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Combined Electrochemical Treatment for

Article · October 2015

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4 authors, including:

Richard Sorgnard PhD Robert Odell Morhea Technologies/Bioenergetics Resea… Neuropathy and Centers of America

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All in-text references underlined in blue are linked to publications on ResearchGate, Available from: Richard Sorgnard PhD letting you access and read them immediately. Retrieved on: 02 July 2016 FEATURE

Combined Electrochemical Treatment For Peripheral Neuropathy This technique uses blocks in conjunction with electric cell signaling treatment (EST) to successfully treat neuropathies of all causes.

Robert H. Odell, Jr., MD, PhD Interventional Specialist Las Vegas, Nevada Richard Sorgnard, PhD Executive Director Morhea Technologies Las Vegas, Nevada Peter Carney, MD Neurosurgeon in Private Practice Elkhart, Indiana Robert Milne, MD Milne Medical Center Las Vegas, Nevada

neuropathy occurs as a result of basic patho- treatments have focused on reduction of symptoms,6 and, logic processes gone awry—either from in the case of diabetes, control or slowing of the progres- injury or disease. The incidence of neu- sion of the underlying disease. ropathy increases with age and its preva- Combined electrochemical treatment (CET) represents lence is growing. In fact, the prevalence a safe and effective therapy for all forms of neuropathy.7 of peripheral neuropathy may be as high We have now documented the reversal of the neuropathic A as 2.4% in the United States.1 A study of process both from clinical observations and from objective people with diabetes estimated the prevalence of diabetic functional (neurodiagnostic) testing and anatomic (epidural peripheral neuropathy (DPN) in patients with type 2 dia- fiber density [ENFD]) data.8 Although our clinics have betes to be 26.4%.2 DPN is often the first indication to the not yet initialized formal double-blinded control studies, patient that they have diabetes.3 Morbidity associated with our clinical outcomes strongly suggest that the CET proto- diabetic and other neuropathies is a major reason patients col is making a substantive difference in patients’ lives and seek medical care and represents a major cost to patients certainly warrants more detailed consideration. and society.4,5 This paper will discuss neuropathic , with It is compelling to note that the course of DPN, as well as a focus on DPN. We will discuss how biochemistry and other neuropathies, generally is progressive. To date, most physics act in concert for healing.

October 2015 | PracticalPainManagement.com 47 Combined Electrochemical Treatment for Peripheral Neuropathy

