spinal cord regeneration a red herring for a greater shortcoming

Gregory C. O'Kelly gokelly at calinet.com
Wed Jun 19 22:19:18 EST 2002

  Research into spinal cord regeneration is a small industry which keeps 
many neuroscientists employed at doing what is called 'basic science', 
and that is science which is not aimed at hypothesis testing, or 
anything at all for that matter. Research into spinal cord regeneration 
is something that should continue even if there is not now anything on 
the horizon that will be remotely of clinical benefit for today's spinal 
cord injured. But the focus on such research as the solution to solving 
the problem of post-sci paralysis masks a greater problem, and that is 
the questionable verisimilitude of the ionic channel school's model of 
nerve impulse propagation and the early 20th century claim that cell 
membrane voltages were the result of an ion concentration gradient. The 
inability to do anything about paralysis can be laid at the feet of this 
model and this hypothesis. Their shortcomings prompt and prolong the 
myopic focus of neuroscience and clinical neurology on the spinal cord 
as the locus of all paralysis following a spinal cord injury, no matter 
how severe. However there is another, far more important consideration 
that needs to be addressed, and that is the deterioration of the body, 
the wasting of muscle, that follows spinal injury and which, if not 
reversed, will result someday in people whose spinal cords have been 
miraculously restored but who remain paralyzed anyway because of 
advanced disuse muscle atrophy or amyotrophy. There is nothing new about 
this sort of paralysis. It follows prolonged bedrest, head injuries and 
strokes, and exposure to weightlessness. In fact in a number of 
instances of enduring paralysis following spinal injury the paralysis is 
due to this muscle atrophy and not to irreversible cord damage. This is 
the case for the majority of quadriplegia and a lesser fraction of 
paraplegia. The disuse atrophy advances during the acute phase of injury 
when the upper motor neurons are not firing because of the presence of 
swelling and bleeding into the nervous tissue, as in a stroke. The acute 
phase can go on for 2 or 3 months, far longer than it takes for an 
astronaut to weaken to the point where he has trouble standing upon 
return to earth.
The question then is what can be done about this, how can the muscles be 
maintained during the acute phase of injury so that the upper motor 
neurons will have healthy lower motor neurons to act upon when they 
themselves come out of shock? The answer involves an understanding of 
the electrochemical nature of the nervous system, and how upper motor 
neuron firing can only be simulated using the anode of the direct 
current. This simulated firing, if provided during the acute phase of 
injury, maintains a structure on the muscle called the transverse 
tubule, the type II muscle fiber. This fiber has its origins in the 
lower motor neurons, and arborizes throughout the muscle to the type I 
fiber, the fiber which does the actual contracting. The type II fiber 
makes up most of the bulk of a muscle. As the muscle atrophies this 
fiber is seen to diminish in cross-sectional area.
Even those who, having suffered a spinal injury of the incomplete sort, 
remained paralyzed for years, can be restored to functionality if their 
muscles are restored. But this takes an exceptionally long time, that 
time being 2 or 3 times as long as the time from the injury depending 
upon the age and general health of the injured. That is why it is 
important to get to the patient while he or she is still in the acute 
phase of injury with at least stable vital signs.
For more details about the research and treatment see the paper below 
which may not come through completely, given space limitations (though 
it is only 5 pages long), but which is available in full by request to 
gokelly at calinet.com .

Muscle Disuse Atrophy, Paralysis, and Electrochemical Stimulation

In the article "Muscle Weakness, Paralysis, and Atrophy after Human 
Cervical Spinal Cord Injury" (Thomas et alii, 1997) it is reported that 
"Severe muscle atrophy was revealed which might reflect disuse," and, 
"Thus, the weak voluntary strength of these partially paralyzed muscles 
is not due to submaximal excitation of higher CNS centers, but results 
mainly from reduction of this input to triceps motoneurons." The 
reduction of this input reflects the diminution of the power 
amplification of the nerve impulse across the synapse. Below this 
reduction of amplification of the power of the nerve impulse will be 
shown to be the result of the disuse atrophy of the muscle. This sort of 
myopathy, motor weakness and paralysis is the same sort of myopathy that 
is found in those exposed to microgravity and long term bedrest.
All spinal and head injuries, no matter how severe, are followed by 
disuse atrophy from at least the level of injury, and, in most cases, 
over the entire body as the acute phase is prolonged and the patient is 
immobilized either mechanically or by failure of the neurons in the cord 
to fire because of the presence of blood, as in a stroke or concussion. 
