Physician's Section
 

The electro-physiology of electro-stimulation with the ReBuilder™

Simplified basis:

•  Nerves become dysfunctional when they cannot forward electrical signals.
•  Signals propagate by a rolling difference in electrical potentials from section to section.
•  Atrophy, chemical burns, anoxia, physical compression, dilution of mineral electrolytes in synaptic fluid all
   contribute to an aberrant, in cohesive polarization of these polarity gradients.
•  The ReBuilder™ sends a much stronger signal that re-polarize and re-establishes these gradients.
•  Since the end points of stimulation are extremely distal, the ReBuilder™  re-educates the nerves to follow  the
   correct paths from nerve cell to nerve cell; one foot is electrically positive while the other is electrically negative. 
   This difference induces a physical "pulling together" of axons and dendrites  which can help reduce the synaptic
   gap.

•  The ReBuilder's warm water footbath with added electrolytes vasodilates the skin and increases the mineral
    concentration of the blood while simultaneously utilizing the muscle stimulation of the calf muscles to infuse these
    newly activated, recharging nerves with the necessary minerals to support the increased metabolism.

Distinct and characteristic morphologic changes have been demonstrated in diabetic peripheral neuropathy including focal and generalized nerve fiber loss, nodal changes, blunted fiber regeneration, and segmental demyelination.  Pathophysiologically, by utilizing the technique of threshold electrotonus, diabetic neurons (myelinated and unmyelinated) display selective reduction of inward rectification of the potassium channel.  Thus, channel closure produces an excess of positively-charged potassium (K+) on the inner side of the nerve membrane leading to depolarization. This also induces the opening of both the voltage and time-dependent calcium (Ca++) channels and sodium (Na+) channels. Evidence suggests that this axonal accumulation of sodium and calcium during dysesthetic peripheral neuropathy is of pivotal importance with respect to symptoms of paresthsiae and burning.  Paresthesiae are believed to be produced by multiple cutaneous or motor axons firing ectopically and cyclically with alteration of Na-K-Cyclic adenosine monophosphate (C-AMP) and ATPase.  Some researchers believe that a final common pathway might be a decrease in the intra-axonal concentration of C-AMP.  Based upon the disappearance and/or significant improvement in the paresthesiae, it is tempting to speculate that this aberrant behavior of the fibers is affected at the cellular level with stabilization.  Since these specific changes are seen to a greater extent in sensory nerves and with advanced age, it is hypothesized that ReBuilder™ bio-stimulation selectively induces hyperpolarization or repolarization with a return to baseline axonal potential in the sensory afferents.  The effects of this ReBuilder™ stimulation on peripheral nerve excitability may depend on a combination of factors including design, strength, intensity, and duration as well as the functional state of the peripheral nerve.  To date it has been difficult to identify electrophysiological changes by the conventional gold standards of serial nerve conductions and SSEP.

Although the cellular mechanisms underlying the mode of action of the ReBuilder™ are speculative, several general principles have emerged from experimental studies. First, electrical stimulation induces ionic gradient changes in the Na-K-ATPase system. Since there are distinct physiologic and neuro-biologic changes noted at the cell membrane level, it is postulated that chronic sub-threshold stimulation of afferents also induces similar ionic changes.  The most plausible explanation is that the ReBuilder™ targets the small C-fibers and induces a change in the firing pattern of the C-fibers by recruitment, synchronization, and possible temporal summation, thereby producing either hyper-polarization or re-polarization. It is well known that the functional C-polymodal receptor afferents are functionally adaptive and can be modulated by drugs and temperature which act or influence their surface membrane receptors.  Similarly, stimulation by either threshold or sub-threshold influences could produce the same effect.  It is recognized that unmyelinated C-fiber axons comprise 75% of the axons in cutaneous peripheral nerves in the sole (epidermis and dermis) and have increased utilization of potassium channels.  By virtue of this defect in the internal rectifying channel, there is an interference with neuronal transmission thereby producing a constant depolarization.  Since dramatic benefits are seen in diabetic patients, it is presumed that ReBuilder™ stimulation induced alteration of the nociceptive threshold depends on voltage-flux, flux density, time, and usage leading to pain modulation. This is the well-known strength duration relationship.

Despite the absence of electrodiagnostic sensitivity, the morphologic and pathophysiologic changes raise several interesting questions.  Axonal damage was seen in all the subjects with 100% loss of sensory action (SNAP) and 60% loss of compound motor potentials (CMAP) with rare demyelination.  Despite this extensive damage, there was dramatic subjective, statistically significant benefit in 90%. Since it is assumed that there is both A and C-fiber damage, the current results suggest that metabolic influences are primary, but the high frequency of regenerating axons may be relevant to the benefits seen.  Specific metabolic abnormalities that have been identified in diabetic neuropathy include a reduction in nerve-free myoinositol, a reduction in the rate of synthesis and transport of intra-axonal proteins, a reduced incorporation of glycolipids and amino acids into myelin, a reduction in nerve Na-K-AT-Pase, and excessive glycogen accumulation.  It has also been documented that elevated glucose levels evoke a rise in the intracellular ATP levels thereby closing the potassium channel.

These observations highlight the role of metabolic modulation.  Serial analysis of glucose levels, glycohemoglobin, and HbA1c of these 4 individuals did not show striking differences over the ensuing months yet implies that this is a current contemporaneous aspect.

The idea that a single ReBuilder™ treatment can induce a change in the firing pattern of the C-fibers is novel and appealing.  However, one cannot ignore the therapeutic benefit over a longer period.  Patients using the ReBuilder™clearly showed an improvement, particularly those with underlying diabetic peripheral neuropathy.

The intriguing issue of neuroprotection needs to be addressed. Does the ReBuilder™treatment delay the progression of peripheral nerve damage?  So far follow up data suggests that it does.

Electrical stimulation alteration of the nociceptive threshold depends on voltage-flux, flux, density, time, and usage.  According to Faraday’s Law, a magnetic field (created by the ReBuilder’s current path) will exert a force on a moving ionic current.  Furthermore, an extension of this physics principle known as the Hall effect, holds that when an electro-magnetic field is perpendicular to the direction of flow, it will generate a secondary intra-cellular voltage and secondary heat.  Since peripheral nerves in diabetic neuropathy have impaired blood flow with endoneurial hypoxia secondary to nerve micro vessel damage, it is tempting to speculate that improvement in the micro vascular circulation is also reflected in the feeling of warmth which may be due to an improvement in local and regional blood flow.