Restless legs syndrome (RLS) is an unpleasant or uncomfortable sensation in your legs and an irresistible urge to move them. Does this sound familiar? RLS is common in people with MS.
Question via email: "Do our MS doctors and fellow patients know of anyone who's successfully getting prescribed Sativex? I don't, and I'm aware MS make us eligible but I haven't found a Dr yet who agrees?"
Yes, Sativex can be prescribed via the NHS for spasticity, which it is licensed for. However, not all NHS Trust's have it on its formulary because of issues regarding payment. It has to be prescribed via specialist services. At Barts-MS we refer our patients to the National Hospital for an assessment and possible prescribing. Several of my patients are on Sativex for spasticity.
Please note we can't use it for pain, RLS, etc. on the NHS.
I know we can now legally get medical cannabis privately in the UK, but it's expensive, and honestly I haven't had the energy. 🤕 Plus I don't even know if it would help me. I wish I could just give it a try. 🤷♂️
The problem lies in finding someone who will actually issue a prescription. I recently moved to Woolwich in south eat London, registered with a new GP and he said "nope"
I have to buy Sativex privately. Yes it definitely helps me but there is a stygma, How can a recreational class B drug have any medical benefits? Its all very frustrating
Aug 24, 2023·edited Aug 24, 2023Liked by Gavin Giovannoni
This all leads to something called “clonus”, a form of spasm (I think).
65 now, MS since facial numbness in 1988, typical relapsing pattern to 1998, Betaseron ’95 to ’17, then Ocrevus until Covid, now no DMT and I “piggyback” the ALA trial. Walking is still my major mode of getting around, quite hampered by right leg problems. I could sit most of the time, but that would cancel my replacement “job” of collectables sales at the local antique market (used to be a Psychologist). Today I’m probably SPMS with returned bladder issues and the walking problem. Other stuff has held up pretty well.
1995, pretty difficult getting around, leg stiffness, I bought a good portable wheel chair. Remitted slowly after that but was never able to run or skip again, for things like hurrying across the street to avoid traffic. And my reflexes had increased, at least at the knees. Otherwise, I did well until 2016. Then a “perfect storm” of PTTD, peroneal neuropathy, “inflamed lower nerve”, “pinched nerve”, a sprain (?), spasms and other things that could never be truly diagnosed or rectified. Went to many specialists, each seeing diagnosis and solution through their own lens. And I’ve had flat feet since a kid (but was still called “speedy” in Little League baseball). The pain aspect of this, 2017 to 2021, got severe with nearly every step but finally improved 95%. My solution was being careful and wearing arches or other inserts, or boots (some expensive); none of which helped immediately and some of which never helped at all. I did use a hand vibrator massager from Homedics and prescription compounded medicine with Amitriptyline, Baclofen, Gabapentin and Ibuprofen. I think those helped but nothing stopped the entire “perfect storm” all at once. I tried NMES too (electrical stimulation), but that didn't seems to do anything. Small ice packs slipped into the sock actually helped quite nicely sometimes. My right leg is more turned outward now than it used to be (called “too many toes”, a sign of PTTD). The problem seems structural, not a relapse that remitted. Haven’t had a relapse (if you call it that) since the 2001 appearance of clonus. I think there were new spinal lesions at the time. (This happened when I temporarily switched to Avonex for 6 months).
This leads finally to “clonus”. I don’t recall where I stumbled upon this definition recently, but the Google definition is “involuntary and rhythmic muscle contractions caused by a permanent lesion in descending motor neurons”. I don’t know about descending neuron damage, but THE KEY in this definition for me, is RHYTHMIC. Yes, there is varying spasticity, infrequent cramps and PLMS, burning-slight aching in the peroneal area, but the biggest challenge in the whole mess is the rhythmic contractions at night sometimes, when trying to get to sleep. They repeat, at predictable intervals, with stimulus, currently at every 12-14 seconds when they occur- an uncontrollable contraction and release. But I can focus on relaxing my peroneal muscle, the time between contractions increases- 20 sec, 30 sec, then I fade off into sleep. When I awake a couple hours later, the clonus has stopped, I eat a couple sugar free cookies with milk and maybe add a 20 mg. tab of baclofen. Baclofen has never been a “life-saver” in terms of spasticity but does have sedative effects, so it helps me sleep. Any, ANY, noise or physical sensation (stimulus) can start the clonus again. The clonus will happen in the day, sitting in the car, if my sock is too tight! And it happens during MRIs, causing body movement which ruins the MRI. Now they use anesthesia and put me to sleep when I get my periodic MRIs (which show no changes for at least 20 years). Many years ago, Clonazepam was a life saver for shaking and trembling. I took the pill, and stopped shaking. So I tried it for clonus )only recently), and it works! I try to avoid a new medicine regiment, so I take it only when needed. When I want the best night’s sleep I can get, I’ll end up taking both Baclofen and Clonazepam, sometimes at full strength, sometimes less.