There is an implication that a great deal of chronic paralysis 
subsequent to such neural trauma may be due to muscle atrophy and not to 
enduring and irreversible neuropathy. During the acute phase of injury 
the blood/brain barrier must be reestablished, and pressure, as from 
swelling or slight vertebral displacement, must be relieved. This takes 
easily many weeks. While blood is still present in the nervous tissue 
and until it is absorbed the horn cells will not fire. This phase of 
recovery easily takes another two or three months more. The severity of 
muscle atrophy that advances during this time is far greater than that 
which routinely leaves astronauts too weak to stand up upon return to 
earth after only a few weeks in space and still using their muscles, 
only minimally.
Disuse muscle atrophy is routinely described as the loss of muscle fiber 
cross-sectional area. In "Hemiplegic Amyotrophy" (Chokroverty, 1976) the 
author states that these fibers are the type II fibers also known as the 
transverse tubule or t-tubule. In "Muscles - Effectors of the Motor 
System," (Ghez, 1991) the author 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."
The t-tubules grow from the post-synaptic motoneurons, arborizing 
throughout the muscle, but maintain the cytoplasmic continuity 
characteristic of the electrical synapse, a device which the t-tubule 
forms as it contacts the sacrcomere, a reservoir of interstitial fluid. 
To understand how loss of cross-sectional area of the t-tubule might 
effect the power of muscle contraction it is only necessary to consider 
the motor unit as an electrochemical circuit, and to remember the 
amplifying characteristic of the peripheral, chemical synapse at the 
neuromuscular junction.
An excitatory, CNS impulse descends the axon. Arriving at the 
synapse/motor endplate region the negative charge draws calcium ions 
[positively charged molecules] across the cleft to break vesicles of 
acetylcholine. This neurotransmitter triggers the creation of another 
action potential postsynapticaly. An action potential is a voltage. A 
voltage is an electrical pressure. What is being pressured is the 
movement of negative electrical charge along the t-tubule to the 
electrical synapse at the sarcomere where calcium ions are again drawn 
by the arriving negative electrical charge from the fluid in the 
sarcomere to initiate the splitting of ATP and the energizing of the 
type I muscle fiber contraction.
The reason for the increase in power of the CNS nerve impulse across the 
chemical synapse is best described by the equations for electrical 
power, and for the inverse, exponential relationship of conductor 
cross-sectional area and resistance to flow. That is, if power = voltage 
x current flow[ p=vi], then to amplify power one must either increase 
voltage or current flow. The power of the nerve impulse is amplified by 
increased current flow made possible by a muscle's transverse tubule 
that is larger than the microtubule which bears the nervous impulse. The 
t-tubule grows out from the motorneurons which were galvanized by the 
release of acetylcholine. To increase i or current flow along it, r or 
resistance must be decreased. Because r = 1/a2 where a is the 
cross-sectional area of the conductor, to reduce r the cross-sectional 
area of the conductor must be increased. On muscle this is done by 
causing the t-tubule to grow thicker. A t-tubule that is twice the cross 
sectional area of a microtubule passes four times the power at the same 
voltage. It is possible then that the CNS excitatory impulse not being 
sufficiently amplified to result in usable muscle contraction because of 
disuse atrophy may be the reason for residual and chronic paralysis in 
those who have suffered concussive but not destructive spinal and 
cerebral injury. And this is in accordance with the findings of Thomas 
et alii mentioned at the start of this essay.
The question then arises, how is a muscle strengthened if it cannot be 
used, that is, how can muscle power be increased if the muscle cannot be 
exercised? Even more, if only a muscle that is used powerfully 
['overloaded', as they say] can be built up, anabolized, then the 
strengthening of weak muscles must be an exceedingly difficult task 
since the ability of a muscle to be used powerfully is dependent upon 
the preexisting good health of that muscle where good health is taken as 
lack of amyotrophy or atrophy. The electrical equation for power, p=vi, 
provides an answer to the question of muscle strengthening of unusable 
muscles. What must be provided to a muscle that cannot be used is a 
simulation of the nerve impulse, the wave of 
depolarization/polarization, that causes the twitch, but that simulation 
must be of greater power than the nervous system is capable of. By 
introducing an electrochemical impulse to the neuromuscular junction 
that is of greater voltage and current flow one is able to overload the 
muscle as if the nervous system had done so. The transverse tubule will 
grow in response so that the energy of contraction of the type I fiber 
will increase.
The field of electrotherapy is severely riddled with misunderstanding 
about what is happening when electrodes send impulses into the body 
transcutaneously. This misunderstanding is most evident in the failure 
to appreciate the importance of amperage and its role in 
electrochemistry. It is apparent too in the mistaken notion that what is 
important for muscle strengthening is muscle contraction, and that the 
way to achieve this most harmlessly is to increase electrical power to 
the muscle by increasing voltage only while de-emphasizing amperage. 
