/ News & Insights / Treatment Toward a Cure: A Paradigm Shift in the Treatment of Diabetic and other Neuropathies

Treatment Toward a Cure: A Paradigm Shift in the Treatment of Diabetic and other Neuropathies

RM Cary, RH Odell M.D.,, R Sorgnard

A nurse helping a diabetes patient check their blood sugar


In the United States and most developed countries, the quality of medical care continues to grow in the treatment of acute disease, many cancers and genetic disease. Sadly, such has not been the case of most chronic disease.  Efforts have largely been in management of symptoms rather than reversal of symptoms or even cure. Diabetes, diabetic neuropathies and other neuropathy associated disease states consume large portions of healthcare resources of the USA and the world.

By and large to date, care has only focused on symptom control and slowing the disease progression. At this time there is no real effective treatment, only symptom management. We have developed a protocol for which compelling evidence exists that the clinical course of diabetic and other neuropathies is actually arrested and likely reversed. To this end, we utilize advanced electronic signaling treatment (EST) to signal cell healing rather than smothering nerve and muscle cells with pharmacological agents. As we also have discovered, these energy medicine techniques are practically devoid of side effects.


Peripheral neuropathy occurs as a component of several common and many rare diseases. It is heterogeneous in etiology, diverse in pathology, and varied in severity. Peripheral neuropathy of the extremities is often undervalued as a significant problem worldwide, and especially in the U.S.

Neuropathy from diabetes and other causes is rampant in the U.S. population (>8 percent by some estimates), and is projected to worsen. Neuropathy, at least subclinically, is often the first sign of diabetes; other end organ damage is less perceivable. Morbidity associated with neuropathy from diabetic and other diseases are a major reason why patients seek medical care and are huge cost to third party payers and the U.S. (and global) societies as a whole. This nerve disease affects millions of people worldwide by causing multiple foot, ankle, hand, wrist as well as other muscular and skeletal disorders.

Components of Diabetic Peripheral Neuropathy

Diabetic peripheral neuropathy (DPN) is a particularly debilitating complication of diabetes mellitus and accounts for significant morbidity by predisposing the foot to ulceration and lower extremity amputation. It is estimated that between 12 percent and 50 percent of people with diabetes have some degree of DPN, which may be asymptomatic in more than 50 percent of cases. Symptoms may be disabling and may be manifested as both “ negative” and “positive” symptoms, including tingling, prickling, pins and needles, numbness, pain (e.g., burning, lancinating, throbbing, stabbing, aching), along with allodynia (other pain or unusual sensation)and loss of proprioception (balance)[i]. In fact, less than 25 percent of patients with diabetic neuropathy have “positive” symptoms of pain, and these are the only symptoms that medication can target.

A predominant feature of DPN is sensory loss, but it is believed that all causes of peripheral neuropathy have a sensory, motor, and autonomic neuropathy component. Sensory neuropathy causes numbness, paresthesias and loss of protective sensation, which can lead to loss of sleep, ulcerations and lower extremity amputations. Motor neuropathy causes imbalance leading to injuries and fractures, some forcing patients to lose their independence. Autonomic neuropathy can alter everyday body functions such as blood pressure, heart rate, bowel and bladder emptying, digestion, and lead to skin ischemia and Charcot events[ii],[iii],[iv]

The costs to the world economy are staggering. In the U.S. alone, the annual total direct medical and treatment cost of diabetes was estimated to be $44 billion in 1997, representing 5.8 percent of total personal healthcare expenditure in the U.S. during that year. The management of DPN and its complications is likely to form a large proportion of this total expenditure, because treatment is often resource intensive and long term. In 2001, the total annual cost of DPN and its complications in the U.S. was estimated to be between $4.6 and $13.7 billion for Type I and Type II diabetesi.

