kangaSue
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Normokalemic periodic paralysis, a variant form of hyperkalemic periodic paralysis?
http://hkpp.org/what-is-periodic-paralysis
Temporary paralysis I need your Insights
- Thread starter Jenny TipsforME
- Start date
http://hkpp.org/what-is-periodic-paralysis
Snow Leopard
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Hi, I'm sorry to hear you had this awful experience and likewise, the poor treatment by the hospital staff!
I don't really know what it could be caused by, but it sounds most like this: https://en.wikipedia.org/wiki/Cataplexy
One possible cause is like the so-called sleep paralysis - the paralysis that we get when entering REM sleep is activated when conscious, a common symptom of those who suffer from narcolepsy. My first questions besides those infection related (fever, meningitis?) would be about sleep quality and rhythms, whether you take melatonin or anything else that effects sleep. Could also be somehow linked to migranes as well.
Interestingly for some starting to wiggle their toes is they only way they can regain functioning.
Guillain-Barre has onset over days to a week or so and takes months to years to recover (if at all), it doesn't come and go rapidly like this.
I don't really know what it could be caused by, but it sounds most like this: https://en.wikipedia.org/wiki/Cataplexy
One possible cause is like the so-called sleep paralysis - the paralysis that we get when entering REM sleep is activated when conscious, a common symptom of those who suffer from narcolepsy. My first questions besides those infection related (fever, meningitis?) would be about sleep quality and rhythms, whether you take melatonin or anything else that effects sleep. Could also be somehow linked to migranes as well.
Interestingly for some starting to wiggle their toes is they only way they can regain functioning.
Guillain-Barre has onset over days to a week or so and takes months to years to recover (if at all), it doesn't come and go rapidly like this.
out2lunch
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As I was reading the thread, this thought came to me as well. Many years ago, I experienced episodes of severe cataplexy, in which I would drop like a rag doll and couldn't move my extremities; just my fingers, toes, and eyelids. In all instances, extreme emotions brought them on, typically fear.
The worst drop attack ever was when my cat got on top of the refrigerator while I was cooking dinner on the stove. I couldn't see him since the refrigerator was behind me. But the little fur ball leaped onto the stove and landed in the frying pan! Next thing I know, I was down on the floor, frozen. It lasted for about a minute. Scared the cat more than me.
But I've had far less severe attacks of all-over muscle weakness that lasted for several hours, where I couldn't stand up and walk. All I could do was sit propped up or slumped over. And drool. I remember the drool. Yuck.
My sleep neurologist diagnosed both of these as cataplexy. I've got the narcolepsy gene, and I've been tested in the sleep lab for daytime sleep latency, but the results were negative. Experts claim cataplexy without narcolepsy doesn't exist, but I'm not the only one with obvious drop attacks who doesn't have narcolepsy. For our patient cohort, I believe the experts are clueless.
The toe thing is more difficult than the finger thing. I've had a couple of these attacks on the freeway, during those near misses when everyone slams on their brakes at the same time and you're absolutely positive you're going to hit the vehicle in front of you. I lose muscle tone in my legs and arms and slump against the steering wheel. What gets me functioning again is wiggling my fingers. Then my hands, lower arms, feet, lower legs, etc. Fortunately, it never lasted for more than about 10 seconds. Put the paralysis was instantaneous, within seconds.
I had Guillain-Barre about 3 years ago, after a really bad gut illness. It came on gradually, just a few weeks after I recovered from the gut bug. It was severe peripheral neuropathy with some mild muscle weakness. Started in my feet and hands and moved slowly up my body. Took over six months for recovery, which wasn't 100%. Still have numbness in my feet and hands, especially my toes and fingers.
I was just hospitalized for a similar issue paralysis etc.....
Low potassium and low phosphates was the issue....
Then it happened again.....in hospital full paralysis cant talk, etc.....hospital staff treated me horribly cause all vitals were fine....
I always have numbness in my throat or what I think is early dyphagia that sometimes feels like throat constrictions....
Sometimes worse sometimes better
Low potassium and low phosphates was the issue....
Then it happened again.....in hospital full paralysis cant talk, etc.....hospital staff treated me horribly cause all vitals were fine....
I always have numbness in my throat or what I think is early dyphagia that sometimes feels like throat constrictions....
