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    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

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Temporary paralysis I need your Insights

duncan

Senior Member
Messages
2,240
@Jenny TipsforME , @Gingergrrl , I fear my knowledge is limited to ATS and the KCNJ2 mutation manifestations. For that particular manifestation, though, the victim does not necessarily have to be hypokalemic (although most are). A significant portion prove to be hyperkalemic, and some can even demonstrate normal potassium levels.

They could not check my wife because her ATS is primarily cardiac. She has LQT and severe arrythmias and cardiomyopathy - so they could not evoke an episode without possibly triggering a cardiac incident. But one of the meds the drs prescribed her LOWERS potassium, so go figure. I have to reach out to them to explain that; I did not realize its effects until after the examination and I had researched them...

My wife has to do this, generate this email conversation, since I am not the patient. She hasn't even set up the account yet. When she does, I will try to get some more insight, and whatever I find out, I will report back here if I can. @anciendaze has been kindly helping explain things to me, as well.
 

anciendaze

Senior Member
Messages
1,841
Folks, I can't explain everything. What I can tell you is that emphasis on levels of potassium only catches some cases, perhaps missing the majority. You are repeating a misunderstanding which turns up in many M.D.s.

The serum ion levels that are easy to measure are a small part of the story. Movement of potassium and sodium ions in and out of cells is highly dynamic. Every time a neuron fires there is movement of potassium, sodium, chloride and calcium ions across membranes. Intracellular concentrations change rapidly.

Calcium is important not just in nerves, but in every situation where biochemicals stored inside vesicles in cells are released when those vesicle fuse with cell membranes. That was why Gingergrrl's doctor tried calcium channel blockers to treat MCAS. He/she was hoping to reduce activity of mast cells. Unfortunately, she had a specific problem with antibodies to N-type calcium channels which this exacerbated.

You also find a great deal of movement of ions into and out of muscle fibers during activity. Sharp distinctions between neurological and metabolic activity only occur in textbooks.

Recently, I've been particularly interested in metabotropic receptors. These are surprisingly complicated. They respond to neurotransmitters and control ion channels, but this is not a simple mechanical operation. Biochemicals called second messengers are involved, and so are protein kinases. There are a number of ways operation can fail, and so far medicine has only addressed some of these in a few locations.

Typical ionotropic receptors operate on a time scale of milliseconds, but metabotropic receptors can function on much longer time scales of seconds. This is still too short to show up on common clinical measurements, where doctors are looking for readings that are stable for hours or days.

Life is a process of managing continual change. Defects in processes can produce changes in levels, but this is far from universal.

I'd liken current medicine to an automobile mechanic who does nothing until the engine in your car is in danger of seizing because the level of oil in the crankcase is too low. Had he paid attention to the oil drips on the driveway he could have seen the pathological process leading to failure, and followed this back to leaking seals. "Nah! We see that all the time. Lots of cars leak oil, and keep on running."
 
Messages
36
I too get temporary paralysis and I therefore appreciate this thread. For me it's associated with adrenal problems and appear if it has been too long since I ate or after a meal when the blood goes to the stomach.

However, a doctor I just met said "we usually call those episodes for Parkinsonism". Is there anyone of you that knows more about that?
 

Jenny TipsforME

Senior Member
Messages
1,184
Location
Bristol
@Lindberg what diagnosis do you have (or should probably have)? I'm finding people who say they get temporary paralysis tend to have POTS (sometimes with ME). I don't know why.

Have your adrenal problems been confirmed with tests when it has been happening?

I've done the saliva test you repeat through the day a few years ago. My morning cortisol was perfect but then went low later (compared to what it should do, it is normal to decrease a bit). My DHEA was also low.
 
Messages
36
@Jenny TipsforME My diagnosis is ME and my doctor and I both assumes I also have POTS, but I haven't done a proper test for it. I need my glass of water with salt, though... :)

My cortisollevel is low but within the threshold for being ok. Everything points to adrenal problems though when I'm crashing. Losing weight, losing water, neverending period, hollow eyes, hyperpigmented spots etc.

The paralysis comes with crashes and during the weeks after if I'm not taking care of the bloodsugar and elektrolyts properly. I was recommended not to go to the emergency room when I was really bad. This was because my doctor didn't understand the severity back then, so I haven't been checked during a crash. I gave myself hydrocortison on the arms, drank a lot of water with salt, ate all the time and tried so survive...
 
Messages
36
@Jenny TipsforME Yes, the cream since that was what I had. I only used it during the worst crashes/days to support the adrenals, didn't dare to use it for any longer period of time. I placed it on the inside of the arms where the skin is thinner and repeated a couple of times per day. Helped everything to calm down, to not be as acute as before.