Up to 27 percent of the direct medical cost of diabetes may be attributed to DPNi. These staggering figures cover the annual cost of DPN only, which is believed to represent only 30 percent of the prevalence of overall peripheral neuropathy, and as such, 70 percent of all the causes of peripheral neuropathy are not related to diabetes. Taken together, not only can Diabetic and other causes of peripheral neuropathy lead to tremendous debilitating complications, such as, amputations, pain, numbness, loss of balance, sleep, strength, quality and length of life, and poly-pharmacy use, but they also account for significant overall morbidity and healthcare costs. Some studies have shown that the costs of caring for the diabetic patient with neuropathy can be as much as $7,000 more per year than caring for the diabetic patient without neuropathy. Sadly, most of this cost is directed to symptom management and control only.

Treatment Options for Peripheral Neuropathy

Diabetic neuropathy is known to develop well before the patient has any symptoms, since many early symptoms are “negative”. The literature states unequivocally that the sooner treatment can be initiated, the greater the chances of reversal of the symptoms. This is a disease of the circulation, and microvascular circulatory deficiencies, caused by errors in glucose metabolism, have direct effects on the circulation to the nerves, as well as direct effects on the nerves themselves. Pain signals, in turn, trigger secondary peripheral and central hyperalgesia (increased pain and sensation) which enhance the body’s response to the microvascular insult. Ephatic transmission (nerve “cross talk”) can generate painful dysesthesias and allow numbness to co-exist with pain at the same locations. On a local level, micro-inflammation and edema around the nerves also contribute to neuropathy and diseases such as carpal tunnel syndrome and Morton’s Neuromas[v].

Several modalities are currently used to treat diabetic or peripheral neuropathy. Modifying risk factors by lifestyle changes, vitamins & supplements, physical medicine, topical medicinal treatments, prescribed oral medications, transcutaneous electrical nerve stimulation (TENS) units, monochromatic infrared light energy (MIRE), Anodyne®, Microvas®, and surgery have all been used to treat PN patients[vi],[vii],[viii],[ix]. The most common approach is oral medications, which only “paper over” the symptoms. According to Berger, 53.9 percent of diabetic PN patients are treated with opioids, 39.7 percent with anti-inflammatory drugs, 21.1 percent with serotonin selective reuptake inhibitors (SSRI), such as Cymbalta, 11.3 percent with tricyclic inhibitors (TCA), such as Nortriptylline, and 11.1 percent with anticonvulsants, such as Neurontin and Lyrica[x]. Many researchers and clinicians have observed that there is no rational reason to treat the neuropathic patient with opiates.

The safety and efficacy of these medications throughout the literature over the years is equivocal at best. These medications have drawbacks. Major adverse effects could include sedation, dizziness, confusion, short term memory impairment, risk of renal impairment, GI bleeding, constipation, nausea, swelling, and physical dependence. Almost some or all of these adverse affects, including the staggering health care costs of iatrogenic complications, are well documented with long-term usage of many of these medications.

Recently, further studies and sub-analysis performed has shown no statistical quality or merit in treatment modalities, such as TENS, MIRE, Anodyne®, Microvas®, and even decompressive nerve surgery.

A New Treatment for Peripheral Neuropathy

For the purposes of a discussion of pathophysiology, neuropathy from diabetes will be used as the model. We will discuss how chemistry and physics, both models that we as humans use to model these smooth running biological systems, act together for healing. On a more basic level, we know that electrons, i.e. electron behaviors, tie together all of electrical and chemical medicine, and thus tie disease and curative medicine conceptually together.

 Alternating current (AC) frequencies reverse and fire at a rate greater than the rate a nerve can fire, i.e., greater than 1,000 Hz.  These depolarizing frequencies have been shown by Knedlitscheck [xi] to stimulate utilization of cAMP. It is well documented that cAMP directs all cell-specific activity, such as the repair of insulted tissue causing the metabolic cascade (leaking arachidonic acid) and decreasing the level of noxious pain mediators (anti-inflammatory effect). The sustained depolarization of the cell increases intercellular levels and utilization of cAMPv.