Sometimes worse sometimes better
Jenny TipsforME
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Asking in other places the common theme seems to be it's people who have POTS who have episodes like this. It isn't actually POTS itself but seems like some sort of chain reaction eg something (virus, heat etc) causes a POTS flare and then some disruption to sensory and motor areas of the brain. It sounds like neurologists with POTS patients see it quite a lot. It seems like a stroke sort of thing but doesn't cause lasting damage.
It definitely felt more POTS like but weird it didn't go lying down. I don't know how often it's a combination of POTS and ME. These 2 conditions seem to create a vicious cycle.
It's always a little hard to tell with random ME viral symptoms but it did seem to develop into a virus. Tomorrow will be a week. Today stopped going hot and cold. Finding it a little more natural to sit up a bit. Neck still stiff and sore but easing.
I think virus onset coincided with too hot shower caused a POTS reaction which generated this weird brain Inflammation reaction. I'll look up other ideas when my brain let's me though. Thank you.
BTW I've written up the full horror of my experience here
https://tipsforme.wordpress.com/2016/05/27/paralysis-and-pace/
It definitely felt more POTS like but weird it didn't go lying down. I don't know how often it's a combination of POTS and ME. These 2 conditions seem to create a vicious cycle.
It's always a little hard to tell with random ME viral symptoms but it did seem to develop into a virus. Tomorrow will be a week. Today stopped going hot and cold. Finding it a little more natural to sit up a bit. Neck still stiff and sore but easing.
I think virus onset coincided with too hot shower caused a POTS reaction which generated this weird brain Inflammation reaction. I'll look up other ideas when my brain let's me though. Thank you.
BTW I've written up the full horror of my experience here
https://tipsforme.wordpress.com/2016/05/27/paralysis-and-pace/
Jenny TipsforME
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I'm still not great but better than I could have been if that makes sense. I can think fairly clearly but getting cognitive fatigue headaches easily so trying to avoid reading (or being more boundaried about how much I read). Dysautonomia symptoms still bad.
Anyway I had an idea this morning that my paralysis could be related to acetylcholine auto antibodies (eg cholinergic crisis). Auto antibodies to acetylcholine receptors is an issue in POTS (also ME?). I'm not well enough to read the relevant journal articles though. What do you think?
Anyway I had an idea this morning that my paralysis could be related to acetylcholine auto antibodies (eg cholinergic crisis). Auto antibodies to acetylcholine receptors is an issue in POTS (also ME?). I'm not well enough to read the relevant journal articles though. What do you think?
anciendaze
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What you describe is not ordinary ME/CFS. Several aspects of your account fit one of the rare periodic paralysis disorders, but it is not possible at this remove to distinguish it from episodic ataxia. At this point your account does not sound like narcolepsy. There is a high probability you have a channelopathy with autoantibodies to some ion channel. Some involve low levels of potassium, some high. Some involve different ion channels altogether.
Autoantibodies to one type of cholinergic receptor are responsible for the classical medical disease myasthenia gravis in which neuromuscular junctions malfunction. There are multiple types of even acetylcholine receptors or enzymes which could be involved, so this is not an easy open-and-shut case. Antibodies to N-type calcium channels which will turn up on a paraneoplastic panel can also interfere with operation of neuromuscular junctions via a different mechanism.
Autoantibodies to one type of cholinergic receptor are responsible for the classical medical disease myasthenia gravis in which neuromuscular junctions malfunction. There are multiple types of even acetylcholine receptors or enzymes which could be involved, so this is not an easy open-and-shut case. Antibodies to N-type calcium channels which will turn up on a paraneoplastic panel can also interfere with operation of neuromuscular junctions via a different mechanism.
Jenny TipsforME
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@anciendaze thanks I've not heard of episodic ataxia. Type 2 episodic ataxia sounds plausible I'll look up my SNPs when I'm more alert. Something I forgot to mention to doctors is early on with the paralysis I felt I had to concentrate to keep my eyes still rather than nystagmus like in REM, when I closed my eyes they oscillates. That's mentioned in episodic ataxia.
I'm pretty sure not narcolepsy, doesn't seem to fit for a few reasons.
Also agree not typical ME (even if other pwme sometimes get this too). The dismissal of the hospital has really upset me. Scary that there's so little investigation when you have ME diagnosis.
Periodic paralysis is possible but they tested potassium while I couldn't move. Think that one was actually on the doctor's radar.
