Just want to chime in with the little I actually know. My main source of information is a patient with hypokalemic periodic paralysis (caused by low potassium levels) I have known for many years. For a long time I didn't realize his problems were caused by that because he didn't get an accurate diagnosis until 2010. Unfortunately, there are multiple types of low potassium channelopathies, and even some which involve hyperkalemic periodic paralysis (too much potassium).
If that were not enough there are many possible types of potassium channels. Some are voltage-gated (though you won't be able to measure the voltage with a common volt meter), some are controlled by ligands which may be neurotransmitters, some even involve
calcium channels controlling potassium channels. There are even the
G protein-coupled inwardly-rectifying potassium channels which allow potassium ions in, when gated by the G-protein receptor, but will not allow them out. The ion pores themselves are often fairly simple, like some kind of valve, but the control mechanisms are not. Recognizing neurotransmitter molecules is more complicated than recognizing particular ions, and recognizing proteins is an order of magnitude harder. A lot can go wrong.
In the problem Gingergrrl experiences the ion channel antibody which has been found interferes with a calcium channel inside a neuron on the pre-synaptic side of a neuromuscular junction. Does calcium cross the synapse? No, the neurotransmitter acetylcholine carries the impulse to the post-synaptic side. If she had antibodies to that receptor, she would have a different neuromuscular disease called
myasthenia gravis. There are then other ion channels inside muscle fibers needed for their operation. Signalling involves ATP as well as potassium and sodium ions. (While we tend to think of ATP and other purines as a kind of molecular fuel for cell metabolism, nature thinks nothing of also using them for signalling. Very little in biology has only a single purpose.)
Ion channels of a single type don't operate alone. Nerves, for example, require pumping sodium and potassium ions in opposite directions before they can fire. When they fire, these ions race back to the other side of the membrane. This happens over and over again, typically many times a second.
When you consider the multiplicity of types, and the many ways they are linked together in cascades to control metabolic processes, you almost wonder if they were designed by Rube Goldberg (or Heath Robinson). Why use calcium ions to cause vesicles containing acetylcholine to fuse with cell membranes and release their contents when these molecules will be picked up a short distance away, and then used to generate another ionic signal which will cause a muscle to contract, if the signal arriving at the presynaptic side was already electrical/ionic and depended on different ions?
One big problem with standard medical thinking is that we prefer linear chains of causation, but all of these mechanisms involve feedback processes, making causation circular. This can mean that an attempt to move things in one direction can do precisely the opposite.
I wish patients with these problems could skip ahead a decade or two to a time when this has been worked out, and proven treatments are available. At present many patients and doctors are involved in fairly random trial and error.
