Temporary paralysis I need your Insights

[Mary]

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?

@Gingergrrl - I don't know. I've never been tested for auto-antibodies. I think I've had mild POTS for years but it's been manageable. But lately my BP and HR are more erratic. Actually my BP is going higher than normal and I feel better that way, although sometimes my HR goes up too high - I don't know what's going on, but again do feel better overall so am just trying really hard to stay on top of potassium, it seems to be my Achilles heel.

 

[Mary]

I can't take anything that stimulates the adrenals, makes me crash. Including worsening of POTS, as you mentioned.

Have you ever tried an adrenal glandular? I've taken a couple of different kinds with good results - they don't deplete potassium like the licorice did. The one I'm currently taking is Drenamin PMG by Standard Process. I generally take a very small dose, but initially had to take quite a bit. And it helped so much. My chiropractor told me that steroids like Cortef push the adrenals to work harder and will deplete them further, but that the adrenal glandular supports them and gives them a rest. But I know we're all different - some people do find them too stimulating.

 

[Mary]

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

True - I believe it stops the heart. But low potassium is also potentially dangerous - it has caused extreme fatigue for me, muscle spasms and a high heart rate, even though on blood work I'm on the low side of the normal range. I suggest people try something like low-sodium V8 before starting a potassium supplement - it's next to impossible to OD on food-based potassium unless your kidneys are damaged.

I used to have a lot more fatigue before I discovered a chronic low potassium problem, when I started taking methylfolate. The methylfolate caused my potassium levels to tank rather badly with severe fatigue but since I'd read Freddd's posts about potassium, I knew what it was. I had had that severe fatigue before but never knew what it was - just thought it was another weird CFS symptom and no point in going to the doctor with it.

 

[Gingergrrl]

I suggest people try something like low-sodium V8 before starting a potassium supplement - it's next to impossible to OD on food-based potassium unless your kidneys are damaged.

This is random but in case anyone has MCAS and cannot eat/drink tomatoes, another huge source of Potassium is coconut water.

And I agree with @anciendaze from earlier post that each person in the thread has completely different needs and abilities as to what they can tolerate or what might be dangerous for them.

I had been curious if potassium channelopathies were similar in treatment recommendations to calcium channelopathies but sounds like they are very different. I know I am supposed to avoid anything that further blocks the calcium channel and try to lower the antibody (easier said than done LOL.)

This is a very interesting thread and makes me wonder if ME/CFS is a channelopathy or if there are a group of us with an ME/CFS diagnosis but actually have a channelopathy issue instead?

(Sorry this was not all directed @Mary, I just quoted her re: the V8 and then realized I had other random thoughts to add .)

 

[Mary]

This is a very interesting thread and makes me wonder if ME/CFS is a channelopathy or if there are a group of us with an ME/CFS diagnosis but actually have a channelopathy issue instead?

@Gingergrrl -- this is all new to me, but considering all the problems we have with POTS and electrolytes and phosphorus too, it's intriguing -- you have some very interesting "random thoughts"!

 

[kangaSue]

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.

Depends on the condition. IVIG or Plasmapheresis is used to treat some with VGKC encephalitis. As a matter of interest, serum alkaline phosphatase tends to be higher in those with VGKC-disease.
http://www.ncbi.nlm.nih.gov/pubmed/27469409

The number and complexity of potassium channels is even greater than for calcium channels. I thought I might have a potassium channel antibody issue when I found that potassium channel opener meds greatly improved on my GI dysfunction for a while but testing actually found the low (normal range) titre of N-type VGCC Ab

 

[anciendaze]

There is a special reason I am super cautious about making recommendations concerning potassium channel problems at the moment. This probably does not apply to most of you, but there are some people out there with extreme problems that don't become apparent until they are given particular drugs.

Patients who have problems with general anesthesia are one kind, and you can check published statistics to see that a small percentage die for unexplained reasons. The people I'm talking about have problems with routine medical procedures like use of muscle relaxants during colonoscopies. Use the wrong type and the patient goes into malignant hyperthermia. In one case where there was a known sensitivity to common anesthetics the surgeon ignored warnings and used a muscle relaxant so he could intubate the patient. The resulting malignant hyperthermia caused the patient to die hours later. Once the response had been triggered there was little medical personnel could do.

I've just had a report from another patient with a severe channelopathy about a colonoscopy which took unusually long -- without anesthesia. After this was over the doctor asked questions which revealed he had only read the instructions directly associated with what he was supposed to do normally during the procedure. He had ignored the pages about what to do, or not, if anything went wrong. The doctor was merely curious about what was going on in a strange case; the patient was alarmed at how close he had been to an agonizing death if the surgeon had done what was customary in a crisis.

I want to emphasize that such cases are extremely rare, just not nonexistent. The patient who survived calls himself "a zebra among zebras" (based on the medical advice to young doctors "when you hear hoofbeats think horses, not zebras.") Using arguments from "evidence-base medicine" to recommend treatments that work for the vast majority will tacitly condemn some number of exceptional patients to death. I'm still waiting for an answer from medical doctors to my question: "what number of excess deaths do you consider acceptable in medical practice?"