It was actually looking at the list of POTS drugs and seeing meds for myasthenia gravis on the list that gave me the idea this morning. I have asked my POTS doctor for this before and he said no. Agreed autoantibodies could be an issue but felt it wasn't established enough as a treatment for POTS. I'll ask again in my August appointment...
Perhaps I should take the tack of asking if I have myasthenia gravis?! I don't think I do but might get relevant testing (think there's biologically quite an overlap with POTS and ME from what I know of it).
I'm pretty sure not narcolepsy, doesn't seem to fit for a few reasons.
Also agree not typical ME (even if other pwme sometimes get this too). The dismissal of the hospital has really upset me. Scary that there's so little investigation when you have ME diagnosis.
Periodic paralysis is possible but they tested potassium while I couldn't move. Think that one was actually on the doctor's radar.
It was actually looking at the list of POTS drugs and seeing meds for myasthenia gravis on the list that gave me the idea this morning. I have asked my POTS doctor for this before and he said no. Agreed autoantibodies could be an issue but felt it wasn't established enough as a treatment for POTS. I'll ask again in my August appointment...
Perhaps I should take the tack of asking if I have myasthenia gravis?! I don't think I do but might get relevant testing (think there's biologically quite an overlap with POTS and ME from what I know of it).
Jenny TipsforME
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@parabola chiari malformation is something I've wondered about. I have a number of the other symptoms generally. The operation sounds scary, although perhaps not as scary as there being no treatment...
I know of someone (online) who had the decompression surgery with no regrets, and no more seizures and blackouts. I suspect I may have it too, currently awaiting a referral to find out if I have a rare connective tissue disorder which can cause it. I get a lot of dull pain at the base of my skull
Jenny TipsforME
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@parabola yes I get that pain too, got it now.
My understanding is that some individuals with potassium channelopathies test normal even when episodic. I suspect a neurologist will order genetic testing if it is considered a serious possibility. Of course, not much is known about some of these channelopathies, so who knows which neurologists know their way around the nuances?
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ahimsa
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@Jenny TipsforME (Hmm, will a username containing spaces generate an alert? I've never tried it)
I'm so sorry that you went through this. I read your posts when it happened but since I had no personal experience of paralysis, and no suggestions, I never posted.
I do get back of the head aching and soreness, sort of like a bruised feeling. It's one of the many symptoms I've mentioned to doctors during the early years of my illness (pretty much don't bother these days).
One time I asked my doctor whether my pain could be from swollen lymph nodes. Because it felt a bit like that kind of pain. She told me there were no lymph nodes in that area! (LOL - Can you tell that I've never taken any anatomy, not even biology in high school? math, physics, etc., but no biology)
It's more likely something to do with blood flow since I have problems with Orthostatic Intolerance (NMH, POTS). But who knows.
At any rate, I hope you find some answers for your paralysis. It is a shame that a diagnosis of ME means the doctors don't do much searching for an explanation when something like this happens. It's one thing to ignore minor symptoms, but PARALYSIS? Sheesh.
I'm so sorry that you went through this. I read your posts when it happened but since I had no personal experience of paralysis, and no suggestions, I never posted.
I do get back of the head aching and soreness, sort of like a bruised feeling. It's one of the many symptoms I've mentioned to doctors during the early years of my illness (pretty much don't bother these days).
One time I asked my doctor whether my pain could be from swollen lymph nodes. Because it felt a bit like that kind of pain. She told me there were no lymph nodes in that area! (LOL - Can you tell that I've never taken any anatomy, not even biology in high school? math, physics, etc., but no biology)
It's more likely something to do with blood flow since I have problems with Orthostatic Intolerance (NMH, POTS). But who knows.
At any rate, I hope you find some answers for your paralysis. It is a shame that a diagnosis of ME means the doctors don't do much searching for an explanation when something like this happens. It's one thing to ignore minor symptoms, but PARALYSIS? Sheesh.
taniaaust1
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Hi Jenny, I've had bouts of paralyses too when I had very severe ME and they are scary. Mine was different thou to what you described. Yours is sounding more to like maybe extreme weakness (where it becomes impossible to lift things like arms as after all you said you could still squeeze doctors hand) along with an issue initiating movements coming more so from the brain.