So yesterday I planted strawberries which involved bending, sitting & shoveling, and carting 2 bags of soil. My lower ankle/foot was giving pain by the end of the day, so I put on the “Arizona” boot which helped. I think maybe I should stop any unnecessary physical activity. But by morning, it’s better/ I’ll wear the boot and/or arches for a while, and see how it goes. The boot adds ankle strength but brings on clonus.
Sorry for the long essay. Perhaps someone can take something from it. :-)
I think ALL pwMS that have any issues related to sleep should do a sleep study. MANY pwMS suffer with sleep apnea. Any time someone says "I'm tired ALL the time", get a sleep study done. If apnea is diagnosed, proper use of a CPAP can help tremendously and be a literal life saver!
I have been taking gabapentin for my symptoms and it has helped quite a bit. I’ve had to increase from the recommended 800 mg to 1200 mg over the past two years. My sleep was being severely impacted by RLS and other MS symptoms started to pop up as a result. My right eye would not open fully along with being really exhausted and increased leg pain during the day. Interrupted sleep was taken seriously by my neurologist. I would be in bad shape otherwise.
Try splitting the dose. Doses above 600mg are poorly absorbed. Try 600mg 2 hours before bed, 600mg just before bed. Join RLS-UK, lots of up to date info and a great help forum at Health Unlocked.
Aug 23, 2023·edited Aug 23, 2023Liked by Gavin Giovannoni
Hi,
One common medication prescribed for insomnia is quetiapine and it's giving me the worst case of RLS whenever I take it (even at a low dosage of 25mg). Not sure why. I end up in a weird state where I'm really tired but I have to move my legs every 15 seconds or so... Really unconfortable!
Quetiapine is a major tranquilliser or antipsychotic and should not be prescribed as a sedative. It is used to treat major psychiatric symptoms. It belongs to the class of agents that causes RLS and/or make RLS worse.
Thanks for answering! I completely agree with your first sentence but it would seem that, in Canada at least according to my personnal experience, some doctors (GPs and psychiatrists) really like quetiapine for insomnia (dont know why). I guess the lower risk of addiction is a plus to doctors.
As for me (pwMs), I have sleep apnea and I need a cpap. Currently treating my insomnia with THC with acceptable results.
You recommend Benzodiazepins, which is addictive and severely affects sleep architecture, but reject Quetiapine, which is sleep-inducing even at very low doses (much lower than in psychiatric patients) without being addictive? That makes no sense to me, dear Prof G.
Quetiapine is a dopamine blocker and as a class these agents cause RLS; they are not a treatment for RLS. Dopamine agonists, the opposite of blocking agents, which stimulate the dopamine receptors are used to treat RLS. There is a weak evidence base to support benzodiazepines as a treatment. You may interested in the following review that fingers Quetiapine as being a common cause of RLS.
Saber et al. Restless Legs Syndrome and the Use of Antipsychotic Medication: An Updated Literature. Cureus . 2022 Aug 9;14(8):e27821.
Restless legs syndrome or Willis-Ekbom disease (RLS/WED) is a sleep-related movement disorder characterized by an urge to move the legs. This impulse is usually accompanied by an uncomfortable and unpleasant sensation in the legs, which worsens at night and during periods of inactivity and is relieved by movement. Several studies in the literature reported the association between RLS and different antipsychotic medications. with Olanzapine, Quetiapine, and Clozapine identified as the most common causes. The literature suggests that the development of RLS in antipsychotic users may be attributed to the inhibition of dopaminergic neurotransmission or the impact of antipsychotics on iron metabolism. Diagnosing antipsychotic-induced RLS remains a substantial challenge in clinical practice, with challenges in the management of this condition also being widely reported in the current literature. In this article, we will review the evidence suggesting the association between RLS and the use of antipsychotic medications, differentiate between RLS and other movement disorders, and give a brief review of the pathophysiology, diagnosis, and management of RLS and its challenges among psychotic patients.