In fact, Kilgore and Bhadra have shown[xii] that nerve block via depolarization does occur at 2,000 to 20,000 Hz. Wyss [xiii],[xiv]clearly showed that depolarization is sustained with the application of these currents, specifically 4,000 Hz[xv].

A new, innovative, and effective treatment has been established for diabetic and other peripheral neuropathies.  This treatment is termedtheCombination Electrochemical Treatment (CET). CET incorporates two well-established procedures combined into a protocol that is showing great promise as a safe and effective treatment solution for diabetic, idiopathic and all other neuropathies.  The CET consists of two procedures, an ankle block performed with local anesthetic, and Electronic Signal Treatment (EST), as delivered by a unique sophisticated electromedical wave generator.

Ankle Block

The peripheral nerve block injections are performed with a low volume and concentration of local anesthetic, and as such are not intended to produce the level of anesthesia required for performing surgery.  Bupivicaine is chosen because it does not fix to the tissues as rapidly; more time is available for the iontophoresis (electronic means of delivering a medication) of the local anesthetic into the tissues by the EST. No steroids are utilized at any time during this procedure. The blocks are aseptically performed and no infections have been reported in thousands of injections.

Electronic Signal Treatment

Electricity has been a powerful tool in medicine for thousands of years. All medical professionals are, to some degree, aware of electrotherapy.  EST utilizes computer controlled, exogenously delivered specific parameter electroanalgesia using both varied amplitudes and frequencies of electronic signals.  This digitally produced electronic sinusoidal alternating current, with associated harmonics produces scientifically documented and/or theoretically reasonable physiological effects when applied to the human body.  The EST medical device that delivers the electronic signals uses sophisticated communications-level technology to produce and deliver higher frequency signal energy in a continually varying sequential and random pattern via the specialty electrodes. This alternation of sequential and random signal delivery eliminates neuron accommodation.  These signals are produced by advanced electronics not possible even 10 years agov.

Brief Overview of Mechanisms of Action

A thorough discussion of the mechanisms of action is beyond the scope of this paper. However, a brief summary is presented here.

When mechanisms are considered, a note needs to be made about neuroanatomy.  While myotomes and dermatomes have been well documented in biomedical literature, as far as we can tell no such maps exist for the distal sympathetic C fibers anywhere in the body.  Still, we know enough about the C fibers to know that these are primary in diabetes pathophysiology:   these efferent fibers control the tone of local arterioles, and thus are the critical contribution to the pathophysiology of small vascular structures and small nerve fibers (which are only viable as a function of these tiny arterioles).  Pathology in the small arterioles and nerve fibers combine to adversely affect the distal tissues of the legs (and later the hands).

Increasing blood flow:  CET has been shown to increase blood flow[v] through several direct vasodilatory mechanisms.  The vasodilatation improves microcirculation, which has a salutary effect on the healing process in these oxygen-deprived nerve cells. The drainage function of the capillary system is improved as a result.  Stimulation of motor nerve fibers results in excitation of the muscle fibers.  This has two effects on the blood flow: energy is used up, the metabolic rate is increased, and blood flow is enhanced in the region of stimulating muscles. In addition, through the contraction activity of the muscle group, an active stimulation of the venous backflow occurs.  Also, the EST directly influences blood flow and lymph transport via sympathetic function imitationv.

Anti-inflammatory action:  EST, as an extension of presently available technology, also has potent anti-inflammatory effects [v].  The potential long-lasting anti-inflammatory effects of some electrical currents are based on basic physical and biochemical facts, namely that of stimulating and signaling effective and long-lasting anti-inflammatory effects in nerve and muscle cells. A full review is available in the references[v].

The electronic frequencies are programmed into the EST device, and sequence through a series of different complex waveforms.  Each individual waveform represents a different mechanism of action.  The electronic signals stimulate superior steroidogenic (anti-inflammatory) effects without the negative side effects of injected steroids.

