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Muscle Weakness, Atrophy, and Chronic Paralysis

Kurt Weir kweir at SLONET.ORG
Thu Feb 25 19:23:26 EST 1999


Below I have presented an abstract of research I have done over the last 20
years which has great impact on the understanding and treatment of
paralysis following concussive nervous system trauma.  I would appreciate
greatly any feedback on the issue, and interest in perhaps doing one's own
verification of the results of this clinical testing on the restoration of
the chronic quadriplegic and the clinical prevention of this state of
affairs in the first place through sound intervention in the acute phase of
injury using direct current stimulation to trigger the anabolization of
somatic proteins - in particular the transverse tubule in muscle.
ATROPHY, MUSCLE STRENGTH, AND CHRONIC PARALYSIS

Gregory C. O'Kelly

In his essay "Control of Movement" (Principles of Neural Science, 1991,)
Claude Ghez states "Muscle weakness may result from disturbances in
descending motor pathways or in the spinal motor neurons themselves."  He
does not say which is involved in the motor weakness of those suffering
from disuse atrophy like that of astronauts returning from weightless
conditions or those confined to prolonged bedrest.  Presumably the wasting
of muscles through atrophy is not a neurogenic condition, but a myopathic
one, though atrophy from disuse always follows both upper and lower motor
neuron lesions.  In 
his "Diseases of the Motor Unit" in the same volume) Lewis P. Rowland
writes "When the sole manifestation of a disease is limb weakness, as often
happens, clinical criteria alone rarely suffice to distinguish between
neurogenic and myopathic diseases."  In the list of examples of myopathic
diseases Rowland does not list muscle atrophy.

Claude Ghez defines muscle atrophy as "loss of muscle volume.  In his 1976
"Hemiplegic Amyotrophy" (Archives of Neurology, Feb.) Sudhansu Chokroverty
notes that in the case of muscle wasting he and others have found a
noticeable diminution of cross-sectional area of type II muscle fibers, and
that this wasting was found usually in cases of prolonged bed rest, and he
suggests that disuse atrophy could be the cause of such degeneration.  For
Dr. Chokroverty the type II muscle fiber was the transverse tubule.   Ghez
writes:  Contraction is set off by the depolarization of the muscle fiber.
When an action potential in a motor axon reaches the neuromuscular junction
it generates an endplate potential, which in turn triggers an action
potential in the muscle fiber.  This action potential is propagated rapidly
over the surface of the fiber and conducted into the muscle fiber by means
of the system of T-tubules.  The T-tubule system insures that the
contraction that follows a single action potential, termed a 'twitch',
spreads throughout the entire fiber."

Ghez also writes, "A key aspect of the electromechanical mechanism by which
the action potential triggers mechanical contraction, a process termed
'excitation-contraction coupling', is a sudden increase in intracellular
Ca++."  The depolarization that takes place is dependent upon the arrival
of a negative electrical charge to attract the positively charged calcium
ions.  This is electrochemistry, a quantum chemical effect which cannot be
adequately modeled appealing to thermodynamics and concentration gradients;
 depolarization is possible only with direct current.  Contractions using
AC do not engage 
'key aspects of the electromechanical mechanism' and so do not involve the
calcium-ion-activated splitting of ATP by actin.  This is easily demonstrated.

The t-tubule is not a myelin-coated cell process, it is a protein, one
which acts as an electron transport chain. The transverse tubules grow from
the synaptic junction at the nerve terminal, arborize extenively so that by
the time they arrive at the sarcomere, as seen in Ghez's diagram, they are
relatively small in relation to the size of the sarcomere.  Yet the
t-tubules are what makes up the bulk, the volume of muscle, the muscle
mass.  With a constant voltage, if the resistance to flow is increased by
diminished conductor size, the 
amount of amperage that draws the calcium ions from the sarcoplasmic
reticulum is diminished, and so too then is the number of calcium ions
reduced.  Consequently the strength of excitation-contraction coupling is
diminished because there is less calcium ion activated splitting of ATP.

It is suggested then that deterioration of the t-tubule is another way in
which muscle weakness may be brought about.  And if the t-tubule is allowed
to deteriorate to the point where it no longer contacts the sarcomere, or
is so small in cross-sectional area that the action potential's charge is
severely diminished, then the resulting sliding of thin and thick filament
as a result of voluntary, acetylcholine-mediated muscle contraction is also
prevented or diminished in energy.  According to Ghez the strength of
muscle contraction is due to the initial length of the muscle or the rate
of movement of the thick and thin filaments.  The concentration of calcium
ions effects the rate of movement of thick and thin filaments through its
influence on the calcium ion activated splitting of ATP, and reduced
concentrations of this ion make for much less energetic movement.

One implication of this explanation of muscle atrophy is that in the case
of chronic paralysis following non-destructive bruising or concussion of
the cord or brain, subsequent paralysis or motor weakness may be the result
of disuse atrophy which advances during the acute phase of injury.  This
deterioraton of the t-tubule is reversible, and may be accomplished through
the triggering of anabolism of muscle tissue by stimulation at the motor
endplate region with transcutaneously-delivered, negative electrical charge
from the anode.  This charge, or, as it is known in physics texts, chemical
energy, acts to trigger the cellular polymerization of proteins, the ones
which make up to t-tubule.  It is suggested then that if the somatic
proteins of the recently injured from concussive nervous system trauma are
maintained during the acute phase, then upon recovery from it they are far
more likely to be restored to functionability.  This mode of
electrotherapy, if prolonged over a period of years, may be able to restore
to functionability muscles long unused because of paralysis.




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