Never had what I’ve heard RLS is, but spasticity and pain ramp up at night, always when I’d love to drift off to sleep, of course. Cramped feet will often waken me at night. Most of my sleep is in a.m. hours now after thrashing around and massaging my legs and feet more nights then not in the wee hours. It’s just spasms to me. I did try cannabis. Nothing like being wide awake, stoned and unable to move or pee! That was like paralyzed hell. (Perhaps I overdid it, but I always hated the stuff, and CBD had no effect.) I’m glad it works for others, though.🌷
That is awful. I am not trying to make light of your spasticity, but sometimes the only thing that helps me is to soak in a bath of Epsom salts for 20 mins. That is a last resort for me. After gabapentin, walking, stretching-a bath in the middle of the night😵💫
No, Sheila, it’s not making light. It’s like whoah, I can’t move! And I can’t even do anything like read, bathe or anything else because my cerebellum packed up and left home. I think I did listen to a meditation tape. So in the spirit of trying maintain some sense of humor, no matter how weird things get, it was pretty funny, all told! I’m glad you have a good strategy for those wee hours!🌷
I don't have RLS, but I have MS & hypernychthemeral syndrome (Non-24-hour sleep-wake disorder). I take Melatonin and use a light box every day. I'm in pain all the time, but none of the meds I've tried have helped. I'm considering medical cannabis, but it's expensive and tiring to get. 🤕
At last! A neurologist who is familiar with RLS and knows the dangers of dopamine agonists. I had to become a patient expert to access the right treatment. All SNRI, SSRI & tricyclical anti depressants and melatonin will worsen RLS, so it's essential to get the DX correct. Please all visit RLS UK website and the Mayo Clinic Algorithm. And do NOT agree to dopamine agonists. Augmentation and withdrawal is hell on earth. Methadone and Buprenorphine are both highly effective at low dose for refractory RLS.
Thank you Prof. Giovanonni for talking about this.
I think you are being a bit harsh on neurologists. Most know about the dangers of dopamine agonists and most RLS updates discuss this and recommend gabapentinoids and the opiods. When I attended a recent RLS session at the American Academy of Neurology the message was loud and clear.
My reference regarding melatonin is not for RLS, but the periodic nocturnal limb movements of sleep (PLMS), which is a different diagnosis. PLMS is classified as one of the so-called non-REM sleep parasomnias, which as a groups respond to melatonin.
The US RLS foundation has been brilliant at raising awareness of Augmentation and Dr Andy Berkowski, Dr Mark Buchfuhrer and Dr John Winkelman have all helped. I think there are still Parkinson's neurologists in the UK who overprescribe DAs and the RLS UK Help forum still has reports of neurologists prescribing these as first line treatment and refusing iron infusions.
15 years of MS, and severe RLS developed about five years ago preventing sleep and interfering with daily life. Low iron and anemia are often part of the issue, and although I do struggle with anemia, my blood iron levels were normal. It was my GP who finally tested for Ferritin and discovered it was extremely low. (ferritin is the iron stored in organs) I now take daily OTC supplements of ferrous sulfate and the symptoms have almost completely diminished.
When I looked up Ferritin/iron deficiency and EBV, I was surprised they were connected. EBV also ties to abnormal liver tests, and I also had that at the same time. They wanted to do a biopsy, but I told them to wait, suspecting it was my MS, and retested in 6 months to find it back to normal. I also had new lesions on my MRI three months prior to figuring out the low Ferritin anemia.
Since MS is EBV-driven, and EBV is known to affect Ferritin when in an active state, why aren't Ferritin levels levels checked as an indicator to MS activity?
Is it true that high ferritin levels (over1000) can exacerbate. RLS? I have clonazepam now which helps, occasionally having to take it during the day as well as at night. I am taking duloxetine 120mg daily. Do you know what causes High ferritin levels? Thank you. Eve
Re: "Is it true that high ferritin levels (over1000) can exacerbate. RLS?"