Peripheral Neuropathy of successfully transmitted nerve sig- testing (QST) such as sweat testing Four primary nerve fibers are import- nals across the junction. When nerve (Sudoscan), thermography, and pos- ant in small fiber (sensory) neurop- signals attenuate because the synap- sibly fMRI, and will be considered in athy: A-delta, afferent C, efferent C, tic cleft widens, necessary conductive future studies. and A-beta. occurs minerals and are no In physics, electron behavior is when normal signaling between adja- longer held in place by naturally-occur- referred to as “organized chaos.” This cent nerve cells attenuates as a result ring electrical tension and are slowly idea unites activities of electrical and of insufficient oxygen transport. The leeched away.12,13 chemical medicine, and thus ties dis- hypo-oxidative state associated with The initial sensory perception ease and curative medicine together neuropathic pain appears to be a pri- associated with atrophying conceptually.16 Although myotomes mary factor, along with demineraliza- and enlarged synaptic clefts often is and dermatomes have been well doc- tion of the synaptic fluid, necessary for reported by the patient as tingling or umented in published biomedical lit- signal transport. 9 electric sensation. This effect most erature, we are unable to find any data Unlike muscles, which use either likely is the result of ephatic firing, detailing existing “maps” for the dis- oxygen or glucose metabolic pathways, defined as some nerve signals being tal sympathetic C fibers in the body. nerve cells are limited to the oxidative misdirected to nearby nerves.12-14 As Still, C fibers are known to have a pri- reductive metabolic system, or Krebs the condition worsens, more signals mary influence in the development of cycle.10,11 The Krebs cycle requires an are misdirected or suppressed, lead- the pathophysiology of diabetes. These immediate defense response to assure ing to increasingly unpleasant sensa- efferent fibers control the tone of local neural integrity and survival during tions such as stinging, burning, and arterioles, and, critically, contribute to a hypo-oxidative state. This defense pain. In time, affected nerve signals can the pathophysiology of small vascu- mechanism also occurs upon expo- become completely suppressed, result- lar structures and small nerve fibers sure to environmental toxins, chemo- ing in numbness. (which are viable only as a function of therapeutic agents, military chemical Ephatic cross firing co-existing these tiny arterioles). in the weapons, insecticides, and other neu- with numbness may also explain why small arterioles and in the nerve fibers rotoxic substances. Contraction, which patients can have pain, , and combines to adversely affect the distal is one such defense mechanism, causes numbness at the same locations at the tissues of the extremities.17 a generalized shrinking of the nerve same time. These conditions often Tests of functional improvement are cells and a widening of the synaptic result in poor tissue perfusion, insecure generally considered more robust than cleft between these cells. gait, balance problems, general muscle anatomic testing. However, ENFD As the synaptic junctions between weakness, and other mobility issues. testing is rapidly becoming an accepted the of one nerve cell and the den- From a diagnostic standpoint, specific standard to measure afferent C fibers drites of the next nerve widen, normal neurodiagnostic testing can directly and unmyelinated A-delta fibers.18 signal transmission can become com- measure this effect, as the increased Thermal evoked potentials and fMRI promised. Signals of normal intensity voltage threshold necessary to fire also can measure the function of C and can no longer bridge this newly wid- enough nerve axons for the patient to A-delta fibers, but ENFD currently is ened gap, resulting in a loss of bioelec- “feel” sensation normally. the most practical method. In our clin- tric integrity. Widening of the synaptic The sensory function of afferent ics, we have employed A-delta NCS gap makes it more difficult for normal A-delta and C fiber is best measured and ENFD biopsies. sensations to propagate and causes a by the A-delta nerve conduction study Despite the many described causes general loss of electrical conductivity (NCS), thermal evoked potentials, and of peripheral neuropathy, the patho- in the synaptic fluid.12 functional magnetic resonance imag- physiology of simultaneous and syner- Conductivity relies on minerals and ing (fMRI). Nerve conduction veloc- gistic decrease in vascular and neuronal specific neurotransmitters in the synap- ity (NCV) testing is less sensitive than function remains constant throughout tic fluid to enable propagation of the A-delta NCS but can also measure all the process and creates a pathological nerve signal. These conductive min- three fibers. A-delta function is effec- cascade. erals and neurotransmitters are deliv- tively measured by A-delta NCS with ered via the perfusion of adjacent tis- 95% accuracy.15 Efferent C fiber func- Basis of CET sues with fresh blood. They are kept in tion, which is a primary pathology, is CET involves the use of local anes- suspension by the periodic ionization best assayed by quantitative sensory thetics to block pain and other nerve

48 PracticalPainManagement.com | October 2015 Combined Electrochemical Treatment for Peripheral Neuropathy

Table 1. Differences Between Electrical and Chemical Nerve Blocks What do nerve blocks accomplish? Electrical—sustained depolarization Chemical—hyperpolarization blockade Neuron blockade Afferent block results in less perceived pain Afferent block results in less perceived pain • Less pain, local muscle relaxation • Less pain, local muscle relaxation • Relaxation, more circulation • Relaxation, more circulation • More circulation • More circulation More nutrients//hormones o o More nutrients/enzymes/hormones Less toxic metabolites o o Less toxic metabolites • Less neurogenic • Less neurogenic inflammation Efferent block results in local vasodilation Efferent block results in local vasodilation • More circulation • More circulation More nutrients/enzymes/hormones o o More nutrients/enzymes/hormones Less toxic metabolites o o Less toxic metabolites • Less neurogenic inflammation • Less neurogenic inflammation They achieve exactly the same physiologic results

