Combined Electrochemical Treatment for Peripheral Neuropathy
A neuropathy occurs as a result of basic pathologic processes gone awry—either from injury or disease. The incidence of neuropathy increases with age and its prevalence is growing. In fact, the prevalence of peripheral neuropathy may be as high as 2.4% in the United States.1
A study of people with diabetes estimated the prevalence of diabetic peripheral neuropathy (DPN) in patients with type 2 diabetes to be 26.4%.2 DPN is often the first indication to the patient that they have diabetes.3 Morbidity associated with diabetic and other neuropathies is a major reason patients seek medical care and represents a major cost to patients and society.4,5
It is compelling to note that the course of DPN, as well as other neuropathies, generally is progressive. To date, most treatments have focused on reduction of symptoms,6 and, in the case of diabetes, control or slowing of the progression of the underlying disease.
Combined electrochemical treatment (CET) represents a safe and effective therapy for all forms of neuropathy.7 We have now documented the reversal of the neuropathic process both from clinical observations and from objective functional (neurodiagnostic) testing and anatomic (epidural nerve fiber density [ENFD]) data.8
Although our clinics have not yet initialized formal double-blinded control studies, our clinical outcomes strongly suggest that the CET protocol is making a substantive difference in patients’ lives and certainly warrants more detailed consideration.
This paper will discuss neuropathic pathophysiology, with a focus on DPN. We will discuss how biochemistry and physics act in concert for healing.
Four primary nerve fibers are important in small fiber (sensory) neuropathy: A-delta, afferent C, efferent C, and A-beta. Neuropathic pain occurs when normal signaling between adjacent nerve cells attenuates as a result of insufficient oxygen transport. The hypo-oxidative state associated with neuropathic pain appears to be a primary factor, along with demineralization of the synaptic fluid, necessary for axon signal transport.9
Unlike muscles, which use either oxygen or glucose metabolic pathways, nerve cells are limited to the oxidative reductive metabolic system, or Krebs cycle.10,11 The Krebs cycle requires an immediate defense response to assure neural integrity and survival during a hypo-oxidative state. This defense mechanism also occurs upon exposure to environmental toxins, chemotherapeutic agents, military chemical weapons, insecticides, and other neurotoxic substances. Contraction, which is one such defense mechanism, causes a generalized shrinking of the nerve cells and a widening of the synaptic cleft between these cells.
As the synaptic junctions between the axons of one nerve cell and the dendrites of the next nerve widen, normal signal transmission can become compromised. Signals of normal intensity can no longer bridge this newly widened gap, resulting in a loss of bioelectric integrity. Widening of the synaptic gap makes it more difficult for normal sensations to propagate and causes a general loss of electrical conductivity in the synaptic fluid.12
Conductivity relies on minerals and specific neurotransmitters in the synaptic fluid to enable propagation of the nerve signal. These conductive minerals and neurotransmitters are delivered via the perfusion of adjacent tissues with fresh blood. They are kept in suspension by the periodic ionization of successfully transmitted nerve signals across the junction. When nerve signals attenuate because the synaptic cleft widens, necessary conductive minerals and neurotransmitters are no longer held in place by naturally-occurring electrical tension and are slowly leeched away.12,13
The initial sensory perception associated with atrophying nerves and enlarged synaptic clefts often is reported by the patient as tingling or electric sensation. This effect most likely is the result of ephatic firing, defined as some nerve signals being misdirected to nearby nerves.12-14 As the condition worsens, more signals are misdirected or suppressed, leading to increasingly unpleasant sensations such as stinging, burning, and pain. In time, affected nerve signals can become completely suppressed, resulting in numbness.
Ephatic cross firing co-existing with numbness may also explain why patients can have pain, dysesthesia, and numbness at the same locations at the same time. These conditions often result in poor tissue perfusion, insecure gait, balance problems, general muscle weakness, and other mobility issues. From a diagnostic standpoint, specific neurodiagnostic testing can directly measure this effect, as the increased voltage threshold necessary to fire enough nerve axons for the patient to “feel” sensation normally.
The sensory function of afferent A-delta and C fiber is best measured by the A-delta nerve conduction study (NCS), thermal evoked potentials, and functional magnetic resonance imaging (fMRI). Nerve conduction velocity (NCV) testing is less sensitive than A-delta NCS but can also measure all three fibers. A-delta function is effectively measured by A-delta NCS with 95% accuracy.15 Efferent C fiber function, which is a primary pathology, is best assayed by quantitative sensory testing (QST) such as sweat testing (Sudoscan), thermography, and possibly fMRI, and will be considered in future studies.
In physics, electron behavior is referred to as “organized chaos.” This idea unites activities of electrical and chemical medicine, and thus ties disease and curative medicine together conceptually.16 Although myotomes and dermatomes have been well documented in published biomedical literature, we are unable to find any data detailing existing “maps” for the distal sympathetic C fibers in the body. Still, C fibers are known to have a primary influence in the development of the pathophysiology of diabetes.
These efferent fibers control the tone of local arterioles, and, critically, contribute to the pathophysiology of small vascular structures and small nerve fibers (which are viable only as a function of these tiny arterioles). Pathology in the small arterioles and in the nerve fibers combines to adversely affect the distal tissues of the extremities.17
Tests of functional improvement are generally considered more robust than anatomic testing. However, ENFD testing is rapidly becoming an accepted standard to measure afferent C fibers and unmyelinated A-delta fibers.18 Thermal evoked potentials and fMRI also can measure the function of C and A-delta fibers, but ENFD currently is the most practical method. In our clinics, we have employed A-delta NCS and ENFD biopsies.
Despite the many described causes of peripheral neuropathy, the pathophysiology of simultaneous and synergistic decrease in vascular and neuronal function remains constant throughout the process and creates a pathological cascade.