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| Fig: Neuromuscular Spindle Cell |
A neuron is one complete nerve cell. It
consists of:
- The cell body with its nucleus
- Along extension called the axon or nerve fiber
- Many short branching extensions (dendrites) that connect the nerve via synapses with nerve receptors or other nerves
- The synapse.
The signal that a nerve conducts cannot
be stronger or weaker. The nerve impulse always has the same strength. The
intensity of a nerve signal is determined by how often the nerve
"fires" per second.
Alpha motor neurons have their origin in the ventral horn of the gray matter of the spinal cord. When a nerve signal from type Ia afferent nerves reaches the spinal cord, the response returns to the muscle along the alpha motor neurons. There are two types of alpha motor neurons. "Tonic" alpha motor neurons innervate postural muscles that are active for extended periods of time. "Phasic" alpha motor neurons innervate phasic muscles that only contract for short periods of time. About 70% of the motor neurons going to the muscles are alpha motor neurons. These innervate the thick extrafusal muscle fibers that are responsible for the force of muscular contraction. The remaining 30% are the gamma motor neurons, which innervate the intrafusal muscle fibers. The intrafusal muscle fibers do not contribute to the strength of muscular contraction. Instead, gamma stimulation causes contraction of the intrafusal muscle fibers, which stretch the neuromuscular spindle. This process produces fine motor control, not raw force. The nerve impulses traveling through gamma motor neurons to the intrafusal muscle fibers originate in the cerebellum.
At
each end of the neuromuscular spindle, the intrafusal muscle fibers attach to
the muscle sheath and are thereby automatically lengthened or shortened with
the rest of the muscle. In the middle of each intrafusal fiber is an area with
no actin and myosin, which therefore does not contract. So when the gamma motor
neurons stimulate the intrafusal muscle fibers to contract, the intrafusal
muscle fibers pull toward each end and thus lengthen the central portion upon which
the Ia nerve receptor fibers are wound.
Ia nerves are afferent nerves. They and
their nerve receptors are called "primary" to distinguish them from
the finer type II nerves. The primary Ia receptors of neuromuscular spindle
cells are always sending signals into the spinal cord. When the central portion
is stretched, the output from the "primary" receptors is increased.
Type Ia nerves are thick and the nerve signals travel through them swiftly.
When the receptor area between the contractile portions of the intrafusal
fibers is suddenly lengthened, it sends an especially intense signal (high
number of nerve firings per second) through its type Ia nerves to the dorsal
horn of the spinal cord. Only one synapse in the spinal cord needs to be
stimulated before the speedy "monosynaptic" response is sent back to
the same muscle to contract. This is the basis of reflex reactions such as the
knee-jerk reflex. This type of response is called "monophasic"
because it occurs once and immediately stops.
"Secondary"
type II afferent nerves connect directly into the contractile portions of the
intrafusal muscle fibers. Type II nerves are slender and slower than type Ia
nerves. They are responsible for the second type of neuromuscular spindle
response which, when stimulated, causes the muscle to raise its tension slowly
and remain in a state of elevated tonus.
During the muscle test or any
weight-bearing activity, there is both alpha and gamma efferent stimulation to
the muscle. Alpha stimulation of the extrafusal fibers produces the force of
contraction. Gamma stimulation of the intrafusal fibers stretches the central
receptor area of the neuromuscular spindle cell. The receptor, which is always
sending impulses, then sends a greater than normal impulse into the spinal cord
and cerebellum. This is, in effect, an order for greater contraction in the
muscle to meet the current demand. This results in a greater nerve signal being
sent back through the alpha motor nerves to the extrafusal fibers of the
muscle, increasing the force of contraction.
The
neuromuscular spindle cells are responsible for signalling the nervous system
to increase the tension in a muscle that is lacking adequate tone. As the
examiner applies more force in the muscle test, the patient's neuromuscular
spindle cells monitor the amount of force applied and signal the nervous system
to produce the appropriate intensity of alpha nerve signal to contract the
muscle enough to hold the limb or other body part in position.
Thus if the neuromuscular spindle cells in a muscle are not sending an adequate
signal, the muscle will test weak.
The
activity of the neuromuscular spindle cells excites its own muscle to contract.
It further facilitates contraction of the muscle's synergists and its
stabilizers. At the same time, the antagonists to the muscle are inhibited. As
mentioned, the reflex excitation of the muscle itself occurs swiftly because
only one single synapse in the spinal cord must be traversed between the
neuromuscular spindle cell and the extrafusal muscles that provide the force of
contraction. This allows the body to protect itself by very quickly jerking
away from potentially damaging stimuli. The neural circuits that facilitate the
synergists and stabilizers and those that inhibit the antagonists, each have
two synapses in the spinal cord to traverse and thus are somewhat slower.