function in the distal lower extremi- higher-dose, specific-frequency EST are treatment of neuropathy include: ties, followed by electrical cell signal- similar with regard to their ability to increasing blood flow and available ing treatments (EST) to both lower block nerve fiber (axon) transmission oxygen, increasing second messen- extremities. First, a low-dose, low-vol- and promote beneficial effects on nerve ger(s) responsible for regenerative tis- ume injection of local nutrient-infused cells (Table 1).24 The afferent block sue effects, and promoting analgesia anesthetic (Na+ channel blocker) is results in less perceived pain; the effer- and anti-inflammatory effects. At a injected into the target region, followed ent block promotes increased blood deeper level, the effects of the local by treatment with the EST device.19 flow through vasodilation. Vasodilation anesthetic (LA) and EST on cyclic The device combines, and simultane- promotes nutrient transfer to the nerve monophosphate (cAMP), ously delivers, frequency-modulated cell and removal of waste products with a second-messenger molecule, cause (FM) and amplitude-modulated (AM) pH normalization; the reduction in the most basic and important mecha- electric cell currents in a pulsed elec- inflammation produces a concomitant nism in reversing neuropathy: activat- tromagnetic fields (EMFs).20-22 reduction in edema and pain. ing the regenerative processes.14 The The concepts of sig- effects of chemically blocking pain also naling, simultaneous nerve stimulation, Key Mechanisms of Action may play a role in early patient com- and timed muscle activation indicate Patients occasionally ask, “How does pliance. Patients become more moti- how physics and pharmacology can the CET treatment fix my numb- vated to continue treatment because work together to promote a physiologi- ness?” The answer to this question is they experience improvements in their cal environment that favors healing.20,23 most likely that the healing process is symptoms and reduced pain or numb- Clinically, we have witnessed extraor- enhanced by factors in the local anes- ness, particularly . dinary results with CET that are con- thetic beyond simply its ability to block sistent with plausible and scientifically sodium channels, arresting degenera- Effects on Increased Blood supportable regenerative and reparative tive pathology and promoting healing. Flow and Oxygen Transport physiologic mechanisms.21,22 The key physiological mechanisms Peripheral neuropathy is most likely The effects of the local anesthetic and of action of CET necessary for the caused by disorders of the circulation,

October 2015 | PracticalPainManagement.com 49 Combined Electrochemical Treatment for Peripheral Neuropathy