I am not aware of this, but it would depend on the cause of the high ferritin levels as some of the conditions that cause a very high ferrtin level may be associated with RLS.
A higher than normal ferritin level can be seen in several conditions. However, diagnosis of these conditions might require additional testing based on your symptoms and physical examination.
Hemochromatosis
Porphyria — A group of disorders caused by an enzyme deficiency that affects your nervous system and skin
Rheumatoid arthritis or another chronic inflammatory disorder
Thank you Prof G for answering my questions. The only thing that comes close in the reasons you have given is Hodgkin's Lymphoma as the others do not apply, and I am now being tested for Multiple Myeloma. I also have POTS. Eve
RLS and spasticity feel very different. I had RLS for a long time in my legs and back, mostly when sitting in an arm chair although turning onto my side in the chair meant I got to sit there for a bit longer before it kicked off, sometimes you just need to sit in a comfy chair! At some point it just stopped happening.
The spasticity is a different beast and despite taking 3 x 10mg Baclofen I am still woken at 5am with the pain because it doesn't last long enough. Have you written about spasticity I couldn't find anything?
My GP diagnosed me with RLS and RAS a couple of years ago - it was agony. I tried Magnesium but this didn’t help although I continue to take a supplement. I currently take Pramipexole, am also on Venlafaxine, Nabilone (for severe nausea) Zolpidem and Gabapentin. I also have an underactive thryoid. My RLS started when I was Menopausal. My RLS/RAS has virtually gone since starting Pramipexole and I only take a low dose,
Is it possible that my RLS could improve now that I am postmenopausal? I also used to have low ferritin but this has resolved now my periods have finished. I am now concerned about taking Pramipexole. Would it worth upping my gabapentin or Nabilone (I only take 500mcg) and stopping the Pramipexole in your opinion?
I have restless leg syndrome or one of the other things that mimic it. I'm lucky that I don't get it very often but I will sometime be suddenly wide awake because my feet are pinging. I do try and get back to sleep but if it continues the only thing I can do it get up. I don't get it often enough to have a major impact but I can see it would be a downward spiral of fatigue.
Aug 24, 2023·edited Aug 24, 2023Liked by Gavin Giovannoni
I had RLS probably 10 years before my MS diagnosis. Magnesium lotion works great thankfully. CBD/THC does not. I have noticed it getting worse this past month. It used to only bother me when I was sitting in a comfortable chair in the evening. Now it follows me to bed.
I have not recommended CBD/THC is a treatment for RLS. It is licensed for spasticity and there is evidence it helps with pain. I am not aware of any evidence suggesting CBD/THC works in RLS.
I had severe RLS years ago sat in long lectures at university. Unbearable sensation of awareness in leg with absolute urge to move it. Completely resolved on leaving the lecture theatre! Would come back when sitting or lying down to sleep at night (but never as bad as when trapped in an audience). I have memory of it being in my left leg only, but maybe I'm mistaken, it was such a long time ago.
At some point it must have (thankfully) gone away.
Years later, with MS, legs twitchy, jerky and heavy but not quite RLS. Until the time I decided to try stopping duloxetine to see if a) made much difference to pain and/or b) improved fatigue. After three weeks of no duloxetine had the worst attack of RLS ever one night in both legs and took hours to go to sleep. Thankfully has never returned since restarting duloxetine. Perhaps it was coincidental and I just had a one-off bad night! Whichever way. RLS is horrible. Be kind to patients presenting with it.
Strange that the cause and physiology of RLS remain unknown. Several vague suggestions from dopamine to iron deficiency anaemia. Could it be caused by MS?
I suspect an MS lesion or lesions in a strategic area could trigger RLS. Not sure MS can cause it outside of this mechanism. I suspect the dopamine and iron hypotheses are correct based on triggers and treatment responses. But the mechanisms need to be worked out.
I forgot to add that coffee and caffeine actually help many RLS UK members. The anecdotal evidence is compelling. I had never drunk coffe in my life. Hated the stuff. But during dreadful augmentation on Ropinirole, I tried EVERYTHING. Nothing helped except drinking coffee during an attack. It improved my RLS. So caffeine is not a trigger for everyone.
Question via email: "Do our MS doctors and fellow patients know of anyone who's successfully getting prescribed Sativex? I don't, and I'm aware MS make us eligible but I haven't found a Dr yet who agrees?"