It is the coupled activity of the
alpha and gamma nerves in the neuromuscular spindle cells that makes muscular
contraction smooth and coordinated. Postural or "tonic" muscles
typically hold relatively high levels of tone for long periods of time. Such
muscles have a high proportion of slow tonic fibers. The activity of such
muscles does not require fine coordination. Therefore, tonic muscles have few
neuromuscular spindle cells. "Phasic" muscles have a higher
proportion of fast "phasic" fibers and far more neuromuscular spindle
cells to provide for their faster, more intricate, finely coordinated
movements.
Normally, the neuromuscular spindle
cells continuously send signals to the nervous system concerning the length of
the muscle. The length of a muscle may be manually adjusted by manipulation of
the neuromuscular spindle cells. Pushing or pinching the neuromuscular spindle
cells together (parallel to the length of the muscle) reduces the tension on
the intrafusal muscle fibers. They then send signals of less intensity than
normal through their Ia afferent nerves to the spinal cord. This temporarily
reduces the level of alpha efferent nerve signalling, which results in less
tension in the extrafusal fibers responsible for muscle strength. Thus,
pinching the spindle cells together will cause a muscle to temporarily test
weak. This may be used to determine whether a muscle is responding correctly.
Stretching and activating the
neuromuscular spindle cells by pushing the two hands or fingers into the belly
of a muscle and pulling apart stretches the intrafusal fibers, increasing their
output to the spinal cord. As a result, more nerve impulses per second are sent
through the alpha efferent nerves to the extrafusal fibers of the muscles,
which then contract more strongly. Thus, pulling the neuromuscular cells apart
increases the tension in a muscle.
When
a muscle (the agonist) acts, the action of its neuromuscular spindle cells
causes its antagonist to be inhibited. When the antagonist to a muscle acts,
the agonist is inhibited. This principle is call "reciprocal inhibition."
Were both the agonist and antagonist to act simultaneously, they would be
fighting against each other, which would be a waste of energy. Also, the two
bones in the joint over which the two muscles act would be jammed together.
Reciprocal inhibition occurs automatically at the level of the spinal cord
where the synapses meet between the afferent nerve from the neuromuscular
spindle cell and the efferent nerve that returns to the antagonist. However,
higher brain centers can override this effect. A conscious decision can be made
in the cerebral cortex to flex whole groups of agonists and their antagonists simultaneously.
This is conveyed to the cerebellum and from there to the appropriate spinal
segments and then on to the muscles. This is what occurs when a bodybuilder
flexes most of his or her muscles at once to make an impressive pose.
It
is normal that while a muscle is active, its antagonists are inhibited. An
incorrectly functioning neuromuscular spindle cell may send impulses so overly strong
that any activity of the muscle causes its antagonist(s) to subsequently test
weak, even after the agonist has relaxed. This condition is called
"reactive muscles." Dysfunctioning
neuromuscular spindle cells will usually therapy-localize (TL). That is, if the
muscle tests
weak because of dysfunction of the neuromuscular spindle cell, touching the
neuromuscular spindle cell will cause the muscle to test strong. Conversely, just
about any normotonic indicator muscle will weaken when a dysfunctioning
neuromuscular spindle cell is therapy-localized.
A
dysfunctioning neuromuscular spindle cell is usually palpable as a hard lump. Locating
it through therapy localization and palpation makes treatment more direct and
easy to perform.
To strengthen a muscle that tests
weak because of a dysfunctioning neuromuscular spindle cell, the examiner
presses his fingers rather deeply into the muscle on each side of the
neuromuscular spindle cell and then pulls his fingers apart from each other
along the direction of the fibers of the muscle. This also can be used to
"wake up" normally functioning muscles and thereby prepare them for
strong contraction before or even during athletic competition.
To
weaken a muscle that tests hypertonic (one that tests strong but cannot be
weakened by usual means) because of a dysfunctioning neuromuscular spindle
cell, the examiner presses his fingers into the muscle on each side of the
problematic neuromuscular spindle cell and then repeatedly presses his fingers
together along the line of the direction of muscular contraction (the line of
the muscle fibers themselves). This effectively "pinches" the
neuromuscular spindle cell together. This type of manipulation of the
neuromuscular spindle cells can swiftly return full extension to shortened,
tight muscles. It is not the most pleasant type of massage, but it is one of
the most effective in promoting the relaxation of overly contracted muscles.