Blocking pain signals:  Another primary mechanism of action of EST is a reactive sustained depolarization of the nerve’s cell membrane.  This occurs because multiple delivered signals fall within the absolute refractory period of the cell membrane.  A pharmaceutical nerve block occurs when the Na channels are completely blocked, resulting in sustained hyperpolarization of the cell membrane. EST produces a sustained depolarization of the cell membrane. All propagated pain and dysesthetic signals are blocked, but all cellular voltage-gated channels are allowed to function at optimum levels to their designated equilibrium point.  Thus, metabolic activity of the cell is continued, the patient’s pain suppression is facilitated, and all aspects of neuropathy can potentially be reversed.

cAMP Activation:  More profound effects happen on a cellular level: the sustained depolarization that occurs has a direct effect to produce an electrical conformational change of the cell membrane and activation of adenylyl cyclase, which converts ATP to cAMP. The positive effects of cAMP were discussed previously. Stimulation also activates the release of pain-suppressing neuro-modulators found in the central nervous system, e.g. endorphin, encephalin and GABA.

CET Outcomes

The first author, a board certified anesthesiologist, interventional pain medicine specialist and Fellow of Interventional Pain Practice (FIPP) of the World Institute of Pain, has been using this block for over five years; the concept of the CET was formally introduced in 2008 to the International Spine Intervention Society at its annual convention.

Diabetic peripheral neuropathy (DPN) and peripheral neuropathy (PN) patients have shown marked symptom reduction and motor function improvement with application of the CET[xvi],[xvii]. Clinically, the largest improvement in symptomology (reversal of pain, restoration of sensation & feeling to the extremities, increase strength, balance and quality of life) has been obtained with patients treated between ten and sixteen weeks. The treatment course is variable depending on the severity of the patient’s neuropathy and overall compliance to the treatment regimen. The goal of therapy during the treatment protocol is to reduce neuropathic symptoms including any pain, paresthesias, dysesthesias, allodynia, numbness.  As many as 80 percent of patients with neuropathic symptoms experience benefits. In some patients, improvement of positive and negative symptoms approaches 100 percent.

Long term goals – including misuse of medications, improvement of balance, sleep, overall function, and quality of life – have also been accomplished in a significant plurality of patients. A retrospective study from our clinic showed that symptom improvement was being maintained in over 51 percent of patients[xviii]. Longer term goals – the prevention of infections and amputations – especially in diabetics, have profound implications in the ability to save precious health care resources.

Objective Data

It is the authors’ position that nerve regeneration is really occurring. Clinical objective human data of nerve regeneration from neuropathy patients in the author’s clinics of the clinics of others have included changes in epidermal nerve fiber testing (ENFD), Neuralscan neurodiagnostic testing, and nerve conduction velocity (NCV) testing. An example is shown in figure 1 of the improvement in A-delta nerve function in a patient who has improvement of symptoms. Figure 2 shows epidermal nerve regrowth in a patient who has successfully undergone the EST protocol.


The safety of electrotherapeutic treatments in general and EST in particular has been established through extensive clinical use

Summary & Conclusion

The clinical experiences of multiple physiciansxii and podiatristsxiii have shown that the application of EST, when combined with the low dose local anesthetic, favorably influences the peripheral vasculature and promotes nerve and cell regeneration. Many forms of neuropathy can be reversed over time with this effective, new treatment.  Clinicians are seeing the nerve regenerative and growth capabilities of this treatment consistent with the above results.  Little or no return of neuropathy symptoms long-term post CET treatment has been observed.  Our current patient treatment success, response rates and lack of relapse are substantial, and are supported by three different kinds of objective proof of neural regeneration.

Further basic science studies regarding the exact mechanisms and clinical studies which would correlate risk factors such as length of time prior to treatment could yield even more effective protocols.

Finally, a paradigm shift in treatment of chronic disease such as what has been presented here may pave the way for true healthcare reform, where the scientific application of energy medicine can effect symptom reversal, true healing in a safe and effective manner.  Outcomes will significantly reduce health care costs’ these, of course, need to be combined with lifestyle and risk avoidance behavior changes.