neural edema (neurogenic inflamma- cell membrane via sustained cell inflammatory mediators. By pro- tion), and altered microcirculation membrane depolarization.19 moting changes to G proteins in cell around nerves. Blood flow is among the Specific signaling produces other sec- membranes, EST may ultimately nor- least discussed and appreciated factor ondary circulatory effects: facilitation malize cell function and neuropathic in pain relief. The influence of blood of diffusion processes and balancing of pathology. flow, especially its diminution, is not metabolic concentration differences; Multiple studies support the belief emphasized enough in the EST-induced activation of metabolism that cAMP will increase from sus- literature.25 by increasing the formation of cAMP, tained depolarization of the cell mem- CET’s promotion of increased blood particularly in the endothelium; and brane.26,27 Schwartz stated that there flow is likely a primary mechanism for activation of muscle pump by motor are “numerous citations that demon- its effectiveness. If blood flow is nor- activity, which results in the centripetal strate … second messenger formation malized, the local milieu is improved, transport of venous blood and lymph within the cell at various ion voltage and healing of A-delta and C fibers nodes.23 gates when exposed to frequency spe- can occur. Increasing blood flow to The EST effects of motor neuronal cific electronic signal currents.”28 This the affected tissue has obvious, well and muscle stimulation produce an direct effect of EST increases avail- published benefits, such as increasing increase in metabolism, followed by able cAMP for normalization of cel- available oxygen content, increasing auto regulatory vascular mechanisms lular metabolism, improvement of local availability of nutrients, facilitating the that result in a decrease of local periph- blood supply and oxygen, improve- elimination of waste, and the overall eral resistance of the vasculature in the ment in cell proliferation, increases in normalization of neural transmitters. stimulated muscle. Post-EST stimula- local blood flow, and equilibration of EST signals, programmed with the tion leads to an overall relaxation effect differences in metabolic concentration. appropriate and time-varying cell sig- and circulatory normalization.19,20,23 naling parameters, as well as appro- A simplified schematic of the sym- Analgesia and Inflammation priate amplitude, influence the circu- pathetic ’s control of Several mechanisms help explain the latory system via several mechanisms circulation is illustrated in Figure 1. analgesia produced by EST. Under of action. By using specific program- Variations in the input at control points the influence of rapidly-alternating ming, EST signals produce the follow- will affect vascular tone. If the affer- polarity, ion movement is enhanced, ing effects on blood flow: ent sympathetic signal is increased, which tends to balance differences in • Slow-frequency nerve stimulation with no other influence on the effer- metabolite concentration, leading to (1-4 Hz) of the sympathetic ner- ent C-fibers, sympathetic tone also will pH normalization and reduction in vous system to produce vasocon- increase. When the efferent C-fibers are tissue acidosis. Formation of cAMP striction of the blood and lymph blocked, including by electric signaling, directs all cell-specific activity toward vessels, accelerating the centripe- the blood flow will increase regardless the repair of cell membranes, inhib- tal transport of venous blood and of the input of the afferent C-fibers. iting the release of arachidonic acid lymph The control exerted will trump affer- from insulted membranes and inhib- • Slightly faster low-frequency sig- ent signals, as the circuitry is in series. iting subsequent (pain nal stimulation of the sympathetic mediator) cascade.19,20,23 nervous system to produce vaso- Second Messenger (cAMP) Specific parameters of the electric sig- constriction (10 Hz) Formation/Activation: nal energy produce repeated excitation • Fast stimulating signal frequen- Normalization of Cell Function of afferent nerve fibers, effecting neu- cies (100 Hz) to produce vaso- EST energy produces a hormone-like ronal signaling processes in the central dilatation via sympathetic func- effect by triggering an electrical confor- nervous system (CNS), thus interfering tion exhaustion of the synaptic mation change to the cell membrane with local pain perception.29 Finally, neurotransmitters G protein. This change influences the EST assists in cell receptor uptake of • Fast non-stimulating frequency activity of adenylate cyclase, resulting beta-endorphin, encephalin, and phyl- signaling (>2,000 Hz), in which in the formation of cAMP. cAMP- lokinin among other substances, which multiple electric signals fall within induced repair processes are nec- modulate or inhibit pain impulses in the absolute refractory period of essary to stabilize the cell mem- the CNS. the cell membrane to inhibit the brane and inhibit continued leakage Direct blocking of afferent pain sig- action impulse capability of the of acids known to trigger pain and nals occurs in several ways:

50 PracticalPainManagement.com | October 2015 Figure 1: Nervous systemCombined control Electrochemical of vasomotor tone Treatment & Influence for Peripheral Neuropathy of Electronic Signal Treatment (EST)

Sympathetic Nervous System

Sympathetic Tone (Located in Thoracolum- (Pre Synaptic) bar )

Sympathetic input Pre-Sympathetic Ganglion (SNS axon) Adrenal Medulla vasomotor tone Release of Epi & NE flow (vasoconstriction) to prolong effects of SNS stimulation Post-Sympathetic Directly Stimulates Ganglion (cell) NE

Stimulatory EA Blocks Middle frequency EA Effects on ganglion ganglion Directly Blocks any NE effects of Effects on nerves: (ACh) vasoconstriction Nerves directly blocked open depletion (30-150 Hz) NE Blocked

Net Effect on Blood Flow:

Stimulatory Frequency: 0.1 – 1000 Hz Vasodilation & Middle Frequency: Healing Effects 2000+ Hz