For example, the application of this technique to a tight upper trapezius
muscle between the neck and shoulder can swiftly reduce tension and pain in the muscle. This is assuming that the
tension in the upper trapezius is primary and not caused only by its
antagonist, the latissimus dorsi, having inadequate tone. Such treatment to the
upper trapezius muscle may lengthen it so much that the shoulder sinks a few centimetres.
Treatment
of neuromuscular spindle cells requires 1-7 kilograms of pressure. Sometimes
even more pressure is required for the desired effect. Patients who have little
tone in their muscles should be treated with less pressure. The pressure should
be applied to a particular neuromuscular spindle cell several times. If the
muscle is very wide and several neuromuscular spindle cells are involved, the
treatment is repeated upon each active spindle cell, or simply across the whole
width of the muscle. After adequate treatment, the neuromuscular spindle cells
should no longer therapy-localize and the muscle should have the proper level
of tension as measured by muscle testing.
If
the same dysfunction of the neuromuscular spindle cell returns, or if there are
neuromuscular spindle a cell problem in many separate muscles, a
nutritional correction is indicated. Goodheart recommends that the patient chew
raw bone concentrate or raw bone nucleoprotein extract. He suspects that the
helpful factor in the bone concentrate is phosphatase. As long
as one has no allergy to the nightshade family of plants (potatoes, tomatoes,
eggplant and peppers), the phosphatase in raw potato also seems to work well
for this purpose.
Correction of a Muscle that Tests Weak Due to Dysfunctioning Neuromuscular Spindle Cells
Indications of possible dysfunction of the neuromuscular spindle cells:
- The muscle has too little tone (is hypotonic).
- The muscle is palpatory hypertonic but tests weak.
- There are firm lumps in the belly of a muscle that hurt when pressed upon.
- The muscle contains neuromuscular spindle cells that therapy-localize.
Test:
- Palpate the muscle for firm l umps. They will usually be in the belly of the muscle but may be located anywhere in the contractile fibers.
- Touch (therapy-localize) the suspect area (on the lumps if any are palpated).
- Test the muscle again while the suspect area is therapy-localized.
- If the previously weak-testing muscle now tests strong, there are dysfunctioning neuromuscular spindle cells in the area therapy-localized.
Correction:
- To raise the tone of a muscle that tests weak because it contains a dysfunctioning neuromuscular spindle cell, push the fingers (or sides of the hands) into the muscle on each side of it and pull the tissues apart along the direction of the muscle fibers. Do this several times with 1-7 kilos of pressure.
- Retest the previously weak-testing muscle. It should now test strong. If not, return to test step 1, check for and correct other areas of dysfunction.
- Therapy-localize the previously dysfunctioning neuromuscular spindle cell and retest the muscle. The muscle should again test strong. If not, repeat correction step 1.
- Have the patient chew raw potato or raw bone concentrate at this time to lock in the correction.
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| Fig: Neuromuscular Cells "Pulling Apart" to increase tension in a muscle |
Correction of a Muscle that is Hypertonic Due to a Dysfunctioning Neuromuscular Spindle
Indications of possible dysfunction of the
neuromuscular spindle cells:
- The muscle has too much tone (palpatory hypertonic) and is hard and painful.
- There are firm l umps in the belly of a muscle that hurt when pressed upon.
- Neuromuscular spindle cells therapy-localize.
Test:
- Palpate the muscle for firm lumps.
- Therapy-localize the suspect area (on the l umps if any are palpated).
- Test another normotonic indicator muscle while therapy localizing the suspect area.
- If the previously normotonic indicator muscle now tests weak, there are dysfunctioning neuromuscular spindle cells in the area therapy-localized.
Correction:
- To correct a muscle that is too tight because of dysfunctioning neuromuscular spindle cells, push the fingers (or sides of the hands) into the muscle on each side of the area that therapy-localized and push the tissues together (pinch the neuromuscular spindle cell together) along the direction of the muscle fibers. Do this several times with 1-7 kilos of pressure.
- Therapy-localize the previously dysfunctioning neuromuscular spindle cell area and retest the indicator muscle. The indicator muscle should now remain strong. If not, repeat correction step l.
- Test if the muscle that could not be weakened previously (hypertonic), now can be weakened (is normotonic).
- Have the patient chew raw potato or raw bone concentrate to lock in the correction.
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| Fig: Neuromuscular spindle cell "Pressing Together" to decrease in a muscle |
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