When I ME paralyse, my limbs cant be moved at all, I cant use any muscles at all, I cant even move a finger. I have the strong actual will there to "move" but its like the message cant get throu to the body part (which feels different to me other bouts where I struggle to move due to my brain functioning wrong and not wanting to initiate). I can still in such a state can move my head, my mouth (though my words may be jumbling and mumbled) and my eyes though they can become very hard to move too as if they have weights on them trying to hold or keep them shut.
It's more like I loose the know how on how to move, I remember one incident from when I was extremely sick where I was staring at my finger trying to use every ounce of my strong will to get it to move during a paralyses incident and it wouldnt even twitch.. it was like my finger could of been on another and not me, no connection with it at all. (I dont know if it had touch sensation at all as I couldnt touch it either to find out).
I think there are several different issues ME patients have with movement
1/ heaviness making it hard or near impossible to move, body parts becoming too heavy to move (or one becoming too weak to move them)
2/ a complete neurological disconnect where the will to move is there but the part wont move
3/ where one looses will to actually move so will then stay in same positions as if paralysed (if think of this kind related to some kind of seizure)
Ive experienced all of these.
.......
sounds like you also could of had some sleep paralyses at some point. Sleep paralyses isnt an uncommon thing even among healthies and is just a state between sleep and awake and one finds one cant move. Focusing on a finger or toe and trying to move that will after a time break a sleep paralayses state.
....
I also have severe POTS but dont connect my past paralysis incidents to it at all, I know they are connected to me ME crashing.
I sympathise over your hospital trip with this. Near everytime I end up in hospital due to the POTS, i end up covered with pee (usually right up to my neck) due to that bedpan over flowing when I have to use it. Ive had to go home in a hospital gown on many occassions due to this (if you get a nice nurse thou, hospitals usually have spare clothes they can give you to go home in but only once have they bothered to do this, often been sent home with my butt showing out of back of the gown).
On one occassion I got a dr who wouldnt give me a saline IV and the hospital then used one of their wheelchairs to force me to leave and they put me onto a taxi and sent me home unable to walk (I live alone too). It was pits, on leaving the taxi I actually had to crawl out in public up my driveway. Fortunately I only have once been sent home in that state, I usually get given a couple of bags of saline when my POTS prevents me from being able to walk.
When I ME paralyse, my limbs cant be moved at all, I cant use any muscles at all, I cant even move a finger. I have the strong actual will there to "move" but its like the message cant get throu to the body part (which feels different to me other bouts where I struggle to move due to my brain functioning wrong and not wanting to initiate). I can still in such a state can move my head, my mouth (though my words may be jumbling and mumbled) and my eyes though they can become very hard to move too as if they have weights on them trying to hold or keep them shut.
It's more like I loose the know how on how to move, I remember one incident from when I was extremely sick where I was staring at my finger trying to use every ounce of my strong will to get it to move during a paralyses incident and it wouldnt even twitch.. it was like my finger could of been on another and not me, no connection with it at all. (I dont know if it had touch sensation at all as I couldnt touch it either to find out).
I think there are several different issues ME patients have with movement
1/ heaviness making it hard or near impossible to move, body parts becoming too heavy to move (or one becoming too weak to move them)
2/ a complete neurological disconnect where the will to move is there but the part wont move
3/ where one looses will to actually move so will then stay in same positions as if paralysed (if think of this kind related to some kind of seizure)
Ive experienced all of these.
.......
sounds like you also could of had some sleep paralyses at some point. Sleep paralyses isnt an uncommon thing even among healthies and is just a state between sleep and awake and one finds one cant move. Focusing on a finger or toe and trying to move that will after a time break a sleep paralayses state.
....
I also have severe POTS but dont connect my past paralysis incidents to it at all, I know they are connected to me ME crashing.
I sympathise over your hospital trip with this. Near everytime I end up in hospital due to the POTS, i end up covered with pee (usually right up to my neck) due to that bedpan over flowing when I have to use it. Ive had to go home in a hospital gown on many occassions due to this (if you get a nice nurse thou, hospitals usually have spare clothes they can give you to go home in but only once have they bothered to do this, often been sent home with my butt showing out of back of the gown).
On one occassion I got a dr who wouldnt give me a saline IV and the hospital then used one of their wheelchairs to force me to leave and they put me onto a taxi and sent me home unable to walk (I live alone too). It was pits, on leaving the taxi I actually had to crawl out in public up my driveway. Fortunately I only have once been sent home in that state, I usually get given a couple of bags of saline when my POTS prevents me from being able to walk.