For the paralysis though I still needed to keep the bloodsugar stable, eat frequently, drink water with salt and to just rest.

Scary feeling getting those paralysis, one is totally dependant on others helping you to get what you need. Feels like one has aged a lot very fast... Or as the body has glued itself in the position you are at. My mimic gets really stiff as well, difficult to speak (besides being weak) and difficult to chew. Would be interesting to know exactly what happens!
 

Mary

Moderator Resource
Messages
17,292
Location
Southern California
@Jenny TipsforME - This is a very interesting thread, but I am so sorry you had to go through 11 hours of paralysis - I can't imagine how terrifying that must have been!

I don't have anything of substance to add here, just that I have some difficulty keeping my potassium levels up where they need to be. I've had a couple of episodes of what I would call self-induced POTS, where something I took (licorice, horsetail) caused my potassium levels to tank and where it took me a day or 2 or even more to figure out what was going on. My heart rate got quite high and BP lower. My potassium also tanked with methylfolate.

So I am learning I need to drink at least 2 glasses of low-sodium V8 a day (900 mg. potassium chloride each glass) plus 800 mg. or more potassium gluconate. I get extra fatigued and muscle twitches, and lately, high HR otherwise.

I hope you get some answers here!
 
Messages
36
@Mary I can't take licorice either, my thougth was that it stimulates the adrenals but they are too weak so they are putting on the breaks instead. I can't take anything that stimulates the adrenals, makes me crash. Including worsening of POTS, as you mentioned.

Interesting also that you get muscle twitches and need extra potassium, it's the same for me. I'm just about to look into some good source for that. Thank you for writing what you are taking!
 

Justin30

Senior Member
Messages
1,065
Over consumption of licorice can result in some paralysis. See articles:
https://scholar.google.com/scholar?...&q=related:RqPqpEXXeIaQVM:scholar.google.com/

Licorice like florinef can deplete potassium and I think mess up phophate levels. If POTS the hypovolemic type is also present than potassium levels need to be kept from what I understand around 4.2 or higher. I am not a Dr though.

I had paralysis issues when potassium depleted from supplements and meds.

High doses of B12 I have heard can also leech potassium.

If you read the symptoms of low potassium paralysis can kind of make sense if its low.

Not a Dr though so my knowledge os just what I have read.
 

Strawberry

Senior Member
Messages
2,079
Location
Seattle, WA USA
Calcium is important not just in nerves, but in every situation where biochemicals stored inside vesicles in cells are released when those vesicle fuse with cell membranes. That was why Gingergrrl's doctor tried calcium channel blockers to treat MCAS. He/she was hoping to reduce activity of mast cells. Unfortunately, she had a specific problem with antibodies to N-type calcium channels which this exacerbated.

Hi anciendaze, I'd like to clarify this post/paragraph for my own issues. My dr prescribed amlodipine for high blood pressure, which is a calcium channel blocker. I have felt worse since being on the medication, yet my heart palpitations went away by 95% after going on the medication. That would mean it was mast cells affecting my palpitations? I have severe palpitations to medicines, and moderate to auto pollution. Also, my local doc didn't know about mast cells at the time of the amlodipine prescription, Dr Kaufman just diagnosed that in the last few months. I denied it at first, but am now pretty positive MCAS is what I have.

Also if I can ask, since I apparently DO have MCAS, would that mean that staying on amlodipine and all the MCAS meds I am now on, that eventually my inability to stand for more than 2 or 3 minutes will get better?

I know you are not a Dr and can't advise me, but I am curious if you have an opinion. I had made the connection to the amlodipine recently, and wondering if this is the right medication for me. My local Dr knows nothing of MCAS...
 

Justin30

Senior Member
Messages
1,065
That would mean it was mast cells affecting my palpitations?

I am curious about this to does MCAS typically cause palpitations...i know this is not part of the topic but pain meds have reduced my palpatations.

I personally think the palpatations are part of dyautonomia ie POTS or NMH. I am going to talk to my POTS Dr in Sept and get input.
 

Strawberry

Senior Member
Messages
2,079
Location
Seattle, WA USA
@Justin30 I honestly don't know, but my suspicion is that when something makes my mast cells degranulate (like meds) it degranulates a chemical that affects my heart. I know I have something orthostatic intolerance wise, but not sure what yet. This is all so new!

Maybe this should be moved to a new thread? We definitely are off topic.

Apologies to the thread and moderator.....
 

kangaSue

Senior Member
Messages
1,849
Location
Brisbane, Australia
So this means that the 23andMe (or other genetic data) could be totally normal and then someone develops a channelopathy later in life?
Inflammation alone is enough to alter ion channel function through alteration in the timing of movement of calcium, potassium, sodium and chloride into and out of cells.

