multiple sclerosis

Ron Apland apland at mala.bc.ca
Sat Oct 26 11:52:31 EST 1996


In article <224 at homostudy.win-uk.net>, gord at homostudy.win-uk.net (G K GRAY) writes:
>  
> In article <327163FC.22EF at indigo.ie>, John King (johnkate at indigo.ie) writes:
>>Is the cause of signs for MS due to demyelination?  Is it due to
>>decreased nerve conduction?  Could nerve conduction increase if the
>>nerve was stimulated more?
>>
> Since it is an observable but inadequately explained fact that
> myelin somehow accelerates the neural impulse the answer to your
> first two questions must be YES! The third question remains
> problematic. In MS the myelin sheath loses contact with the axon,
> whose ion pores are clustered where the Nodes of Ranvier have been,
> and none over the internodal lengths.  This is unlike unmyelinated
> axons whose ion-pores are evenly distributed. Hence hyper-
> stimulation is unlikely to reap any benefit, but sometime this might
> be worth an experiment.

I read an article in New Scientist some 8-10 years ago that suggested 
a reason for a series of remissions accompanying a slow deterioration
with MS.  In a nutshell it suggested that degeneration of function is
the result of demyelination to the point that an action potential can
no longer make it from one Node of Ranvier to the next somewhere along
the axon because of the absence of ion channels between the nodes.  As
the axon adjusts (whatever that means) to the deterioration new ion
channels begin to appear between the nodes fostering the action potential
and returning some function.  Does anyone know of this hypothesis (finding?)
and what status it has now?  I'm a casual reader in this area and have
not again seen mention of it. On the otherhand, if it is accurate it would
suggest that repeated stimulation of the axon might indeed have some
beneficial effect.



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