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Jenny TipsforME
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@taniaaust1 do we pee a lot or are bedpans too small?! Did hear nurse comment on volume of liquid. I think my regulation of fluid balance is often off kilter.
Even worse that they'd discharge you with no one to help at the other end.
Do you ever get saline when your blood electrolytes are OK? My understanding is it is to boost blood volume in POTS, so not relevant whether the bit of blood they measure has electrolytes. Is that right?
From feedback elsewhere, paralysis doesn't seem to be POTS itself strictly speaking, but it is people who have POTS who get it (some of them also have ME like us). People with POTS have been found to have autoantibodies to acetylcholine receptors, as do people with myasthenia gravis (which has paralysis issues). There's drugs for this so worth trying to work out if that is it.
It did feel more like a POTS flare than an ME flare. Eg my ME can be only moderate and I have trouble speaking coherently without big pauses. I was able to talk better than average, didn't have brain fog. Of course afterwards my ME is worse but there was a gap before the PEM set in.
Generally I'm starting to notice that PEM follows from high heart rate/POTS. I know other people are observing this since more of us are wearing heart rate monitors. Probably means controlling POTS main focus for me to also control ME.
Even worse that they'd discharge you with no one to help at the other end.
Do you ever get saline when your blood electrolytes are OK? My understanding is it is to boost blood volume in POTS, so not relevant whether the bit of blood they measure has electrolytes. Is that right?
From feedback elsewhere, paralysis doesn't seem to be POTS itself strictly speaking, but it is people who have POTS who get it (some of them also have ME like us). People with POTS have been found to have autoantibodies to acetylcholine receptors, as do people with myasthenia gravis (which has paralysis issues). There's drugs for this so worth trying to work out if that is it.
It did feel more like a POTS flare than an ME flare. Eg my ME can be only moderate and I have trouble speaking coherently without big pauses. I was able to talk better than average, didn't have brain fog. Of course afterwards my ME is worse but there was a gap before the PEM set in.
Generally I'm starting to notice that PEM follows from high heart rate/POTS. I know other people are observing this since more of us are wearing heart rate monitors. Probably means controlling POTS main focus for me to also control ME.
Jenny TipsforME
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@ahimsa yes neck pain could be blood flow (that sort of pain is also called coathanger pain, top of neck, into shoulders). Can be simply Tech Neck. Can be viral related.
Jenny TipsforME
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@duncan I've got 23andme data so can have a look at SNPs to see what's likely.
3 hetero risks for myasthenia gravis
No SNP riskfor Thyrotoxic hypokalemic periodic paralysis, the other periodic paralysis will be harder to look up
Possible risk for Type 7 episodic Ataxia but not sure I'm reading this right, seems fairly common anyway and episodic ataxia is rare. Not enough CACNA1A information to work out Type 2
Anyway I've run out of spoons for that activity (and formatting text!)
3 hetero risks for myasthenia gravis
No SNP riskfor Thyrotoxic hypokalemic periodic paralysis, the other periodic paralysis will be harder to look up
Possible risk for Type 7 episodic Ataxia but not sure I'm reading this right, seems fairly common anyway and episodic ataxia is rare. Not enough CACNA1A information to work out Type 2
Anyway I've run out of spoons for that activity (and formatting text!)
Jenny TipsforME
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I've got a few risk SNPs for Acetylcholine autoantibodies which are associated with ME/CFS. Brain not up to working out how likely this is in general population. Here are mine:
The nAChR ones weren't on my 23andme.
Don't know if mAChRM3 receptors can bear any relation to temporarily being unable to move?
If you've got no idea what this means it's from http://www.la-press.com/examination...rphisms-in-acetylcholine-recept-article-a4862
"The mAChRM3 receptors are located in the gastrointestinal tract and are controlled in part by the parasympathetic nervous system through the vagus nerve.75 Moreover, clinical data report that nAChRs are involved in inflammatory bowel disease.76 CFS/ME patients often exhibit gastrointestinalassociated issues, such as irritable bowel syndrome and constipation.12,28
Dysregulation of mAChRM3 receptors may affect metabolic and cardiac responses. In normal pancreas, mAChRM3 receptors play a role in regulating insulin and glucagon secretion.77,78 Muscarinic ACh receptors expressed by pancreatic β cells have been reported to play a significant role in maintaining proper insulin release and whole-body glucose homeostasis.77 Changes in Ca2+-mediated channels may result in adverse glucose metabolic outcomes as implied in CFS/ME patients.79 Pancreatic β cells rely on transient changes in Ca2+ to initiate the complex sequence of events resulting in insulin secretion following glucose exposure. Thus, it may be argued that aberrant intracellular Ca2+ concentrations through permissive AChR activity will impede the usual and necessary sequence of events required to initiate insulin response to glucose in CFS patients.