Yes, Sativex can be prescribed via the NHS for spasticity, which it is licensed for. However, not all NHS Trust's have it on its formulary because of issues regarding payment. It has to be prescribed via specialist services. At Barts-MS we refer our patients to the National Hospital for an assessment and possible prescribing. Several of my patients are on Sativex for spasticity.
Please note we can't use it for pain, RLS, etc. on the NHS.
I know we can now legally get medical cannabis privately in the UK, but it's expensive, and honestly I haven't had the energy. 🤕 Plus I don't even know if it would help me. I wish I could just give it a try. 🤷♂️
The problem lies in finding someone who will actually issue a prescription. I recently moved to Woolwich in south eat London, registered with a new GP and he said "nope"
I have to buy Sativex privately. Yes it definitely helps me but there is a stygma, How can a recreational class B drug have any medical benefits? Its all very frustrating
This all leads to something called “clonus”, a form of spasm (I think).
65 now, MS since facial numbness in 1988, typical relapsing pattern to 1998, Betaseron ’95 to ’17, then Ocrevus until Covid, now no DMT and I “piggyback” the ALA trial. Walking is still my major mode of getting around, quite hampered by right leg problems. I could sit most of the time, but that would cancel my replacement “job” of collectables sales at the local antique market (used to be a Psychologist). Today I’m probably SPMS with returned bladder issues and the walking problem. Other stuff has held up pretty well.
1995, pretty difficult getting around, leg stiffness, I bought a good portable wheel chair. Remitted slowly after that but was never able to run or skip again, for things like hurrying across the street to avoid traffic. And my reflexes had increased, at least at the knees. Otherwise, I did well until 2016. Then a “perfect storm” of PTTD, peroneal neuropathy, “inflamed lower nerve”, “pinched nerve”, a sprain (?), spasms and other things that could never be truly diagnosed or rectified. Went to many specialists, each seeing diagnosis and solution through their own lens. And I’ve had flat feet since a kid (but was still called “speedy” in Little League baseball). The pain aspect of this, 2017 to 2021, got severe with nearly every step but finally improved 95%. My solution was being careful and wearing arches or other inserts, or boots (some expensive); none of which helped immediately and some of which never helped at all. I did use a hand vibrator massager from Homedics and prescription compounded medicine with Amitriptyline, Baclofen, Gabapentin and Ibuprofen. I think those helped but nothing stopped the entire “perfect storm” all at once. I tried NMES too (electrical stimulation), but that didn't seems to do anything. Small ice packs slipped into the sock actually helped quite nicely sometimes. My right leg is more turned outward now than it used to be (called “too many toes”, a sign of PTTD). The problem seems structural, not a relapse that remitted. Haven’t had a relapse (if you call it that) since the 2001 appearance of clonus. I think there were new spinal lesions at the time. (This happened when I temporarily switched to Avonex for 6 months).
This leads finally to “clonus”. I don’t recall where I stumbled upon this definition recently, but the Google definition is “involuntary and rhythmic muscle contractions caused by a permanent lesion in descending motor neurons”. I don’t know about descending neuron damage, but THE KEY in this definition for me, is RHYTHMIC. Yes, there is varying spasticity, infrequent cramps and PLMS, burning-slight aching in the peroneal area, but the biggest challenge in the whole mess is the rhythmic contractions at night sometimes, when trying to get to sleep. They repeat, at predictable intervals, with stimulus, currently at every 12-14 seconds when they occur- an uncontrollable contraction and release. But I can focus on relaxing my peroneal muscle, the time between contractions increases- 20 sec, 30 sec, then I fade off into sleep. When I awake a couple hours later, the clonus has stopped, I eat a couple sugar free cookies with milk and maybe add a 20 mg. tab of baclofen. Baclofen has never been a “life-saver” in terms of spasticity but does have sedative effects, so it helps me sleep. Any, ANY, noise or physical sensation (stimulus) can start the clonus again. The clonus will happen in the day, sitting in the car, if my sock is too tight! And it happens during MRIs, causing body movement which ruins the MRI. Now they use anesthesia and put me to sleep when I get my periodic MRIs (which show no changes for at least 20 years). Many years ago, Clonazepam was a life saver for shaking and trembling. I took the pill, and stopped shaking. So I tried it for clonus )only recently), and it works! I try to avoid a new medicine regiment, so I take it only when needed. When I want the best night’s sleep I can get, I’ll end up taking both Baclofen and Clonazepam, sometimes at full strength, sometimes less.