 

[anciendaze]

@Gingergrrl,

I'm still trying to pull together a post on the variety of ways neuromuscular junctions can fail, which isn't easy. I am particularly aiming at common "diagnostic tripwires" which appear to be based on the absurd assumption that there is no interaction at all between the various problems at such junctions.

What may be relevant to you personally is the extent to which I now suspect you have autoantibodies to both beta-adrenergic receptors and muscarinic acetylcholine receptors. A great deal about your strange medical history would be explained if this were true. Whatever causes autoimmune response in patients with antibodies to N-type calcium channels, but without detectable small-cell lung cancer, probably induces antibodies to muscarinc acetylcholine receptors. The two seem to go together, even if nobody can explain this.

 

[Gingergrrl]

Depends on the condition. IVIG or Plasmapheresis is used to treat some with VGKC encephalitis.

KS, thanks and IVIG and PP were both recommended for me by the doctor who ordered the test that discovered my VGCC Ab (but he is no longer my doctor and it was more of a one-off consult than anything ongoing). You answered my question that some of the same treatments could be used for the VGKC Abs depending on the cause.

The number and complexity of potassium channels is even greater than for calcium channels.

Wow, and I did not realize this. Your comment just made me recheck my PAVAL test again to confirm that I was negative on all of the Potassium Channel Abs and I am.

Patients who have problems with general anesthesia are one kind, and you can check published statistics to see that a small percentage die for unexplained reasons. The people I'm talking about have problems with routine medical procedures like use of muscle relaxants during colonoscopies. Use the wrong type and the patient goes into malignant hyperthermia. In one case where there was a known sensitivity to common anesthetics the surgeon ignored warnings and used a muscle relaxant so he could intubate the patient. The resulting malignant hyperthermia caused the patient to die hours later. Once the response had been triggered there was little medical personnel could do.

AD, thank you for this phenomenal info that I know will be very useful to Jenny and also to me even though I do not have the potassium Abs. I just bookmarked your page on malignant hyperthermia which I had never heard of before. One of the neuros that I saw after learning of the antibody said that I should never have an anesthesia that blocks the calcium channel and the doctors (if I ever needed surgery in future) would have to truly understand that I have this Ab and what it could mean. I am 45 and colonoscopies are not advised in the US until age 50 so I am safe for now!

I'm still waiting for an answer from medical doctors to my question: "what number of excess deaths do you consider acceptable in medical practice?"

This question gave me chills b/c I had a baby sister who died of medical malpractice in a lung related surgery. Even one death is one too many but (some) doctors do not see it that way. Of course there are some phenomenal doctors out there too so I don't want to over-generalize.

@Gingergrrl, I'm still trying to pull together a post on the variety of ways neuromuscular junctions can fail, which isn't easy. I am particularly aiming at common "diagnostic tripwires" which appear to be based on the absurd assumption that there is no interaction at all between the various problems at such junctions.

Thank you and I saw where you re-posted this in my ER thread so I replied there instead of here and also bookmarked it for the future to show my doctors. I know it is just a theory but we need theories right now very badly! I think a lot of the OP, Jenny, experiencing hours (days?) of paralysis and docs just dismissing it as "part of her ME." How is this acceptable? It is not.

 

[anciendaze]

@Gingergrrl,

I feel the need to take exception to one aspect of that article I linked. While patients with identified defects in that gene will definitely be vulnerable to malignant hyperthermia, the idea that the problem is restricted to them is probably wrong.

We see a pattern in many medical problems with identified genes. At first it looks like only those patients with the identified genetic variation are vulnerable. As more data come in the number of identified variant sequences increases, but the percentage of patients with identified sequences exhibiting the problem goes down. In the case of HKPP it now looks like only 10% of patients in North America with objective evidence of the problem have a known genetic variation.

What I believe is going on is that most of the cases are probably the result of autoantibodies attacking variations which would not be serious functional problems by themselves. The target molecule plus antibody is completely non-functional.

Added: Just to avoid panic, I want to say that this particular problem (MH) is extremely rare. There is a definite association, however, with some rare diseases. When other factors tell you this patient is a "zebra", you need to proceed with caution.

 

[Gingergrrl]

What I believe is going on is that most of the cases are probably the result of autoantibodies attacking variations which would not be serious functional problems by themselves. The target molecule plus antibody is completely non-functional.

So, do you (or do doctors at this point in time) know what makes the combination of genetics plus auto-antibody switch from non-functional to pathogenic? I was discussing this with Hip in another thread but we were not sure. Actually I shouldn't say "we" b/c I had no clue about this until that thread!

Added: Just to avoid panic, I want to say that this particular problem (MH) is extremely rare. There is a definite association, however, with some rare diseases. When other factors tell you this patient is a "zebra", you need to proceed with caution.