Reference://www.ehs.net/2231/pdf/autonomic.pdf

Figure 1. Schematic drawing of nervous system control of vasomotor tone and the influence of EST. EA, ; Epi, epinephrine; EST, electrical cell signaling treatments; NE, norephinephrine • At low, stimulatory frequen- blocks axon information (pain “blocking the dieseling effect” cies, EST produces Na+ channel signal) transport analogy). exhaustion of neurotransmitters • EST “resets” or “reboots” primary Pure electric nerve blocks have been occurs and secondary mech- performed clinically for years to block • At the application of higher doses, anisms (wind-up)19,20,23,28 pain and increase local blood flow, higher frequency non-stimulating • EST blocks conduction in both with success similar to that of chemi- EST electric cell signals induces a directions, since efferent pain sig- cal blocks.30 sustained depolarized state across nals can be associated with periph- EST signal energy works to reduce multiple Nodes of Ranvier and eral (the so-called inflammation by initially facilitating

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H+ pH 6.9 H+ H+ H+ normal pH 7.4 H+ H+ normalized region pH 7.4 H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ +/- +/- H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+ H+

Figure 2. Influence of alternating current (electric field) on the concentration of hydrogen ions. Note how low pH (6.9) creates an area of inflammation. Based on reference 23.

the natural inflammatory process within tissues.10,13,19,20,28 This rebal- the nerve axon.32-35 toward a swift, organized, and natural ancing results in the dilution of toxic, resolution. While complex, all concepts pain and/or inflammatory mediators; Synergistic Interaction above fit together when taken into the an increase in tissue clearance by an Of EST and Anesthetics context of electric cell signaling and improvement in the efficacy of the local Local anesthetics are known to depress of normalization of cAMP. However, blood flow; and an overall improve- mitochondrial function by hyperpolar- the basic signaling mechanism could ment of diffusion and reabsorption ization, a “locking down” of the cell’s easily be the EST-driven ionic action between the intra- and extra-capillary voltage channels.14,32 However, EST has on cAMP. Through this and the other fluids.23 been shown to increase the number, size, mechanisms, cellular derangements and overall activity of mitochondria.33,34 return to normal in optimum phys- Distal Phenomena Increased mitochondrial activity allows iological time. An entire focused Axon Circulation for substantially more energy for bio- review has been devoted to the ben- Neuropathies also may result from utilization and regeneration of cells. eficial effects of CET on inflamma- interference in axon transport by prod- This physiologic benefit of EST is tion.23 By alternating the electronic ucts of glucose metabolism, such as extremely important, because increas- signal frequency parameters, inten- sorbitol.31 Axon transport problems ing production and use of energy are sities, and dwell times of the applied also are accompanied by inflammation. central to the healing process. EST treatment energy, the movement Some unique factors must be used to of inflammatory mediators and meta- explain nerve hypofunction, which Clinical Markers and Results bolic end-products away from the area depends on how distal that section of Formal studies and clinical experience of inflammation is enhanced, leading to nerve is from the CNS. The circulatory with CET have shown improvement in the reduction of inflammation. concepts of axon transport, including 80% to 85% of patients with periph- Figure 2 shows the influence of an afferent movement of nutrients and eral neuropathy, and a major functional alternating current on the concentra- efferent movements of waste, appear improvement in 75% of patients.7,21 tion of hydrogen ions and how an area to be an important factor. The difficulty in defining improvement of inflammation with low pH is nor- Does decreased axon circulation arises because neuropathy is more mul- malized under the effects of electric decrease nerve function, or does tidimensional than chronic pain in its signaling.23 decreased nerve function decrease presentation. Symptoms include pain, circulation? Perhaps both occur. dysesthesia, paresthesia, as well as loss Restoring Metabolic However, at this time, we cannot iden- or impairment of sensory function, Equilibrium tify which is first. Nonetheless, inflam- numbness, dry skin, gait instability Equilibration of differences in met- mation probably plays a major role in and fall risk, erectile dysfunction, and abolic concentration by alternating- interference of this circulation. The incontinence.35 Signs of peripheral neu- polarity EST will result in an increase largest manifestation of these distur- ropathy include decreased vibration, in the redistribution of ions and water bances occurs at the distal aspect of reflexes, protective sensation to pain,

52 PracticalPainManagement.com | October 2015 Combined Electrochemical Treatment for Peripheral Neuropathy

Table 2. Relationship of Symptom score (NRS) to Neuralscan Score (NS) NS improved NS same or not improved Totals NRS improved 16 11 27 NRS same or not improved 4 3 7 Totals 20 14 34 McNemar’s odds Ratio = 2.7

