multiple sclerosis

G K GRAY gord at
Sun Oct 27 06:20:18 EST 1996

In article <1996Oct26.095231 at>, Ron Apland (apland at writes:
>In article <224 at>, gord at (G K GRAY) writes:
>> In article <327163FC.22EF at>, John King (johnkate at 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!
 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.
>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?  
>       On the otherhand, if it is accurate it would
>suggest that repeated stimulation of the axon might indeed have some
>beneficial effect.
Hmm - - problematic - I've watched one MS patient slowly
deteriorate and die after long suffering and I know another going
the same way now. The two patterns are slightly different, however.
In the first case it was only the limbic system that seemed to be
affected - the brain was sharp right to the end but he graduated
from a car fitted with complete hand controls to a more restricted
electric wheel-chair because he was losing control of the arms.
The one still living seems to be losing brain function as well.
This seems to mean that Schwann myelin and Oligodendrocytic are
differently affected, and might be expected because the first is
formed in the foetus much earlier than the second, which forms
during the 9th month of pregnancy. The known part of the mechanism
is failure of the Blood-Brain Barrier, a failure which is thought
to have a genetic basis. Some recent german work (sorry, I
have yet no ref.) indicates that a bacterium attacks the velcro-like
material that holds the lamellae in place.
        If repeated and persistent stimulation causes axonal ion
channels to migrate, filling the internodal areas, that
would alleviate the condition, but it could not restore the higher
effective impulse velocity afforded by myelin or any other
beneficial functions due solely to myelin. Which means it could
never produce a full recovery. The treatment would end in a blind
alley and might very probably impede more effective ones.

Cheers! Gord 

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