For my possible MIS-diagnosis in 2003, of Parkinson's disease...
Has anyone ever heard of channelopathy?

I think that is the same thing as an "ion channel disorder". Ion channels are (if I remember right) tiny tubes that pass through the cell wall and serve as pathways for the particular ions (electrolytes) to be moved in and out as needed. If the channels are not formed properly then this movement is impeded.

I (and Laura too, I suspect) have wrestled with this for the last couple of years. It is beastly complicated but it really may explain PD as, at least in part, a problem with electrolyte imbalance.


1. Fortschr Neurol Psychiatr. 1997 Nov;65(11):481-8.

[Ion channel diseases in neurology].

[Article in German]

Lerche H, Mitrovic N, Lehmann-Horn F.

Abteilung Angewandte Physiologie, Universität Ulm.

Since 1990, many mutations, in genes encoding ion channels have been discovered
to cause disorders characterized by hyper- or hypoexcitability of skeletal muscle
or the central nervous system (CNS): i) mutations in the muscle chloride channel
gene lead to a loss or change of function of the channels and cause an abnormally
low total chloride conductance resulting in hyperexcitability of the muscle fiber
membrane in the dominant and recessive form of myotonia congenita; ii) numerous
dominant point mutations in the gene encoding the muscle sodium channel
alpha-subunit cause incomplete sodium channel inactivation. Dependent on the
inactivation parameter altered and the degree of the gain of function induced by
a given mutation, the muscle episodically becomes hyper- or hypoexcitable (i.e.
stiff or weak), particularly in response to elevated serum potassium
(potassium-aggravated myotonia, hyperkalemic periodic paralysis) or cold
environment (paramyotonia congenita); iii) dominant point mutations in the gene
coding for the muscle L-type calcium channel alpha(1)-subunit can cause episodes
of muscle inexcitability (i.e. weakness), particularly in response to lowered
serum potassium (hypokalemic periodic paralysis); despite the recently discovered
etiology of the disease, the pathogenesis of the weakness is still unknown; iv)
dominant mutations in a voltage-gated potassium channel expressed in the CNS
cause episodic ataxia type 1 presumably by antagonizing repolarization of the
cell membrane; v) dominant mutations in a neuronal calcium channel alpha-subunit
may cause either episodic ataxia type II or familial hemiplegic migraine by a so
far unknown pathomechanism; vi) the first mutation in an ion channel associated
with an inherited form of epilepsy, nocturnal frontal lobe epilepsy, was found in
the alpha(4)-subunit of a neuronal nicotinic acetylcholine receptor.

PMID: 9480290 [PubMed - indexed for MEDLINE]

And the really humorous (not) part? Levodopa has hypokalemia "sometimes severe" as one of its side effects!