Amperage is given so little attention that in the attempts to avoid it 
those using DC stimulation to cause muscle to contract use voltages ten 
times higher than necessary so that minuscule amperages can be spurted 
in microsecond bursts. Amperage is a rate of current flow; it has a time 
factor in it. Voltage is nearly instantaneous while amperes passed 
depend upon a time factor. Microsecond pulses are too short to let much 
current pass.
Worse still are those who make muscle contract using AC or biphasic 
current that in effect passes no amperage at all. The contractions 
triggered by biphasic current are triggered as a result of voltage 
transmission, and do not involve any sort of biochemical change. In 
addition electrotherapists who rely upon AC or biphasic current do not 
seem to grasp that the stimulus must also be provided to the 
neuromuscular junction [motor endplate region] and not to the surface of 
the muscle in general. Traditional electrotherapeutic approaches to 
building muscle fail to consider that what is happening on the muscle is 
that electrons are being driven by an action potential originating in 
the post-synaptic motor neurons, that these electrons are traveling on 
the t-tubule to the sarcomere, and that the more of these electrons that 
arrive at the sarcomere the more powerful the muscle contraction. The 
failure to grasp this distinction is the reason why traditional 
electrotherapy has never been able to affect the building of muscle, and 
why it is not used by any athletes or NASA to prevent muscle wasting or 
to build muscle. It places emphasis on muscle contraction triggered by 
voltage transission using AC as if the contraction and not how it was 
triggered is what is important. Emphasis should be instead on increasing 
amperage to increase electrical power to a muscle, not voltage, since 
this is more like the action potential itself. And this is done by 
stimulating at the endplate region with the anode of the DC or 
monophasic current, thereby triggering anabolism, the building of tissue 
through the energizing of the synthesis of proteins. It is the anode 
that delivers electrons, it is the cathode that carries them off. This 
is the key to understanding electrochemistry and the functioning of a 
Electrochemistry involves oxidation/reduction reactions. These are 
reactions that involve the movement of an electron from the catabolic, 
oxidizing reaction to the anabolic, reduction reaction. This implies 
then two chemical reactions which are separated by a barrier, like a 
cell wall, and across which a voltage may be measured. A voltage is an 
electrical pressure, that is, a pressure which tends to drive electrons 
to where they are lacked. The movement of electrons is the flow of 
chemical energy. Reduction reactions necessary for the building of 
carbon/hydrogen bonds like those of all organic molecules, need to be 
energized, need electrons. These electrons are harvested by the cell and 
the multicellular organism through oxidative, catabolic, corrosive 
reactions like those in which stomach acids breakdown organic molecules. 
These reactions are seen in mitochondrial respiration in the cell, and 
in the breathing and gastrulation [digestion] of the multicellular 
organism. Every chemical reaction either takes energy to happen, or 
gives off energy as it happens. Chemical energy is electrons, once known 
as cathode rays, and presently known as alpha radiation. This sort of 
energy is like that which is given off by a battery. A battery is 
powered by chemical reactions which take place inside of it. These 
reactions are catabolic, corrosive or oxidative reactions, and are those 
kinds of reactions which give off energy, cathode rays, rather than 
requiring it. The cell is likened to a battery because it can give off 
energy as a result of oxidation through the breakdown of ATP taking 
place inside of it
The energy gotten from a battery can be used to power those reactions 
that take energy rather than giving it off. In 1800 Alessandro Volta 
announced his new invention to the Royal Society, the battery. Chemists 
started to play with it immediately because by using it the energy could 
be provided which would cause chemicals to break down into their 
constituent elements, and the chemists wanted to find out what these 
were. The classical example was the putting of a battery's electrodes 
into water and turning it on, causing hydrogen to form at one pole and 
oxygen at the other as the water broke down in what came to be known as 
hydrolysis, the general process for all chemicals being described as 
Electrochemists then spoke of oxidation-reduction reactions, which were 
reactions which involved the movement of electrons, as in direct 
current. Reduction is, in organic chemistry, the combination of carbon 
and hydrogen, a process which takes energy rather than liberates it. All 
biological molecules are based upon carbon and hydrogen bonds. What the 
electrochemists were speaking of by oxidation-reduction reactions were 
two reactions involving the movement of electrons from one to the other, 
the one an oxidative or catabolic one which liberated electrons, and the 
other a reduction reaction which needed electrons.
Multicellular organisms with nervous systems use those nervous systems 
to direct the flow of chemical energy liberated by respiration and 
digestion, catabolic reactions. This flow is directed to the organs and 
muscles of the organism so that it can continue in the search for more 
energy sources. This energy is delivered by the nerves to the synapses 
which cause both anabolism, the building of tissue, and motor 
functioning necessary for escape and search. Anabolism and anode are 
related words. The anode is the source of electrons from a battery. Just 
as the cell is compared to a battery, so the organism made up of cells 
is like a battery. Direct or galvanic current in pulses from the anode 
delivered by transcutaneouis electrodes to points in the body where 
there are clusters of synapses [ganglia and motor endplate regions], 
simulates the nerve impulse and stimulates the building of tissue just 
as would follow from exercise. And that is electrochemistry and its 
application to the body.