This lower odds ratio reflects the fact that while A-delta nerve condution study can predict clinical improvement; other nerves (afferent and efferent C fibers, and A-beta fibers) also play roles in an individual patient’s progress. Because objective improvements of A-delta nerves have been observed, there would also likely be improvements in afferent and efferent C-fibers resulting from improvements in the microvascular environment. A-beta improvement is measured by a reduction in allodynia, but no objective test exists. pressure, and thermal stimulation, as improvement (including those with of 62%.15 well as decreased proprioception. All no recordable responses). When sen- The spf A-delta test device is capa- of these symptoms can be measured sory nerves did show a pretreatment ble of assessing a wide variety of poly- but can be difficult to reproducibly response, however, they improved in neuropathies and compressive/entrap- quantify from provider to provider 82% of patients. In some cases, nerves ment syndromes. Regional mapping and clinic to clinic. that had no response did, in fact, begin techniques in the hands and feet can to have a measurable NCV. Since a be easily employed. In peripheral neu- Objective Testing placebo effect would be unlikely in ropathies, standard points The effectiveness of interventions this setting, Cernak et al stated that measured at L4, L5, S1, S2 and in the can only be self-reported by patients. “These trends in motor nerve func- feet appear hypoesthetic. However, numerous difficulties exist in tion may represent a decline in neu- The spf-NCS technology can objec- describing, standardizing, and quanti- rological morbidity of DPN as nerve tively track the progress of the patient fying pain and the other aspects of neu- function improves. In both sensory by repeat testing. The A-delta NCS ropathic symptoms in clinical evalua- nerves tested … over 40% of patients score Deviation Index is a numerical tions. Objective measures of improved did show an improvement in peroneal means of measuring outcomes and the neurological function and regeneration sensory nerve conduction while more extent of a neuropathy. Improvements should satisfy even the most skeptical than 31% showed an improvement in in nerve function are represented by of government regulators, stakeholders their sural sensory nerve.”21 decrease in hypoesthesia and are iden- and third party payers, and should pave tified as positive numbers; worsening the way for more widespread usage of spf (A-delta) NCS results, as negative numbers. Numbers CET and EST. Three diagnostic tests spf A-delta NCS testing is based on close to 0 indicate little or no change in have demonstrated reproducible func- the behavior of A-delta nerves in A-delta nerve function (Figure 3, page tional and anatomic objective improve- the pain processing system and has 54). In the example, the Neural scan ment of neurological function after the gained traction in the medical com- score improved by +34. Table 2 (above) CET protocol in treating peripheral munity over the past 15 years. The shows the relationship between symp- neuropathy. A-delta NCS system has 2 compo- tom relief and test score improvement. nents: an electrical stimulator that NCV generates neuroselective signals specific ENFD Skin Biopsies Cernak et al reported trends in to A-delta nerves; and a detector that ENFD punch biopsies are gaining wide increased amplitude and decreased records in real-time the micro-voltage acceptance for diagnosing and follow- latency of motor function when changes of the threshold action poten- ing patients with neuropathy.18 The test patients treated with CET were tested tial signal at muscles. The A delta- measures the density of intra-epidermal at least 1 month post-procedure—3.8% NCS measures the voltage required to nerve fibers at various sites in the leg. of peroneal motor nerves, and 49% of fire peripheral A-delta nerves, and has The measurements usually are taken in tibial motor nerves, showed improve- been shown to be reproducible with the lateral mid-foot, 10 cm above the ment.12 Sensory function in the pero- localization of nerve root injury sen- lateral malleolus, and 10 cm above the neal and sural nerves showed a 36% sitivity of about 95% and a specificity lateral epicondyle. Loss of nerve fibers

October 2015 | PracticalPainManagement.com 53 Combined Electrochemical Treatment for Peripheral Neuropathy

Clinical course: The patient is a 72-year-old male who presents with pain and numbness in the toes and bottoms of his feet. Cause of his neuropathy was either idiopathic or pre-diabetic. Over the course of 6-weeks, the patient had improvement in his symptoms, including numbness, by 80% to 90%. His sleep improved as well. He discontinued his medications and continued to improve after August 2012. He remains almost symptom free through mid-2015.