I think that's called altered gene transcription rather than a genetic mutation which 23andME tests for.

Both inherited gene mutations and altered gene transcription of ion channels in disease states or following tissue insult have collectively been termed as “channelopathies”
We just cross posted at the exact same moment! How strange that the calcium channel SNP causes hypokalemic PP! Am hoping @kangaSue or @anciendaze will explain this to us!
I wish.
 

anciendaze

Senior Member
Messages
1,841
General comment on calcium channels affecting things: every time a cell releases chemicals stored in a vesicle by fusing the vesicle with the cell membrane some kind of calcium channel is involved. Mast cells are only one such type of cell, there are many others. Neurons use voltage-gated calcium channels when they release neurotransmitters, and at the moment we believe there are 5 types of these. They are quite different from the types found in mast cells, but there are common subunits which can be targets of antibodies.

@Strawberry the subject of how calcium channels affect the heart is pretty substantial. I don't have to make any assumptions about mast cells to explain problems. Yes, there might be some such effect, but there are plenty of alternative explanations. You need an expert on MCAS to decide if your problems can be traced to mast cells. It takes a detailed review of medical history and test results to untangle these diagnostic messes.
 

Gingergrrl

Senior Member
Messages
16,171
My wife has to do this, generate this email conversation, since I am not the patient. She hasn't even set up the account yet. When she does, I will try to get some more insight, and whatever I find out, I will report back here if I can.

@duncan when you initially posted that someone close to you was diagnosed with ATS, I had no idea it was your wife and am so sorry to hear this. It sounds like you are really there for her and are a great support and husband. I am hoping she was able to set up the account and get the info that she needed re: the medication and potassium. It is so frustrating trying to solve all of these complex puzzles on our own and am so grateful for PR.

Calcium is important not just in nerves, but in every situation where biochemicals stored inside vesicles in cells are released when those vesicle fuse with cell membranes. That was why Gingergrrl's doctor tried calcium channel blockers to treat MCAS. He/she was hoping to reduce activity of mast cells. Unfortunately, she had a specific problem with antibodies to N-type calcium channels which this exacerbated.

I wanted to clarify this in case it helps anyone else in the thread. My former cardio had me try the calcium channel blocker (Diltiazem) in 2014 for POTS at least a year before I had overt MCAS. I had a disastrous reaction as Anciendaze stated and I suspect this is b/c of having the calcium auto-antibody but I just did not know it yet. I was officially diagnosed with MCAS in mid 2015 (but had subclinical symptoms all my life). So the CCB was not for the MCAS, it was to try as an alternative to a beta blocker for POTS, except that I did not tolerate it at all (it lowered my BP to where I vomited and almost fainted which the BB does not do.)

I don't have anything of substance to add here, just that I have some difficulty keeping my potassium levels up where they need to be.

Mary, I am the same in that I only maintain potassium levels by supplementing prescription Potassium 20 MEQ every night. I do not know how or if this relates to the auto-antibodies?

Inflammation alone is enough to alter ion channel function through alteration in the timing of movement of calcium, potassium, sodium and chloride into and out of cells.

I think that's called altered gene transcription rather than a genetic mutation which 23andME tests for.

Both inherited gene mutations and altered gene transcription of ion channels in disease states or following tissue insult have collectively been termed as “channelopathies”

Thank you @kangaSue and that is really helpful. I had wondered if obtaining genetic info would be helpful vs. just accepting that I have a channelopathy now and treating it moving forward. I had a MAJOR tissue injury to my arm from Levaquin and wonder if this led to the "gene altered transcription" type of channelopathy that you mention.

Lastly I have a question for @anciendaze @duncan @kangaSue re: Jenny and her possible potassium channelopathy. Would the same types of treatments used for calcium channelopathies be used for potassium channelopathies? Am asking in general and not meant as treatment advise for anyone.
 

anciendaze

Senior Member
Messages
1,841
@duncan...
Lastly I have a question for @anciendaze @duncan @kangaSue re: Jenny and her possible potassium channelopathy. Would the same types of treatments used for calcium channelopathies be used for potassium channelopathies? Am asking in general and not meant as treatment advise for anyone.
At this point I would say no, without knowing if we are dealing with autoantibodies or inherited genes or some combination. There are non-selective ion channels which handle potassium, sodium or calcium ions indiscriminately, but I would not bet on any treatment affecting them avoiding other problems. There are many classes of ion channels which are quite different in their chemical characteristics and functions, even when they handle the same simple ion. Here is a table for comparison of just calcium channel types. It is not complete.

Before anyone starts "throwing potassium at the problem" I want to remind people that KCl is used in lethal injections.