So yesterday I planted strawberries which involved bending, sitting & shoveling, and carting 2 bags of soil. My lower ankle/foot was giving pain by the end of the day, so I put on the “Arizona” boot which helped. I think maybe I should stop any unnecessary physical activity. But by morning, it’s better/ I’ll wear the boot and/or arches for a while, and see how it goes. The boot adds ankle strength but brings on clonus.
Sorry for the long essay. Perhaps someone can take something from it. :-)
I think ALL pwMS that have any issues related to sleep should do a sleep study. MANY pwMS suffer with sleep apnea. Any time someone says "I'm tired ALL the time", get a sleep study done. If apnea is diagnosed, proper use of a CPAP can help tremendously and be a literal life saver!
Good Morning
I have been taking gabapentin for my symptoms and it has helped quite a bit. I’ve had to increase from the recommended 800 mg to 1200 mg over the past two years. My sleep was being severely impacted by RLS and other MS symptoms started to pop up as a result. My right eye would not open fully along with being really exhausted and increased leg pain during the day. Interrupted sleep was taken seriously by my neurologist. I would be in bad shape otherwise.
Try splitting the dose. Doses above 600mg are poorly absorbed. Try 600mg 2 hours before bed, 600mg just before bed. Join RLS-UK, lots of up to date info and a great help forum at Health Unlocked.
Thank you for the info.
Hi,
One common medication prescribed for insomnia is quetiapine and it's giving me the worst case of RLS whenever I take it (even at a low dosage of 25mg). Not sure why. I end up in a weird state where I'm really tired but I have to move my legs every 15 seconds or so... Really unconfortable!
Quetiapine is a major tranquilliser or antipsychotic and should not be prescribed as a sedative. It is used to treat major psychiatric symptoms. It belongs to the class of agents that causes RLS and/or make RLS worse.
Thanks for answering! I completely agree with your first sentence but it would seem that, in Canada at least according to my personnal experience, some doctors (GPs and psychiatrists) really like quetiapine for insomnia (dont know why). I guess the lower risk of addiction is a plus to doctors.
As for me (pwMs), I have sleep apnea and I need a cpap. Currently treating my insomnia with THC with acceptable results.
You recommend Benzodiazepins, which is addictive and severely affects sleep architecture, but reject Quetiapine, which is sleep-inducing even at very low doses (much lower than in psychiatric patients) without being addictive? That makes no sense to me, dear Prof G.
Quetiapine is a dopamine blocker and as a class these agents cause RLS; they are not a treatment for RLS. Dopamine agonists, the opposite of blocking agents, which stimulate the dopamine receptors are used to treat RLS. There is a weak evidence base to support benzodiazepines as a treatment. You may interested in the following review that fingers Quetiapine as being a common cause of RLS.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9481228/
Saber et al. Restless Legs Syndrome and the Use of Antipsychotic Medication: An Updated Literature. Cureus . 2022 Aug 9;14(8):e27821.
Restless legs syndrome or Willis-Ekbom disease (RLS/WED) is a sleep-related movement disorder characterized by an urge to move the legs. This impulse is usually accompanied by an uncomfortable and unpleasant sensation in the legs, which worsens at night and during periods of inactivity and is relieved by movement. Several studies in the literature reported the association between RLS and different antipsychotic medications. with Olanzapine, Quetiapine, and Clozapine identified as the most common causes. The literature suggests that the development of RLS in antipsychotic users may be attributed to the inhibition of dopaminergic neurotransmission or the impact of antipsychotics on iron metabolism. Diagnosing antipsychotic-induced RLS remains a substantial challenge in clinical practice, with challenges in the management of this condition also being widely reported in the current literature. In this article, we will review the evidence suggesting the association between RLS and the use of antipsychotic medications, differentiate between RLS and other movement disorders, and give a brief review of the pathophysiology, diagnosis, and management of RLS and its challenges among psychotic patients.