History & Clinical Course:

  • 66 y/o female with 10-11 year history of diabetic neuropathy
  • Symptoms included burning and aching on the plantar surfaces of the feet
  • Underwent 16 CETs and 8 EA treatments, stopping to have a TKR
  • Reduction of 70% in burning pain noted
  • Patient weaned self of Lyrica
  • Repeat ENFD done 3 months after last visit



About the Author

Portrait 3

RH Odell M.D., Ph.D.1; R Sorgnard, Ph.D2.; RM Cary1, PA-C, M.Ed., DFAAPA

1Neuropathy and Pain Centers of America, Las Vegas, NV

2Moorhea Technologies, Las Vegas, NV



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[ii] Shy ME. Peripheral neuropathies. In: Goldman L, Ausiello D, eds. Cecil Textbook of Medicine. 23rd ed. Philadelphia: Saunders Elsevier; 2007: 446.

[iii] Wilson J.  Type 2 diabetes. In the clinic, Ann Intern Med. 2007; 146(1): ITC1-15.

[iv] Benarroch E, Freeman R, Kaufman H. Autonomic nervous system. In: Goetz CG, eds. Textbook of Clinical Neurology. 3rd ed. Philadelphia: Saunders Elsevier 2007: chap 21.

[v]Odell RH, Sorgnard R.  Anti-Inflammatory Effects of Electronic Signal Treatment; Pain Physician 2008: 11:891-907

[vi]Barrett S, DeHeer P, Offutt S. Point-Counterpoint: Nerve Decompression in Diabetic Patients: Should It Be Done? Podiatry Today 2005: 18(6): 44-50

[vii]Leonard DR, Farooqi MH, Myers S. Restoration of sensation, reduced pain, and improved balance in subjects with diabetic peripheral neuropathy: study with monochromatic near-infrared treatment. Diabetes Care 2004: 27(1):168-172

[viii]Lavery L. Diabetes Watch: A Closer Look At The Research Behind MIRE Therapy. Podiatry Today 2007: 20(7): 22-29

[ix]Harkless L, LaFontaine J, Shibuya H. A Randomized Controlled Study Assessing the Safety and Efficacy Of The MicroVas Device in the Treatment Of Patients With DPN in the Lower Extremities: a Preliminary Outcome Report. UNTHSC, June2007; Available at . Accessed November 19, 2013

[x]Berger A, Dukes EM, Oster G. Clinical characteristics and economic costs of patients with painful neuropathic disorders. J Pain. 2004: 5:143-149

[xi] Knedlitscheck, G. Cyclic AMP Response in Cells Exposed to Electric Fields of Different Frequencies and Intensities; Radiation Environmental Biophysics 1994: 32:1-7).

[xii]Kilgore KL, Bhadra N.  Nerve conduction block utilising high-frequency alternating current. Med Biol Eng Comput2004: 42:394-406

[xiii]Wyss, OAM. Nervenreizung mit Mittelfrequenzstromstossen. Helvetica Physiologica Acta  1967: 25: 85-102

[xiv] Wyss, OAM. Prinzipien der elektrischen Reizung. Zurich: Leemann 1962

[xv]Woessner J; The Electric Nerve Block.  In:  Boswell M, Cole E, Eds. Weiner’s Pain Management 7th Ed 2006: 1233-1242

[xvi] Odell RH, Sorgnard RE. New Device Combines Electrical Currents and Local Anesthetic for Pain Management; Practical Pain Management 2011: 11 (6): 52-68

[xvii]Cernak C, Marriott E, Martini J, Fleischmann J. Electric Current and Local anesthetic Combination Successfully Treats Pain Associated With Diabetic Neuropathy. Practical Pain Management; 2012: 23-36

[xviii]  Odell RH, Zhan Z. Clinical Outcomes utilizing the Combined Electrochemical Treatment for Peripheral Neuropathy:  A Retrospective Study from a Western Clinic, Submitted for publication in October 2013, Pain Medicine



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