A New & Effective Treatment for Peripheral Neuropathy
The Integrated Nerve Block (InB) incorporates two well established procedures that have been combined into a protocol that is showing great promise as an effective treatment solution for diabetic and idiopathic neuropathies.
The InB 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 sensory peripheral nerve block injections are performed with a lower volume and concentration of local anesthetic, and as such are not intended to produce the level of anesthesia required for performing surgery. No steroids are utilized.
Robert H. Odell, Jr., MD, PhD, a Board Certified interventional pain medicine specialist who has been using this block for several years, introduced the concept of the Integrated Block to the International Spine Injection Society at its annual convention last July in Las Vegas. The only chemical utilized is the local anesthetic. Sequential and random signal delivery eliminates neuron accommodation.
Dr. Cynthia Cernak, DPM
Dr. Alex Scholl, DPM
Dr. Desiree Scholl, DPM
Another primary mechanism of action (besides the anti-inflammatory effect) 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.
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. 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)1. The sustained depolarization of the cell increases intercellular levels and utilization of cAMP.
Stimulation also activates the release of pain-suppressing neuro-modulators found in the central nervous system, e.g. endorphin, encephalin and GABA.
Vasoconstriction and vasodilatation work hand in hand in a complex manner to achieve these effects. Vasoconstriction pushes intravascular fluid in a central direction to the heart, reduces the influx from arteries and reduces edema. Exogenous stimuli at specific pulse rates induce synchronous synaptic release of the neurotransmitter norepinephrine without depletion. Norepinephrine stimulates α-receptors to contract vessel smooth muscles. Vasoconstriction is necessary to treat the inflammation and edema normally present in any type of neuropathy.
Vasodilatation improves microcirculation, which has a salutary effect on the healing process in these oxygen deprived cells. The drainage function of the capillary system is improved as a result. Stirnulation 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 imitation.
COMPONENTS OF NEUROPATHY
Neuropathy involves both positive and negative symptoms. Numbness and pain can exist simultaneously, along with allodynia, dysesthesias and loss of proprioception. These symptoms are significant components of all neuropathies, and all can be improved with this treatment. Diabetic Neuropathy is known to develop well before the patient has any symptoms, and the literature states unequivocally that the sooner treatment can be initiated, the greater the chances of reversal of the symptoms. Microvascular circulatory deficiencies, caused by errors in glucose metabolism, for example, have direct effects on the circulation to the nerves, and there are direct effects on the nerves themselves. Pain signals, in turn, trigger secondary peripheral and central hyperalgesia which enhance the body's response to the microvascular insult. On a local level, microinflammation and edema around the nerves also contribute to the neuropathy.
THERAPEUTIC INJECTION SERIES
Case histories by a number of MDs and DPMs using the protocol have discovered that a concentrated number of treatments in the first three weeks are necessary to maintain a sustained suppression of the neuropathy and pain; these are critical in breaking the pain cycle. Specific electronic signal frequencies (EST), applied immediately post-injection, produce a number of effects, two of the most important of which are to reduce the inflammation and to enhance cellular repair mechanisms.
ELECTRONIC SIGNAL THERAPY
Immediately post injection (within 15 minutes), the Electronic Signal Treatment is applied exogenously through electrodes that are housed in vasopneumatic suction cups. The sucking action of the cups draws blood to the surface creating a blood pool beneath the cups and expanding the electrical field around the area being treated. This vasopulse effect also lowers skin resistance.
The electronic frequencies being applied are programmed into "Smart Card" computer chips, and sequence through a series of different complex waveforms. Each individual waveform represents a different mechanism of action. The electronic signals stimulate superior steroidogenic effects without the possible negative side effects of the injected steroid.1
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.
Another primary mechanism of action (besides the anti-inflammatory effect) 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.
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. 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)1. The sustained depolarization of the cell increases intercellular levels and utilization of cAMP.
Stimulation also activates the release of pain-suppressing neuro-modulators found in the central nervous system, e.g. endorphin, encephalin and GABA.
Vasoconstriction and vasodilatation work hand in hand in a complex manner to achieve these effects. Vasoconstriction pushes intravascular fluid in a central direction to the heart, reduces the influx from arteries and reduces edema. Exogenous stimuli at specific pulse rates induce synchronous synaptic release of the neurotransmitter norepinephrine without depletion. Norepinephrine stimulates α-receptors to contract vessel smooth muscles. Vasoconstriction is necessary to treat the inflammation and edema normally present in any type of neuropathy.
Vasodilatation improves microcirculation, which has a salutary effect on the healing process in these oxygen deprived cells. The drainage function of the capillary system is improved as a result. Stirnulation 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 imitation.
SUMMARY AND CONCLUSION:
Our clinical experience with MDs and DPMs has shown that the application of EST, when combined with the low dose local anesthetic in the integrated block, favorably influences the peripheral vasculature and promotes nerve and cell nutrition. Many of forms of neuropathy can be reversed.
Since the local anesthetic and EST have opposite effects on the nerve cell membrane, some of the beneficial physiologic changes are thought to be due to changing localized depolarization-repolarization cycles in the cell membranes; further studies regarding the exact mechanisms could yield even more effective protocols.
Patient case studies, the results of which are summarized below in the graph, were performed by Robert H. Odell Jr, MD, PhD, DABA, DABPM, FIPP in 2008
Six or less non steroid chemical nerve blocks with EST once every 3rd visit, on patients with diabetic & idiopathic neuropathy, LBP w & w/o radiculopathy
Odell RH, Sorgnard R. Anti-Inflammatory Effects of Electronic Signal Treatment; Pain Physician 2008; 11:891-907