Thanks and at present, these things are very helpful vs. causing panic (although in the event that I actually need surgery/anesthesia that will change very quickly and I will be asking you guys a lot of questions)!

 

[anciendaze]

So, do you (or do doctors at this point in time) know what makes the combination of genetics plus auto-antibody switch from non-functional to pathogenic? I was discussing this with Hip in another thread but we were not sure. Actually I shouldn't say "we" b/c I had no clue about this until that thread!...

Some functions are absolutely vital, so blocking them is pathological, if not immediately lethal. As to what causes the body to manufacture antibodies to such important molecules, at this point we scarcely have a clue.

What I can say with some confidence is that once you find several autoantibodies attacking unrelated targets you have to assume there will be others caused by the same pathological process. Since mast cells could be called the "border guards" of the immune system, my guess is that they play a substantial role in cases where there are multiple false alarms. Mast cells are involved in a LOT of chemical communication with other immune cells, which we hardly understand.

This is, however, only my personal opinion.

If you need anesthesia, and a good anesthetist is aware of your history, I think you will be OK. They don't need to know the reasons behind a response to be aware that it is dangerous. This is one class of medical professionals who find out very quickly when they make such a mistake. They also continuously monitor vital signs so they know when things start to go bad while it is still possible to intervene. They do their best to avoid lawsuits for malpractice.

 

[Gingergrrl]

As to what causes the body to manufacture antibodies to such important molecules, at this point we scarcely have a clue.

Thanks and I was just curious how far the science is with these types of issues.

Since mast cells could be called the "border guards" of the immune system, my guess is that they play a substantial role in cases where there are multiple false alarms. Mast cells are involved in a LOT of chemical communication with other immune cells, which we hardly understand.

This makes a lot of sense and I think Mast Cells play a big role with many things we are not aware of.

If you need anesthesia, and a good anesthetist is aware of your history, I think you will be OK. They don't need to know the reasons behind a response to be aware that it is dangerous. This is one class of medical professionals who find out very quickly when they make such a mistake. They also continuously monitor vital signs so they know when things start to go bad while it is still possible to intervene. They do their best to avoid lawsuits for malpractice.

Agreed and if I ever needed surgery, unless I could actually speak with the anesthesiologist first, I would not do it. I agree (at least in the US) that they do their best to avoid lawsuits and if someone had two rare things (MCAS and ion channelopathy) that this would grab their attention, even if the sole motivator was to avoid a lawsuit.

 

[Jenny TipsforME]

Oh I didn't get alerts for the last flurry of responses. Wonder why?

 

[Gingergrrl]

Oh I didn't get alerts for the last flurry of responses. Wonder why?

How weird but good to hear from you and I have been hoping you were okay.

 

[Sushi]

Oh I didn't get alerts for the last flurry of responses. Wonder why?

If you miss clicking on one response you will have to "re-watch" the thread.

 

[Jenny TipsforME]

@Gingergrrl I've been a bit up and down which is how it goes, but I've not had the paralysis again thankfully. I saw my POTS (cardiologist) doctor today and he says I need to see a neurologist. He hadn't heard of other POTS folk getting this which is slightly odd as online it does seem to be POTS patients who get this (sometimes overlapping ME). He seemed to nod at the NMJ and Periodic Paralysis stuff but said it's not his area (which it's not).

 

[Gingergrrl]

@Gingergrrl I've been a bit up and down which is how it goes, but I've not had the paralysis again thankfully. I saw my POTS (cardiologist) doctor today and he says I need to see a neurologist. He hadn't heard of other POTS folk getting this which is slightly odd as online it does seem to be POTS patients who get this (sometimes overlapping ME). He seemed to nod at the NMJ and Periodic Paralysis stuff but said it's not his area (which it's not).

Jenny, am glad that you have not had the paralysis again and am hoping it never happens again! I agree that a Neuro would be the best person to help if you can find a good one who takes this seriously. I saw two absolutely horrible mean-spirited Neuro's back to back until I finally found a good one who I was referred to by my cardio. She is the ultimate reason that I got approved to try IVIG and took the antibody seriously.

My understanding, which is minimal, is that many of these antibodies can cause a paraneoplastic syndrome (PNS) which can lead to all sorts of symptoms including dysautonomia/POTS so this could be the connection although the average doctor does not know squat about any of this. I'm now having doctors/nurses asking me to explain things which is insane if you really knew the level of science that I came into this with.

 

[Nemesis]

I have Hemipleg migraine it caused me in the past temporary paralyzing, or temporary blindness, or temporary deafness or temporary speaking problems, thinking temporary unfeeling with pain, also vasomotor or vasco dilation can cause that

 

[Jenny TipsforME]

@Nemesis I do get migraines, although a lot less on POTS meds. How long have you had temporary paralysis at a time? Is it with other migraine symptoms? I'm generally intolerant of electric light but that day I was ok with hospital lights.