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Muscle Weakness, Atrophy, and Chronic Paralysis

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  • Muscle Weakness, Atrophy, and Chronic Paralysis

    Presented in the following paper is an explanation
    of atrophy based upon an understanding of muscle
    fine structure and electrochemistry. Everythhing
    is taken directly from texts, though some of these
    texts are physics texts. Direct current stimulation
    is discussed; it is an area which is still generally
    uninvestigated despite its import for the treatment of
    atrophy. The claims made in the paper for this treat-
    ment are based upon 19 years of experimentation. The
    author can recommend to the incredulous self-experiments
    which can be performed to verify the claims made. The
    author would like to see this area of medical research
    receive more attention, and has written a 38 page paper
    discussing the history of electrotherapy, and the use of
    direct current stimulation in the treatment of chronic
    paralysis and the degenerative diseases of aging. Your
    responses and interest are welcome. Gregory C. O'Kelly
    The following paper is an abstract on the noted results of 19 years of experimentation using direct current stimulation on the non-denervated muscles of the chronic paralytic following concussive spinal injury. It attempts to explain the nature of muscle atrophy and its effects on motor weakness, and suggests that much chronic paralysis following non-destructive nervous trauma is not due to irreversible neuropathy but to easily reversible myopathy in the form of atrophy which takes place during the acute phase of injury.
    The paper is being presented over the internet in this way for lack of interest in the biological, biomechanical, and neuroscientific community. Its implications for the treatment of chronic paralysis, the maintenance of fitness especially under weightless conditions, and reversal of the degeneration of aging should be apparent to the knowledgeable. If the reader has any questions the author, Gregory C. O'Kelly, is available for questions, comments, and criticism at the e-mail address of the paper's origin.


    In his essay "Control of Movement" (Principles of Neural Science, 3rd ed., 1991, p.545) 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 (p.246) 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"(p.546). Neither Dr.Ghez nor any other physician in Principles of Neural Science gives any indication just what it is that might be lost to result in this loss of volume. What is being lost when volume diminishes? When Ghez speaks of muscle volume he refers to its contents and not the muscle size or capacity. What are these contents?
    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 shown by Dr. Ghez on p.549 of Principles... in his essay "Muscles - Effectors of the Motor System". 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 action of Ca++ is also what is critical at the neuromuscular junction to break up the vesicles of acetylcholine, thereby resulting in the endplate potential which creates the subsequent action potential carried out from the junction to the sarcomeres on the transverse tubules where Ca++ is drawn from the sarcoplasmic reticulum. In both instances, at the motor endplate region or the sarcomere-t-tubule junction, 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, and it is possible only with direct current, not alternating current, the current of choice for those who think that making a muscle contract strengthens it no matter what method is used to make it contract. 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. AC does not depolarize anything unless it has first been rectified to DC; the ionization of the skin commonly found with DC stimulation is not a factor with electrotherapy using AC.
    Ghez writes: "The depolarization of the T-tubule system acts on the specialized voltage sensitive channels in the terminal cisterns located in the apposing regions of the sarcoplasmic reticulum membrane. By mechanisms that are not fully understood, these local voltage-sensitive channels cause the release of Ca++ throughout the membrane of the sarcoplasmic reticulum." The mechanisms are not fully understood only because of the failure to grasp that the action potential is pushing a negative electrical charge longitudinally down the fiber or axon, and it is this, electrochemistry, which draws the calcium ions.
    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. Appealing then to the laws of electricity one sees that since the t-tubules support the movement of electrical charge which appears to the voltmeter observer as an action potential, that the amplitude of this charge is directly influenced by the cross-sectional area of the tubule since resistance to the passing of an electrical current is inversely proportional to the square of the cross-sectional area of the conductor. 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 the aforementioned 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 mode of electrotherapy, if prolonged over a period of years, is able to restore to functionability muscles long unused because of paralysis. It is suggested that this kind of paralysis, from myopathy/atrophy, is what is involved in over 95% of all quadriplegia, all hemiplegia, and up to half of all paraplegia.