Cardiac mAChRM3 receptors perform an array of pathological and physiological functions. mAChM2 is not the only muscarinic receptor involved in cardiac function. Rather, mAChRM3 parasympathetic control of cardiac function is well established.48 A report by van Borren et al80 has shown the effect of muscarinic AChR stimulation on Ca2+ transients, cAMP production, and pacemaker frequency in sinoatrial (SA) nodes of the rabbit. These findings imply that muscarinic agonism will have an effect on SA node function, exacerbating disturbances of proper cardioregulatory mechanisms, particularly in an environment where Ca2+ intracellular concentrations are likely to be altered due to the direct effects of receptor activity. Clinical consequences such as altered orthostatic cardiovascular responses could be predicted and could align with symptom presentation in CFS/ME
...
Conclusion
In conclusion, we report for the first time the presence of SNPs in receptors for ACh in patients with CFS/ME. Many detrimental consequences for physiological homeostasis are possible through aberrant AChR function in these patients. These scenarios require further investigation to establish whether the AChR SNPs identified in this study result in changes of function and conceivably may be associated with CFS/ME pathomechanisms and symptomatology"
Does this mean it is the likely cause of my POTS at any rate?!
The nAChR ones weren't on my 23andme.
Don't know if mAChRM3 receptors can bear any relation to temporarily being unable to move?
If you've got no idea what this means it's from http://www.la-press.com/examination...rphisms-in-acetylcholine-recept-article-a4862
"The mAChRM3 receptors are located in the gastrointestinal tract and are controlled in part by the parasympathetic nervous system through the vagus nerve.75 Moreover, clinical data report that nAChRs are involved in inflammatory bowel disease.76 CFS/ME patients often exhibit gastrointestinalassociated issues, such as irritable bowel syndrome and constipation.12,28
Dysregulation of mAChRM3 receptors may affect metabolic and cardiac responses. In normal pancreas, mAChRM3 receptors play a role in regulating insulin and glucagon secretion.77,78 Muscarinic ACh receptors expressed by pancreatic β cells have been reported to play a significant role in maintaining proper insulin release and whole-body glucose homeostasis.77 Changes in Ca2+-mediated channels may result in adverse glucose metabolic outcomes as implied in CFS/ME patients.79 Pancreatic β cells rely on transient changes in Ca2+ to initiate the complex sequence of events resulting in insulin secretion following glucose exposure. Thus, it may be argued that aberrant intracellular Ca2+ concentrations through permissive AChR activity will impede the usual and necessary sequence of events required to initiate insulin response to glucose in CFS patients.
Cardiac mAChRM3 receptors perform an array of pathological and physiological functions. mAChM2 is not the only muscarinic receptor involved in cardiac function. Rather, mAChRM3 parasympathetic control of cardiac function is well established.48 A report by van Borren et al80 has shown the effect of muscarinic AChR stimulation on Ca2+ transients, cAMP production, and pacemaker frequency in sinoatrial (SA) nodes of the rabbit. These findings imply that muscarinic agonism will have an effect on SA node function, exacerbating disturbances of proper cardioregulatory mechanisms, particularly in an environment where Ca2+ intracellular concentrations are likely to be altered due to the direct effects of receptor activity. Clinical consequences such as altered orthostatic cardiovascular responses could be predicted and could align with symptom presentation in CFS/ME
...
Conclusion
In conclusion, we report for the first time the presence of SNPs in receptors for ACh in patients with CFS/ME. Many detrimental consequences for physiological homeostasis are possible through aberrant AChR function in these patients. These scenarios require further investigation to establish whether the AChR SNPs identified in this study result in changes of function and conceivably may be associated with CFS/ME pathomechanisms and symptomatology"
Does this mean it is the likely cause of my POTS at any rate?!