain this now.
There are a lot of people who say that homeopathy actually helped them. Maybe placebo, maybe not. I will give it a try.
Hyland's sells those preparations: "Restful legs", "Leg Cramps" and "Leg Cramps PM". I searched online and found some postings in drug forums where people wrote, it alleviated or stopped their restless legs syndrome.
I do not think that it will help me, but I will buy "Restfull Legs" and try it.


There are a lot a similarities between RLS and Parkinson's Disease. Maybe the problem is a dopamine deficiency in the brain (or in some parts of the brain) or a neurotransmitter imbalance. This could be possible because low dopamine levels are not only a problem of Parkinson patients but also of drug addicts during withdrawal.
I will try to increase my brain's dopamine levels.
Dopamine is not able to pass the blood-brain-barrier. So Parkinson patients will get L-dopa which is the precursor of dopamine. It is able to pass the BBB and gets then converted to dopamine. That's the theory.
It seems to be possible to supplement Mucuna pruriens which contains a lot a L-dopa. Those mucuna extracts are sold in order to raise dopamine levels. But actually that does not really happen.
L-dopa will get metabolized too early to dopamine in the body. This results in high dopamine levels in the body but not in the brain because when converted to dopamine, it is no more able to pass the BBB.
It has to be prevented that L-dopa gets metabolized already in the body. This shall only happen in the brain when L-dopa has passed the BBB.
In order to reach this, doctors give their patients not only L-dopa but L-dopa plus a decarboxylase inhibitor (like Carbidopa).
This way it is possible that L-dopa reaches the brain (without being metabolized to dopamine) and there it becomes dopamine then.
Unfortunately Carbidopa is a prescription-only medicament and I have no idea what to tell my doctor in order to get it. Every test would show that I have no Parkinson or something else.
So I searched for herbal decarboxylase inhibitors. There is only one herb that maybe could do the job: green tea. But probably it is not enough to drink just some cups of tea. So I ordered the strongest green tea extract, high in EGCG, I could find. (And maybe I will try to take it together with quercetine).
Then I will not use Mucuna pruriens because a found pure (and cheap) L-dopa on ebay.
I found some texts that say that the effects L-dopa supplementation (in healthy persons) can first be felt after 5-7 days. So I will try it for a little more than a week before reducing my methadone dose.

It seems that Parkinson's disease is not only related to dopamine alone.
MDMA (which has effect on serotonin) helped Parkinson patient and I think, in Russia those patients are also treated with GABA-drugs. I read advices of using phenibut and picamilon.
Maybe taking phenibut or picamilon could help to alleviate or stop my withdrawal RLS. I also read posting where people wrote that gabapentin, baclofen and pregabalin helped to reduce withdrawal severity.
But all of those medicaments are only to get on prescription (at least in Germany).

GHB/GBL is able to nearly stop opioid withdrawal symptoms completely. It also helps to sleep and stops RLS. It reduced the severity of all my withdrawal to maybe 10%. And made withdrawal quite easy. Escpecially because I was able to sleep.
Although it will not metabolize to GABA, it shall increase the GABA effects.
Benzodiazepines also work on GABA receptors but on the wrong type, as it seems. Benzos did not help me during opoiod withdrawal.

Another natural thing which helped a lot of people is "exercise" or "movement".
People suffering from "normal" RLS tell that their symptoms are less severe the more they moved their legs. To go for a longer walk over the day seems to alleviate the symptoms during the night. Exercising shall do the same.
I was not able to try this. I have a really bad leg injury. Some weeks it was inpossible to stand up for me. I am lucky that I can walk on crutshes now but I am still always in pain. It is not possible for me to go for a walk or to exercise with my leg.

How and cold showers seem to help some patients when RLS gets too strong during the night. I cannot try this, too, because of my injury´and my wound dressings/bandages that cover my feet and half the leg.

To promote wound healing, I take some herbal remedies to improve vein-related blood flow. For example I take horse chestnut pills since nearly half a year. Some doctors advice their RLS-patients to try these pills, too.
It seems not to influence my RLS.
There are some other herbal remedies to improve blood circulation that shall help some patients with RLS but I forget the names of the herbs.

Supplemention with 300 I.E. Vitamin E per Tag is said to help. But there is not a single study that proves any effect on RLS. I am not sure if this really helped somebody. But I read this some times.
I had no idea how much 1 I.E. is (I.E. is the German abbreviation for "Internationale Einheit" = international unit. So probably the English abbreviation is I.U..) - so I looked it up. I do not know how this system works. It seems to be a different amount for every vitamin. For vitamin E 1 IU means 910mcg dl-alpha-tocopherol or 670mcg d-alpha-tocopherol.
Vitamin E is often given to oil capsules in order to longer the sell-by-date. I eat Nigella sativa capsules to reduce the pain of my leg injury. The package says every gel capsule contains 500IU of d-alpha-tocopherol. So I took 1500IU per day and this did not help with RLS.