Figure 3: Example of Neuralscan with clinical improvement. Normal nerves lie between bottom single line and the lowest line in the left (hypoesthetic) set. In this case, the Neuralscan score has improved significantly, which is readily seen by comparing the graphs. Improvement in objective testing correlates well with the patient’s clinical improvement; notable is the fact that this patient, a functional medicine advocate, takes optimal care of himself.

is associated with increased neuropathic is demonstrated in 50% (11 of 22) of superficial burns have been reported pain. In our experience, nearly half of biopsied nerves, and 75% of patients from adhesive-type electrodes when patients with a painful condition had showed at least 1 nerve regrowth. After excessive power density is applied. evidence of small fiber neuropathy as 3 months, nerve regrowth was present These problems have been resolved noted with the skin biopsy.36 The diag- in 63% of all nerves biopsied. These by using a venturi-type vacuum cup nostic efficiency of skin punch biopsy results are remarkable when one con- electrode system. There have been no is about 88%, whereas findings on rou- siders that there could not be a placebo reports of infection to date. tine nerve conduction studies and elec- effect because of the natural history of In a study comparing CET to pre- tromyography typically are normal.37 this disease. Neuropathies of all kinds gabalin (Lyrica), Carney demonstrated One laboratory, Corinthian Research are represented here and a significantly that CET is “superior” to treating dia- Lab, has developed the Prevalence larger study is underway. betic nerve pain; CET “decreased the Registry in Small Fiber Treatment in average pain score 54% more than pre- Neuropathic Evaluations (PRISTINE). Safety of CET gabalin (P=0.00006), and was 62% Various clinics using the CET neurop- CET has a remarkable track record more effective than in athy protocol have registered their pre- of safety. Clinics that have used our reducing the average pain score by 50% and post-treatment biopsy results. Data protocol for patients with neuropathic (P=0.003)” without side effects.22 in this registry are helping to improve pain in the feet and legs have rarely, if our understanding of the relationship ever, observed side effects. In our expe- Summary between clinical profiles and reduced rience, there has been an occasional The time has come for a paradigm shift ENFD in patients with neuropathic allergy to bupivacaine, which is easily in the approach to chronic disease. pain (Table 3). In a preliminary analy- solved by switching to xylocaine with Although complex, the basic mech- sis, definitive epidermal nerve regrowth no loss of efficacy. Occasional mild, anisms of cell signaling could easily