Never had what I’ve heard RLS is, but spasticity and pain ramp up at night, always when I’d love to drift off to sleep, of course. Cramped feet will often waken me at night. Most of my sleep is in a.m. hours now after thrashing around and massaging my legs and feet more nights then not in the wee hours. It’s just spasms to me. I did try cannabis. Nothing like being wide awake, stoned and unable to move or pee! That was like paralyzed hell. (Perhaps I overdid it, but I always hated the stuff, and CBD had no effect.) I’m glad it works for others, though.🌷
That is awful. I am not trying to make light of your spasticity, but sometimes the only thing that helps me is to soak in a bath of Epsom salts for 20 mins. That is a last resort for me. After gabapentin, walking, stretching-a bath in the middle of the night😵💫
No, Sheila, it’s not making light. It’s like whoah, I can’t move! And I can’t even do anything like read, bathe or anything else because my cerebellum packed up and left home. I think I did listen to a meditation tape. So in the spirit of trying maintain some sense of humor, no matter how weird things get, it was pretty funny, all told! I’m glad you have a good strategy for those wee hours!🌷
🌸
I don't have RLS, but I have MS & hypernychthemeral syndrome (Non-24-hour sleep-wake disorder). I take Melatonin and use a light box every day. I'm in pain all the time, but none of the meds I've tried have helped. I'm considering medical cannabis, but it's expensive and tiring to get. 🤕
At last! A neurologist who is familiar with RLS and knows the dangers of dopamine agonists. I had to become a patient expert to access the right treatment. All SNRI, SSRI & tricyclical anti depressants and melatonin will worsen RLS, so it's essential to get the DX correct. Please all visit RLS UK website and the Mayo Clinic Algorithm. And do NOT agree to dopamine agonists. Augmentation and withdrawal is hell on earth. Methadone and Buprenorphine are both highly effective at low dose for refractory RLS.
Thank you Prof. Giovanonni for talking about this.
I think you are being a bit harsh on neurologists. Most know about the dangers of dopamine agonists and most RLS updates discuss this and recommend gabapentinoids and the opiods. When I attended a recent RLS session at the American Academy of Neurology the message was loud and clear.
My reference regarding melatonin is not for RLS, but the periodic nocturnal limb movements of sleep (PLMS), which is a different diagnosis. PLMS is classified as one of the so-called non-REM sleep parasomnias, which as a groups respond to melatonin.
The US RLS foundation has been brilliant at raising awareness of Augmentation and Dr Andy Berkowski, Dr Mark Buchfuhrer and Dr John Winkelman have all helped. I think there are still Parkinson's neurologists in the UK who overprescribe DAs and the RLS UK Help forum still has reports of neurologists prescribing these as first line treatment and refusing iron infusions.
15 years of MS, and severe RLS developed about five years ago preventing sleep and interfering with daily life. Low iron and anemia are often part of the issue, and although I do struggle with anemia, my blood iron levels were normal. It was my GP who finally tested for Ferritin and discovered it was extremely low. (ferritin is the iron stored in organs) I now take daily OTC supplements of ferrous sulfate and the symptoms have almost completely diminished.
Nice example of iron responsive RLS. Some patients need IV iron.
When I looked up Ferritin/iron deficiency and EBV, I was surprised they were connected. EBV also ties to abnormal liver tests, and I also had that at the same time. They wanted to do a biopsy, but I told them to wait, suspecting it was my MS, and retested in 6 months to find it back to normal. I also had new lesions on my MRI three months prior to figuring out the low Ferritin anemia.
Since MS is EBV-driven, and EBV is known to affect Ferritin when in an active state, why aren't Ferritin levels levels checked as an indicator to MS activity?
Is it true that high ferritin levels (over1000) can exacerbate. RLS? I have clonazepam now which helps, occasionally having to take it during the day as well as at night. I am taking duloxetine 120mg daily. Do you know what causes High ferritin levels? Thank you. Eve
Re: "Is it true that high ferritin levels (over1000) can exacerbate. RLS?"
I am not aware of this, but it would depend on the cause of the high ferritin levels as some of the conditions that cause a very high ferrtin level may be associated with RLS.
From: https://www.mayoclinic.org/tests-procedures/ferritin-test/about/pac-20384928
A higher than normal ferritin level can be seen in several conditions. However, diagnosis of these conditions might require additional testing based on your symptoms and physical examination.