L-Tryptophan is an amino acid that helped some people. While it does not work for some patients, it is a wonder medicine for others.
(Sandryk, R., L-Tryptophan in the treatment of RLS. Letter to the publisher. Am J. Psychlat. 143 (4) 534..., 1986
It is a natural, essential amino acid. It is possible to eat foods that are high in tryptophan but I am not sure if this helps because I think tryptophan competes with other amino acids to pass the blood brain barrier. Probably it is the best to take L-tryptophan without (protein rich) food on empty stomach.
Supplemention of 2-3g L-tryptophan in the night time lead to a dramatically improvement of sleep and RLS.
L-tryptophan gets metabolized to 5-HTP and this then to serotonin.
I knew that dopamine deficiency can cause RLS but never heard that serotonin could help.
When this really helps, then probably supplementation with 5-HTP + decarboxylase inhibitor would do the same. Perhaps serotonin reuptake inhibitors can also help. Perhaps could St. John's wort supplementation help, too. I have to get more information on this.
Maybe I will try this before trying to increase my dopamine levels.


These are my reflections and trials until now.
If somebody tried other things or had success with one of the remedies that did not work for me, please write.
I am looking forward to read your thoughts to this topic.
 
This is perhaps the best synopsis on akathisia is read thus far. It is true that the symptoms of opiate withdrawal are somewhat hidden from the clinician as the most terrible symptoms, i.e.: akathisia, from an objective point of view does not convey the torment the withdrawal syndrome confers upon the unfortunate addict. The fact that this contributor discerns that this aspect of withdrawal presents during periods of attempted rest. I have seen withdrawal so dominated by akathisia that the patient, in an attempt to rest, throws themselves upon their cot to only rise up again to pace the floor. This process was repeated indefinitely. These individuals were attempting to withdrawal from Methadone-over 200mg/day. Due to the very extended half-life of Methadone HCL, it was theorized that transferring them over to a short acting mu agonist with a relatively short half-life, such as morphine extended release (600mg/day), the long half-life of Methadone could be overcome following a period of about 30 days. The clearance of Methadone was verified by the absence of metabolites via ELISA and only morphine sulfate ER remained. It was found that although a shorter time was required to achieve relative absence of withdrawal symptoms, no diarrhea, vomiting, etc..., the continued occurrence of akathisia at bedtime was so severe that the re-establishment of Methadone maintenance was required. In retrospect, the use of sufficient benzodiazepine may have curtailed the severity of the akathisia but would have negated any possible relevance the study may have provided. It should be noted that though the use of Zoloft and clonidine was used in a palliative manner and that the Zoloft was thought to have prevented vomiting, the clonidine was thought to have had some positive results with respect to all symptoms of the opioid withdrawal syndrome. It may be that the clinical benefits of clonidine, to be fully exploited, may require dosages so high as to require ICU inpatient monitoring of the blood pressure.
 
I am on one month and one week of going off 25 methadone. I thought I was out of the woods at about day 25 but last night, I went into acute for NO REASON!!! I was so freaked out. RLS, achey, threw up, muscle cramping, weak, etc... Terrible. I got up and took Kratom and some RLS stuff and laid down. Went to sleep and woke up feeling way better but so stiff. I was disheartened that at 37 days I can suffer still.
 
I am on one month and one week of going off 25 methadone. I thought I was out of the woods at about day 25 but last night, I went into acute for NO REASON!!! I was so freaked out. RLS, achey, threw up, muscle cramping, weak, etc... Terrible. I got up and took Kratom and some RLS stuff and laid down. Went to sleep and woke up feeling way better but so stiff. I was disheartened that at 37 days I can suffer still.

That sucks :!

Hang in there, you should continue to even out as time since your last dose continues to pass.

While Kratom no doubt may aid you during the worst days, I've found through some considerable amount of trial and error that high therapeutic range doses of Pregabalin (Lyrica) - 225 to 300mg TID in my case - can almost completely numb the muscle aches and pains, and, that some Clonidine (Catapres) - 0.1 to 0.3mg Q6h - in combination with Isopropryl (Rubbing) Alcohol applied Q6h onto the forehead, neck, chest and lower back can significantly alleviate the excessive sweating, restless legs, hypertension and insomnia associated with OWS.

P.S: I REALLY don't want to cause you any further pain and suffering; so please, only read the following if you're not easily discouraged (it's not worth it if you'll lose sleep as a result, so to speak).

NSFW:
My methadone doc has told me that he knows of one ex patient (obviously he didn't name him or her) who continued to report acute withdrawal symptoms (mild to moderate severity) up to 87 days since stopping. But I'm guessing that this person probably had an impaired liver from Hep C, which could have resulted in the half-life of the methadone being increased, which might prolong withdrawal (possibly).


Edit: DL-Phenylalanine is a precursor amino acid to Dopamine IIRC.
 
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