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Table 3. Comparison of Epidural Nerve Fiber Biopsy in 8 patients (Preliminary) # NRS NRS NFI NFI #CET #EA ENFD Pre-Treatment ENFD Post-Treatment Results pre post max post foot calf thigh Time foot calf thigh # improved/ At least one from last total biopsied improved treatment AS 8 0 24% 2% 0 19 0 0.1 11 0 0 0 5.9 0/3 no EB 5 3 28% 10% 16 20 0 0 3.5 0 0 0 4.7 1/3 yes MB 10 3 62% 29% 16 15 0 0.5 3.4 5 mos 0.1 0.2 4.5 2/3 yes LC 10 5 49% 52% 20 15 0 0 2.9 3 mos 0 0 1.6 0/3 no JD 10 1 8% 4% 20 20 1.6 3 mos 0.5 3.2 6.1 1/1 yes EG 8 2 80% 44% 20 36a 0.7 2.3 0.3 6 mos 0.9 2.3 3.4 2/3 yes JS 9 2 48% 24% 16 11 0 1.7 4.8 3 mos 3.4 3.1 5.4 3/3 yes DY 5 3 54% 30% 20 10 5.5 8.3 11.8 6.5 mos 6.4 10.3 5.3 2/3 yes a over 15 month period Of the total number of nerves biopsied, 11 of 22 showed nerve growth. Six of the 8 patients (total # of patients) had at least 1 nerve growth. Ten of 16 nerves biopsied after 3 months showed nerve growth. CET, Combined Electrochemical Treatment; EA, electroanalgesia; ENFD, Epidermal Nerve Fiber Density; NFI, neuropathy function index; NRS, numerical pain/numbness (symptom score) be the normalization of cAMP, which promising when EST is used in con- are indicated, and correlation of out- leads to the opening of voltage-gated junction with spine blocks, including comes with length of time of known channels in pain and the sym- epidural, paravertebral, and medial neuropathic symptoms must be done. pathetic nervous system. Vessels then branch blocks using local anesthetics CET and EST are an important first vasodilate, increasing local circula- only. This approach has the potential to step in the overall treatment picture, tion, allowing incoming nutrients and be superior to current practice, because but they should not be expected to a “washing out” of waste products. This the combination of local anesthetics stand alone. Nutritional support, diet, cascade eliminates the primary chem- and EST does not require the injection exercise, and other lifestyle changes all ical causes of local pain. In addition, of particulate matter (from steroids) are necessary for successful long-term signaling cAMP also leads to decreased near the medullary arteries. Slowing, outcomes. firing of afferent C-fibers, which in stopping, and even reversing the pro- turn decreases ephatic cross firing of gression of the neuropathic process Author’s Info: Robert H. Odell, Jr., afferent A-delta fibers. has been observed clinically. Even in MD, PhD (biomedical engineering), We postulate that signaling the dis- patients whose symptoms do not seem practices interventional pain manage- tal nerve axons to normalize function to be reversed, we have seen evidence ment and anesthesiology in Las Vegas, and circulation may be precisely what of stabilization and/or slowing of the Nevada. Dr. Odell is a diplomat of is required to rebalance the system and progression of disease. As a result, the the American Board of Anesthesiology, break the pathogenic cycles of neurop- issue of early intervention is critically the American Board of Pain Medicine, athy. In the CET neuropathy protocol, important. and the American Academy of Pain electrodes are placed on the gastroc- One question that our experience Management. He is a fellow of nemius, which has the largest-diam- and observations have not been able to Interventional Pain Practice (FIPP) eter blood vessels, and on the feet. In answer is when neuropathy becomes from the World Institute of Pain. this way, circulatory and signaling phe- irreversible. Some patients with symp- Richard Sorgnard, PhD (molecu- nomena work synergistically to effect toms for greater than 10 years have lar biology), is Executive Director for tissue healing. experienced substantial improve- Morhea Technologies, LLC, a medical Preliminary results have been ment. Longitudinal studies certainly technology development and engineering

October 2015 | PracticalPainManagement.com 55 Combined Electrochemical Treatment for Peripheral Neuropathy

firm in Las Vegas, Nevada. nerves destroyed by PPN. his medical degree. He spent three years Peter Carney, MD, is a neurosurgeon As a pioneer in Integrative Medicine, of residency at the University of Texas- who now focuses his practice on the accu- Robert Milne, MD, recognized the poten- Southwestern, John Peter Smith Hospital, rate diagnosis and treatment of patients tial of using complementary methods. where he was chief resident and in addi- with chronic pain. For the last 5 years Dr. Milne’s interest in complementary tion was awarded Board Certification he has had a special interest in the use medicine began when his young daugh- in Family Practice. Dr. Milne has pub- of the principles of quantum mechanics ter became very ill and was unable to lished several books and has also traveled to treat patients with painful periph- be helped with prescription drug med- extensively to Europe in his continued eral neuropathy (PPN). His recent work icines. Dr. Milne received his under- search for methods to help his patients. documents that the principles of quan- graduate degree from the University of He holds 2 patents on medical devices, tum mechanics not only treats PPN more Southern California. After three years in the Elast Allergy Testing Device and effectively and more safely than pharma- the Peace Corps in Paraguay, he attended Micro-Vibration Therapy (MVT) for cological methods but also demonstrates the University of Missouri-Columbia the treatment of pain. He is also a fre- that these principles help to regenerate School of Medicine where he received quent lecturer on Integrative Medicine.

References

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