The reason for the preference of AC or biphasic current in 
electrotherapy over DC or monophasic current has its origins in the 
middle of the 19th century. AC was preferred over DC because the former 
would make the muscle contract strongly no matter where the electrode 
was placed on the muscle, no matter how badly atrophic the muscle was, 
and for as long as the current ran. The latter would make the muscle 
contract strongly only if the muscle were already healthy, only if the 
stimulus were provided at the endplate region, and only with the 
initiation of current flow. The muscle would relax after each pulse even 
if the current were allowed to continue. The current had to be stopped 
and restarted for each new contraction. But more important still was a 
phenomenon given little attention by traditional electrotherapists who 
sought to avoid it by minimizing amperage passed. This phenomenon was 
the ionization of the skin which showed up as blistering at the anode 
and pitting at the cathode. So the preference of AC to DC for 
electrotherapy was driven by the desire to avoid skin damage and by the 
ease of use of AC in causing strong muscle contractions even on weak 
muscles without having to repeatedly stop and start current flow.
When a muscle is exercised over a period of time using the anode of the 
DC to bombard the synapses at the motor endplate region with electrons, 
it will be seen that at first, if the muscle is weak, the contractions 
triggered will also be weak. If the muscle is exercised regularly and 
for an extended period of time, the muscle's contractions will be seen 
to grow stronger, the muscle will have more bulk, and whereas its 
contraction formerly caused only the movement of tissue, after numerous 
sessions of electrochemical stimulation the muscle's contractions will 
start tomove a limb.. The muscle may be made to twitch 2000 times per 
second. At this rate it takes only one second to exercise the muscle, to 
overload it with depolarizing pulses of electrons that trigger the 
building of the transverse tubule, and thereby the strengthening of the 
muscle. At rates higher than this the muscle does not contract as 
strongly since it does not have the time to re-polarize fully before the 
next pulse. Current strengths can be as low as 5 to 15 milliamperes, and 
voltages as low as 20 to 60 volts. Pulse widths can be .25 milliseconds, 
with time in between pulses being the same. To let the pulses be 
delivered for longer than a few seconds per motor endplate region at the 
rate of 2000 herz causes a longer reddening of the skin which may, if 
the stimulus is prolonged beyond a point results in the blistering of 
the skin. Although the cathode used, being greater in surface area than 
the stimulating electrode, can be allowed to remain in one place far 
longer than the stimulating electrode, it too needs to be moved from 
time to time to prevent pitting of the skin beneath it. The dispersive, 
cathodic electrode is between 9 and 16 square inches while the 
stimulating electrode is round with a diameter of 12 to 15 millimeters.
Because with the use of DC what is involved is the delivery of electrons 
or chemical energy to the body, it is important that the number of 
electrons delivered by the anode be more than the number of electrons 
carried off by the cathode. To insure this it is important that the 
cathode be made of what is called a sacrificial metal, and that is a 
metal which corrodes, oxidizes or rusts as its electrons are drawn from 
the metal rather than from the body. These electrons are then delivered 
to the body by the anode for a net increase in chemical energy to the 
body delivered in a way simulating the body's own nervous, delivery 
system, i.e., the electrons are delivered to the peripheral chemical 
synapses found in all motor endplate regions and ganglia of the body.
There are 1,152 motor endplate regions and ganglia in the body. Spending 
one second on each with the stimulating electrode every 2 or 3 days 
maximizes the rate at which the muscle can be built given the 
limitations on the muscle resulting from the state of health of the 
body's other subsystems like the vascular system. In other words a 
healthy young person will build muscle more quickly that an older, 
disabled person. But as that older person builds muscle and restores the 
body the rate of recovery will increase. The problem of disuse atrophy, 
whether in the astronaut, the bed-ridden patient, or the spinal cord or 
brain injured patient, can only be ameliorated through the use of DC 
stimulation, through the provision of negative electrical charge at the 
site of the motor endplate region using the anode. It is only through 
electrochemical intervention and not voltage transmission that the 
t-tubule can be made to grow.

Dr. Sudhansu Chokroverty et alii (1976) Archives of Neurology, vol.23, 
no.6, February
Dr. Claude Ghez (1991), Principles of Neural Science , 3rd ed., Kandel, 
Jessell, Schwartz, Appleton and Lange, Norwalk, Connecticutt, 1991, p.549.
Dr. C.K.Thomas et alii (1997), Experimental Neurology, vol.148, no.2, 

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