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This is where
@anciendaze is the expert IMO and I am not sure how frequently someone with PP would have episodes or at what age they might start. I do not have PP but have an antibody that blocks the calcium channel. I honestly do not know when I developed this antibody (and all of the others) but suspect they were all post-viral...
I'm not an expert, but I know someone who is. This subject is a work-in-progress, and I am encouraged that this doctor said there are many different forms of periodic paralysis. This is much better than claiming it does not exist.
I'm now rethinking some previous assumptions after learning about "nutcracker syndrome" or "superior mesenteric artery syndrome", though I have no idea if this applies here. "Real cases", in the minds of doctors, tend to involve both pain and hematuria. This is a combination of a serious complaint with a conspicuous clinical sign. Nothing in nature demands this. My guess at the moment is that a great deal of variability in presentation is due to immune response to occult bleeding. (Localized ischemia causing sterile cell death may also provoke an autoimmune response.)
Powerful immune responses to cancers of the ovaries or testes are known to cause paraneoplastic syndromes. I am speculating that bleeding in the same organs could provoke an identical response.
W.R.T. age at onset of PP, this typically shows up in late teens. Most patients go years before recognizing triggers, so clinical presentation tends to be very uneven, depending on what they were doing just prior to seeing a doctor. Most patients find some pattern of behavior which minimizes problems before getting a professional diagnosis. (Some have gone 30 years without a correct diagnosis.) Not all of these behaviors makes sense, and some may be like a gambler's lucky socks. Others are definitely connected with problem foods or activities. You don't have to psychoanalyze the patient to find out why they are generating new behaviors in response to a condition that leaves them paralyzed.
Early studies in Europe suggested there might be identifiable genetic causes in 30% of cases. Studies extended to North America, with a highly-varied and more mobile population, have recently found only 10% with identified genetic factors. You can't depend on genetic testing any more than you can in type III Ehlers-Danlos Syndrome. Response to changes in electrolytes, carbohydrate loads and/or exercise, seen on objective tests, will clearly distinguish patients with life-threatening disease, but we are still in the dark about the incidence of less severe conditions.