Hemochromatosis
Porphyria — A group of disorders caused by an enzyme deficiency that affects your nervous system and skin
Rheumatoid arthritis or another chronic inflammatory disorder
Liver disease
Hyperthyroidism
Leukemia
Hodgkin's lymphoma
Multiple blood transfusions
Alcohol abuse
Taking too many iron supplements
Thank you Prof G for answering my questions. The only thing that comes close in the reasons you have given is Hodgkin's Lymphoma as the others do not apply, and I am now being tested for Multiple Myeloma. I also have POTS. Eve
RLS and spasticity feel very different. I had RLS for a long time in my legs and back, mostly when sitting in an arm chair although turning onto my side in the chair meant I got to sit there for a bit longer before it kicked off, sometimes you just need to sit in a comfy chair! At some point it just stopped happening.
The spasticity is a different beast and despite taking 3 x 10mg Baclofen I am still woken at 5am with the pain because it doesn't last long enough. Have you written about spasticity I couldn't find anything?
https://gavingiovannoni.substack.com/p/case-study-are-you-a-zombie-because
Thank you
My GP diagnosed me with RLS and RAS a couple of years ago - it was agony. I tried Magnesium but this didn’t help although I continue to take a supplement. I currently take Pramipexole, am also on Venlafaxine, Nabilone (for severe nausea) Zolpidem and Gabapentin. I also have an underactive thryoid. My RLS started when I was Menopausal. My RLS/RAS has virtually gone since starting Pramipexole and I only take a low dose,
Is it possible that my RLS could improve now that I am postmenopausal? I also used to have low ferritin but this has resolved now my periods have finished. I am now concerned about taking Pramipexole. Would it worth upping my gabapentin or Nabilone (I only take 500mcg) and stopping the Pramipexole in your opinion?
If it isn't broken it does need fixing ;-)
I have restless leg syndrome or one of the other things that mimic it. I'm lucky that I don't get it very often but I will sometime be suddenly wide awake because my feet are pinging. I do try and get back to sleep but if it continues the only thing I can do it get up. I don't get it often enough to have a major impact but I can see it would be a downward spiral of fatigue.
I had RLS probably 10 years before my MS diagnosis. Magnesium lotion works great thankfully. CBD/THC does not. I have noticed it getting worse this past month. It used to only bother me when I was sitting in a comfortable chair in the evening. Now it follows me to bed.
Re: "CBD/THC"
I have not recommended CBD/THC is a treatment for RLS. It is licensed for spasticity and there is evidence it helps with pain. I am not aware of any evidence suggesting CBD/THC works in RLS.
I had severe RLS years ago sat in long lectures at university. Unbearable sensation of awareness in leg with absolute urge to move it. Completely resolved on leaving the lecture theatre! Would come back when sitting or lying down to sleep at night (but never as bad as when trapped in an audience). I have memory of it being in my left leg only, but maybe I'm mistaken, it was such a long time ago.
At some point it must have (thankfully) gone away.
Years later, with MS, legs twitchy, jerky and heavy but not quite RLS. Until the time I decided to try stopping duloxetine to see if a) made much difference to pain and/or b) improved fatigue. After three weeks of no duloxetine had the worst attack of RLS ever one night in both legs and took hours to go to sleep. Thankfully has never returned since restarting duloxetine. Perhaps it was coincidental and I just had a one-off bad night! Whichever way. RLS is horrible. Be kind to patients presenting with it.
Strange that the cause and physiology of RLS remain unknown. Several vague suggestions from dopamine to iron deficiency anaemia. Could it be caused by MS?
Re: "Could it be caused by MS?"
I suspect an MS lesion or lesions in a strategic area could trigger RLS. Not sure MS can cause it outside of this mechanism. I suspect the dopamine and iron hypotheses are correct based on triggers and treatment responses. But the mechanisms need to be worked out.
Yes, I think MS causes atypical RLS and also lowers the threshold for developing typical RLS. RLS is very common in pwMS.
I forgot to add that coffee and caffeine actually help many RLS UK members. The anecdotal evidence is compelling. I had never drunk coffe in my life. Hated the stuff. But during dreadful augmentation on Ropinirole, I tried EVERYTHING. Nothing helped except drinking coffee during an attack. It improved my RLS. So caffeine is not a trigger for everyone.