SUBJECTION

1. The restrictive inflammation is reduced by the movement of electricity as outlined in the NCTP©
2. There is such a large amount of current that it "fools" the CNS causing it to send the appropriate chemicals to "repair" the damaged area of the axon which has been demyelinated and "has a leak".

Because of years working with electrical stimulation we understand there are three primary conductors for the electrical current within the human body. They are, in order of capacitance:

1. Water (i.e. interstitial fluids, etc.)
2. Muscle fiber
3. Nerve fibers

Other body tissues have more resistance than capacitance. It is also a known fact that electricity goes to the point of least resistance. The myelin possesses high electrical resistance and low capacitance and thus acts as an insulator around axons.¹

In a normal, undamaged state, the myelin around the axon protects the electrical signal from outside interference and at the same time keeps a "clean" undisturbed canal or pathway for the signal from the Central Nervous System CNS) to travel through to the extremities. However, when the myelin is permeated by fluids due to lesions, the signal from the CNS dissipates to other regions, causing paralysis beyond that point. (The degree of the paralysis is in relationship to the degree of permeation.)

Studies suggest that axonal damage may be associated with inflammation. And note a relation between axonal injury and inflammation, suggesting that a reduction in the inflammatory response might result in the loss of fewer axons and thus in less clinical deficit. ^{1 2 3}

It has recently been recognized that in some patients with traumatic (nonpenetrating) spinal cord injury there are residual axons that maintain continuity through the lesion but fail to conduct impulses as a result of demyelination. These findings have been reported in some patients with "clinically complete" lesions (i.e., those with no function below the level of the lesion), which are classically considered to be due to transection of the spinal cord and its constituent axons within the lesion. The demonstration of these preserved, but demyelinated, axons suggests that in spinal cord injury, at least some degree of functional recovery might be achieved by strategies that restore impulse conduction along demyelinated axons. ^{1 4-6}

Recognition that spinal cord injury is, in part, a disorder of myelin should trigger a critical rethinking of these disorders and provides us with new targets for therapy. Ideally, future studies will tell us whether the protection of axons from injury in multiple sclerosis and the repair of demyelinated axons in spinal cord injury are therapeutic strategies that will help preserve neurologic function in patients with these disorders. ¹

This can be related to the results being seen in the SCI patients using the Neuro Care™ Treatment Program©. These patients are seeing results! In some cases, the paralyzed patient is walking again. The patients are all individuals who are diagnosed paraplegic or quadriplegic and at least 1-3 years post injury. They have all been told they would be permanently paralyzed. However, during their treatment period they are all seeing changes in their paralyzed state. Feeling and sensation is returning and they are proceeding to strengthen and re-educate the muscular structure to support their weight. Then they are learning to walk again.

Although each patient has an individual recovery schedule, there is a pattern of recovery developing as the pathway reopens/repairs.

After reviewing studies like these of Dr. Waxman, it is thought that either the myelin is re-depositing or the body is producing sufficient Sodium and Potassium levels to compensate for the loss of myelin. Perhaps there is a prevention of axonal loss: Axonal function and integrity can be preserved after acute insults by means of neuroprotective interventions that block or modulate injurious ion fluxes at several stages within this molecular death cascade or that interfere with "downstream" degenerative events such as activation of calpains and other destructive enzymes. It is suggested that further studies will be needed to determine whether the reduction in inflammatory responses or the neuroprotection of axons can limit or prevent axonal degeneration in multiple sclerosis or SCI. If so, whether this will reduce or prevent the acquisition of persistent neurologic deficits.¹

Even though the results we are seeing at this time is anecdotal, the effect in multiple sclerosis and SCI patients suggests what Dr. Waxman is seeing is possible. Using the Neuro Care Treatment Program© is an effective medium for achieving it. We are not sure whether the pathway is reopened via a reversal of the demyelination or the depositing of sodium or potassium levels at the axon. In either case we are seeing the reversal of many of the symptoms of SCI over a period of time, from weeks to months. In most cases, less than one year. Due to these anecdotal results we feel further study is warranted.

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